r/Steroids Wiki
Compiled by u/OsmiumOG
Vol. 1
1
Table of Contents
Overview .....................................................................................19
Helpful Links
Books and Publications
AAS Related Acronyms
Talking Points
19
19
20
23
What Are Steroids? ....................................................................30
Catabolic Steroids (Glucocorticoids)
Anabolic Steroids (AAS)
How Do Anabolic Steroids Work?
Are AAS Dangerous?
Are There Any Long-Term E ects?
Should I Begin Taking Anabolic Steroids?
Can I Do This Naturally?
Why Young Men Should Not Take AAS
Women & AAS
Tips For Interpreting Scienti c Studies
30
30
31
31
32
32
33
33
38
38
Original Stories ..........................................................................41
Hall of Fame
41
A Pin Story
The Rage Story
Massive Attack
Signal Story
The Loss Story
The Dirty Bulk Story
The Pituitary Story
You Wanna Be A Freak?
41
45
51
57
60
67
70
75
Hall of Shame
80
First Tren Cycle
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Abuse of DNP
Wasted First Cycle Cutting
84
92
Frequently Asked Questions (FAQ) ..........................................96
Compound Usage
96
How much weight can I expect to gain during my rst cycle?
96
Are the gains from steroid use temporary?
96
Can steroids make me look like a professional bodybuilder?
97
How dangerous is an isolated cycle of steroids?
97
How dangerous is long-term steroid use?
98
Can steroids be used to enhance an athletic career safely?
98
What are the safest steroids for men?
99
What steroids will not cause hair loss?
99
What are the safest steroids for women?
99
Do androgen receptors down-regulate?
100
Is there a limit to how muscular someone can get with unlimited gear?
100
What do the anabolic and androgenic reference numbers under the pro le for
each steroid mean?
101
Can I just do a oral only cycle?
101
What about just a Prohormone or Designer Steroid cycle?
101
Compound Handling and Mixing
102
How Do I Mix And Run My HCG?
My Gear Crashed…How Do I Fix It?
My Gear Has Particles Floating In It?
I need to travel during my cycle/blast/cruise. What do?
Cycle Complications
102
103
103
103
104
When I go to donate blood they ask about steroid use. Am I possibly harming
someone else?
104
I got sick while on cycle. What do?
104
I'm getting unbearable back / shin / calf / etc. pumps. What can I do?
104
Injecting
105
My Injection Spot Is Red, Itchy, Or Sore?
Is It Normal To Bleed After An Injection?”
Is Aspirating Required?
Does Injecting Build Up Scar Tissue?
105
105
105
106
How Do I Open Ampules?
106
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Can I Re-Use Syringes?
How Fast Should I Inject?
Is It Dangerous To Inject Small Air Bubbles?”
Ancillaries
107
107
108
108
Q: Can Nolvadex (Tamoxifene) and Arimidex (Anastrozole) be used together? 108
Q: Can Nolvadex (Tamoxifene) and Letrozole be used together?
109
Q: Does Aromasin need to be taken with fat?
109
HGH
110
Does using HGH shut down natural HGH production?
General
110
111
Does ejaculation reduce my testosterone levels?
Are American military personnel tested for steroids?
Can steroids increase the size of my penis?
Are fat cells ever lost?
Why do steroids make your traps and shoulders pop out that much?
111
111
112
114
114
Medicinal Use of AAS ..............................................................116
Anxiety
Cerebral Palsy
Collagen Synthesis
COPD
Cystic Fibrosis
Hepatitis C
Hypogonadism
Immune therapy
Multiple Sclerosis
Post Traumatic Stress Disorder (PTSD)
116
116
119
119
120
121
121
121
121
122
Safe Injections .........................................................................124
Injection Methods
The Injection
Types Of Syringes
The 3 Variables
Standard Syringe Speci cations
Gauge Numbers
124
124
125
125
126
126
Needle Lengths For Injection Sites
127
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CC & mL
Syringe Size
Syringe, Needles, etc. Suppliers
Rotating Injection Sites
Injection Frequency
Sterilization
WHO: Alcohol swab skin prep is unnecessary
Using A Draw Needle
Insulin Needles & BackLoading
Disposal Of Used Needles/Syringes.
Is Aspirating Required?
Safe Injecting Technique
Single Vial
Multiple Vials
Ampoules
Ampules To Sterile Vial
Ampules To Preloaded Insulin Syringes
Special Injection Techniques
Z-track Technique
Air Bubble Technique
PIP (Post Injection Pain)
128
128
128
129
129
130
131
131
132
133
134
135
135
136
137
139
140
141
142
142
143
What Causes (Non-Infectious) Injection Pain?
How do I prevent pain before I inject?
Where Do I Inject?
143
144
145
Glutes (Dorsogluteal)
Ventro Glutes
Quads (Vastus Lateralis)
Delts (Deltoid)
Chest (Pecs)
Lats (Latissimus)
Traps (Trapezius)
Triceps
Biceps
Calves
146
146
147
148
148
148
148
149
149
149
Subcutaneous (SubQ)
Volume Each Site Can Hold
149
149
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Frequently Asked Questions (FAQ)
My Injection Spot Is Red, Itchy, Or Sore?
Is It Normal To Bleed After An Injection?”
Is Aspirating Required?
Does Injecting Build Up Scar Tissue?
How Do I Open Ampules?
Can I Re-Use Syringes?
How Fast Should I Inject?
Is It Dangerous To Inject Small Air Bubbles?”
My Gear Crashed…How Do I Fix It?
My Gear Has Particles Floating In It?
150
150
150
151
151
152
152
152
153
153
153
Testosterone Replacement Therapy (TRT) ............................157
Categorization of Low Testosterone (T)
Primary Hypogonadism
Secondary Hypogonadism
157
157
157
Symptoms of Low Testosterone
What is TRT?
Getting On TRT
158
159
159
Finding a Doctor; Getting Blood Work
Understanding your Blood Work Results
160
161
Common TRT Prescriptions
163
Testosterone
Gels/Creams
Injections
Pellets
Nasal Gel
Lozenges
HCG/HMG
Testosterone vs. HCG
Clomid
Aromatase Inhibitors (AIs)
Medication Dosages-General
163
164
165
166
167
167
168
168
169
169
169
HCG and TRT
What to Expect While On TRT
170
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The First 1-3 Months
3-Months and On
General Tips While on TRT
Injection Tips
Coming O TRT
171
172
172
173
174
Bene ts of TRT
Side E ects of TRT
Related Posts
Studies
174
175
176
177
Anabolic Steroids and the Law ..............................................179
United States
179
State vs. Federal
179
Austria
Australia
Belgium
Canada
Czech Republic
Denmark
France
Greece
Israel
New Zealand
Norway
Sweden
United Kingdom
References
180
180
180
180
181
181
181
181
181
182
182
182
182
183
Cycle Information ....................................................................185
Things to Know
The Cycle
Pre-cycle Check list
Planning the Cycle
185
185
186
Calculating Total Amount Needed
Example
186
187
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Calculating Dosage
Finding A Source
Blast and Cruise
Additional Topics
187
187
188
188
Your First Cycle
190
BEGINNER FAQ
190
Can I Just Do An Oral Only Cycle?
190
What About A Prohormone Or Designer Steroid Cycle?
191
Is my gear bunk?
191
Is (random UGL that has existed for one week) Pharma legit?
193
I don’t feel anything, I have zero side e ects, my training and nutrition is perfect
and I’ve still not gained a single pound
195
The Basic Bulk
196
What You Will Need
Essentials
Optional Items
Why 4 Vials of Testosterone?
Testosterone Enanthate Or Testosterone Cypionate?
WhEn DoEs tHe TeSt KiCk In?
Testosterone Peaks
Arimidex or Aromasin?
How Much AI Do I Need?
When Should You Start Your AI?
Estradiol Rise
Study Disclaimer
Putting It All Together.
References
SERM On Cycle?
Injecting Your Gear
Post Injection Pain
Frontloading Test?
OPTIONAL: What Oral Steroid Should I Use?
Suggested Orals
When Should I Take It?
196
196
197
197
197
198
198
198
199
199
200
201
201
202
203
203
204
204
204
205
206
Half-Life Method
Pre-Workout Method
206
207
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Hybrid Method
How Often Should I Pin (Inject)?
Post Cycle Therapy (PCT)
Human Chorionic Gonadotrophin (HCG)
Why Should I Use HCG?
How Do I Mix And Run My HCG?
Blood Work
Nutrition
Dosing
The Basic Cut
207
207
207
208
208
208
209
209
210
212
SUPPLEMENTAL COMPOUNDS
Salbutamol
Clenbuterol (Clen)
ECA Stack
213
213
214
215
Intermediate Bulk Cycle
Cut/Recomp Cycles
216
216
Silver Standard
Gold Standard
216
218
Equipoise (Boldenone) Cycles
219
Beginner EQ Bulk
Intermediate EQ Bulk
Advanced EQ Bulk
Beginner EQ Cut
Intermediate EQ Cut
Advanced EQ Cut
220
221
221
222
223
223
Power Lifting Cycle
Estrogen Suppression Cycle
Very Advanced Insulin Cycle
224
224
225
WOMEN & PEDs ......................................................................229
DISCLAIMER
229
OTC Fat Burners
230
Ephedrine
230
Non-OTC Fat Burners
230
Clenbuterol (Clen)
230
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Thyroid Medication: T3 and T4
Anti-Estrogens
Human Growth Hormone (HGH)
231
233
236
Anabolic Androgenic Steroids (AAS)
Virilization
Anavar (Oxandrolone)
Winstrol (Stanozolol)
Turinabol (Tbol)
Primobolan (Methenolone)
Proviron (Mesterolone)
Masteron (Drostanolone Propionate)
Boldenone (EQ, Bold A, Bold C, etc.)
Nandrolone Phenylpropionate (NPP)
Testosterone Propionate
Trenbolone Acetate
Post Cycle Notes
237
237
239
241
243
245
247
248
249
250
251
253
253
Things to Remember
254
AAS and Birth Control
256
Androgen De ciency In Women
258
FAQ
258
Related Studies
259
The Estrogen Handbook .........................................................261
Gyno Mechanics
Estrogen (E2)
261
261
Low Estrogen Sides
High Estrogen Sides
262
263
Aromatase
264
Aromatase Inhibitors (AIs)
Suicidal AI vs. Non-Suicidal/Binding AI
Arimidex (Anastrozole)
Aromasin (Exemestane)
Letrozole
Selective Estrogen Receptor Modulators (SERMs)
Nolvadex (Tamoxifen)
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265
266
266
268
268
269
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Raloxifene (Evista)
Nolvadex vs. Raloxifene for HGH/IGF-1
Nolvadex vs. Raloxifene for Gyno
Clomid
Prolactin Support
269
269
270
271
272
What Is Prolactin?
Cabergoline (Dostinex)
Pramipexole (Mirapex)
272
276
276
Post Cycle Therapy (PCT) .......................................................279
The Purpose of PCT
The HPTA: How It Works
Determining Factors In Di culty Recovering the HPTA
Individual Response
Type of Anabolic Steroid(s) Used
Length of Cycle
PCT Medications
SERMs
286
Dosing
288
Nolvadex:
Clomid
Torem
SERM Dosing Note
288
289
290
290
hCG
Dosing
291
292
Mixing hCG
Running hCG
1. Over The Entire Cycle
2. Weeks Leading Up To PCT
3. 1-2 Weeks Before PCT
4. First 1-2 Weeks Of PCT
292
293
293
294
294
295
Aromatase Inhibitors: Aromasin (Exemestane) Above All Else
Dosing
295
297
Drug Interactions
Side E ects
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280
283
283
283
284
284
297
297
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What to Expect from PCT
When NOT to Run PCT
When to Start PCT
Very Long Ester AAS & PCT Transition
Very Long Ester Testosterone & PCT Transition
When to Start Your Next Cycle
Blood Work
The Danger
302
302
PCT for Women
303
Michael Scally (former) M.D.'s Thoughts:
O cial /r/steroids PCT Protocols
SERM Dosing Note
Optimal/Primary PCT Options
Nolvadex
Clomid
Torem
303
304
304
306
Nolvadex
Clomid
Torem
306
307
307
Minimalist PCT Options
308
Nolvadex
Clomid
Torem
308
308
308
Post Blast & Cruise Recovery Not Endorsed By /r/steroids
ASRM Guidlines For Physicians To Prescribe
Original Power PCT
New Power PCT
Controversy
308
308
309
310
310
Jcaesar369 Recommended PCT Protocol
TL;DR:
Controversy
Triptorelin PCT
313
313
313
314
A Doctor's Recommended PCT (TRT Clinic)
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303
304
305
305
Secondary PCT Options
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298
299
299
300
301
302
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12
Miscellaneous Findings
315
Triptorelin/GnRH
Misc.
315
315
References
316
Nutrition ....................................................................................320
Macronutrients
321
Protein
Carbohydrates
Fats
321
323
326
Eating "Healthy"
329
Videos
Web Resources
References
329
329
329
Steroids Pro les, Androgenic and Anabolic Rating .............332
Compound Short-cuts
332
Quick List
Extended List
FAQ
What is the di erence between Testosterone Enanthate and Testosterone
Cypionate?
Hepatotoxicity
Drug Induced Hepatotoxicity
341
342
342
343
344
Cholestasis
345
Liver Function Tests
Liver Protection
347
348
TUDCA / UDCA
NAC (N-acetylcysteine)
Choline & Inositol
Milk Thistle
348
351
353
354
Liv.52 (LiverCare)
354
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341
Drug Metabolism
Anabolic Androgenic Steroids
C17-Alpha Alkylation & What It Does
Trenbolone
ff
333
335
339
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A Final Word
References
355
355
Ancillaries / Related
359
FAQ
362
Q: Can Nolvadex (Tamoxifene) and Arimidex (Anastrozole) be used together? 362
Q: Does Aromasin need to be taken with fat?
363
Esters
366
A Primer On Esters And How They Work
Actions Of Di erent Esters
Esters Active Half-Life Table
Esters And The Active Dose
Sustanon: The "King" Of Testosterone Blends
Ester Pro les
373
Acetate ( C2 H4 O2 )
Propionate ( C3 H6 O2 )
Phenylpropionate ( C9 H10 O2 )
Isocarpoate ( C6 H12 O2 )
Caproate ( C6 H12 O2 )
Enanthate ( C7 H14 O2 )
Cypionate ( C8 H14 O2 )
Decanoate ( C10 H20 O2 )
Undecylenate ( C11 H20 O2 )
Undecanoate ( C11 H22 O2 )
Laurate ( C12 H24 O2 )
Conclusion
373
373
374
374
374
374
375
375
375
376
376
376
Human Growth Hormone (Somatotropin)
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Use/Dosing
Dosing Schedule
Dosages
Ramping
Duration
Administration
Post Cycle Therapy
Side E ects and Risks
380
380
382
382
383
383
383
383
Does using HGH shut down natural HGH production?
385
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367
368
369
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HGH Brands List
References
385
386
Peptides ....................................................................................388
BPC 157
CJC-1295 with DAC
CJC-1295 w/o DAC
DSIP
Epitalon
Follistatin
GHRP-2
GHRP-6
Hexarelin
HGH Fragment 176-191
IGF1-DES
IGF1-LR3
Insulin
Ipamorelin
MGF (Mechano Growth Factor)
PEG-MGF
PT-141 Bremelanotide
Selank
Sermorelin (GRF 1-29)
Thymosin Beta 4 (TB-500)
388
388
389
389
390
390
391
391
392
392
393
393
393
394
394
395
395
396
396
397
The Body's Growth Hormone System & Peptides
Growth Hormone Releasing Hormones (GHRH):
Which GHRH?
Growth Hormone Releasing Peptides, Ghrelin-mimetics (GHRP):
Which GHRP?
Dosing Schedules
Administration
398
399
399
400
400
401
402
BPC 157 & Healing Your Body
402
What is BPC 157?
What Does BPC 157 Do?
How Much BPC 157 To Take
402
402
404
How To Inject BPC 157 Or Take BPC 157 Orally
404
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How Long To Take BPC 157
Use In The Medical Field
Studies and Other Links
405
405
405
Side E ects ..............................................................................408
General
408
Trenbolone
408
Solutions
409
Acne
Blood Pressure
Gynecomastia
Lactation (Galactorrhea)
Liver Stress
Painful Pumps
"Test Flu"
409
416
419
419
420
421
421
Bloodwork ................................................................................424
How Do I Get Bloodwork?
What Bloodwork do you need before Your First Cycle?
Where To Get Private bloodwork
In the USA
Australia, New Zealand
United Kingdom (UK)
Canada
426
429
429
429
Additional Notes
Related Posts
Health Markers
432
434
437
Alanine amino-transferase (ALT)
Albumin
Alkaline Phosphatase (ALP)
Apolipoprotein A-I (apoA-I)
Apolipoprotein B (apoB)
Aspartate amino-transferase (AST)
Basophils
437
437
437
437
437
438
438
Bicarbonate
Bilirubin
438
438
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425
426
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Blood Urea Nitrogen (BUN)
BUN/Creatinine Ratio
C-reactive Protein (CRP)
Carbon Dioxide (CO2)
Calcium
Chloride
Cholesterol, Total
Cholesterol, HDL
Cholesterol, LDL
Cholesterol, VLDL
Cholesterol, LDL/HDL Ratio
Creatine Kinase
Creatinine
Eosinophils
Estradiol
Follicle Stimulating Hormone (FSH)
Gamma-Glutamyl Transpeptidase (GGT)
Globulin
Glucose (fasting)
Hematocrit
Hemoglobin
Homocysteine
Iron
Lactic Acid Dehydrogenase (LDH)
Luteinizing Hormone (LH)
Lymphocytes
Mean Corpuscular Volume (MCV)
Mean Corpuscular Hemoglobin (MCH)
Mean Corpuscular Hemoglobin Concentration (MCHC)
Monocytes
Neutrophils
Phosphorous
Platelet Count
Potassium
438
438
439
439
439
439
439
439
440
440
440
440
440
441
441
441
441
441
442
442
442
442
442
443
443
443
443
443
444
444
444
444
444
445
Prolactin
Prostate-speci c antigen (PSA)
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Red Blood Cell Count
Red Cell Distribution Width (RDW)
Sodium
T3 Uptake
Testosterone, Total
Testosterone, Free
Thyroid-Stimulating Hormone (TSH)
Thyroxine (T4)
Thyroxine, Free Index
Total Protein
Triglycerides
Urea
Uric Acid
White Blood Cell Count
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445
446
446
446
446
446
446
447
447
447
447
447
448
18
Overview
The r/steroids Wiki provides a unique and comprehensive compendium of
knowledge on anabolic steroids, as well as speci cs about our community,
r/steroids, which is the largest steroid community in the English-speaking
world.
Helpful Links
•
•
•
•
•
•
•
SteroidPlanner - Plot and Graph your cycles
SteroidPlotter - Another option for graphing cycles
HRT Calculator - Peptide and HRT/TRT/Cycle Calculator
Steroid Powder Calculator - Help calculating homebrew recipes
Fitness Calculators - Basic tness calculators (BMI, Calorie, etc.)
TDEE Caldulator - Basic TDEE calculator
Lift Vault - Free workout programs and spreadsheets
Books and Publications
ANABOLICS, 10th edition, William Llewellyn
A Compilation of Anabolic and Nutritional Supplements Steroids
Underground Steroids Handbook II, Daniel Duchaine
The Endocrine Society's Clinical Guide: Testosterone Therapy in Adult
Men with Androgen De ciency Syndrome. ( Scribd )
• Why are Steroids Illegal in the USA? ( Scribd )
• Testosterone: Action, De ciency, Substitution, 3rd Edition (pp. 405-444).
Cambridge University Press, New York.Behre H.M., Nieschlag E.,
(2004).
•
•
•
•
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AAS Related Acronyms
Acron
ym
X/X/
Y/Y
AAS
Meaning
Week 1
daily dose/
Week 2
daily dose/
Week 3
AnabolicAndrogenic
Steroids
Notes
Example: 40/40/20/20 = 40mg per day for week
1, 40mg per day for week 2, 20mg per day for
week 3, 20mg per day for week 4. Used in
reference to Nolva, Clomid, or Torem PCT.
Adrol
Anadrol
AI
Aromatase
Inhibitor
compounds that stop Gyno
ALT
Alanine
transaminas
e
Aspartate
Aminotransf
erase
An enzyme found in the highest amounts in the
liver. Injury to the liver results in release of the
substance into the blood.
Low levels of AST are normally found in the
blood. When body tissue or an organ such as
the heart or liver is diseased or damaged,
additional AST is released into the bloodstream.
The amount of AST in the blood is directly
Alternating between a bulk cycle with high AAS
use and a TRT cruise.
AST
B&C
Blast and
Cruise
BMR
Base
Metabolic
Rate
Dianabol
Dbol
Deca
DMZ
DOM
S
ED
Deca
Durabolin
(Nandrolone
Decanoate)
Dymethazin
e
Delayed
Onset
Muscle
Every Day
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When your muscles get sore 2-3 days after
exercising
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EOD
E#D
Epi
EQ
FSH
Gear
GH
Gyno
Every Other
Day
Every "#"
Days.
Epistane
Equipoise
(Boldenone
Undecylenat
e)
Folliclestimulating
hormone
Anabolic
steroids or
other things
that are
used during
Growth
Hormone
Gynecomast
ia
E3D = Every 3 Days: Take, skip two days, take.
Side effect resulting from increased prolactin
and/or estrogen production
Halo
Halotestin
HCG
Human
Chorionic
Gonadotropi
Human
Growth
Hormone
Human
Menopausal
Gonadotropi
n
Hormone
Replacemen
t Therapy
Luteinizing Hormone provided to facilitate
production of testosterone by gonads. Standard
Dose: 250 IU EOD
Intramuscular
injection
Luteinizing
hormone
An injection that goes into the muscle tissue
HGH
hMG
HRT
IM
LH
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Luteinizing hormone and Follicle-stimulating
hormone to facilitate the production of
testosterone and spermatozoa by the gonads
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Mast
Masteron
PCT
Post Cycle
Therapy
Pins
Syringes /
Needles
Post
Injection
Research
Chemical
PIP
RC
Subq
Subcutaneo
us Injection
Sust
Sustanon
Sdrol
Superdrol
Tbol
Oral
Turinabol
Total Daily
Energy
Expenditure
Testosteron
e
Trenbolone
TDEE
Test
Tren
TRT
The method to recover from an AAS cycle.
Pain felt in the area of an injection
Drugs made for "research" purposes, very often
highly underdosed
An injection that goes into the fatty tissue
The average amount of energy you need to do
your daily activities
Using exogenous Test to mimic natural
production levels
Var
Testosteron
e
Replacemen
t Therapy
Anavar
VG
Ventro Glute
A very common muscle in which to inject
Winn
y
Winstrol
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Talking Points
/u/MittRomneysCampaign wrote (original):
So far, I have had two discussions that went very well that involved
layperson subreddits.
I like the way these discussions went because few of the responses were
outright dismissive (something like "lol ok juicehead" without even listening
to you would be dismissive), and to the extent they were opposing steroids,
they were based on misinformation -- not outright contempt for the idea.
But once this misinformation was corrected, the commenters/voters seem
largely receptive.
I am linking these with "np" because the last thing we need is a "roid rage
brigade."
• Futurology: https://np.reddit.com/r/Futurology/comments/3afjpa/
the_male_pill_is_coming_and_its_going_to_change/csccdrq
• SubredditDrama: https://np.reddit.com/r/SubredditDrama/comments/
3btepe/i_simply_say_name_one_single_initiative_feminism/
csprvow
You and I both know that most of these drugs are ne. So we're on the
same page. I don't need to convince you because I'd be preaching to the
choir.
Any time you are talking with a layperson about steroids, you need to try to
avoid saying anything that paints you as a Roid User Stereotype.
If you are too angry, you can be accused of "roid rage" and instantly
dismissed, because they will think "if I take it I will act like this guy." We all
know roid rage isn't a thing, but they don't. So your job is to convince them
rational people exist who use these things.
If you come off as too enthusiastic, you run the risk of looking like a junkie.
People think steroids = needles = heroin = steroids are as harmful as
heroin. It doesn't matter if they're wrong. They think it and they vote.
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But how you frame anabolics matters a lot too, so here's an unassorted list
of points to remember and/or emphasize:
• Don't say "steroids." Say "male hormones."
Yes, I realize that steroids are male hormones, and YOU realize that
steroids are hormones, but the average person barely knows anything
about this, and hasn't bothered to make the connection that testosterone =
male hormone = steroid. You have a limited amount of time to convince
people, usually, so make sure you don't lose their attention.
• Mention that estrogen is a steroid also, and in the birth
control pill
Many women take the pill and advocate for its availability. The reasoning I
use is something like "estrogen is a steroid, it's just not an anabolic steroid,
because it's not a male hormone, and male hormones tend to help build
muscle."
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So, rules of conversation that are important in everyday civilized discussion
become even more important when trying to make the case that a
hormone attributed to anger and destruction should be legal.
• Try your best not to swear or seem angry. If you do swear, make sure it's
very strategic swearing. If you do seem angry, make sure it comes off as
a professional kind of outrage, like a doctor who is outraged that a
bene cial treatment is not allowed -- because that's what doctors would
do if TRT were outright illegal.
• Make sure to NEVER insult your opponent. Only respond to their
reasons, and respond to their reasons with evidence. Don't say "you
have no idea what you're talking about" or "you're an idiot" or anything
like this. If avoiding these things makes you seem like a robot, that's
ne. It's preferable to seeming angry. If you are so angry you can't have
the discussion any more, POLITELY leave.
• At the same time, don't be condescending. Normal people already feel
threatened by you because you lift. And I'm pretty sure this applies to
99% of this board because for however much you don't think you lift,
normal people really really don't lift. Regardless of how silly it is, "bigger
than me" means "person who could maybe beat me up" in caveman
logic. The last a regular person needs is a lecture from a person who is
both stronger AND smarter than them.
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The average person does not realize that estrogen = steroid, and that
testosterone = steroid, just that testosterone happens to be a steroid that
builds muscle.
You will get a lot of support from women who nd this hypocritical. Many
women I've talked to don't realize that estrogen is in the birth control pill, so
they don't bother to think "hey, my sex hormones help me not get pregnant,
so why wouldn't giving men their sex hormones help them not impregnate
me?" I've been able to convince a lot of the women I know this way. (The
women I associate with are pretty open-minded, but still. They'd be against
it if I hadn't said anything.)
• Frame testosterone in terms of birth control.
I realize that testosterone is not primarily used as birth control, but it has
been used as such before. Trestolone is also useful to mention, because
of how it's been used for birth control purposes and can also be used for
muscle-building.
• Avoid the "cheating" debate by mentioning that athletics
would be unfair even if they were drug free.
I'm just going to copy-paste this: "the anti-cheating stance is a losing battle
since (a) it's been a losing battle for decades, tests are extremely
beatable and (b) athletes are already at some kind of genetic advantage
anyway if they're winning. They'd have to be -- the number of things you
can do to make yourself better at a sport is nite, while genetic variation will
continue all the way along the top level. (Examples of this variation include
factors like your predisposition to building muscle, your natural testosterone
levels, your maximum vo2max, and so on.) ... The idea that drugs give an
unfair advantage and genetics don't would be true assuming equal genetic
advantage, but when you're looking at the highest levels of the sport you're
looking at the athletic height of 7 billion people, which is a ton of genetic
variation to pool from. Reducing all advantages period would be a really
losing battle, so it's more consistent to just say "athletes will take these
anyway, so let's see what they can do when they don't have to hide it."
• Mention that steroids already were legal for a long time
without many consequences, and that criminalizing them
produces consequences of its own.
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This is what I said: "Arnold did steroids more safely because the drugs
were legal and he knew what he was getting. When you don't know the
product you're getting, there is a much greater risk of dilution,
contaminants, etc. Also, this isn't like, say, LSD, which was a craze then
was illegal pretty much everywhere before we could even study it. We have
a pretty good idea of what it'd look like if these drugs were legal again
because they were before, and they still are legal in something like a dozen
countries and decriminalized in others."
• Mention that the AMA, FDA, NIDA, NIH, and DEA actually
testi ed in opposition to the inclusion of male sex
hormones under the Controlled Substances Act.
Most people are under the impression that steroids are illegal for health
reasons, and not for sporting reasons.
When I say things like this, most people give me weird looks, because they
are still under the impression that drug laws are scaled to drug harm: "The
primary roadblock to male birth control is that they all involve male sex
hormones like testosterone. Ergo, you can take these to be better at sports.
If you can take them to be better at sports, this is a fast-track to their
criminalization. So the issue isn't really developing male birth control, it's
developing male birth control that doesn't help you be better at sports."
• Mention the inconsistencies in scheduling as support for
this being about sports.
Metenolone is grouped with testosterone and trenbolone, despite
metenolone being extremely unharmful and trenbolone being harmful in at
least some respects. The only commonality they have is that they bene t
an athlete. If these drugs were illegal for purely health reasons, they'd be in
different schedules.
• Mention that testosterone is produced by your body, so it
must be safe at some doses.
Most women I've talked to don't know that they have testosterone. When I
say "your testosterone levels", they look at me with this blank expression
on their face like they didn't know that was possible.
• Attack the category "anabolic steroid" for being misleading
in this kind of discussion.
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The category "anabolic steroid" is as useful to assess safety/unsafety as
"pain-killer" is, because "pain-killer" includes both ibuprofen and heroin.
Saying "anabolic steroids are harmful" is like saying "painkillers are
harmful." Well, yes, some are, in certain dosages, but as a category? No.
• Mention that drug laws do not have to correspond to drug
harm.
Here is a comparative drug harm chart by David Nutt. Steroids rank
toward the bottom.
Virtually everyone is aware that cannabis is mostly harmless. They think
steroids are toward the top of harm, so this is a clear discrepancy in
perception. If you stress that they're less harmful than cannabis, this will
change perceptions.
• Try to use chemical names instead of steroid slang.
Saying "tamoxifen" or "clomifene" might be annoying, but you sound more
credible to regular people when you do this. If you say "you can treat sideeffects with tamoxifen, HCG, and an aromatase inhibitor" you sound
immensely more believable than a person who says "you won't get sides if
you PCT with HCG and pop some nolva or clomid." If this sounds
pretentious to you or you never talk this way, just roll with it.
• You will need to prioritize some steroids and throw others
under the bus.
Think about the most harmless hormones we can take. Those are the
steroids you should be advocating for.
So: testosterone, nandrolone, methenolone (primo), oxandrolone (anavar),
and maybe MAYBE methandrostenolone (dbol).
But testosterone comes rst, then nandrolone/methenolone/anavar, then
everything else.
DO NOT try advocating for making tren or halo legal. This is suicide.
People will google trenbolone and say "wtf, they give this to cattle? and
you're putting that in your body?" OR someone will mention that tren killed
Zyzz which will lead to a discussion about what really killed him, and so on.
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I'm in favor of making all of this shit legal or at least decriminalized, but you
will not win this battle by having an all-or-nothing approach. You need to
take the most defensible stance you can take and "legalize cattle hormones
that killed some 22 year old" is not that.
Even if you run tren, I'm not judging you. Just don't mention tren or act like
tren is great. Focus on the basics and the stuff with the least side effects.
• Stress that since you already have estrogen and
testosterone in your body, there are "roids" in your body.
This is why testosterone is the hormone you need to focus on the most.
When people think of steroids, they think of that shit they give Bane to
make him instantly monstrous.
It's very dif cult to, with a straight face, oppose a hormone that's in your
body as we speak.
Other useful links
• Why roid rage is a myth: http://examine.com/faq/what-is-roidrage.html
• About the SAC: http://www.steroid.com/The-Steroid-Control-Act.php
Anyway, it's possible to convince laypeople that these hormones are ne. In
a perfect world, we could just give everyone a textbook and have them
learn how these drugs work, so then they'd say "what's the big deal?" -but, no one is going to read that textbook, so you need to do the
convincing.
It's very possible. You just need to avoid certain pitfalls when making your
arguments and make sure to stress certain points over others.
I hope this helps, because all of us bene t.
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What Are Steroids?
The term “steroids” refers to a class of hormones with a classic polyphenol
ring structure that are derived from the cholesterol molecul. There are two
types of steroids. They are often confused: *Anabolic** and Catabolic.
These two steroids serve different medical purposes.
Catabolic Steroids (Glucocorticoids)
A group of steroid hormones produced in the adrenal cortex or made
synthetically. They have various metabolic functions and are used to treat
in ammation.
Glucocorticoids are utilized to treat:
• Arthritis
• Asthma
• Autoimmune diseases such as lupus and multiple sclerosis
• Skin conditions such as eczema and rashes
• Some kinds of cancer
Side effects of glucocorticoids can include fat gain (particularly trunk),
muscle atrophy, weakened bones, and cataracts.
Anabolic Steroids (AAS)
A synthetic steroid hormone that resembles Testosterone in promoting the
growth of muscle. Such hormones are used medicinally to treat some forms
of weight loss and by some athletes and others to enhance physical
performance. The proper term for these compounds is Anabolic-Androgenic
Steroids (AAS).
Use of anabolic steroids can have side effects including: * Acne and
cysts * Breast growth and shrinking of testicles in men * Voice deepening
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and growth of body hair * Heart problems, including heart attack * Liver
disease, including cancer * Aggressive behavior
See Additional Sides
How Do Anabolic Steroids Work?
There are generally considered to be three mechanisms of action of AAS.
1. By binding to the androgen receptor located in the cytoplasm, AAS
stimulate protein synthesis in the muscle.
2. AAS bind to the glucocorticoid receptor, blocking the catabolic actions
of cortisol on muscle (protein breakdown).
3. Psychological effects include increased motivation and aggression,
leading to increased training intensity.
See Pharmacology of AAS.
Are AAS Dangerous?
The general consensus is that if used properly, in conjunction with blood
tests, AAS can be used safely. However, the potential side effects can be
extreme if they are used incorrectly. Most commonly, a lipid pro le
imbalance which favors plaque deposition in the arteries occurs. The strict
diet of most bodybuilders means this is minimized by a low fat intake.
Liver problems can occur with the use of 17α-alkylated oral anabolic
steroids. Rare cases of hepatic peliosis (blood lled cysts in the liver), more
commonly known as a liver cancer, have been associated with the use of
oral AAS. While these cases have been rare, they emphasize the need for
blood testing during a cycle.
Gynecomastia can occur as a result of high levels of Testosterone being
partially converted to estrogen, the primary metabolite being estradiol (E2).
The enzyme responsible for this conversion is called aromatase. It can be
inhibited by a class of drugs called Aromatase Inhibitors (AI). Another class
of drugs called a Selective Estrogen Receptor Modulator (SERM), such as
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Raloxi ne or Nolvadex, can also be used because it blocks estrogen from
binding with the estrogen receptor, rather than the binding with the enzyme
that metabolizes from Testosterone to Estrogen.
Are There Any Long-Term E ects?
AAS have been used in humans to improve performance since the 1930s.
This was a crude extract from male dog urine. Nazi paratroopers were
thought to be the rst to take Testosterone for performance. In the fties,
drug development company Ciba developed Dianabol—and the race was
then on to nd the best steroid in terms of anabolic-androgenic
dissociation.
The long history of use by many thousands of people has shown that if
used reasonably, most people do not experience any long-term adverse
effects. However, there is a distinct lack of research in this area, with the
occasional case study in the medical literature. The mass media likes to
sensationalize the death of any past steroid user.
The fact is, the most likely problem would be an increase in arterial plaque
deposition as a result of an unfavorable blood lipid levels. This does not
affect all users, hence another reason for blood testing.
There is strong evidence to suggest that brief exposure to anabolic
steroids might have long lasting performance-enhancing effects:
A cellular memory mechanism aids overload hypertrophy in muscle
long after an episodic exposure to anabolic steroids
Should I Begin Taking Anabolic Steroids?
The generally accepted criteria for starting AAS is as follows:
• Research until you have a very good understanding of what you are
considering putting into your body. Do this PRIOR to your cycle.
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• Do not run a cycle without having a PCT and an AI on hand. If you can't
afford either, you can't afford to cycle.
• The best rst cycle is a simple rst cycle. KISS (Keep It Simple Stupid!).
As more experience is gained and you learn how your body reacts to
gear, cycles can become more complex. Adding two previously unused
elements to a cycle makes it impossible to know which thing may be
causing issues. One new compound at a time, and grow into your dose.
You don't need grams and grams of gear.
• Steroids are not magic. The key is a very good caloric surplus, healthy
diet and progressive overload exercise regime. With these factors in
place, keep your expectations reasonable and you'll be happy.
• For your cycle duration, remain aware of how your body is reacting both
physically and emotionally. If something feels "off" or "not right", and it's
not a known side, it probably isn't right. Typical beginner cycles make
people feel very good overall.
Can I Do This Naturally?
You will eventually reach a genetic potential maximum (calculate yours
here) with regards to strength and size. There are often people giving
advice to "reach your genetic maximum potential rst" before using gear.
Some at /r/steroids give and promote this advice, some do not. This
advice is preference.
Information about how steroids help vs natural
• Steroids vs Natural
• Natural Bodybuilder Cut Study
• Natural Muscle Building: A Look At Potential, Genetics & Arm Size
Why Young Men Should Not Take AAS
Introduction
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Until then it is advised that individuals train naturally. Those suffering from
low testosterone symptoms should rst address lifestyle practices and
environmental factors that may be causing issues. After underlying issues
have been addressed with no results; Clomid monotherapy or hCG-only
cycles function as far safer alternatives to taking steroids. Read the Wiki
section on hypogonadotropic hypogonadism (HH). Consult with a family
physician for a referral to an endocrinologist.
Young adults up into their early twenties are at peak Testosterone output,
peak natty growth potential, and the perfect time to bulk naturally.
MRI scans show that the adolescent brain and neuroendocrine system
growth and development continues until the age of 25. The last regions to
nish growing are the absolute most important—those associated with
consciousness, sense of self, abstract reasoning, conscientiousness, highbandwidth emotional processing, higher cognition and impulse control.
While still under the age of 25, the fragile connections that make up your
newly-forged neural pathways are far more exposed and vulnerable to the
potential for permanent damage than previously set, well-worn and
established pathways.
What's safe?
For hypogonadal patients under the age of 25 the standard of care medical
professionals advise for the treatment of low Testosterone levels is either
(a) hCG or (b) Clomid monotherapy. Each option has its own unique side
effects, relative merits and disadvantages—but either one of these two
options are far safer, and nowhere near risking the debilitating negative
side effects that can come as a consequence of AAS mismanagement or
abuse.
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Exogenous androgens act as epigenetic growth signaling termination
factors. What this translates to is that it isn't just your height that's stunted.
It's your IQ. AAS can atrophy brain development and higher cognitive
functions. Clinical studies showed this can lead to long-term aggression,
anxiety, depression, cognitive de cits and memory problems—among
others.
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What are the different risks?
“Anabolic steroids have been reported to induce psychiatric side effects
such as aggression and depression. Adolescence represents an
extremely sensitive neurodevelopmental period to in uence by
detrimental effects.”
– Side Effects of Drugs Annual
“AAS use by teenagers is a primary concern because of the potential
side effects where remodeling of the brain and behavioral maturation
occurs.”
– Journal of Behavioral Processes
“AAS use impaired spatial learning and memory, and this effect was not
rescued by exercise. The harmful effects of AAS on learning and
memory should be taken into account when athletes decide to use them
for performance or body image improvement.”
“Testosterone and anabolic steroids have been found to affect the
central nervous system (CNS) in humans and laboratory animals. The
locations they affect include centers that regulate mood, sexuality and
aggression. People who use steroids in excessive doses often
experience mood disorders that meet the criteria of psychiatric disease
categories such as depression, anxiety, psychotic reactions and
cognitive deterioration.”
– Anabolic Steroids Cause Longstanding Changes in the Brain
Until you're around the age of 25,1, 2 your brain and endocrine system are
still developing. This should be obvious as you are still going through the
end of puberty, getting acne, etc. During this time period, supplementing
with exogenous hormones is extremely dangerous.
Taking anything before completely nishing puberty can have negative side
effects. While still maturing, the brain, organs, and cells are consistently
gauging the overall development of the body. When a foreign substance is
introduced, the body’s ability to truly judge how far along your maturation is,
resulting in the possibility of premature shutdown or stunting your growth
and development processes.
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Don't Short-Circuit Your Natural Blast
The body is already pumping out blast levels of Testosterone as part of the
natural course of late adolescence. It's the highest that it's ever going to be.
During this time there is a 30 fold increase in testosterone production
priming them for growth. During this time the body needs to 'learn' to create
these hormones and to stabilize their production. By introducing exogenous
hormones this inhibits the body from adequately forming the ability to
perform this function on its own. This can create the possibility of
decreased quality of life down the line.
There's a serious potential for long-term side effects. People oft-say “I've
stopped growing, so it's okay.” No: it's not okay. The rest of you hasn't
nished developing yet. There are many other potential side effects
besides simply your growth plates. Here are a few; Brain Function,
Memory, Alzheimers Disease…
It's well known that hormones play a role in the development of cognitive
brain function. Your neuroendocrine system is still developing until around
the age of 25.
Premature Closing of Growth Plates
This one is the most known about. Even if you think you've stopped
growing, there still is a potential for height increase over time. Scientists
have found that growth plates don't fuse completely in some cases until
individuals are past 22. Don't be deterred just because you haven't grown
taller in awhile. You grow out as well as up. Do you want broader
shoulders, or do you want to stay stuck with what you've got now?
Cancer, Liver, Kidney Disease
You hear all the time teenagers say “Well, my friends did it and they got big
and nothing happened to them.” Really? How do you know? Have they
been to a doctor and had their liver and kidney values checked? Just
because a person looks okay on the outside doesn't mean that they don't
already host serious problems on the inside. If treated improperly or in an
untimely manner, liver and kidney damage can eventually be fatal.
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Impotence
Your neuroendocrine system is still developing. Supplementing with
hormones while you are still growing can potentially cause permanent
impotence and fertility issues in teenagers. When you add testosterone,
estrogen and a wealth of other synthetic androgens to your body it can
cause problems with your normal testicular growth and function.
Remember, some of these effects are more than just temporary.
Gyno, or “Bitch Tits”
Androgen usage in teens increases the risk of gyno. Gyno has already
been known to happen naturally in many teenagers because of uctuating
hormones. When you add more hormones to the mix, you dramatically
increase the problems. Remember once you have gyno, it's very hard to
get rid of. Unless you take the proper precautions up front, you'll have to
resort to surgery and go under the knife.
Hair Loss, Acne, Prostate Dysfunction
Tracking Neurological Development
Maturation of the Adolescent Brain
Neuromorphological, neurochemical, neurophysiological,
neurobehavioral, and neuropharmacological evidence suggests that the
brain remains in its active state of maturation during adolescence. Such
evidence supports the hypothesis that the adolescent brain is
structurally and functionally vulnerable to environmental stress, risky
behavior, drug addiction, impaired driving, and unprotected sex.
Computed tomography and MRI studies also provide evidence in
support of this hypothesis. Brain maturation occurs during adolescence
due to a surge in the synthesis of sex hormones implicated in puberty
including estrogen, progesterone, and testosterone. These sex
hormones augment myelinogenesis and the development of the
neurocircuitry involved in ef cient neurocybernetics. Although
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tubulinogenesis, axonogenesis, and synaptogenesis can occur during
the prenatal and early postnatal periods, myelinogenesis involved in the
insulation of axons remains under construction in adolescence. Sex
hormones also signi cantly in uence food intake and sleep
requirements during puberty.
In addition to dramatic changes in secondary sex characteristics, sex
hormones in uence learning, intelligence, memory, and behavior of
adolescents. The development of excitatory glutamatergic
neurotransmission occurs earlier in the developing brain as compared to
GABAergic neurotransmission, which makes the pediatric population
susceptible to seizures. The development and maturation of the
prefrontal cortex occurs primarily during adolescence and is fully
accomplished at the age of 25 years. The development of the
prefrontal cortex is very important for complex behavioral performance,
as this region of the brain helps accomplish executive brain functions.
Women & AAS
Just as seen in adolescents, the side effects seen in women can be
permanent. AAS can lower voice, facial hair growth, and induce clitoral
enlargement. For this reason, AAS administration to women must be used
very cautiously, at more conservative doses, but is possible.
For more information please visit the Women's Wiki Page and visit r/
steroidsxx for specialized advice for women.
Tips For Interpreting Scienti c Studies
The number one tip, is “Who stands to gain from this?” This is particularly
relevant if you found the study quoted by some supplement site, for
example. You should also check at the end of the article to see if there is
any disclosure of con ict of interest from the researchers. There should
also be information on the source of funding. If it was funded commercially,
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and one or more of the authors have an interest, beware. Most good
journals will cite these things.
You can also look at the reputation of the journal itself. There is a ranking
system or journals, but without being a scientist, it is hard to know. For
those wanting to read more see Impact factor.
Another factor of course is how relevant the research is. Was it in mice?
Was it in elderly women? Was the study well designed to test what you
want to know?
One interesting area is the reference section. Here you can nd yourself
valuable information on studies that might be more relevant to what you
want. Throughout the text assertions are made that are backed up by prior
research. This is then referred to the reference section. PubMed is
wonderful at this as there are related citations to the right side.
References
• Testosterone dose-response relationships in healthy young men
• Androgen receptor up-regulation by androgen treatment
• Performance-enhancing Drugs on the Web: A growing publichealth issue.
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Hall of Fame
A Pin Story
Laying in bed at the in-laws house and feeling lethargic after a long day of
family activities; I get myself up to go to the kitchen. I have to take care of
this before bed.
This trip has really made me aware of my body dysmorphia as no one in
the house is over 160 lbs and I'm a pretty solid 205 of muscle, bone and
organs. It's always obvious when traveling to other countries. Most places
that I go in this country, I'm the biggest guy there and typically in the best
shape. Meanwhile, I'm on a strict diet doing a cut cycle trying to get from
14% BF to 8%. Public bathrooms with big mirrors are rough as everyone
next to me looks small in comparison. I imagine them looking at me as I
look at some guys in my gym. Jesus Christ that guy is big. Sometimes it
seems like people just move out of your way.
I hover around the group until I can silently signal my SO that it's time to pin
me. I head back to the room, telling everyone good night and, like
clockwork, she arrives 5 minutes later.
"Which side did you do last night?"
"I don't know, it's your job to track."
I feel my right and left medial glutes. "Right side today." I adjust myself
onto the bed so that she has access to my right ass cheek, hand her the
alcohol wipe and hold the pin by the needle protector for her to unsheath
when ready. Like the professional she is, she nds the muscle, uses her
petite hands to measure the distances, quickly swabs and swiftly jabs.
"That was a good one. Didn't feel a thing." I hope she didn't hit any scar
tissue.
There is really a lot of silence in the time it takes to push 2ml of viscous
uid down a 25g needle. It seems to take forever; longer if you're high like I
am now. It's almost all done, I can tell by the pressure. Here it comes. Shit.
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It starts as a little itch, deep in your esophagus. It's almost negligible. It
didn't start until the end of the pin, shouldn't be that bad. Good night kisses
and "I love you's" are exchanged as I hold in the cough as long as possible.
I never told her about Tren cough. The itch is creeping up my throat,
becoming unbearable. I make my way to the bathroom quickly as she
disappears back to the group. The coughing begins slowlly and my throat
tenses up, no more swallowing for a bit, so I spit in the toilet instead. My
eyes are getting watery. The coughing escalates. I may puke.
The coughing is worse, but somewhat controlled, still spitting in the toilet
and sink. I look in the mirror. Tears are going down my face. I think I inhaled
some saliva. I let out a round of coughs as I watch in the mirror. Holy shit,
my traps and chest look good when I cough. When will this end?
It's been about 2 minutes, but It's hard to say in high-time. The coughing
turns violent.
Fuck, I may die this time.
How did I get into this situation?
If someone read my truthful story about dying in this bathroom from Tren
cough, they wouldn't believe that anyone could be this stupid.
I start recounting how ridiculous it is.
You bought illegal drugs from an unground vendor.
You illegally had them shipped to you!?
You carried them to another country where they are illegal?
You secretly are injecting them at your family's house!?
And you're going to choke to death.
When will this coughing end?
How will it end?
All this risk, why are you such a dumb ass to die for this?
And just like that, it stopped; no more coughing. My throat still itches, but
it's able to be ignored. I slowly wipe up my eyes, clean the sink, ush the
toilet and hope that no one heard me. I pause for a second to listen and
take a quick mirror check before exiting the bathroom.
When I see myself, I closely inspect my body.
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"You are an undersized fatass. Time for bed."
I make my way back to the bedroom. The family is, apparently, unaware of
my near death experience. I'm tired. I need to fall asleep before Tren
makes it impossible. One more pin left for this trip and all I can do is hope
that it goes better than this last one.
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The Rage Story
Why do they make childrens beds so damn stiff? What the fuck is wrong
with those people? Or maybe something is wrong with me because I
purchased this fucking thing. The tiny pillow on which I'm resting my head
is soaking wet from the sweat and oils that heavy Trenbolene usage incites.
I ip the pillow over, only to nd that the other side is equally as wet. I have
no recollection of having ipped it previously. Fuck it. The pillow ies past
my feet, hitting the wall with a nearly inaudible fwop and sinks to the oor.
Resting my head on the stiff mattress, I discover that it's wet as well and
simply rest my head in the wetness. At least it's not on my neck.
"Daddy, when is my next birthday?" Her tiny and excited voice piercing
through the noise from the party in the next room.
"Well, today was just your birthday party. Your real birthday is
Tuesday and then you'll have another one in a year. You need to
sleep; It's late"
"Tomorrow?"
"No, in three days. The day after gymnastics. Now lets try to sleep."
She has to be exhausted from all of the activities today.
The noise from the next room consistently escalates, the volume of
laughter and mumbled talk following the graph of the number of wine
bottles opened over time. I glance at the glowing yellow clock that also
serves as a nightlight. 10:27pm. I've been laying here for two hours trying
to get her to sleep. My heart begins pounding hard and fast, hands
unsteady. I try to take my pulse, but can't really coordinate the counting,
timer and placement of my ngers on my neck for an entire minute. I decide
to do a six second estimate. Eleven. That puts me at 110 beats per minute,
resting. Typically being bradycardia, this is unwelcome news.
Remembering back to the previous weekend's ght with my SO when I
smashed a bone china bowl on our granite counter top, I recognize that my
temper has higher peaks than usual. I have been removing pieces of bone
china from drywall all week and do not want to repeat it, especially not in
front of family and friends.
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You're not going to say shit; Let it pass. Control your breathing, relax. I put
my ever-present head set into my ears, re up Pandora and select the
Mozart Piano Quartet channel. I can feel my heart beat in both of my ears.
My blood pressure is elevated. Focusing on my breathing and listening to
the apropos song "Intervention" by Helen Jane Long, I'm able to slow my
heart rate down.
I wrap my arm around my tiny daughter and she rests her head on my
bicep. A few songs pass and I believe that she may have fallen asleep,
unable to hear her breathing due to my head set.
"I don't want your arm." She moves to her own pillow. It's uncomfortable
for her neck because of the size.
The door to the hallway opens and the loudness of the party spills into the
room, overtaking the music in my head set. You're not doing shit. My heart
rate begins to climb again. The noise continues to pour into the room,
seemingly louder and louder. They forgot to shut the door. JUST go shut
the door. You're not saying shit. I get up.
"Where are you going Daddy?"
"I'll be right back."
"Don't go."
"I'll be right back."
I exit the room and take the four steps to the hallway door. My SO and I
lock eyes and, with a penetrating stare, I swing the door shut harder than I
intended. It slams and the noise from the party stops for a brief second as
the room sees me walk away. I hope they all got the point. My heart is
racing again.
I lay back down into my spot on the bed that is nearly a puddle of sweat.
Listening to the relaxing music and focusing on my breathing for ten
minutes, I'm unable to slow my heart rate. Physically feeling my pulse in my
ears, hands unstable and uncomfortable. This is fucked up. This is unusual.
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What would I say at the hospital? I'd rather die here than go to the hospital,
fuckit. I need this party to end. I text my SO.
"Come in here."
Laying there, still trying to control my heart rate, it continues to climb higher
despite my efforts. I can feel my body getting hotter. I call her. It rings up
until the point that I think that it will go to voicemail before she answers.
"Hello Honey." She's tipsy.
"Get in here."
"Ok."
She arrives in our daughter's room, nearly immediately. My heart is racing
as if I were doing wind sprints. I estimate it at 160 BPM, laying still on the
bed.
"Why do we have to have an infant's birthday party last twelve
hours?" I'm catching my breath as I talk, unable to complete the sentence
fully in one breath.
"What do you mean? It's only 11:00, it's just family and close friends."
She's standing back, away from the bed and me. I know that she can feel
the heat and seriousness of my stare through the darkness of the room.
"Shut it down. You have 15 minutes, or I will shut it down and kick
every single person, including family, friends and children, out of this
fucking house." I'm nearly panting. Heart racing, hands shaking
underneath the covers.
"What is wrong with you? Why are you being like this?"
With the seriousness and implied nality of a military command I insist.
"Shut it the fuck down, or I will. Fifteen minutes, starting now." She
sees me look at my phone for the time. It's 10:57. I am going to go nuclear
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at 11:12. If the lights were on, my heartbeat would be visible, moving the
blanket which rests on my chest.
She turns and quietly leaves the room. I need to calm down before I have a
heart attack. Maybe my last electrocardiogram was wrong and I do have an
abnormality. I do not fucking care, this party needs to end. I can hear her
announce the news to the room.
"He says that we have 15 minutes to end the party."
The disappointment of the group is verbal and strong.
"Why is he being like that?"
"It's only eleven o'clock."
She's trying to be quiet, but I hear her response.
"He's being mean again."
That fucking did it; I'm going to shut these fuckers up. I launch out of the
bed, wearing only my boxer briefs, and proceed to the kitchen. My body is
red and hot, veins swollen and exposed, muscles engorged with blood as I
walk into the room of fteen people. My heart wants to pound a hole
through the front of my chest wall. There is no way that I could utter a
sentence right now without panting. Absolute silence befalls the room
immediately as all eyes are on me for my next action. Fear can be felt in
the air and a few people shift in their chair, uncomfortably. With the stare of
death, I go person to person making eye contact as I walk, slowly and
deliberately. Family members, in-laws, close friends, it doesn't matter. Dare
they say a fucking word and I'll explode. I'm prepared to lay waste to
anything or anyone in my path.
No words, complete silence; staring at me in awe of the control that I took
over the room. I walk to the kitchen cabinet and open it, pulling out a large
red cup that was stolen on some drunken night, from some greasy diner. I
proceed to the ltered water and ll up the cup, slowly, still looking people
in the eyes. Cup lled with water, I go to exit the room.
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"Party. Over. Now."
It's as much as my racing heart would allow me to say. And without a single
audible word, people leave and family members go to bed. Jesus Fucking
Christ, I was too close to making a huge mistake with loved ones. Time for
PCT.
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Massive Attack
"If everybody jumped off a cliff," my father used to say, "would you?" This
was a few years ago. It was the summer a wild cougar killed a jogger in
Sacramento. The summer my doctor wouldn't give me anabolic steroids.
A local supermarket used to offer this special deal: if you bought fty bucks
worth of receipts, you could buy a dozen eggs for a dime, so my best
friends, Ed and Bill, used to stand in the parking lot asking people for their
receipts. Ed and Bill, they ate blocks of frozen egg white, 10-pound blocks
they got at a bakery supply house, egg albumin being the most easily
assimilated protein. Ed and Bill used to make these road trips to San
Diego, then cross the border on foot at Tijuana to buy their steroids, their
Dianabol, and smuggle it back. This must've been the summer the D.E.A.
had other priorities.
Ed and Bill are not their real names.
We were road-tripping down through California, and we stopped in
Sacramento to visit some friends. At this point the cougar was still running
wild. This was the countryside, but not. The wilderness platted into 2.5-acre
mini estates. Somewhere was a female cougar with cubs, squeezed in
among the soccer moms and swimming pools. This was less of a vacation
than a pilgrimage from one Gold's Gym franchise to the next along the west
coast. On the road, we bought water-packed tuna and ate it dry, tossing the
empty cans in the back seat. We washed it down with diet soda and farted
the length of Interstate 5.
Ed and Bill shot the pre-loaded syringes of D-ball, and I did everything else.
Arginine, Ornithine, Smilax, DHEA, saw palmetto, selenium, chromium,
free-range New Zealand sheep testicle, Vanadyl, orchid extract... At the
gym, while my friends bench-pressed three times their weight, pumping up,
shredding their clothes from the inside, I'd hover around their giant elbows.
"You know," I'd say, "I think I'm putting on real size with this yohimbe bark
tincture."
Yah, that summer.
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The only reason they let me hover was for contrast. It's the old strategy of
choosing ugly bridesmaids so the bride looks better. Mirrors are only the
methadone of body-building. You need an audience. There's that old joke:
"How Many Bodybuilders Does It Take to Screw in a light bulb?" Three: one
to screw in the bulb and two to say, "Really, dude, you look massive!" Yeah,
that joke. That's not really a joke.
The Sacramento people we visited, on our way home from Mexico, we
stopped by their house again, and they pulled us inside and locked the
doors. They were throwing a barbecue for some friends who'd been away
at a men's retreat. On this retreat, somebody explained, each man was
sent out into the desert to wander until he had a revelation. Now while the
tiki torches ickered and the propane barbecue smoked, one man stood
clutching some kind of shriveled baseball bat. It was the desiccated
skeleton of a cactus he'd found on his quest, but it was more. "I realized,"
he said, "that this cactus skeleton was me. This was my manhood, abrasive
and hard on the outside, but brittle and hollow." Everybody else around the
deck closed their eyes and nodded. Except my friends, who turned the
other way with their jaws clenched to keep from laughing. Their huge arms
folded across their chests, they elbowed each other and wanted to walk up
the road to see some historical rock. The hostess stopped us at the gate
and said, "Don't! Just don't." Clutching her wine cooler and looking into the
darkness beyond the steam of the whirlpool and the light of the tiki torches,
she said a cougar had been prowling around.
The cougar had been right up next to their deck, and she showed us in the
shrubs, a scattering of short, coarse, blond hair. That year, everywhere we
drove, that whole trip, there were already fences and property lines and
names on everything.
Ed juiced and lifted for a couple more years until he blew out his knees. Bill,
until he ruptured a disk in his back. It wasn't until last year when my father
died, my doctor nally came across. I lost weight and kept losing weight
until he whipped out a prescription and said, "Let's try you on 30 days of
Anadrol."
So I jumped off the cliff, too.
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People squinted at me and asked what was different. My arms got a little
bigger around, but not that much. More than the size, the feeling was
enough. Anadrol is an anabolic steroid, a synthetic derivative of
testosterone. Possible side effects include: testicular atrophy, impotence,
chronic priapism, increased or decreased libido, insomnia, and hair loss.
One hundred tablets cost eleven-hundred bucks. Insurance does not cover
it. But the feeling does. Your eyes are popped open and alert. The way
women look so good when they're pregnant, glowing and soft, and so much
more female, Anadrol makes you look and feel that much more male. The
raging priapism part - that was the rst couple weeks. You are nothing but
the real estate between your legs. It's the same as those old illustrations in
Alice in Wonderland where she's eaten the cake marked "eat me" and
frown until her arm sticks out the front door. Except it's not your arm that
sticks out, and wearing bicycle pants is totally out of the question.
About the third week, the priapism subsided or seemed to spread to my
entire body. Weightlifting gets better then sex. A workout becomes an orgy.
You're having orgasms, cramping, hot, rushing orgasms in your delts, your
quads, your lats and traps. You forget about that lazy old penis. Who needs
it? In a way it's a peace, an escape from sex. A vacation from libido. You
might see a hot woman ant think, "Grrrrrrr," but your next egg white omelet
or set of squats are a lot more attractive.
I didn't go into this stupid. This is a kind of weird aside, but a friend in
medical schoolmate me a deal that if I introduced her to Brad Pitt, she'd
sneak me in to help her dissect some cadavers. She met Brad, and I spent
a long night helping her disassemble dead bodies so rst-year pre-med
students could study them. Our third cadaver was a 60-year-old physician.
He had the muscle mass and de nition of a man in his twenties, but when
we opened his chest, his heart was almost the size of his head. I held his
chest open and my friend poured in Formalin until his lungs oated. My
friend looked at his freaking big heart, and his equally freaky big dick, and
she told me: testosterone. Self administered for years. She showed me the
coiled little wires and the pacemaker buried in his chest and told me he had
a history of heart attacks. About this time, a bodybuilder magazine ran an
occasional little feature in its back pages, a catch-up pro le about a star
bodybuilder from the 1980s. Back then, these stars posed and gave
interviews swearing they were blessed with great genetics and
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determination, they just worked hard and ate well, they never used
steroids. They swore. In the update features, these same guys were pale
and doughy, battling health problems from diabetes to cancer. And they
admitted they had been using steroids.
I knew all this, and I still jumped off the cliff.
My father was dead, Ed and Bill were a mess, and I was fast losing faith in
tangible shit. Here I'd written a story, a make-believe book, and it was
making me more money than any real work I'd ever done. I had about a 30day window of free time between my book obligations and the opening of
the Fight Club movie. Here was a 30-day experiment, an updated Jack
London adventure in a little brown bottle. My friends didn't stop me. They
only told me to eat enough protein to make the investment worthwhile. Still,
I didn't buy the 10-pound blocks of egg white. I never lled my fridge with
rows and rows of foil-wrapped boneless, skinless chicken breasts and
baked potatoes the way Ed and Bill used to. I just took the little white pills
and worked out and one day in the shower, I noticed my nuts were
disappearing. Okay, I'm sorry. I promised a lot of friends I wouldn't go here,
but this was the turning point. When the old goose eggs shrink to ping-pong
balls, then to marbles, then your doctor asks if you want a re ll on your
Anadrol script, it's easy to say no. Here you are looking great, bright and
alert, pumped and ripped you're looking more like a man than you ever
have, but you're less of a man where it counts. Besides, the appeal of
being a freaky, massive pile of muscle had already started to wane. Sure,
at rst it would be fun, like owning a rambling Victorian mansion, but after
the rst couple weeks the constant maintenance would eat up my life. I
could never wander very far from a gym. I'd be eating egg protein every
hour. All this and the whole project would still collapse some day.
I jumped off the cliff because it was an adventure. And for 30 days I felt
complete. But just until the tiny white pills ran out. Temporarily permanent.
Complete and independent of everything. Everything except the Anadrol.
the woman in Sacramento, hosting that barbecue all those years ago, she'd
said, "Those friends of yours, they're crazy." Beside the swimming pool, the
man cradled the brittle cactus skeleton of his masculinity, the woman still
stared at her clumps of bleached "cougar fur." Pumped and huge in their
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tanktops, Ed and Bill disappeared, lumbering down the road. Out in the
dark was the cougar. Or other cougars.
Ed used to wear a T-shirt that said, "Fuck Moderation."
The hostess said, "Why do men have to do such stupid things?" "As long
as America has a frontier," Thomas Jefferson used to say, "there will be a
place for America's mis ts and adventurers." Now Ed and Bill are fat
eyesores, but that summer, really dude, they were massive. A good pump,
my father, the Anadrol, all that's left is the intangible story. The legend. And
okay, that thing about frontiers, maybe it wasn't Thomas Jefferson, but you
get the idea.
There will be cougars outside. It's such a chick thing to think life should just
go on forever.
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Traveling around, as I always do, I just happen to be in Hawaii this week. I
can’t get over this shit; it chases me from place to place to place. Waking
up from a sun drenched nap next to a pool that is built to look like a beach,
I immediately see another swole dude a few chairs over. I calculate his
stats immediately in my mind.
5’11, 210, 12-13%. Mad capped Delts, oversized traps, . . . de nite gear
user. I wonder what his r/steroids name is. That could be /u/Mak_Ultra.
Every time I nd myself wondering if this swole dude in front of me is one of
you.
Went to a Luau in Paradise Cove the other night. It has the standard girls in
coconut bras and metrosexual to manlet looking performers.
Anavar and Clen, for sure. Which r/steroids member would he be? /u/
roidie? Naah. Did I answer one of this guy's questions?
Pretty high and, not quite, drunk the rest of the night, I sat around trying to
gure out a signal that the community could use to identify each other. With
more sobriety, my senses sharpened and came to reason.
Why the fuck would we signal each other? The conversations would be
super awkward.
Ya, so, you're a member.
Dude, you look like your running some serious Tren with those
sweats.
Nah man, it's just hot here.
Awh, cool. Hey, I got a couple extra viagra and some dbol if you need
it.
Alright, I'll hook you up with some legit Primo!
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No one is going to fucking signal anyone and have those idiotic
conversations. The fuck am I thinking. Two slow taps on the head. That’s
the stupidest idea in the world.
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The Loss Story
”What will your cycle do to your sperm production?”
”I should be ne for the rst 15 weeks or so due to the sequestration
of testosterone by the gonads in the presence of FSH.” She’s in the
medical eld, she’ll understand
”Are you sure? You know that I’m getting older. Chances are less.”
”It’ll be ne, nothing to worry about.”
The familiar ow of our negotiations proceed without aw. A concern,
followed by an explanation; A re-iterated concern and a comfort. These
things can become more deeply entrenched than the Donner Pass in
marriage. Each person knows what the other is doing, wether placating or
telling the truth, it doesn’t matter if a ght is avoided. She knows that I’m
placating.
—
When the doctor opened the door, I could see that the room was tiny. It
never helps my body dysmorphia to be put into a very small room, with a
very small woman to sit in a close quarters. I feel oversized and
uncomfortable, mutant-esque. We both enter the room and I squeeze by
her, navigating to the back where patients and family intuitively sit to hear
the pertinent medical news. "Please, have a seat." She promptly begins.
"As you know, your wife's endometriosis didn't get better by the six
months of birth control or the medication that was prescribed.
Therefore we performed laparoscopic surgery to remove her right
fallopian tube."
"Yes."
"Well, while we were in there, we wanted to check the left fallopian
tube to ensure it's health. Unfortunately, it appears to have signs of
endometriosis as well. She may not be able pass an ovum through it
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and therefore pregnancy may be impossible. I would suggest an ink
test to determine if a non-assisted pregnancy is still possible."
"You mean, we may not be able to have more children without invitro?”
"Yes. The tests would give us more clarity."
She places the photographs that were taken onto the back lit glass panels
so that we can view them. She shows me the fallopian tube and points out
the areas that it appears matted and attened.
"If you're going to attempt to get pregnant naturally, do it quickly. You
are both getting older and this condition isn’t going to get any better.”
I’m not sure that I want another child.
”Ok.”
She walks me through the post-surgical recovery process and what I
should expect over the next few days in terms of care for my wife. The
printed pages of standardized recovery information, with the important
information circled in red, are handed to me and reviewed. She leads me
back to the empty recovery area where I sit and wait. Not long after my
return, my wife is wheeled in on a gurney, looking groggy, but awake. With
no words, I give her a kiss and just look at her to assess her condition.
”Can I have some ice chips?”
The nurse quickly leaves to fetch them. As if the request was pre-planned
to obtain some privacy for her next question, she darts out. ”What did the
doctor say?”
”Lets talk about it later, when you’re feeling better.”
”I’m ne, tell me.”
I recount what the doctor told me regarding her other fallopian tube,
childbearing and the chance of infertility. Her mood is visibly dampened.
She really wants another. The nurse returns with the ice chips during a long
and contemplative pause. The business of the surgical recovery continues
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as the conversation hangs in the air. It’s continuation is not triggered by a
private moment, or a certain look or feel; it’s triggered by a song.
Upon release and pick up at the patient exit, we hear the song “Do you
want to build a snowman?” from the movie “Frozen.” Somehow, the mood
deepens and becomes more serious as the song progresses. Anna sings
the words, “We only have each other, it’s just you and me.” and the
pressure releases.
”Do you think that we should do the ink test?”
”What would you want to do if it’s blocked?”
”I’m not sure.”
”Well, if it is blocked, we’d have to go through in-vitro.”
”I know, but don’t you think that we should see if it’s even possible?”
”I like trying, even if it can’t happen. If we’re not going to do in-vitro,
there’s no need to have the test.”
The massive increase in libido while I’m on a bulk cycle ensures that the
“trying” part of getting pregnant is taking place, daily. On this bulk cycle I’m
keeping my estrogen low which increases my libido even more. Several
weeks later, while cooking pancakes and bacon on a Saturday morning, I
get the call from the bathroom, “Honey, can you come here, please!?”
There is an undertone of distress mixed with a sprinkle of playfulness.
“There’s something on the counter that you should see.” Looking
around the counter, I don’t see anything. ”The other counter.” I swing my
head left to see the pregnancy test with what looks like a “+” on it. Oh, shit.
I grab it and double check the instructions. A + symbol means pregnant.
Fuck, this is really happening. Here we go. You see, my previous cycle put
a lot of stress on our marriage. Fights, crying and a near divorce due to an
interesting side effect that high doses of Trenbolone has for me; it makes
me stop tolerating bullshit. Trenbolone helped me say things that I had
been avoiding for years. Trenbolone helped push me to x things that had
been broken. And, unfortunately, Trenbolone urged me to do it all at once.
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With my marriage on the rocks, I don’t want to have another kid. We are
still recovering from the damage that repairing things creates; wounds
healing. Where I live today, a man’s paternal rights to raise his child are
unequal and easily removed. I could hear her lawyer in family court already.
“He’s a drug user! Alcoholic. Injects steroids daily!”
“He’s been violent and broken things.”
“He scared all of our family and friends on our daughter’s birthday.”
“Smashed a porcelain bowl and almost hurt us.”
“He, . . .”
My missteps would be listed forever and I would never see either of my
children again. The pregnancy test represented risk in a way that nothing
else could. At the same time, I was happy. My daughter would have a
sibling. My wife and I would have another intimate bonding time during her
pregnancy. I would have another child to love and love me. This time I have
more experience and am better prepared for this baby. Should be easy.
We hold each other in elation, thinking about the new child. For those few
moments, miracles were real. ”I took two tests at work yesterday and
they were both positive.” Over time, the news settles in and the
implications start to present themselves. The money, time, and effort. The
joy, bonding, love, and happiness. The advantages of having a designated
driver for ten months. The upcoming additional stop every morning and
evening. Sleepless nights and fun lled days.
The regime of doctors appointments begin and everything is ne. No
morning sickness this time presents a great relief. At about ten weeks the
doctor begins using the doppler handheld ultrasound to hear the child’s
heartbeat. It can be dif cult to hear, depending on the size, position, shape
of the uterus, and actual conception date of the fetus. When the doctor was
unable to nd the heartbeat at week ten, it wasn’t a big deal. ”This is
pretty common. Sometimes we just can’t nd it. Nothing to worry
about.” She’s worried. By week fourteen, however, the heartbeat is
typically apparent.
”We tried to check the heartbeat today, but couldn’t nd it.”
”Ok. . ?”
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”We immediately did an ultra-sound to check things further.” It’s not
good. ”The ultra-sound determined that it’s a blighted-ovum.”
”What does that mean?”
”It’s a fertilized egg that implanted into my uterus but didn’t develop
for some reason or another. Most often it’s due to a genetic defect.”
Being in the medical eld often makes medical news less dramatic due to
knowing how common these things are and simple familiarity. The pace of
my meal consumption slows to a crawl as my appetite leaves me. Eating
my salmon, brown rice and asparagus becomes more of a chore than
usual. This fucking bulk, I need to get this food in. I choke down the rest of
my plate and make a 75g protein shake with 40g of Waximaize. Shaking
the blender ball cup vigorously due to the large amount of powder and then
chugging it makes that familiar bloated, lled up to my throat feeling
apparent.
”What happens next?”
”It needs to be removed; I’m scheduled for a D&C next Monday.”
”Ok, I’ll take some time off.”
The conversation is all business, but I know that there’s pain there; She
has wanted this for so long. That night, we just hold each other in peace.
The piercing quiet, soft stroking of her thumb in my hand, sweat dripping
down my legs where-ever two pieces of skin touch, and weary heavyheadedness make for a dif cult several hours. It’s hard to hold back my
tears. It’s hard to not speak. There is nothing to say. I eventually fall asleep
before the sun rises. A few days later I am slowly engulfed by the
realization.
Sperm have less motility while on steroids.
Sperm have less viability while on steroids.
Sperm have higher rates of genetic defects while on steroids.
My steroid use probably caused this.
Not only am I killing myself earlier, but I’m hurting my loved ones.
For what? To look good?
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I remain with my head in my hands, on the ground, rigorously motionless,
thinking these thoughts for what seemed like hours. The guilt and shame
lling my every cell, stealing what little self-worth I maintained. If only the
ceiling would collapse on me. Maybe this cycle will give me a myocardial
brillation. When my daughter returns home from school and jumps on top
of me, I snap out of it. I didn’t even hear her come in the house. I hug her
tightly and go to greet my wife. She can tell that I’m upset.
The next morning after my traditional cold shower, I need to pin for my bulk.
Pinning after my shower is a taciturn sacrament. The sacrament has a
speci c place for the implements, an order and cadence — not today. The
syringe's orange tip means that it’s delts day. When I nally get the pin
unsheathed and placed on my right delt, I set it on the skin slowly,
intentionally. The thoughts from my time on the oor, the previous day, ll
my head. The pin, still pressing on my skin, hurting me with it’s sharp poke.
You’ve sent your wife to the hospital because of this. The pain of the needle
on my skin is screaming at me to pull it away. I see myself in the mirror. As
usual, I inspect my body closely. You are an undersized fatass. And, at that
moment, the needle pierces my epidermis and sinks slowly into my muscle.
With my left nger and thumb I push the oil into my body, feeling that slight
bit of pressure inside the muscle as it enters.
I pull the needle out slowly, guiltily. Fumbling with the sheath, I eventually
cap it and hold it in my hand. Overwhelmed with sorrow and pain, I stand
there, over the sink, with my used steroid syringe in my hand, crying.
Untouched tears streaming down my face, chest heaving for gulps of air.
——————
As with any story, creative license is taken. This is a not an actual,
literal account of what happened. Liberties were taken with
conversations, ow and almost everything in order to make it more
interesting, readable, emotional, and shorter.
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I’m hurting everyone around me for my aesthetics.
I’ve now sent my wife to surgery for visible abs.
I’m a horrible, sel sh and vane asshole.
I deserve to die.
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The Dirty Bulk Story
There was a time at the Old Westside gym where I couldn't gain weight to
save my fucking life.
There was this dude who trained there who could just put on weight like
fucking magic. He'd go from 198 to 308 and then to 275 and back down to
198. And he was never fat. It was amazing.
I nally asked him one day how he did it.
"You mean I never told you the secret to gaining weight? Come
outside and I'll ll you in."
Now remember, we're at Westside Barbell. And this guy wants to go
outside to talk so no one else can hear. Think about that for a minute. What
the hell is he going to tell me? This must be some serious shit if we have to
go outside, I thought.
So we get outside and he starts talking.
"For breakfast you need to eat four of those breakfast sandwiches
from McDonalds. I don't care which ones you get, but make sure to
get four. Order four hash browns, too. Now grab two packs of
mayonnaise and put them on the hash browns and then slip them into
the sandwiches. Squish that shit down and eat. That's your
breakfast."
At this point I'm thinking this guy is nuts. But he's completely serious.
"For lunch you're gonna eat Chinese food. Now I don't want you
eating that crappy stuff. You wanna get the stuff with MSG. None of
that non-MSG bullshit. I don't care what you eat but you have to sit
down and eat for at least 45 minutes straight. You can't let go of the
fork. Eat until your eyes swell up and become slits and you start to
look like the woman behind the counter."
"For dinner you're gonna order an extra-large pizza with everything
on it. Literally everything. If you don't like sardines, don't put 'em on,
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but anything else that you like you have to load it on there. After you
pay the delivery guy, I want you to take the pie to your coffee table,
open that fucker up, and grab a bottle of oil. It can be olive oil, canola
oil, whatever. Anything but motor oil. And I want you to pour that shit
over the pie until half of the bottle is gone. Just soak the shit out of
it."
"Now before you lay into it, I want you to sit on your couch and just
stare at that fucker. I want you to understand that that pizza right
there is keeping you from your goals."
This guy is in a zen-like state when he's talking about this.
"Now you're on the clock," he continues. "After 20 minutes your brain
is going to tell you you're full. Don't listen to that shit. You have to try
and eat as much of the pizza as you can before that 20-minute mark.
Double up pieces if you have to. I'm telling you now, you're going to
get three or four pieces in and you're gonna want to quit. You fucking
can't quit. You have to sit on that couch until every piece is done.
And if you can't nish it, don't you ever come back to me and tell me
you can't gain weight. 'Cause I'm gonna tell you that you don't give a
fuck about getting bigger and you don't care how much you lift!"
Did I do it? Hell yeah. Started the next day and did it for two months. Went
from 260 pounds to 297 pounds. And I didn't get much fatter. One of the
hardest things I've ever done in my life, though.
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The Pituitary Story
"That motherfucker.”
I toss the paper and envelope onto the island. My doctor skipped a few
check boxes on my blood work order. Fuckit, checking them myself. I nd a
black pen and check the missing boxes.
☒ Estradiol
☒ Prolactin
Asking the doctor to mail me the blood order lets me review it and not have
to go to a doctors of ce visit. Getting the blood drawn takes ten minutes in
the hospital. And, a few days later, I get a message from my doctor to call
him about the results. I decide to go there and just ask for a copy.
"Hi, I'm DL. I'd like a copy of my latest lab results."
"We can't give you a copy until the doctor signs off on them."
"What? They're the results from me, I paid for them." Be nice, she's
probably just following bosses orders.
"The doctor still has to sign off on them and by state law we don't
have to give them to you until he has done that. Sit down and I'll be
with you in a minute." da fuk
After about ten minutes, they bring copies of the results.
Test
Amount
TSH
3.4
Serum Test
586
T4
1.2
Free Test
159
T3
0.80
Estradiol
59.8
HDL
40
Prolactin
23.1
LDL
170
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Test
I just glance at them and stick them in my bag, forgetting that they are even
there. Before I make it home, I get a call and glance at my phone.
Dr. GP
I answer it and after a little small talk, he moves abruptly to the point of the
call.
”DL, your results look ok. You need to start taking your statin again
for the LDL until you can get your HDL up into the 50’s or 60’s. The
TRT dose seems to be working well, Thyroid is in range. Uhh, huh.
”There is one thing concerning here. Your elevated prolactin levels
are very abnormal; I don’t see this often. You’re going to need to go
and have an MRI taken of your pituitary.”
”What’s that? I need to have a brain MRI?”
”Yes. Unfortunately. We need to see if there is anything going on in
your pituitary gland. It is over-producing prolactin and this usually
indicates swelling and / or prolactinomas. It could be very serious,
and I want you to get this MRA as soon as you are able. Can you
come and pick up the order?”
”Wait a minute. So, my pituitary may possibly be swollen, have a
tumor, cancer or similar — causing it to over-produce prolactin. What
is the typical treatment for prolactinomas?”
”If that’s the case, which I’m not saying it is, you’ll need to see a
neurologist and probably have your pituitary gland removed. That’d
put you on hormone replacement for the rest of your life.” Well, I’m
already there today.”
”Is there any way that opiates from my recent surgery could cause
this?”
”I don’t believe so. Even if it did, we couldn’t determine it conclusively
without the MRI. So, you need to get this MRI immediately.”
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Prolactinomas
Prolactinomas develop when one of these normal cells develops a mutation
that allows the cell to divide repeatedly, resulting in a large number of cells
that produce an excessive amount of prolactin. About 10 percent produce
growth hormone as well as prolactin.
Symptoms
•
•
•
•
•
•
Low Testosterone
Decreased Sperm production
Lethargy
Loss of libido
Loss of muscle mass and strength
Decreased hematocrit
Fuck. I fucking have all of those when I’m not on TRT. Every symptom lines
up and was there for three years of not running gear, including not being
able to impregnate my wife a second time. This explains so much of my life
path, being on TRT, some of my decisions to use gear regularly to maintain
muscle and strength. It ts perfectly.
...
As I lay in a hospital bed, bare-assed, the neurosurgeon explains (for the
fth time).
”After you are comfortably put to sleep, we’re going to be entering
your brain through your nose. We’ll make a small incision, insert a
probe, and visually verify what we saw in the MRI. If it is as we
suspect, we’ll be removing the pituitary. The nurses will give you all of
the after care instructions and your medications to take after surgery.
Any questions?” I’ve researched this exhaustively at this point. I may still
die.
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Research, research, research, research, research, research, research,
research, research, research, research, research, research, research,
research, research, research, research, research, research, research,
research, research, research, research, research, research, research
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”Nope. I understand.”
”Everything is going to be ne.”
As the doctor leaves the area, the anesthesiologist comes up.
”We’re going to be putting you to sleep now to go to surgery.”
”Ok, I’ve been told that I have a high tolerance. You may want to take
that into consideration.”
”Yes, I was informed. Don’t worry, you’ll be out.”
I glance over at my wife who is grinning from having warned them. I just
smile back. I’m trying to stay awake as long as I can, to feel the effects. I
want to feel the onset.
”Ok, will you count to 30 for me?”
”One… Two… Three… Four… Five…”
I faintly hear my wife’s voice, as she touches my arm softly.
”I lovvv”
——————
As with any story, creative license is taken. This is a not an actual, literal
account of what happened. Liberties were taken with conversations, ow
and almost everything in order to make it more interesting, readable,
emotional, and shorter.
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I'm not banned. Tren does give you horri c sides.
But only at high dosages over long periods.
You wannabe a bodybuilder?
Everyone wants it..
Wanna be a freak?
Want to be a freak? You're in luck. I'm drunk and going totell you but let's
face it. You don't really want this do you? Want to be a FREAK?
Really?
Want the girls dropping their jaw when you walk in the room?Want the guys
saying WTF when they see you? Want her down on her knees in frontof
you telling you how hot your abs look before she takes you in her mouth?
Really?
Yeah, most guys do but they don't want to work for it. Faceit. Most guys are
lazy, don't want to sacri ce and can't eat strict for aweek. I'm not going to
bullshit you guys in this thread. I will lay it all outbut the truth is we don't
really want it bad enough. We say we do until we are45 minutes into our
tenth cardio session that week. WE say it until our muscleshurt so bad
there are tears in our eyes and we give up. We want it until wehave to eat
sh for the 4th time that day...I say I want it but I fucking lovebeer more, so
I drink...I say I want to be a FREAK but I don't want to work forit. I'm 10
weeks into a blast and my will feels broken...I can't go on, or canI??? Do I
really want this life? No time but time to train. Time to cook, Timeto grocery
shop, Time to tan. Fuck!!! Not sh and shakes again...FUCK my life.
I walk past the mirror and catch a glimpse. MY oblique’s arechiseled. My
veins look like spider webs all over my body. I catch her lookingat me at
work, at the store, at the gym. Guys ask me what I'm on. I can't takeit. i'm
on a FUCKING starvation diet and a shit load of cardio but that's notwhat
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they want to hear. They want to hear what drugs to take...You PM me
everyfucking day. Same questions over and over. ITS NOT THE DRUGS
DUMMY!!! Or isit??? Yes and no. Can you take the sides?
Really??? 2 fucking weeks from now you will PM me againwhining. I can't
sleep. I can't eat like this. I can't do that much cardio. Ican't. I can't... THEN
STOP PM'ing ME!!!! I can't help you. You don't fuckingwant this! Just admit
it! You don't fucking want this. Its hard. It hurts. Youhave no social life. You
are in the gym when your buddies are drinking beer.You are doing cardio
when guys are lying on the couch. You spend your last $50on protein
powder and a bottle of prop. I know all this because I am you. Iwant it for
2-3 months then I give up. Fuck 10 sessions of cardio a week. Fuckeating
sh. Fuck taking pills so I can sleep from all the insomnia from the TREN.
It’s ok. Get some sleep. Wake up and pin. Fuck I love topin. Push in more
oil. I love it. My lunches are packed. Off to work. Trainafter work. Get the
pump. Here they come. What are you on??? Not this again...I'm on a crazy
train. Fuck my life but fuck I look good and I can lift a shitload of weight. Go
ahead, fuck with me. I will make fast work of you...The trenis in my head. Is
she cheating on me? How much sleep did I get last night? 5hours max. Pin
some GH and prop and tren. Fuck, I need some caffeine. Ok,double
espresso. Time to train.
So IF IF IF you can handle the work, cardio and diet not tomention the
sides. Then what??? Drugs of course.
You want that freaky bodybuilder look and your genetics areaverage like
me??
Its actually quite simple but it takes a focus so strong andfocused most give
up in a few months if not sooner
Fuck, where am I? Oh yeah the drugs. One word... Trenbolone.How lo0ng
can you take it??? Don't cry to me in 3 weeks when you can't sleep. Idon't
give a fuck. I can't sleep either. Time for some Xanax. Maybe somewhiskey.
Most guys give up on tren right when its getting good. 9 weeks in andman
your body is changing. The girls want you. Give me some Cialis, prop
andmore tren...How high can I go. 1050mg tren per week and I look in the
mirror.Who is this??? I don't even look the same. I need some mast, maybe
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some win,var, halo. Fuck I look like carved stone…I’m drunk but its all true.
Do youwant to be a freak? Man the fuck up and start working for it bitch.
Prop, tren and an oral is a good start. The question is HOWLONG CAN
YOU RUN THIS??? Tren at 9 weeks 1050mg per week and you are crazy.
Eat,train, pin, sleep....over and over. I’m feeling insane just 6 more weeks.
Its 4months now..... Im sub 10% and huge. Not skinny. Huge and
lean...How muchlonger can I go. I want to look like the guy on the cover of
the magazine.REALLY??? Eat some more sh and do some more
cardio...Fuck Fuck...
]Do you really want to be a freak??? Really..?
I walk past them every day at the gym. Same guys doing thesame routine
looking the exact same as they did 3 months ago. Talking duringsets and
even while doing cardio. It isn't work, it's fucking social time forthem. I can't
be social at the gym. I'm not built for it and I don't want it.I'm there to work,
to train, to push my body beyond what the average guy can do.
A few guys are there working like a bulldozer at aconstruction site. Heavy
ass poundage's, sweat running down and out of breaththey push another
rep. I see the pain in their faces and the strain on theirbodies. My turn
mother fucker. Time to WORK. I warm up imagining the set beforeI do it.
The steroids are pulsing through my body. The tabs dissolved under
mytongue. God how I love the taste of D-bol or Anadrol while walking in the
gym.I have been pushing the caffeine and getting in the food. I'm ready. I
don'tpin pussy ass doses. I'm jacked to the max. A gram is child's play. I
need topush in just a little more oil.2200mg, 2500mg that week. Maybe a
bit more.Fuck it, just ll the barrel all the way and shoot. I am making
changeseveryday. I don't want to be the same. I can't be the same.
The steel is cold in my hands. I pump out a few fast sets.Load the weight
up. Maybe I will get 4 reps. Maybe 5. I look at the guy pickingup a chick at
the gym. He weighs a buck fty. What a fucking joke. This isn'ta bar its a
fucking place of employment. I'm here to WORK. Fuck the chicks. Idon't
need a girl right now. I need to train. I lift the weight off and itfeels heavy. I
grind out 6 reps. Hell yeah! I'm just getting started. OH fuck.Here comes
some guy telling me how good I look. Looks like he has never traineda day
in his life. I ignore his questions and turn up my iPod. I'm trying
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toconcentrate. Get the fuck away from me my mind screams. I have to be
cool.Don't want to get kicked out of the gym....again...I feel rage inside me.
Good.Channel it. Put it to use. Hit the set again. I don't want to be the guy
whoshows up and goes through the motions. I want to make changes. God
the pain isbad tonight. Lactic acid is heavy in my muscles. Ok, enjoy the
pain. Like it.Its good. Trick your mind. I like the pain. I want the pain. I'm
grinding outslow heavy ass reps. It burns but I tell myself its good. My rest
between setsis minimal. I have done 5 sets but the guy talking to the chick
has done none.Fuck he is tiny.
I walk over to the next bench and load up some more weights.I see a
monster walking by. He is covered in sweat. He nods. I nod back.Nothing is
said. We are both in the same place. We are there to train not talk.He asks
for a spot with one word. spot? I nod and ask how many. He says 5
reps.He pushes out 8 with a few forced reps. My turn. The night goes by
slow. Itswork. Its hard but I have a pump. Time for cardio. I take a piss and
get on thetreadmill. Bump up the incline and speed. The guy two machines
down is walkinglike he is strolling through the park. He's reading a fucking
book. Hell, I canbarely read the numbers in front of me on the machine. I
am feeling my lungsburn. Just 40 more minutes to go...Fuck my life. Ok, go
to that place in yourmind far away. I look down and 15 minutes has gone by
in what seems likeseconds. Good. Go to that place some more. I am
absolutely covered in sweat. Myshirt looks like I pulled it out of a bucket of
water. I nally nish and getoff the treadmill.
Its late and I'm hungry. I feel dizzy. I walk out of thegym. and go get some
food. Everyone is obese. I can't believe how fat everyoneis. They are pigs. I
am in a world of fat people. How can these lazy fucksstand it? I feel hate.
Why do I hate these fat asses? Its weird but I feel likeyelling at them to
wake up. The girls are looking at me again. One stops me andtouches the
ropes for veins in my arm and says nurses must love me when theydraw
my blood. Its funny but she is right. They do say that. I'm a freak. Itsexactly
what I want. I'm walking art. My art. My sculpture. Its who Iam....Just
another day...a day of work to become a FREAK
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Hall of Shame
First Tren Cycle
Hello guys,
I am currently suffering from a lot of side effects after a 16 week tren cycle
and am turning to you guys for your help because some of this stuff is
really making my life horrible.
It was a tren cycle with Tren A (10 weeks) rst and then tren E (6 weeks).
Tren dosages were moderate (350-500) and test was at 250.
It was my rst cycle and supposed to be a cut/recomp. I gained some
muscle but I was still having a lot of trouble losing fat.
I took some T3 in the middle of the cycle. 500mcg didn't do much so I
upped it to 1000mcg (typo, it was: 50mcg and 100mcg). Didn't really make
much difference so for the last two weeks I stopped.
Now, during the cycle I started noticing a whole bunch of symptoms:
cramps, very fast fat regain if I took 2-3 days off, huge appetite, waking up
very early in the morning and not being able to fall asleep afterwards.
The rst two weeks after the cycle were pretty bad. I did and still am doing
PCT with Nolva (40/40/20/20).
All of the aforementioned symptoms got worse. To recap here's what I am
currently suffering from:
• constant feeling of fatigue/feeling of sickness ( u like) which goes away
in the evening. This is the only symptom that has faded after two weeks.
I am feeling better now and able to function.
• huge appetite: after the cycle I had 2-3 days of binging and afterwards
am eating +1000 cals over maintenance and I still dream of food almost
every night.
• fast weight gain, especially right after the cycle (and I was already sort of
bloated): 5 kgs in 10 days. I think it's partially water retention because I
doubt you can synthesize so much fat so fast. Also the fat is much
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•
•
•
•
•
•
squishier. My gut sometimes changes shape: in the evening it may get
bigger and the next morning be much thinner. I think these are water
uctuations.
weight gain patterns: moon face, enlargement of the neck and different
patterns of fat gain (compared to how I usually gain fat) at the gut level;
always waking up after 4-5 hours of sleep and can't go to sleep
afterwards, even when taking 5-10mg of melatonin.
low sex drive
muscle fatigue and lower back pain: when I walk for more than 5
minutes, my legs (anterior shin splints) hurt to the point where I have to
slow down. Muscle fatigue in the quads as well.
elevated blood pressure during the cycle (15-17); it has now subsided a
little bit
right after the cycle, when the symptoms were the worst, I was also quite
anxious for no reason.
All of these seemed like tell-tale signs of high cortisol levels.
I saw my general physician to get some tests done. Here are the results:
• Cortisol at 8 in the morning : 504.6 nmol/L (normal range: 218 to 615)
• Rest of the bloods taken at 10 am.
• Blood sugar: 0.95 g/L (0.70 to 1.05)
• Sodium: 141 (135 to 145)
• Potassium: 5.18 (3.50 to 5.10) - the slight elevation is probably due to
the fact that I supplemented with potassium and magnesium in order to
help with the cramps
• Chlorine: 101 (98 to 107)
• Creatinine: 13.9 (7 to 12)
• Creatinine clearance (Cockroft-Gault): 94.54 (normal when higher than
60).
Liver:
• ASAT: 126 (should be lower than 40)
• ALAT: 72 (should be lower than 41)
• GGT: 27 (should be lower than 60).
Lipids (all in g/L):
• Total cholesterol: 2.58 (should be lower than 2)
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• Triglycerides: 0.98 (0.50 à 1.50)
• HDL Cholesterol: 0.17 (should be 0.55 to 1.10)
• LDL Cholesterol: 2.21 (should be lower than 1.30)
Other:
• CRP: 0.3 (should be lower than 5)
• Serum protein: 67.3 (66 to 87).
• TSH: 1.430 was 2.390 in april 2015.
• Leucocytes: 4,480 (4000 to 11 000). There's other stuff related to
haematology but it's all in range.
Didn't do test or E2 since I didn't tell my general physician about the cycle.
I also saw an endocrinologist to whom I didn't speak about steroids. He
said everything was ne with regard to my concerns with cortisol since it
was in range. Moreover he said that he didn't see any hormonal problems. I
don't really trust his analysis given that I didn't tell him about AAS usage
and also since he didn't really seem to care about any of my symptoms at
all.
Will see another doc soon for liver and lipid related issues. I will probably
need to nd someone to whom I can speak freely about AAS.
The only upside is that during this last week things got better in terms of
general health.
I guess that maybe when test production will restart it will help with ghting
what I think is elevated cortisol and that the symptoms will slowly go away.
I am open to any and all suggestions to how to solve this thing.
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Abuse of DNP
NEW IMPORTANT UPDATE!: I just realized something important, during
this incident, I was also taking 1000mg of Naringin for several weeks (due
to its alleged bene ts towards hematocrit levels) which as I found out
"taking naringin supplements can result in higher-than-expected levels of
[certain] drugs in the blood, which may cause a variety of unwanted sideeffects. As a result, patients should not take any drugs with naringin or
grapefruit juice without rst consulting a licensed health care provider. In
addition, the effects of taking naringin and/or drinking grapefruit juice are
cumulative; the more naringin that is ingested, the greater its interaction
with certain drugs and other nutrients."
This could absolutely be the cause of why my blood level of DNP exploded
with such a little amount. Could be, maybe, maybe not. I don't recall if I was
taking Naringin during my old DNP cycle, but certainly wasn't taking it as
regularly as I do now! Be extremely careful if you are taking Naringin of
these bizarre interactions! That is theory #2, so, perhaps the purity of the
DNP had nothing to do with it at all! De nitely worth noting this! Stay safe
gentlemen!
___
TL;DR is at the bottom of the post, the last three bullet points are the
takeaway lessons. To make things clear, as a lot of folks are messing up,
this incident happened WITHOUT T3 and Clen and over a month apart
from the 1200mg DNP cycle. They are unrelated events as far as I know.
That is the whole point of the post - to warn you about the unpredictability
of this substance if you are not careful. Also, this did NOT happen after
eating pizza, there were no pizza leftovers from my previous day's cheat
day! I ate the leftovers with my regular meal! Stop it already! I count it as
one single cheat day if I have leftovers on the next day, so please stop
criticizing my diet! We're all gonna make it brahs. Happy lifting!
___
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This is sort of a PSA for those of you who are venturing into the use of DNP
for fat loss - it is long and detailed - just FYI, I am the last person on earth
who would say "drugs are bad mmkay" and tell you not to take it just
because there's inherent risk. However, I feel like this experience can
bene t many who nd themselves in the same position as me: want to try
out the compound yet aren't exactly sure of what to expect due to so many
different opinions out there. Whether you believe my story to be true or not,
or misattribute it to something other than DNP, sharing this interesting
occurrence can help shed some light on the substance, as well as help
people be completely prepared for stuff that can go very, very wrong.
First and foremost, for those who think I'm a nobody who just hopped in
this product before doing his due diligence, I had put in a gigantic amount
of research: from forums to research papers across the web, I was very
prepared to take the dive into this very controversial compound.
I am 263lbs. I was 280 when I started using it. You see, I had cycled this
compound for a few months prior to this incidence from a seller who
claimed his DNP was for agricultural purposes. With how hard it is to nd
this substance, I just bought it from him. I press my own pills, and I have a
very expensive high-end scale for very precise dosages in my pills. Well, I
started off with the typical. 100mg/d for 1wk, nothing serious, minor weight
loss. Did a three week cycle after resting 2 weeks where I eventually
ramped up to 600mg/d. I did another 2-3wk where I eventually ramped up
to 1200mg/d. I was taking all the supplements people recommended: Alcar,
Vit C, Vit E, electrolyte drinks (Propel water, in my case), taurine, etc. Well,
I did feel like shit during a lot of the cycle, and I knew right off the bat by
doing a burn test of the substance that it was highly diluted. By how much,
who knows, I estimated 70%-ish was DNP, God knows what the ller was.
So I gured if I'm taking 1200mg, this must mean I'm taking 800-900mg
DNP. Still a very high amount, and even though I was feeling like shit (as
people do while on DNP), it was nothing I would consider life-threatening,
especially while taking my supplements. The weight loss was not superdramatic either. But I did manage to lose about 20lbs over the course of 2-3
cycles. I even included Clen and T3 to my cycle while going as high as
1200mg/d of the diluted DNP. Note, that at 1200mg my top rectal
temperature only reached 101.8F, and this was after my workout's warmup.
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However I was worried that the ller might be something toxic, so I decided
to nd someone who had pure DNP.
Well, I did. Much, much pricier than the original but at least I had the peace
of mind there could be no "biocides" as ller, as the new seller suggested
could be present in the agricultural dnp. I dried out the powder (175F for 2
hours on a paper plate in the oven), then after leaving it out one day I set a
little bit on re. The thing blew up like a reball, while the agricultural DNP
just barely cracked and popped, only sometimes completely burning up.
This is pure DNP, I thought, so it gave me peace of mind. I pressed 100mg
pills despite the temptation of pressing higher amounts. And before anyone
tries to tell me that my pills were probably incorrectly dosed, I did a triple
con rmation, weighed and reweighed, have 2 separate calibration weights
of different weights and on top of my years of pill-pressing experience, the
possibility that the pills are pressed have a margin of error of more than 5%
is nihil. They are 100% 100mg-ish pills, no doubt.
Now, this step that I did next is quite possibly the only thing that saved my
life. I decided not to go reckless by hopping on a 500mg/d or more cycle. I
decided to test the waters and see how I react, so I decided to start with
200mg/d as a warmup, divided in to doses, am and pm. After the rst
100mg dose only, and you'll have to take my word as someone who has
dosed many times before, I started feeling the warmth and sweating just 6
hours or so after ingestion. I was de nitely warming up but I thought this
was mostly my imagination, after all, it took me 500-600mg of old DNP to
feel this. Regardless, I thought, no way this is too much a dose. And I took
the other 100mg dose at night.
The next day happened to be a cheat day. Based on previous experience
with this whole "carbs will make your heat worse", I thought it was an
exaggeration. I had cheat meals with 1200mg DNP before, eating an entire
pizza and much more without an extreme reaction. So I gured I shouldn't
worry. I took the 100mg along with my meal and thought not much of it.
Skip forward to the next day. Yes, this ordeal happened merely on the 2nd
day of DNP, after my third dose. I had just come back from Costco with my
van still loaded with groceries. I decided to pack my groceries after eating
my second cheat meal (leftovers from the previous cheat day) along with
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100mg DNP. So I did, and before I started loading up my groceries, I was
feeling uncomfortably warm, but thought not much of it. I started feeling
hotter and hotter the more trips I was taking, as well as the trips to taking
out the trash and whatnot. What hit me next was so intense I kind of not
even remember it all properly. I started feeling hotter and hotter so I'm like,
whatever, I'll take my shirt off and stand in front of the AC for a while to cool
off. Then my heart beat started ramping up. I noticed my hands started
going numb and cramping (big red ag for a potassium-related issue). I
started feeling confusion all of a sudden, I'm like, OK. This is de nitely the
DNP but this isn't enough to cause anything serious. I hop into the shower,
feeling progressively more "out of it", my heart beating faster, starting to get
shaky and nervous. I got into the cold water but it didn't seem to cool me off
as much. I took my rectal temperature: 101.8F, I had reached the same
temperature as I did with 1200mg DNP, which wasn't extreme. Perhaps this
is what sort of triggered some panic within me. I was getting extremely
dizzy in the shower, wasn't able to think straight, my heart was pounding
out of my chest. I felt I might collapse any moment. Despite my best efforts
to stay calm, I was drifting into a panic attack. "This is impossible, this
amount is peanuts, if I actually die from this, I'd be the person who died
from the lowest amount, I'm a big dude, this shouldn't hit me so strong."
I took my nger pulse, it was 165bpm, the highest I had ever seen despite
taking Clen and T3 on previous cycles. I gured this is an electrolyte
problem, so I frantically go my bedroom, trying to stay focused and calm,
and pick up some magnesium pills and potassium pills. Took a few of them.
Now, whenever I encountered similar disturbances in my old cycle, I would
just have some powerade ready and my body absorbed it so quickly it
would provide super-fast relief. However, here is my fatal mistake. I forgot
to buy electrolytes from Costco. I gured I would have no need for them
during such a low-dose testing period. Stupid stupid stupid. I was drinking
3-5 gatorades during my previous cycles although I did so only because I
thought I was taking high amounts. Well, I then took .5mg of Xanax (which I
believe, was the true savior here. Had I not taken this, I might have
panicked so much I'd had made dumb decisions). All wet and still out the
shower, I blasted the A/C on max while standing in front of it. I put on a bag
of frozen vegetables on my chest and the fact that it didn't feel as cold as
I'd imagined made was frightening, I had never felt this way before, but I
tried to regain composure. "This can't happen with this little DNP, and it isn't
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even my rst time. I'll be ne". However, panic and regret started haunting
me, as I gured "This. This is exactly how people die from DNP. This kicked
harder than a fucking mule seemingly out of nowhere. This is what must
have happened to those who died from apparently low doses. This is
horrible".
During this time, I was scared that I might pass out or something or that a
heart problem may be triggered (I had experienced A-Fib in the past) so I
considered calling and ambulance. I actually told Alexa to call 911, and she
said she couldn't. I had no idea where my phone was. Despite this, the
Xanax helped me keep my mind under control. Little by little I started
feeling less panicky and my heart rate was dropping, which made me feel I
was gonna be ne. However the electrolyte problem was a big one. Yes I
took the mineral pills but how long will it take for my body to absorb? I
needed gatorade. I considered calling a family member (despite being
11pm) to bring me some from the store just to weather out this episode. I
felt like I really couldn't walk away from the AC or I'd start heating up like
crazy again, the AC was barely cooling me.
Eventually, my BPM lowered to the 120s and then 110s which gave me
tremendous peace of mind all while standing in front of the fan. I grabbed
my water and walked to the nearest 24hr store and picked up some
gatorade. I chugged 3 bottles and as usual, starting feeling good relief as
soon as I started drinking, placebo or not. Not to mention the heaps of
water I drank before getting to the gatorade. Came back and took my anal
temperature again which was now at 100.6F. After that, I tried to relax, and
nothing major happened. Thank fuck.
So, the takeaway? Well, as to how such a low dose in so little time could
have phased me so deeply tells me there likely are very different
pharmacokinetics with DNP that depend on the concentration taken.
In other words, some people might tolerate 33mg better of DNP with 67mg
of ller (like Taurine) in the pill, three times a day, rather than someone who
takes pure DNP (100mg with no ller, once a day). Same net amount,
taken in different concentrations. That's just a theory. Of course, this might
also prove that Electrolyte treatment is imperative in some people
regardless on how low the dose one might consider to be taking. Of course,
it is possible that the agricultural DNP had far, far less DNP than I thought
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(although I can assure you, from chemical and burn tests, that there was in
fact DNP in it, just unsure how much). Even if it were 10% DNP 90% ller,
at 1200mg that's still only 60mg more than what I was taking before, no
way it can trigger such a strong response. It just doesn't make sense. It
must be a different pharmacokinetic factor that happens when one does not
dilute the DNP.
You may believe I was an overreacting sissy, or that this was purely
anxiety-related and very little involvement from DNP's presence, but I can
assure you, all those scary stories I had heard from DNP overdosing
seemed to match what I was feeling. This is was something that I would not
wish on my worst enemy. As to whether or not I will try DNP again, I will
say, most likely no, for the time being. However...... I am thinking if I dilute
the DNP in 1 part DNP, 3 parts Taurine, I could severely minimize such a
sudden and unexpected event like this from happening again. Then I can
start with 200mg pills twice a day (which would actually be 50mg DNP/
150mg Taurine each). This should be a much safer alternative which after
at least a 2 week break I might consider. Also, the big takeaway from this is
ALWAYS HAVE EASILY ABSORBED ELECTROLYTES HANDY
regardless of the dose you are taking. This stuff can seriously mess up your
body during the time of its effects and if you nd yourself unprepared to
deal with them this can turn out to be a living nightmare. Again, I will
reiterate that all of this happened with a total dose of 300mg Pure DNP
spread out over the course of 2 days. Please be careful out there folks.
Please be aware that this is a monster of a substance, and I am very very
happy that I was prudent enough to have only taken small amounts. If I had
done something like starting off with 600mg/day, I could very well have
died, collapsed on the bathtub and had no one to take me to a hospital in
time before I cooked myself. It can happen at any dose, so if you still feel
like giving this substance a shot, please keep in mind everything I just
discussed and don't think that it can't happen to you.
Main takeaway points:
1. Dangerous reaction may happen at any dose, perhaps depending on the
type (concentration) of DNP you are taking. These can be such as
dehydration and electrolyte de ciency (which can severely affect your
heart, nerves, muscles and mind), so keep electrolytes handy always.
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2. The quality and concentration of your DNP may vary - greatly. Test out
your substance! If you obtain a source from a new vendor, try as small of
an amount as you can possibly take whilst taking all precautions: don't
start with stupid doses and be patient - if you have anxiety, keep a
benzo or similar substance nearby, I can very well tell the difference
between an anxiety attack from actually going up in a blaze as I did that
day. It can happen easier than you think!
3. Symptoms can be hard to identify and can come on suddenly. You may
not actually feel dehydrated, just a little thirsty, and just a little warm. If
you are about to venture with this compound, play it safe: drink as many
electrolyte drinks as you can in a day, drink ridiculous amounts of water
and have ice and frozen packs ready at all times. Also keep in mind a
bad diet (my cheat day for example) can trigger a strong reaction even
with low dosages.
Hope this helps everyone be aware and I'm open to any honest questions.
Please treat this substance with respect and never think you are above it. I
would not wish this experience to my worst enemy.
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Wasted First Cycle Cutting
Cycle Log
Testosterone E 250mg/ML Week 1 Started with 300mg/week in mind until I
got convinced by rude redditAors to up to 500mg/week. Also bought steroid
test kits to make sure all my test was real! Monday Feb-14 First injection 150mg Thursday Feb-17 150mg Felt increased anxiety, sleep was hard rst
night but then sleep became amazing rest of the week
Week 2 Upped it to 500mg/week Monday Feb-21 250mg Thursday Feb-24
250mg Sleep was decent but started having panic attacks about the littlest
things, started taking Arimidex 0.25mg ed after noticing sore/puffy Nipples.
Week 3 Switched it up to 250mg/e3d, so approximately running 583.3mg/
week now Sunday Feb-27 250mg Wednesday Mar-2 250mg Saturdayy
Marc-5 250mg Felt panicky occasionally but felt somewhat euphoric on
some days, so far has felt like an emotional rollercoaster and am not able
to fully determine whether e2 is too high or low will get blood work soon
though.
Week 4 Blood work came back as Total Test- 2287(ng/dl) Estradiol- 41(pg/
ml) PSA Total- 0.30 (ng/ml) Tuesday Mar-8 250mg .25mg of adex Friday
Mar-11 250mg No more adex unless I absolutely need it since my test to
estro ratio was 55:1 :(
Week 5 Monday Mar-14 250mg Not really feeling too much by now so
hoping week 6 will knock my socks off with results Thursday Mar-17 250mg
Week 6 Sunday Mar-20 250mg Monday Mar-21 Started taking 10mg of
Cardarine ed with 2250mg of L-carnitine ed (since it has a oral
bioavailability of ~15%) Wed Mar-23 250mg Saturday Mar-26 250mg
Started to feel major strength gains this week with going from 8 reps of 75
db bench to 8 reps of 85 on db bench
Week 7 Tuesday Mar-29 250mg So far feel the same as week 6 but still no
visible changes except some veins showing on biceps
Week 8 - 11 250mg e3d Added Anavar 30(rest days)-50 mg(training days)
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Week 12 Got bloods done with total test coming back at 1900 ng/dL so my
supply was underdosed so switched brands and increased dose to 125mg
Ed totaling at 875mg test a week
Week 13 125mg ed
Week 14- 125mg ed. nipples started getting out of control and been having
to take Nolva 10mg ed and 1mg of adex split into 3 doses throughout the
week. Never running high test again, too hard to control e2 but did give me
a nice look overall even though it was only 3ish weeks of high test.
Week 15 Dropped down to 200mg a week split on Mondays and
Thursday’s at 100mg x 2
Week 16 Overall highly disappointed with my rst teat cycle, my brand
could have been the factor that ruined it but overall was not impressed in
the slightest. Did gain some lean muscle as I was cutting during cycle while
yes probably should have bulked but was already too fat tbh. I look and feel
better so that’s all that matters, never got hungry at all though which is
surprising for a test cycle.
After cycle cruiseStarted cruise on week 15 and plan on cruising until next cycle in October/
November. As of right now it’s May 27 and I do have some 300 long cut
coming in which consists of 100mg test e, 100mg tren e, 100mg masteron.
I plan on starting this within next 2 weeks when it comes in and will be
taking half a mL Monday and another half Thursday with some extra test e
added in for a “cruise” at 200mg test e, 100mg tren e, 100mg masteron e
weekly for 6-8 weeks so try and get absolutely shredded before my
vacation this summer. For reference ending numbers before cruise,
physique are 6’2 220 15~17% bf
Edit: starting stats 6’2 237 22% bf Also I’ve been diagnosed as
hypogonadal and have had a test level of 360ish since I was 18 now 22
and have tried clomid but didn’t work, also I’ve cut all the way down to 170
before and bulked up to 237 and I’ve run many programs for strength
training and hypertrophy training so I DO KNOW HOW TO DIET AND
TRAIN, but thanks to being born with cesspool genetics I had to use test to
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actually gain muscle or at least keep it while I was cutting so consider this
before you go to heavy on roasting me plz also look at my before and after
photos and tell me if I still messed up this cycle completely??!? Here’s
before and after photos
https://imgur.com/a/IDkQvH5
Edit 2: after reading all of y’all’s encouraging comments I decided to hop on
test/tren/mast in a couple weeks. I will make a new post in 10 weeks from
now and I expect to hear all the lovely things you’ve said to me on here 10
Fold :)
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Frequently Asked Questions
(FAQ)
Compound Usage
How much weight can I expect to gain during my rst
cycle?
Provided dosing is suf cient, a steroid user can expect to make the most
signi cant progress during their rst cycle. Although this will vary from
person to person, it is not uncommon for someone to gain 20 pounds of
weight or more during a rst cycle of AAS use. Some of this may be water
retention, although a solid gain of more than 10-15 pounds of muscle mass
is possible.
Are the gains from steroid use temporary?
Yes, and no. Steroids can help you do two basic things with regard to
muscle growth. First, they can allow you to more rapidly reach your genetic
limits for muscle growth. Provided you continue to train actively, eat
properly, and use an effective PCT program, you should be able to maintain
at your genetic limit inde nitely. So in this regard, the early gains do not
have to be temporary.
Later, steroids can allow you to push well beyond your genetic limits. It is
important to emphasize this, as extreme physical development cannot be
maintained long-term without the repeat administration of anabolic
substances. The body will always revert back towards its normal metabolic
limits once AAS are removed. In this context, some of the gains will not be
permanent.
Steroids do permanently alter the physiology of your muscles by adding
more cellular nuclei. With higher nuclei content, each muscle cell can
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manage its volume more ef ciently, which allows more rapid expansion.
Even after a long period of complete abstinence from training and AAS, the
nuclei remain. This may provide a “muscle memory” effect, allowing you to
reach your genetic limit (perhaps a slightly extended limit) faster than if you
had never used AAS in the past. So in this regard, there are lasting bene ts
beyond the temporary increase in muscle size itself.
Can steroids make me look like a professional
bodybuilder?
If you have the underlying genetics to allow for this extreme muscle growth,
this may be possible with a lot of hard work and dedication. Genetics are a
big factor in determining the ultimate limits to your physique, even in an
enhanced state. Many people use steroids and look very big and
impressive because of it, but very few users are able to make it to the stage
of a professional bodybuilding show.
How dangerous is an isolated cycle of steroids?
Anabolic/androgenic steroids are among the safest drugs available, at least
in a short-term sense. Fatal overdose is not reasonably possible, and the
negative health changes such as alterations in cholesterol, blood pressure,
hematocrit, and blood clotting (among other things) are very unlikely to
manifest in serious bodily harm or death after an isolated cycle. There are
rare deaths from such things as stroke and liver cancer in short-term
abusers, but such occurrences are statistically extremely rare in light of the
millions of people that use these drugs. If you had to comparatively rate the
acute risks of AAS abuse, they would be slightly higher than marijuana, but
far less than virtually all other illicit narcotics.
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How dangerous is long-term steroid use?
The long-term use of steroids for non-medical reasons can be a unhealthy
practice. It has been dif cult, however, to quantify the exact risk. The main
issue is the fact that AAS abuse can promote heart disease, the number
one killer of men. Heart disease is a slow progressive disease, which may
build for decades without symptoms. Steroid abuse may accelerate the
silent process of plaque deposition in the arteries, and also induce other
changes in the cardiovascular system that can increase susceptibility to
stroke or heart attack. If death nally occurs, however, it will be dif cult for a
medical examiner to pinpoint AAS as the cause; too many variables play a
role in the etiology of cardiovascular disease. The vast majority of deaths
where AAS have contributed go unreported for this reason. The exact
mortality rates of long-term steroid abusers have, likewise, been dif cult to
calculate. It is especially important to closely monitor cardiovascular
disease and other health risk factors if long-term steroid use is a practice
you will follow.
Can steroids be used to enhance an athletic career
safely?
The non-medical use of AAS by de nition cannot be de ned as a safe
practice. However, it can be argued that anabolic/androgenic steroids can
be used with high relative safety, even over a period of many years. The
guidelines of steroid harm reduction are important to minimizing the
negative health effects of these drugs. Provided an individual follows these
guidelines and is careful with drug selection, dosages, and durations of
intake, follows a diet low in saturated fats, cholesterol, sugar, and re ned
carbohydrates, actively trains with both resistance and cardiovascular
exercise, and uses cholesterol support supplements such as sh oils and
others during all cycles, it may be dif cult in many cases to argue high
tangible health risks. It takes a great deal of involvement and planning to
use AAS in this manner, which is always advised.
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Testosterone, whatever the form, tends to be the safest steroid for men.
When the dose remains within the moderately supratherapeutic range,
alterations in cardiovascular risks factors are noticed, but not extreme.
Some of this has to do with the bene cial cardiovascular effects of estrogen
in men.
What steroids will not cause hair loss?
For those with a genetic predisposition to hair loss, all anabolic/androgenic
steroids are capable of accelerating the process. Slowing the onset of this
during AAS use requires a focus on reducing relative androgenicity in the
scalp. This can be accomplished with the use of predominantly anabolic
drugs. Alternately, moderate doses of testosterone can be used with
nasteride, a drug that reduces DHT conversion (and androgenic
ampli cation) in the scalp. Still, those genetically prone to hair loss can
have problems with any steroid, and are always advised to limit dosing,
drug intake durations, and monitor effects on the hairline closely.
What are the safest steroids for women?
Women are generally most concerned h the virilizing (masculinizing) effects
of anabolic/androgenic steroids.
The least virilizing agents are not in any way whatsoever those with the
highest relative anabolic to androgenic effect, such as nandrolone,
oxandrolone, turinabol, and methenolone. Anabolic/Androgenic ratios, while
a useful measure to scientists, have little to no carryover in terms of
virilization potential in women. In fact, nandrolone—despite having an
androgenic rating of only 37—is extremely virilizing in women.”
Care must always be taken, as all AAS are based on male sex steroids,
and as such they can cause masculinizing effects in women.
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What are the safest steroids for men?
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Do androgen receptors down-regulate?
Conclusions from Scienti c Research
There is no scienti c evidence to support the popular view that AAS use
might be expected to result in downregulation of the AR relative to receptor
levels associated with normal androgen levels.
Conclusions from Bodybuilding Observations
While there are no studies showing downregulation in human skeletal
muscle resulting from high-dose AAS use, there are some studies in cell
culture, and sometimes in vivo, which seem to indicate that downregulation
can occur, though not as a result of increase in androgen from normal to
supraphysiological.
All of these studies, however, are awed from the perspective of the
bodybuilder wishing to know if downregulation of the AR has ever been
observed in any cell in response to increase of androgen from normal to
supranormal levels.
Upregulation in human muscle tissue, in vivo, is not directly proven but
seems to t the evidence and to provide a plausible explanation for
observed results.
Is there a limit to how muscular someone can get with
unlimited gear?
Yes, myostatin inhibits extremely large growth in humans. It is speculated
that some of the biggest bodybuilders have mutations that cause them to
produce very low levels of myostatin. Read more here.
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What do the anabolic and androgenic reference
numbers under the pro le for each steroid mean?
These numbers come from early studies measuring the effect of each
steroid on certain muscle and sex organ tissues of animals, usually mice.
These numbers are useful for assessing the relative anabolic to androgenic
balance of each drug in humans. They are not as accurate at assessing the
total muscle building potential of each steroid, however, and should not be
taken as absolute ratings of potency.
Can I just do a oral only cycle?
You can. Should you? Probably not. Oral steroids are still going to suppress
your natural Test pretty hard. You may nd you don't feel the best or
symptoms of low testosterone. if you choose to do a oral only cycle, you
should still look into getting a SERM (like Nolvadex/Clomid or the sorts)
for a proper PCT, as well. You should consider reading through this Wiki
and potentially consider doing a real cycle, complete with Testosterone, as
you'll nd better results, as well as feeling better overall too.
What about just a Prohormone or Designer Steroid
cycle?
Again. You can. Should you? Probably not. Prohormones & Designer
Steroids are going to suppress your natural Test pretty hard. You may nd
you don't feel the best or symptoms of low testosterone. Prohormones &
Designer Steroids are no better (or even worse in some cases) than using
a traditional oral steroid. The supplemental PCT crap they sell with these
Prohormones / Designer Steroids is predominantly bogus stuff and if you
choose to do a Prohormone / Designer Steroid cycle, you should at least
look into getting a SERM (like Nolvadex/Clomid or the sorts) for a real PCT.
You should consider reading through this Wiki and potentially consider
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doing a real cycle, complete with Testosterone, as you'll nd better results,
as well as feeling better overall too.
Compound Handling and Mixing
How Do I Mix And Run My HCG?
Mixing 2ml bac water with 5000iu hCG will provide 250iu for every tenth of
a ml/cc. This will provide you 20 250iu hCG doses.
Generally hCG will come with a vial of lyophilized powder and an ampule of
either sodium chloride solution or bacteriostatic water. You want the
bacteriostatic water. Bac water is intended for multiple uses and will inhibit
bacteria growth. The sodium chloride solution is intended for female fertility
use purposes and is to be used in a single injection. If used over multiple
injections it may begin to grow bacteria.
When you check your vial of lyophilized hCG it will generally be 5000 IU,
although it can come in other amounts.
Using 5000 IU as the most common example; if you take 2mL of Bac Water
and inject that slowly into your vial of 5000 IU hCG, you then have 250 IU
per tenth of a mL (cc). So every tenth of your 1mL insulin syringe would be
250 IU.
The other form hCG might come in is a liquid form. This is hCG in a
solution with a preservative to keep it active. You may add bacteriostatic
water to this in order to adjust your dosage if you need.
In either case, hCG should be kept in the refrigerator after reconstitution to
preserve its shelf life. It should be refrigerated within 72 hours of mixing it
with bac water. hCG should be good for around 60 days when refrigerated.
After that time it will lose potency at about ten percent per week as time
goes on.
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Answer: Gear can crash due to storing the product in colder than
recommended temperatures (or in shipment)…or because the ratio of AAS
to oil is out of balance (this can be either a manufacturer error or a personal
error if home brewing). This does not damage the steroid. In order to
correct the problem, simply run the vial under warm water until the products
reverts back to its normal state. Clean with alcohol swab after drying off.
My Gear Has Particles Floating In It?
Answer: You can choose to either dispose of the product or you can relter it by using a Whatman lter. While opinions will differ on this subject,
the opinion of re- ltering is still available and a suitable solution in many
cases, assuming the product is not badly polluted. In cases where it is
apparent that the product is very poor quality and contains a large amount
of foreign material, it would be wise to dispose of the product. This should
not occur with reputable UGL’s and will never occur with Pharm-grade
versions, although an occasional speck may occur with UGL products here
and there and is usually not a big deal.
I need to travel during my cycle/blast/cruise. What do?
Answer: A solution would be to switch over to testosterone Undecanoate.
With a half life of 20 days, it makes for an excellent and risk free choice.
You could also frontload your choice of cypionate/enanthate ester for a
shorted trip. Use Steroid Planner to plan it out. However, the rapidly
dropping levels of this choice make it dif cult to manage estrogen properly.
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Cycle Complications
When I go to donate blood they ask about steroid use.
Am I possibly harming someone else?
The primary concerns for steroid users giving blood are infectious disease
transmission. Given that users self-administer injections there is a concern
about knowledge of proper needle handling and use. People with HIV /
AIDS or Hepatitis should not give blood.
Reference
I got sick while on cycle. What do?
Assuming it's not just "Test Flu", you have two choices. Cruise on a low
dose or PCT. Of course a lot of factors play in with if you got sick near the
beginning, in the middle, or near the end. In the beginning most will opt to
cruise instead of "PCT-ing" so early. In the middle most will opt to cruise
instead of "PCT-ing" and cutting the cycle so short. Near the end can be
tricky. Most still choose to cruise and potentially extend the cycle longer
than originally intended, but if it's really close to the end some may choose
just to go ahead and PCT. Obviously this all depends on the severity of
your illness. Also if it's something that you'll get over within a week, most
will just continue their dosages as normal.
I'm getting unbearable back / shin / calf / etc. pumps.
What can I do?
The rst line of action should be:
• Taurine (3-10g pre-workout, you may also add 3-5g AM/PM depending
on when you workout)
• Magnesium (200-500mg pre-workout, you may also add 200-500mg AM/
PM depending on when you workout)
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• Potassium (200-300mg pre-workout, you may also add 200-500mg AM/
PM depending on when you workout)
• Upping your water intake (1-2 gallons ED)
If none of this helps, anecdotally, Cialis (10-15mg ED) has been known to
help.
Injecting
My Injection Spot Is Red, Itchy, Or Sore?
Answer: Get to a doctor for some antibiotics if it is red, itchy, or hot. If it is
simply sore and/or swollen it is probably going to be okay see: Post
Injection Pain (PIP). If in doubt, get some antibiotics; a common thing to
tell your doctor is that you injected B12.
Is It Normal To Bleed After An Injection?”
Answer: Yes, it is common to occasionally nick a vein close to the surface
of the injection site, which will cause blood to leak from the surface. The
amount of blood which can seep from an injection site can be anywhere
from a drop or two, to a very light stream which slowly ows down that body
part. Even in the event a larger vein is hit when doing an injection, this type
of bleeding is relatively easy to stop and will not pose any harm to the
individual.
Is Aspirating Required?
Answer: Many AAS users do not aspirate when injecting. It is considered a
bit of an out-dated methodology, but it never hurts to do it.
According to the CDC:
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Aspiration - Aspiration is the process of pulling back on the plunger of
the syringe prior to injection to ensure that the medication is not injected
into a blood vessel. Although this practice is advocated by some experts,
the procedure is not required because no large blood vessels exist at
the recommended injection sites."
STTI International Nursing Research Congress Vancouver, July 2009:
"Aspiration is not indicated for SC injections."
"Aspiration is not indicated for IM injections."
Organizations which state aspiration is not necessary:
• Centers for Disease Control (CDC)
• Advisory Committee on Immunization Practices (ACIP)
• Department of Health Services (DHS)
• American Academy of Family Physicians (AAFP)
• U.K. Department of Health (DoH)
• World Health Organization (WHO)
References located at the bottom of the page.
Does Injecting Build Up Scar Tissue?
Answer: Yes, repeated Intramuscular injections can cause the muscle to
build up scar tissue. Generally there is no in ammation or inclusion in the
tissue. In an effort to minimize scar tissue build up, users will rotate through
many injection sites. If you're interested, here is a case study of a
woman in an extreme case, it includes stained muscle biopsies
How Do I Open Ampules?
Answer: Ampules can be aided in opening by scoring (some ampules
come pre-scored). Scoring is a process in which in a ne line is ground
away around the neck of the ampule. Scoring makes it much easier to snap
the top of the ampule off without breaking the vial and spilling the oil.
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Normally, a scoring tool is used for this process, although sometimes
knives or other objects can be used.
An amp opener can be used, which is the fastest and the least time
consuming methods.
If you don't have an ampule opener. Grasp the ampule between thumb and
fore nger of one hand. Move liquid from the neck to the body of the ampule
by tapping (thumping) the ampule sharply. Using gauze pad (or similar),
grasp stem (the part above the neck) with other hand. Break stem away
from you and discard safely. This is a very helpful video that shows the
process
Lastly, the tape-method can be employed, as well. The tape method
involves taping the entire vial all the way up to the neck line. Several layers
of tape should surround the vial, so that it is properly secured. The point of
taping the vial is two-fold. One purpose is to prevent the contents of the
ampule from spilling, should the ampule break somewhere other than the
neckline. The other purpose is to reinforce the ampule, so that it is more
likely to break at the neckline. One can combine both the tape method and
the scoring, which is the best way to ensure that the oil contained in the
ampule will not be spilled.
Can I Re-Use Syringes?
Answer: Absolutely not. You should never take a needle which has entered
the body and re-insert it back into a steroid product, as this can result in
bacteria build-up and cause potential future infections.
How Fast Should I Inject?
Answer: As a general rule, 30 seconds per mL/cc.
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Is It Dangerous To Inject Small Air Bubbles?”
Answer: No, a small amount of air will do no harm. Air bubbles injected
into muscle tissue is of no concern. Even if the individual were to thread a
vein and inject the entire contents of the syringe into the vein, the small air
bubbles contained within it would be the least of that person’s worries. In
reality, several cc’s of air would have to be injected directly into a vein all at
once, in order to cause cardiac arrest. Even injecting 2-3 cc’s of air directly
into a muscle would be largely inconsequential. Of course, such an action
is not recommended, but you get the point.
Ancillaries
Q: Can Nolvadex (Tamoxifene) and Arimidex
(Anastrozole) be used together?
A: Yes, they can when needed. Taking Arimidex with Nolvadex decreases
the serum concentration of anastrozole by 27%, but has no effect on the
pharmacodynamics of either
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362190/
In conclusion, the results of this study con rm that anastrozole does not
affect the pharmacokinetics of tamoxifen when the two drugs are given
in combination to post-menopausal women with early breast cancer. In
addition, the oestradiol suppressant effects of anastrozole appear
unaffected by tamoxifen.
http://publications.icr.ac.uk/629/
As a result of (a) the lack of effect of anastrozole on tamoxifen and DMT
levels and (b) the observed fall in blood anastrozole levels having no
signi cant effect on oestradiol suppression by anastrozole, we conclude
that the observed reduction in anastrozole levels by tamoxifen is unlikely
to be of clinical signi cance when anastrozole and tamoxifen are
administered together.
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The actual ATAC trial that this information comes from. Pharmacokinetic
details can be found here
http://www.nature.com/bjc/journal/v85/n3/pdf/6691925a.pdf
"...the observed fall in blood anastrozole levels having no signi cant
effect on oestradiol suppression by anastrozole, we conclude that the
observed reduction in anastrozole levels by tamoxifen is unlikely to be of
clinical signi cance when anastrozole and tamoxifen are administered
together.”*
Q: Can Nolvadex (Tamoxifene) and Letrozole be used
together?
A: Yes, they can when needed. Just be aware that taking Letrozole with
Nolvadex decreases the serum concentration of Letrozole by 35-40%.
https://pdfs.semanticscholar.org/e492/
c9fb67a771779ac3be19faf14ea3b458e03a.pdf
Pharmacokinetic analyses of the combination of tamoxifen and letrozole
have revealed that these drugs interact, resulting in letrozole
concentrations approximately 35-40% lower than when letrozole is used
alone.
...
...letrozole has no impact on tamoxifen concentrations.
Q: Does Aromasin need to be taken with fat?
A: It works better when taken with a high fatty meal, yes.
http://www.rxlist.com/aromasin-drug.htm
Exemestane is freely soluble in N, N-dimethylformamide, soluble in
methanol, and practically insoluble in water
http://www.rxlist.com/aromasin-drug/indications-dosage.htm
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the recommended dose of AROMASIN is 50 mg once daily after a meal.
http://www.drugs.com/monograph/aromasin.html
High-fat meal increases plasma exemestane concentrations by
approximately 40%.
http://labeling.p zer.com/showlabeling.aspx?id=523
Absorption: Following oral administration of radiolabeled exemestane, at
least 42% of radioactivity was absorbed from the gastrointestinal tract.
Exemestane plasma levels increased by approximately 40% after a
high-fat breakfast.
http://www.drugs.com/monograph/aromasin.html
Dosages >25 mg daily not shown to provide substantially greater
suppression of plasma estrogens but may increase adverse effects
HGH
Does using HGH shut down natural HGH production?
Answer:
The mechanism by which chronic exposure to hGH leads to tolerance,
dependence, and a withdrawal syndrome is unclear and does not
involve the suppression of hormone secretion. During the nadir of
growth velocity, which follows the withdrawal of prolonged drug therapy,
serum GH levels remain normal, as do serum IGF-I and IGF-binding
protein-3 levels (4). Moreover, endogenous pulsatile secretion of GH
resumes within days even after long-term hGH therapy (7).
http://press.endocrine.org/doi/full/10.1210/jcem.87.8.8721
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General
Does ejaculation reduce my testosterone levels?
Temporarily, yes, it does. However, not ejaculating will eventually decrease
the levels even more. For peak levels, only ejaculate every seven days.
A research on the relationship between ejaculation and serum
testosterone level in men.
http://www.ncbi.nlm.nih.gov/pubmed/12659241
The purpose of this study is to gain understanding of the relationship
between ejaculation and serum testosterone level in men. The serum
testosterone concentrations of 28 volunteers were investigated daily
during abstinence periods after ejaculation for two phases. The authors
found that the uctuations of testosterone levels from the 2nd to 5th day
of abstinence were minimal. On the 7th day of abstinence, however, a
clear peak of serum testosterone appeared, reaching 145.7% of the
baseline ( P < 0.01). No regular uctuation was observed following
continuous abstinence after the peak. Ejaculation is the precondition and
beginning of the special periodic serum testosterone level variations,
which would not occur without ejaculation. The results showed that
ejaculation-caused variations were characterized by a peak on the 7th
day of abstinence; and that the effective time of an ejaculation is 7 days
minimum. These data are the rst to document the phenomenon of the
periodic change in serum testosterone level; the correlation between
ejaculation and periodic change in the serum testosterone level, and the
pattern and characteristics of the periodic change.
Are American military personnel tested for steroids?
Steroids are not part of the standard drug panel. However, users should be
aware that their superiors have the ability to order steroid-speci c testing if
an individual is suspected of using. PCT drugs will also not appear on the
test.
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hGH: It is very likely that it can and will with prolonged usage.
Effect of human growth hormone therapy on penile and testicular size
in boys with isolated growth hormone de ciency: rst year of
treatment.
http://www.ncbi.nlm.nih.gov/pubmed/6406387
The response of genital and gonadal growth during the rst year of
treatment with human growth hormone (hGH) was studied in 20 boys
with isolated growth hormone de ciency (IGHD) (11 of hereditary origin
and 9 sporadic cases). Prior to hGH treatment, 13 of the 15 prepubertal
boys had a penis length below the normal mean, 3 of which were more
than 2 SDS below the mean. The boys with hereditary IGHD had a
greater de cit in penile size than did the sporadic cases. hGH treatment
improved the penile length in all but two boys aged 14 and 15 yr, and led
to growth up to normal size in the three boys with very small penises.
Three of the hereditary IGHD patients had subnormal testes and all of
the other prepubertal boys had a testicular volume in the normal range.
hGH treatment increased testicular size, particularly in the prepubertal
boys. Of three additional untreated adults with IGHD, one had a
subnormal-size penis and two had penises of low-normal size. Our
ndings constitute further evidence that hGH de ciency is associated
with decreased penile growth and, to some extent, decreased testicular
size, and that hHG treatment improves the growth of the genitalia and
gonads. Since these effects were also observed in prepuberty, it seems
that not all the hGH or, rather, somatomedin effect on sex organs is
androgen mediated.
Testosterone: There is evidence that in infants and young children that it
can increase size.
Congenital hypogonadotropic hypogonadism and micropenis: effect
of testosterone treatment on adult penile size why sex reversal is not
indicated.
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Can steroids increase the size of my penis?
http://www.ncbi.nlm.nih.gov/pubmed/10228293
Micropenis is commonly due to fetal testosterone de ciency. The clinical
management of this form of micropenis has been contentious, with
disagreement about the capacity of testosterone treatment to induce a
functionally adequate adult penis. As a consequence, some clinicians
recommend sex reversal of affected male infants. We studied 8 male
subjects with micropenis secondary to congenital pituitary gonadotropin
de ciency from infancy or childhood to maturity (ages 18 to 27 years).
Four patients were treated with testosterone before 2 years of age
(group I) and four between age 6 and 13 years (group II). At
presentation, the mean penile length in group I was 1.1 cm (-4 SD;
range, 0.5 to 1.5 cm) and in group II it was 2.7 cm (-3.4 SD; range, 1.5
to 3.5 cm). All patients received one or more courses of 3 intramuscular
injections of testosterone enanthate (25 or 50 mg) at 4-week intervals in
infancy or childhood. At the age of puberty the dose was gradually
increased to 200 mg monthly and later to an adult replacement regimen.
As adults, both group I and II had attained a mean nal penile length of
10.3 cm 2.7 cm with a range of 8 to 14 cm (mean adult stretched penile
length for Caucasians is 12.4 2.7 cm). Six of 8 men were sexually active,
and all reported normal male gender identity and psychosocial behavior.
We conclude that 1 or 2 short courses of testosterone therapy in infancy
and childhood augment penile size into the normal range for age in boys
with micropenis secondary to fetal testosterone de ciency; replacement
therapy at the age of puberty results in an adult size penis within 2 SD of
the mean. We found no clinical, psychologic, or physiologic indications
to support conversion of affected male infants to girls. Further, the
results of this study do not support the notion, derived from data in the
rat, that testosterone treatment in infancy or childhood impairs penile
growth in adolescence and compromises adult penile length.
Role of parenteral testosterone in hypospadias: A study from a
teaching hospital in India
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183705/
Additionally, a father decided to treat his infant son with Testosterone for
increased penis size.
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Are fat cells ever lost?
The number of fat cells in your body is set in childhood and early
adolescence. Those fat cells will shrink or expand to hold more fat as
required.
http://www.ncbi.nlm.nih.gov/pubmed/18454136
Obesity is increasing in an epidemic manner in most countries and
constitutes a public health problem by enhancing the risk for
cardiovascular disease and metabolic disorders such as type 2 diabetes.
Owing to the increase in obesity, life expectancy may start to decrease
in developed countries for the rst time in recent history. The factors
determining fat mass in adult humans are not fully understood, but
increased lipid storage in already developed fat cells (adipocytes) is
thought to be most important. Here we show that adipocyte number is a
major determinant for the fat mass in adults. However, the number of fat
cells stays constant in adulthood in lean and obese individuals, even
after marked weight loss, indicating that the number of adipocytes is set
during childhood and adolescence. To establish the dynamics within the
stable population of adipocytes in adults, we have measured adipocyte
turnover by analysing the integration of 14C derived from nuclear bomb
tests in genomic DNA. Approximately 10% of fat cells are renewed
annually at all adult ages and levels of body mass index. Neither
adipocyte death nor generation rate is altered in early onset obesity,
suggesting a tight regulation of fat cell number in this condition during
adulthood. The high turnover of adipocytes establishes a new
therapeutic target for pharmacological intervention in obesity.
Why do steroids make your traps and shoulders pop
out that much?
There are more androgen receptors in those areas. Related study.
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Medicinal Use of AAS
Due to the culturally engrained stereotype of AAS use, medicinal use of
AAS has just recently began to be investigated. This page seeks to
document areas where AAS may be bene cial to patients with disease.
Anxiety
There is a large amount of anecdotal evidence that increased
Testosterone levels can assist with anxiety relief.
Cerebral Palsy
Consensus seems to be forming that hGH is bene cial for use for Cerebal
Palsy patients.
Is treatment with growth hormone effective in children with cerebral
palsy?
Dev Med Child Neurol. 2004 Aug;46(8):569-71.
http://www.ncbi.nlm.nih.gov/pubmed/15287249
Children with cerebral palsy (CP) often have poor linear growth during
childhood, resulting in a diminished nal adult height. Here we report a
female with CP and short stature but without growth hormone (GH)
de ciency who exhibited increased growth during treatment with GH.
We also report two other children with CP who were treated with GH:
one female with a history of leukemia, and a male with Klinefelter
syndrome. These two children were both found to be GH-de cient by
insulin provocative GH testing and responded to treatment with
increased growth rate. Growth improved to a greater extent in the two
children with apparent GH de ciency. In summary, it is felt that GH
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therapy might be bene cial for children with CP and warrants further
investigation. Growth hormone de ciency in two children with
cerebral palsy.
Dev Med Child Neurol. 1995 Nov;37(11):1013-5.
http://www.ncbi.nlm.nih.gov/pubmed/8566448
The authors describe two children with cerebral palsy and linear growth
failure secondary to growth hormone de ciency. One of the children was
successfully treated with growth hormone replacement therapy. His
linear growth velocity increased from 3cm/year before therapy to 8.3 cm/
year during the rst two years of therapy. Potential complications such
as worsening orthopedic status did not occur. Psychosocial bene ts
were noted. The authors conclude that growth hormone de ciency may
play a role in linear growth failure in some children with cerebral palsy
and that some of these children may bene t from growth hormone
therapy.
Growth hormone de ciency and cerebral palsy
http://www.dovepress.com/articles.php?article_id=5238
Cerebral palsy (CP) is a catastrophic acquired disease, occurring during
development of the fetal or infant brain. It mainly affects the motor
control centres of the developing brain, but can also affect cognitive
functions, and is usually accompanied by a cohort of symptoms
including lack of communication, epilepsy, and alterations in behavior.
Most children with cerebral palsy exhibit a short stature, progressively
declining from birth to puberty. We tested here whether this lack of
normal growth might be due to an impaired or de cient growth hormone
(GH) secretion. Our study sample comprised 46 CP children, of which
28 were male and 18 were female, aged between 3 and 11. Data
obtained show that 70% of these children lack normal GH secretion. We
conclude that GH replacement therapy should be implemented early for
CP children, not only to allow them to achieve a normal height, but also
because of the known neurotrophic effects of the hormone, perhaps
allowing for the correction of some of the common disabilities
experienced by CP children.
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Growth Hormone Therapy Improves Bone Mineral Density in Children
with Cerebral Palsy: A Preliminary Pilot Study
http://press.endocrine.org/doi/full/10.1210/jc.2006-0385
Context: Cerebral palsy is associated with osteopenia, increased
fracture risk, short stature, and decreased muscle mass, whereas GH
therapy is associated with increased bone mineral density (BMD) and
linear growth and improvement in body composition. Objective: We
conducted a pilot study to evaluate the effect of 18 months of GH
therapy on spinal BMD, linear growth, biochemical markers, and
functional measures in children with cerebral palsy.
Design and Setting: The study was a randomized control trial,
conducted from 2002–2005 at the University of California, Los Angeles,
Orthopedic Hospital’s Center for Cerebral Palsy.
Patients: Patients included 12 males with cerebral palsy, ages 4.5–15.4
yr. Intervention: We compared 18 months of GH (50 μg daily) vs. no
treatment. Primary Outcome Measures: Spinal BMD (dual-energy x-ray
absorptiometry scan), height, growth factors, and bone markers were
assessed.
Results: Ten subjects ( ve in each group) completed the study. Preand post-average height z-scores were −1.47 ± 0.23 and 0.8 ± 0.2 (GHtreated group) vs. −1.35 ± 1.26 and −1.36 ± 1.27 (control group) (Δ sd
score, 0.67 vs. −0.01; P = 0.01). Average change in spinal BMD z-score
(Δ sd score corrected for height) was 1.169 ± 0.614 vs. 0.24 ± 0.25 in
the treated and control groups, respectively (P = 0.03). Osteocalcin,
IGF-I, and IGF-binding protein 3 levels increased during GH therapy.
There was no change in quality of life scores as measured by the
Pediatric Orthopedic Disability Inventory.
Conclusions: This small pilot study suggests that 18 months of GH
therapy is associated with statistically signi cant improvement in spinal
BMD and linear growth.
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Collagen Synthesis
Testosterone decreases collagen synthesis, reducing the strength, exibility
and structural integrity of skin and joints. There are ways to mitigate this.
Boldenone (Equipoise), Methenolone (Primobolan), Nandrolone (Deca),
oxandrolone (Anavar) and human growth hormone (hGH) each enhance
collagen synthesis, which helps to offset testosterone's negative impact.
Options
Procollagen III is a primary indicator used to determine the rate of collagen
synthesis:
• Boldenone at 3 mg/kg increases procollagen III by
approximately 340% within one week.
• Nandrolone at 3 mg/kg a week increases procollagen III
levels by 270%.
• Primobolan at 5 mg/kg increases collagen synthesis by ~180%.
• HGH at 6 iu/day increases the collagen deposition rate by
around 250% in damaged collagen structures.
• Stanozolol boosts collagen production 40340-9/full) and
mRNA.
• Anavar is prescribed post-surgery and has hundreds of
scienti c studies demonstrating increased collagen synthesis,
accelerated wound healing and enhanced recovery.
• Estrogen plays an integral role in keeping tendons and joints
strong.
COPD
It doesn't appear that AAS are effective for COPD.
http://www.ncbi.nlm.nih.gov/pubmed/18684793
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Patients with severe chronic obstructive pulmonary disease (COPD)
commonly develop weight loss, muscle wasting, and consequently poor
survival. Nutritional supplementation and anabolic steroids increase lean
body mass, improve muscle strength, and survival in patients enrolled in
comprehensive rehabilitation programs. Whether anabolic steroids are
effective outside an intensive rehabilitation program is not known. We
conducted a prospective, double-blind, placebo-controlled, 16-week trial
to study the bene ts of anabolic steroids in patients with severe COPD
who did not participate in a structured rehabilitation program. Biweekly
intramuscular injections of either the drug (nandrolone decanoate) or
placebo were administered. Sixteen patients with severe COPD were
randomized to either placebo or nandrolone decanoate. The placebo
group weighed 55.32 +/- 11.33 kg at baseline and 54.15 +/- 10.80 kg at
16 weeks; the treatment group weighed 68.80 +/- 6.58 at baseline and
67.92 +/- 6.73 at 16 weeks. Lean body mass remained unchanged, 71
+/- 6 vs. 71 +/- 7 kg in placebo group and 67 +/- 7 vs. 67 +/- 7 in
treatment group, at baseline and 16 weeks respectively. The distance
walked on 6 min was unchanged at baseline, 8 weeks, and 16 weeks in
placebo (291.17 +/- 134.83, 282.42 +/- 115.39, 286.00 +/- 82.63 m) and
treatment groups (336.13 +/- 127.59, 364.83 +/- 146.99, 327.00 +/173.73 m). No improvement occurred in forced expiratory volume in one
second, forced vital capacity, maximal inspiratory pressure, maximal
expiratory pressure, VO(2) max or 6-min walk distance or health related
quality of life. Administration of anabolic steroids (nandrolone
decanoate) outside a dedicated rehabilitation program did not lead to
either weight gain, improvement in physiological function, or better
quality of life in patients with severe COPD.
Cystic Fibrosis
This thread has some information
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Hepatitis C
Sexual dysfunction in males with chronic hepatitis C and antiviral
therapy: interferon-induced functional androgen de ciency or
depression?
Hypogonadism
See Testosterone Replacement Therapy (TRT)
Immune therapy
http://www.medibolics.com/litref2.htm
Multiple Sclerosis
Not to be confused with glucocorticoid use to treat in ammation produced
by MS, anabolic steroids also can play a role.
Users Letter
Dr. Terry Wahls discusses dietary treatment of MS in a TED Talk.
Need access to these:
The treatment of multiple sclerosis with anabolic steroids
Results of combined administration of anabolis steroids in patients
with multiple sclerosis
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Post Traumatic Stress Disorder (PTSD)
Joe Rogan Experience #574 - Dr. Mark Gordon, Matthew Gosney &
Jason Hall (TL;DW - Doctor is treating PTSD patients with hormone
therapy) - [139:56]
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Safe Injections
Injection Methods
• Intramuscular injection: An injection into muscle tissue.
• Subcutaneous injection: An injection into the region between
the skin and the muscle, also known as a “SubQ” injection.
AS far as performance enhancement is concerned, there are two primary
injection methods. These are the intramuscular injection method and the
subcutaneous injection method. An intramuscular injection is exactly as it
sounds; it is an injection given directly into a muscle. A subcutaneous
injection is an injection which is placed between the skin and the muscle.
Which method is utilized will depend on the drug being administered and
the goals & preferences of the user. The overwhelming majority of
individuals choose to administer their AAS by way of IM (intramuscular)
injection, although they can be injected subcutaneously, if desired, although
it is not recommended to inject over ½ cc/mL of AAS. HGH, Insulin, HCG,
and Peptides) are typically administered subcutaneously.
The Injection
The injection process itself is relatively straightforward. Perhaps nothing
causes more anxiety for AAS users than their rst injection. This fear is far
more psychological than physical, as the act of performing an injection,
especially when utilizing proper technique and the correct pin size, can be
relatively painless. Some muscle groups are more prone to causing
discomfort than others and the possibility of hitting a nerve, scar tissue, or a
sore spot is a reality, but in general, an injection should not be considered a
“painful” experience. With the information presented in this document, you
have been presented with everything you need to know in order to properly
perform an injection. For an abbreviated step-by-step walk through, see
Safe Injection Technique.
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Types Of Syringes
For a beginner, the many different types of syringes and their associated
terminology can be confusing. Let us look at these differences which de ne
the various types of syringes. Generally, syringes are de ned by the
following 3 things: Gauge size, how many cc’s a syringe can hold, and
needle length. By learning what these things mean, you will have no
problem selecting the appropriate syringe for your needs.
You may have heard of a syringe type known as an “insulin syringe” or "slin
pin." Regardless of whether a syringe is classi ed as an insulin syringe or
not, ALL syringes, including insulin syringes, are categorized by the 3
variables listed above. Insulin syringes are named as such due to the
original purpose for which they were produced, which was to administer
insulin to diabetics. Because diabetics will often need to perform multiple
daily injections into the SubQ region, a smaller & shorter needed was
needed in order to increase patient compliance through more tolerable, and
relatively painless, injections.
The 3 Variables
• Gauge: The gauge of the syringe refers only to the thickness of
the needle itself. The lower the gauge number, the thicker the
needle. The higher the gauge number, the thinner the needle.
• CC: A cc refers only to how much volume a syringe can hold.
The average syringe will hold anywhere between 1-3 cc’s. The
more cc’s a syringe holds, the larger the barrel will be.
• Needle Length: Needle length refers to just that…the length of
the needle. This is not a measure of the entire syringe, but only
the needle itself. The average needle will measure between
5/16th’s of an inch and 1.5 inches in length.
Typically, the syringes normally used for injecting AAS (non-insulin
syringes) come individually wrapped and can be purchased as little as one
at a time. Insulin syringes come in individually wrapped or a plastic bag, but
regardless they come in packs.
Selecting The Syringe Needed
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Standard Syringe Speci cations
Most common syringe specs for steroid injections:
• 18-22g for drawing and 23-27g for injecting
• 1/2" to 1.5 inch needle length
• 3 cc syringe
Note: If your syringes come with the needles already attached, order the
drawing needle to come on them. Otherwise, you'll have to switch needles,
each time you want to draw from a vial.
Most common syringe specs for peptide injections:
• 28-31 gauge
• 5/16th" to ½ inch needle length
• ½-1 cc syringe
Gauge Numbers
Most of the steroid products on the market are oil-based. As an “oil-based”
steroid, the steroid molecule has been suspended in oil, with the oil being
used as a carrier. Since AAS are measured in mg amounts and are a solid
in their natural form, they require a carrier if they are to be effectively
delivered into the body by injection. Since oil is signi cantly more resistant
to bacterial proliferation than water, and is also inexpensive, it is a logical
choice. However, oil also has a higher viscosity than water, which means it
will resist ow under applied force to a greater degree than water. The
higher the viscosity of an injectable product, the thicker the needle will need
to be in order to be able push the uid through the needle.
When talking about needle “thickness,” which one of the three previously
mentioned variables am I referring to? If you thought “gauge,” you thought
correctly. The “gauge” of a syringe pertains solely to the thickness of the
needle. Choosing the correct gauge is the an important factor in needle
selection, because if you choose a gauge number which is too high, the oil
will not t through (or at least be very dif cult to force through) and if you
choose a gauge number which is too low, you will be piercing your tissue
with an unnecessarily thick needle and cause more tissue damage,
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scarring, and trauma than necessary. The most basic rule to follow when it
comes to gauge selection for your injection needle is to choose the highest
gauge number possible, BUT which will still allow the oil to ow through the
needle easily. This will make the injection nominally invasive, while
reducing discomfort and minimizing scar tissue buildup. There is no
machismo in using a needle which is thicker than necessary—only idiocy.
Today, almost all steroids will t through a 25 gauge syringe, so this gauge
size should be your automatic go-to choice when the viscosity of a steroid
is unknown. This gauge is relatively thin in comparison to the syringes used
back in the day. Not too long ago the viscosity of many oil-based steroids
was much higher than it is today, requiring the use of 21-22 g. needle for
basically every injection—and in some cases, such as when injecting crude
forms of Testosterone suspension or injectable Winstrol, an 18 g. syringe
would be required just to be able to t the steroid crystals through the
needle without clogging it. For those of you who are trying to mentally
picture an 18 g. needle without a reference point, it is more like a small nail
than a needle. Today, things are much easier.
Needle Lengths For Injection Sites
The recommendations below are the “average” needle lengths used for
each body part listed.
• Glutes: 1-1.5 inch (For one's rst purchase, unless you are
exceptionally lean, it's best to stay with 1.5" needles for Glutes
to make sure you inject deep enough into the muscle.)
• Ventro Glutes: 1 inch
• Delts: 1 inch (some individuals can get away with ½ inch)
• Quads: 1 inch (some individuals can use as small as a ½ inch
needle when injecting into the quads, depending on how lean
they are).
• Chest: ½-1 inch
• Biceps: ½-1 inch
• Triceps: ½-1 inch
• Calves: ½ inch
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• Traps: ½-1 inch
• Lats: 1 inch
CC & mL
The term “cc” stands for cubic centimeters and is a unit of measurement for
determining injection volume. It is important to note that the term “cc” and
“mL” (milliliter) are identical and interchangeable with each other. 1 cc = 1
mL.
While syringes will indicate measurement in cc’s, steroid products (vials/
bottles/ampules) will almost always use ml’s as their unit of measurement.
So, if your steroid product says it contains 10 ml per bottle at 250 mg/mL,
you know it also contains 10 cc’s per bottle at 250 mg/cc. Therefore, if you
wanted to inject 500 mg of that steroid, you would need to inject 2cc’s (2
mL’s) of that product.
Syringe Size
Most 23-27 g syringes hold 3 cc’s, although some will occasionally hold
less, so you when ordering you should always specify exactly what you
want to purchase. Since 3 cc syringes are no more costly than their smaller
counterparts and being that many steroid users will often inject more than 1
cc at a time, it makes sense to strictly purchase 3 cc syringes for steroid
injections (with the exception for the rare occasion you need larger).
Syringe, Needles, etc. Suppliers
• [Apollo Lab Supply](www.apollolabsupply.com)
• GPZ Med Lab
• Total Diabetes Supply
• Medical Laboratory Supply
• Androusa
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Rotating Injection Sites
One issue which may eventually arise if the individual continues injecting
AAS long enough is the issue of scar tissue build-up. Scar tissue is a
dense, brous, connective tissue which forms over a wound or cut, either
external or internal. In the case of injection, the scar tissue formed is
internal. Scar tissue can impede contraction (make the muscle weaker),
impair local muscle growth, decrease exibility, and increase the possibility
of re-injury.
Some scar tissue formation is unavoidable, as every time an injection is
administered, scar tissue is formed. The bottom line is that excess &
problematic scar tissue is not something you want to have to deal with at
any point. Fortunately, we can take steps to minimize the appearance of
scar tissue through rotating injection sites. Scar tissue is much more likely
to form to a greater degree if you repeatedly and frequently use the same
injection site. For this reason, it is a good idea to start a “rotation”, in which
injections sites are routinely transferred from one site to the next in a
systematic fashion. Typically, the individual will select at least 3 body parts
to include in this rotation, while also altering the sites within each bodypart,
in order to decrease the number of times the same area is injected into per
rotation.
Injection Frequency
How often a particular steroid should be administered will depend on a few
factors, with injection frequency being governed primarily by the half-life of
each steroid. Obviously, longer-acting AAS will require a less frequent
injection schedule, while the opposite holds true for shorter acting versions.
With injectable steroids, the length of time it will stay active in the body
depends on the type of ester which has been attached to the steroid.
Esters are molecular modi cations to a steroid hormone, which have been
added solely to extend the life of the drug within the body.
When attempting to determine the injection frequency of a particular
steroid, examine the ester and you will have your answer. While there is
some dispute regarding the proper injection frequency required among the
various esters, the differences in opinion are minimal.
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Below is a list of some common esters used, along with the most
commonly recommended injection frequencies for each one:
• Acetate: ED
• Propionate: ED
• Phenylpropionate: ED or EOD
• Caproate: E3D or E3.5D
• Isocaproate: E3D or E3.5D
• Enanthate: E3D or E3.5D
• Cypionate: E3D or E3.5D
• Decanoate: E3D or E3.5D
• Undecanoate: E3D or E3.5D
• Undecyclenate: E3D or E3.5D
Note: These are just suggestions. If you choose to do less frequent
injections you may be more susceptible to side effects due to uctuations in
blood levels. If you wish to inject more frequently, regardless of ester, then
it is perfectly ne; it will only help blood levels be more stable.
Some injectable AAS have no ester, such as the various suspensions &
bases, such as Injectable Anadrol, Injectable Winstrol, Trenbolone No Ester
(TrNE) or Testosterone No Ester (TNE). These compounds are typically
injected 30 to 90 minutes preworkout.
Sterilization
Sterilization is a critically important part of the injection process, as
unsanitary injection practices pose the greatest risk in terms of acquiring
serious infections & abscesses. As described above, these are health
problems you want to avoid at all costs and investing a little extra time and
consideration into this aspect of your program can go a long way towards
ensuring you remain problem free.
There are 3 key components you have control over and which need to
remain sterile at all times. They are the needle(s) being used, the injection
site(s), and the rubber stopper(s) of each vial you will be drawing from. It is
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your job to make sure these components do not come in contact with
anything other than the intended object. When it comes to ensuring sterility,
alcohol is your weapon of choice. Alcohol kills more germs & bacteria
safely, than any other household product. Sterilizing an injection site or
object is a simple process. Prior to sterilization, clean the area of any debris
so that it appears visually clean. Afterwards, grab a alcohol pad or wet a
cotton swab with alcohol and wipe the intended area. After the area/object
has been sterilized, it should not come in contact with any other unsterilized
object.
Note: The World Health Organization (WHO) states in their latest
advice that swabbing with alcohol beforehand, like aspiration, is an
unnecessary and outdated practice so long as the surface is visibly
clean.
According to the medical establishment, an injection site should be covered
with an appropriate bandage post-injection. While this will help further
ensure that bacteria does not enter the injection site and cause infection,
this practice is rarely employed among AAS users, typically with little to no
negative consequences.
WHO: Alcohol swab skin prep is unnecessary
The procedure is super uous so long as you're in a relatively clean
environment—not in an infectious diseases wing or exposed high-risk
patients in an ICU ward.
Multiple trials were conducted and there was no difference in the infection
rate. Swabbing has gone the way of aspirating your pins.
• Skin antisepsis does not reduce incidence of infection
• Routine skin prep with alcohol swab: Is it necessary? (No)
• Intramuscular injections: To swab or not to swab
• Effectiveness of Alcohol Swabs for Preventing Infections
Using A Draw Needle
In order to properly load your syringe correctly, it will require 2 different
syringes or more speci cally, two different needles. One needle will be
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required for drawing the steroid into the barrel, while the other needle head
will be used to inject the steroid.
The primary reason for using two different needles is due to the delicacy of
needles, in general. Pushing a needle through a rubber stopper or into
muscle tissue just a single time will dull the needle considerably. In fact,
when viewing enhanced images of needles which have already pierced
human muscle tissue, the viewer can clearly see that the tip of the needle
has been bent. The act of injecting is already an invasive process and in
order to minimize both discomfort, as well as scar tissue build-up, a fresh
needle head should be used every time when doing an IM injection. Close
up view of a needle after penetrations.
A secondary reason for using one needle to draw with and another to inject
is that it can take a long time to draw a few cc’s of oil through a 25g.
syringe or smaller. By using a lower gauge number to draw with (usually
18-22g.), it cuts down on the amount of time required to draw the oil into
the barrel. It's recommended using no smaller than a 21-22g pin to draw
with is because bigger pins can damage the rubber stopper after repeated
uses, potentially allowing little pieces of rubber to break away from the
rubber stopper and fall into the vial. A 21-22g pin is suf cient for quick
drawing and will more thoroughly maintain the integrity of the rubber
stopper.
Insulin Needles & BackLoading
While performing a sub-q inject with a dull 39-30 g. insulin syringe is not
going to be as unpleasant as performing an I.M. injection with a dull 23 g.
syringe, the user can still take steps to ensure that ever injection is
performed with a fresh, sharp needle. Due to insulin syringes being so
much smaller and more fragile than their 23-25 g. counterparts, they dull
much more quickly. The act of pushing an insulin syringe through a rubber
stopper even one time will signi cantly dull the needle head.
However, since the needle head of an insulin syringe can not be removed,
as they can be with larger pins, the only way to inject with a fresh needle
head is by back-loading. The practice of back-loading is self-explanatory.
You simply load the pin through the back end instead of loading the pin
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through the needle head. This is easily accomplished by using one insulin
syringe (or any other syringe) to draw with and a second insulin pin for the
injection.
In order to back-load, begin by getting out 2 insulin syringes and setting
them in front of you. Select one as your drawing syringe and one as the
injecting syringe. Load your drawing syringe as you normally would and
then set it down on a table, etc. Pick up your injecting syringe and remove
the back plunger. You then want to carefully squirt the contents of the
loaded syringe into the back of the injecting syringe without letting any spill
out the back. At that point, pick up the plunger, gently press it back into the
barrel, but not fully inserting. Then, you ip the needle and wait for ALL the
liquid to go to the bottom. Once it does, you may now fully insert the
plunger and you are done.
Very Helpful Video On Back-Loading
Disposal Of Used Needles/Syringes.
When disposing of used syringes, it is of primary importance that the
original protective covering be placed back on the syringe prior to
discarding. This will prevent anyone from accidentally coming in contact
with the syringe and accidentally piercing their skin. No one wants to be
pulling a used needle out of their hand, because the user was negligent in
his responsibilities.
In addition, most individuals will place their used syringes in a medical
sharps storage container designated only for syringes, in order to minimize
the occurrence of someone coming into contact with a stray needle. But
there are people who are negligent and use empty protein containers,
plastic milk containers, juice containers, etc., for disposal of their used
syringes. Regardless of which method you employ, nd out how to legally
dispose of your pins.
Aspiration
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Note: The World Health Organization (WHO) states in their latest
advice that aspirating is unnecessary, and frequently causes more harm
than good.
The act as aspirating was traditionally performed as safety measure to
prevent one from accidentally injecting directly into a blood vessel. In order
to perform this simple procedure, one must have fully inserted the needle
into the injection site. Once the needle has been fully inserted, but before
depressing the plunger, gently draw (pull) back on the plunger by a few
millimeters. If no blood enters the barrel, you are safe to proceed with the
injection. If blood pours back into the barrel, you have entered a blood
vessel and need to relocate the syringe.
Seeing traces or specks of blood is not indicative that you have entered a
blood vessel. Typically, when a vein (blood vessel) has been threaded,
blood will pour into the barrel when pulling back the plunger. If you do
thread a blood vessel, you do not necessarily have to completely remove
the syringe and start over again. First, try pulling the needle out 1/4-1/2
inch and then try aspirating again. If blood does not pour into the barrel
after this 2nd attempt, then you have exited the blood vessel and are safe
to proceed. If blood does continue to enter the barrel, you will have to
remove the needle and nd a new injection site.
Aspiration is no longer recommended by any of the major health
organizations.
Is Aspirating Required?
Answer: Many AAS users do not aspirate when injecting. It is considered a
bit of an outdated methodology.
The reason aspiration is no longer taught is that the major injection sites
lack nerves or signi cant surface blood vessels. Furthermore, even a tiny
shift in movement while pinning can make the difference between hitting a
blood vessel or missing, so even if you aspirate, you can still end up hitting
a vessel.
The act of aspirating also involves signi cant movement which causes
further trauma to the muscle. If by chance you inject into a vein, it will
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nearly immediately collapse, and is entirely harmless. It's nearly impossible
to inject intravenously while injecting IM at a ninety degree angle.
According to the CDC:
Aspiration: “Aspiration is the process of pulling back on the plunger of the
syringe prior to injection to ensure that the medication is not injected into a
blood vessel. Although this practice is advocated by some experts, the
procedure is not required because no large blood vessels exist at the
recommended injection sites.”
STTI International Nursing Research Congress Vancouver, July 2009:
"Aspiration is not indicated for SC injections."
"Aspiration is not indicated for IM injections."
Organizations which state aspiration is not necessary:
• Centers for Disease Control (CDC)
• Advisory Committee on Immunization Practices (ACIP)
• Department of Health Services (DHS)
• American Academy of Family Physicians (AAFP)
• U.K. Department of Health (DoH)
• World Health Organization (WHO)
References located at the bottom of the page.
Safe Injecting Technique
Single Vial
1. Use A Draw Needle: Without one, you will dull your pin needle to the
point that it'll be very painful and potentially give a pip.
Note: If your syringes come with the needles already attached, order
the drawing needle to come on them. Otherwise, you'll have to switch
needles, more than necessary. Close up view of a needle after
penetrations.
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2. Clean The Vial: Wipe top of the vial with an alcohol pad/swab and let
dry.
3. Draw Air: Uncap the needle and ll the syringe with as much air as you
plan to withdraw in liquid. (i.e. If you plan to inject 1.5 mL/cc of liquid,
you will draw 1.5 mL/cc of air.)
4. Inject The Air Into The Vial: Inject the air into the vial to create positive
pressure inside the vial. This will assist and make drawing easier.
5. Draw The Liquid: Draw your required mL/cc of liquid while ensuring to
keep the needle point in the liquid.
6. Change To Your Injection Needle: Cap the drawing needle and
remove the drawing needle from the syringe. Attach your injection
needle to the syringe.
7. Clean The Area: Clean the area you want to inject with a new alcohol
swab in an outward going circular motion and let dry. Uncap your
injection needle.
8. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert
the needle. This serves to decrease the chances of muscle spasms.
9. Insert The Needle: Insert needle in a fast and precise motion, push
needle in until 2 mm or so is exposed.
10. Aspiration (OPTIONAL): Gently draw (pull) back on the plunger by a
few millimeters. If no blood enters the barrel, proceed. If blood pours
into the barrel, see [Aspiration]( )
11. Push The Plunger: Push the plunger on the syringe, injecting the liquid
into the muscle slowly and smoothly.
Note: As a general rule of thumb, always inject slowly; take 30 seconds
per mL.
12. Pull The Needle Out: Pull the needle out and cap it, then swab the
area with a alcohol pad/swab.
13. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.
Multiple Vials
1. Use A Draw Needle: Without one, you will dull your pin needle to the
point that it'll be very painful and potentially give a pip.
Note: If your syringes come with the needles already attached, order
the drawing needle to come on them. Otherwise, you'll have to switch
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needles, more than necessary. Close up view of a needle after
penetrations.
2. Clean The Vials: Wipe all of the vial tops with alcohol pad/swab, and
let them dry.
3. Draw Air & Inject Air: Uncap the draw needle and ll the syringe with
as much air as you plan to withdraw in liquid for the 1st vial. (i.e. If you
plan to inject 1.5 mL/cc of liquid, you will draw 1.5 mL/cc of air.) Then,
Inject the air into the vial and pull out the needle. Repeat for each vial.
4. Draw The Liquid: Pick the "most important" compound to draw rst.
(i.e. the one that I want the dose to be the most exact). Load the pin
with that compound. Going down the line of "importance", in the rest.
Note: Pick the "most important" compound to inject air into last. This
way you can immediately start drawing after injecting the air.
5. Change To Your Injection Needle: Cap the drawing needle and
remove the drawing needle from the syringe. Attach your injection
needle to the syringe.
6. Clean The Area: Clean the area you want to inject with a new alcohol
swab in an outward going circular motion and let dry. Uncap your
injection needle.
7. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert
the needle. This serves to decrease the chances of muscle spasms.
8. Insert The Needle: Insert needle in a fast and precise motion, push
needle in until 2 mm or so is exposed.
9. Push The Plunger: Push the plunger on the syringe, injecting the liquid
into the muscle slowly and smoothly.
Note: As a general rule of thumb, always inject slowly; take 30 seconds
per mL.
10. Pull The Needle Out: Pull the needle out and cap it, then swab the
area with a alcohol pad/swab.
11. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.
Ampoules
This is a very helpful video.
1. Grasp The Ampule: Grasp the ampule between thumb and fore nger
of one hand.
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2. Move All Liquid To The Bottom: Move liquid from the neck to the body
of the ampule by tapping (thumping) the ampule sharply.
3. Break The Ampule: Using gauze pad (or similar), grasp stem (the part
above the neck) with other hand. Break stem away from you and
discard safely. Note: Another option is to get an ampule opener.
4. Set Ampule Upright: Set ampule upright on a at and sturdy surface.
5. If Necessary, Reconstitute: If your ampule came unconstituted,
reconstitute the compound with bacteriostatic water or whatever liquid
you are using. Make sure ampule is fully reconstituted before drawing.
Note: To nd out dosing for HCG use this HCG calculator.
6. USE A SPECIAL FILTER NEEDLE TO DRAW LIQUID
7. Insert Filter Needle Into Ampule: Remove lter needle cap and insert
the lter needle into the liquid.
8. Draw The Liquid: If needle is suf ciently long, draw the liquid with the
ampule in the upright position. If a short needle is used invert the
ampule and draw the liquid.
9. Set Ampule Aside: If you are drawing multiple times to different noninsulin syringes, set the ampule in an upright position. If you are - see
below, otherwise, discard safely.
10. Remove Filter Needle: Draw (pull) back the plunger slightly to remove
any liquid from the lter needle. Place the needle cap back on and
remove the lter needle.
11. Change To Your Injection Needle: Cap the lter needle and remove
the lter needle from the syringe. Attach your injection needle to the
syringe.
12. Clean The Area: Clean the area you want to inject with a new alcohol
swab in an outward going circular motion and let dry. Uncap your
injection needle.
13. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert
the needle. This serves to decrease the chances of muscle spasms.
14. Insert The Needle: Insert needle in a fast and precise motion, push
needle in until 2 mm or so is exposed.
15. Push The Plunger: Push the plunger on the syringe, injecting the liquid
into the muscle slowly and smoothly.
Note: As a general rule of thumb, always inject slowly; take 30 seconds
per mL.
16. Pull The Needle Out: Pull the needle out and cap it, then swab the
area with a alcohol pad/swab.
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17. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.
Ampules To Sterile Vial
1. Grasp The Ampule: Grasp the ampule between thumb and fore nger
of one hand.
2. Move All Liquid To The Bottom: Move liquid from the neck to the body
of the ampule by tapping (thumping) the ampule sharply.
3. Break The Ampule: Using gauze pad (or similar), grasp stem (the part
above the neck) with other hand. Break stem away from you and
discard safely. Note: Another option is to get an ampule opener.
4. Set Ampule Upright: Set ampule upright on a at and sturdy surface.
5. If Necessary, Reconstitute: If your ampule came unconstituted,
reconstitute the compound with bacteriostatic water or whatever liquid
you are using. Make sure ampule is fully reconstituted before drawing.
Note: To nd out dosing for HCG use this HCG calculator.
6. USE A SPECIAL FILTER NEEDLE TO DRAW LIQUID.
7. Insert Filter Needle Into Ampule: Remove lter needle cap and insert
the lter needle into the liquid.
8. Draw The Liquid: If needle is suf ciently long, draw the liquid with the
ampule in the upright position. If a short needle is used invert the
ampule and draw the liquid.
9. Set Ampule Aside: If you are drawing multiple times to different noninsulin syringes, set the ampule in an upright position. If you are - see
below, otherwise, discard safely.
10. Remove Filter Needle: Draw (pull) back the plunger slightly to remove
any liquid from the lter needle. Place the needle cap back on and
remove the lter needle. Attach any normal needle to the syringe.
11. Clean The Vial: Wipe the vial top of your STERILE vial with alcohol
pad/swab, and let them dry. Note: Most places that sell syringes/
needles will also sell sterile vials.
12. Inject The Liquid Into The Sterile Vial And Store Properly Until
Needed.
When Needed, Draw and Inject:
1. Clean The Vial: Wipe top of the vial with an alcohol pad/swab and let
dry.
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2. Draw The Liquid: Uncap the insulin syringe and insert the needle
through the stopper of the vial. Draw your required iu/mL of liquid while
ensuring to keep the needle point in the liquid. Remove and replace the
cap on the insulin syringe.
3. Clean The Area: Clean the area you want to inject with a new alcohol
swab in an outward going circular motion and let dry. Uncap your insulin
needle.
4. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert
the needle. This serves to decrease the chances of muscle spasms.
Note: This is not necessary for subcutaneous injections
5. Insert The Needle: Insert needle in a fast and precise motion, push
needle in until ~2 mm is exposed.
6. Push The Plunger: Push the plunger on the syringe, injecting the liquid
slowly and smoothly.
7. Pull The Needle Out: Pull the needle out and cap it, then swab the
area with a alcohol pad/swab.
8. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.
Ampules To Preloaded Insulin Syringes
Here's Is An Alternate Way Of Preloading Insulin Syringes vs. Using A
Sterile Vial. Taken From This Thread
1. Grasp The Ampule: Grasp the ampule between thumb and fore nger
of one hand.
2. Move All Liquid To The Bottom: Move liquid from the neck to the body
of the ampule by tapping (thumping) the ampule sharply.
3. Break The Ampule: Using gauze pad (or similar), grasp stem (the part
above the neck) with other hand. Break stem away from you and
discard safely. Note: Another option is to get an ampule opener.
4. Set Ampule Upright: Set ampule upright on a at and sturdy surface.
5. If Necessary, Reconstitute: If your ampule came unconstituted,
reconstitute the compound with bacteriostatic water or whatever liquid
you are using. Make sure ampule is fully reconstituted before drawing.
Note: To nd out dosing for HCG use this HCG calculator.
6. USE A SPECIAL FILTER NEEDLE TO DRAW LIQUID.
7. Insert Filter Needle Into Ampule: Remove lter needle cap and insert
the lter needle into the liquid.
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8. Draw The Liquid: If needle is suf ciently long, draw the liquid with the
ampule in the upright position. If a short needle is used invert the
ampule and draw the liquid.
9. Set Ampule Aside: If you are drawing multiple times to different noninsulin syringes, set the ampule in an upright position. If you are - see
below, otherwise, discard safely.
10. Remove Filter Needle: Draw (pull) back the plunger slightly to remove
any liquid from the lter needle. Place the needle cap back on and
remove the lter needle.
11. Insert Insulin Needle: Remove the cap on the insulin syringe. Put the
insulin syringe into the top of the syringe you used to draw the liquid
with; where the needle would normally attach to the syringe.
12. Slowly, carefully, push the liquid up so that you can suck it out with the
insulin needle. Cap the insulin needle and repeat until done. Store
properly until needed.
When Needed, Draw and Inject:
1. Clean The Area: Clean the area you want to inject with a new alcohol
swab in an outward going circular motion and let dry. Uncap your insulin
needle.
2. Inhale, Then Exhale Slowly: Inhale deeply, and while exhaling insert
the needle. This serves to decrease the chances of muscle spasms.
Note: This is not necessary for subcutaneous injections
3. Insert The Needle: Insert needle in a fast and precise motion, push
needle in until ~2 mm is exposed.
4. Push The Plunger: Push the plunger on the syringe, injecting the liquid
slowly and smoothly.
5. Pull The Needle Out: Pull the needle out and cap it, then swab the
area with a alcohol pad/swab.
6. Legally Dispose: Dispose of your medical sharps (needles) properly.
Note: Find out how to legally dispose of your pins.
Special Injection Techniques
The purpose of the below injection techniques is to seal the injected
compound deep within the muscle, by allowing no exit path back into the
subcutaneous area and skin. While using these techniques is not essential
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to performing a proper injection, they will allow the user to minimize oil loss
due to seepage.
• Z-track Technique: A technique utilized to prevent leakage of
the injected substance post-injection.
• Air Bubble Technique: A technique utilized to prevent leakage
of the injected substance post-injection.
Z-track Technique
The Z-track method requires temporarily displacing the skin &
subcutaneous tissue prior to injection and immediately releasing the tissue
post-injection. In order to perform the Z-track method, prepare your syringe
and be ready to inject. Once the syringe is in hand, use your free hand to
pull the skin at the injection site ½-1 inch away from its original location.
While continuing to hold the skin in this stretched position, administer the
injection into the original location. Immediately after removing the syringe
from the injection site, release the skin which was being held in place. The
Z-track method works best at locations where there is a greater amount of
lose skin. Utilizing locations with taut skin will be more dif cult.
Very Helpful Video To See Technique
Air Bubble Technique
The air bubble technique involves injecting a small amount of air at the end
of an injection. In order to perform this technique prepare your syringe and
be ready to inject. When the syringe is in hand, pull ½ cc/mL of air into the
syringe. Just prior to and throughout the injection, make sure the needle is
pointing down, so that the air oats to the top of the barrel (near the
plunger) and is the last thing to be injected into the muscle, as it is this
small air bubble which will help to seal off the opening and prevent leakage.
This is also used by some to make sure all of the liquid they are injecting is
out of the needle.
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PIP (Post Injection Pain)
What Causes (Non-Infectious) Injection Pain?
• The Shorter The Ester, The Higher The Melting Point
• The Concentration Of The Gear
• The Solvents Used
• Injecting Too Quickly
• Virgin Muscle
The Shorter The Ester, The Higher The Melting Point
One thing that can cause pain is when the oil/solvents are absorbed by the
body and crystals are left behind. Short esters (Propionate, Acetate, etc.)
are harder, more painful crystals with melting points in the 100c range. A
hormone with a longer ester (excluding Cypionate - Cyp is a long ester, but
also has a high melting point) can have a melting point in the 20c-40c
range; not far off from human body temp.
The Concentration Of The Gear
Pain can also be caused by concentration of your gear. Building off of point
1: Hypothetically, let's say it takes the body 24 hours to absorb 1mL of a
certain oil/solvent blend and 24 hours to absorb 50mg of Testosterone
Propionate. If 50mg (or less) of Testosterone Propionate is in 1mL of that
oil, this injection should be painless. On the other hand, if 100mg of
Testosterone Propionate is in that same 1mL of solution, then after 24
hours the body will have absorbed 50mg and 1mL, leaving 50mg behind in
the injection area, crystalized and painful.
It's better to shoot 3mL of 50mg/mL low concentration Testosterone
Propionate than 1mL of 150mg/mL high concentration Testosterone
Propionate: the high concentration is more likely to cause pip.
This is also why water based suspensions (Testosterone base/no ester,
Winstrol, etc.) hurt the most; water is very easily absorbed in the body.
The Solvents Used
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The solvents used can cause pain in two ways. Benzyl alcohol (BA) is used
at 1-2% as a preservative and antiseptic. If the alcohol content is too high
the gear will burn. Pain in the rst 24 hours is usually caused by heavy
solvents, pain in the next few hours is usually cause by crystallization.
Another way is a bad recipe. If someone used 2% BA, and the rest of the
solution oil, the mg/mL would have to be low due to oil's weak ability to hold
crystals. On the other hand, a recipe like 2% BA, 5% Guaiacol (super
solvent), 10% Benzyl Salicylate (liquid aspirin) with the ller split 50:50
between Ethyl Oleate (oil/solvent hybrid) and normal oil should be far less
painful.
Injecting Too Quickly
If you inject too quickly, it can potentially tear tissue.
Virgin Muscle
If your muscle is new to the hormone, it will absorb the hormone slowly, but
absorb the oil/solvent quicker. This will cause more crystallization and pain.
As your muscles recognize the hormones, they will be absorbed more
quickly, thus less pain. The deeper you inject into the center of a muscle
group, the better.
How do I prevent pain before I inject?
• Cutting The Oil With Sterile Oil
• Warming Up The Oil
• Inject Slowly
• What If None Of Those Help?
Cutting The Oil With Sterile Oil
Cut your shots 50:50 with sterile ltered oil. If you want to use 50mg of
Testosterone Propionate and you have 100mg/mL Testosterone Propionate
- pull 0.5mL of your Test Prop and 0.5mL of sterile ltered oil to shoot 1mL
of 50mg/mL Testosterone Propionate. This is the #1 best way. Don't bother
with B-12, as it’s water based and absorbed so quickly it will have little to
no impact.
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Warming Up The Oil
Before you shoot, it can help to warm your gear (especially suspensions).
Carefully making sure the vial stopper (top) doesn't touch the water, you
can put the vial in the bathroom sink and let hot water run over the vial for
~2 minutes and shake well. This will lower the oils viscosity also making it
easier it pull into the syringe. One way some will make sure the vial doesn't
touch the water, is to put the vial inside a zip lock bag. If you don't want to
constantly be reheating the entire vial each time, alternatively you can do
the same once you've drawn the oil into the syringe. If you heat the syringe
it is recommended to use a zip lock bag or the likes to protect the syringe
from being exposed to the water.
Injecting Slowly
Inject slowly; take 30 seconds per mL. Use a 25g pin to inject so it forces
you to move slower.
What If None Of Those Help?
If none of these work, you could have dirty gear. It’s possible there could be
particles (although bacteriostatic) in the gear that made it through the lter
and is causing infection, although mild. Alternatively, if using higher
concentration gear, your gear is just too high concentration to be tolerable
for you.
How do I deal with pain once I have it?
The worst thing you can do is ice it. Cold will help the crystals fall out of
solution/suspension. It’s okay to take some ibuprofen to decrease the
swelling and help with pain. Also being in a hot tub, jacuzzi, or warm bubble
bath will help melt the crystals down. Using a heating pad can help as well.
Where Do I Inject?
Inevitably, one of the rst questions many individuals will ask themselves
shortly before their 1st injection is “where do I inject?” While there is no
right or wrong answer, the most commonly injected muscle among rst time
users are the Glutes. It is a muscle group that's relatively painless
(potentially), does not have any major veins/arteries near the surface, and
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contains a lower density of nerves. The twisting and turning can be a
problem for some, in which case injecting Ventro Glutes is another option. If
that is too hard to nd for you, try Quads, but there is a slightly larger
margin for error in regard to hitting nerve clusters and puncturing large
veins. But you should aim to have as many injection sites as possible to
avoid building scar tissue.
Basically, any muscle can be injected into, although larger, thicker muscles
are typically superior to small, shallow muscle groups. An example of a
body part which falls into the latter category would be the forearms. This
body part is rarely ever injected into and is a poor choice all the way
around, so avoid them. Never inject into the hands, feet, or neck
Locations To Inject
Noteworthy Sites For Injection Descriptions:
• Spot Injections
• IPED Info
Glutes (Dorsogluteal)
When people talk about injecting Glutes, they are referring to injecting into
the Gluteus Maximus / Gluteus Medius via dorsogluteal.
Diagram For Injection Area Glutes Injection Photos (Thanks to Spot
Injections)
Helpful Dorsogluteal Injection Video
Another Helpful Glutes Video
Ventro Glutes
Ventro Glutes is the common term, but in actuality we are injecting into the
Gluteus Medius via ventrogluteal.
Start by nding three bony landmarks - the greater trochanter (at your hip
joint), the iliac crest (top of your pelvis), and the anterior superior iliac spine
(front of your pelvis). Diagram for reference. Now that you've found these
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markers it's time to nd the injection spot. We'll be injecting the gluteus
medius. Think of an imaginary line between the iliac crest (IC) and the
greater trochanter (GT); now imagine another line intersecting that one
from the anterior superior iliac spine (ASIS). Where those lines meet is your
spot.
• A Picture For Reference
• Diagram For Reference
• Additional Diagram For Reference
• Additional Diagram For Reference
• Additional Diagram For Reference
• Penis Pic... Just To Be Sure.
This spot may feel hard, almost like bone; but as long as you stay in the
prescribed spot you will be ne. Here are some techniques to further clarify
the injection spot.
• Lay on your side and put your hand on the prescribed area. Now
raise your leg like so. You will feel a muscle ex. That is your
gluteus medius.
• Stand up and place your hand on the prescribed area. Now shift
your weight from one foot to the other. You will feel a muscle
tense. This is your gluteus medius.
When you're con dent you've found the correct spot begin your injection
routine.
Excellent Video On The Process Of Finding Vento Glutes
Quads (Vastus Lateralis)
When injecting into the Quads it can be a bit trickier. Never inject into the
inner-thighs…only inject into the actual quadriceps muscles themselves,
particularly the Vastus Lateralis. The Rectus Femoris can also be injected,
but most users will nd it more painful and increases the risk of hitting a
nerve (causing the muscle to "twitch"). Lastly, the Vastus Medialis
(teardrop) can be injected into as well, although it is not a preferred area,
especially for a beginner.
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Quads Injection Photos (Thanks to Spot Injections)
Very Helpful Video Of Locating The Vastus Lateralis
Delts (Deltoid)
When injecting into the delts, all 3 heads are suitable, although the side &
rear heads are a bit more comfortable, on average.
Diagram For Injection Area
Delts Injection Photos (Thanks to Spot Injections)
Helpful Delt Injection Video
Chest (Pecs)
The diagram below shows the places on your Chest (Pec) where you can
inject. In the Photos they just use the upper options. In the video below he
uses the lowest option. It is just a preference thing; try them all and see
what you like best.
Diagram For All Three Injection Areas
Chest Injection Photos (The Upper Options) (Thanks to Spot
Injections)
Helpful Chest Injection Video (He Does The Lowest Option)
Lats (Latissimus)
Diagram For Injection Area
Lats Injection Photos (Thanks to Spot Injections)
Very Helpful Lats Injection Video
Traps (Trapezius)
Diagram For Injection Area
Traps Injection Photos (Thanks to Spot Injections)
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Triceps
For Triceps, there are three heads you may inject in: The outer (horseshoe)
tricep head, the lower rear tricep head, and middle rear tricep head.
Diagram For Injection Area (Horseshoe)
Diagram For Injection Area (Lower Rear)
Diagram For Injection Area (Middle Rear)
Triceps Injection Photos (Horseshoe) (Thanks to Spot Injections)
Helpful Triceps Injection Video
Biceps
For Biceps, there are two heads you may inject in: The outer bicep head,
and outer bicep head.
Diagram For Injection Area (Inner)
Diagram For Injection Area (Outer)
Biceps Injection Photos (Thanks to Spot Injections)
Calves
Diagram For Injection Area
Calves Injection Photos (Thanks to Spot Injections)
Subcutaneous (SubQ)
SubQ is excellent for TRT or cruising purposes. See Injection Tips in the
TRT page.
Volume Each Site Can Hold
Site
Volume
Glutes (Dorsogluteal)
3-5 mL/cc
Ventro Glutes
3-5 mL/cc
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Quads (Vastus Lateralis)
3-5 mL/cc
Delts
2-3 mL/cc
Chest
2 mL/cc
Lats
2 mL/cc
Traps
2 mL/cc
Triceps
1.5 mL/cc
Biceps
1.5 mL/cc
Calves
1.5 mL/cc
Subcutaneous (SubQ)
< .5 mL/cc
Frequently Asked Questions (FAQ)
Below are common questions and answers regarding injecting.
My Injection Spot Is Red, Itchy, Or Sore?
Answer: Get to a doctor for some antibiotics if it is red, itchy, or hot. If it is
simply sore and/or swollen it is probably going to be okay see: Post
Injection Pain (PIP). If in doubt, get some antibiotics; a common thing to tell
your doctor is that you injected B12.
Is It Normal To Bleed After An Injection?”
Answer: Yes, it is common to occasionally nick a vein close to the surface
of the injection site, which will cause blood to leak from the surface. The
amount of blood which can seep from an injection site can be anywhere
from a drop or two, to a very light stream which slowly ows down that body
part. Even in the event a larger vein is hit when doing an injection, this type
of bleeding is relatively easy to stop and will not pose any harm to the
individual.
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Is Aspirating Required?
Answer: Many AAS users do not aspirate when injecting. It is considered a
bit of an out-dated methodology, but it never hurts to do it.
According to the CDC:
Aspiration - Aspiration is the process of pulling back on the plunger of the
syringe prior to injection to ensure that the medication is not injected into a
blood vessel. Although this practice is advocated by some experts, the
procedure is not required because no large blood vessels exist at the
recommended injection sites."
STTI International Nursing Research Congress Vancouver, July 2009:
"Aspiration is not indicated for SC injections."
"Aspiration is not indicated for IM injections."
Organizations which state aspiration is not necessary:
• Centers for Disease Control (CDC)
• Advisory Committee on Immunization Practices (ACIP)
• Department of Health Services (DHS)
• American Academy of Family Physicians (AAFP)
• U.K. Department of Health (DoH)
• World Health Organization (WHO)
References located at the bottom of the page.
Does Injecting Build Up Scar Tissue?
Answer: Yes, repeated Intramuscular injections can cause the muscle to
build up scar tissue. Generally there is no in ammation or inclusion in the
tissue. In an effort to minimize scar tissue build up, users will rotate through
many injection sites. If you're interested, here is a case study of a woman
in an extreme case, it includes stained muscle biopsies
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How Do I Open Ampules?
Answer: Ampules can be aided in opening by scoring (some ampules
come pre-scored). Scoring is a process in which in a ne line is ground
away around the neck of the ampule. Scoring makes it much easier to snap
the top of the ampule off without breaking the vial and spilling the oil.
Normally, a scoring tool is used for this process, although sometimes
knives or other objects can be used.
An amp opener can be used, which is the fastest and the least time
consuming methods.
If you don't have an ampule opener. Grasp the ampule between thumb and
fore nger of one hand. Move liquid from the neck to the body of the ampule
by tapping (thumping) the ampule sharply. Using gauze pad (or similar),
grasp stem (the part above the neck) with other hand. Break stem away
from you and discard safely. This is a very helpful video that shows the
process
Lastly, the tape-method can be employed, as well. The tape method
involves taping the entire vial all the way up to the neck line. Several layers
of tape should surround the vial, so that it is properly secured. The point of
taping the vial is two-fold. One purpose is to prevent the contents of the
ampule from spilling, should the ampule break somewhere other than the
neckline. The other purpose is to reinforce the ampule, so that it is more
likely to break at the neckline. One can combine both the tape method and
the scoring, which is the best way to ensure that the oil contained in the
ampule will not be spilled.
Can I Re-Use Syringes?
Answer: Absolutely not. You should never take a needle which has entered
the body and re-insert it back into a steroid product, as this can result in
bacteria build-up and cause potential future infections.
How Fast Should I Inject?
Answer: As a general rule, 30 seconds per mL/cc.
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Answer: No, a small amount of air will do no harm. Air bubbles injected
into muscle tissue is of no concern. Even if the individual were to thread a
vein and inject the entire contents of the syringe into the vein, the small air
bubbles contained within it would be the least of that person’s worries. In
reality, several cc’s of air would have to be injected directly into a vein all at
once, in order to cause cardiac arrest. Even injecting 2-3 cc’s of air directly
into a muscle would be largely inconsequential. Of course, such an action
is not recommended, but you get the point.
My Gear Crashed…How Do I Fix It?
Answer: Gear can crash due to storing the product in colder than
recommended temperatures (or in shipment)…or because the ratio of AAS
to oil is out of balance (this can be either a manufacturer error or a personal
error if home brewing). This does not damage the steroid. In order to
correct the problem, simply run the vial under warm water until the products
reverts back to its normal state. Clean with alcohol swab after drying off.
My Gear Has Particles Floating In It?
Answer: You can choose to either dispose of the product or you can relter it by using a Whatman lter. While opinions will differ on this subject,
the opinion of re- ltering is still available and a suitable solution in many
cases, assuming the product is not badly polluted. In cases where it is
apparent that the product is very poor quality and contains a large amount
of foreign material, it would be wise to dispose of the product. This should
not occur with reputable UGL’s and will never occur with Pharm-grade
versions, although an occasional speck may occur with UGL products here
and there and is usually not a big deal.
Related Posts
• How To Inject For Noobs.
• Aftermath Of An Abscess
References
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Is It Dangerous To Inject Small Air Bubbles?”
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Atkinson, W. L., Pickering, L. K., Schwartz, B., Weniger, B. G., Iskander, J.
K., & Watson, J. C. (2002). General Recommendations on Immunization:
Recommendations of the Advisory Committee on Immunization Practices
(ACIP) and the American Academy of Family Physicians (AAFP). Morbidity
and Mortality Weekly Report, 51, RR2. 1-33.
Chiodini, J. (2001). Best practice in vaccine administration. Nursing
Standard, 16(7), 35-38.
Diggle, L. (2007). Injection technique for immunization. Practice Nurse,
33(1), 34-37.
Gammel, J. A. (1927). Arterial embolism: an unusual complication following
the intramuscular administration of bismuth. Journal of the American
Medical Association, 88, 998-1000.
Ipp, M., Taddio, A., Sam, J., Goldbach, M., & Parkin, P. C. (2007). Vaccine
related pain: randomized controlled trial of two injection technique Archives
of Disease in Childhood,92,1105-1108.
Li, J.T., Lockey, R. F., Bernstein, I. L., Portnoy, J. M., & Nicklas, R. A.
(2003). Allergen immunotherapy: A practice parameter. Annuals of Allergy,
Asthma, & Immunology, 1-40.
Livermore, P. (2003). Teaching home administration of sub-cutaneous
methotrexate. Paediatric Nursing, 15(3), 28-32.
Middleton, D. B., Zimmerman, R. K., & Mitchell, K. B. (2003). Vaccine
schedules and procedures, 2003. The Journal of Family Practice, 52(1),
S36-S46.
Nicoli, L. H., & Hesby, A. (2002). Intramuscular injection: An integrative
research review and guidelines for evidence-based practice. Applied
Nursing Research,16(2), 149-162.
Ozel, A., Yavuz, H., & Erkul, I. (1995). Gangrene after penicillin injection: A
case report. The Turkish Journal of Pediatrics, 37(1), 567-71.
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Peragallo-Dittko, V. (1995). Aspiration of the subcutaneous insulin injection:
Clinical evaluation of needle size and amount of subcutaneous fat. The
Diabetes Educator, 21(4), 291-296.
Roger, M. A., & King, L. (2000). Drawing up and administering
intramuscular injections: A review of the literature. Journal of Advanced
Nursing, 31(3), 574-582.
Talbert, J. L., Haslam, R. H. & Haller, J. A. (1967). Gangrene of the foot
following intramuscular injection in the lateral thigh: A case report with
recommendations for prevention. The Journal of Pediatrics, 70(1), 110-114.
Workman, B. (1999). Safe injection techniques. Nursing Standard, 13 (39),
47-53.
World Health Organization (2004). Immunization in Practice, Module 6:
Holding an immunization session. Immunization in Practice: A practical
resource guide for health workers –2004 update,1-29.
Center for Nursing History at Misericordia University: http://
www.misericordia.edu17. Levels of Evidence, Canadian Medical
Association & Centre for Evidence-Based Medicine (2001). Available
at:http://www.cebm.net/index18. Melnyk, B. M., & Fineout-Overholt, E.
(2005). Evidence-Based Practice in Nursing & Healthcare: A Guide to Best
Practice. Philadelphia: Lippincott, Williams & Wilkins.
Reference For A Lot Of Info Here
Reference For Volume
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Testosterone Replacement
Therapy (TRT)
Welcome to r/steroids' wiki on testosterone replacement therapy (TRT).
This wiki explores TRT for treating low testosterone (aka low T).
For a medical reference, see The Endocrine Society's "Clinical Guide:
Testosterone Therapy in Adult Men with Androgen De ciency
Syndrome." ( Original PDF | Scribd )
Categorization of Low Testosterone (T)
Before we get into testosterone replacement therapy for treating low T, let’s
look at the categories of male hypogonadism (low T).
Primary Hypogonadism
This type on low T is caused by a problem with your testicles. The testicles
are still receiving the message from the brain to produce testosterone, but
the testicles aren't working properly and cannot produce enough
testosterone. This form of hypogonadism is usually due to injury to the
testicles or radiation exposure from chemotherapy.
Secondary Hypogonadism
This type of low T is caused by a problem with you pituitary or
hypothalamus, two glands in the brain that tell the testicles to produce
testosterone. Basically, the messaging system is broken. [As a side note,
physicians and online references generally group pituitary and
hypothalamus problems together. If they don’t, problems with the pituitary
may be referred to as secondary hypogonadism and problems with the
hypothalamus may be referred to as tertiary hypogonadism.]
Secondary hypogonadism is far more common than primary hypogonadism
and many more things can cause it. It can be caused by pituitary or
hypothalamic disorders or a pituitary tumor. Fortunately, only about 0.25%
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of these pituitary tumors are cancerous, the rest are benign. But, they still
may effect testosterone production. Secondary hypogonadism may also be
caused by obesity, diabetes, and the use of certain medications.
Lastly, normal aging may cause secondary hypogonadism. The truth of the
matter is that aging gradually wears down all the systems of the body. One
system that gets particularly worn down is the messaging system for the
production of testosterone. As a result, testosterone levels gradually
decline with age. This natural decline in testosterone production leads to
the prevalence of low testosterone in middle-aged and older-aged men. It is
estimated that between 20-40% of older men have low testosterone and/or
suffer from symptoms associated with low T.
Symptoms of Low Testosterone
Some advertisements for testosterone replacement products may lead you
to believe that simply feeling tired or cranky is a sign of low T. In reality,
symptoms tend to be more involved than that. Regardless of your age, low
T symptoms can include:
• Erectile dysfunction, or problems developing or maintaining an
erection
• Other changes in your erections, such as fewer spontaneous
erections
• Decreased libido or sexual activity
• Infertility
• Rapid hair loss
• Reduced muscle mass
• Increased body fat
• Enlarged breasts
• Sleep disturbances
• Persistent fatigue
• Brain fog
• Depression
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Many of these symptoms can also be caused by other medical conditions
or lifestyle factors. If you’re experiencing them, make an appointment with
your doctor. They can help you identify the underlying cause and
recommend a treatment plan.
What is TRT?
Testosterone replacement therapy (TRT) is the administration of
testosterone to men to treat low T. It is a prescription treatment overseen by
a physician. The main goal of therapy is to reestablish normal testosterone
levels. Physicians typically aim to reestablish a testosterone level between
500 ng/dL and 1000 dg/nL.
Men sometimes confuse anabolic steroid usage (testosterone cycles) for
the purpose of bodybuilding with TRT. TRT uses normal, physiological
dosages to increase low testosterone levels back to normal levels. The
testosterone preparation is taken regularly, oftentimes for the rest of an
individual’s life. On the other hand, testosterone cycles for the purpose of
bodybuilding use above normal, supraphysiological dosages to increase
testosterone levels above normal for a period of time. Users of testosterone
cycles for the purpose of bodybuilding typically cycle on and off
testosterone to give their bodies a break from these supraphysiological
testosterone levels.
• A Guide to Hypogonadism - National Library of Medicine
• Androgen Replacement Therapy - Medscape
• Testosterone Therapy in Adult Men - Endocrine Society
• Testosterone Replacement Therapy - Elite Men's Guide
• Testosterone Wiki - Testosterone Subreddit
Getting On TRT
To get a prescription to go on TRT, you're going to have to get blood work
that shows that you have low testosterone. The blood work will at a
minimum measure your total testosterone level. It may also measure your
free testosterone and sex hormone binding globulin levels. Any test
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providing all three values will provide more information than the total
testosterone level alone, so ask for the most comprehensive test possible.
The test requires a blood sample to be taken from a vein. The best time for
the blood sample to be taken is between 7 a.m. and 10 a.m because
testosterone levels uctuate throughout the day and early morning tests
offer the most reliable results. A second sample is often needed to con rm
a result that is lower than expected.
Additional tests of use include a measurement of LH (luteinizing hormone)
levels, FSH (follicle stimulating hormone) levels, prolactin levels, and a full
thyroid panel.
• Testosterone Testing - LabTestOnline
• Testosterone Testing - MedLinePlus
Finding a Doctor; Getting Blood Work
TRT has really only recently gone mainstream. Some physicians know
quite a bit about it; some know very little. Some physicians wholeheartedly
support it; some look at it very skeptically. Most will be somewhere in the
middle. Thus, it’s important to nd a physician that you feel comfortable
with and that has a good understanding of and respect for TRT.
If you suspect you have low testosterone because you have some
symptoms of low T, start by talking about these symptoms with your doctor.
Then, ask your doctor for a simple blood test to measure your testosterone
levels. If your doctor won’t perform a blood test, either get a different doctor
or get some blood work done yourself. Plenty of companies now offer
hormone panel testing services Any Lab Test Now, DirectLabs,
DiscountedLabs, ZRT Laboratory. While you can’t get a TRT prescription
from them, you can arm yourself with the results by guring out whether or
not your levels are low.
Here are the different doctors that you can see that most often treat men
with low testosterone (ordered by ease of access and knowledge of TRT).
In any case, a male doctor is more likely to prescribe testosterone than a
female doctor:
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• Low T Centers/Men’s Health Clinics – These clinics speci cally
cater to testing for and treating men with low testosterone. They
charge a monthly fee for access to physicians. Insurance may or
may not cover these providers, so check. (Companies with the
most locations are Low T Center, BodyLogicMD, and
LowTestosterone.com). Note: These centers and clinics do not
prescribe testosterone to any man that comes in complaining of
low testosterone symptoms. They perform blood tests and only
prescribe testosterone therapy to men with clinically diagnosed
low testosterone.
• Anti-Aging/Longevity Clinics – These clinics typically also
prescribe HGH as well as other hormones. They are expensive
because they typically only take cash and do not charge to
insurance.
• Naturopathic Doctors (NMDs) – Some are licensed to prescribed
hormones; some are not. If they are licensed to prescribe
hormones, they are likely to prescribe TRT fairly easily. They are
often cheaper than anti-aging clinics, but may not work with
insurance, so check.
• Endocrinologists - Can be covered by insurance; some
specialize in TRT, but some are not as knowledgeable about
TRT. They also help manage diabetes and obesity. If you have
diabetes and/or are obese, they can help with both issues.
• Urologists - Often treat low testosterone and other related men’s
health issues like sexual dysfunction. If you have sexual
dysfunction issues, they can help with both issues.
• General Practitioner/Primary Care Manager – They may treat
you if they are comfortable with prescribing testosterone and
comfortable with you. They are also the most likely not to have a
good deal of knowledge of or experience with TRT.
Understanding your Blood Work Results
The normal range for total testosterone levels in men is approximately 300
ng/dL to 1050 ng/dL. There is no absolute consensus among different
medical organizations for the exact cutoff for low testosterone. In general,
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the cutoff ranges from high 200s to low-to-mid 300s ng/dL. This range is
over a broad age range and there is no “normal” testosterone level based
on age that men can look to as a reference.
The of cial recommendations of the major professional organizations are:
Organizati
on
The
Endocrine
Society
Suggest Total Testosterone Level for Treatment
2010 guidelines suggest 300 ng/dL as a common
threshold for symptoms in many men, but state that “the
threshold testosterone level below which symptoms of
androgen de ciency and adverse health outcomes occur
and testosterone administration improves outcomes in the
2002 guidelines suggest men with symptomatic
hypogonadism and a total testosterone level of less than
200 ng/dL may be potential candidates for therapy.
American
Organizati
on of
Clinical
Endocrinol
ogists
European
< 350 ng/dL
Associatio
n of
Urology
Japanese
2008 guidelines suggest that total testosterone be ignored
Urological
and diagnoses be made purely from free testosterone.
Associatio
n
As mentioned above, your free testosterone level is as important, if not
more important, as the total testosterone level. The normal range for free
testosterone in men is 5 ng/dL to 21 ng/dL. It should be noted that labs use
different assays and methodologies to measure free testosterone levels. A
free testosterone (direct) test will yield values outside of the above range if
you try to convert the values. In this case, use the reference range for free
testosterone provided by the lab. Compare your lab results directly to the
lab provided range to assess where you stand. For example,
AnyLabTestNow provides a free (direct ) range of 35 to 155 pg/mL (3.5 to
15.5 ng/dL).
Two important points should be noted regarding the normal range for
testosterone. First, the normal range for testosterone is quite large. One
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man can have nearly three to four times the testosterone as another man
and both men can be considered “normal”. The size of the change in
testosterone levels over a lifetime can be just as important as the actual
clinical value for the development of low T symptoms. While low T is
generally de ned as total testosterone below 300 ng/dL, men with levels
above this cutoff value may still experience symptoms of low T because
they experience big individual declines over their lifetime. Some men start
to experience the symptoms of low testosterone at merely low-normal
levels; anecdotal reports include some men suffering symptoms of low
testosterone at levels as high as 450 ng/dL.
Second, testosterone levels naturally decline. Total testosterone levels
decline nearly 30% between the ages of 25 and 75. Free testosterone
levels decline nearly 50% between the ages of 25 and 75. But, the normal
range is applied to both a 25-year-old and a 75-year-old man. There is no
clinically “normal” testosterone level based on age that men can look to as
a reference. Some studies do measure average total and free testosterone
with age, so that you can compare your levels with the average study
levels. Elite Men’s Guide Normal Testosterone Levels article provides
more detail on testosterone levels.
Common TRT Prescriptions
Testosterone
There are a few different forms of testosterone for TRT. These forms can
be broken down into four categories: 1) injectable oil-based testosterone, 2)
testosterone gels/creams, 3) testosterone lozenges, and 4) implantable
testosterone pellets. The two most common forms are injectable oil-based
testosterone and testosterone gels. Testosterone may also come in
transdermal patches or troches, but both forms are not used often.
Right now, there are no FDA-approved oral pill forms of testosterone in the
US. In general, oral pill forms may cause liver damage and should be
avoided for TRT. The only safe oral form for long-term use is testosterone
undecanoate, which again is not available in the US. For men outside the
US, it is marketed under several brand names including Andriol, Undestor,
and Nebido among others.
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Most docs will rst recommend Testosterone in the following forms and
generally (but not always) in this order:
Gels/Creams
Testosterone gels deliver testosterone through daily skin applications. The
gels consist of a hydro-alcoholic base medium with 1 or 1.62% active
testosterone. These formulations deliver 25, 50, or 100 mg of testosterone
per day. This form of testosterone is relatively new with the rst
testosterone gel introduced in 2000. As such, most gels are sold under a
brand name only and are typically more expensive than generic injectable
testosterone cypionate and enanthate. Androgel, Axiron, Fortesta,
Testim, and Vogelxo. Recently, generic versions, such as Bio-T-Gel have
become available.
Recently, testosterone gel usage has surpassed injectable testosterone
usage for TRT. Approximately 60% of TRT users use testosterone gels,
while 35% use injectable testosterone (according to Endo Pharmaceuticals
FDA ling for Aveed). Gels will likely be the rst recommendation by any
physician. It’s important to know that the surge in their usage may be
largely attributed to the heavy advertising by the pharmaceutical companies
promoting these gels not the actually effectiveness of these gels.
Overall, gels mimic the natural release of the body, but many men complain
that testosterone gels do not fully raise T levels back up to normal desired
levels. Experience has shown that some patients may never absorb
enough testosterone from gels to improve symptoms of low T.
Pros: Easy to use; dosage can be easily modi ed; many available gels;
mimic physiological release Cons: Expensive; inconsistent dosage; can rub
off on others; doesn't work well if you sweat a lot; must be applied daily;
may not raise levels to desired levels.
Products: Androgel, Axiron, Bio-T-Gel, Fortesta, Testim, and Vogelxo
Dosage: 2.5-10 grams of gel spread over the application site daily
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Injections
Testosterone injections involve the injection of oil-based testosterone into
the muscle (usually the thighs, glutes, or deltoids). The testosterone is then
absorbed via the muscle into the blood stream over time. Intramuscular
testosterone preparations have been the mainstay of testosterone
replacement therapy since the 1950s, and they are one of the most popular
forms of testosterone for TRT.
The two most common forms of injectable testosterone are testosterone
enanthate (TE) and testosterone cypionate (TC). TE and TC are modi ed
forms of testosterone. Speci cally, they have an ester molecule attached to
the T molecule. This attachment slows the absorption of testosterone and
increases the half-life. Due to their long half-lives, both TE and TC provide
a sustained release of testosterone into the bloodstream. The most
commonly recommended dosing regimen for TRT is 100 mg to 200 mg
every one to two weeks. If your doctor tells you to inject every other week,
half the dose and inject every week. Lower dosages injected more
frequently lower the uctuations in testosterone levels between injections.
For more info on testosterone esters, see r/steroids A Primer on Esters.
Overall, injections of testosterone enanthate and testosterone cypionate
are inexpensive and safe. Since both forms have been around for so long,
generic versions of these medications are available. Most men that use
injectable testosterone for TRT swear by it because they get T levels back
to normal and deliver results.
While injectable testosterone is safe, know about two potential drawbacks.
First, T injections can cause uctuations in T levels following administration.
Following an injection of testosterone enanthate or testosterone cypionate,
T levels exceed normal physiological levels for the rst 2 to 3 days. They
then steadily decline to levels below physiological levels just prior to the
next injection. To minimize this issue, just shorten the interval between T
injections and lower the dose proportionally to minimize this cyclical nature
of highs and lows. (See the dosage instructions) Second, injectable
testosterone increases red blood cell production more than other forms of
testosterone. To address this potential side effect, just get regular check-
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ups with your doctor after starting TRT to monitor red blood cell levels.
Then, your doctor can address any issues preemptively.
Of note, the FDA recently approved a new injectable testosterone ester
(testosterone undecanoate) called Aveed by Endo Pharmaceuticals. Like
testosterone enanthate and cypionate, testosterone undecanoate has an
ester attached to it. Unlike testosterone enanthate and cypionate, which
need to be injected every week or every other week, testosterone
undecanoate needs to be injected once every 10 weeks. Studies show that
testosterone injections of 750 mg Aveed maintain normal levels between
300 and 1000 ng/dL for up to 10 weeks.
Pros: Inexpensive; consistent dosage; easy to adjust dosage. Cons: Need
to inject; some doctors may not want you to inject on your own; T levels
may uctuate if you inject infrequently; may experience injection site pain.
Products: Testosterone cypionate (generic); testosterone enanthate
(generic); testosterone undecanoate aka Aveed (branded product by
Auxilium Pharmaceuticals, Inc.)
Dosage: 100 – 200 mg every one to two weeks. If your doctor tells you to
inject every other week, half the dose and inject every week. Lower
dosages injected more frequently lower the uctuations in testosterone
levels between injections. For injecting info, see r/steroids Safe Injecting
Technique
• Testosterone Cypionate - FDA AccessData
• Testosterone Enanthate - FDA AccessData
• Aveed Full Prescribing Information - Endo Pharmaceuticals
Inc.
Pellets
Testosterone pellets are implanted underneath the skin in the subdermal fat
layer by a physician. The pellets slowly release a steady infusion of
hormone into the body testosterone as they dissolve over the course of
three to six months.
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Pros: Easy to use; need to administer very infrequently; no risk of transfer.
Cons: Needs to be surgically inserted and removed; may extrude/push out
of your skin on their own; dif cult to adjust dosage once implanted.
Products: Testopel (branded product by Auxilium Pharmaceuticals, Inc.)
Dosage: 6-8 pellets implanted every 3-6 months
• Testopel Full Prescribing Information - Auxilium
Pharmaceuticals Inc.
Nasal Gel
Testosterone nasal gel is administered into each nostril three times a day
every day.
Pros: Convenience; ease of use
Cons: Must be taken three times per day, every day, preferably at the same
time each day. Additionally, it failed to restore testosterone levels to normal
in 10% of men in the phase 3 clinical trial.
Products: Natesto ((branded product by Endo Pharmaceuticals, Inc.)
Dosage: One spray in each nostril three times per day (5.5 mg per spray;
33 mg per day)
• Natesto by Endo Pharmaceuticals
• Natesto Full Prescribing Information
Lozenges
Transbuccal testosterone lozenges are placed under the tongue or against
the surface of your gums. The lozenges release testosterone, which is then
absorbed through the mucous membranes of the mouth. The lozenge lasts
for 12 hours after which time it must be replaced with another lozenge for a
total of two lozenges per day.
Pros: Less liver toxicity than oral forms because it is absorbed through the
gums not swallowed. Cons: Must be kept in the mouth all day; may
aggravate gums.
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Products: Striant (branded product by Auxilium Pharmaceuticals, Inc.)
Dosage: 2 lozenges per day
• Striant Full Prescribing Information - Auxilium
Pharmaceuticals Inc.
• FDA Patient Insert on Striant
If you can get injections, do it. Everybody on /r/steroids will recommend
the same. When the doc recommends the gel/cream you can mention that
you're worried about it getting on your girlfriend or kids and they'll usually
understand. You may also want to mention that you tend to sweat a lot or
that you hear it's less effective and more expensive than injections. For /
injection locations and information, see the Wiki.
HCG/HMG
HCG is injected either intra-muscularly or subcutaneously. It can be used
alone or in conjunction with Testosterone. Dosage varies, but it typically
comes in a 5000iu vial of lyophilized power which needs to be mixed with
bacteriostatic water. (NOTE: hCG typically comes with a sodium chloride
solution, intended for a single injection; not bacteriostatic water) Mixing 2ml
bacteriostatic water in a 5000iu vial of hCG will provide twenty 250iu doses.
Each tenth of a cc/ml will be 250iu.
HMG is very similar to HCG, the key difference being that HCG acts as a
synthetic LH (luteinizing hormone). hMG mimics both of the two key
hormones produced by the testes to stimulate spermatogenesis: LH and
FSH, making it more effective in maintaining fertility. However, hMG is often
signi cantly more expensive than HCG.
As of March 23, 2021 the FDA has deemed hCG a biologic product and
compounding pharmacies will no longer be allowed to provide this service
Testosterone vs. HCG
Testosterone is the most common, but has the potential to cause infertility
and testicular atrophy during TRT use. HCG can be used in it's place or in
conjunction at low doses to maintain fertility and testicular size. Whereas
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testosterone directly puts exogenous testosterone into your blood stream,
HCG tells your body to create more endogenous testosterone.
Clomid
Clomiphene is sometimes used in place of testosterone/HCG. It is
sometimes used in an attempt to restart HPTA, as well. Like HCG, it helps
TRT-users maintain fertility. However, it can sometimes have unwanted
side effects. It comes in an oral form and dosage can be 25-50mg ED, but
may be tapered down based off BW.
Aromatase Inhibitors (AIs)
Testosterone can be converted in estrogen via the aromatase enzyme.
Consequently, taking testosterone via TRT may increase estradiol levels.
Most men on TRT dosages will not experience high estradiol levels.
However, some genetically susceptible men may experience high levels.
These high estradiol levels may lead to symptoms of high estrogen such
as uid retention and gynecomastia. As such, it is important to routinely test
estradiol levels during TRT.
If estradiol levels are found to be too high, the most common treatment is
Anastrozole (Arimidex) or Aromasin. Arimidex inhibits the aromatase
enzyme, and thus it inhibits the conversion of testosterone to estrogen.
Common medication and doses are 0.25-0.5mg Arimidex E3-7D or
12.5-25mg Aromasin E3-7D (depending on estrogen levels and response).
Normal estrogen range is about 7-42 pg/mL. Most users on this sub report
that they feel best when they're at 20-30. However, many on this sub also
feel that an AI isn't needed until/unless you notice symptoms of high
estrogen.
Medication Dosages-General
Most docs have a "standard" dosage for each medication that they start
you at (that will vary slightly from doc to doc). Some docs may adjust these
doses after a month or so of use depending on your BW results and how
tell them your mood and libido respond.
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HCG and TRT
HCG is commonly co-prescribed with testosterone. Practically speaking,
HCG is prescribed primarily to men looking to maintain fertility during TRT.
Some physicians and testosterone clinics argue that all men taking
testosterone should also take HCG because HCG helps enhance the
effects of testosterone therapy. There is no consensus, however, on using
HCG for this purpose.
To begin, The Endocrine Society’s Clinical Guidelines for Testosterone
Therapy do not recommend for the use of or against the use of human
chorionic gonadotropin (HCG) during testosterone therapy. They basically
do not offer any opinion either way.
With that being said, some physicians and some low testosterone centers/
clinics do prescribe HCG along with TRT, especially for maintaining fertility.
HCG is an FDA-approved drug, and it is recommended by the American
Association of Clinical Endocrinologists as the rst therapy for the
treatment of low sperm production. As such, some physicians prescribe
HCG alongside testosterone therapy to maintain fertility in men during TRT.
Why does testosterone therapy cause infertility in men? Exogenous
testosterone shuts down the body’s natural production of testosterone by
the testes. Testosterone levels in the body remain normal because of the
exogenous testosterone but testosterone levels within the testes drop
below normal. Since sperm production requires high levels of testosterone
within the testes, testosterone therapy reduces sperm production. In some
men, this reduction may be enough to cause fertility issues. Be aware of
this potential side effect and discuss your options with physician if you are
looking to conceive a child.
Besides stopping TRT or lowering the dosage, one potential way to
maintain fertility during TRT is to take HCG. In men, HCG stimulates the
testes to produce testosterone, which raises the intratesticular testosterone
level and allows for the production of sperm.
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According to the American Association of Clinical Endocrinologists
Clinical Guidelines HCG should be the initial therapy of choice for
increasing sperm production for at least six to twelve months. Therapy with
HCG is generally begun at 1,000 to 2,000 IU injected intramuscularly two to
three times a week, and it is taken alongside testosterone. Also, two
studies with men speci cally on testosterone replacement therapy show
that 500 IUs every other day also maintains normal sperm production.
If sperm production has not been initiated within six to twelve months of
therapy with HCG, the AACE recommends that administration of FSH in a
dosage of 75 IU injected intramuscularly three times a week along with the
HCG regimen. After six months, if sperm are not present or are present in
very low numbers (<100,000/mL), the human menopausal gonadotropin (or
FSH) dosage can be increased to 150 IU intramuscularly three times a
week for another six months.
It should be noted that HCG must be properly stored because it is a peptide
not a discrete molecule, like testosterone. Typically HCG comes in the form
of a powder in a sterile ampule to prolong its shelf life. In order to use, HCG
must be reconstituted/remixed with bacteriostatic water.
In general, HCG should be kept in the refrigerator away from food. If
unmixed, the shelf life of HCG is generally up to 18 months in the
refrigerator. If mixed, the shelf life of HCG is up to 2 months in the
refrigerator. If unrefrigerated, unmixed HCG typically only lasts 60 days,
whereas mixed HCG typically only lasts 48 hours.
What to Expect While On TRT
The First 1-3 Months
• Doctor visits: Most docs will have you come in every couple of
weeks for the rst 2-3 months and then once every year.
• Time to notice effect: You can notice some effects on libido
within the rst few hours (although it may be placebo). Effects
on mood may take more like 2-3 weeks.
• Mood Effects: Increase in energy and overall a better sense of
well-being.
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• Libido Effects: Greater desire for sex. More frequent erections,
especially during sleep.
• Negative Side Effects: In this time, you'll probably get some night
sweats. You may also get some acne breakouts. You probably won't
notice a whole lot of other negative effects at this point.
3-Months and On
• Fewer doctor visits
• Night sweats and acne should decrease
• First 1-3 days after injection, you'll feel great. Next 4-8 days
you'll feel good. The next 8-14, you'll still probably feel slightly
better than before you started. That's why I recommend E7D
injections or more frequent--it evens it out so you feel great
consistently.
• Mood is likely more consistently good.
• Libido effects may be slightly less than in the rst 1-3 months,
but still a big improvement.
• Somewhat Common Positive Effects: Some TRT-users also may
experience a loss of fat, increased muscle, Increase in strength,
a deeper voice, and increase in facial and body hair.
• New Negative Side Effects: It's possible that you might
experience high estrogen at this point, so watch out for
estrogen sides. If you experience increased headaches, nipple
lactation, or worsening vision, talk to a doctor; this could indicate
a pituitary tumor that is increasing in size due to the medication.
General Tips While on TRT
• Get blood work. It's the only way to con rm low T and whether
or not estrogen and/or prolactin are causing side effects.
• Keep a daily log of your injections, your sex drive, and your
mood. It can be useful to show to a doctor if you're trying to
argue for/against adjusting medication. Plus, it can help
determine if you're actually experiencing effects of the
medication since the change is generally pretty gradual.
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• If you have problems telling other people you're on TRT that
you'd like to open up to: remember that this isn't much different
than having poor eyesight and getting glasses or lasik. You have
abnormally low testosterone. The medication is helping you be
"normal." That being said, some people may still view it as
steroids and you won't be able to say anything to sway them.
Depends on the person you're telling.
Injection Tips
• Z-Track injection method is helpful, but not 100% necessary.
• Quad injections are easy, but many prefer ventrogluteal.
• You may also want to consider subcutaneous injections. They
use a smaller needle and the absorption rate is a little slower,
evening out your T levels.
Subcutaneous injection is excellent for TRT purposes. Subcutaneous
injection sites.
The subcutaneous that I refer to here is not the same as an IM injection
"leaking" and doesn't have the associated pain. An intentional sub-q
injection is actually into the subcutaneous fat. It tends to form a small
nodule which is easily absorbed. An injection which leaks gets between the
muscle fascia and the subcutaneous fat. It absorbs more slowly and
causes more irritation.
The easiest sites to use are near the umbilicus (belly button) or in the
oblique fat pads (love handles) for e3d injections. It's easy to see what you
are doing and both hands are available. Because of this, it's much easier
than IM for regular small injections and just as effective. If the volume is 0.3
cc or less, it's completely painless and doesn't leave any visible signs
unless you are very lean. At around 10% one may need to stop using the
belly sites and stick to obliques. Even with 2 sites, each will be completely
absorbed before you return to it.
There is less discomfort than IM. With good gear (eg: pharma) there is no
PIP. It might sting for a few minutes but that's it.
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A 29G 1/2" slin pin with 0.5cc syringe is a good size. They are low dead
space needles, meaning there is less wasted gear. The only downside is
that drawing can take a while, but since it's such a low volume it doesn't
really add up to much time.
For instructions on doing the shots, watch this video: SUBCUTANEOUS
TESTOSTERONE INJECTIONS - THE CUTTING EDGE WITH DR. JOHN
CRISLER
The video and shows the belly and oblique sites.
Dr. Crisler recommends a 5/8" 25G needle. I had some leakage with a
larger needle and the syringe / needle had a larger dead space that wasted
gear. I'm much happier with 29G. His fears about a high-pressure jet are
unfounded due to the viscosity of the oil.
Coming O TRT
You may want to come off of TRT for a number of reasons (cost, sick of
pinning, no longer wanting to be swole, etc). If it's solely for fertility
concerns, you may not need to (see info above about HCG/HMG/Clomid).
Otherwise, you'll want to make sure that you don't come off cold turkey and
instead do an actual PCT. Coming off cold turkey, you risk having your
HPTA remain shut down, tanking your test, and suffering depression, ED,
and other low T side effects. See the Wiki for TRT-speci c PCT
recommendations.
Bene ts of TRT
Testosterone replacement therapy in men with low testosterone produces
many positive bene ts. These bene ts can be broken down into conclusive
bene ts and inconclusive bene ts. Conclusive bene ts are bene ts that are
relatively certain, whereas inconclusive bene ts are bene ts that are not
certain.
Conclusive Bene ts: Testosterone replacement therapy has consistently
shown to positively alter body composition. It increases muscle mass (via
increased muscle synthesis) and decreases fat mass (via increased fat
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lipolysis), especially abdominal fat mass. It also slows or even reverses the
loss of bone mineral density due to aging. TRT also increases libido.
Inconclusive Bene ts: Testosterone replacement therapy may also improve
sexual function (improve erectile function), improve mood, reduce
depression. However, TRT has not been shown to conclusively improve
erectile function and mood. The primary reason why TRT may not help with
erectile dysfunction or mood/depression is because both conditions can be
related to one or more of many potential underlying medical conditions
unrelated to testosterone levels. Without addressing such underlying
conditions, testosterone alone will likely not improve erectile dysfunction or
mood/depression.
Side E ects of TRT
The following are potential side effects of TRT.
• Polycythemia – Polycythemia occurs when red blood cell production
increases too much. Testosterone stimulates the production of red blood
cells. Thus, TRT may increase red blood cell levels beyond normal. High
red blood cell levels cause the blood to thicken and clot, which can
potentially lead to a stroke. Oftentimes, if red blood cell production rises
to dramatically, TRT dosages must be lowered or stopped. Additionally,
your physician may perform a phlebotomy (a withdrawal of blood to
lower red blood cell levels). The risk appears to be higher with IM
preparations and may be due to the supraphysiologic levels that are
seen with infrequent injections.
• Infertility – TRT interrupts the body’s normal release of testosterone. It
also impairs the production of sperm. While infertility is usually
reversible, it is important for men who wish to preserve their fertility to
talk with their physician prior to commencing TRT.
• Sleep Apnea – TRT may worsen sleep apnea in men who have been
previously diagnosed.
• Gynecomastia – TRT may alter the balance of testosterone and
estrogen in the body in certain men. Some men’s bodies metabolize
testosterone in estradiol more readily than normal. This aromatization
causes the breast tissue to swell. It is important to address any issues
with gynecomastia quickly. Unfortunately, medical treatment of
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gynecomastia that has persisted beyond a year is often ineffective.
Gynecomastia Wiki - Gynecomastia Subreddit
• Fluid Retention - Fluid retention may occur in the arms and legs at the
beginning of therapy. It generally resolves after the rst few months of
treatment.
• Alteration of Lipid Levels - Testosterone therapy may adversely affect
cholesterol levels, slightly lowering HDL cholesterol and slightly raising
LDL cholesterol. Most cases of adverse affects to cholesterol deal with
supraphysiological doses of testosterone, not replacement doses.
The Endocrine Society Clinical Practical Guidelines detail the conditions in
which testosterone administration is associated with a high risk of adverse
outcome and in which testosterone should not be administered:
Very high risk of serious adverse outcomes
• Metastatic prostate cancer
• Breast cancer
Moderate to high risk of adverse outcomes
• Unevaluated prostate nodule or induration
• PSA >4 ng/ml (>3 ng/ml in individuals at high risk for prostate
cancer, such as African-Americans or men with rst-degree
relatives who have prostate cancer)
• Hematocrit >50%
• Severe lower urinary tract symptoms associated with benign
prostatic hypertrophy as indicated by AUA/IPSS >19
• Uncontrolled or poorly controlled congestive heart failure
• TRT Side Effects - Medscape
Related Posts
Word of caution to the naturally low-T crowd.
/u/sixxsix creates this entry
After 1 year on TRT
The Epically Long TRT Story
10 pins in and smiling
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The journey to good TRT
4 Months starting TRT TRT is amazing
10 Things to look for in a doctor for TRT
Subcutaenous Test Injection Sites - Self Experiment (For Science)
Studies
Subcutaneous administration of testosterone. A pilot study report.
CONCLUSION: Therapy with weekly subcutaneous testosterone
produced serum levels that were within the normal range in 100% of
patients for both peak and trough levels. This is the rst report, which
demonstrated the ef cacy of delivering weekly testosterone using this
cheap, safe, and less painful subcutaneous route.
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Anabolic Steroids and the Law
United States law prohibits the possession of anabolic steroids without a
legal medical prescription, imparting severe penalties (including ne and/or
imprisonment) for those that choose to violate these laws. Under in uence
of U.S. government of cials, World Anti-Doping Agency (WADA) members,
and public criticism following numerous doping scandals, a growing number
of countries are following the U.S. by adopting their own laws against the
possession of anabolic steroids and other sports doping drugs. In many
cases similar severe criminal penalties have been enacted. The following
section discusses in more detail various national laws that concern the
personal use of anabolic steroids and other related drugs.
United States
Anabolic steroids have been classi ed as controlled substances in the
United States since 1991, with passage of the Anabolic Steroid Control Act
of 1990 (Pub. L. No. 101-647, Sec. 1902, 104 Stat. 4851, 1990). This law
makes it a criminal offense to sell, distribute, manufacture, or possess
anabolic steroids without proper legal authorization. The outlined penalties
for possession without a legal prescription include a maximum of 1 year of
imprisonment and/or a minimum ne of $1,000. This may be increased to 2
years of imprisonment and/or a $2,500 minimum ne for individuals with a
prior drug conviction. Note that this law was amended in 2005 following
passage of the Anabolic Steroid Control Act of 2004. The new law added
26 new steroid compounds to the list of controlled substances, and also
removed the legal requirement that a compound be proven anabolic in
humans before it can be added. This “promotes muscle growth” clause was
the key roadblock to removing many of the “legal steroids” of the late 1990s
and early 2000s.
State vs. Federal
Criminal laws against the possession of anabolic steroids exist at both the
federal and state level in the U.S. Depending on the circumstance, an
individual may be charged with a steroid related crime by either the federal
government or the state government where the crime took place. Unless
the crossing of state lines was involved, most criminal prosecutions for
steroid related crimes take place at the state level in accordance with state
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laws. Most often the state laws mirror federal statutes very closely although
this is not always the case. There can also be a great deal of variability in
how punishments are determined between one state and another. If you
are not obtaining medications legally through a physician’s prescription, it is
advisable to study the steroid laws closely, particularly those of your
individual state.
Austria
The possession of anabolic steroids is not a criminal act according to
Austrian law. In 2008, Austrian government of cials announced intent to
place criminal penalties on steroid possession.
Australia
It is a criminal act to import, supply, use, or possess anabolic steroids in
Australia without a prescription from a medical practitioner, dentist, or
veterinarian (Poisons and Drugs Act Amendment of 1994). The outlined
penalties for possession without a legal prescription include a maximum of
6 months of imprisonment and/or a ne of $5,000.
Belgium
It's a criminal act to manufacture, transport, acquire, or possess doping
substances including anabolic steroids, human growth hormone, and
erythropoietin.Penalties for selling is imprisonment ranging from 1 month to
5 years and a ne that ranges from 3000 to 100,000 euros. Penalties for
transport, import, export, possession, usage and manufacturing are one of
the penalties for selling instead of both (either imprisonment or the ne). If
you are found to possess one of said substances it is equaled to using.
Some of the substances you are allowed to use and possess of course if
you have a prescription. Belgium also "muscle pro les". “Muscle pro ling”
is the practice of identifying suspected anabolic steroid users based simply
on their appearance, then arresting them on that basis and forcing them to
submit to urine tests.
Canada
Anabolic steroids are included in the Canadian Controlled Drugs and
Substances Act as Schedule IV substances. It is illegal to sell,
manufacture, or import anabolic steroids into Canada without proper legal
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authorization. Possession of anabolic steroids for personal use is not a
criminal act.
Czech Republic
In 2008 it became a criminal act to manufacture, import, export, store, or
distribute anabolic steroids in the Czech Republic. The potential penalties
include a maximum of 3 years in prison. It is not a crime to possess
steroids for personal use.
Denmark
In Denmark it is a crime to manufacture, import, export, market, dispense,
distribute, or possess doping substances including anabolic steroids,
human growth hormone, and erythropoietin without proper medical or
scienti c reason (The Act on Prohibition of Certain Doping Substances No.
232 of 21 April 1999). The potential penalties for possession include a
maximum of 2 years in prison.
France
In 2008 it became a criminal offense to manufacture, transport, acquire, or
possess doping substances including anabolic steroids, human growth
hormone, and erythropoietin in France. The potential penalties for
possession include a maximum of 5 years imprisonment and/or a 75,000
Euro ne.
Greece
The possession of anabolic steroids is not a criminal act according to
Greek law. In 2008, government of cials announced intent to place criminal
penalties on steroid possession in Greece.
Israel
In Israel, under the provisions of the Pharmacy Ordinance, it is prohibited to
import anabolic steroids that are not approved by the Ministry of Health,
and their sale without a physician’s prescription is prohibited. The Division
of Enforcement and Inspection in the Ministry of Health is working with
elements of customs and the police to locate and seize anabolic steroids
that are illegally imported and/or manufactured in Israel. The Division is
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also working for the prosecution of traders and vendors of these
substances. Offenders also face tax evasion charges (on sales value of
steroids).
New Zealand
It is a criminal act to import, supply, use, or possess anabolic steroids in
New Zealand without a prescription from a medical practitioner. As it so
happens, steroids fall broadly under the Medicines Act as opposed to the
Misuse of Drugs Act. The Misuse of Drugs Act is what de nes drugs as
Class A,B or C etc, and decides which punishments should be given to
their sale or use. Some Medicines also fall under Both Acts as they are
deemed to have a high risk of abuse potential, or are considerably more
dangerous. If you are caught with steroids or other medicines in your
possession without a prescription, or you are selling them without
permission you could face potentially years in prison or thousands of
dollars in nes.
Norway
It has always been illegal to import, export and sell anabolic steroids in
Norway. The Medicinal Products Act was amended on June 14, 2013 & in
force as of July 1, 2013, to make the use and purchase of anabolic steroids
illegal, as well.
Sweden
In Sweden it is a crime to import, manufacture, transport, sell, possess, or
use doping substances such as anabolic steroids and growth hormone
without proper legal authorization (The Swedish Act prohibiting certain
doping substances (1991,1969). The potential penalties include a
maximum of 2 years in prison. Possession for personal use is usually
regarded as a petty offense and given a maximum penalty of 6 months
imprisonment.
United Kingdom
Anabolic steroids are controlled as Class C substances under the Misuse
of Drugs Act 1971. There is no possession offense, but it is illegal to
manufacture, supply or possess/import/export steroids with the intent to
supply, without a license to do so. The maximum penalty for these offenses
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is 14 years in prison and/or a heavy ne. The “supply” offense can mean
something as simple as sharing anabolic steroids with someone else, even
if you don’t sell them. There were changes to UK steroid law as of April 23,
2012 that pertained to importing anabolic steroids. Following advice from
the ACMD, anyone wishing to import these drugs from outside the UK will
have to do so in person (“personal custody”). It will no longer be permitted
to buy steroids and associated drugs from outside the UK, through internet
and mail order sites and have the products delivered. There has been a
great deal of pressure in recent years from the U.S. and World Anti-Doping
Agency to place criminal penalties on the possession of anabolic steroids
without a prescription.
References
• Llewellyn, William, Anabolics 2010, 2003-4
• https://www.health.gov.il/English/Topics/PharmAndCosmetics/
pharm_crime/Pages/steroids.aspx
• http://www.israelnationalnews.com/News/Flash.aspx/270013
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Cycle Information
Things to Know
The Cycle
Typical AAS usage comes in pre-planned lengths of time that a person is
taking any compounds. The idea is to achieve a set of goals and then allow
the body to get back to stasis and ensure that there are no medical issues
before doing it again. There is also some controversy about possible
decreased effectivity of long term use of AAS use. Cycles range in lengths
from short (8 weeks) to long (20 weeks).
There are several different items that need to be understood to execute a
good cycle.
Pre-cycle Check list
The following check list has been created to help new users ensure that all
bases are covered.
1. Cycle goals: What are your goals for the cycle? The goals of the cycle
are imperative to planning a complete cycle with compounds, length
and recovery.
2. Eating plan: How many calories are you planning per day? If you're
cutting, will you re-feed? How often?
3. Exercise plan: Generally, your recovery period after exercise will
decrease. This will allow more physical exertion while on cycle. Try to
take advantage of this to get the most out of your cycle and plan more
time in the gym.
4. Blood work: The hallmark of all safe cycles, blood work is required to
ensure user safety.
Pre-cycle: It is strongly recommended that blood work be done before
a cycle to ensure good health and to obtain an accurate measure of
pre-cycle testosterone production.
On-cycle: Depending on the length of your cycle and trust in your
source, you may want to get blood work done while on cycle. This
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would verify that gear is working correctly and ensure that you remain
in good health.
Post-cycle: After PCT, newer users or users with unknown sources
should get blood work done to ensure a return of natural testosterone
production.
5. Gear list: What gear needs to be purchased? Consider planning to
purchase a little more than needed as accidents (dropping a vial, etc)
happen.
6. AI list: Different cycles require different AI's. It's always recommended
to have one on hand, even if not actually used during cycle. If you
cannot afford an AI, you cannot afford to run a cycle.
7. PCT List: Your natural production of testosterone will, more than likely,
cease during cycle. A de nitive plan needs to be put into place to
ensure a return to stasis and normal testosterone production after
cycle.
8. Pins, storage and disposal: How many pins do you need? How will
you store them? How will you dispose of them? Find out how to
legally dispose of your pins.
9. Questions: During cycle you will probably gain a lot of mass. You may
have friends and family ask how you are doing it. Be prepared to
answer these questions.
10. Clothes: Yes, you'll probably need some new ones while on cycle.
Planning the Cycle
When planning your cycle, you will need to know how much of each
substance you will be using for the entire duration of the cycle. It can
greatly help to plot your blood levels of the various compounds.
Calculating Total Amount Needed
1. To calculate the total amount needed to be purchased:
X mg desired * number of days / week(s) * number of weeks total =
total amount needed
2. Calculate the total mg per vial:
total ml * #mg / ml = total mg per vial
3. Then calculate the vials needed:
total needed / mg per vial = total vials
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4. Round up and add one to be sure:
total vials, rounded up +1 = total purchase amount
Example
1-12 Test Prop 150mg EOD
Source provides 10 ml vials of 100mg / ml Test Prop.
1. To calculate the total amount needed to be purchased:
150 mg * (7 injections / 2 weeks) * 12 weeks = 6,300 mg total needed
2. Calculate the total mg per vial:
10 ml of 10g mg/ml vial = 10 ml * 100mg /ml = 1000 mg per vial
3. So for a Test P cycle, 150 mg, EOD:
6,300 mg / ( 1000mg / vial ) = 6.3
4. Round up and add one to be sure:
(6.3 round up =) 7 + 1 = 8 total vials needed
Calculating Dosage
Most vials come in 10ml vials. The label will typically tell you the number of
milligrams per milliliter (mg / ml). For example, a vial of Testosterone
Propionate can come in a 10ml vial with 100mg / ml. That means that the
entire vial contains 1000mg of the substance. If you want to inject 150mg of
the substance EOD, you will inject 1.5ml.
X mg desired / (N mg / ml) = Total ml needed per injection.
For a Testosterone Propionate vial at 100 mg / ml and a user wanting
150mg E0D:
150mg / (100 mg / ml) = 1.5 ml
For a Testosterone Ethanate vial at 250 mg / ml and a user wanting 150mg
E2D:
150mg / (250 mg / ml) = .6 ml
Finding A Source
// As is posted everywhere, this forum is not the appropriate place to
look for a source. There are multiple other ways to nd a source; Reddit is
not one of them. Asking will result in a ban from r/steroids.
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Blast and Cruise
Some users decide that they do not want to waste time with PCT, and
instead want to keep using steroids for a longer period. What they will then
do is run a cycle (blast), and then run a TRT dose (cruise). This allows the
body to heal from the stress placed under it during the blast, allowing the
liver/kidneys to rest and letting their cholesterol normalize. Once they are
back within healthy parameters, they may then proceed to do another blast.
This allows you to avoid going through PCT, which in and of itself is rather
harsh on the body. This also prevents the muscle loss often seen in PCT.
There are downsides, of course. You will likely be either infertile or have a
very low sperm count during this period, and the longer you stay on the
higher the chances are of you staying that way should you PCT. These
cases are rare, but it has happened.
Additional Topics
Example Cycles
Safe Injection Technique
Post Cycle Therapy (PCT)
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Your First Cycle
So, you got interested in steroids and are now trying to gure out where to
start. Beginners have one rule: KISS.
That stands for Keep It Simple, Stupid. The more chemicals you toss in at
once, the bigger your chances of going down in a aming reball. A big,
bloated, gyno-y reball. BUT most potential side effects can be avoided
entirely if the cycle is followed correctly and the proper precautions are
taken.
Contrary to what a lot of people say, /r/steroids does not believe that you
have to have reach your full natural potential before running a cycle. What
is recommend is that you have a good amount of experience and
knowledge when it comes to training and nutrition and that you start off
fairly lean – It is recommend that you are under 15% body fat and ideally
closer to 10%.
This wiki page will include how to administer the steroids, recommended
doses and durations, how to prevent and counteract side effects, and what
you can expect to gain from your rst cycle.
BEGINNER FAQ
-Contributions by u/DLTBB2
Can I Just Do An Oral Only Cycle?
You can. Should you? Absolutely not. Oral steroids are going to suppress
your natural Testosterone production hard.
ALL steroid cycles need to be taken together with a base of
Testosterone to replace your natural production, which will be shut
down.
Without a Testosterone base, you will feel weak, tired, depressed, low
libido, erectile dysfunction, muscle loss and weakness—all the
symptoms of low testosterone.
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As you won't have any Testosterone to support the muscles you're building,
you'll lose all your newfound, hard-earned gains just after you've gotten
them.
If you choose to do a orals-only cycle against all sound advice, you should
look into getting a SERM (like Nolvadex/Clomid or the sorts) for a proper
PCT, as well. You should consider reading through this Wiki and doing a
real cycle, complete with Testosterone, as you'll nd better results, as
well as feeling better too.
What About A Prohormone Or Designer Steroid Cycle?
Again. You can. Should you? Probably not. Prohormones & Designer
Steroids are going to suppress your natural Test pretty hard.
You need to take ANY CYCLE* together with a base of Testosterone to
replace your natural production, which will be shut down. Without a
testosterone base you may nd you don't feel the best or you feel
symptoms of low testosterone.
Prohormones & Designer Steroids are no better (or even worse in some
cases) than using a traditional oral steroid. The supplemental PCT crap
they sell with these Prohormones is predominantly bogus stuff and if you
choose to do a Prohormone / Designer Steroid cycle, you should at least
look into getting a SERM (like Nolvadex/Clomid or the sorts) for a real
PCT. You should consider reading through this Wiki and doing a real cycle,
complete with Testosterone, as you'll nd better results, as well as feeling
better overall too.
Is my gear bunk?
It's a question we see almost daily on the forum. The author's cycle isn't
living up to their expectations and more often than not, the rst thing they'll
do is blame the gear for their underwhelming results. But are they doing
everything that is required from them to make gains? Are they using the
correct metrics to evaluate whether their gear is legit? And have they
started the cycle with realistic expectations? In most cases, absolutely not.
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I don’t feel anything from it.
You won’t necessarily feel different on gear. I don’t, regardless of what
compound/dose I’ve used, I always feel the same, laid back and easygoing. When you read about people feeling superhuman when they start
injecting a bit of Testosterone, the chances are they’ve suffered from low
Test without necessarily realising for their whole lives and are nally
experiencing normality, which they think feels fantastic.
But I’m not getting any side effects!
Good. That’s what you want. You don’t have to suffer from side effects for
your gear to be legitimate. Consider yourself lucky. Would you prefer to be
covered in acne, bloated and balding to help con rm you’re actually
injecting hormones? If you’re asking this question in the rst place, the
chances are you’re new to using PEDs and using moderate doses of 1-2
mild compounds. It’s more common not to suffer sides at all than it is to be
riddled with them with this kind of cycle.
I’ve not gained any weight/have gained very little weight!
What’s your maintenance calorie intake? How did you reach this gure?
Please don’t say you used a shitty generic online calculator. How active are
you day to day? How many calories do you burn during training? Are you
doing cardio? Combine all of this. That’s your maintenance calorie intake. If
you want to gain weight, you need to be in a calorie surplus daily. Don’t
think you’re a special snow ake who will do an insane recomp at
maintenance calories during your rst cycle. You’ll spend the whole cycle
spinning your wheels and have nothing or very little to show for it at the
end.
But I’m eating roughly 2300-3300 calories every day and still not gaining
Roughly won’t cut it. It needs to be consistent. If you’re spending half of
your days at -500 calories and half at +500 calories, you’re at maintenance
over the course of the week and that’s why you’re gaining next to nothing.
Your surplus needs to be consistent over the week if you wish to gain
consistently.
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My bench press hasn’t suddenly shot up by 50KG..
It won’t. Sure, you’ll gain strength faster than you would naturally. But
you’re not going to turn superhuman overnight or even during one full
cycle. You need to tailor your routine so it’s focused on progression and
work on adding small increments in weight, extra reps or additional time
under tension to your lifts each week over the course of the cycle. The
small and consistent increments will add up and it’s possible to boost your
numbers considerably in 15 weeks, but you’re not going to turn in to Larry
Wheels. Look at the volume and frequency of your training and make sure
it’s right for you and you’re able to recover in between sessions. Focus on
progression. Get rid of all of that junk volume where you’re lifting with little
to no intensity and aimlessly trying to pump the muscle thinking it’s going to
explode. That kind of training might work for a select few with superb
genetics, but you’re better off focusing on the bread and butter and getting
stronger over low to moderate volume.
Is (random UGL that has existed for one week)
Pharma legit?
REMEMBER THAT THERE WILL BE NO SOURCE DISCUSSIONS
ALLOWED ON THIS FORUM
There’s countless threads on the forum already with reviews. You’ll see
certain labs mentioned and praised daily. Outside of putting out a bad batch
due to dodgy raws or somebody producing identical replicas, you’re more
than likely going to be good to go with those labs. If they’ve put out a shit
batch, you’ll have probably heard about it already. If you’re buying from
some obscure lab that nobody has ever heard of despite having dozens of
well reviewed labs at your disposal, that’s on you.
Should I add X, Y and Z to make up for the fact that this might be bunk?
No. You’re brand new to gear. It might not be bunk and could be a training/
nutrition issue. Throwing in another compound is going to give you more
potential side effects to worry about and require you to add additional
ancillaries to counteract them. You’re only just learning how you respond to
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Test by itself and if you’re ticking all the boxes, you can make great gains
on that alone with little to no sides.
I’m using (extremely high)mg of AI and on (relatively low)mg of Test and
feel like shit, this Test must be bunk!
You’ve been using a high dose of AI from the offset and have crushed your
E2. That’s why you feel like shit. Use your AI when it’s required at the
lowest dose you can get away with using and ideally, have bloods done to
determine when it’s required or you’re going to be blindly throwing super
strong medication to x a problem which may not exist, risk crashing your
E2 and ruining your whole cycle.
I don't feel extremely horny 24/7 and don't want to shag every woman in
sight, this must be bunk, right?
Not necessarily, no. It's all a ne balancing act. Your Test could be sky high
but your E2 or a range of other different hormones could be slightly out of
whack, creating a ratio that your body doesn't like and having a negative
impact on your libido. Over time, you'll learn what levels/ratios work for you
and help you feel on point and you'll be able to achieve them through a
proper dosing schedule/can use blood work to dial them in. Not only that,
but your Test levels aren't the only thing that will impact your sex drive. Are
you stressed at work? Hate your job? Anxious? Depressed? Worried about
the cost of living increasing? Having trouble sleeping? Think your Mrs is
having an affair with your mate? You're hardly going to want to shag every
woman within a 2 mile radius while you've got dozens of issues and stress
bubbling away under the surface. There's more to a healthy libido than
Testosterone levels.
I haven't been able to replicate ( tness in uencer)'s physique even though
I've used the same cycle as them, my gear must be bunk!
There is a million things separating your physique from theirs other than
your cycle. Your height, weight, frame, insertions, muscle bellies,
muscularity, body fat percentage, body fat distribution, calorie/macro/ uid/
mineral intake, training volume/frequency/intensity/style and countless
other factors will differ from theirs. And what's to say they are being honest
about their cycle and dose to begin with? It's common for somebody in the
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public eye to downplay their cycle/doses to pay homage to their work rate,
genetics and consistency. You are naïve if you think you will mimic
somebody's exact physique by simply copying their gear protocol.
I don’t feel anything, I have zero side e ects, my
training and nutrition is perfect and I’ve still not gained
a single pound
Get a blood test from MediChecks while on cycle and post your results. If
the gear is bunk or severely under dosed, your blood work will show this
quite clearly and then we can all agree that the gear is indeed bunk. I’ve
been blasting and cruising for upwards of 8 years and I can’t ever recall
using any gear that was blatantly bunk and I’ve used every lab under the
sun, so I don’t think it’s as common as the constant bunk gear threads are
suggesting. If you’re using a compound which won’t show on a blood panel,
send a sample to Janoshik or a similar lab for testing. That will identify the
exact contents of your gear and you'll know if it's accurately dosed, under
dosed or bunk. Most of the time, it’s a training/diet issue and people are
blaming it on the gear before accepting they might not be ticking all the
boxes. If in doubt and you’re doing everything right, get a blood test or a lab
test and you’ll know for sure.
Don’t go in to this with your expectations too high. If your diet consists of
one solid meal a day and 5 snacks that are t for a primary school student’s
lunchbox, you’re not going to look like Nick Walker any time soon. In fact,
you’ll probably never look like him, or even a low level IFBB Pro. Your
genetics will dictate 95% of your potential and even if you do
EVERYTHING perfectly, you’ll nish your rst cycle looking like a slightly
thicker, fuller, stronger version of your natural self with slightly rounder
delts, more prominent traps and a couple of extra veins running down your
upper arm when you’ve got a good pump. Maybe 1 in 50 of you will be a
great responder and nish the cycle looking dramatically different, but you’ll
never need to ask this question because it’ll be clear your gear is real from
the offset.
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The Basic Bulk
The Basic Bulk, that is recommend, is a 12–20 week cycle of Testosterone
while running a moderate calorie surplus with emphasis on gaining as
much lean muscle tissue as possible and progressively adding weight to
your lifts.
Testosterone is a powerful tool, if used correctly and can put on a good
+8-12 lbs of LEAN mass (excluding water and fat gain) over the course of
16 weeks. Testosterone is a relatively mild compound that causes little to
no issues with side effects. Again, most potential side effects can be
avoided entirely if the cycle is followed correctly and the proper precautions
are taken.
Read Other Experiences With Testosterone:
• 1st Compound Experience Thread
• 2nd Compound Experience Thread
When purchasing your AI (Aromatase Inhibitor) and SERMs (Selective
Estrogen Receptor Modulator) it is advised to buy pharmaceutical grade
products whenever possible. Your Testosterone can be pharmaceutical
grade or from an underground lab (UGL). Just make sure you do plenty of
research of the brand before you spend any money to make sure they have
good reviews.
NO SOURCE TALK
REMINDER: NO SOURCE TALK. This forum is not the place for you to
do research or request source information.
What You Will Need
Essentials
• Testosterone Enanthate or Cypionate - 4 x 10 mL Vials (generally
dosed 250-300mg per mL)
• An Aromatase Inhibitor (AI) like Arimidex or Aromasin
• PCT Medication
|--- /r/steroids Recomended PCT
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• Syringes and Needles
|--- Luer Lock Syringes
|--- 21g Needles (1" to 1.5") for drawing
|--- 25g Needles (1" to 1.5") for injecting Glutes
|--- 25g Needles (1") for injecting anywhere else (Not necessary if only
injecting Glutes.)
|--- Alcohol injection swabs
Optional Items
• An Oral Steroid
• HCG (Learn more on the PCT wiki page)
|--- Bacteriostatic Water
• SERM in case of a gyno air-up
|--- Raloxifene
or
|--- Nolvadex
Why 4 Vials of Testosterone?
On a lot of forums the rst cycle advised to new steroid users is 10-12
weeks. 10 weeks is slightly too little. 12 weeks is ne, but you will have Test
left in the vial. For this reason, you may go up to 16–20 weeks. Given this
is your rst cycle and will likely yield some of the most dramatic results,
(assuming diet, training and rest are on point) you want to strike a balance
between maximizing your gain and minimizing the time it will take to
recover from the cycle and any potential side effects. It is always
recommended to at least PCT for your rst cycle vs. Blast & Cruise.
Testosterone Enanthate Or Testosterone Cypionate?
What's The Difference?
Approximately nothing. De nitely nothing that is going to make a difference
in choosing one or the other for our purposes. Read the speci cs below:
• The ester weights are almost identical, with Cypionate being ever soslightly heavier.
Meaning there is ever so-slightly more actual testosterone hormone
(~1%) in Enanthate.
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• The terminal half-life is also almost identical.
Enanthate is 4.5 days.
Cypionate is 5 days.
This will result in ever so-slightly more stable bloods with Cypionate.
• For some, they may experience a slight difference in potential Post
Injection Pain (PIP). This is due to Cypionate having a higher melting
point than Enanthate, making Cypionate more prone to being able to
cause PIP. This all depends on how your Testosterone was brewed by
your source/supplier. Read more on Post Injection Pain (PIP): Here.
Please See Our Esters Wiki Page: Here
WhEn DoEs tHe TeSt KiCk In?
Be patient. It's a marathon, not a sprint.
Testosterone Peaks
Blood serum concentrations quickly rise to supraphysiological levels.
• Testosterone Enanthate levels have been shown to peak as soon as
~6-10 hours after injection.1
• Testosterone Cypionate has been shown to have pharmacokinetics very
similar to the pharmacokinetics of Enanthate, with peak serum
concentrations occurring shortly after injection.1
• Just because your T levels are high doesn't mean you'll transform into
The Hulk overnight. Enhanced protein synthesis is directed from the cell
nucleus and is a long-term recursive metabolic process.
• Testosterone E and C both take between 14-19 days to fully
saturate, depending on your individual metabolism.
• You probably will start noticing enhanced recovery and mild weight gain
around Weeks 3–4.
• You probably won’t notice much aside from greater recovery unless
you had low T levels to begin with.
Arimidex or Aromasin?
You should read the AI portion of The Estrogen Handbook, as well as the
compound pro les for each, and make that choice on your own.
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• Arimidex compound pro le
• Aromasin compound pro le
If you choose Arimidex: Just be aware the blood levels of Arimidex
can drop a bit when used alongside Nolvadex. (In case of a gyno airup. See more below)
If you choose Aromasin: TAKE WITH FATS
How Much AI Do I Need?
Hopefully none!
How much AI is required can vary from person-to-person, as a guide it
advised you get bloodwork to dial in your dose. You will basically need to
use trial and error to nd your ideal AI dose to get your Test:Estrogen
balance at your personal ‘sweet spot.’ MOST users will nd 0.5 mg of
Arimidex or 12.5 mg Aromasin E3D or E3.5D to be a good dose. Some
may need more frequent (EOD) dosing. Some may even need less than
E3.5D.
Some don't need any AI at all. This is something that varies widely from
person-to-person.
In The Estrogen Handbook, it gives an idea of side effects for both low
and high Estrogen levels which may help you gauge an idea of where
you’re at should you become confused and not want to have bloods taken,
BUT blood work will be the only way to know 100%.
It is HIGHLY UNLIKELY that you will need this dose on 500mg of
Testosterone, but it is suggested to have enough to run the Arimidex 1mg
EOD or Aromasin 25mg EOD, this will give you more than what you
realistically should need.
REMEMBER: Get bloodwork to dial in the AI dose you may need.
When Should You Start Your AI?
There are two different trains of thought:
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• Dose preventatively (i.e., before you get high bp, spicy nips, etc.)
• Dose only when you start to notice sides (acne, bloating/water
retention, high blood pressure, nips that are a bit zesty) (PREFERRED)
The preferred method is only to take an AI only when sides necessitate.
Why?
Estrogen (E₂) is highly anabolic, cardioprotective and neuroprotective, and
essential for normal physiological functioning.
Crashed E₂ sides are far worse than the inverse, and estrogen should be
proportionally high just as test, so long as sides don't get out of hand.
Gyno takes weeks to develop, and new gyno can effectively be taken care
of with SERMS while continuing the cycle.
Estradiol Rise
With this testosterone peak, Estradiol (E2) has been found to correlate
directly.[5] This is no surprise as aromatization will occur, causing Estradiol
to peak shortly after as well.
See below:
• One study found that after a 200mg Test E injection, E₂ values rose
signi cantly in just 6hrs post injection in eugonadal men and that peaked
at 2 days after injection (base serum E2 was 23 ± 4 pg/ml, peaked at
day 2 (45 ± 4 pg/ml). Alternatively, hypogonadal men were also studied
and found to increase signi cantly in just 6hrs as well and peaking the
day after the injection, but bringing them to a more optimal range (base
serum E₂ was 7.2 ± 2 pg/ml, peaked at day 1 to 29 ± 4 pg/ml).[2]
Another study supports this level of change in Hypogonadal men.[4]
• Another study found that after a 200mg Test C injection, E₂ values rose
signi cantly from a mean of 26.2 ± 14.9 pg/ml to 76.9 ± 26.3 pg/ml on
days 4 to 5.[3]
The above two studies are strange showing that despite them being similar,
Test E seems to peak E₂ much faster than Test C (Side note: Test C is
shown peaking Test levels much slower than seen in other studies as well.
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One factor that you’ll notice from the rst bullet point is the difference
between raise in Estradiol in eugonadal vs hypogonadal. For most
individuals starting their rst cycle it can be assumed you are eugonadal
unless you have been properly diagnosed as hypogonadal, thus your
Estradiol can spike close to the upper range after your rst shot of Test. If
you are doing the “Your First Cycle” outlined on this wiki page then your
rst shot will be 250mg. That's 50mg over that of the study.
Another point of consideration is your age. It has been shown in individuals
~65 y/o that the aromatization is far greater than that of someone in their
20s. This was even the case when controlling percentage fat mass as that
can increase aromatase.[5][6] So if your Gramps is wanting to do his rst
cycle, he may want to watch for high estrogen sides sooner. Likewise If you
are entering your 40s-50s, you may want to watch for sides slightly earlier,
but otherwise you'll be ne with the below.
Study Disclaimer
The problem with these studies for us as anabolic steroid users are we’re
not just injecting once. We are injecting weekly, and with that we don’t have
cold hard data for right at the beginning of the cycle—how E₂ is affected
injection by injection. The best we have is a table showing 300 mg and
600mg injected weekly for 5 months, but the table with the data is just the
average over the 5 months, this doesn’t show us each point of data that
they took. It would be interesting to see the rst few weeks of the study.
Putting It All Together.
• Assuming you are a healthy eugonadal male
• Assuming you’re using Test E or C
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It's important to remember how much variance we have as individuals).
It’s important to note that these peaks shown above are just that, the peaks
— the levels begin to drop off after them, but with each new injection you
will reach a new peak, until nally around the time saturation levels are
reached. Note that you should reach close to ~94% saturation by the
beginning of the fourth week, and with that, by week 5 you should know if
your AI dosing is working for you or not, but week 5 or 6 get blood work
done to con rm.
[1]
• Assuming you are of decent BF% (ideally less than 15%)
• Assuming that you are a young male (20s-30s).
• Assuming pre-cycle blood work did not show that you have borderline
out-of-range high E₂ to begin with.
• You would typically start to experience high estrogenic sides somewhere
after your third injection.
Example:
If you're injecting on Mondays and Thursdays:
• You do your rst AAS injection on Monday
• You would start your AI only if showing unambiguous sides on or after
the following Monday's injection
Get regular blood work if you are unsure of anything.
References
1. Behre HM, Nieschlag E. 1998 Comparative pharmacokinetics of
testosterone esters. In: Nieschlag E, Behre HM, eds. Testosterone:
Action, De ciency, Substitution, ed 2. Berlin: Springer-Verlag;
329–348.
2. Sokol R, Palacios A, Camp eld A, Saul C, Swerdloff R. 1982
Comparison of the kinetics of injectable testosterone in eugonadal
and hypogonadal men. In: Fertility and Sterility, 425-430
3. Nankin H. 1987 Hormone kinetics after intramuscular testosterone
cypionate. In: Fertility and Sterility, 1004-1009
4. Nakazawa R, Baba K, Nakano M, Katabami T, Saito N. Hormone
Pro les after Intramuscular Injection of Testosterone Enanthate in
Patients with Hypogonadism. In: Endocrine Journal 2006, 53 (3),
305-310
5. Kishore M. Lakshman, Beth Kaplan, Thomas G. Travison, Shehzad
Basaria, Philip E. Knapp, Atam B. Singh, Michael P. LaValley,
Norman A. Mazer, Shalender Bhasin; The Effects of Injected
Testosterone Dose and Age on the Conversion of Testosterone to
Estradiol and Dihydrotestosterone in Young and Older Men, The
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Journal of Clinical Endocrinology & Metabolism, Volume 95, Issue
8, 1 August 2010, Pages 3955–3964
6. Cohan P.G.; Aromatase, adiposity, aging and disease. The
hypogonadal-metabolic-atherogenic-disease and aging
connection. In: Medical Hypotheses, Volume 56, Issue 6, June
2001, Pages 702-708
SERM On Cycle?
I thought SERMs were just for PCT, why do I need Raloxifene or
Nolvadex for on cycle?
Raloxifene and Nolvadex will both bind to the Estrogen receptor at the
breast site and be your rst plan of attack against uncontrollable gyno
sides. If your Estrogen is wildly out of control and you are developing puffy,
sore, or itchy nipples, UP your AI dose and start taking your SERM (Rolax 60mg ED) (Nolva - 20mg ED). It usually will subside after a 7-12 days.
Continue the SERM for 3 days after the symptoms have subsided before
you drop the SERM.
Note: If you choose Arimidex as your AI, just be aware the blood levels
of Arimidex can drop a bit when used alongside Nolvadex. To avoid
this, you may choose Raloxifene.
This isn't required, but it is de nitely RECOMMENDED. It's always better to
have it and not need it rather than need it and not have it.
Injecting Your Gear
The injection process itself is relatively straight forward. Perhaps nothing
causes more anxiety for AAS users than their 1st injection. This fear is far
more psychological than physical, as the act of performing an injection,
especially when utilizing proper technique and the correct pin size, can be
relatively painless. Some muscle groups are more prone to causing
discomfort than others and the possibility of hitting a nerve, scar tissue, or a
sore spot is a reality, but in general, an injection should not be considered a
“painful” experience.
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To Learn Step-By-Step On How To Inject Safely, Click Here
For a rst cycle, the easiest not to mess up is Glutes, a nice big muscle
with decent circulation and low risk of hitting any nerve clusters. The
twisting and turning can be a problem for some in which case shooting
Ventro Glutes is another option. If that is too hard to nd for you, try
Quads, but there is a slightly larger margin for error in regard to hitting
nerve clusters and puncturing large veins. But you should aim to have as
many injection sites as possible to avoid building scar tissue.
Visit our injection page to learn all about Safe Injection Technique.
Post Injection Pain
To Learn All About Potential Post Injection Pain, Click Here
Frontloading Test?
Frontloading simply means to take a calculated, especially high dose on
the rst day (or week) for injectable AAS. This allows blood levels of the
compound to reach a stable level faster. The problem is taking a large
amount of Test can be hard to control estrogen.
Should I Frontload My Test?
No, this is your rst cycle and we want to keep things as simple as
possible, that includes managing sides; the optional oral is already pushing
things.
OPTIONAL: What Oral Steroid Should I Use?
Again, an oral steroid is completely optional. Oral steroids can add
greater complexity to cycles if we start throwing in more compounds.
It's suggested either to use dry orals or, to use aromatizing ones such
as dianabol only if you can commit to properly managing the added
complexity in managing your estrogen levels.
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If one has preexisting pubertal gyno, or if you are prone to massive
aromatization, there's better choices. Aromatizing orals might be better
as nishers once you've already learned E2 management. But if you can
keep your estrogen under control, and aren't afraid of the added
complexity, they can certainly be fun to run in the beginning.
Dry orals such as anavar or turinabol can be added to your rst cycle
without the extra E2 concerns.
If you use a wet oral such as Dianabol, you'll nd AI dosing starts to
become more complicated. Not only do you need to nd your dosing for
Dianabol and Testosterone, but then you also need to readjust once you
come off the Dianabol. Regardless, it's a timeless classic that has been
used for rst cycles for a long time.
Other options include Anadrol or Superdrol, both of which do not aromatize,
but have been known to cause Gyno by some other mechanism. If you
choose to use Anadrol or Superdrol, it is recommended to have Raloxifene
on hand in case of a Gyno Flair-Up.
In the end, the choice is personal in nature.
Suggested Orals
• Dianabol (Dbol) is a very "wet" compound, which means that it converts
to estrogen and at a high rate at that. It is highly recommended to use
an AI from day one of this cycle in order to prevent heavy water
retention, gynecomastia, and other high estrogen side effects.
(Sides). Don't use Dianabol unless you know how to manage E2, or
you can afford the extra time and attention to properly dial it in. For
this reason it's oft-best left mid-cycle, or as a nisher when you have
your E2 under control, unless you can commit to the added estrogen
management from the start.
• Anadrol (Adrol) is considered a "dry" compound, which means that it
doesn't convert to estrogen. Despite this, individuals using this
compound will often report pronounced estrogen related side effects
such as gynecomastia and water retention, among others. (Sides.)
• Superdrol (Sdrol) is considered a "dry" compound, which means that it
doesn't convert to estrogen. Despite this, some individuals using this
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compound still report gynecomastia symptoms. There are theories on
why this may happen, but nothing has ever been proven. Sdrol is also
known to cause lethargy in some. It is a DHT derivative, so hair loss can
be a concern. (Sides.)
• Turinabol (Tbol) is considered a "dry" compound, which means that it
doesn't convert to estrogen. It also doesn't convert to DHT. It is also one
of the most "side-effect free" compounds, but it is also not known for
putting on as much potential mass as Dbol or Adrol. You should still
review the compounds side effect pro le. It does still affect lipids
negatively, but most oral steroids do.
• Anavar (Var) is considered a dry compound, which means that it doesn't
convert to estrogen. It also doesn't convert to DHT. Strength increases
are common and mixed with less than dramatic weight gains. The
compound is very bene cial to athletes participating in sports that have
weight divisions, or where extra weight can be a hindrance.
Note: These are just some of the suggested orals based on their
properties. You may also use any of the orals in The Basic Cut.
Anecdotally, some have reported just as good (if not better) size gains from
the orals listed in The Basic Cut as Turinabol (Tbol).
When Should I Take It?
There are two trains of thought when it comes to this, and a third if you mix
the two. Whatever you decide, if you experience gastrointestinal
discomfort, you can avoid this by taking your oral steroids with meals when
possible.
Half-Life Method
Oral steroids have a short half-life of just a few hours. One classic method
says that they should be split throughout the day. So you'd start dosing as
soon as you wake up and then every 4 hours or so (as much as you can
split it up) throughout the day.
Off Days: Same as above.
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Pre-Workout Method
One recent trend which has become quite popular lately is the pre-workout
method, in which the individual administers the entire day’s dose of oral
AAS immediately before training; usually around ~1.5 hours pre-workout.
Off Days: Either all upon waking or the Half-Life Method.
Hybrid Method
A third option is to mix the two above methods. What you would do is take
a small dose throughout the day, but pre-workout (~1.5 hours pre-workout)
you will take a slightly higher dose.
Off Days: Use the Half-Life Method.
How Often Should I Pin (Inject)?
It is suggested on /r/steroids that you should at least inject every three
days (E3D) or every 3.5 days (E3.5D) to keep blood levels as stable as
possible for Testosterone Enanthate or Cypionate. This will minimize side
effects and make controlling estrogen easier. You may do once a week, but
it is not optimal.
Here is an example of blood levels with 500mg of Test Enanthate
injected once a week (E7D). This was plotted with SteroidPlotter.
Here is an example of 250mg Test Enanthate injected every 3.5
days, also plotted with SteroidPlotter. As you can see the release rate,
in which Testosterone is released into your blood, is more stable.
Post Cycle Therapy (PCT)
After you did your 12-15 week cycle, you have to begin your Post Cycle
Therapy (PCT). The rst two weeks after your last injection you do not take
any drugs, as the endogenous testosterone is still disrupting your natural
endocrine system.
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Then, you will either do a /r/steroids Recomended PCT
Human Chorionic Gonadotrophin (HCG)
Why Should I Use HCG?
Running a small dose of HCG will help to keep the testes full and will aid
with recovery once you come to the end of your cycle and need to PCT. It’s
not 100% necessary, but if you have access to some and don’t mind
spending a small amount of money to speed up your recovery then it is
probably worth looking at.
Suggested Dose: Run 250 IU EOD throughout the full cycle.
Learn more on the PCT wiki page.
How Do I Mix And Run My HCG?
Mixing 2ml bac water with 5000iu hCG will provide 250iu for every tenth of
a ml/cc. This will provide you 20 250iu hCG doses.
Generally hCG will come with a vial of lyophilized powder and an ampule of
either sodium chloride solution or bacteriostatic water. You want the
bacteriostatic water. Bac water is intended for multiple uses and will inhibit
bacteria growth. The sodium chloride solution is intended for female fertility
use purposes and is to be used in a single injection. If used over multiple
injections it may begin to grow bacteria.
When you check your vial of lyophilized hCG it will generally be 5000 IU,
although it can come in other amounts.
Using 5000 IU as the most common example; if you take 2mL of Bac Water
and inject that slowly into your vial of 5000 IU hCG, you then have 250 IU
per tenth of a mL (cc). So every tenth of your 1mL insulin syringe would be
250 IU.
The other form hCG might come in is a liquid form. This is hCG in a
solution with a preservative to keep it active. You may add bacteriostatic
water to this in order to adjust your dosage if you need.
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In either case, hCG should be kept in the refrigerator after reconstitution to
preserve its shelf life. It should be refrigerated within 72 hours of mixing it
with bac water. hCG should be good for around 60 days when refrigerated.
After that time it will lose potency at about ten percent per week as time
goes on.
Blood Work
Regular blood work is STRONGLY encouraged. It is recommend getting
blood work before starting your cycle (to assess your baseline Testosterone
levels and general health), during your cycle (to con rm that your
Testosterone is legitimate and properly dosed), and after your cycle (to
assess how well you have recovered). The wiki page regarding blood
work can be found here and some help in how to understand your
results can be found here.
When Should I Get Bloodwork?
The standard recommendation for Test E/C injections is to get bloodwork
drawn 36-48 hours after your last injection, in order to try to get a
representative picture of your PEAK testosterone levels. Actual
pharmacokinetic calculations speculate the peak plasma levels of
testosterone will happen at about 35-40 hours post last injection, but you
must remember that everyone responds slightly differently to gear and that
injection site (ie glute or delt) may make a small difference.
Nutrition
It is recommended to eat about TDEE + 30%. Go nd multiple TDEE
calculators and calculate your TDEE on each. /r/steroids highly
recommend the 3-Suns Adaptive TDEE Spreadsheet. It gets more
accurate the longer you use it, but by week 3 or 4 it should be really close
and closer than any online calculator. Just remember it's better to over eat
than under gain.
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Dosing
Note: For this example we are using the time frame for the 15 weeks. If you
wish to end it sooner, obviously all your ending weeks will change and the
week you start PCT will as well.
• Weeks 1-15: Testosterone E or C, 250 mg every 3 or 3.5 days (E3D or
E3.5D) for a total of 500 mg per week.
• Weeks 16-17: Nothing (This allows the exogenous testosterone to clear
your body to a reasonable amount).
• Weeks 18-Til: Whatever PCT protocol you choose.
• Throughout Cycle (or at least on hand): An AI like Arimidex or
Aromasin. Again, dosing is user dependent and you should get blood
work to dial in your dose, but MOST users will nd .5 mg of Arimidex or
12.5 mg Aromasin E3D or E3.5D to be a good starting dose. Some may
need more frequent (EOD) dosing or some may even need less than
E3.5D; this is really something that varies person-to-person too much.
Watch out for signs of low or high estrogen - especially high estrogen,
like excessive bloating or itchy nipples.
Oral Steroid Options / Additives:
Test E & C takes about six weeks to fully saturate the blood (i.e., kick in). If
you don't want to wait that long and you want to aid in your bulk, a popular
thing to do is start the oral from day 1 (kickstarting). Another popular thing
to do is to run your oral at the very end of your cycle, leading up to PCT
( nisher). You can run your oral anytime during the cycle though. You may
pick one of the following:
• For 6 Weeks: Dianabol (Dbol), 30–60 mg, ED or
• For 6 Weeks: Anadrol (Adrol), 50–100 mg, ED or
• For 4 Weeks: Superdrol (Sdrol), 10–20 mg, ED or
• For 6 Weeks: Turinabol (Tbol), 40–80 mg, ED or
• For 6 Weeks: Anavar (Var), 30–50 mg, ED
Note: These are just some of the suggested orals based on their
properties. You may also use any of the orals in The Basic Cut.
Anecdotally, some have reported just as good (if not better) size gains
from the orals listed in The Basic Cut as Turinabol (Tbol).
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Why 500mg?
We answer this question ten times a day.
500mg is recommended for your rst cycle.
500 mg is a low dose. Gains are log-linear up to 600 mg and well beyond. If
you're going with 300mg, you're still shutting yourself down—and you're
leaving a lot of free gains on the table for nothing.
There's little to no difference in sides between 300 and 500. There's no
difference in shutdown between 300 and 500.
Some low responders need as much as 250mg just to reach normal levels
of Testosterone as addressed by TRT.
500mg is a low dose in that you can take well over ten times that amount
without any Ill effects. 500mg is a low dose in that bodybuilders have long
started from there and worked up. 500 is low. 750 is intermediate. 1000+ is
a little bit more advanced.
At 300mg, you're putting yourself in the no-man's land just between TRT
and a full-on blast where it's dif cult to dial in your aromatase inhibitor (AI).
Managing your estrogen with an AI is one of the most important things you
can learn from your rst cycle. This dosage is recently picked up popularity
by YouTube and tness in uencers who have stakes in TRT/HRT clinics
that cannot legally prescribe more than 300mg.
The r/steroids wiki incorporates thousands of clinical studies and case
reports to come to its numbers. Test is a very benign compound. Unlike
some of the synthetics, your body immediately recognizes it and knows just
what to do.
Taking a higher dose than it's naturally accustomed to simply results in
adaptation to temporarily produce relatively higher levels of aromatase to
accommodate for the in ux of hormone and attain equilibrium.
The immediate byproduct of that adaptive response—17β-Oestradiol (E2)
is highly anabolic, cardioprotective, neuroprotective, important for lipid
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balance and libido, and essential for normal physiological functioning. No
acute toxicity or organ stressors manifest themselves, even at doses
hundreds of times that of normal.
Your body knows how to handle testosterone. It's been synthesizing it since
before birth. It's essential for normal physiological functioning. The Wiki
recommends 500mg on your rst cycle for good reason.
The Basic Cut
The Basic Cut differs very slightly from The Basic Bulk, mainly in dosing.
The standard rule of thumb is to not cut while off cycle as some hard
earned muscle mass could be lost. Most users anecdotally notice less bloat
with Testosterone Propionate, so it's often used for cuts, but overall you
can use Test E or C just ne as well.
Dosing:
• Weeks 1-12: Testosterone Propionate, 30-50 mg (ED) OR
• Weeks 1-12: Testosterone Enanthate or Cypionate, 100-200
mg (E3D or E3.5D). PCT differs from propionate protocol below.
• Weeks 13: Nothing the rst 2-3 days (This allows the
exogenous testosterone to clear your body). PCT should start
day 3 or day 4 due to test propionate's active life of ~0.8 days.
• Weeks 13-til: Starting day 3 or 4. Whatever PCT protocol you
choose.
• Throughout Cycle (or at least on hand): An AI like Arimidex or
Aromasin. Dosing is user dependent and you should get
bloodwork to dial in your dose. Watch for signs of low or high
estrogen—especially high estrogen, such as excessive bloating
or itchy nipples.
• Take AI only when sides necessitate. Estrogen is highly
anabolic, cardioprotective and neuroprotective, and essential for
normal physiological functioning. Low E2 is far worse than high
E2, which should be proportionally out of range just as test.
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Gyno takes weeks to develop and can be taken care of with the
AI on hand.
Note: You can extend up to 20 weeks. If you wish to extend it, all your
ending weeks will change and the week you start PCT will as well.
SUPPLEMENTAL COMPOUNDS
Salbutamol
Salbutamol tablets are also effective while being far less dangerous than
Clen:
• Be sure to get Salbutamol tablets, rather than Albuterol inhaler
spray, which is just a recipe for shakiness and nausea.
• Positive effects of oral albuterol on serum lipids and
carbohydrate metabolism in healthy men Increased HDL,
Decreased LDL
• More fat burnt in a cardio session with Salbutamol
• Acute effects of nebulized salbutamol on resting energy
expenditure in patients with chronic obstructive pulmonary
disease and in healthy subjects 11.4% increase in resting
energy expenditure among healthy subjects with Salbutamol
• Combination of salbutamol, caffeine and high-calorie diet:
more muscle, less fat
During a low-calorie slimming diet, pharmacological strength athletes
sometimes use beta-2 agonists such as salbutamol to lose more fat and at
the same time retain more muscle. According to obesity researchers at
the American Pennington Biomedical Research Center, salbutamol can
also improve body composition during a high-calorie diet if you combine
salbutamol with caffeine.
Salbutamol Stack
Even more effective than an ECA stack is Salbutamol with caffeine. This
stack is more effective than ephedrine while being far safer than
clenbuterol.
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• Last 4-6 Weeks: Salbutamol/Caffeine, 4mg/200mg, up to 3xED
Clenbuterol (Clen)
Clenbuterol is prescribed as a bronchodilator for asthma, but also has the
additional effect of increasing metabolism. The claim is a 10% increase in
metabolism over ECA, which claims a 3% increase in metabolism. (This
often quoted, but never found an original study to back this up.) Clenbuterol
has a 36-39 hour half-life – meaning if you take it, or worse, too much, you
have to ride it out for about a day and a half. Some people panic if they
take too much, and head to the Emergency Room, where the doctors will
still just tell you that you need to ride it out until it wears off. There is
nothing you can take to “make it stop” before then.
Clenbuterol has also been called “anti-catabolic” – meaning it does not
promote muscle loss as part of the increase in metabolism to reduce
bodyfat.
Some additional considerations when using clenbuterol:
• Supplement with (3-5g ED) L-Taurine – Clenbuterol tends to inhibit LTaurine in your system, producing cramps
• Using Ketotifen with Clenbuterol (2-3mg ED) - Ketotifen is an
antihistamine that inhibits down regulation of beta receptors, but you
should do more outside research before using.
Common Clenbuterol Cycles
• 2 weeks ‘on’ / 2 weeks ‘off’ for 8-12 weeks – Starting at 20mcg,
increasing by 20mcg units as you can handle, until what you can handle
or a maximum of 100mcg per day, and then stay at that amount for the
duration of the two weeks. Then stop and go off for 2 weeks, substituting
your favorite OTC thermo, and then repeating the 2 weeks ‘on’, again
starting at 20mcg.
• Continued ‘on’ for 8-12 weeks, include ketiotifen – Starting at 20mcg
for a week, increase by 20mcg per week until what you can handle or a
maximum of 100mcg per day, and then stay at that amount for the
duration of the cycle
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ECA Stack
Another thing to consider is using a ECA (ephedrine, caffeine, aspirin) or
EC (ephedrine, caffeine) stack. This will function as an appetite
suppressant and accelerate your metabolism and hence aid tremendously
on a cut:
• Last 4-6 Weeks: ECA or EC Stack, Up To 3xED
If you use Test E & C, it takes about six weeks to fully saturate the blood
(i.e. kick in). If you don't want to wait that long and you want to aid in your
cut, a popular thing to do is start the oral from day 1 (kickstarting). Another
popular thing to do is to run your oral at the very end of your cycle, leading
up to PCT ( nisher). You can run your oral anytime during the cycle though.
You may pick one of the following:
• For 6 Weeks: Winstrol (Winny), 40-80 mg, ED or
• For 6 Weeks: Epistane (Epi), 40-80 mg, ED or
• For 6 Weeks: Anavar (Var), 40-80 mg, ED
ADDITIONAL WARNINGS:
• Winstrol (Winny) is considered a "dry" compound, which
means that it doesn't convert to estrogen. It is a DHT derivative,
so hair loss can be a concern. (Sides)
• Epistane (Epi) is considered a "dry" compound, which means
that it doesn't convert to estrogen. It is a DHT derivative, so hair
loss can be a concern. (Sides)
• Anavar (Var) is considered a "dry" compound, which means that
it doesn't convert to estrogen. It also doesn't convert to DHT. It is
one of the most side-effect free compounds, but does affect
lipids negatively, as most oral steroids do. You should still review
the compound side effects. (Sides)
Nutrition:
It is recommended to keep your caloric intake at no less than 80% TDEE.
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Intermediate Bulk Cycle
By now, you have probably put on a fair bit of mass, and want to see how
how much you are capable of. This is a solid second cycle, perfect for
putting on mass quickly with minimal side effects. Nandrolone also
provides excellent joint support, allowing you to push your body a bit
harder. At this point you have a bit of a feel for how your body responds to
testosterone. You can extend the cycle a bit.
• Weeks 1-16: Testosterone Enanthate or Cypionate, 500 mg/
week split E3.5D.
• Weeks 1-16: NPP (Nandrolone), 50-75 mg/day (350-500mg
weekly)
• Weeks 16-18: Nothing (This allows the extraneous testosterone
to clear your body).
• Throughout Cycle (or at least on hand): An AI like Arimidex
or Aromasin. Dosing is user dependent and you should get
bloodwork to dial in your dose. Watch out for signs of low or
high estrogen, especially high estrogen, like excessive bloating
or itchy nipples. Do not take AI preemptively.
• Take AI only when sides necessitate. Estrogen is highly
anabolic, cardioprotective and neuroprotective, and essential for
normal physiological functioning. Low E2 is far worse than high
E2, which should be proportionally out of range just as test.
Gyno takes weeks to develop and can be taken care of with the
AI on hand.
You can extend for up to 20 weeks. If you wish to extend it, obviously all
your ending weeks will change and the week you start PCT will as well.
Cut/Recomp Cycles
Silver Standard
The following cycle is considered to be a very solid cutting cycle that
maintains lean body mass while burning fat. Keep your caloric intake at no
less than 80% TDEE.
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• Weeks 1-12: Trenbolone Acetate, 50-100 mg, every day (ED)
to your tolerance level
• Weeks 1-12: Testosterone Propionate (or Testosterone
Enanthate), 50 mg ED
• Weeks 1-12: Arimidex, .5mg E3D, watch for E2 crash, adjust
accordingly.
• Weeks 13-14: Nothing (This allows the extraneous testosterone
to clear your body).
• On Hand Throughout Cycle: An AI like Arimidex in case signs of
excessive bloating or itchy nipples occur.
• On Hand Throughout Cycle: A Dopamine Agonist like Caber or
Prami to stop prolactin production.
• Take AI only when sides necessitate. Estrogen is highly
anabolic, cardioprotective and neuroprotective, and essential for
normal physiological functioning. Low E2 is far worse than high
E2, which should be proportionally out of range just as test.
Gyno takes weeks to develop and can be taken care of with the
AI on-hand.
Q: What should my protein/carb/fat percentages be during this cut?
A: It depends on your goals.
• You're planning to eat below your TDEE for a true cut.
Get in your standard bulk protein and balanced nutrients. The rest does not
matter. In a caloric de cit, your body will not attempt to convert incoming
food to fat. Trenbolone is highly anabolic and will tell your body to not burn
muscle for fuel (catabolism).
People have regularly ran caloric de cits of 1,500 calories below TDEE
without losing strength. You'll notice a loss in energy, but not strength.
• You're planning to eat above your TDEE in an attempt to gain
muscle while losing fat.
Trenbolone has the capability to stop the creation of new fat (de novo
lipogenesis) from carbohydrates. This only happens when blood plasma
levels of estrogen are low. Regularly dose your AI's to control estrogen. It
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will not stop storage of fat from intake in a caloric surplus. Therefore, above
your TDEE, you want to consume extra carbohydrates to avoid fat storage.
When excess carbs are eaten, Trenbolone will push them into the
mitochondria of your cells, generating heat and producing sweat. If your
sweating is excessive, you are eating too many carbs. Adjust your carb
intake so as to only have a small amount of Tren sweats. It is recommend
to not eat carbs at night and only light carbs (vegetables) for dinner. The
requirement for low estrogen for Tren to do it's magic is why /r/steroids
recommends high Tren/low Test cycles for cuts and recomps.
Gold Standard
Works best when body fat is below or at 12%.
Add in the following to the Silver Standard Cut / Recomp Cycle:
• Weeks 1-12: Masteron Propionate, same mg as Testosterone
Propionate
Contra Costa Contest Prep
Taken from this video (video taken down) by Michael Pacini. The weeks
column is for the number of weeks away from your contest.
• WARNING: 19-nor metabolites (Tren/Deca/etc.) are highly
suppressive for up to six months or more. Nobody should be
taking nandrolone or other 19-nor compounds unless they're on
blast and cruise, because full recovery from PCT will be
rendered largely ineffective for as long as half a year—so long
as to be impractical.
Weeks
Compound
Amount
Frequency
Weeks 14-8
Test C
500mg
EW
Weeks 14-8
NPP
600mg
EW
Weeks 14-8
1-Test C
(DHB)
500mg
EW
Weeks 8-5
Test C
250mg
EW
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Weeks 8-5
NPP
300mg
EW
Weeks 8-5
1-Test C
(DHB)
250mg
EW
Weeks 14-0
Anavar
10mg
7xED
Weeks 14-0
Proviron
25mg
2xED
Weeks 14-0
Adex
0.5mg
ED
Weeks 14-0
Nolva
10mg
ED
Weeks 5-0
Salbutamol
4mg
3xED
Weeks 5-0
Oral Primo
25mg
2xED
Weeks 5-0
Winstrol
25mg
2xED
Weeks 14-1
GH
2IU
3xED
Equipoise (Boldenone) Cycles
Equipoise (EQ) is a fantastic compound that can be utilized in any cycle
for almost any purpose. EQ tends to give users a very healthy-looking
reddish-brown hue to their skin tone, almost like a very light base tan.
Equipoise tends to visibly increase vascularity in those who are less than
15% body fat, and will grow the delts and traps in a way that makes them
look volumized and very full. Some forums have put EQ into their Top 5 list
of most important bodybuilding hormones. EQ is equally used in
powerlifting circles for the increased rate of recovery and dense dry gains
that don't pack on 15+ lbs of water during a cycle.
Some users report an increase in cardiovascular endurance, along with a
signi cant increase in appetite. One of the reported negative side effects of
EQ is that some users experience mild anxiety that will increase with the
dose. This is due to the aromatase-inhibiting effects of EQ metabolites
ADD, ADT and 1-AD. Have something on-hand to bring estrogen levels
back up in case of crashed E2: test no ester (TNE or short-ester test,
Dianabol, HCG or Trestolone will all do the trick.
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For EQ to really shine, it needs to be run longer and at higher doses than
any other steroid, but it is incredibly mild in terms of side effects and
shouldn't be considered in the same class of “mega-dosing,” as with other
steroids. 1–1.5 grams is a good dose for the positive properties of EQ to
really come into their own. Even a cycle with 2–3 grams of EQ would still
be mild.
EQ is best run as an accessory compound in a bulk cycle for those looking
for that extra pop in their delts.
EQ can be run as an accessory to tren on a cut cycle to help mitigate the
reduction in cardiovascular capacity that comes along with tren use, while
keeping muscle fullness, and helping to avoid looking at.
EQ really shines as the main compound in a recomposition cycle, where it
allows you to keep your muscle fullness and vascularity while building a
few pounds of muscle and dropping a few percent body fat. ALWAYS RUN
A TEST BASE.
Beginner EQ Bulk
For those with minimal AAS experience this cycle will add around 10–15 lbs
of dry lean gains and you won't lose much (if any) during PCT.
• Weeks 1-16: Equipoise, 200 mg, E3D
• Weeks 1-24: Testosterone Enthanate, 300 mg, E3D
• Run Testosterone for 8 weeks after dropping EQ to allow
the Uncdeylenate ester to clear.
• On-hand Throughout Cycle: An AI like Arimidex in case signs of
excessive bloating or itchy nipples occur. Also have something
to bring estrogen levels back up in case of Crashed E2: test no
ester (TNE) or short-ester test, Dianabol, or HCG will all do the
trick.
• Take AI only when sides necessitate. Estrogen is highly
anabolic, cardioprotective and neuroprotective, and essential for
normal physiological functioning. Low E2 is far worse than high
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E2, which should be proportionally out of range just as test.
Gyno takes weeks to develop and can be taken care of with the
AI on hand.
Intermediate EQ Bulk
Keep an AI on hand but you shouldn't need it.
• Weeks 1-16: Equipoise, 200 mg (E3D)
• Weeks 1-24: Testosterone Enthanate, 300 mg every three
days (E3D)
• Run Testosterone for 8 weeks after dropping EQ to allow
the Uncdeylenate ester to clear.
• On-hand Throughout Cycle: An AI like Arimidex in case signs of
excessive bloating or itchy nipples occur. Also have something
to bring estrogen levels back up in case of crashed E2: test no
ester (TNE or short-ester test, Dianabol, or HCG will all do the
trick.
• Take AI only when sides necessitate. Estrogen is highly
anabolic, cardioprotective and neuroprotective, and essential for
normal physiological functioning. Low E2 is far worse than high
E2, which should be proportionally out of range just as test.
Gyno takes weeks to develop and can be taken care of with the
AI on hand.
Advanced EQ Bulk
This cycle ups the dose a bit on the test and EQ and adds in some
masteron to help keep the estrogen down and the water off. Recommend
running Aromasin proactively to hold down E2
• Weeks 1-20: Equipoise, 200 mg (E3D)
• Weeks 1-28: Testosterone Enthanate, 300 mg every three
days (E3D)
• Weeks 1-20: Masteron Enanthate, 250 mg every three days
(E3D)
• Weeks 1-20: Deca-Durabolin, 200 mg (E3D)
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• Weeks 1-20: Aromasin, 12.5 mg, E3D — Adjust as needed
• On Hand Throughout Cycle: An AI like Arimidex in case signs of
excessive bloating or itchy nipples occur. Also have something
to bring estrogen levels back up in case of crashed E2: test no
ester (TNE or short-ester test, Dianabol, or HCG will all do the
trick.
• Run Testosterone for 8 weeks after dropping EQ to allow the
Uncdeylenate ester to clear.
• Take AI only when sides necessitate. Estrogen is highly anabolic,
cardioprotective and neuroprotective, and essential for normal
physiological functioning. Low E2 is far worse than high E2, which
should be proportionally out of range just as test. Gyno takes weeks to
develop and can be taken care of with the AI on hand.
Beginner EQ Cut
Surprisingly, the same dosages as the Beginner Bulk, however, adjust your
calories to be in a caloric de cit no more than 80% of your TDEE.
• Weeks 1-16: Equipoise, 200 mg (E3D)
• Weeks 1-24: Testosterone Enthanate, 300 mg, E3D
• On Hand Throughout Cycle: An AI like Arimidex in case signs of
excessive bloating or itchy nipples occur. Also have something
to bring estrogen levels back up in case of crashed E2: test no
ester (TNE or short-ester test, Dianabol, or HCG will all do the
trick.
• Take AI only when sides necessitate. Estrogen is highly
anabolic, cardioprotective and neuroprotective, and essential for
normal physiological functioning. Low E2 is far worse than high
E2, which should be proportionally out of range just as test.
Gyno takes weeks to develop and can be taken care of with the
AI on hand.
• RUN TESTOSTERONE FOR 8 MORE WEEKS after dropping
EQ to allow the Uncdeylenate ester to clear.
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Intermediate EQ Cut
The effect of Tren and EQ on your physique during a cut is nothing short of
freakish. Estrogen is kept low so de novo lipogenesis is strongly inhibited,
Tren leans you out while both Tren and EQ give that huge boulder shoulder
and traps look.
• Weeks 1-16: Equipoise, 200 mg, E3D
• Weeks 1-24: Testosterone Enthanate, 300 mg (E3D)
• Weeks 4-16: Trenbolone Acetate, 50-100 mg, every day (ED)
to your tolerance level
• RUN TESTOSTERONE FOR 8 MORE WEEKS after dropping
EQ to allow the Uncdeylenate ester to clear.
• On Hand Throughout Cycle: An AI like Arimidex in case signs of
excessive bloating or itchy nipples occur. Also have something
to bring estrogen levels back up in case of crashed E2: test no
ester (TNE or short-ester test, Dianabol, or HCG will all do the
trick.
• On Hand Throughout Cycle: An Dopamine Agonist like Caber or
Prami to stop prolactin production and eventual lactation.
• Take AI only when sides necessitate. Estrogen is highly
anabolic, cardioprotective and neuroprotective, and essential for
normal physiological functioning. Low E2 is far worse than high
E2, which should be proportionally out of range just as test.
Gyno takes weeks to develop and can be taken care of with the
AI on hand.
Advanced EQ Cut
Ensure that you have run several cycles with these compounds before
attempting.
• Weeks 1-20: Equipoise, 200 mg (E3D)
• Weeks 1-28: Testosterone Enthanate, 300 mg (E3D)
• Weeks 4-20: Trenbolone Acetate, 50-100 mg, ED to your
tolerance level
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• Weeks 1-20: Masteron Propionate, 200 mg (E3D)
• RUN TESTOSTERONE FOR 8 MORE WEEKS after dropping
EQ to allow the Uncdeylenate ester to clear.
• Weeks 1-20: Aromasin, 12.5 mg, E3D -- Adjust as needed
• On Hand Throughout Cycle: An AI like Arimidex in case signs of
excessive bloating or itchy nipples occur. Also have something
to bring estrogen levels back up in case of crashed E2: test no
ester (TNE or short-ester test, Dianabol, or HCG will all do the
trick.
• On Hand Throughout Cycle: An Dopamine Agonist like Caber or
Prami to stop prolactin production.
• Take AI only when sides necessitate. Estrogen is highly
anabolic, cardioprotective and neuroprotective, and essential for
normal physiological functioning. Low E2 is far worse than high
E2, which should be proportionally out of range just as test.
Gyno takes weeks to develop and can be taken care of with the
AI on hand.
Power Lifting Cycle
• Excerpt from Brandon Lily's Cube Method.
Estrogen Suppression Cycle
• Effects of aromatase inhibition in hypogonadal older men: a
randomized, double-blind, placebo-controlled trial
• Estrogen suppression in males: metabolic effects
• Arimidex vs Femara (Letro)
• Aromatase inhibitors for male infertility
• Hormonal Approaches to Male contraception
• Hormonal approaches to male contraception: approaching
reality
• Changes in hormonal pro le and seminal parameters with
use of aromatase inhibitors in management of infertile men
with low testosterone to estradiol ratios
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Very Advanced Insulin Cycle
Read the Insulin Compound Description Page
WARNING: Insulin use is VERY DANGEROUS. You can, quite literally,
DIE FROM IT if not done properly. This guide is to serve as only an
example of what some people do in order to start using it.
|------------ READ -------------------------------------------------------------------------|
• Insulin can easily kill you if mis-used. Do not fuck around.
• BUDDY SYSTEM ALWAYS! Have a knowledgeable buddy
with you
• DO NOT go to sleep for two hours after insulin use
• Keep emergency glucose tablets on hand. If you feel like
shit, you need more glucose.
• You must have your eating plan tuned to near perfection
|------------ THIS -------------------------------------------------------------------------|
I’ll use the 5 day training split as an example here. That will give you 20
days “on” insulin.
Day 1: 5 IU insulin / 50g Dextrose
Day 2: 5 IU insulin / 50g Dextrose
Day 3: 5 IU insulin / 50g Dextrose
Congratulations!! You’ve survived thus far. I assume(hope) you’ve been
monitoring your BG levels. You probably have noticed that you are in the
higher range using 50 g of dextrose PWO. Now it’s time to drop the carbs
slightly. Don’t fret. This should be more than ample amounts(of carbs) to
get you through to your PPWO meal.
Day 4: 5 IU insulin / 40g Dextrose
Day 5: 5 IU insulin / 40g Dextrose
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Let’s up the dose …
Day 6: 6 IU insulin / 50g Dextrose
Day 7: 6 IU insulin / 50g Dextrose
By this point in time you should be feeling good (i.e. more con dent) but
still respectful to Insulin. Let’s test the waters for three days to give you the
feel of things. By that I mean we’ll drop the carb intake slightly so you can
nd a comfortable ratio in regards to IU’s vs. carbs per gram.
Day 8: 6 IU insulin / 40g Dextrose
Day 9: 6 IU insulin / 40g Dextrose
Day 10: 6 IU insulin / 40g Dextrose
Now, the above ratios are safe and effective. You can stop right here and
continue on for the next 10 days at the above doses/ratios. Or you can
move forward slightly.
Day 11: 7 IU insulin / 50g Dextrose
Day 12: 7 IU insulin/50 g Dextrose
Day 13: 7 IU insulin/50 g Dextrose
Day 14: 7 IU insulin/50 g Dextrose
Day 15: 7 IU insulin/50 g Dextrose
If you felt con dent with the above protocol, you could experiment on days
14-15 and drop your dextrose to 40g. If you do so, please monitor your BG
levels every 15 minutes or so. Have glucose tabs, or another source of
quick carbs handy (like orange juice) to stave off any possible signs of
hypoglycemia. Should this happen, don't panic, just drink a glass of orange
juice, or similar, and in 10 minutes the symptoms will have subsided.
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At this point you should have a good idea of how you react with Insulin in
terms of blood glucose (BG) levels vs. carbohydrate intake .
OK, on to your nal week.
Day 16: 8 IU insulin / 60g Dextrose
Day 17: 8 IU insulin / 60g Dextrose
Day 18: 8 IU insulin / 60g Dextrose
Day 19: 8 IU insulin / 60g Dextrose
Day 20: 8 IU insulin / 60g Dextrose
Congratulations! You just completed your rst cycle/experience with
Insulin in a safe an effective manner. I stopped at 8 IU, being that is enough
to get your feet wet with the drug. You can experiment later on. This was
simply a guide.
One last thing. Guys ask “Which way is better?” to take your Whey/
Dextrose in one shake, or Dextrose rst, and whey 15 minutes later”?
Bottom line, it’s just preference.
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WOMEN & PEDs
DISCLAIMER
This is an overview of all the various supplements and hormones that
women have been known to use towards “ tness goals”. This wiki is in the
interest of giving you a starting place to do the basic research so you can
make your own informed decisions instead of relying on some guy you
know (guys have different body chemistry than women) – regardless of
how experienced they are with their own cycling and supplementation, it
doesn’t necessarily translate into anything useful for you as a female. It is
beyond critical for YOU to own your own decisions – your goals, your
results, your sides. This is not a case where because you know someone
who "you trust and would never hurt you”, it is YOUR decision and YOUR
responsibility. No one else is going to experience the results AND the
sides. No one can guarantee what will or won’t happen – you are literally
your very own petri-dish. YOU need to educate yourself so you can make
informed choices. There are no quick xes or magic pills. None of this
stuff matters if you don’t already have a solid and performing diet, training,
cardio & recovery program. And even in having this information available,
just because it’s there or you have access to it, doesn’t mean it is the
appropriate path to your goals. You need to have reasonable expectations.
The body simply can’t support changes that are forced on it faster than it
can accommodate. “Drugs aren’t always the answer.”
Always remember that steroids are NOT particularly fat burners (even if
some may have fat burning properties). If you aren’t already lean or your
diet isn’t optimized already, you may nd yourself “thick” when everyone
else told you [ ll in the steroid] would lean you out & tone you up. You’re
screwing with your hormone pro le. Women’s hormone balance is much
more complex than men’s, and doesn’t work the same. Additionally
women’s bodies can be much more complex in their response to something
as simple as just the diet. All sorts of metabolic fun can result from any sort
of extreme. Going into desperation mode and throwing more drugs on to
force a result you want, but your body isn’t ready to produce yet, is just
going to aggravate the situation.
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OTC Fat Burners
Ephedrine
If you want to go back to basics, you can build your own ECA or EC stack.
To Build Your Own Stack
• EC Stack: Typical is 20-30mg Ephedrine + 200mg Caffeine
• ECA Stack: Adding in Aspirin is typically used to help prevent clotting,
but the other two compounds share the same anti-clotting mechanisms.
Overall the difference to the stack is negligible without the Aspirin.
Recommendations for Aspirin are typically baby aspirin (81mg).
Another variation is Ephedrine / Caffeine / Yohimbine HCl (ECY).
Yohimbine is great as an appetite suppressant, but too much of it can leave
you feeling sick to your stomach.
• ECY: 20-30 mg ephedrine + 200 mg caffeine + 5 mg Yohimbine.
You can take any of these combinations at 2-3 times ED, but it is generally
recommended to not take anything after 3pm, or determine how late into
the day the last dose affects you, and make that the latest time of your last
dose so you can sleep. Anything that affects your sleep will reduce your
quality recovery time and can begin to negate any progress you make from
the compound you’re taking.
Non-OTC Fat Burners
Women are often more interested in ‘fat loss’ before they are interested in
muscle growth, particularly for competition prep. The following compounds
are explicitly not steroids, but they are generally controlled substances or
by prescription only. These are some of the other supplements that women
start to “lose fat” or “lean up”.
Clenbuterol (Clen)
Clenbuterol is prescribed as a bronchodilator for asthma, but also has the
additional effect of increasing metabolism. The claim is a 10% increase in
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metabolism over ECA, which claims a 3% increase in metabolism. (This
often quoted, but never found an original study to back this up.) Clenbuterol
has a 36-39 hour half-life – meaning if you take it, or worse, too much, you
have to ride it out for about a day and a half. Some people panic if they
take too much, and head to the Emergency Room, where the doctors will
still just tell you that you need to ride it out until it wears off. There is
nothing you can take to “make it stop” before then.
Clenbuterol has also been called “anti-catabolic” – meaning it does not
promote muscle loss as part of the increase in metabolism to reduce
bodyfat. Here are a couple studies that imply that clenbuterol, interestingly
on a restricted diet, does promote some amount of muscle growth (or
preservation) in research animals:
Some additional considerations when using clenbuterol:
• Supplement with (3-5g ED) L-Taurine – Clenbuterol tends to inhibit LTaurine in your system, producing cramps
• Using Ketotifen with Clenbuterol (2-3mg ED) - Ketotifen is an
antihistamine that inhibits down regulation of beta receptors, but you
should do more outside research before using.
Common Clenbuterol Cycles
• 2 weeks ‘on’ / 2 weeks ‘off’ for 8-12 weeks – Starting at 20mcg,
increasing by 20mcg units as you can handle, until what you can handle
or a maximum of 100mcg per day, and then stay at that amount for the
duration of the two weeks. Then stop and go off for 2 weeks, substituting
your favorite OTC thermo, and then repeating the 2 weeks ‘on’, again
starting at 20mcg.
• Continued ‘on’ for 8-12 weeks, include ketiotifen – Starting at 20mcg
for a week, increase by 20mcg per week until what you can handle or a
maximum of 100mcg per day, and then stay at that amount for the
duration of the cycle
Thyroid Medication: T3 and T4
The thyroid hormones thyroxine (T4) and triiodothyronine (T3), are
tyrosine-based hormones produced by the thyroid gland primarily
responsible for regulation of metabolism. T4 converts to T3, with T3 being
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3-4 times stronger than T4. Synthetic T4 is often prescribed for people
diagnosed with hypothyroidism (“sluggish thyroid”).
On a side note, thyroid disease is not uncommon in women. I would
hesitate to blame “can’t lose weight” on the thyroid, as people often look for
pills-based solutions or some excuse before they’ll spend the time revisiting
their diet & training programs. But that said, if you feel there is an issue, by
all means, talk to your doctor about it and get a thyroid panel done.
T3 is frequently suggested as part of a fat-loss protocol. It is important to be
conservative with use of T3 if you choose to go that route. You are
manipulating your thyroid via self-medication. Too much and you will
immediately feel lethargic. General guidance also suggests to be slow in
your dosing – taper off when you are coming off instead of just dropping it
cold. The body generally can adapt to small changes, but tends to rebound
with large, sudden changes.
Another very important consideration with T3 is that bumps up
metabolism… but that means metabolism of everything – both lean muscle
mass and bodyfat. Women tend to be so focused on “fat loss” that they
forget about the importance of muscle mass. Building and preserving
muscle mass has nothing to do with “looking like a man” or “getting huge”,
but rather about the keeping the body component that helps you burn
bodyfat more ef ciently, and it also goes into what makes up a bodyfat
percentage. “What’s your bodyfat?” means what is the ratio of lean muscle
mass to bodyfat in your body? It is great to drop bodyfat, but if you are
sacri cing muscle mass, your overall bodyfat percentage will not drop the
way you want it to. The lack of muscle mass can contribute to a higher
bodyfat percentage (what we often call “skinny-fat”) just as higher bodyfat
percentage.
To this end it is not generally recommended to cycle T3 without an anabolic
support. Either an AAS or, a very common stack is with clenbuterol, which
has been shown to be anabolic, or at least anti-catabolic.
Typical Cycle
It is not recommended to run T3 by itself. Combine the following with an
AAS cycle.
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• 12.5-50mcg per day, for the duration of your cycle
• Start at 12.5mcg for a week. You can either keep it here or increase.
Increases shouldn't be more than 12.5mcg per week until a maximum of
75mcg (high dose - advanced users only). At the end, taper back down
by 12.5mcg every 3 days.
Anti-Estrogens
There are two classes of estrogen manipulators that often fall under the
term “anti-estrogens”. The rst are Selective Estrogen Receptor
Manipulators (SERMs). The only current example out there is Tamoxifen
Citrate (Nolvadex). This operates speci cally on the ovarian-driven
estrogen process. The second category that falls under “anti-estrogens” are
Aromatase Inhibitors (AI’s) that operate not on ovary-originating estrogen,
but rather that resulting from aromatization (or conversion to estrogen) of
testosterone. Examples of testosterones that convert are exogenous
testosterones (anabolic androgenic steroids) such as Testosterone,
Nandrolone, or Dianabol. There is also a natural source of androgen that
converts to estrogen – that produced by the adrenal glands, in both men
and women. When women enter menopause and their ovary-originating
estrogen is no longer produced, the only remaining source of naturally
produced estrogen is that resulting from the adrenals. Examples of AIs are
Arimidex, Aromasin, and Letrozole. In practice, both these and Nolvadex,
are all primarily prescribed as breast cancer treatment for post-menopausal
women.
Women are more likely to use a SERM like Nolvadex to address the
bodyfat associated with estrogen – speci cally the stuff that tends to collect
around the hips, thighs, lower abdomen and butt. It is important to note that
each person has her own distribution of fat – estrogen tends to promote a
higher concentration of fat cells in those lower areas as part of a natural
preservation strategy to protect a fetus and also to provide an extra storage
of energy source (bodyfat) to help support a growing fetus and the mother if
there is any issue with available food sources (i.e. a drought scenario).
This is by design and using an anti-estrogen as a weight-loss strategy
is not a good idea. Estrogen is one of the three basic hormones that make
up who we are, and drive everything from moods to how we look and feel.
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Estrogen is there for a purpose and should not be completely suppressed
only for the purpose of fat loss.
Nolvadex acts to fake out the estrogen receptors (envision a safety
protector that you put into outlets as part of baby-proo ng your house) and
essentially cutting off the estrogen process, instead of literally turning it off.
For cycle duration, it is recommended to keep it to 4-8 weeks maximum.
Long-term use of Nolvadex has the potential to introduce health issues as
described in this article: Side effects of long-term use of tamoxifen. In
the extreme, full estrogen shut down in women can lead to what is often
referred to as the “Female Athlete Triad” – basically estrogen shutdown as
a result of an eating disorder such as anorexia, which leads to reduction in
calcium, and eventually to brittle bones and a host of other issues related to
a stopped period. Here is an overview of this particular issue. Though
this discussion is not focused on eating disorders, the end result, if
someone decided to use medical estrogen suppression as a long-term
weight loss protocol, is the same. This is just to reinforce that this is not a
good idea.
The estrogen process tends to be fairly resilient so coming off a reasonable
duration cycle can produce an estrogen rebound when the process is no
longer inhibited. There isn’t much documentation about this rebound, but
general guidance is to taper off a cycle by reducing the dose (i.e. in half,
every 3 days).
In the context of this article, Aromatase Inhibitors are more speci c to the
estrogen produced as a result of using an aromatizing steroid. This means
that the steroid cycle is more aggressive and will produce side effects such
as water retention and potentially more mood swings, as the converted
estrogen may be adding to natural estrogen levels, enhancing typical
estrogen effects that might be experienced during a menstrual cycle. AI’s
are more commonly used by men who cycle as the increase in estrogen
can produce such side effects in men as gynecomastia (enlarged breast
tissue), water retention, mood swings, etc. Estrogen suppression can help
to create a tighter look (i.e. for competition), but full suppression can
produce too much dryness, including painful joints. Plus you typically want
some estrogen for other bene ts.
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Generally speaking AI’s are not recommended for pre-menopausal
women who are new to steroid cycling or using non-aromatizing
compounds. If they choose to use an AI, it needs to be very
conservatively used, as it is very easy to shut down estrogen with
these compounds.
Typical Use
Primarily Nolvadex is used during the last 4-8 weeks of a contest prep to
help reduce bodyfat in the hips / thighs / waist area. Again, it will not do the
heavy lifting, but will support a tight contest prep. It is possible to
experience either immediate interruption of menstrual ow, or breakthrough
bleeding within 4 weeks of starting the cycle. Also once coming off, the
effects will not be maintained and the estrogen-pattern bodyfat depositing
will continue again. “Estrogen rebound” is often experienced as well, thus
the taper down is recommended. Because of the potential of this rebound it
is recommended to cycle Nolvadex with a speci c end / target date in mind,
followed by an expected rebound while your body recovers from the prep
phase.
More aggressive aromatase inhibitors are not generally recommended
unless you are an experienced cycler running aromatizing compounds such
as NPP. If your cycle is intended for a bulk phase, then don’t use the AIs as
you need the estrogen to build muscle mass and the water gain is minimal
with most compounds women use.
Typical Cycle
• Nolvadex: 10-20mg ED, split in half AM and half PM for maximum of 8
weeks.
• Arimidex: 0.5mg EOD (only with an aromatizing AAS) for maximum of
6-8 weeks – AIs are very aggressive and will produce dry-feeling joints.
If you experience aggressive hot/cold ashes and feeling sick, taper off
over a couple days and stay off.
• Aromasin: 12.5-25mg EOD (only with an aromatizing AAS) for a
maximum of 6-8 weeks – AIs are very aggressive and will produce dryfeeling joints. If you experience aggressive hot/cold ashes and feeling
sick, taper off over a couple days and stay off.
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Human Growth Hormone (HGH)
Growth Hormone is often recommended for “fat loss”. It is not a “fat burner”
in the same sense as clen or ephedrine, but instead falls under the larger
category of “anti-aging” compounds or “hormone replacement therapy”. In
these contexts, it is intended to be dispensed under the supervision of a
quali ed physician based on constant monitoring of IGF-1 levels. This is
the indicator used to track growth hormone production by the
hypothalamus. Essentially this is what drives “youthfulness”. The
hypothalamus produces optimal levels of growth hormone around age
18-21. These levels begin to decrease after age 30-35 as the
hypothalamus shrinks with age. The idea behind supplementing with HGH
is to return the levels of growth hormone to optimal levels, as if you were
still in the prime of your life.
In practical use, as mentioned above, HGH is used for its anti-aging
properties, as a maintenance protocol for older folks, or to promote those
youthful properties with speci c interest in promoting fat loss, or rather not
promoting age-related fat depositing, or stacked with an AAS cycle to
enhance the overall effect.
Typical Use
GH is often recommended for women for ‘weight loss’. By itself, GH does
NOT promote muscle growth in the same sense as AAS, as it is not sex
hormone. Instead, it will work to promote those youthful features such as
healthy hair, improved skin elasticity, better sense of well-being, better
healing capability (Study), and more optimized metabolism to promote a
preference for less bodyfat depositing (Study). It might also be viewed as a
support during the extremes of competition prep for the body. With a steroid
cycle, such as anavar, it would work to enhance the effects of that
compound. The effects of a GH cycle are not immediate and dramatic, but
rather subtle and slow to show over time.
Typical Cycle
Dose:
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• For non-competition use, and more for general maintenance and
youthfulness: 1 iu ED
• For competition / with a cycle: 2-3 iu ED
Primarily for cost purposes, 6 days on / 1 day off or 5 days on / 2 days off
(not two days in a row) can be used as well.
Duration: 4-6 months is ideal. Very short cycles such as a month, are not
really going to show any particular results for the cost.
Potential Sides
• Water retention is a common experience.
• At higher doses (i.e. 4 iu) wrist pain similar to carpal tunnel syndrome is
commonly experienced
• Very aggressive use may fall into the extreme category of acromegaly
Anabolic Androgenic Steroids (AAS)
/r/steroids is hesitant to recommend stacking any AAS with more
AAS. It is done, but should only be after you have experience with
each individual compound in the stack. For this purpose, we will only
cover one compound at a time. But you may add in a Fat Burner or
HGH if your goals could bene t from them.
Virilization
When it comes to steroids and women, there is a universal fear; turning into
a man. As you know, anabolic androgenic steroids derive from the primary
male sex hormone testosterone, and as such, while no woman will turn into
a man, if she’s not careful she can easily display masculine traits. Many
anabolic steroids cause what is known as virilization, speci cally put,
changes that occur due to the high presence of androgens in the body.
Androgens are hormones we all produce, both men and women, and
essentially so with Testosterone and Dihydrotestosterone being primary. Of
course, men require about ten times the amount as women, and when
androgen production goes beyond the needed amount for a female,
masculine traits can manifest. The most common virilizing effects include:
• Body-Hair Growth
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• Clitoral Enlargement
• Deepening of the Vocal Chords
There is hardly a woman alive who would enjoy such effects, but guess
what; plenty of women supplement with anabolic steroids and never
experience a single one. The reason is simple; they’re informed. They’ve
done their homework; they understand which hormones to take and which
ones to avoid. They understand if virilization symptoms begin to show then
that particular steroid is not for them; we’ll explain shortly.
Avoiding Virilization
When steroids and women coexist if we’re going to avoid virilization, and
we’re assuming you want to, the rst order of business is to choose
anabolic steroids that carry low virilizing properties. Some steroids carry
higher virilizing properties, and logic tells us, we’ll need to avoid these; this
isn’t rocket science. Even so, let’s be clear; all anabolic steroids carry a
level of virilization concern, some higher and some lower than others.
When we choose anabolic steroids that carry low virilizing properties, in
most cases, most women will be ne, but there is still a risk. As we are all
unique individuals, some women will not tolerate some steroids at all even
though another woman may tolerate it perfectly. Look at it like dairy
products; most of us can drink all the milk and eat all the cheese we want,
but some of us get sick if we even think about a cow; some of us are
lactose intolerant, but most of use aren’t.
The key to avoiding virilizing symptoms is straightforward; choose steroids
that carry a low rate of probability in this regard. Second, if for any reason
virilization symptoms begin to show, discontinue use immediately. Once
you discontinue use, the effects will dissipate rapidly. If you ignore the
symptoms and let them set it, this is where true damage is done, and in
many cases, where they cannot be reversed. At any rate, if symptoms
show discontinue all steroid use; in your next go around do some
examining of your prior use. Was your dose of a certain steroid too high?
Maybe you simply need a lower dose that is more tolerable; maybe you
need a different steroid altogether. In any case, if you’re smart and pay
attention to your body you can supplement without these effects becoming
problematic.
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A note about available steroid information:
Most of what is out there on muscle forums and even medical studies is
primarily written with men in mind. The subject of women and steroids is
much less studied and published. The detail written here is based on both
published and anecdotal information, and some good guesses based on
“what seems to work”. This puts more of the onus on women to educate
themselves to make informed choices for themselves. Always remember:
YOUR body, YOUR results, YOUR sides. Well-intentioned husbands /
boyfriends / male friends / guys from the gym, even experienced, are not
necessarily going to be giving you the best or right information on which to
base your decisions. The basic chemistry is different, the dosing is different
and the risks are different. At the end of the day, it is always your own
personal chemistry experiment and no one can take the risks for you.
And a last note on what should be the obvious thought – ANY supplement
– over-the-counter, prescribed or illegal, is always only going to be a
SUPPLEMENT to an already existing and functioning diet and training
program. There are no quick xes and nothing is for free. You will not get
the results you envision using any supplement if you don’t already have
your diet and training in place and working. If this is not true, chances are
you are going to end up in a place worse than better. Always consider your
diet, training, cardio & recovery to be your foundation. Constantly optimize
these before trying to " x” things with drugs.
Compound Pro les
This section will include links to the standard steroid pro les for the
technical details, with most of the discussion focused on use, speci cally
for women. Please note that most steroid pro les are written with men in
mind as the target audience and relative to male hormone pro les. Any
dosing recommended is not going to be appropriate for women unless
otherwise speci ed.
Anavar (Oxandrolone)
Anavar (Var) is probably the most commonly used AAS by women. It might
be used by competitors for off-season building with an appropriate diet, or
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during contest prep for cutting, preservation of muscle during a cutting diet,
and improved recovery.
Typical Use
Anavar promotes lean muscle mass with minimal sides and occasional
water retention. It is a oral steroid, though used in small enough doses that
its impact on the liver is typically minimal for women. It will mess up your
lipid pro le though, as oral steroids do. It is also attractive to women and
beginners who are not interested in dealing with needles. The predictable
and minimal sides are also attractive points to those not wanting to deal
with the more individual and androgenic sides of most other AAS.
Typical Cycle
• Dose: 5-10mg ED – split the dose ½ in the AM, ½ in the PM
• Duration: 6-8 weeks for beginners and up to 10-14 weeks for more
experienced users
• No need to taper down the dose or follow with post cycle therapy (PCT).
It is generally suggested to start the cycle at 5mg ED (splitting doses
as above) for the rst 10-14 days to identify any adverse reaction.
(This is strongly suggested if this is your rst time with the
compound.) After that time, you can increase to 10mg ED.
Suggested maximum dose is 20mg ED (though more is not better – often
10mg is suf cient). As the dose increases, sides may increase and results
don’t necessarily increase. Anecdotally, if the cycler is interested in going to
doses above 20mg, the sides can begin to accumulate and the impact on
your liver becomes more of a consideration. Based on this and the cost
(anavar is typically one of the more expensive compounds), if you are
looking for more aggressive results, this is the point where people will move
to a more aggressive, cheaper, injectable compound.
Potential Sides
• Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
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• You may still experience usual menstrual sides (cramps, bloating, etc.)
on your regular menstrual schedule
• Mild acne / bacne
• Clitoral enlargement and increased sensitivity
• Oily hair
• Increased body hair growth
• Sore or scratchy throat / cracky or deepening voice
• Some experience water retention (though not due to aromatization)
Be careful w/ using diuretics to manage this – continued use of even OTC
diuretics is not recommended.
• May cause vaginosis / yeast infection (most any AAS has this potential)
• Occasionally people experience nose bleeds or headaches (due to
increased blood pressure – you can google for OTC supplements to
help with BP
Winstrol (Stanozolol)
Winstrol (Winny) comes in both oral and water-based injectable form (but
also very rarely an oil based). It is attractive to women or recommended for
women because it is an oral, it has a relatively short half-life and detection
time (i.e it clears the system relatively quickly, reducing the duration of any
undesirable sides following completion of a cycle), and promotes lean
muscle mass without water retention. It is most commonly viewed as a
“cutter” for competitors. Winstrol is also attractive as it tends to be both
cheaper and more readily available than others like anavar or primobolan.
Because of this, it is also less likely to be faked.
Winstrol is often grouped with anavar as a good steroid for “beginners" or
those who don’t want to go into the more aggressive compounds (i.e.
injectables). However it is more androgenic than anavar and sides are less
predictable and more unique to the individual, with the potential of being
very androgenic. Because of this, anavar would generally be the better
recommendation, but winstrol is seen as a viable alternative. And is also
known to have a "fat burning" effect.
Typical Use
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Typical Cycle
Oral Winstrol: Can be cycled similarly to anavar.
• Dose: 5-10 mg/day- split the dose ½ in the AM, ½ in the PM
• Duration: 6-8 weeks for beginners and 8-12 weeks for more experienced
It is generally suggested to start the cycle at 5mg ED (splitting doses
as above) for the rst 10-14 days to identify any adverse reaction.
(This is strongly suggested if this is your rst time with the
compound.) After that time, you can increase to 10mg ED if desired.
Suggested maximum dose is 15mg ED (though more is not better – often
10mg is suf cient). As the dose increases, sides may increase and results
don’t necessarily increase. Anecdotally, if the cycler is interested in going to
doses above 15mg, the sides can begin to accumulate and the impact on
your liver becomes more of a consideration.
If chosen to include in a competition cutting stack, schedule towards the
nal weeks of prep. It usually takes about 2 weeks to really start to “show”
itself.
Potential Sides
• Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
• May still experience usual menstrual sides (cramps, bloating, etc.) on
your regular menstrual schedule.
• Mild to aggressive acne on face or shoulders
• Clitoral enlargement and increased sensitivity
• Oily skin / hair
• Hairloss – A shampoo like Nizoral or Nioxin ( nd next to the dandruff
shampoo in most stores) can help minimize this.
• Increased body hair growth
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Winstrol is most commonly used both by men and women, as a cutter
during competition prep. It promotes lean, hard muscle mass without water
retention. One might see competitors running a winstrol-only cycle, or a
more advanced physique competitor using it in a stack towards the nal
weeks of a competition prep.
•
•
•
•
Sore or scratchy throat / cracky or deepening voice
Dry joints (result of the anti-estrogenic aspect of winstrol)
May cause vaginosis / yeast infection (most any AAS has this potential)
Occasionally people experience nose bleeds or headaches (due to
increased blood pressure – you can google for OTC supplements to
help with BP
Turinabol (Tbol)
Turinabol (Tbol) is an oral steroid that has recently become more widely
used by women.
Typical Use
Tbol is good to cycle for both cutting or bulking off-season. Lean gains are
good for a women looking to build some size.
Typical Cycle
• Dose: 5-10mg ED – split the dose ½ in the AM, ½ in the PM
• Duration: 6-8 weeks for beginners
• No need to taper down the dose or follow with post cycle therapy (PCT).
It is generally suggested to start the cycle at 5mg ED (splitting doses
as above) for the rst 10-14 days to identify any adverse reaction.
(This is strongly suggested if this is your rst time with the
compound.) After that time, you can increase to 10mg ED if desired.
Suggested maximum dose is 15mg ED (though more is not better – often
10mg is suf cient). As the dose increases, sides may increase and results
don’t necessarily increase. Anecdotally, if the cycler is interested in going to
doses above 15mg, the sides can begin to accumulate and the impact on
your liver becomes more of a consideration.
Potential Sides
• Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
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• You may still experience usual menstrual sides (cramps, bloating, etc.)
on your regular menstrual schedule
• Mild acne / bacne
• Clitoral enlargement and increased sensitivity
• Oily hair
• Increased body hair growth
• Sore or scratchy throat / cracky or deepening voice
• Some experience water retention (though not due to aromatization)
Be careful w/ using diuretics to manage this – continued use of even OTC
diuretics is not recommended.
• May cause vaginosis / yeast infection (most any AAS has this potential)
• Occasionally people experience nose bleeds or headaches (due to
increased blood pressure – you can google for OTC supplements to
help with BP
Anadrol (Oxymetholone)
Anadrol (Adrol) is an oral steroid that has recently become more widely
used by women when bulking.
Typical Use
Adrol is good to cycle for bulking off-season. Lean gains are good for a
women looking to build some size. It has been found to be a good choice
for women who wish to be conservative yet have very effective results. The
medical doses are pretty astonishing. The reason that 50 mg is the tablet
size is because that’s the standard minimal medical dose, including for
women and children! It used to be used extensively for improving red blood
cell count. But for bodybuilding purposes, we will always start low with any
AAS.
Typical Cycle
• Dose: 12.5-25mg ED – split the dose ½ in the AM, ½ in the PM
• Duration: 6-8 weeks for beginners
• No need to taper down the dose or follow with post cycle therapy (PCT).
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It is generally suggested to start the cycle at 12.5mg ED (splitting
doses as above) for the rst 10-14 days to identify any adverse
reaction. (This is strongly suggested if this is your rst time with the
compound.) After that time, you can increase to 25mg ED, which has
been found to be a safe dose for women.
Suggested maximum dose is 37.5mg ED (though more is not better – often
25mg is suf cient). As the dose increases, sides may increase and results
don’t necessarily increase. Anecdotally, if the cycler is interested in going to
doses above 25mg, the sides can begin to accumulate and the impact on
your liver becomes more of a consideration. These are just the suggested
dosages, medically Anadrol has been given to women at higher dosages
and been ne.
Potential Sides
• Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
• You may still experience usual menstrual sides (cramps, bloating, etc.)
on your regular menstrual schedule
• Mild acne / bacne
• Clitoral enlargement and increased sensitivity
• Oily hair
• Increased body hair growth
• Sore or scratchy throat / cracky or deepening voice
• Some experience water retention (though not due to aromatization)
Be careful w/ using diuretics to manage this – continued use of even OTC
diuretics is not recommended.
• May cause vaginosis / yeast infection (most any AAS has this potential)
• Occasionally people experience nose bleeds or headaches (due to
increased blood pressure – you can google for OTC supplements to
help with BP
Primobolan (Methenolone)
Primobolan (Primo), comes in both oral and injectable form. The
injectable is most commonly used. Oral form, primobolan acetate, has
recently become more available.
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Typical Use
Primo has been listed as one of the top favorites for women. Because it
does not aromatize, again it is a favorite cycle both for cutting or bulking
off-season. Lean gains are good for a women looking to build some size,
but not get “too swole”. Oral Primo is unique in that the oral form is one of
the few orals that is not hard on the liver, but at the same time, it loses a
degree of its strength as it passes through your system, thus higher doses
are required.
Typical Cycle
Injectable Primo:
• Dose: 50-150mg / week
• Duration: 6-12 weeks
It is generally good to start the cycle at 50mg / week for the rst 4
weeks to identify any adverse reaction. (This is strongly suggested if
this is your rst time with the compound.) After that time, you can
increase the dose if desired.
Suggested maximum dose is 150mg / week (though more is not always
better). As the dose increases, sides may increase and results don’t
necessarily increase.
Oral Primo:
• Dose: 50-75mg ED – split the dose ½ in the AM, ½ in the PM
• Duration: 6-12 weeks
• No taper or post-cycle therapy is needed.
It is generally good to start the cycle at 50mg ED (splitting doses as
above) for the rst 10-14 days to identify any adverse reaction. (This
is strongly suggested if this is your rst time with the compound.)
After that time, you can increase the dose if desired.
Suggested maximum dose is 15mg ED (though more is not always better).
As the dose increases, sides may increase and results don’t necessarily
increase.
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Potential Sides
• Notorious for hairloss – A shampoo like Nizoral or Nioxin ( nd next to the
dandruff shampoo in most stores) can help minimize this.
• Acne
• Increased body hair growth
• Sore or scratchy throat / cracky or deepening voice
• Clitoral enlargement and increased sensitivity
• Oily hair
• Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
• May still experience usual menstrual sides (cramps, bloating, etc.) on
your regular menstrual schedule.
• May cause vaginosis / yeast infection (most any AAS has this potential)
Proviron (Mesterolone)
Proviron is a highly androgenic compound that is used primarily during the
nal weeks of a competition cutting phase to help lean out in the midsection. It is often stacked with Nolvadex to lean out the hips/thighs/waist
further. Being fundamentally androgenic (as opposed to anabolic), proviron
will not promote muscle growth as much as it promotes leanness and
hardness. For short cycles (i.e. 4-8 weeks maximum), sides are minimal.
Typical Use
Proviron would often be stacked with Nolvadex as a nal 4-8 week dial into
a competition date.
Typical Cycle
• Dose: 25 mg ED – split the dose ½ in the AM, ½ in the PM
• Duration: 4-8 weeks
• No need to taper the dose when the target date or cycle end date is
over.
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This is often the primary component of a prep phase. It can be run all the
way up to a show without promoting water retention issues.
More experienced cyclers will often stack with winstrol or anavar.
Potential Sides
•
•
•
•
•
•
•
•
•
Water retention
Acne (face or shoulders)
Oily skin
Hairloss
Increased body hair growth
Sore or scratchy throat / cracky or deepening voice
Facial hair growth
Clitoral enlargement and increased sensitivity
Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
Masteron (Drostanolone Propionate)
Masteron (Drostanolone Propionate) is a highly androgenic compound
that is used primarily during the nal weeks of a competition cutting phase
to help lean out in the mid-section. It is often stacked with Nolvadex to lean
out the hips/thighs/waist further. Being fundamentally androgenic (as
opposed to anabolic), Masteron (Mast) will not promote muscle growth as
much as it promotes leanness and hardness. For short cycles (i.e. 4-8
weeks maximum), sides are minimal.
Typical Use
Masteron would often be stacked with Nolvadex as a nal 4-8 week dial
into a competition date.
Typical Cycle
• Dose: 7-15mg ED or 14-30mg EOD
• Duration: 4-8 weeks
• No need to taper the dose when the target date or cycle end date is
over.
Potential Sides
• Water retention
• Acne (face or shoulders)
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•
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•
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•
Oily skin
Hairloss
Increased body hair growth
Sore or scratchy throat / cracky or deepening voice
Facial hair growth
Clitoral enlargement and increased sensitivity
Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
Boldenone (EQ, Bold A, Bold C, etc.)
Equipoise (EQ) (Boldenone Undecylenate) is an injectable steroid that
includes a small amount of aromatization. It is seen as a nice compound
that produces good gains with minimal water retention. EQ is the most
readily available (and used), but a shorter ester would be optimal. /r/
steroids suggests going with the short ester version of this
compound, Boldenone Acetate (Bold A). This will allow the compound to
clear much faster if sides occur.
Typical Use
For an experienced cycler, as an off-season bulker with low water retention,
or at the beginning of a contest prep, again with low water retention.
Anecdotally, some people experience an increase in hunger on EQ, so it
might t well with a bulker phase.
Typical Cycle
Bold A:
• Dosage: 5-7.5mg ED or 10-15mg EOD
• Duration: 4-10 weeks
It is generally suggested to start the cycle at 5mg ED (or 10mg EOD)
(splitting doses as above) for the rst 10-14 days to identify any
adverse reaction. After that time, you can increase to 7.5mg ED (or
15mg EOD) if desired.
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Suggested maximum dose is 15mg ED (though more is not better – often
10mg is suf cient). As the dose increases, sides may increase and results
don’t necessarily increase.
Equipoise (EQ):
• Dosage: 50-75 mg / week
• Duration: 6-10 weeks
It is generally suggested to start the cycle at 50mg / week for the rst
6 weeks to identify any adverse reaction. After that time, you can
increase to 75mg / week if desired.
Suggested maximum dose is 150mg / week (though more is not better). As
the dose increases, sides may increase and results don’t necessarily
increase.
Potential Sides
•
•
•
•
•
•
•
Acne
Oily skin
Hairloss
Clitoral enlargement and increased sensitivity
Sore or scratchy throat / cracky or deepening voice
Increased body hair growth
Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
• May cause vaginosis / yeast infection (most any AAS has this potential)
Nandrolone Phenylpropionate (NPP)
There are several different forms (esters) of Nandrolone available. NPP is
the shorter-acting Deca Durabolin (Nandrolone Decanoate) that would
be more likely recommended for women. The longer acting Deca will
anecdotally produce more water retention and due to the longer ester it will
take longer to clear if sides pop up. This is a more aggressive cycle for
women with some water retention and longer detection time than the more
commonly used injectables such as primo.
Typical Use
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For women, NPP falls into the scope of really only for those experienced
who are looking for signi cant growth and are prepared to deal with the full
scope of potential sides. It might be considered an off-season cycle for a
female bodybuilder or used at the beginning of a 16 week prep, to be later
dropped and replaced with a non-aromatizing compound.
Typical Cycle
• Dose: 5-8mg ED or 10-16mg EOD
• Duration: 8-10 weeks
It is generally suggested to start the cycle at 5mg ED (or 10mg EOD)
(splitting doses as above) for the rst 2-3 weeks to identify any
adverse reaction. After that time, you can increase to 8mg ED (or
16mg EOD) if desired.
Suggested maximum dose is 15mg ED (though more is not better – often
10mg is suf cient). As the dose increases, sides may increase and results
don’t necessarily increase. As we get into the much more aggressive
cycles, it becomes more of a personal preference on dosing based on
goals and any other stacked compounds
Potential Sides
•
•
•
•
•
•
•
•
Water retention
Acne
Oily skin
Hairloss
Sore or scratchy throat / cracky or deepening voice
Increased body hair growth
Clitoral enlargement and increased sensitivity
Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
Testosterone Propionate
There are several esters of testosterone, but only the Propionate ester, also
known as Testosterone Propionate (Test P), would be recommended for
women. The other variations commonly used by men, Testosterone
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Cypionate, Testosterone Enanthate (Test E), or Sustenon, are
considerably longer-acting esters, producing anecdotally much more water
retention and more aggressive sides, taking a much longer to clear the
system.
Typical Use
For women, Test P falls into the scope of really only for those experienced
who are looking for signi cant growth and are prepared to deal with the full
scope of potential sides. It might be considered an off-season cycle for a
female bodybuilder or used at the beginning of a 16 week prep, to be later
dropped and replaced with a non-aromatizing compound. It is reasonably
short-acting so will begin to produce results (and sides) fairly quickly. This
compound does aromatize a bit. There is no real need for an aromatase
inhibitor with this compound, but be aware that it does still produce some
water retention.
Typical Cycle
• Dose: 3-6mg ED or 6-12mg EOD
• Duration: 4-6 weeks
As we get into the much more aggressive cycles, it becomes more of a
personal preference on dosing based on goals and any other stacked
compounds
Potential Sides
Water retention
Acne
Oily skin
Hairloss
Sore or scratchy throat / cracky or deepening voice
Increased body hair growth
Clitoral enlargement and increased sensitivity
Interrupted period / ow – may take a few months for the ow to come
back as normal. Note this does NOT mean you won’t get pregnant.
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Trenbolone Acetate
Trenbolone Acetate (Tren A) is more recently, being mentioned more
frequently with women. It is a favorite among men because it promotes
strength while allowing great cutting results with no aromatization. The
issue is that this compound is extremely androgenic and also can have
effects on the liver. Very experienced female cyclers may use trenbolone
acetate as part of a cutting cycle, but should be very careful and diligent
with their bloodwork afterwards.
/r/steroids hesitates to include cycle information her, because you
should already have an idea of the cycle details if you are at a point
where you are considering running a tren cycle. Virilization is a major
risk here.
Post Cycle Notes
Generally women don’t run aggressive cycles and can just end the AAS
cycle. The compound(s) will attenuate over time as their individual half-lives
run their course. During that time, just as at the beginning of the cycle,
there is a big ux in the hormone pro le. Drawing a comparison to “that
time of the month”, the sides can seem more pronounced and in particular,
some moodiness may result. The range of this is something that is very
unique to each person, and even unique to each compound plus each
person’s unique body chemistry.
Anticipating this, pay attention to your general state of mind post-cycle. If
you nd yourself getting depressed or moody, step back and acknowledge
that it is most likely the effect of the hormones, and not something else
happening in your daily life. If you happened to be using prescription antidepressants, I would suggest you be particularly aware of your state of
mind. One OTC option to help even out your moods is Inositol. This is
essentially just a B-vitamin, ideally in powder form. For more information
about inositol and depression treatment, here is an article, or you can just
google “inositol, depression” for a bunch of information. Powder inositol is
recommended over inositol tabs/caps.
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Another obvious effect of coming off a cycle is the reduction (or back to
“normal”) in recovery ability and strength and maybe some of the increased
sense of well-being that comes with AAS at times. The loss of these can be
both humbling and frustrating, however it’s important to keep things in
perspective as you can’t stay on a cycle forever without hitting some point
of negative effects. It is supposed to be a “cycle” – a phase with a speci c
goal, and then letting your body adapt to the change and retain as much as
possible. Again, monitor yourself as the compound(s) clear out of your
system in terms of strength and recovery – adjust your training and your
expectations to match this phase of your progress to avoid burnout or
injury.
Things to Remember
In summary, some basic things to keep in mind if you want to play on the
dark side:
• Make sure your goals and expectations are appropriate. Just
because someone suggested a particular drug or it is available, doesn’t
mean its the right thing to get to your goal.
• More is NOT always better. It’s about nding a workable balance for
YOUR hormone levels, your goals and your experience.
• Never forget that you are self-medicating with hormones – it is
always your own personal experiment. Slow & low is your best
approach.
• Don’t stack a pile of stuff you’ve never run each individually before
– you have no idea how these compounds affect your body so you can’t
make judgments on what to cut / what is bad / what is good for your
body chemistry. Also there is an accumulated effect when you are
throwing all sorts of stuff in the pile. Fundamentally you are jacking up
the amount of DHT in your system. Know the half life of each compound
you are interested in – some are much longer than others so if you don’t
like the sides, on longer esters, tough tit. Now you have to wait for the
compound to clear your system before the sides go away.
• Know the potential sides – anything is possible in any degree – there
is no such thing as “no sides”- only those that you don’t experience – it
is very individual so you are still running your own personal experiment.
• You need to accept the potential of sides – you either accept them or
you don’t. You can’t pick which ones you want & which you don’t and
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you can’t predict what you will experience until you try it. It’s more about
managing risk by educating yourself, staying at conservative doses and
watching how your body responds. If you can't accept the risk of sides,
you have no business cycling.
Don’t listen to other people – especially guys. They will have a
completely different experience with different doses & different
compounds. A tiny little amount of anything will have dramatic effects on
women compared to men. YOU are responsible for YOUR cycle.
Women do not need to worry about post-cycle therapy (PCT) like
guys do. Women can generally just end a cycle. There is no need to
taper. The compound will clear at the rate speci ed by its half-life.
Think in the long term – just like a bulking or cutting diet – it has a
place in the ongoing cycle of change that happens over time. You can’t
maintain the state of being “on” so you have to also come off, expect to
lose a little of what you gained, but you will have made a change to your
over all body composition.
Watch your diet – if you are going to bother putting this stuff in your
body, you should respect your body enough to not think you can get
away with eating shit – IF the diet is tight, then you will also get the
leaned out effect that everyone wants – but sloppy diet will get you more
big than lean.
Time off = Time on. The general rule of thumb is to allow at least as
long as your cycle, to clear your system and let your body re-establish
its own homeostasis. People tend to want to “try more”, but it is
important to remember that there are impacts to your body not
immediately apparent that you need to pay attention to, i.e. kidneys,
liver, blood pressure, etc.
AAS can promote yeast infections / vaginosis. Any AAS or sex
hormone manipulator (including AIs) can promote yeast infections. It is
always recommended to supplement with Acidophilus to help prevent
these.
AAS and Birth Control do not interact. However the effects they each
promote are opposing – birth control works to regulate estrogen
(including estrogen-pattern bodyfat depositing) while AAS promotes lean
muscle mass.
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AAS and Birth Control
One of the most common questions asked is about AAS and Birth Control.
Women typically experience an interruption of their menstrual cycle while
on any sex hormone-manipulating cycle (AAS or “anti-estrogen”). This does
NOT mean that you cannot get pregnant. Despite the lack of ow, other
typical menstrual sides can be present when “that time of the month” is
expected – including bloating, breast sensitivity, moodiness, etc.
There is very little to nothing published on the topic of the interaction of
birth control and anabolic androgenic steroids so it is hard to say how they
truly interact. For the usual purpose of women using steroids, to cut, it is
more than that the effects of birth control and steroids promote opposing
results, so the end result is less than completely optimal effects of either.
Birth control’s purpose is to regulate estrogen levels. For some this may
mean controlling higher levels during a period, or for others this might
mean promoting more if they experience irregular periods. This also
includes the usual water retention and estrogen-pattern fat depositing
around the stomach, hips and thighs areas. While a steroid is trying to
promote lean muscle mass, and in some cases, even a ‘fat burning’ effect.
Even while the steroid may interrupted the menstrual ow, the birth control
will still support prevention of pregnancy.
If a cycle is used for off-season mass-building, the need for staying lean is
less of an issue. However for competition cutting, it can be an issue. The
trade-off is to continue using birth control, and possibly not get the full
effect of the cutting in the stomach / hips / thighs area, but still getting the
pregnancy prevention or dropping the birth control, using a back-up birth
control method (i.e. condoms) and have less of an impact from the
estrogen-pattern fat depositing. Another option for many is an intra-uterine
device (IUD). The copper IUD is completely non-hormonal, or another
option such as Mirena, has a low-dose of slow-release progesterone to
help address bleeding which can be an issue with the copper IUD. IUDs
must be inserted by your OB/GYN and can last 3-6 years for progestin
IUDs and up to 12 years for copper IUDs. This is something you need to
discuss with your OB/GYN. The cost tends to vary and may or may not be
covered by your health insurance.
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Another concern that women often with steroid use is recovery of the
menstrual cycle. Noting I have yet to see a published study on this, the
following paragraphs come with a caveat that this is from anecdotal and
observational information and suggested as practical guidance and not a
medical verity. If you have lost your period for an unusually long time and
are concerned, always consult your OB/GYN.
The menstrual cycle tends to be sensitive to changes in its environment –
ranging from stress, to increased physical activity, sudden weight or
bodyfat drop, introduction of steroids, or an estrogen manipulator such as a
new birth control dose or use of an anti-estrogen. It will tend to turn off ow
(and in the extreme, amenorrhea) or have breakthrough bleeding or
sporadic periods while it deals with the change in its environment. When
things have returned to a state of homeostasis, things will generally return
to normal, including the usual monthly ow and the usual side effects of
estrogen-pattern bodyfat depositing, water retention, cramps, etc.
To gauge roughly how long it should take for an interrupted menstrual cycle
to return, look rst at the compound you are using and its half-life. This will
help you get an idea of a point where the concentration of the compound
has dropped to where the rest of the body is comfortable and ready to turn
things back on. And then, keeping in mind that the menstrual cycle works
on a 28-day schedule, it will generally want a full month of a stable
environment before it may start up again. If you have concern, always
consult your OB/GYN. There are prescriptions that are available to help
reintroduce a period.
A last comment is about steroids and pregnancy. Again there are no
medical studies available, but general guidance is to allow a good six
months after a cycle to clear before attempting to get pregnant. Be sure to
work closely with your personal physician if you plan to get pregnant and
ensure that all of your basic blood work, and everything else is in order.
The concern is that the presence of steroid compounds in the female
system while a fetus is growing, can affect the sex hormones of the fetus,
producing androgenic fetal abnormalities. Some of this mentioned here,
but all in all, you would want to ensure a steroid-free environment for your
child. There are many women who have cycled, who then stopped, cleared
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out and have had healthy children with no problem. Steroid use will not
leave you infertile.
If the father is using steroids when the mother gets pregnant, there is no
effect on the fetus itself. The concern for men using steroids is more related
to the steroid-driven suppression of natural testosterone production, and in
the potential for infertility. Again, that said, there are many men who have
conceived while on cycle with no issue.
Androgen De ciency In Women
If you are a woman and taking non-IUD hormonal birth control and don't
take DHEA or some other kind of androgen replacement you are very
probably living with suboptimal hormone levels. More on this: Here.
Obviously this doesn't really apply when on AAS.
FAQ
Will AAS affect my birth control? Short answer: No. There is little/no
evidence to show that anabolic or catabolic steroids will cause your birth
control to stop working. However, you may stop ovulating and therefore
stop having menstrual periods while using AAS.
Do women need PCT? For most female cycles, it is advised to simply
taper down your dose or stop completely. Women do not need to use
SERMs and AIs and taking them can have very damaging effects.
What is virilization? Technically, virilization refers to the development of
male traits by females. For example, the growth of body hair and loss of
hair on head, enlargement of genitals, deepening of voice, acne,
irregularity/loss of menstrual cycle, loss of breast size, and increase in sex
drive. Virilization is caused by an increase of androgens. It is possible to
avoid and prevent unwanted virilization by avoiding compounds that are
more androgenic than anabolic, by taking the lowest possible doses to
achieve desired results, and by closely monitoring your body for unwanted
physical changes.
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What about my genitals? Many women experience an enlargement of the
clitoris while using AAS. Examples: 1, 2
Depending upon the length and dose of the cycle, most women report that
this engorgement is only temporary and that their genitals return to normal
within a short period after their last dose. It is a myth that the common, lowdose cycles will result in "growing a dick."
Am I going to get too bulky/huge? You will only get as big as your eating
and training allows. The compounds and dosages that most women will
use will not result in incredible mass.
Related Studies
Most of this wiki page was taken from a blurb written by Sassy69.
Related Thread - Female Cycle Thread.
On the pill, watch out for injuries
Effects of follicular versus luteal phase-based strength training in
young women
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The Estrogen Handbook
Gyno Mechanics
First of all there are three different types of Gynecomastia (Gyno): Estrogen
induced, Progesterone induced and Prolactin induced. Of course, you can
avoid all three types of Gyno by keeping Estrogen (E2) within the normal
range (unless using a 19-nor). The precursor to any type of Gyno is almost
always Estrogen! Once you let Estrogen build up you signal to your brain
that you have conceived, it doesn’t matter if you are a man or woman, your
body at this point will have to go through certain processes to prepare you
for lactation. Firstly your body will rush to use that Estrogen and build up
breast tissue (which will form a lump) which is mandatory for the lactation
process. Once this stage has been completed and you have let Estrogen
still high your Progesterone will increase (Estrogen can still remain high)
which is an attempt from your body to make the tissue larger and also
make your aerolas bigger (puffy and enlarged nipples) again to get them
ready for lactation. Last stage of Gyno is Prolactin lactation, all previous
stages were preparing the body for this moment at this point your
Progesterone and Estrogen will drop and your Prolactin will spike, this is
when someone starts lactating.
Estrogen (E2)
Estrogen is commonly referred to as “E2”. Estrogens are made up of
Estrone (E1), Estradiol (E2), and Estriol (E3) (though the one we’re
concerned with is E2 speci cally). It is ne to simply refer to these as
Estrogen, but it’s more important that you know how to control your own
and have a basic understanding of the topic.
The mechanisms through which E2 interacts with sexual reproductive
organs and other hormones in the male body is actually much more
complex than in a woman’s body. This is mainly because we have so little
E2 compared to our female counterparts. The same can be said of
Testosterone in women; a slight change in levels can trigger huge changes.
A lot of people know the term “aromatase” or “aromatization”, but do people
know exactly what it is?
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The most challenging hormone for the steroid user is Estrogen by far. It is
the cause of any changes in your nipple/pecs (gyno), mood, libido,
hardness, bloat, skin, prostate, appetite – you name it, when you feel off
90% of the time is due to low/high Estrogen levels.
When you hit your sweet spot you will know, you can’t miss it. You will feel
happy, content, you will sex like a champ, eat like a champ and train like a
champ and to top it off everybody around you will be happy as well.
Here is an indicators of low/high Estrogen levels:
Low Estrogen Sides
• Dry skin/lips
• Feeling of dehydration
• Loss of libido
• Erectile Dysfunction
• Loss of sensitivity
• Dry glans (penis)
• White glans
• Loss of girth
• Irritability/Mood swings
• Crying for no reason
• DHT rage (aggression you take out on others)
• Dull orgasm
• Hesitation just before urinating
• Night sweats
• Loss of appetite
• Constant fatigue
• Lethargy
• Constipation (due to dehydration)
• Diuretic effect (pissing more water than you are consuming)
• Itchy scalp
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• Obsessive thoughts
Low and high Estrogen sides are very alike, the more experienced you get
the easier it is to differentiate between them, but it will always be tricky. The
best way to tell is always to get your Estradiol (E2) checked though blood
work.
High Estrogen Sides
• Acne
• Loss of libido
• Water retention (Bloat)
• Moon face
• Scrotum hanging too high
• Extreme oiliness all over
• Moodiness (Aggression, depression, increased irritability)
• Lethargy
• Insomnia
• Soft erections
• Extreme cravings for sugar/chocolate
• High BP
• BP spikes
• Enlarged prostate
• Pressure in lower abdomen when urinating
• Thin stream when urinating
• Constipation (from water retention)
• Itchy nipples
• Gynecomastia
When you get one side effect, it is just an indication use this list to
potentially make a full picture. Never go by one side only, being bloated
only means nothing, having dry skin only means nothing again. Again, the
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best way to tell is always to get your Estradiol (E2) checked though blood
work.
Aromatase
Aromatase is an enzyme that converts testosterone to estradiol and
androstenedione to estrone. Similarly, 17-ketosteroid reductase is an
enzyme that is capable of converting androstenedione to testosterone and
estrone to estradiol. Aromatase is named based upon the fact that it
removes a methyl group on the 19th carbon and rearranges ring A into an
aromatic ring, hence it aromatizes the testosterone molecule.
Aromatase is found in many different cells in the body, however it is
primarily found in adipose tissue. The liver, skin, and testes are also
primary sites of aromatization. In the testes, you have two different cells
that respond to the gondaotropic hormones (LH and FSH). Leydig/
interstitial cells respond to LH and initiate the synthesis of testosterone.
Sertoli/sustentacular cells respond to FSH and initiate and support
spermatogenesis. Sertoli cells do not produce testosterone but they contain
FSH-dependent aromatase. The estradiol produced in Sertoli cells binds to
E2 receptors in Leydig cells and the estradiol will suppress the Leydig cell’s
response to LH stimulation. Aromatase activity in other cells are not FSHdependent. Much of the brain contains aromatase, except the pituitary
gland.
Aromatase Regulation
Aromatase is decreased endogenously by prolactin and anti-Mullerian
hormone, although AMH is irrelevant and concentrations are almost nonexistent in adult males. It is also decreased exogenously by aromatase
inhibitors, nicotine, zinc, vitamin E, and resveratrol. The enzyme is
increased endogenously by gonadotropins, insulin, testosterone, and
androstenedione. Increased adipose tissue increases quantity of
aromatase in body.
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Aromatase Inhibitors (AIs)
Keep in mind Estrogen is good for you in many ways (libido, mood, skin
quality, hair, nails etc). But, most importantly, Estrogen is good for your
lipids. I am sure you have heard how Arimidex and Letrozole are bad for
your lipid values while Aromasin is ‘better’, in reality all AI’s are as bad as
each other for your liver values. The more you lower Estrogen, the worse
your liver values will get – it doesn’t matter which AI you use, all that
matters is how much you are lowering your Estrogen. If you lower your
Estrogen by 10 pg/mL you won’t notice much difference. If you crash your
Estrogen down to single digits I guarantee you that your HDL/LDL will be
completely out of whack no matter which AI you used.
Suicidal AI vs. Non-Suicidal/Binding AI
Arimidex and Letrozole are non-suicidal AI’s, all they do is bind any
Estrogen you convert directly on your aromatase enzyme. Each AI binds a
different percentage of Estrogen, Letrozole binds more than Arimidex of
course. The problem with binding AI’s is that once you cease use, all of the
Estrogen that had accumulated when you were using that AI suddenly gets
released – this process is called "Estrogen rebound" and I am sure you
know it can be far worse than Estrogen while on a cycle since normally
when you drop your AI you either cruise with a low dose of Test or PCT. In
both cases you have far less Test in you and once all that Estrogen is
released you got a much higher chance of getting Gyno and of course you
are going to be bloated and feel soft for weeks till your Estrogen comes
down to normal levels.
Aromasin is the new generation of AI and it is suicidal, the difference
between Aromasin and the other AI’s is Aromasin will actually destroy/kill a
certain percentage of your aromatase enzyme so by doing so it also 'kills'
any estrogen that was attached to that enzyme. This means when you stop
using Aromasin you won’t rebound at all like you would with the binding
AI’s. If anything, you will have to wait for a while for your body to start
producing more aromatase (very bad if you crashed your Estrogen
comparing to using the other AI’s). Each person is different in the rate they
create new aromatase; it can take one to three weeks.
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Arimidex (Anastrozole)
Arimidex (Adex) will lower your Estrogen by about 50-60%. Of course, if
you keep taking it that percentage accumulates so you lower 50% by
another 50% and so on, you can easily end up with your Estradiol in the
singles if you take it for long enough at a high enough dose and you aren’t
converting much Estrogen from aromatizing gear (using low dose of Test
and high dose AI). Arimidex is a good for new steroid users as if they
overestimate their dosing for AI and get symptoms of low E2, they will
bounce back back up fairly quickly and adjust as needed.
Dosage on cycle: dosing is user dependent and you should get blood
work to dial in your dose, but MOST users will nd .5 mg of Arimidex E3D
or E3.5D to be a good starting dose for 500-600 mg Testosterone (just for a
reference). Some may need more frequent (EOD) dosing or some may
even need less than E3.5D; this is really something that varies person-toperson too much and without blood work there is no way to know for sure
what dosage you need.
Aromasin (Exemestane)
Aromasin (Asin) is an orally available suicidal aromatase inhibitor.
Because Aromasin is steroidal this gives it a favorable Estrogen
suppression pro le and confers a few really awesome bene ts over other
anti-estrogens both on paper and in real experience. Steroidal antiestrogens have the bene t of being lipid-friendly and they all lower SHBG
which increases the ratio of free to bound Testosterone, which as many
experienced bodybuilders know can have a relatively profound, positive
impact on gains.
It is important to understand how drugs work in order to properly dose
them, Aromasin is a suicidal aromatase inhibitor, this means that it binds
with aromatase enzymes and as it does so permanently disables the
enzyme and destroys it. Hence the “suicidal” this compound. Just beware,
if you crash your estrogen on Aromasin, it can take a long time waiting for
your E2 to rise again (compared to the non-suicidal AIs), which will have a
negative impact on lipid pro le, joint integrity, mental health, libido and
overall gains.
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There is a great study on the pharmacokinetics of Aromasin in men
which found the following:
• 24 hours after one 25mg dose estrogen levels are reduced by
58 ± 21%
• 3-6 days after initial dose estrogen levels return to baseline
(without rebounding)
This means that you can nd the timing and dosage that works for you; this
exibility is what makes Aromasin such a versatile Anti-E.
BUT WAIT, there’s more. In males, Aromasin was found to increase total
testosterone by ~60% after 10 days @ 25mg/day, however the same study
found that while it increased total testosterone by 60%, free testosterone
was increased by over 100 percent! that’s right, it DOUBLES bio-available
testosterone (in naturals of course). With all this said, it is an option to be
ran into PCT like the study, when utilizing HCG right before or the rst
couple week of PCT. See the PCT wiki page for more info.
The Good:
• Lowers SHBG, increasing free test & makes all other anabolic
steroids more bio-available (i.e. more gains)
• Increases IGF-1
• No adverse changes in lipid pro les for men (unless you crash
estrogen - studies were also not on cycle and may be different)
• Is not liver toxic
• No Estrogen rebound
The Bad:
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Aromasin’s half life in the male body is actually very short (~9 hours) and it
is quickly eliminated, however, since as soon as it enters your bloodstream
it quickly destroys the aromatase enzymes present in your body, it is
effective in maintaining signi cant reductions in estrogen for up to +72
hours after a single 25mg dose. Estrogen levels only begin to rise again
after your body has begun to make new aromatase enzymes to replace the
ones destroyed by Aromasin.
• Typical aromatase inhibitor issues here, include stiff joints and
possibly lethargy if E2 gets too low
• If you crash your E2 levels, it will remained crashed until your
body makes more aromatase at it's own rate.
• Typically more expensive than Arimidex or Letrozole
• Alopecia. The other two AI’s have hair loss/hair thinning as a
side effect, but not full blown Alopecia.
Dosage on cycle: dosing is user dependent and you should get blood
work to dial in your dose, but MOST users will nd 12.5 mg of Aromasin
E3D or E3.5D to be a good starting dose for 500-600 mg Testosterone (just
for a reference). Some may need more frequent (EOD) dosing or some
may even need less than E3.5D; this is really something that varies personto-person too much.
Letrozole
Letrozole is by far the harshest of all AI’s, not necessarily because your
Estrogen will be too low but because Letrozole as a compound/active
ingredient is really harsh. The main applications for Letrozole is for Contest
Prep or apart of Gyno Reversal (along with a SERM) as this is the nuclear
option. Whenever used, always be sure to taper off to avoid rebound.
On cycle dosage: This AI is very easy to crash your estrogen with. It is not
typically recommended as your main AI
Selective Estrogen Receptor Modulators (SERMs)
After your cycle is complete and the steroid esters start to clear the system,
a post cycle therapy (PCT) is done to help get the pituitary glands running
again. SERM's work by blocking estrogen going into the pituitary glands,
which cause a rise in LH/FSH and testosterone levels, temporarily. This
helps give a boost after cycle, and it helps maintain gains.
Keep in mind all 3 SERMs will work in favor of your liver (Agonists) since
they are mild Estrogens, like stated earlier Estrogen is good for your liver
so adding a SERM will always improve your HDL/LDL. All SERMs don’t
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lower Estrogen, in fact they will increase your total Estrogen. They also
block your Estrogen in the nipple area.
Nolvadex (Tamoxifen)
Agonist: Liver, Uterus (female)
Antagonist: Breast/Nipple
Nolvadex is more suited for PCT purposes rather than Gyno Flair-Ups or
Gyno Reversal, as it increases natural Test levels by 60%, but will
decrease IGF-1 levels +25%.
Dosage on cycle: 20-40mg ED
Dosage for PCT: See PCT
Raloxifene (Evista)
Agonist: Liver, bone (increases bone density and is a recognized
treatment for osteoporosis)
Antagonist: Breast/nipple
Raloxifene doesn’t affect IGF-1 levels whatsoever, also it increases bone
density. It is the ideal SERM for Gyno Flair-Ups or Gyno Reversal since its
an agonist for your bones, doesn’t affect IGF-1 levels, and is perfectly safe
to run with a 19-Nor. Raloxifene shouldn’t be used in PCT since it raises
natural test levels by 40% only, 20% less than Nolvadex.
Dosage on cycle: 60mg-120mg ED
Nolvadex vs. Raloxifene for HGH/IGF-1
Taken from this study
Conclusions: Tamoxifen, but not Raloxifene, reduces IGF-I levels. Both
SERMs stimulate the gonadal axis, with tamoxifen imparting a greater
effect. We conclude that in therapeutic doses, Raloxifene perturbs the GH
and gonadal axes to a lesser degree than Tamoxifen.
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Nolvadex vs. Raloxifene for Gyno
Taken from this study
Conclusion: Inhibition of estrogen receptor action in the breast appears to
be safe and effective in reducing persistent pubertal gynecomastia, with a
better response to Raloxifene than to tamoxifen. Further study is required
to determine that this is truly a treatment effect.
Gyno Flare-Up Protocol
If your Estrogen is wildly out of control and you are developing puffy, sore,
or itchy nipples, UP your AI dose and start taking your SERM.
Note: If you choose Arimidex as your AI, just be aware the blood levels of
Arimidex can drop a bit when used alongside Nolvadex. To avoid this, you
may choose Raloxifene.
Dosing: Pharmaceutical Raloxifene 60mg ED or Pharmaceutical Nolvadex
20mg ED. It usually will subside after a 7-12 days. Continue the SERM for
3 days after the symptoms have subsided before you drop the SERM. It is
suggested to use Raloxo ne over Nolvadex when possible, due to
Nolvadex decreasing IGF-1 as seen above.
Gyno Reversal Protocol
If your Gyno is pubertal, as seen above, this potentially could help, but
most likely surgery is your best option. If your Gyno is from AAS use, this
has worked for multiple users on our board:
Dosing: Pharmaceutical Raloxifene 120mg ED - split the dose ½ in the
AM, ½ in the PM for a month, then 60mg ED - split the dose ½ in the AM, ½
in the PM until you've seen suf cient reduction in size.
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Clomid
Agonist: Liver
Antagonist: Breast/nipple
Clomiphene is a harsh drug, if you get the visual sides/blurry vision from
clomid they stay for life. They are rare, but do happen.
Clomiphene is a mixed agonist/antagonist. This is due to the fact that
Clomiphene is composed of two isomers: enclomiphene (trans-clomiphene)
and zuclomiphene (cis-clomiphene). Enclomiphene is an Estradiol receptor
antagonist. Zuclomiphene is an estradiol receptor agonist. In all likelihood,
the net antagonist effect might be due to the composition being 70% trans
(enclomiphene) and 30% cis (zuclomiphene). Nolvadex/Raloxifene is more
of a strict anti-estrogen, decreases the effect of estrogen in the body, and
potentiates the action of clomiphene. This combination came about after
100s of clinical experience.
So Nolvadex/Raloxifene is more of an antagonist, than Clomid is. They are
better at blocking the ER than Clomid is. Clomid also seems to exert
agonistic effects in parts of the brain that control emotion. That would
explain why some turn into women on periods during there experiences
with Clomid.
Tamoxifen is also made of slightly more isomers, the cis isomer of
tamoxifen (inactive one) trans-tamoxifen and trans-4-OHT isomer.
All you really need to know about clomid can be learned here:
Product Information: Clomid(R), Clomiphene citrate. Aventis
Pharmaceuticals, Kansas City, MO, 96.
Here is the clomiphene drug monograph
• If you want to learn about any drug, the manufacturer PRODUCT
INFORMATION and DRUG MONOGRAPH are excellent and probably
the best way to learn about any drug, especially these PCT medications,
as these sources are FDA approved and studied in large clinical trials.
• The FDA recommended dosage for clomid for male hypogonadism
(what we are trying to beat with PCT) is 25 mg EOD or every day,
titrated up to 50 mg EOD MAXIMUM for HPTA restart.
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Dosage for PCT: See PCT
Prolactin Support
Of all the potential side effects connected to AAS use, decreased libido and
sexual dysfunction are regarded as two of the most undesirable and for
good reason. Not only do they interfere with one of man’s most prized
activities. Although excess estrogen and testosterone de ciency are often
responsible for these side effects, elevated prolactin, which has begun to
af ict steroid users with increasing frequency, also deserves its share of the
blame. When it comes to the latter, we can fairly point the nger at 19-Nors
like Trenbolone and Nandrolone - two mainstays in the world of AAS.
Although steroids are the primary culprit when it comes to prolactin-induced
side effects, certain Growth Hormone (GH) peptides also have the potential
to increase prolactin levels, although to a much smaller extent than the
aforementioned AAS. Generally speaking, the increase in prolactin
witnessed with this class of supplementation is inconsequential, as levels
do not rise high enough to cause problems. In fact, this effect is so mild that
levels usually remain within a normal physiological range. However, when
combined with other prolactin elevating drugs, they may add further fuel to
the re, giving cause for consideration. Lest anyone decide to shy away
from GH peptides for this reason, when used alone - and often even when
used with other prolactin elevating drugs - the bene ts far outweigh the
risks. It is only when one’s prolactin levels are already high that they
increase the potential for side effects. Of the different GH peptides on the
market today, only GHRP-6, GHRP-2, and Hexarelin are capable of
increasing prolactin levels.
What Is Prolactin?
Most commonly referred to as the lactation hormone, prolactin is
responsible for the production of breast milk in nursing mothers and also
plays a critical role in the growth & development of the mammary glands.
Despite its connotation with pregnancy, it is a diverse hormone, having
in uence over a large number of functions and being implicated in over 300
separate actions. When it comes to steroid users, most are interested in
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circumventing just two of these—the development of glandular tissue in the
breast (gyno) and lactation.
However, prolactin also encourages bodyfat storage by directly increasing
the production of a speci c protein called lipoprotein lipase (LPL).
Lipoprotein lipase plays an important role in fuel metabolism by hydrolyzing
triglycerides from circulating plasma chylomicrons (chylomicrons are fat
globules which transport dietary triglycerides from the small intestine into
circulation) and other low-density lipoproteins, providing free fatty acids to
adipose tissue for storage. The higher one’s LPL levels, the more likely one
is to accumulate bodyfat. Prolactin has also been shown to increase
estrogen receptor concentration within breast tissue, increasing one’s
sensitivity to circulating estrogen and making the individual more
susceptible to gynecomastia and other estrogenic side effects.
When reviewing the effects of elevated prolactin on the male body, it
becomes readily apparent that it is in one’s best interest to keep this
hormone under control. While some of the side effects associated with
increased prolactin are readily recognizable, others, such as increased
bodyfat and estrogen receptor proliferation, are frequently attributed to
other causes or not recognized at all. Regardless of one’s awareness,
excess prolactin will wreak hormonal havoc on the body, directly working
against our bodybuilding goals while simultaneously initiating the
development of female secondary sex characteristics. All bad—all
preventable.
Choosing Your Medicine
Until recently, alleviating hyperprolactinemia (excess prolactin) involved the
routine administration of one of various side effect-laden pharmaceutical
preparations. In many cases, the accompanying side effects were worse
than the primary condition one was trying to treat, negating the drug’s
bene cial effects and leaving the you between a rock and a hard place. For
years Bromocriptine was the go-to of defense when it came to lowering
prolactin for dopamine agonists. It was effective, readily available, and
reasonably priced, but many found the resultant side effects just too much
to handle. But today, most will either use Cabergoline (Dostinex) or
Pramipexole (Mirapex)
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First Line Of Defense
When you're wanting to preventatively take action against prolactin, a
Dopamine Agonist may not be the best choice to start with as they come
with many unwanted sides and can be harsh drugs. You should always
have a Dopamine Agonist on hand if you wish to take a 19-Nor, but if you
wish to run something preventatively, you should start with some
supplements.
Supplements To Help Control Prolactin:
PLEASE READ: Prolactin-Inhibiting Supplements Wiki Page
• Vitamin B6 (Pyridoxine Hydrochloride & P-5-P) - To lower prolactin
levels it's recommend you take 50-200mg of P-5-P a day, in divided
doses. If you want to take regular B6, which can sometimes cause
minor side effects, take 300-1000 mg per day in divided doses.
Read the label before you buy B6 (if you choose not to get P-5-P),
because the Pyridoxine Hydrochloride type of B6 (in most
supplements) has been shown to be a prolactin inhibitor, but
Pyridoxal Hydrochloride has been shown to be ineffective at
lowering prolactin – make sure you buy the right type!
• Vitamin B6 - Examine Page
• Vitamin E - When using Vitamin E as a prolactin inhibitor, it's
recommended that you take 300-400 IU per day of natural Vitamin E –
this can be raised up to dosages such as 1000 IU for greater prolactin
control, but be aware of the possible side effects outline here
Natural Vitamin E is labelled D-Alpha Tocopherol whereas synthetic
is labeled DL-Alpha Tocopherol – the natural form works best. DAlpha Tocopherol with mixed natural tocopherols or D-Alpha
Tocopherol with mixed natural tocotrienols are the absolute best
forms to take.
• Vitamin E - Examine Page
• SAM-e - Take 400-1200 mg a day of SAM-e along with Vitamin B6 and
Vitamin E. An added bonus is SAM-E's ability to detoxify the liver.
• SAM-e - Examine Page
• Other Effective Prolactin-Inhibiting Supplements
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Remember, only use your Dopamine Agonist if blood work shows elevated
levels or if your nipple(s) leak ON THEIR OWN. Do NOT squeeze your nips
and force liquid out, even natural guys can do this, by doing this you will
stimulate and cause an increase in prolactin.
DO NOT TOUCH YOUR NIPS.
The Dopamine Connection
Anti-prolactin drugs work by mimicking the activity of a substance in the
brain called dopamine, thereby classifying them as dopamine agonists.
Dopamine itself is a neurotransmitter; a chemical messenger between
nerve cells in the brain. When levels of this neurotransmitter are normal the
body functions properly, but if levels become imbalanced serious problems
can develop, such as Parkinson’s or Restless Leg Syndrome.
However, in order for dopamine to have an effect it must rst attach to
dopamine receptor sites, which are found on the surface of the cell. Once
attached, the receptor receives, recognizes, and responds to this chemical
signal. Dopamine Agonists works by stimulating these same receptor sites,
thereby producing the same effects as dopamine, but you may be
wondering, how is this relevant to prolactin?
As one of the predominant regulators of prolactin, dopamine has a direct
impact on its production. More speci cally, dopamine works to reduce
prolactin levels by attaching to D3 receptors, which inhibit the production of
prolactin by lactotrophs (lactotrophs are prolactin producing cells located in
the pituitary). Acting as a dopamine substitute, dopamine agonists works
through the same mechanism, fooling the body into thinking that dopamine
levels are high. This shuts down, or reduces the production prolactin,
depending on the dosage administered.
Exactly how the steroids trenbolone and nandrolone increase prolactin
levels, we can’t be sure, but one thing we do know is that many who use
these drugs have experienced dramatic elevations of this hormone—
sometimes far above normal levels. This can and often does lead to one or
more of the aforementioned side effects. Dopamine agonists works to
address the issue directly, shutting down prolactin production at its root.
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Cabergoline (Dostinex)
Cabergoline (Caber) will lower both progesterone and will inhibit prolactin/
lactation. It’s a dopamine agonist means it wont allow your body to lactate
since it will occupy your dopamine receptors which are responsible for
lactation. Caber is the best prolactin support when running any 19-Nor
since the side effects are minimal – no drowsiness, doesn’t affect sleeping
patterns, and in general as far as dosing goes is far more exible than
Pramipexole or Bromo. Also there is no withdrawal when ceasing use of
Caber like with Prami.
Caber is a recognized ED med, it reduces downtime (not to be confused
with multiple orgasm) so if you need 24 hour recovery between sessions
two weeks after taking Caber you will see a signi cant decrease in
downtime you will need 12-16 hours to be ready for the next session, if you
need 2 hours you will need 1 hour with Caber.
Also its known for its potential multiple orgasm effect - when you ejaculate
you will feel as if you are releasing two or three loads at the same time.
This needs some input for the user though its not instant, the more you
hold it in the more orgasms you will potentially have in the end.
Common Dose On Cycle: 0.25-.5mg E3D or E3.5D
Common Does To Stop Lactation: 1-1.5mg E3-5D
Pramipexole (Mirapex)
Pramipexole (Prami), like Caber, will decrease progesterone and will inhibit
prolactin/lactation. It’s a dopamine agonist, like Caber, so it will occupy
dopamine receptors which are responsible for lactation.
Pramipexole (Prami) is a very peculiar drug! You need to taper up really
slowly to get to the desired dose and also taper down slowly to avoid the
mild withdrawal effect it will cause. Prami is an addictive substance and /r/
steroids is hesitant recommending it, as the more you use it the harder it
will be to come off it, also you will nd you will want to increase the dose to
maintain the ed effect. Prami’s ED effect is not as good as Caber. It does
reduce downtime like Caber does but that’s about it there is not potential
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enhancement in your orgasm or your libido contrary to caber. Only
advantage of Prami over caber is that if taken at the right time (2-3 hours)
before bedtime it can work as good as a Benzo to knock you out to sleep.
Which when running Tren is a bonus. If, however, you dose it wrong
(unwillingly of course) say 30 minutes – 1 hour before bed time you will nd
that after 2-3h of sleep you will be wide awake and probably sweating since
the dopamine you suppressed 4 hours ago rebounds and you feel as if you
just had a hit of coke in your sleep, not a good feeling. Also every time you
up the dose it takes some adjusting even if you are used to the substance.
Sleep sides like vivid dreams and waking up mid night can be avoided by
taking Prami at the right time so you got to experiment with this (the earlier
you take it the better). Make sure you never take Prami in the morning or
too early in the evening you are going to feel drained, dizzy, nauseous and
like a zombie all you will think its when the time comes to go to sleep.
The worst part with Prami starts when you quit, for the rst few days after
you quit, you will wake up in your sleep many times as if you were quitting
cigarettes or weed even, then you will have the lightest sleep ever as if you
were sleeping with your eyes open and the dreams will be negative and
intense. Basically you get all the Prami sides you had earlier only they cant
be avoided since you don’t take Prami anymore. This will subside
completely after 5 – 7 days.
Common Dose On Cycle: taper up from 0.125mg to 0.25mg-0.50mg (the
high dose only if you are stacking two 19-Nors or high dose of tren). After
you are done with your cycle taper down even slower from 0.50mg to
0.125mg and stay one week on each increment then quit. No matter what
you do expect some discomfort the rst 3-5 days after you quit.
Dose To Stop Lactation: You would probably need 1-2mg per day to stop
lactation, but wouldn’t recommend it, it would take ages to rump up to that
dose, if you are already lactating, use Caber worse thing that could happen
when jumping to a high dose of caber would be to get a ush face that lasts
12-14h (annoying but much better than puking your guts of for hours).
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Post Cycle Therapy (PCT)
Post Cycle Therapy or PCT is a period of medication treatment that follows
the use of anabolic steroids. Post Cycle Therapy is also one of the most
confusing topics for many steroid users; this is largely due to
misconceptions. When to start PCT, which meds to use, how long to use
them and what you should expect, these are all common questions and
ones we’ll address here.
RECOMMENDED PCT: 10mg Nolvadex, 6-8 weeks
The Purpose of PCT
When we supplement with anabolic steroids we suppress our natural
testosterone production. Testosterone, the primary male hormone, is
essential to our very well being. Most men who supplement with anabolic
steroids will always include at least a minimal amount of testosterone in
their cycle due to this suppression factor.
Following the use of exogenous anabolic steroids, the majority of users will
experience what has been dubbed a “hormonal crash” or “post cycle
crash”, which is a bodily environment in which key hormones essential to
the retention of the newly created muscle mass has been suppressed or
shut down.
The key hormones in question are LH (Luteinizing Hormone), FSH (Follicle
Stimulating Hormone), and subsequently (and most importantly),
Testosterone. LH and FSH are known as gonadotropins, which are
hormones that signal the gonads (testes) to begin or increase the
manufacture and secretion of Testosterone.
Alongside low levels of these hormones, the overall balance of total
hormones will be essentially thrown off, whereby Testosterone levels will be
low, and most of the time (depending on many factors), Estrogen levels will
be higher, and levels of Cortisol (a steroid hormone that destroys muscle
tissue) will be at normal levels. With Testosterone levels low and Cortisol
levels in the normal (or high) range, Cortisol now becomes a threat to the
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newly created muscle that was created during the recent anabolic steroid
cycle (Testosterone properly suppresses and counteracts Cortisol’s
catabolic effects on muscle tissue).
SHBG (Sex Hormone Binding Globulin) is a concern here as well, as it
binds to sex hormones (Testosterone) and renders them inactive,
essentially ‘handcuf ng’ them and preventing them from exerting their
effects. SHBG will also normally be elevated during the post-cycle weeks
as a result of the supraphysiological levels of androgens from the recent
anabolic steroid cycle.
The human body will normally restore this imbalance of hormones and
recover its endogenous Testosterone levels on its own over time with no
assistance, but studies have demonstrated that without the intervention of
Testosterone stimulating agents, this will occur over the course of up to 4
months or so. This is quite evidently enough time for the hormonal
imbalance to wreak havoc on the body and result in any individual losing
most or all of the newly gained muscle during this time. Therefore, all
anabolic steroid users should be concerned with the fastest possible
hormonal recovery, assisted and boosted with the use of Testosterone
stimulating compounds in the proper manner.
Furthermore, the attempt to allow the body to recover on its own will
present a very high probability of long-term endocrine damage to the HPTA
over time whereby the individual will develop anabolic steroid induced
hypogonadism (the inability to manufacture proper levels of Testosterone
for the rest of their life). It is therefore paramount that a proper post cycle
therapy that includes multiple recovery compounds be utilized so as to not
only restore the HPTA function to normal levels as quickly as possible, but
to avoid any possible permanent damage, which takes priority over the
concern of maintaining the recently gained muscle mass.
The HPTA: How It Works
The HPTA is the Hypothalamic Pituitary Testicular Axis, which is an axis
of interconnected endocrine glands in the body that deal with and control
Testosterone production.
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Click here for an HPTA Diagram
Outlined above is a diagram of the HPTA. The HPTA regulates how much
Testosterone is manufactured and circulating the body at any one given
time. Every individual is essentially programmed by their genetics (DNA) as
to how much maximum Testosterone they will manufacture, and this is the
prime determining factor. There exist other factors that determine how
much Testosterone an individual will produce as well, and these include:
age, diet, body composition, lifestyle habits, and physical activity. All of
these factors play a role in how much Testosterone an individual will
generate overall.
The HPTA functions under what is known as the negative feedback loop,
whereby the body will reduce its manufacture and secretion of Testosterone
if too much Testosterone is detected circulating in the body, and will also
adjust as such if insuf cient amounts of Testosterone are detected. This
detection and adjustment, known as the negative feedback loop, is
controlled by the hypothalamus, which is essentially considered the
‘master’ gland for all endocrine and hormonal functions in the body.
The negative feedback loop is ultimately the body’s attempt to maintain
hormonal homeostasis, which refers to the regulation of a system (in this
case, the internal systems of the body) in order to maintain stable and
constant favorable conditions. All endocrine glands operate by way of the
negative feedback loop in one way or another, and to varying degrees. In
the case of post cycle therapy, the concern is primarily with the negative
feedback loop of the HPTA.
Within the HPTA, the concern during PCT is the restoration and regulation
of the following 5 hormones to homeostasis:
• GnRH (Gonadotropin Releasing Hormone)
• LH (Luteinizing Hormone)
• FSH (Follicle Stimulating Hormone)
• Testosterone
The HPTA begins with the rst axis point, the hypothalamus, which will
detect a need for the human body to manufacture more Testosterone, and
will release varying amounts of GnRH. GnRH is a hormone that signals the
next axis point, the pituitary gland, to begin the manufacture and release of
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two important gonadotropins: LH and FSH. LH and FSH are two hormones
that work to signal the third axis point, the testes, to begin production and
secretion of Testosterone. This is the nal stage of Testosterone production
in the HPTA.
There are two primary hormonal factors that serve to inhibit, reduce,
suppress, or shut down Testosterone production in the HPTA:
• Excess Testosterone
• Excess Estrogen
Although there exist other hormones that serve to inhibit and suppress
HPTA function (such as Progestins and Prolactin), these are the two
primary conditional hormones that are of concern.
When the hypothalamus detects excess levels of Testosterone and/or
Estrogen in the body (either from the use of exogenous androgens on an
anabolic steroid cycle or otherwise), the hypothalamus will act to attempt to
restore a balance by essentially doing the opposite of what was previously
described. The hypothalamus will reduce or stop its production of GnRH,
which halts production of LH and FSH, which ultimately reduces or halts
production of Testosterone.
Until the hypothalamus’ ideal hormonal environment is restored, the
production of the various signaling hormones within the HPTA will not
begin, and this will often require months of time for the body to do this on
its own without the intervention of any Testosterone stimulating agents. The
reason as to why the recovery of the HPTA naturally takes such a long time
should be very clear due to the described workings of the HPTA.
This very basic understanding of the mechanisms of the HPTA and
negative feedback loop described above is essential to understanding how
and why a proper PCT program must be developed and utilized following
an anabolic steroid cycle.
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Determining Factors In Di culty Recovering the
HPTA
With anabolic steroid use, there are several different major determining
factors in how much dif culty an individual will experience in recovery of
their HPTA and endogenous Testosterone function during PCT. They are
the following factors, in no particular order of importance:
• Individual Response
• Type of Anabolic Steroid(s) Used
• Length of Cycle (Degree of Testicular Desensitization)
Individual Response
Every single individual will respond in a different manner to any chemical,
compound, anabolic steroid, food or drug in existence.
While some individuals might experience absolutely no HPTA suppression
or shutdown at all, other individuals might experience severe HPTA
suppression and shutdown to the extent where they might require far
longer periods of time to ensure full recovery than most. This, like anything
else, is a spectrum whereby there are the very ‘lucky’ individuals that
recover very quickly and easily on one end of the spectrum, and the
‘unlucky’ individuals that have extreme dif culty recovering during post
cycle therapy. In between the two extremes is the average.
Once again, this is due to the individual’s genetic programming as to how
the HPTA will respond and attempt to maintain homeostasis.
Type of Anabolic Steroid(s) Used
All anabolic steroids exhibit suppression or shutdown of the HPTA through
the mechanisms of the negative feedback loop, and there are no
exceptions to this. It’s often said that if you take any anabolic steroid you
now produce no testosterone, but this isn’t exactly true.
Various anabolic steroids are known as being mildly suppressive
(something like Anavar), while others are known as being heavily
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suppressive (something like Nandrolone Decanoate). In any case, no
matter how mild or severe an anabolic steroid exerts HPTA suppression, all
anabolic steroids when utilized for typical cycle lengths of weeks at a time
will eventually cause the HPTA to shut down, or at the very least severely
suppress its hormonal signal processes.
Even if suppression may not reach 100%, it will still be enough in every
case for there to be a need for testosterone supplementation during
use due to putting your testosterone into a low level state.
Important Note: the need for testosterone supplementation during
anabolic steroid use DOES NOT APPLY TO WOMEN nor does the need
for PCT. See the PCT For Women Section below.
Length of Cycle
This is perhaps the most important and most in uential factor. As the length
of anabolic steroid use continues, the majority of the Leydig cells of the
testes remain dormant and inactive, and the longer these interstitial cells
remain dormant and inactive, the greater the dif culty in essentially getting
these cells to respond to the stimulus of LH and FSH once again.
It has been discovered in studies that the issue of recovery of the Leydig
cells following anabolic steroid use is not due to a lack of LH, but due
instead to the desensitization of the Leydig cells to LH.1 In one study in
which exogenous Testosterone was administered to male test subjects for
21 weeks, LH levels were suppressed shortly after beginning
administration. However, at the end of the 21 week period, LH levels were
observed to rise within 3 weeks once the exogenous Testosterone
administration stopped, but Testosterone levels did not rise until many
weeks later in most of the test subjects.
PCT Medications
The main testosterone stimulating agents for HPTA recovery during PCT
are:
Primary
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• SERMs (Selective Estrogen Receptor Modulators)
Secondary:
• hCG (Human Chorionic Gonadotropin)
• Aromatase Inhibitors
SERMs: Classes of drugs in the SERM category include: Nolvadex
(Tamoxifen Citrate), Clomid (Clomiphene Citrate), Raloxifene, and Torem
(Toremifene Citrate). The nature of a SERM is that it exhibits mixed
Estrogen agonist and Estrogen antagonist effects on the body. This means
that although a SERM might block the effect of Estrogen at the cellular
level in certain tissues, it can enhance Estrogenic effects in other areas of
the body. These can be positive effects as well as negative effects.
In terms of the effect of SERMs on endogenous Testosterone stimulation,
they serve to act as an Estrogen antagonist at the pituitary gland, triggering
the release of LH and FSH as a result. Elevated levels of Estrogen in men
can and does suppress the output of endogenous Testosterone via the
negative feedback. Using SERMs for this purpose are an absolutely
essential addition to any PCT protocol and are not to be excluded under
any circumstance.
hCG: Human Chorionic Gonadotropisynthetic is an LH mimetic. It is a
protein hormone manufactured in high amounts by pregnant females that
contains a protein subunit that is 100% identical to LH, and therefore when
administered to men, it will mimic the action of LH in target tissues, such as
the testes. What results is an increase in Testosterone production via
stimulation of the Leydig cells by hCG.
hCG should never be utilized alone, as its nature as a gonadotropin will
itself trigger a negative feedback loop whereby once hCG is utilized, the
pituitary gland will halt output of LH until hCG use has discontinued.
Therefore, hCG must be utilized prior to PCT or with a SERM, oft-times
with an aromatase inhibitor, as hCG has demonstrated to increase
aromatase activity in the testes, resulting in rising Estrogen levels.3
Aromatase inhibitors: These are compounds such as Aromasin
(Exemestane), Arimidex (Anastrozole), and Letrozole (Femara). Rather
than block the activity of Estrogen at the cellular level in different tissues,
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aromatase inhibitors (AIs) serve to lower total circulating Estrogen levels in
the body by way of inhibiting the aromatase enzyme, which is the enzyme
responsible for the conversion of androgens into Estrogen.
The conversion of androgens into Estrogen results in excess Estrogen
levels, which, as explained earlier on this wiki page, will trigger the negative
feedback loop leading to suppression of Testosterone production. By way
of lowering total circulating blood plasma Estrogen levels, AIs will engage
the negative feedback loop in a positive manner and result in the release of
LH and FSH for the manufacture and secretion of more Testosterone. This
is essentially due to the hypothalamus realizing that circulating Estrogen
levels are too low, and will attempt to increase circulating levels of
Testosterone in order for a portion of the Testosterone secreted to be able
to become aromatized into Estrogen in order to restore the hormonal
balance.
The main importance of aromatase inhibitors is the ability to mitigate the
Estrogenic effects of HCG, if HCG is utilized in certain ways that will be
expanded on later. It is important to note, however, that the majority of
aromatase inhibitors have known drug interactions with Nolvadex that will
reduce blood levels of those AIs. Very speci c choices should be made in
regards as to which AI is used during PCT with what SERM.
SERMs
The question is often asked among the anabolic steroid using community:
Clomid or Nolvadex? Which one for PCT? But there are also relatively
newer SERMs as well. Toremifene (Torem) & Raloxifene (Ralox).
First of all, we will look at the two main SERMs people use for PCT -Nolvadex & Clomid. Nolvadex on a mg for mg basis is far more effective
than Clomid in stimulating endogenous Testosterone production, as well as
being a more cost-effective choice than Clomid itself.
Studies have demonstrated that 150mg of Clomid (Clomiphene Citrate)
administered daily raised endogenous Testosterone levels of 10 healthy
males by approximately 150%, while incidentally, 20 mg of Nolvadex
(Tamoxifen Citrate) daily raised endogenous Testosterone levels by the
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same amount.11 It is very evident here that Clomid is very effective for this
purpose, but Nolvadex seems to be a more cost-effective choice seeing as
though it is more effective than Clomid when compared mg for mg. In the
same study, they directly examined the effects of Nolva and Clomid on the
pituitary. They infused the men with 100mcg of GnRH and then measured
LH output from the pituitary.
The men taking Nolvadex at 20 mg/day had a signi cantly increased LH
response to GnRH. In contrast, the men taking Clomid had reduced LH
output, a decreased sensitivity to GnRH. The researchers stated that "a
role of the intrinsic estrogenic activity of Clomid which is practically absent
in Tamoxifen (Nolva) seems the most probable explanation."11 Likewise,
Clomid actually has been studied to exhibit Estrogen agonist effects at the
pituitary in vitro.12
What all this means is that Clomid potentially will work in varying
degrees as an Estrogen at the pituitary gland, triggering the negative
feedback loop and reducing the output of Testosterone stimulating
gonadotropins (LH and FSH). This is a problem during post cycle
therapy, which is a period in which individuals are trying to recover their
HPTA function rather than halt it even further. Ideally, one would want a
SERM that exhibits almost 100% Estrogen antagonistic effects on the
pituitary gland.
In addition to all this, vision sides are common with Clomid and could
may cause irreversible changes.18 Nolvadex may potentially cause some
vision sides as well,19 but they are known to be far more prominent in
Clomid than Nolvadex.16 More on Side Effects below.
Despite all of this, it should still be noted that the FDA recommends
Clomid for treatment of male hypogonadism and that high doses are
unnecessary to bring hypogonadal men into range.14, 17
To touch lightly on Torem & Ralox, they have all been compared and
studied alongside Nolvadex.15 The study looked at the effects of each
SERM in just under 300 infertile men with low sperm count and low
testosterone levels. The men were given 20 mg Nolvadex, 60 mg
Toremiefene or 60 mg Raloxifene every day for three months. See Figure 1
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SERM
FSH
LH
Testostero
Sperm
Normal
(mIU/
(mIU/
ne (ng/dL)
concentration
sperm
mL)
mL)
(x 106 / mL)
forms (%)
Nolva
5.72 to
4.54 to
496.59 to
32.08 to 41.94 18.91 to
dex
8.42
7.84
763.34
(+30%)
31.64
(+47%)
(+72%)
(+53%)
(+67%)
Torem 5.64 to
4.05 to
498.96 to
25.84 to 37.82 23.09 to
9.53
6.54
743.92
(+46%)
31.73
(+69%)
(+61%)
(+49%)
(+37%)
Ralox
6.39 to
4.18 to
583.55 to
27.01 to 32.64 14.72 to
6.87
4.75
604.35
(+20%)
21.86
(+7%)
(+13%)
(+3%)
(+48%)
As demonstrated, Nolvadex came out on top here in LH, Testosterone &
Normal sperm forms. Torem topped Nolva in FSH and Sperm
concentration. Both are very suitable PCT options (as already known with
Nolva, but this shows Torem as a viable option as well). Ralox was
unfavorable and is probably best used just for gynecomastia treatment.
IMPORTANT NOTE: Be sure to check out Drug Interactions, as this
contains important information for those using SSRIs and SERMs.
Dosing
Nolvadex:
PCT 5–10mg/day (Recommended)
In all studies involving Nolvadex, for doses used to stimulate endogenous
Testosterone production, only 20–40 mg daily of Nolvadex was utilized, and
it has in fact been shown that doubling the dose to 40 mg or higher will not
produce any signi cant difference in endogenous Testosterone secretion.
The only reason why many elect to higher daily doses of Nolvadex for the
rst 1-2 weeks of a PCT is for the purpose of achieving optimal peak blood
plasma levels more quickly, so as to ensure more rapid HPTA recovery.
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from the study here showing results month to month or see the table
below with the medians and results after three months:
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This isn't necessary and just further increases your risk of potential side
effects.
Furthermore, the rst week of PCT, there may be lingering suppressive
AAS still in the bloodstream, simply leading to greater oxidative stress on
the body by taking more compounds.
Recent studies have found that even lower doses than traditionallyprescribed are equally as effective.
STUDIES SHOW PEAK EFFICACY AT 5mg PER DAY
• A weekly low-dose tamoxifen vs raloxifene vs placebo in
premenopausal women with estrogen receptor-positive breast
cancer — This study examined the ef cacy of doses at 1mg and 5mg
per day and found the two lower doses are just as effective as the
previous standard of 20mg per day. “Considering results of our previous
studies we are now focusing on Tamoxifen at 5mg per day. A weekly
dose of 10mg/week is suggested as an alternative.”
• Randomized dose trial of Tamoxifen at low doses in hormone
replacement therapy — This study examined the ef cacy of tamoxifen
at doses of 1mg, 5mg and 10mg per day. “A dose of 5 mg/day was the
most effective and has been selected for a phase III trial in HRT users.”
• Randomized trial of low-dose tamoxifen on breast cancer
proliferation and estrogen biomarkers — “We compared the effects of
tamoxifen at 1 mg/day and 5 mg/day with those of the standard dose of
20 mg/day. The effects of lower doses … were comparable to those
achieved with the standard dose.”
PCT dosing with Nolvadex has been updated (2020) as follows:
• 6–8 Weeks at 5–10 mg ED. Doses can be taken as low as 5
mg/day if sides are a concern.
Clomid
According to the study previously mentioned,14 and thus recommended by
the FDA, Clomid for hypogonadism should be run at 25 mg EOD, 25 mg
ED, or 50 mg EOD. Again, the side effects of Clomid can be quite
bothersome and bad. Why risk vision changes or vision loss running
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+50-150 mg ED when you could just do 25mg ED or 50mg EOD and get
fantastic results? Dosing of a PCT including Clomid is as follows:
• 6-8 Weeks: 25mg ED or 50mg EOD
Enclomiphene Citrate
Clomid consist of two isomers; zuclomiphene and enclomiphene.
Enclomiphene is the transisomer in Clomid that is responsible for
recovery from hypogonadism in men., whereas zuclomifene is
antigonadotropic due to activation of the estrogen receptor and reduces
testosterone levels in men., and is thought to cause some of the side
effects that have been associated with clomiphene citrate. It was also
shown to have pernicious effects to male reproductive organs in mice.
• The dosage for enclomiphene is still debatable; studies show increased
total and free testosterone (without increasing DHT disproportionately)
with daily administration from 12.5mg to 25mg.
• Although rare, Enclomiphene Citrate is becoming more available and
would be the prefered choice over Clomid. It should be mentioned that
no studies have been conducted (at date of writing) that compare the
enclomiphene isomer to other widely available SERMs.
Torem
In the study above comparing Nolva, Torem, & Ralox, 60mg was the
dosage used and found to be very suf cient for PCT purposes. 60mg ED is
the FDA recommended dosage and they found no bene t upon doubling
the dose in women with breast cancer. Again, doubling the dose for the
purpose of achieving optimal peak blood plasma levels quicker isn't
necessary and just further increases your risk of potential side effects.
Dosing of a PCT including Torem is as follows:
• 6-8 Weeks: 60mg ED
SERM Dosing Note
Note: As you've noticed above, /r/steroids recommends 6-8 weeks of
SERMs. It is common for a lot of PCT options to only be 4 weeks. These
protocols usually used double the dose for the rst week or two.
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The only reason why many elect to utilize doubling the dose for the rst 1-2
weeks of a PCT program is for the purpose of achieving optimal peak blood
plasma levels quicker so as to ensure HPTA recovery quicker. This isn't
necessary and just further increases your risk of potential sides. It has been
studied that the longer you are on SERMs, the better your results of
stimulating Testosterone.15 So to prevent unwanted sides as well as
potentially achieve better results, we choose to suggest lower dosing over
a longer period than 4 weeks.
hCG
The majority of anabolic steroid users from the 1960s–mid 1980s did not
even utilize any compounds for the purpose of hormonal recovery, and the
term PCT did not even exist at that time. When the use of hCG became
increasingly popular (circa 1980), it was the only compound utilized. Since
then, the medical and scienti c understanding of such things has increased
exponentially and there should be no reason for any informed and properly
educated individual to utilize hCG on its own for PCT. When utilized in
conjunction with one of the other two categories of compounds (an AI and a
SERM), the dynamics change considerably.
hCG mimics LH and therefore actually keeps the testicles producing
testosterone even when anabolic steroids are present. However, it does not
induce the production of actual LH. The use of hCG on cycle, this is
primarily done so that post-cycle recovery is easier. hCG is also used on
cycle to prevent or at least minimize testicular atrophy that occurs due to
the use of anabolic steroids. The testicular atrophy that occurs is not
permanent, but will reverse once steroid use is discontinued and natural
testosterone production begins again.
It has been mentioned already that much of the dif culty in recovering the
HPTA following an anabolic steroid cycle is the result of Leydig cell
desensitization. hCG is essentially an analogue of LH, and the testes after
a prolonged anabolic steroid cycle would be as equally desensitized to
hCG as they are to LH. The human body, however, produces LH amounts
on its own that are far too inef cient for proper and rapid Testosterone
production.
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The body’s natural increase of LH and FSH following an anabolic steroid
cycle is also not a rapid peak, but a very slow and steady incline, as
evidenced by the study referenced earlier in which it was not until 3 weeks
when LH levels only began to reach the normal physiological
measurements following the cessation of exogenous Testosterone.
Therefore, the body’s own natural LH production does not provide a high
enough dose for stimulation, nor an immediate stimulation to the testes
required for the initial increase in Testosterone needed during the post
cycle therapy weeks.
We will be utilizing a SERM which will stimulate FSH/LH, but most will nd
recovery being a smother transition when hCG is utilized. Studies have in
fact demonstrated the incredible effectiveness of hCG for this purpose, and
it is even suggested clinically that hCG be utilized for the purpose of
treating anabolic steroid induced hypogonadism.\4])
If you choose to include hCG in your PCT protocol, the best possible
SERM for the PCT protocol is Nolvadex, as studies have demonstrated that
hCG and Nolvadex utilized together have exhibited a remarkable
synergistic effect in terms of stimulating endogenous Testosterone
production, and that Nolvadex will actually work to block the desensitization
effect on the Leydig cells of the testes caused by high doses of hCG .10
Dosing
Mixing hCG
Mixing 2ml bac water with 5000iu hCG will provide 250iu for every tenth of
a ml/cc. This will provide you 20 250iu hCG doses.
Generally hCG will come with a vial of lyophilized powder and an ampule of
either sodium chloride solution or bacteriostatic water. You want the
bacteriostatic water. Bac water is intended for multiple uses and will inhibit
bacteria growth. The sodium chloride solution is intended for female fertility
use purposes and is to be used in a single injection. If used over multiple
injections it may begin to grow bacteria.
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When you check your vial of lyophilized hCG it will generally be 5000 IU,
although it can come in other amounts.
Using 5000 IU as the most common example; if you take 2mL of Bac Water
and inject that slowly into your vial of 5000 IU hCG, you then have 250 IU
per tenth of a mL (cc). So every tenth of your 1mL insulin syringe would be
250 IU.
The other form hCG might come in is a liquid form. This is hCG in a
solution with a preservative to keep it active. You may add bacteriostatic
water to this in order to adjust your dosage if you need.
In either case, hCG should be kept in the refrigerator after reconstitution to
preserve its shelf life. It should be refrigerated within 72 hours of mixing it
with bac water. hCG should be good for around 60 days when refrigerated.
After that time it will lose potency at about ten percent per week as time
goes on.
Running hCG
HCG is ran a couple different ways:
• Over The Entire Cycle
• Weeks Leading Up To PCT
• 1-2 Weeks Before PCT
• First 1-2 Weeks Of PCT
1. Over The Entire Cycle
This is the preferred option, as it keeps the Leydig cells active, reducing
atrophy and the reactive oxygen species (ROS) free radical damage
incurred by prolonged shutdown. HCG can be ran over the entire length of
the cycle to make PCT easy and ef cient, if desired:
• Over Entire Length Of Cycle: 250 IU EOD
• Stop HCG use before starting PCT (SERM)
Important Note: 250 IU 2x/week is used by some, but there have been
studies on maintaining intra-testicular testosterone in healthy men with
gonadotropin suppression. This study found 125 IU EOD (437.5 iu/week)
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was 25% less than baseline. Alternatively, 250 IU EOD (875 iu/week) was
found to only be 7% below baseline.13
For this reason, it is recommended to use 250 IU EOD. If desiring to be
as close to baseline as possible, you would need more than 875 IU/week
(7% less than baseline) and less than 1750 IU/week (26% above baseline).
This is where the 500 IU 2x/week comes in, but without a study comparing,
we are only speculating and you could need more. Alternatively, if money is
a factor, it is best to use some hCG rather than no hCG, and you may do
less than the recommended: 500-750 IU/week.
If only taking it for PCT, and not regularly:
2. Weeks Leading Up To PCT
This is the preferred method after Option 1, especially for those that are
coming off a long cycle or blast and cruise.
Starting 6 weeks before PCT:
• Weeks 6-4: 500-1000 IU 3x/week
• Weeks 3-1: 250-500 IU 3x/week
• Week 0: Start PCT (SERM)
3. 1-2 Weeks Before PCT
Typically this will be run in the ~2 weeks leading up to PCT after your last
injection, while you are waiting for your AAS esters to clear (assuming long
esters such as Test E or C). If using short esters (Prop and/or Ace), nothing
changes. You just start the HCG while on cycle (1-2 weeks before PCT).
If you chose to utilize hCG in this fashion (unless using short esters (Prop
and/or Ace), there is one remaining issues to be addressed:
• The fact that hCG causes increased production of aromatase,
leading to increased Estrogen levels. See Below
This is where the AI is to be utilized as a supportive compound for hCG use
in this 1–2 week period, and after hCG is discontinued early on in PCT, only
the SERM to be used in order to carry along the hormonal recovery
process. hCG utilized in this fashion will be ran:
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• 1-2 Weeks Before PCT: 1000-1500 IU EOD
• 1-2 Weeks Before PCT: AI will be used only as long as HCG
4. First 1-2 Weeks Of PCT
Some will say hCG shouldn't be ran into PCT as it's suppressive, but as
noted above in the study with Nolvadex, it has shown to be effective when
run simultaneously with Nolvadex.10
If you chose to utilize hCG in this fashion, there is one remaining issue to
be addressed:
• The fact that hCG causes increased production of aromatase,
leading to increased Estrogen levels. See Below
This is where the AI is to be utilized as a supportive compound for hCG use
in this 1–2 week period, and after hCG is discontinued early on in PCT, only
the SERM to be used in order to carry along the hormonal recovery
process. hCG utilized in this fashion will be run as follows:
• First 1-2 Weeks Of PCT: 1000-1500 IU EOD
• First 1-2 Weeks Of PCT: AI will be used only as long as HCG
Aromatase Inhibitors: Aromasin (Exemestane)
Above All Else
This Section Is Optional, UNLESS Utilizing hCG dosing 3 or 4.
As noted above in hCG dosing 3 & 4, one issue that needs to be
addressed will be the fact that hCG will trigger increases in testicular
aromatase expression, and result in Estrogen increases in the body. If you
are on cycle, as you would be with HCG dosing 1 & 2, you will already be
taking an AI and be taking care of this.
It should also be noted that hCG will also cause an increase in testicular
progesterone levels. Estrogen rising is of course undesirable during PCT,
as it has already been explained that Estrogen will trigger suppression of
endogenous Testosterone production, and there is no doubt that any
individual wishes to encounter Estrogenic side effects during PCT either.
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Therefore, the option here is to include an aromatase inhibitor. However,
there exists a problem in regards to the other two of the three major
aromatase inhibitors (Arimidex and Letrozole). The issue is the fact that in
a PCT program that includes the use of Nolvadex, Arimidex and Letrozole
have direct negative interactions with Nolvadex.
The potential problem here is that Arimidex & Letrozole both have
decreased blood plasma concentrations when used alongside a
Nolvadex.5, 20, 21 Aromasin completely circumvents this problem, as it has
been demonstrated to have no interactions what so ever with Nolvadex,
unlike the other two aforementioned aromatase inhibitors. In one study,
Aromasin displayed no such reduced effectiveness or any reduced blood
plasma levels when utilized with Nolvadex.6 The conclusion here is that the
use of Arimidex or Letrozole would be last resort options for controling
Estrogen during hCG dosing 3 & 4 use.
The other bene t of selecting Aromasin over all other AIs is the fact that
Aromasin has demonstrated in several studies to impact cholesterol
pro les in a negative manner far less than other aromatase inhibitors have,
where in one particular study on cancer patients, 24 weeks of Aromasin
(Exemestane) administration held no impact on cholesterol pro les.7 Some
other studies have also demonstrated a nil effect on cholesterol pro les
from the use of Aromasin.8 Although there have also been some studies
that have demonstrated a negative effect on cholesterol pro les resultant
from Aromasin use, it is evident that there is not as a signi cant or as a
negatively impacting effect from Aromasin on cholesterol as other
aromatase inhibitors.9
Finally, in addition to these bene ts from Aromasin, it is very clear that
Aromasin holds the ability to increase Testosterone levels in males as
demonstrated by studies. For example, one particularly notable study
selected 12 healthy young male test subjects, and were administered
random Aromasin doses of 25mg and 50mg for a 10 day period, and not
only was Estrogen suppressed by a signi cant amount (38%), but
Testosterone levels in the test subjects were observed to have increased
by an incredible 60%.8
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Dosing
Note: This is a lot of Aromasin, but has clinically be shown to be effective.
You may end up experiencing low E2 sides. Most common include the
possibility of stiff joints and lethargy. If you wish to avoid this, consider
skipping the need for this and utilizing hCG dosing 1 or 2
Following these details, Aromasin would be the best possible aromatase
inhibitor of choice in order to combat the increased aromatase activity
caused by hCG. Therefore, Aromasin would then be utilized up to a full
25mg ED, and only while HCG is utilized in hCG dosing 3 or 4. Once
hCG is discontinued, Aromasin too should be halted.
This section is optional, UNLESS utilizing hCG dosing 3 or 4.
Drug Interactions
As with all drugs you use, you should always check for Drug Interactions.
One known issue during PCT is with people taking SSRIs. Nolvadex and
Toremifene have both been shown to have major interactions with one
another.
Most notably, SSRIs have been shown to reduce effectiveness of Nolvadex
and SSRIs when taken with Toremifene have been shown to cause
irregular heart rhythm that may be serious and potentially life-threatening,
although it is a relatively rare side effect. In any case, if you're on a SSRI, it
is best to use Clomid.
Side E ects
Common post-cycle complaints include depressive mood alterations,
fatigue, lethargy, insomnia, and decreased libido.22 As stated earlier, vision
sides are common for both Clomid and Nolva, more so with Clomid. Hot
Flashes, Nausea are two common side effects of Clomid, Nolva, & Torem.
Depression is known to affect many in PCT and is an actual listed side
effect of Nolva. Please make sure you are aware of this and in a good
place mentally before ever starting a cycle as you will be faced with
the potential of depression in PCT.
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What to Expect from PCT
As stated above in the Side Effects section above, common post-cycle
complaints include depressive mood alterations, fatigue, lethargy,
insomnia, and decreased libido.22 You should be fully prepared to go
through these symptoms if you chose to run a cycle.
The biggest problem with most PCT plans is the individual having
unrealistic explanations. Most PCT plans will last 4-8 weeks and many men
expect everything to be back to normal once this 4-8 week period is
complete. PCT does not work this way. Many men also expect for all their
gains be they weight or strength gains to be maintained post-PCT if the
PCT plan was proper and appropriate. Again, PCT does not work this way.
A good PCT plan will help you protect and maintain some of the progress
you made, but if the high in ux of hormones is no longer there (the high
in ux of hormones that helped you make your gains), without that support
system you will lose some of your gains. A good way to look at is as we
look at food – the nutrients you eat help you buildup your body. The
nutrients you eat become the support system. Take away the nutrients and
the support system goes away with it and the “building” begins to collapse.
For this reason it’s not uncommon for some men to begin consuming extra
calories during PCT in order to protect their gains—in simplistic terms
they’re substituting nutrients for the hormones that have been taken away.
This can help maintain weight but it’s not always a good idea. Weight is just
weight and if it’s not weight that’s muscle tissue it’s rather useless. It’s not
uncommon for some men to put on a good bit of body fat during this phase
due to their desperation to hang onto gains.
As stated, the primary purpose of PCT is to stimulate natural testosterone
production. Some gains may be lost during this period, but it’s not the end
of the world. For the steroid user he will be on cycle again one day. For the
present period he should focus on his hormone recovery, continue to train
and eat properly protecting the gains he can without putting on excess
body fat.
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When NOT to Run PCT
If you’re a steroid user that is on cycle more than you’re off, running a PCT
can be counter productive. For example, a man completes a cycle,
implements PCT and then jumps back on cycle right after or soon after
PCT. This is a very harsh practice and terrible for your body.
You are shutting down your natural testosterone production, stimulating it
through PCT and then shutting it right back down. You’ve put yourself on a
never ending rollercoaster with your hormone levels that’s going to wreak
havoc on your body. For such an individual he would be better off running a
low dose of testosterone, therapeutic levels, during his time between
cycles. This is not an approach most men should take. Most men who use
steroids need to come off and stay off after PCT is complete for a time if
long-term health is important to them.
Another time not to run PCT is if you are prescribed Testosterone
Replacement Therapy (TRT). A low testosterone patient has been found by
a medical professional to no longer have the natural ability to produce
enough testosterone on his own, which is why he needs testosterone
supplementation. If he happens to implement a cycle at some point during
his treatment, once the cycle is over he should simply continue on with his
previous Testosterone Replacement Therapy (TRT). If you implement a
PCT plan, you’re attempting to stimulate your natural ability that medical
professional has deemed to not be enough, and it will serve no purpose.
When to Start PCT
Timing is a very important factor when it comes to PCT. You want to start
PCT around the time the compound will be exiting your body and no longer
a major factor in causing suppression. In the medical eld, after 4 half-lives
the amount of drug (6.25%) is considered to be negligible regarding its
therapeutic effects. The chart below is based on known terminal half-lives
of AAS esters, as well as some theoretical half-lives (as some haven't been
studied). You will choose the ester that will require the most amount of
time before starting PCT (SERM).
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IMPORTANT NOTE: This is just the time the compound itself will be low
enough to start PCT. This does not take into account for metabolites that
have been found to have a correlation to LH & FSH recovery in nandrolone.
\23]) This could very well happen in other compounds as well. Be sure to
get post PCT blood work to ensure recovery. See Below
Ester
Time To Wait After Last Pin Before Starting PCT (SERM)
Acetate
3-4 day
Propionate
3-4 days
Phenylpropio
nate
5-6 days
Isocaproate
14-16 days
Enanthate
14-18 days
Cypionate
14-20 days
Decanoate
26-30 days
Undecylenat
e
52-56 days
Undecanoat
e
80-84 days
As you can see, if using a compound like Nandrolone Decanoate (Deca),
Sustanon (Testosterone Decanoate is its longest ester), Boldenone
Undecylenate (EQ), or Testosterone Undecanote, there is a very long
waiting period before starting PCT.
Very Long Ester AAS & PCT Transition
If using Nandrolone Decanoate or Boldenone Undecylenate, most will opt
to continue running Testosterone up until the point the half-lives will both be
considered negligible at the same time.
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For Example: In a Testosterone Cypionate and Boldenone Undecylenate
cycle you will continue to run the Testosterone Cypionate for 8 weeks
AFTER your last Boldenone Undecylenate injection.
On cycle, you can are taking supraphysiological doses of Testosterone.
When you are doing this transition into PCT you may either choose to
continue with your supraphysiological doses or drop your Testosterone
down to TRT doses (80-200 mg/week).
Very Long Ester Testosterone & PCT Transition
If you are using Sustanon or Testosterone Undecanote, you may want to
transition into a shorter ester to make the waiting period for the Decanoate
or Undecanoate ester to clear. Otherwise, due to the ester, it will get rid of
the exogenous Testosterone much slower and with that it will be releasing
VERY small minuscule amounts that will get very low at the end and will not
be optimal. Due to this using a Testosterone Enanthate or Propionate could
be very bene cial to you, your well being, and allowing the most successful
PCT possible (you wouldn't want to start early wile the compound is still
aiding in suppression).
Important Metabolites Note
The table above is just the time the compound itself will be low enough to
start PCT. This does not take into account for metabolites that have been
found to have a correlation to LH & FSH recovery—particularly, in one
study involving Nandrolone Decanoate.23
In the study researchers found that even after six months LH and FSH
were both still repressed. The recovery of LH and FSH was correlated to
the urinary level of the nandrolone metabolite 19-norandrosterone (19-NA).
19-NA was detectable for several months after the last nandrolone
administration, and there was a large inter-individual variation in the
excretion rate. Some individuals still tested positive (>2 ng/mL) even one
year after their last nandrolone dose and still sustained suppression of LH
and FSH during that time. Limitations are that this study did not state a post
cycle therapy was used by any of the steroid users. We do not know much
a proper PCT would have sped up recovery.
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This could very well happen in other compounds as well. Be sure to
get post PCT blood work to ensure recovery.
When to Start Your Next Cycle
For optimal health the general rule to follow is time on + PCT, equals time
off. If your cycle last 12 weeks, you wait 2 weeks to start PCT, and your
PCT plan lasts 6 weeks, then you will wait 20 weeks before starting a new
cycle. A mistake many men make is saying testosterone levels have
recovered shortly after PCT and it is now okay to start a new cycle. If you
do this you have not allowed your body time to normalize. True recovery
means your levels can hold without any type of supplementation, if not then
full recovery has not been reached.
Blood Work
It’s always a good idea to get blood work done after PCT to see where your
body is at; however, this won’t be the full story. When we run a PCT we are
arti cially stimulating natural testosterone production -- the stimulation
would not exist without the implementation of SERMs. The true tale of the
tape is where your numbers are good after a bit of time has passed since
cessation of the SERM; say several months.
The earliest time to check blood work would be a minimum of one month
after cessation of SERM's. You will be looking for LH/FSH returning to fairly
normal, as well as total and free testosterone levels alongside estradiol.
How do you know what normal i for you? If your cycle was run properly, you
should have gotten pre-cycle natural blood work. What were you levels on
that blood work? That will be your base point you are attempting to get
back to with PCT.
The Danger
If you’re going to supplement with anabolic steroids there is one single truth
you need to understand: risks exist. One of these risks is permanently
lowering your natural testosterone production and forever being in need of
TRT. Even with the best PCT plan this risk exists. The point of PCT is to
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help and minimize this risk; it does not completely remove it. If this is
something you cannot accept then anabolic steroid use is not for you.
PCT for Women
Michael Scally (former) M.D.'s Thoughts:
In the case of pre-menopausal females, tapering the anabolic-androgenic
steroids (AAS) would be the best treatment. Anabolic steroid
administration, like males, causes the HPGA to shutdown. However,
stopping the AAS will produce menopausal like symptoms, therefore
tapering until menses returns is best. The labs follicle stimulating hormone
(FSH), luteneizing hormone (LH), progesterone (P) and estradiol (E2) will
be the best indicator. They will show if the HPGA is affected adversely. In
marked contrast to a man, the period typically returns within 1-2 months
and will occur while tapering.
I would NOT suggest “selective estrogen receptor modulators” (SERMs) or
aromatase inhibitors (AIs) for a woman! NEVER! It is the equivalency of
forcing them into menopausal symptoms. The HPGA/HPTA are very
different. In fact, SERM/AI (such as Nolvadex and Arimidex) are used in
Breast Cancer, which includes a signi cant number of adverse effects.
Decreasing E2 in a man is far different from doing the same in a female. E2
and P are the main female hormones. Just imagine how a man feels that
receives Androgen Deprivation Therapy (ADT) for Prostate Cancer.
O cial /r/steroids PCT Protocols
These are the of cial /r/steroids recomended PCT Protocols. In general,
the longer that you have been on cycle and not producing your own natural
Test, the greater precaution you should take in your PCT.
When something is written as "X/X/Y/Y", think of it as Week 1 daily dose/
Week 2 daily dose/Week 3 daily dose/Week 4 daily dose/etc., etc..
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SERM Dosing Note
Note: As you've noticed in our SERMs Dosing section, as well as below, /
r/steroids recommends 6-8 weeks of SERMs. It is common for a lot of
PCT options to only be 4 weeks. These protocols usually used double the
dose for the rst week or two. The only reason why many elect to utilize
doubling the dose for the rst 1-2 weeks of a PCT program is for the
purpose of achieving optimal peak blood plasma levels quicker so as to
ensure HPTA recovery quicker. This isn't necessary and just further
increases your risk of potential sides. It has been studied that the longer
you are on SERMs, the better your results of stimulating Testosterone.\15])
So to prevent unwanted sides as well as potentially achieve better results,
we choose to suggest lower dosing over a longer period than 4 weeks.
Optimal/Primary PCT Options
This is the PCT plans you should use if you want PCT to be as as effective
as possible. This is highly recommended to those that have been on cycle
a long time or that are coming off a Blast & Cruise.
Nolvadex
Option 1
Starting at the beginning of the cycle.
• Over Entire Length Of Cycle: 250 IU EOD
• Stop hCG Before Starting SERM
• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)
Option 2
Starting 6 weeks before PCT (SERM).
• Weeks 6-4: 500-1000 IU 3x/week
• Weeks 3-1: 250-500 IU 3x/week
• Week 0: Stop hCG & Starting SERM
• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)
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Clomid
Option 1
Starting at the beginning of the cycle.
• Over Entire Length Of Cycle: 250 IU EOD
• Stop hCG Before Starting SERM
• 6-8 Weeks: Clomid 25mg ED or 50mg EOD =
25/25/25/25/25/25 (/25/25)
Option 2
Starting 6 weeks before PCT (SERM).
• Weeks 6-4: 500-1000 IU 3x/week
• Weeks 3-1: 250-500 IU 3x/week
• Week 0: Stop HCG & Starting SERM
• 6-8 Weeks: Clomid 25mg ED or 50mg EOD =
25/25/25/25/25/25 (/25/25)
Torem
Option 1
Starting at the beginning of the cycle.
• Over Entire Length Of Cycle: 250 IU EOD
• Stop HCG Before Starting SERM
• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)
Option 2
Starting 6 weeks before PCT (SERM).
• Weeks 6-4: 500-1000 IU 3x/week
• Weeks 3-1: 250-500 IU 3x/week
• Week 0: Stop hCG & Starting SERM
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• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)
Secondary PCT Options
This is the PCT plans you should use if you were in a position where hCG
wasn't an option until something changed and you now have access to it at
the VERY end of your cycle.
Note: Aromasin is added in to combat the E2 sides from HCG. Previously
hCG was utilized on cycle and you'd just adjust AI as necessary. Since you
are no longer on cycle, we will use Aromasin. This is a lot of Aromasin, but
has clinically be shown to be effective in aiding to stimulate testicular
function. You may end up experiencing low E2 sides. Most common
include the possibility of stiff joints and lethargy. If you wish to avoid this,
consider skipping the need for this and utilizing the Optimal/Primary PCT
Options
Nolvadex
Option 1
Taking hCG right before PCT.
• 1-2 Weeks BEFORE PCT: hCG 1000-1500 IU EOD
• 1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See
Section)
• Stop HCG Before Starting SERM
• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)
Option 2
Taking HCG and SERM together.
• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)
• First 1-2 Weeks Of PCT: HCG 1000-1500 IU EOD
• First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See
Section)
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Clomid
Option 1
Taking HCG right before PCT.
• 1-2 Weeks BEFORE PCT: HCG 1000-1500 IU EOD
• 1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See
Section)
• Stop HCG Before Starting SERM
• 6-8 Weeks: Clomid 25mg ED or 50mg EOD =
25/25/25/25/25/25 (/25/25)
Option 2
Taking HCG and SERM together.
• 6-8 Weeks: Clomid 25mg ED or 50mg EOD =
25/25/25/25/25/25 (/25/25)
• First 1-2 Weeks Of PCT: HCG 1000-1500 IU EOD
• First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See
Section)
Torem
Option 1
Taking HCG right before PCT.
• 1-2 Weeks BEFORE PCT: HCG 1000-1500 IU EOD
• 1-2 Weeks BEFORE PCT: Aromasin up to 25mg ED (See
Section)
• Stop HCG Before Starting SERM
• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)
Option 2
Taking HCG and SERM together.
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• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)
• First 1-2 Weeks Of PCT: HCG 1000-1500 IU EOD
• First 1-2 Weeks Of PCT: Aromasin up to 25mg ED (See
Section)
Minimalist PCT Options
This is the PCT plans you should use if you were in a position where HCG
isn't an option. It may not be as effective as the other plans, but it is
suf cient and will aid tremendously.
Nolvadex
• 6-8 Weeks: Nolvadex 10 mg ED = 10/10/10/10/10/10 (10/10)
Clomid
• 6-8 Weeks: Clomid 25 mg ED or 50 mg EOD =
25/25/25/25/25/25 (/25/25)
Torem
• 6-8 Weeks: Torem 60mg ED = 60/60/60/60/60/60 (/60/60)
Post Blast & Cruise Recovery Not Endorsed By /r/
steroids
These are PCT protocols listed are NOT endorsed by /r/steroids and
should be used for information purposes only. They have proven effective
for some, but optimally you will use a PCT protocol listed above
ASRM Guidlines For Physicians To Prescribe
Based on this 2014 paper by the American Society for Reproductive
Medicine this is what they recommend physicians prescribe for anabolic
steroid–induced hypogonadism (ASIH):
• Before Starting: Initial blood work will be taken and will include:
hormonal panel (LH, FSH, E2, T, freeT, SHBG, and PRL), complete
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•
•
•
•
•
blood cell count, lipid pro le, prostate-speci c antigen, and a
comprehensive metabolic pro le.
Week 1-4: For the severely symptomatic patients, a 4-week tapered
course of transdermal or injectable TRT may provide immediate
symptom improvement (i.e. those that have been off for a while and
have not recovered or are experiencing Low T symptoms).
Simultaneous administration of a SERM (such as clomiphene citrate, 25
mg every other day) will interact at the hypothalamus causing
stimulation of LH and ultimately increase intratesticular T. For patients
with ASIH-induced gynecomastia, 10–20 mg tamoxifen daily will block
the breast estrogen receptors and stimulate HPG axis recovery.
Week 5-8: After 4 weeks of treatment with TRT and/or a SERM,
repeated hormone panels should be obtained. If the patient has had
either a poor gonadotropin response or a poor T response, the authors
commence a 4-week course of hCG (1,000–3,000 IU, 3 times per week)
while continuing daily treatment with a SERM at the initial starting dose.
If a patient develops gynecomastia while on hCG, Tamoxifen aka
Nolvadex 10 mg b.i.d. (twice a day) or Anastrazole (Arimidex) may be
commenced.
After Week 8: After 8 weeks of hCG and adjunctive treatment, you
should get blood work again and hormone levels should once again be
assessed.
If the total serum T remains low and the patient continues to be
symptomatic: primary testicular failure is likely. These patients will
require a longer duration of TRT to avoid permanent ASIH.
If appropriately increased serum T and gonadotropin levels are
observed: the SERM may be reduced to 50% of its starting dose at 10
weeks of treatment and continued through weeks 12–16 or until target
serum T level is achieved. Recovery of hormonal function may be limited
in men with testicular failure, and close monitoring is recommended.
Original Power PCT
by Michael Scally (former) M.D.
• hCG - 2500 IU EOD – rst 16 days
• Clomid - 100 mg ED - split the dose ½ in the AM, ½ in the PM
for the rst 30 days
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• Nolvadex - 10 mg ED – entire 45 days
NOTE: Clomid and hCG dosing are extremely high, 50 mg Clomid should
be the upper limit as you should never need more. Blasting high doses of
hCG could lead to desensitization of receptors.
The above is a documented and approved PCT plan by former Dr. Scally.
This can be found in Anabolics 10th Edition by William Llewellyn.
New Power PCT
by Michael Scally (former) M.D.
• HCG - 2000 IU EOD – ( rst 20 days)
• Clomid - 100 mg ED - split the dose ½ in the AM, ½ in the PM
( rst 30 days)
• Nolvadex - 10 mg ED – (entire 45 days)
NOTE: Clomid and hCG dosing are extremely high, 50 mg Clomid should
be the upper limit as you should never need more. Blasting high doses of
hCG could lead to desensitization of receptors.
The above is a documented and approved PCT plan by former Dr. Scally.
You Can See Both The Original And New PoWeR Protocols: Here
Controversy
Aside from the high Clomid and hCG dosages, it should be noted that there
is some controversy on whether using two SERMs at once is bene cial or
not.
This is one of the explanations that Dr. Scally has given:
Clomid acts as an estrogen, rather than an anti-estrogen, by sensitizing
pituitary cells to the action of GnRH. Although tamoxifen is almost as
effective as Clomid in binding to pituitary estrogen receptors, tamoxifen has
little or no estrogenic activity in terms of its ability to enhance the GnRHstimulated release of LH. The estrogenic action of Clomid at the pituitary
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represents a unique feature of this compound and that tamoxifen may be
devoid of estrogenic activity at the pituitary level.
Some strongly disagree with Dr. Scally's reasoning behind the use of
Clomid. What he is describing here is believed to be "estrogen priming," the
concept that estrogen makes the pituitary more sensitive to GnRH from the
hypothalamus, so that more LH is released for a given GnRH stimulus. This
is well known to occur in females leading up to ovulation. Unlike females,
however, men don't have a preovulatory period or spikes in LH. The
research is fairly clear that estrogen priming does not occur in males. For
starters, take a look at an authoritative reference work like Grossman's
Clinical Endocrinology, which states (pg. 99):
Progesterone, acting synergistically with oestrogens, exerts negative
feedback on the hypothalamus during the luteal phase, thus limiting GnRH
pulsatility and slowing LH pulse frequency. The mechanism of positive
oestrogen feedback at the time of the LH surge has been much debated.
There is now evidence that enhancement of both hypothalamic GnRH
pulse generator activity and pituitary responsiveness to GnRH are involved.
All species so far studied have shown an increased 'self-priming' effect of
GnRH on the pituitary during the preovulatory period... In males, the
situation is more straightforward. Since LH surges do not occur, only
negative feedback effects are relevant. testosterone (and its active
metabolite dihydrotestosterone, DHT) exerts major suppressive effects on
both LH and FSH secretion, largely by inhibiting the GnRH pulse frequency
generator, but possibly also by direct pituitary actions. Oestrogens in the
male reduce pituitary responsiveness to GnRH.
That states clearly that there is no priming in males, only negative
feedback. The last emboldened sentence in this quote directly contradicts
Dr. Scally's quote above. If Clomid were to produce estrogenic action in the
pituitary, it would only serve to inhibit LH secretion.
Grossman's statement is corroborated by the more recent research on
the speci c effects of androgens and estrogen on the pituitary and
hypothalamus of healthy men. Here, it was shown that estrogenic action at
the pituitary has an inhibitory effect on LH output. In other words, estrogen
decreases pituitary sensitivity to GnRH. Estrogen does not produce positive
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feedback as seen in estrogen priming in females. The paper stated in its
conclusion that: "These data con rm previous work from our group which ...
showed [estrogen] has both hypothalamic and pituitary sites of negative
feedback in the male." In fact, "negative feedback at the pituitary requires
aromatization," as testosterone itself doesn't produce negative feedback at
the pituitary.
This older paper had a very interesting nding:
The positive estrogen feedback was found to be a relatively sex-speci c
reaction of the hypothalamo-hypophyseal system in rats as well as in
human beings. It is dependent--most of all--on the estrogen convertible
androgen level during sexual brain differentiation, but also on an estrogen
priming effect in adulthood. The lower the estrogen convertible androgen or
primary estrogen level during brain differentiation, the higher is the
evocability of a positive estrogen action on LH secretion in later life. In
clinical studies, we were able to induce a positive estrogen feedback on LH
secretion in most intact homosexual men in clear-cut contrast to intact
hetero- or bisexual men. These ndings were strongly con rmed by Gladue
and associates.
In other words, estrogen levels during brain development are responsible
for the sex-speci c differences in gonadotrophin secretion and estrogen
feedback at the pituitary. The important point of this research is that males
(with the exception of homosexuals) were not found to have any positive
feedback from estrogen. Those results that were "strongly con rmed."
Finally, there's this research (that was referenced above), which couldn't
have been any more relevant. It directly examined the effects of Nolva and
Clomid on the pituitary of human males. They infused the men with 100
mcg of GnRH and then measured LH output from the pituitary. The men
taking Nolvadex at 20 mg/day had a signi cantly increased LH response to
GnRH. In contrast, the men taking Clomid had reduced LH output, a
decreased sensitivity to GnRH. The researchers stated that "a role of the
intrinsic estrogenic activity of Clomid which is practically absent in
Tamoxifen seems the most probable explanation."
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Jcaesar369 Recommended PCT Protocol
Please Read The Original Post Here
TL;DR:
Last 6 Weeks of Your Cycle / Blast & Cruise:(including the time needed
to allow all compounds to clear)
We will count down the last 6 weeks (plus 3 days - 45 days total). You will
start the SERM's after day 0.
• T-minus 45 to 24 Days: 500–1000 IU HCG 3x weekly (IM) for 3 weeks
• T-minus 23 to 2 Days: 250-500 IU HCG 3x weekly (IM) for 3 weeks
• T-minus 2 to 0 Days: Wait 3 days before starting SERM's
Starting The SERMs
SERMs should be run for a much longer time period, depending on the
time of your Cycle or Blast and Cruise (i.e., total time on steroids). Use your
head and think about this one. If a standard 12–16 week cycle uses 4
weeks of SERM's, how long should a 3-year BnC PCT be? There is no
right answer, but you will probably want to err on the side of caution and
run at least 8–12 weeks of SERMs.
• 10 mg Nolvadex (Tamoxifen) everyday OR 60 mg Toremifene everyday
AND
• 25 mg Clomid (Clomiphene) everyday
Controversy
It should be noted that there is some controversy on whether using two
SERMs at once is bene cial or not, with consensus leaning towards the
latter.
How long to wait to check blood work to see if you've recovered?
Answer: ONE MONTH after cessation of SERM's. You will be looking for
LH/FSH returning to fairly normal, as well as total and free testosterone
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levels. How do you know what normal is? What your levels were that you
got with your pre-cycle natural self blood work.
Disclaimer: All of these RECOMMENDATIONS (not mandatory) are to be
used as advice. All of the suggestions by Jcaesar369 are based off of
clinical FDA trials and studies, found in the original post for reference.
Triptorelin PCT
• Triptorelin 50–100 mcg injected intramuscular ONCE
Pick one:
• Nolvadex 10/10/10/10
• Toremi ne 30/30/15/15
The reason for the Nolvadex or Toremi ne is to prevent the estrogen
rebound that is common with Triptorelin, one may also use an AI such as
Armidex or Aromasin.
A Doctor's Recommended PCT (TRT Clinic)
/u/DeludedOldMan's TRT doctor recommend this plan when coming off a
9-month cruise:
Weeks 1-2 (last 2 weeks of injecting test)
• Test C/E (normal TRT dose)
• 400 IU HCG E3D
• 20 mg Clomid EOD
Weeks 3-4
• 400 IU HCG E3D
• 20 mg Clomid EOD
Weeks 5 - 6
• 20 mg Clomid EOD
Week 7-8
• 20 mg Clomid E3D
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Miscellaneous Findings
Triptorelin/GnRH
A newer approach receiving recent attention is Triptorelin, the GnRH
agonist. This is used in a continuous manner to chemically castrate a man,
but in a one off dose, has been reported to kick start the PTA in a
hypogonadic BB. Triptorelin is a synthetic analogue of GnRH. It causes
constant stimulation of the pituitary gland and by acting as such, it
stimulates the pituitary gland to pump out LH and FSH. The dose needed
to cause chemical castration is much greater than the dose one would use
to restart HPTA.
The way Triptorelin hinders gonadotropin release is similar to how hCG will
hinder test production in the testes. A small amount of hCG will stimulate
the Leydig cells to produce testosterone, but too much will desensitize the
Leydig cells. This is what GnRH does, but with the pituitary gland.
Triptorelin has been studied to restore full HPTA function in a steroid user
who cycled for 13 years. Due to it's nature it is advised that Triptorelin only
be used if coming off long-term blasting and cruising or if one plans to
cease AAS forever.
Anecdotal evidence claims that Triptorelin is capable of restoring HPTA
function to those diagnosed with hypogonadism.
• Anabolic steroids purchased on the Internet as a cause of
prolonged hypogonadotropic hypogonadism
• Pituitary gonadotropin-releasing hormone receptors.
Effects of castration, steroid replacement, and the role of
gonadotropin-releasing hormone in modulating receptors in
the rat
• Effects of castration on luteinizing hormone and folliclestimulating hormone secretion by pituitary cells from male
rats
Misc.
Mechanism by which Nolvadex works:
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• While the literature is scant in this eld, a recent paper has shed some
light on this mechanism: Short-Term Aromatase-Enzyme Blockade
Unmasks Impaired Feedback Adaptations in Luteinizing Hormone
and Testosterone Secretion in Older Men
• How Clomid affects the eyes: Effect of clomiphene on [Ca2+]i rises
and cell viability in rabbit corneal epithelial cells
• Explains the possible cause behind vision effects: Oxidative stress
plays an important role in the pathogenesis of drug-induced
retinopathy
References
[1] Mauss J, Börsch G, Bormacher K, Richter E, Leyendecker G, Nocke W.
Effect of long-term testosterone enanthate administration on male
reproductive function: Clinical evaluation, serum FSH, LH, Testosterone
and seminal uid analysis in normal men. Acta Endocrinol (Copenh). 1975
Feb;78(2):373-84. Link
[2] Faloon, W. “Dangers of Excess Estrogen In the Aging Male”. Life
Extension Magazine, November 2008. Link.
[3] Valladares LE, Payne AH. Acute stimulation of aromatization in Leydig
cells by human chorionic gonadotropin in vitro. Proc Natl Acad Sci USA
76:4460-3/1979. Link.
[4] Gill GV. Anabolic steroid induced hypogonadism treated with human
chorionic gonadotropin. Postgrad Med J. 1998 Jan;74(867):45-6. Link.
[5] Boeddinghaus IM, Dowsett M. Comparative clinical pharmacology and
pharmacokinetic interactions of aromatase inhibitors. J Steroid Biochem
Mol Biol. 2001 Dec;79(1-5):85-91. Link.
[6] Zaccheo T, Giudici D, Di Salle E. Inhibitory effect of combined treatment
with the aromatase inhibitor exemestane and tamoxifen on DMBA-induced
mammary tumors in rats. J Steroid Biochem Mol Biol. 1993
Mar;44(4-6):677-80. Link.
[7] Atalay G, Dirix L, Biganzoli L, Beex L, Nooij M, Cameron D, Lohrisch C,
Cufer T, Lobelle JP, Mattiaci MR, Piccart M, Paridaens R. The effect of
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exemestane on serum lipid pro le in postmenopausal women with
metastatic breast cancer: a companion study to EORTC Trial 10951,
'Randomized phase II study in rst line hormonal treatment for metastatic
breast cancer with exemestane or tamoxifen in postmenopausal patients'.
Ann Oncol. 2004 Feb;15(2):211-7. Link.
[8] Mauras N, Lima J, Patel D, Rini A, di Salle E, Kwok A, Lippe B.
Pharmacokinetics and dose nding of a potent aromatase inhibitor,
aromasin (exemestane), in young males. J Clin Endocrinol Metab. 2003
Dec;88(12):5951-6. Link.
[9] Engan T., Krane J., Johannessen D. C., Kvinnsland S. Plasma changes
in breast cancer patients during endocrine therapy — lipid measurements
and nuclear magnetic resonance (NMR) spectroscopy. Breast Cancer Res.
Treat., 36: 287-297, 1995. Link.
[10] Smals AG, Pieters GF, Drayer JI, Boers GH, Benraad TJ, Kloppenborg
PW. Tamoxifen suppresses gonadotropin-induced 17 alphahydroxyprogesterone accumulation in normal men. J Clin Endocrinol
Metab. 1980 Nov;51(5):1026-9. Link.
[11] Vermeulen A, Comhaire F. Hormonal Effects Of An Antiestrogen,
Tamoxifen, In Normal And Oligospermic men. Fertil Steril. 1978
Mar;29(3):320-7. Link.43160-2/pdf)
[12] Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Disparate effect of
clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Am J
Physiol. 1981 Feb;240(2):E125-30. Link.
[13] Coviello AD, Matsumoto AM, Bremner WJ, Herbst KL, Amory JK,
Anawalt BD, Sutton PR, Wright WW, Brown TR, Yan X, Zirkin BR, Jarow
JP. Low-dose human chorionic gonadotropin maintains intratesticular
testosterone in normal men with testosterone-induced gonadotropin
suppression. J Clin Endocrinol Metab. 2005 May;90(5):2595-602. Epub
2005 Feb 15. Link.
[14] Katz DJ1, Nabulsi O, Tal R, Mulhall JP. Outcomes of clomiphene citrate
treatment in young hypogonadal men. BJU Int. 2012 Aug; 110(4):573-8
Link.
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[15] Tsourdi, E., Kourtis, A., Farmakiotis, D., Katsikis, I., Salmas, M., &
Panidis, D. (2009). The effect of selective estrogen receptor modulator
administration on the hypothalamic-pituitary-testicular axis in men with
idiopathic oligozoospermia. Fertility and Sterility, 91(4), 1427–1430.
Link.01280-6/pdf)
[16] Dobbs M. R. (2009). Clinical Neurotoxicology: Syndromes,
Substances, Environments. pg 106. Link.
[17] Teodósio Da Ros C. Twenty- ve Milligrams Of Clomiphene Citrate
Presents Positive Effect On Treatment Of Male Testosterone De ciency - A
Prospective Study. Vol. 38 (4): 512-518, July - August, 2012. Link.
[18] Purvin VA. Visual Disturbance Secondary to Clomiphene Citrate.
1995;113(4):482-484. Link.
[19] Alfred R. Ashford MD Irina Donev MD Ram P. Tiwari MD T. J. Garrett
MD, FRCP(C), FACP. Reversible ocular toxicity related to tamoxifen
therapy. 1988. Link.
[20] The ATAC Trialists’ Group. Pharmacokinetics of anastrozole and
tamoxifen alone, and in combination, during adjuvant endocrine therapy for
early breast cancer in postmenopausal women: a sub-protocol of the
‘Arimidex™ and Tamoxifen Alone or in Combination’ (ATAC) trial. British
Journal of Cancer (2001) 85(3), 317–324. Link.
[21] Dowsett M. Drug and hormone interactions of aromatase
inhibitors. Endocrine-Related Cancer (1999) 6 181-185.
[22] Cyrus D. Rahnema, B.S., Larry I. Lipshultz, M.D., Lindsey E. Crosnoe,
B.S., Jason R. Kovac, M.D., Ph.D., and Edward D. Kim, M.D. Anabolic
steroid–induced hypogonadism: diagnosis and treatment
[23] Gårevik, N., Strahm, E., Garle, M., Lundmark, J., Ståhle, L., Ekström,
L., & Rane, A. (2011). Long term perturbation of endocrine parameters
and cholesterol metabolism after discontinued abuse of anabolic
androgenic steroids. The Journal of Steroid Biochemistry and Molecular
Biology, 127(3-5), 295–300.
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There are many schools of thought on nutrition, especially when it comes to
strength and power athletes. Unfortunately there are no human studies on
nutrition involving supraphyisiological doses of AAS making most
"bodybuilding" and "powerlifting" diet advice anecdotal.
If you've never considered nutrition or diet, /r/ tness has a very good
breakdown for you
To paraphrase however, speci c food choices are less important, in terms
of muscular gains/fat loss, than overall calories and macronutrient
ratios
As a reminder- 1g Carbohydrate -> 4kCal
1g Protein -> 4kCal
1g Fat -> 9kCal
1g Alcohol -> ~7kCal
All successful diet programs are based around one thing, whether or not
they agree on macronutrient ratios, or timing, is another issue entirely. This
single goal is consuming a surplus of calories in order to gain muscle mass
or eating at a caloric de cit in order to lose fat.
Common thought among users is that during cycles it is possible to diet at
a very high caloric de cit without losing much if any muscle mass. On the
ip side, with high doses of AAS it is possible to eat at a higher caloric
surplus than a natural athlete without gaining as much fat, because the
nutrients will be partitioned more favorably for glycogen storage and
muscle growth/repair.
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Macronutrients
A macronutrient is an essential nutrient required in relatively large amounts,
such as carbohydrates, fats, proteins, or water. Some minerals are
sometimes included as well.
Protein
Protein is necessary for muscle repair/growth, as well as normal function
and is sometimes used as an energy source. Protein is not "stored" in
humans like fat (in adipose) or carbohydrates (glycogen).
Due to this increased ef ciency in nutrient partitioning there have
developed two trains of thoughts when it comes to protein intake
The rst is that, because consuming 1g protein/lb (2.2g/kg) of bodyweight
is more than enough for natural athletes, consuming more than that amount
of protein for AAS users is seen as a waste of calores/money. The
increased nutrient partitioning will allow the body to build more muscle off
of less of this macronutrient.
The second is that due to the increased ef ciency it makes sense to
increase protein intake because the body will be able to utilize more of the
macronutrient than it could normally.
I urge you to try out both methods and decide for yourself what works best
or you like the most
(Needs work on aminos, complete sources, sources-complimentary)
Varied Protein Types.
From this article:
Protein intake that exceeds the recommended daily allowance is widely
accepted for both endurance and power athletes. However, considering
the variety of proteins that are available much less is known concerning
the bene ts of consuming one protein versus another. The purpose of
this paper is to identify and analyze key factors in order to make
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responsible recommendations to both the general and athletic
populations. Evaluation of a protein is fundamental in determining its
appropriateness in the human diet. Proteins that are of inferior content
and digestibility are important to recognize and restrict or limit in the diet.
Similarly, such knowledge will provide an ability to identify proteins that
provide the greatest bene t and should be consumed. The various
techniques utilized to rate protein will be discussed. Traditionally,
sources of dietary protein are seen as either being of animal or
vegetable origin. Animal sources provide a complete source of protein
(i.e. containing all essential amino acids), whereas vegetable sources
generally lack one or more of the essential amino acids. Animal sources
of dietary protein, despite providing a complete protein and numerous
vitamins and minerals, have some health professionals concerned about
the amount of saturated fat common in these foods compared to
vegetable sources. The advent of processing techniques has shifted
some of this attention and ignited the sports supplement marketplace
with derivative products such as whey, casein and soy. Individually,
these products vary in quality and applicability to certain populations.
The bene ts that these particular proteins possess are discussed. In
addition, the impact that elevated protein consumption has on health
and safety issues (i.e. bone health, renal function) are also reviewed.
TL;DR Vary your protein intake types for best results.
Bio-availability of Protein
From this article:
Protein Type
Bio-Availability Index
Whey Protein Isolate
Blends
Whey Concentrate
104
Whole Egg
100
Cow's Milk
91
Egg White
88
Fish
83
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Beef
80
Chicken
79
Casein
77
Rice
74
Soy
59
Wheat
54
Beans
40
Peanuts
43
Max usable protein
It is often claimed that "anything over 30g of protein in one hour is unusable
by the body." This is untrue.
http://examine.com/faq/how-much-protein-can-i-eat-in-one-sitting.html
There really is no literature to indicate this number as a 'holy grail' of
protein absorption.
It may have arisen from looking at the rate of amino acid transporters,
assuming 10g/hour as a standard, and applying that to the typical minimeal approach to bodybuilder nutrition (with a meal every three hours).
and
Research done on Intermittent Fasting supports the theory that your
body can cope with far more protein than most people think, with two
studies showing that the consumption of an average of 80-100g of
protein in 4 hours yielded no differences in lean mass
Carbohydrates
Carbohydrates are the body's main source of energy. The muscles, and
liver, store carbohydrates in the form of glycogen, a branched
polysaccharide. AAS increase the amount of glycogen that will be stored in
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the muscle giving it a larger appearance and more energy from which to
draw during workouts. Carbohydrates are also muscle/protein sparing.
Glucose, Insulin and Glucagon after a high carb meal.
During mass gaining phases carbohydrates are generally exaggerated in
AAS users due to the increase in gylcogen storage capabilities. In fat loss
phases carbohydrates are generally the rst macronutrient to be
manipulated to decrease overall calorie intake.
When lowering one's carbohydrates signi cantly it is worth noting that
during high fat/low carb (ketogenic-type) diets, T3, the active thyroid
hormone (or essentially one's metabolic rate) is lowered more than when
compared to high protein/low carb.1 The average minimum carbohydrate
intake recommended is 130 grams per day, with less promoting ketosis,
Carbohydrates can be broken into two basic groups. Fast-acting (mono- &
disaccharides) and slow-acting (polysaccharides). The biggest difference is
how long the carbohydrate takes to get broken down by the body. Fastacting carbohydrates (sugars) illicit a more pronounced glycemic response
by the body, requiring higher levels of insulin, providing the body with
energy in the short term. (Re ned sugars can also increase cholesterol,
LDL, and risk of cardiovascular disease).5 Traditionally "fast" carbs are
placed before, during, and after a workout in order to supply the muscles
with energy as well as promote nutrient uptake following a workout. "Slow"
carbohydrates (some sources include brown rice, sweet potato, and oats)
are then traditionally placed everywhere else in one's diet, including before
a workout, especially if the workout in question will take more than an hour.
These carbohydrates illicit a smaller, and more long-term insulin response,
keeping the body at more stable blood-glucose levels.
Fiber
Fiber contains a different bond between saccharides than other
polysaccharides like glycogen or starches (beta vs. alpha). The body has
trouble breaking down these beta-glycosidic bonds and this creates the
idea of "Net Carbohydrates". Some people consider "net carbs" while
others do not. Net carbohydrates are determined by taking the total
carbohydrate intake and subtracting it by the amount of ber ingested. The
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resulting carbohydrate is the "net" and that number is used to calculate
calories as opposed to the total carbohydrate intake.
Fiber can be broken into two types, insoluble and soluble. Insoluble ber
(sources are hole grains) are not fermented by bacteria in the colon and
add bulk to the stool. Soluble ber (sources are psyllium, rice, beans, fruit,
oats, bran, soy) CAN be fermented and thus can count towards total calorie
intake (though some still choose not to, or assign it 2kCal/g). Soluble ber
holds water and binds to cholesterol, it has positive effects in cholesterol
ratios.
The recommended amounts of ber are 25g for women and 38 for men.
Too much ber (>60g) will require extra uid intake, bind to certain
minerals, impairing absorption, and cause excess bloating.
Dietary ber slows glucose absorption, decreasing the risk for type 2
diabetes by modulating blood glucose and decreases hypertension. This
should be a concern for AAS users since high blood pressure is a common
side effect of anabolic steroids.
High Fructose Corn Syrup
High fructose corn syrup (HFCS) is a major sweetener in the US. It is
composed of 55% fructose and 45% glucose and is sweeter than sucrose.
HFCS is thought to contribute to obesity for a few proposed reasons.
1) In the liver, fructose is more easily converted to glycerol/fatty acids which
form triglycerides, which are transported in the blood and stored in adipose
tissue.
2) Fructose does not stimulate insulin release in the way glucose does,
which in turn will reduce leptin production and does not suppress ghrelin, a
peptide hormone that contributes to feelings of hunger.
No/Low Cal Sweetners
Sugar Alcohols: Each sweetener (sorbitol, xylitol, mannitol) is somewhere
between 1.5-3 kCal/g. They are absorbed and metabolized at a reduced
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rate when compared to sucrose and large amounts can cause diarrhea,
and bloating.
Saccharin (Sweet N Low): A 0 Calorie sweetener derived from coal tar and
is 150-300x sweeter than sucrose, with a bitter aftertaste.
Aspartame (NutraSweet or Equal): 180-200x sweeter than sucrose and 4
kCal/g. Only very small amounts are needed to sweeten however. As a
component is Phenylalanine it is not recommended for those with PKU.
Many people seem to believe that Aspartame is incredibly toxic. Although a
small amount are sensitive to aspartame (causing nausea, headaches,
dizziness etc...) there is no need to be concerned if one does not have
PKU. Methanol, (methyl ester of phenylalanie) gets converted by the liver
into formeldahyde which is itself a toxic by product, however when
compared to diet sodas, fresh fruit/juice such as tomatoes and bananas
have between 1-2x more methanol.
Sucralose: More than 600x sweeter than sucrose, chemically it is sucrose
with chlorine as opposed to hydroxyl groups, this allows it to mostly bypass metabolism. Sucralose has about 2kCal per teaspoon.
Truvia (Stevia): 200x sweeter than sucrose, stevia doesn't issue any
glycemic response.
Fats
Fat is another one of they body's energy sources, certain lipids, and
consumption amounts are also important for hormone production,
maintenance of organs, and keeping joints healthy.
Excess in calories are converted and stored as fat in adipose tissue, the
body's fat stores.
According to the USDA, in order to properly maintain one's organs, joints,
and hormones fat consumption should be between 20-35% percent of the
overall caloric intake.
Because users create and manipulate major hormones on their own it is
common for users to lower fats to below 20%. In order to stay healthy it is
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not advised to dip fats too drastically for long periods of time. It is always
better, for health and safety, to err on the side of caution.
Saturated Fatty Acids
Saturated fatty acids are characterized by having all carbons between the
omega (terminal, methyl) end and the alpha (beginning, carboxyl) end
"saturated" with hydrogens. Saturated fats are generally solid at room
temperature (lard, butter, coconut oil etc...). Saturated fats are not
necessarily bad to include in one's diet. There seems to still be some
controversy over whether or not saturated fats are unhealthy. One one
hand saturated fats can increase LDL2,3 but on the other, diets with
reduced saturated fats have a higher amount of LDL receptors in a
complementary concentration to the amount the saturated fat was reduced
by.4 One's target for saturated fats should be no more than 10% of total fats
because unsaturated fats in fact do have healthier properties.
Unsaturated Fatty Acids
Unsaturated Fats have one (mono) or more (poly) double bonds between
carbons, this creates a "kink" in the otherwise linear structure. Unsaturated
fats are generally liquid at room temperature (olive oil, canola oil, sh-oils
etc...). When a diet that was once high in saturated fats has much of the
saturated fats replaced by mon- and poly-unsaturated fats LDL, cholesterol,
and risk of cardiovascular disease decreases.5
Here is a chart of various oils and their fat makeup
Essential Fatty Acids
These are polyunsaturated fatty acids and are necessary because the body
can only create a double bond at the 9th carbon from the omega end
(hence omega 9). The number (3,6) refers to the location of double bonds.
In the omega 9 fatty acid there is one double bond at the 9th carbon from
the omega end. In the omega 6 there are double bonds at the 6th and at
the 9. In the omega 3 there are double bonds at the 3rd, 6th, and 9th
carbons.
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Essential fatty acids are necessary for immune function, vision, cell
membranes, brain growth, and production of hormones.
Omega 3 and omega 6 fatty acids work in opposition in certain respects.
Omega 3s decrease blood clotting, reduce heart attack, and decrease
in ammation. Omega 6s increase blood clotting and increase in ammatory
responses. Due to this the target ratio for 6s/3s should be <4g/1g. Common
sources for omega 3 fatty acids include: sh, ax, and hemp oils. Common
sources for omega 6 fatty acids include: nuts, walnuts, peanuts, poultry,
corn, and soybean oils.
Trans Fats
For all intents and purposes all that should be noted about trans fats are
two things: The double creates a "trans" relationship between two
hydrogens, thus maintaining the linear fatty acid structure while still having
a double bond. The "more important" aspect of trans fats are that ingesting
1 or more grams of trans fats per day increases LDL, decreases, HDL,
increases cholesterol, decreases insulin sensitivity, and increases risk for
heart disease.6 If a food contains <0.5g of trans fats it legally does not need
to report trans fats. Look for "trans fat free" and steer clear of "partially
hydrogenated" oils in ingredients.
Water
Notable Macronutrient Minerals
(Na, K, Ca)
Micronutrients
Water Soluble Vitamins
Fat Soluble Vitamins
Minerals
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Eating "Healthy"
Common Dieting Strategies
Videos
Fat Head - A Documentary that debunks much of the conventional wisdom
about health and examines the reality of Morgan Spurlock’s work Super
Size Me Gary Taubes Lecture - Why We Get Fat and historical references
to the truth Doctor's Discussion of Keto - Andreas Eenfeldt, M.D. discusses
the parameters of Ketogenic Diets Sugar: The Bitter Truth - Robert H.
Lustig, M.D. discusses the issues and dangers with sugar Robb Wolf on
Paleo - Robb Wolf answers community questions on the bene ts of lowcarb/paleo The Paleo Solution - Robb Wolf discusses ancestral nutrition
and “Western” diseases Your Leaky Gut and Grain - Loren Cordain
discusses auto-immunity and Western diet How Bad Science and Big
Business Created the Obesity Epidemic - David Diamond explains how
industrial in uences have shaped our diet and health care infrastructure
King Corn - A documentary following the effects of the corn industry on
rural America and her inhabitants Dr. Mary Vernon Lecture - A video playlist
of great information and resources.
Web Resources
My Fitness Pal - An online and smartphone application to track
macronutrients and calories. The TDEE calculator in this is not very good.
References
1. Ullrich IH, Peters PJ, Albrink MJ. Effect of low-carbohydrate
diets high in either fat or protein on thyroid function, plasma
insulin, glucose, and triglycerides in healthy young adults. J Am
Coll Nutr. 1985;4(4):451-9.
2. Faghihnia N, Mangravite LM, Chiu S, Bergeron N, Krauss RM.
Effects of dietary saturated fat on LDL subclasses and
apolipoprotein CIII in men. Eur J Clin Nutr.
2012;66(11):1229-33.
3. Dreon DM, Fernstrom HA, Campos H, Blanche P, Williams PT,
Krauss RM. Change in dietary saturated fat intake is correlated
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with change in mass of large low-density-lipoprotein particles in
men. Am J Clin Nutr. 1998;67(5):828-36.
4. Mustad VA, Etherton TD, Cooper AD, et al. Reducing saturated
fat intake is associated with increased levels of LDL receptors
on mononuclear cells in healthy men and women. J Lipid Res.
1997;38(3):459-68.
5. Siri-tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fat,
carbohydrate, and cardiovascular disease. Am J Clin Nutr.
2010;91(3):502-9.
6. Trumbo PR, Shimakawa T. Tolerable upper intake levels for
trans fat, saturated fat, and cholesterol. Nutr Rev.
2011;69(5):270-8.
Reading
Title
Author
ISBN
Burn the Fat, Feed the
Muscle
Venuto, Tom
978-0804137843
The New Atkins for a
New You
Westman, Phinney,
Volek
978-0091935573
Wheat Belly
William David
978-1609611545
Why We Get Fat
Gary Taubes
978-0307272706
Good Calories, Bad
Calories
Gary Taubes
978-1400033461
The Paleo Diet
Loren Cordain
978-0470913024
The Paleo Solution
Robb Wolf
978-0982565841
The Primal Blueprint
Mark Sisson
978-0982207703
The Ketogenic Diet
Lyle McDonald
978-0967145600
Ultimate Keto Food List
Arcita, Joseph
http://document.li/
S01S
Nutrition Crowdsource
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Steroids Pro les, Androgenic
and Anabolic Rating
Anabolic steroids, technically known as anabolic-androgenic steroids
(AAS), are drugs that are structurally related to the cyclic steroid ring
system and have similar effects to testosterone in the body. They increase
protein within cells, especially in skeletal muscles.
Anabolic steroids also have androgenic and virilizing properties, including
the development and maintenance of masculine characteristics such as the
growth of the vocal cords, testicles (primary sexual characteristics) and
body hair (secondary sexual characteristics). The word anabolic comes
from the Greek ἀναβολή or anabole, "that which is thrown up, mound", and
the word androgenic from the Greek ἀνδρός or andros, "of a man" +
-γενής -genes, “born”.
See also pages for Insulin, hGH, and other Peptides.
Compound Short-cuts
• Nandrolone aka Deca, NPP — 19-nortestosterone (19-nor). Rated
125:37. Second only to testosterone in terms of popularity as a bulking
compound. Water retention, collagen synthesis, joint relief, more gains.
Experience thread.
• Boldenone aka EQ, Equipoise, Parenabol — Testosterone
derivative. Rated 100:50. Metabolites include DHB (dihydroboldenone).
Steady, dry, lean moderate mass gains, EPO-like stamina, strength and
endurance, appetite increase, collagen synthesis, potent aromatase
inhibition, IGF-1 boost, stringent estrogen management requirements.
Compound De nition. Comprehensive EQ Guide, Top-level thread.
Experience thread.
• Methenolone aka Primo, Primobolan — DHB/DHT derivative. Rated
88:57. Mild. No sides, dry, lean gains, collagen synthesis, immune
system bene ts, “The perfect steroid.” Pricy (±3× test). Experience
thread.
• Drostanolone aka Mast, Masteron — DHT derivative. Rated 62/25.
Mild, lean, dry gains. Considered a cutting steroid. As with other DHT
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analogues, masteron yields increased libido, aggression and strength
enhancement in the gym; general con dence and well-being
enhancement outside of the gym. Experience thread.
• Trenbolone aka Tren, Parabolan — 19-nortestosterone (19-nor)
derivative. Rated 500/500. Recomp, super-effective nutrient
partitioning, massive strength gains, dry, grainy look, sides from hell,
toxic, tough to out-eat on bulk. Experience thread.
• Trestolone aka MENT (7α-methyl-19-nortestosterone) — 19nortestosterone (19-nor) derivative. Rated 2500:650. Some refer to
this compound as a hybrid of Test, Tren and Deca. Lean gains, super
anabolic at 10x more myotropic than test. Aromatizes to methylestrogen. Can be side heavy. Brie y studied as a male contraceptive,
however all studies were halted 2013 with unclear reasons as to why.
Experience thread.
• Methyltrienolone aka Mtren, Oral Tren — 19-nortestosterone (19nor) derivative. Rated 12000:6000. One of the strongest AAS in
existence—second only to its double methylated cousin,
dimethyltrienolone. Said to rank equally to trestolone for rapid, overnight
changes in aesthetics and appearance. Extreme surge in strength and
aggression. Oft-utilized as a pre-workout or for brief cycles of 3-4 weeks.
Warning: Highly hepatotoxic. Can be used orally or injected. For toxicity
reasons, injection route is highly recommended. Experience thread.
Quick List
The following compounds are used more often.
Compound
Androg
enic
Anab
olic
45
320
24
322-6
30
100
Anadrol 50
(Oxymetholon
e)
Anavar
(Oxandrolone)
Androgel
(Testosterone)
100
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Melti
ng
Point
(°C)
177180
Notes
Detectable for 2 months
Detectable for 2 weeks
333
DecaDurabolin
(Nandrolone
Decanoate)
Dianabol
(Methandroste
nolone)
Durabolin
(Nandrolone
Phenylpropiona
Dymethazine
(Mebolazine)
125
30-3
5
90-21
0
165166
125
92-9
6
210
N/A
50
100
liqui
d
91
1,100
130.7
850
1,900
228230
Detectable for 2 months
25-40
62-13
0
124126
Detectable for 2 months
Methylstenbol
one
Oral Turinabol
90-170
660
None
100
Primobolan
(Methenolone
Acetate)
44-57
88
225230
141143
Proviron
(Mesterolone)
30-40
100-1
50
202206
Detectable for 3 weeks
20
400
223225
Detectable for 3 months
100
100
100
100
98-1
04
Detectable for 3 months
Equipoise
(Boldenone
Undecylenate)
Epistane
(Methylepitiost
anol)
Halotestin
(Fluoxymester
one)
Masteron
(Drostanolone
Propionate)
37
40-60
37
95-96
Superdrol
(Methyldrostan
olone)
Sustanon 100
& 250
Testosterone
Cypionate
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Detectable for 19 days.
Detectable for 5 months
Pros only.
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Testosterone
Enanthate
100
100
32-3
6
Detectable for 3 months
Testosterone
Propionate
100
100
118122
Detectable for 2 weeks
Trenbolone
Acetate/
Enanthate &
Blends
500
500
94-9
7&
72-7
8
Winstrol
(Stanozolol)
30
320
228242
Detectable for 5 months,
Use Montelukast to avoid
respiratory weakness.
Tren is being considered
for addition to androgen
replacement therapy due
to its ability to increase
muscle mass while
Detectable for 2 months
Extended List
The following compounds are more exotic in nature and we do not see
them used much.
Compound
1-Testosterone
Androg
enic
Anabolic
Melti
ng
Point
(°C)
Notes
100
200
Anabolicum Vister
(Quinbolone) (oral
Boldenone)
50
100
Anadur (Nandrolone
Hexyloxyphenylpropionate)
37
125
122124
Detectab
le up to
18
months
Anapolon
45
320
177180
Detectab
le up to 2
months
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Anatro n (Stenbolone
Acetate)
107-14
4
267-332
Andractim
(Dihydrotestosteron)
30-260
60-220
Andriol (Testosterone
Undecanoate)
100
100
Androderm (Testosterone)
100
100
Boldabol (Boldenone
Acetate)
50
100
Cheque Drops
(Mibolerone)
Danocrine (Danazol)
1,800
4,100
37
125
Deposterona (Testosterone
Blend)
100
100
Dihydroboldenone
100
200
Dimethandrolone/
Dimethylnandrolone
(DMAU)
No
Data
Dimethyltrienolone
10,000
10,000
Dinandrol (Nandrolone
Blend)
37
125
Dynabol (Nandrolone
Cypionate)
37
125
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[Bioorg
Med
Chem
Lett. 2005
Feb
15;15(4):1
213-6]
Very
new,
similar to
Tren
Under
develop
ment as
male
birth
control
pill
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Esiclene (Formebolone)
No
Data
No Data
Ethylestrenole
No
Data
No Data
210.
5 °C
Detectab
le for 2
months
Detectab
le for 3
weeks
Genabol (Norbolethone)
17
350
Hydroxytestosterone
25
65
Laurabolin (Nandrolone
Laurate)
37
125
187
1,200
25
46
Mestanolone
78-254
107
Methenolone Enanthate
44-57
88
Detectab
le for 5
months
300
Detectab
le for 5
months
Madol
(Desoxymethyltestosterone )
Megagrisevit-Mono
(Clostebol Acetate)
Methandienone
60
Methandriol
(Mythelandrostenediol)
30-60
20-60
Methyl-1-Testosterone
100-22
0
910-1,600
Methyldienolone
200-30
0
1,000
281
1304
Methylhydroxynandrolone
(MHN)
Methyltestosterone
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94-130
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337
Metribolone (MTren/
Methyltrienolone)
6,000-7
,000
12,000-30,
000
Miotolan (Furazabol)
73-94
270-330
Myagen (Bolasterone)
300
575
Nilevar (Norethandrolone)
22-55
100-200
Noretadrolone
No
Data
No Data
Omnadren (Testosterone
Blend)
Orabolin (Ethylestrenol)
Oranabol (Oxymesterone)
Orgasteron
(Normethandrolone)
Parabolan (Tren
Hexahydrobenzycarbonat
e)
Primobolan Depot
(Methenolone Enanthate)
Prostanozol
100
20-400
330
110-125
500
90-9
5
88
66-7
1
44-57
n/a
Protabol (Thiomesterone)
61
456
Sanabolicum (Nandrolone
Cyclohexylpropionate)
37
125
Steranabol Ritardo
(Oxabolone Cypionate)
20-60
50-90
Synovex (Testosterone
Propionate & Estradiol)
100
100
Test 400
100
100
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Detectab
le for 3
weeks
200-400
500
n/a
Detectab
le for 5
weeks
100
50
325-58
0
130136
338
THG (Tetrahydrogestrinone)
No
Data
No Data
Trenavar (Trenbolone
prohormone)
No
Data
No Data
Trestolone (MENT/7αmethyl-19-nortestosterone
Acetate)
650
2,300
FAQ
Some answers to common questions.
What is the di erence between Testosterone
Enanthate and Testosterone Cypionate?
Approximately nothing. De nitely nothing that is going to make a difference
in choosing one or the other for our purposes. Read the speci cs below:
• The ester weights are almost identical, with Cypionate being ever soslightly heavier.
Meaning there is ever so-slightly more actual testosterone hormone
(~1%) in Enanthate.
• The terminal half-life's are also almost identical.
Enanthate is 4.5 days.
Cypionate is 5 days.
• For some, they may experience a slight difference in potential Post
Injection Pain (PIP). This is due to Cypionate having a higher melting
point than Enanthate, making Cypionate more prone to being able to
cause PIP. This all depends on how your Testosterone was brewed by
your source/supplier. Read more on Post Injection Pain (PIP): Here.
What are esters?
Please See Our Esters Wiki Page: Here
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Hepatotoxicity
It is a well-known fact that most oral anabolic steroids, as well as a select
few injectable anabolic steroids induce a measure of liver toxicity (properly
referred to as hepatotoxicity) in the body. The range of hepatotoxicity that
these compounds can cause varies a great deal, ranging from very minor
to serious life-threatening damage. The word "liver toxicity" and
"hepatotoxicity" is thrown around a lot in bodybuilding circles and
throughout the anabolic steroid using community, but how many people
actually understand what these terms mean? How many people actually
know what speci cally it is that is "toxic" about the anabolic steroid in the
liver? What is it that actually happens to the liver cells (hepatocytes)? The
majority of people who throw around the words "liver toxic" will not be able
to answer those questions at all. This is where that should change. After
reading through this post, you will understand why certain anabolic steroids
cause hepatotoxicity, what hepatotoxicity actually is, and how it affects the
body, and most importantly: what you can do about it and what liver
protectants to take.
Drug Metabolism
When it comes to drug metabolism, the liver’s primary function is to
metabolize the drug into a form that is suitable for elimination by the
kidneys. The main goals of this metabolism is to reduce fat solubility, make
the drug water soluble, and to decrease its biological activity so that it stops
working. This occurs for not only foreign substances (known as xenobiotics,
which drugs are considered), but also endogenous chemicals. Drug
metabolism in the liver exists in two main phases, phase I and phase II.
• Phase I: Phase I metabolism happens primarily in the smooth
endoplasmic reticulum of hepatocytes. The main purpose of this phase
is to make lipid soluble compounds water soluble. This typically renders
the metabolites of the drug to be inactive, but not always. This is the
phase that we want to focus on with oral steroids, and is where the
C17aa comes into play in protecting the steroid from being degraded by
the liver.
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• Phase II: Phase II metabolism takes place in the cytosol of hepatocytes.
In this phase, the products from phase I will undergo conjugation to
increase their water solubility.
The ef cacy of the enzymes used in drug metabolism are age-dependent.
In newborns and the geriatric, the ability to metabolize drugs is greatly
decreased. Smoking can increase the ef cacy of drug metabolism through
the inhalation of polycyclic aromatic hydrocarbons. This is most noticeably
manifested in the increased metabolic activity of caffeine.
Anabolic Androgenic Steroids
C17-Alpha Alkylation & What It Does
It's common knowledge that oral steroids are known as being liver toxic,
while injectable anabolic steroids are not (at least not to as great of an
extent as orals are). There is a reason for this, and that is: C17-alpha
alkylation (C17aa). Without the C17aa modi cation, very little of the
anabolic steroid when ingested will survive hepatic metabolism (liver
metabolism), and not enough of it will reach the bloodstream to produce
any noticeable effects. It was then discovered at one point, that by
modifying the chemical structure by adding a methyl group (also known as
an alkyl group) to the 17th carbon on the steroid structure (also known as
carbon 17-alpha), it would allow the anabolic steroid to become more
resistant to the hepatic metabolism that would previously render the
majority of the ingested steroid into inactive metabolites. This chemical
bonding of a methyl group onto the 17th carbon is what is known as C17alpha alkylation. It is because of C17-alpha alkylation, that the anabolic
steroid becomes orally active and bioavailable – without it, the anabolic
steroid would not survive liver metabolism. However, the negative
downside in this case is that of increased hepatotoxicity (increased liver
toxicity). C17-alpha alkylation allows an anabolic steroid to become more
resistant to hepatic breakdown, and any compound that is further resistant
to hepatic breakdown will always have greater hepatotoxicity associated
with it for various reasons. But how does this happen?
C17aa effectively alters the chemical structure enough to block the enzyme
17beta-hydroxysteroid dehydrogenase (17beta-HSD) from interacting with
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the hormone in the liver, which would normally metabolize the steroid into
an inactive metabolite. However, the liver is now forced to metabolize the
anabolic steroid through other means. At this point in time, it is unknown as
to how exactly the C17aa modi cation causes hepatotoxicity, but it is
strongly hypothesized that because the liver contains a high concentration
of androgen receptors[1] , the now unaltered and unmetabolized anabolic
steroid (which is now instantly highly active) that is making the rst pass
through the liver will exhibit heavy amounts of androgenic activity in the
liver because its metabolism has been blocked. Because it is being
ingested orally, and therefore makes the rst pass through the liver, the
liver then becomes exposed to massive concentrations of these active
anabolic steroids immediately, rather than through the injection route of
administration where the anabolic steroid does not have to make a rst
pass through the liver (and therefore the liver is not exposed to massive
amounts of active androgens all at once). The fact that studies have
demonstrated that the greater the androgenic strength an oral anabolic
steroid exhibits, the worse the hepatotoxicity is, lends credence to the
theory that androgenic activity is correlated with hepatotoxicity in oral AAS.
[2][3]
Trenbolone
Trenbolone does not possess C17-alpha alkylation, however, it is known to
possess ever so small amounts of hepatotoxicity. This is believed to be
because of the nature of Trenbolone’s chemical structure, which causes
Trenbolone to exhibit a higher resistance to hepatic metabolism and
breakdown even though it is not C17-alpha alkylated. The small amount of
hepatotoxicity is not a large cause for concern at all, as Trenbolone’s
minute amount of liver toxicity does not even reach the amounts of toxicity
exhibited by oral C17-alpha alkylated anabolic steroids. The slight
hepatotoxicity can be a concern for individuals with pre-existing liver
problems (known or unknown) and this should be kept in mind. Every
potential Trenbolone user should always have blood work (see Liver
Function Tests below) done in order to monitor liver enzyme readings
regardless, and a proven liver support supplement (see Liver Protection
below) can be utilized during a Trenbolone cycle for the extra assurance of
proper liver function.
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Drug Induced Hepatotoxicity
Drug induced hepatotoxicity can have many causes. Some medications
cause direct damage to hepatocytes while others block certain metabolic
processes. As an example, acetaminophen itself is not the source of
hepatotoxicity, but rather one of its metabolites. When taken in extreme
quantities, this metabolite accumulates because the enzymes required are
unable to keep up in phase II metabolism and cell damage occurs.
Likewise, mitochondrial damage can increase oxidative stress which can
damage hepatocytes.
These causes are categorized in seven general categories based on the
mechanism of hepatotoxicity. The main categories where AAS and
ancillaries are implicated are:
• Steatosis: Steatosis is the accumulation of triglycerides in the liver.
Liver function tests (LFTs) are unreliable when it comes to the diagnosis
of hepatic steatosis. Often will have an AST/ALT ratio < 1. Imaging and
possible biopsy is required to make an accurate diagnosis. AST and ALT
both upwards of 4 times ULN. Tamoxifen and Raloxifene have been
shown to induce hepatic steatosis.
• Zonal Necrosis: Zonal necrosis is essentially the death of cells in a
speci c zone of the liver. This is the most common manifestation of
hepatotoxicity. This will cause an increase in ALT with normal ALP
levels. This can be caused by C-17-alpha-alkylated (C17aa) steroids.
• Cholestasis: Cholestasis is the impediment of biliary ow from the liver
through the biliary tract. This is the cause of jaundice. The increase in
bilirubin causes a yellowing of the skin and that is occurs with itching.
C17aa steroids may cause hepatotoxic cholestasis. This can be seen on
labs as normal levels of ALT and > 2 times ULN ALP. The mechanism of
this is not well known. Testosterone and 19-nortestosterone compounds
have been implicated in cases of hyperbilirubinemia, but rarely to the
point of jaundice. (More on this below).
• Hyperplasia and Neoplasia: C17aa compounds have been implicated
in cases of hepatic hyperplasia and neoplasia, essentially cancer.
However, non-C17aa steroids have also been noted as a cause of liver
cancer in medical case reports.
• Vascular Lesions: These vascular lesions are known as Peliosis
Hepatis. These lesions are present on endothelial cells of hepatic
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vasculature and is typically asymptomatic. This can eventually lead to
hepatomegaly (enlarged liver) and frequently death if untreated.
Effects of liver damage include jaundice, ankle edema, gynecomastia,
increased bleeding due to decrease in clotting factor synthesis. Most of
these effects come from de ciencies in synthesis of their respective plasma
proteins. For example, damage to hepatocytes that are responsible for
synthesis of SHBG will result in a decrease in SHBG. This will alter the free
estrogen/free androgen ratio, potentially inducing gynecomasta. Likewise, a
decrease in plasma proteins will change the blood colloid osmotic pressure,
causing a change in capillary net ltration pressure leading to edema in the
lower extremities.
Cholestasis
Cholestasis is the most common form of liver damage that is characteristic
of the use/abuse of oral anabolic steroids.[4] As already stated, it is the
condition whereby bile is unable to properly ow throughout the liver and
into the duodenum (the rst section of the small intestine that connects to
the stomach). This can occur as the result of a physical (also known as a
mechanical) blockage, such as gallstones or a tumor formation causing
blockage. The other form of blockage is in the form of a chemical blockage
(also known as metabolic cholestasis), which is cholestasis that is resultant
of a disruption of the hepatic cells' ability to properly manufacture and ow
bile. C17aa anabolic steroids cause metabolic (chemical) cholestasis.
Metabolic cholestasis can also be the result of a hereditary genetic
dysfunction, and there are plenty of other substances, drugs, and
medications that can cause cholestasis as well. In order to understand
cholestasis, it is important to know what bile is and what it does for us.
Bile is a dark green/yellow to brown uid that is manufactured by the cells
of the liver, and consists of 85% water, 10% bile salts, 3% muscuous and
pigments, 1% fats, and 0.7% inorganic salts. The primary function of bile is
to digest fats that are consumed in food, making it a very important
component in the digestion and processing of food. Because it is involved
in the digestion and breakdown of fats, it is very important for the proper
breakdown and absorption of fat-based and fat soluble compounds (such
as many types of vitamins). In addition to this, bile serves to act as an
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excretion vehicle for the transport of metabolites out of the liver, such as
bilirubin which is a metabolic byproduct as a result of the liver cells
recycling red blood cells. Finally, an additional function that bile serves (and
this is very important) is the neutralizing of acidity of the contents of the
stomach (as a result of stomach acid) before it enters the intestines. A
simultaneous role bile plays in that process is also a disinfectant, killing
bacteria that could be in the ingested food.
When the C17aa anabolic steroids inhibit the ow of bile in the liver, bile will
build up in the small bile ducts of the liver forming plugs (known as
canalicular bile plugs). The cells of the liver (hepatocytes) will continue to
attempt to excrete bile as they normally would, but as bile accumulates due
to the plugs, enough pressure will build until the lining cells of the bile ducts
rupture. As a result, bile spills out onto other cells and tissue, resulting in
cell death. Cells will begin to build up with bile as well (more common in
intrahepatic chemical/metabolic cholestasis), and without proper ow of
bile, the cells will die. This build-up of bile is known as a bile pool, and while
not all of the bile acids contained in the bile pool are hepatotoxic, most of
them are, and this is why the bile pool accumulation results in liver cell
death. C17aa anabolic steroids cause intracellular bile retention within the
hepatocytes (bile accumulation inside the liver cells).
Symptoms of Cholestasis:
• Nausea
• Malaise
• Anorexia, loss of appetite
• Vomiting
• Abdominal pain/burning (almost like heartburn/burning sensations due to
the lack of bile being excreted to neutralize the acidity of stomach
content entering the duodenum).
VERY IMPORTANT: what is commonly mistaken for heartburn by many
people while using oral C17aa anabolic steroids is actually varying
stages of cholestasis.
• Pruritus (itching)
• Clay colored dark stool
• Pale stool (strong indication of physical/mechanical cholestasis rather
than metabolic/chemical cholestasis)
• Dark amber colored urine
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• Jaundice (strong indication of physical/mechanical cholestasis, but can
occur with metabolic/chemical intrahepatic cholestasis if it reaches
worsened stages)
Although cholestasis can normally be recovered from if C17aa steroids are
halted early enough, the body might require months before liver function is
properly restored, and this is why it is very important to maintain proper
liver function during the use of C17aa compounds with the supplementation
of a proper liver support compound.
Liver Function Tests
Liver Function Tests can be done to assess hepatic function. These are not
exactly conclusive and require some sort of follow up to assess the degree
of severity. Often this will be some sort of imaging or biopsy. Most of these
biomarkers are assessed in a multiplication of the upper limit of normal
(ULN), which is the top end of the normal range.
Aminotransferases: Aminotransferases are enzymes that are used in the
synthesis of amino acids. There are two aminotransferases that are
checked as part of an LFT.
• Aspartate Transaminase (AST): Reference range: 8 - 40 IU/L. While
AST is found in the liver, this enzyme is also found in great quantities in
cardiac and skeletal muscle. Because of these other sources, AST alone
is not a good indicator of liver damage. Essentially, AST does not require
the entire cell to be damaged for it to enter the plasma, where ALT does.
This is due to its location within the cell. If AST is elevated then there is
a good possibility that the source of the AST is from muscle damage.
This can be caused by myocardial infarction (heart attack),
rhadomyolysis, and even resistance training. This is why slightly
elevated AST levels should not be of concern if you lift frequently.
• Alanine Transaminase (ALT): Reference range: ≤ 52 IU/L. Much like
AST, ALT is an enzyme used to catalyze the synthesis of amino acids.
Unlike AST, ALT is found predominantly in the liver and requires
signi cant damage to hepatocytes for it to be released in to the plasma.
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AST to Platelet Ratio Index (APRI): This typically won’t be included in lab
tests, but it is easy to gure out. An online calculator can be found here.
APRI has been shown to be a predictor of liver cirrhosis.
Alkaline Phosphatase (ALP): Reference rage: 30 - 120 IU/L. ALP is an
enzyme that is located within hepatic biliary ducts. Elevations in plasma
concentrations of this enzyme are indicative of either cholestasis or biliary
obstruction. In these pathologies, ALT and AST may remain unaffected.
Total Bilirubin: Reference range: 0.1-1.0 mg/dL. Bilirubin is a byproduct of
hemoglobin catabolism. The heme group of hemoglobin is broken down
into biliverdin, then bilirubin, which is transported to the liver for the
production of bile salts along with urobilin (the pigment that makes urine
yellow) and stercobilin (the pigment that makes feces brown). High hepatic
sources of bilirubin are indicative of cirrhosis or hepatitis.
5'-nucleotidase (5'NTD): Another biomarker used int he diagnosis of
cholestasis.
Liver Protection
TUDCA / UDCA
For Additional Information & Studies, Be Sure To Visit The Examine
Page
Tauroursodeoxycholic acid (TUDCA) and Ursodeoxycholic acid (UDCA) are
bile acids themselves that are non-toxic to the liver and in fact have been
proven to exhibit the exact opposite - they assist in bile ow through
various different pathways which will be covered shortly. TUDCA is simply
the taurine conjugate of UDCA (UDCA with a taurine amino acid bound to
it), which has been claimed to exhibit greater oral bioavailability, but both
variants have been proven to work very effectively. TUDCA and UDCA
used to be extracted from the liver of bears, but synthetic methods have
since been developed in order to manufacture these compounds, as well
as the ability to derive them from other sources.
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By far the most effective liver support compound available, TUDCA and
UDCA are compounds that serve to speed up the metabolic transition of
toxic bile acids to less toxic bile acids, and they also serve to increase the
manufacture of non-toxic bile acids from cholesterol.[5] The result is a
decrease in the toxicity of the bile pool. Remember when I mentioned
above that liver toxicity from oral anabolic steroids (in the really bad stages)
results in bile building up in the hepatocytes (liver cells) until they rupture
and bile spills out onto other cells killing them? Well, the bile being spilled
out consists of mostly toxic bile salts. TUDCA and UDCA are bene cial
non-toxic bile salts that will essentially balance out the toxicity of the bile
pool and serve to neutralize the toxicity making it less toxic to the
surrounding resident liver cells. TUDCA and UDCA have also shown to
increase amounts of the bile salt export pump (a transporter protein) in the
liver cells, thus increasing the ow of bile as a result.[6] What this means is
that they will facilitate the ow of bile in the liver so that the bile pool will not
remain stagnant damage the surrounding liver cells. A good analogy to
explain this is using the 'hot potato' analogy where a group of people in a
circle are throwing a hot potato around from person to person fairly quickly.
As long as the hot potato is passed around at a constant pace, no single
person's hand will get burned, but if the hot potato is to remain in one
person's hand for too long, they will end up doing damage to their hands by
being burned (which is much like a stagnant bile pool in the liver damaging
the surrounding cells). These compounds have also demonstrated to serve
as antiapoptotics in liver cells, which means they effectively block the
transcription factor known as AP-1, which is activated during cholestasis
due to various toxic bile salts that will activate death receptors on liver cells.
[7]
TUDCA and UDCA are by far the best quintessential treatments for both
the prevention of cholestasis, as well as the recovery from it. They are,
quite literally, the compounds speci c to the treatment and mitigation of oral
C17-alpha alkylated anabolic steroid liver toxicity - this cannot be said of
any other liver support supplement/compound. In addition to treating
cholestasis very effectively, it has demonstrated in studies to also reduce
the risk of hepatitis B, where they had signi cantly decreased the risk of
having abnormal serum alanine aminotransferase activity at the end of
treatment compared to the beginning.[8] Other studies have also shown that
UDCA and TUDCA are bene cial in the treatment necroin ammatory liver
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disease, such as (and especially for) hepatitis C-related chronic hepatitis in
which bile duct damage and some degree of cholestasis are frequently
seen at histology, and the study had observed that TUDCA had signi cantly
improved the biochemical expression of chronic hepatitis.[9] In general,
TUDCA seems to prevent hepatic cell death.[10]
Dosing of TUDCA and UDCA: 500-1000mg daily for the maintenance of
healthy liver function during the use of a C17aa oral during a cycle.
1,000mg or higher daily for the purpose of repairing the liver following
heavy hepatotoxicity and hepatocyte damage from cholestasis (and/or for
individuals with serious liver disorders).
IMPORTANT: Do not exceed 8 weeks of TUDCA/UDCA use, as it can
increase negative cholesterol values and decrease HDL. It is
recommended to use these bile salts only during a cycle of oral C17aa
anabolic steroids, or for the purpose of liver repair following periods of
signi cant hepatotoxicity from the use of these compounds. Other
compounds should be sought after for general year-round liver support.
According to this study (taken from Examine), TUDCA has been shown
to decrease HDL levels when taken for extended periods of time. In normal
people, this really isn't a big deal. In people who are constantly using
steroids, like blasting and cruising (B&C), it can become counter-intuitive to
run TUDCA for no reason due to decreased HDL levels. For example, on a
cruise one wants to let their body recover, and ideally see good bloodwork
before blasting again. One key reading on the bloodwork is the HDL, as
HDL is one marker that almost always drops signi cantly while taking
exogenous steroids in large dosages.
Also, according to the FDA as listed in UDCA's medication safety pro le
(two sources below), UDCA should not be taken without direct indication to
do so, i.e. gallstones or primary biliary cirrhosis. The pros of taking TUDCA
and UDCA while not on oral steroids or having one of the aforementioned
indications do not outweigh the cons. TUDCA should not be used for year
round general liver support, as there are other options (discussed below)
which do not have these negative drawbacks, thus making the choice clear.
• Product Information: URSO 250(R) oral tablets, ursodiol oral
tablets. Aptalis Pharma US, Inc. (per FDA), Bridgewater, NJ, 2013.
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• Product Information: URSO Forte(R) oral tablets, ursodiol oral
tablets. Aptalis Pharma US, Inc. (per FDA), Bridgewater, NJ, 2013.
NAC (N-acetylcysteine)
For Additional Information & Studies, Be Sure To Visit The Examine
Page
NAC (N-acetylcysteine) is an excellent liver protectant/support compound
that has demonstrated effectiveness in mitigating hepatotoxicity[11] as well
as successfully treating acetaminophen (Tylenol) induced hepatotoxicity,[12]
which is an added bene t for NAC that TUDCA does not do. NAC has also
demonstrated some pretty good effectiveness at mitigating and preventing
cholestasis as evidenced by studies. One particular study administered
300mg/kg of NAC orally to rats for 28 days, and not only did NAC
administration reduce elevations of liver enzyme values that would
otherwise be high without NAC administration, it also seemed to improve
renal (kidney) function as well![13] That same study indicated, though, that
NAC's activity in ameliorating cholestasis is not through the same pathway
as TUDCA. NAC's ability to prevent or cure cholestasis stems from its
antioxidant and immunomodulatory properties. Acetylcysteine serves to
increase the glutathione reserves in the body and, together with
glutathione, they both directly bind to toxic metabolites. This serves to
protect hepatocytes (liver cells) from succumbing to toxicity from Tylenol or
cholestasis. TUDCA instead operates through the direct action of
essentially 'balancing' the content of bile salts (TUDCA is itself a bile salt),
and while it does assist in mitigating cholestasis, it does not do anything for
Tylenol-related toxicity. Another study also investigated NAC's ability to help
alleviate cholestasis, which focused a little more on the observation of the
renal (kidney) related effects, and found that in addition to improved liver
enzyme values, NAC had the ability to vastly improve markers of kidney
function and was actually able to even double the rate of sodium excretion.
[14] This would also strongly indicate that NAC might prove very useful for
the elimination of sodium and its related water retention in the body, which
is something that might be of particular interest for anabolic steroid using
individuals who might be having problems with water retention during a
cycle.
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The problem, however, with NAC is that it has demonstrated very poor oral
bioavailability,[15] and this is the reason as to why high oral doses of NAC
were utilized in studies for the treatment of Tylenol poisoning compared to
when the subjects were administered NAC through the IV (intravenous)
route of administration. Aside from NAC's ability as a nephroprotective
(kidney protecting) and hepatoprotective (liver protecting) agent, it is well
documented to serve a myriad of other bene ts to the body. Although these
bene ts of NAC do not pertain to the main topic at hand (liver support
during anabolic steroid use), it is very informative and helpful to know and
understand that NAC has potential applications that are extremely far
reaching beyond simply liver and kidney function.
Dosing of NAC: As previously mentioned, there are issues in regards to
poor oral bioavailability with NAC. IV and inhalation formats of NAC do
exist, but are generally prescription-only, depending on which country.
However, the oral format of NAC is generally widely available for purchase
almost anywhere. Be sure to look for a NAC product that has chelated it to
an element or compound to provide greater bioavailability. With that being
said, a proper dose for the purpose of maintenance of liver health during a
cycle of C17-alpha alkylated anabolic steroids would be in the range of
1,000mg - 2,000mg of NAC per day. NAC can be used year-round as a
general liver support, and should be run at 1,000mg per day or less when
not utilizing C17-alpha alkylated oral anabolic steroids.
IMPORTANT: Studies have demonstrated that high doses of NAC can
cause lung and heart damage in mice[16] due to the fact that NAC is
metabolized in the body to S-nitroso-N-acetylcysteine (SNOAC). In large
enough amounts, SNOAC leads to signi cantly increased blood pressure in
the lungs and the right ventricle of the heart. This is why it is advised to not
exceed the standard dose of 1,000mg - 2,000mg per day while on C17aa
oral anabolic steroids. Other than this warning, it should be mentioned that
the implications of long-term NAC use (at any dose range) are currently
unknown and have not been investigated. This is not to say that long
term use is a bad thing, but that we simply do not know if the outcome is
indeed good or bad.
What About Other Liver Protectants?
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Choline & Inositol
For Additional Information & Studies On Choline, Be Sure To Visit The
Examine Page
Choline can be used as a daily supplement for general health and/or a liver
protector while on oral steroid course. Choline cannot replace TUDCA and
should be used in addition to TUDCA while taking oral steroids. Choline
should be used in conjunction with Inositol and many products that you will
nd will contain both anyway.
De ciency in dietary choline can lead to triglyceride accumulation (hepatic
fatty acids) and impair TG release from the liver due to less
phosphatidylcholine being made.
For general liver health take 250-500 mg of choline once per day
For liver protection while on oral steroids take 1-2 g in two even doses per
day (ie 1000mg or 1 g is 500 mg twice a day, 12 hours apart or so)
For Additional Information & Studies On Inositol, Be Sure To Visit The
Examine Page
Inositol may also be used as both a daily supplement for general health
and/or as adjunct liver protection to TUDCA while on oral steroids. Again,
taking inositol and choline together is important.
Inositol the word itself refers to a group of 9 molecules that all have similar
structures, termed stereoisomers. The key isomer that we are focusing on
is MYO-INOSITOL and this is the isomer that we want to supplement and
take. Pretty much all OTC supplements with inositol will be this isomer, but
always double check to be sure you are getting the right one.
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TUDCA and UDCA should be considered rst above all else when using
hepatotoxic anabolic steroids, as they treat the mechanisms speci c to
cholestasis. NAC is very bene cial as well. The other options, are just
secondary aids as they are not nearly as bene cial for C17aa.
For general liver health and oral steroid protection, inositol doses will
typically be in the 2g-4g range, and it is advised to take these doses in two
split even doses per day, roughly 12 hours apart.
Milk Thistle
For Additional Information & Studies, Be Sure To Visit The Examine
Page
Milk thistle, which contains silymarin and silybin are known as being
powerful antioxidants in the liver in particular. Many studies have been
conducted on the ef ciency and have demonstrated them to exhibit a
plethora of bene cial properties in liver tissue. However, milk thistle is not
very effective for treating cholestasis in particular. As a general liver health
support, it is not too bad. However, almost all of the studies performed on
milk thistle’s effectiveness had administered the test subjects the
compound via injection, which would provide near 100% bioavailability. Milk
thistle consumed orally is a different story. Milk thistle can serve as a
bene cial addition to TUDCA and UDCA, but should not be substituted as a
rst-line treatment for cholestasis. TUDCA should be reserved for the rstline treatment of cholestasis and should be the primary liver protectant
while on a cycle of C17-alpha alkylated oral anabolic steroids.
Liv.52 (LiverCare)
Liv.52 is an herbal medicine used widely in Europe and Asia to support
metabolic and liver health. While in some countries this product is regarded
as a drug, it contains all natural ingredients including capparis spinosa,
terminalia arjuna, cichorium intybus, achillea millefolium, solanum nigrum,
tamarix gallica, and cassia occidentalis. There have been medical studies
have been conducted on Liv.52 in recent years, many of which involve its
ability to protect the liver from damage by alcohol or other toxins. Note that
while these studies lend support for the use of a natural remedy like Liv.52
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Inositol shows promising effects in restoring insulin sensitivity and
decreasing LDL and acne, and has many other slight positive bene cial
effects which can be found under the "Human Effect Matrix" category on
the examine.com page linked just above.
during hepatotoxic steroid administration, they do not provide complete
assurance that this remedy can prevent liver damage. Also some of the
studies may have some bias, so be sure to use caution when reviewing
them.
A Final Word
• TUDCA or UDCA should be every anabolic steroid user's rst
choice for on-cycle liver protection during the use of oral C17alpha alkylated anabolic steroids.
• Following this, NAC is an excellent choice to go along TUDCA / UDCA,
and also is a great choice for year-round general liver protectant.
• Another great choice for year-round general liver protectant is Choline &
Inositol, but it shouldn't be your choice for liver protection during use of
oral C17-alpha alkylated anabolic steroids.
• Milk Thistle & Liv.52 (LiverCare) can provide some bene ts, but they in
NO WAY should be your only liver protection during use of oral C17alpha alkylated anabolic steroids.
References
The majority of this wiki page was taken and expanded from this thread by
/u/canal_of_schlemm, as well as a thread by DanC
• Cellular distribution of androgen receptors in the liver. Hinchliffe
SA, Woods S, Gray S, Burt AD. J Clin Pathol. 1996
May;49(5):418-20.
• Liver toxicity of a new anabolic agent: methyltrienolone (17alpha-methyl-4,9,11-estratriene-17 beta-ol-3-one). Kruskemper,
Noell. steroids. 1966 Jul;8(1):13-24.
• T. Feyel-Cabanes, Compt. Rend. Soc. Biol. 157, 1428 (1963).
• anabolic-androgenic steroids and liver injury. M Sanchez-Osorio
et al. Liver International ISSN 1478-3223 p. 278-82.
• Ursodeoxycholic acid and bile-acid mimetics as therapeutic
agents for cholestatic liver diseases: an overview of their
mechanisms of action. Poupon R. Clin Res Hepatol
Gastroenterol. 2012 Sep;36 Suppl 1:S3-12. doi: 10.1016/
S2210-7401(12)70015-3.
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• Tauroursodeoxycholic acid inserts the bile salt export pump into
canalicular membranes of cholestatic rat liver. Dombrowski F,
Stieger B, Beuers U. Lab Invest. 2006 Feb;86(2):166-74.
• Tauroursodeoxycholic acid reduces bile acid-induced apoptosis
by modulation of AP-1. Pusl T, Vennegeerts T, Wimmer R, Denk
GU, Beuers U, Rust C. Biochem Biophys Res Commun. 2008
Feb 29;367(1):208-12. doi: 10.1016/j.bbrc.2007.12.122. Epub
2007 Dec 27.
• Bile acids for viral hepatitis. Chen W, Liu J, Gluud C. Cochrane
Database Syst Rev. 2007 Oct 17;(4):CD003181.
• Tauroursodeoxycholic acid for the treatment of HCV-related
chronic hepatitis: a multicenter placebo-controlled study.
Crosignani A, Budillon G, Cimino L, Del Vecchio Blanco C,
Loguercio C, Ideo G, Raimondo G, Stabilini R, Podda M.
Hepatogastroenterology. 1998 Sep-Oct;45(23):1624-9.
• Effect of tauroursodeoxycholic acid on bile acid-induced
apoptosis in primary human hepatocytes. Benz, Angermüller,
Otto, Sauer, Stremmel, Stiehl. European Journal of Clinical
Investigation Volume 30, Issue 3, pages 203–209, March 2000.
• The protective effects of n-acetylcysteine against acute
hepatotoxicity. Sahin S, Alatas O. Indian J Gastroenterol. 2013
Mar 10.
• The biochemistry of acetaminophen hepatotoxicity and rescue:
a mathematical model. Ben-Shachar R, Chen Y, Luo S, Hartman
C, Reed M, Nijhout HF. Theor Biol Med Model. 2012 Dec
19;9:55. doi: 10.1186/1742-4682-9-55.
• Anti brotic and antioxidant effects of N-acetylcysteine in an
experimental cholestatic model. Galicia-Moreno M, Favari L,
Muriel P. Eur J Gastroenterol Hepatol. 2012 Feb;24(2):179-85.
doi: 10.1097/MEG.0b013e32834f3123.
• Acute cholestasis-induced renal failure: effects of antioxidants
and ligands for the thromboxane A2 receptor. Holt S, Marley R,
Fernando B, Harry D, Anand R, Goodier D, Moore K. Kidney Int.
1999 Jan;55(1):271-7.
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• Pharmacokinetics of N-acetylcysteine in man. Borgström, L.;
Kågedal, B.; Paulsen, O. (1986). European Journal of Clinical
Pharmacology 31 (2): 217–222. doi:10.1007/BF00606662.
PMID 3803419.
• S-Nitrosothiols signal hypoxia-mimetic vascular pathology.
Palmer, Lisa A.; Doctor, Allan; Chhabra, Preeti; Sheram, Mary
Lynn; Laubach, Victor E.; Karlinsey, Molly Z.; Forbes, Michael
S.; MacDonald, Timothy; Gaston, Benjamin (2007). Journal of
Clinical Investigation 117 (9): 2592–601. doi:10.1172/JCI29444.
PMC 1952618. PMID 17786245.
• Drug Induced Cholestasis
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Ancillaries / Related
Compounds in this section are sometimes used to support AAS use in
general. They cover a wide range of uses, and, as with most AAAS use,
these are typically used for purposes which are off label. Therefore,
information and actual studies are hard to obtain.
Compound
Type
Notes
Accutane
Albuteral
Arimidex
(Anastrozole)
Acne prevention. Do not
give blood if using.
β2-adrenergic receptor
agonist
AI, Reversible, nonsteroidal
Standard AI, FAQ.
Aromasin
(Exemestane)
AI, Irreversible, steroidal
Take with fatty meal, not
water soluble.
Bazedoxifene
SERM
Need usage info
Dopamine Receptor
Agonists
Sympathomimetic Amine
Anti-prolactin
Cabergoline
Clenbuterol
Cialis
Clomid
SERM
Cyclofenil
SERM
Cytadren
(Aminoglutet
himide)
Dantrolene
Dimethyl
sulfoxide
(DMSO)
DNP (2,4Dinitrophenol
)
Ephedrine
fl
Cutter, Detectable for 4
days, seperate doses by
3-4 hours
Helps blood ow
Used for PCT
AI, Irreversible, steroidal
Has cortisol reducing
effect
Muscle Relaxant
May be able to help for
DNP overdose
Possibly dangerous,
controversial joint pain
relief.
Cutter (See Datrolene)
Dinitrophenols
Sympathomimetic Amine
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prostate
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ECA or EC
Stack
Ephedrine / Caf ne /
Asprin (Optional)
Cutter
Fulvestrant
AI, selective estrogen
receptor down-regulator
(SERD)
Synthetic LH
No information on usage
during cycles.
HCG
Humog (hMG)
Letrozole
Liv 52
Ostarine
(Enobosarm)
Pramipexole
LH and FSH
AI, Reversible, nonsteroidal
Liver Protection
SARM
Dopamine Receptor
Agonists
SERM
Anti-prolactin
Raloxifene
SERM
Melatonin
Neurohormone
Can treat some gyno from
puberty
Sleep regulation
SERM
Used for PCT, FAQ.
SINGULAIR
(montelukast
sodium)
Leukast
Can prevent respiratory
weakness from Tren
Testolactone
AI, Reversible, nonsteroidal
Thyroid Hormone
Old, weak AI
Precursor to T3
SERM
Used in PCT
Thyroid Hormone
Cutter
GnRH Agonist
One shot PCT, with risk of
infertility
Lasofoxifene
Nolvadex
(Tamoxifen)
T4 (Thyroxine)
Toremifene
T3
Triptorelin
TUDCA
Liver Protection
UDCA
(Ursodiol)
Viagara
Liver Protection
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Powerful AI
Need Info
Helps blood ow
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Aromatase Inhibitor (AI), Reversible, Non-steroidal -- These drugs
inhibit aromatization by reversible competition for the aromatase enzyme.
By using up the aromatase molecules in the system, it is unavailable to
participate in the aromatization of Testosterone which greatly slows down
the process.
Aromatase Inhibitor (AI), Irreversable, Steroidal -- These drugs form a
permanent and deactivating bond with the aromatase enzyme. This
prohibits the aromatase molecule from participating in the aromatization of
testosterone.
Dinitrophenols -- A group of non-naturally occurring chemical compounds
which are nitro derivatives of phenol.
Dopamine Receptor Agonists -- A chemical that binds to the dopamine
receptor and triggers a response. Used to stop the production of prolactin.
GnRH Agonist (Gonadotropin-releasing Hormone Agonists) -- A
synthetic peptide modeled after the hypothalamic neurohormone GnRH
that interacts with the gonadotropin-releasing hormone receptor to elicit its
biologic response, the release of the pituitary hormones FSH and LH.
Leukotriene Receptor Antagonist (Leukast) -- Block the actions of
cysteinyl leukotrienes at the CysLT1 receptor on target cells such as
bronchial smooth muscle.
SARMs (Selective Androgen Receptor Modulators) -- SARMs are
intended to have the same kind of effects as androgenic drugs like anabolic
steroids but be much more selective in their action, allowing them to be
used for many more clinical indications than the relatively limited legitimate
uses that anabolic steroids are currently approved for.
SERMs (Selective Estrogen Receptor Modulators) -- This class of drugs
are estrogen antagonists and do not lower the amount of estrogen that is
in the system; they act by binding to the estrogen receptor without
generating a biological response. Different SERMs can block the estrogen
receptors in different areas of the body. The ones listed block them in
breast tissue.
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Sympathomimetic Amine -- Sympathomimetic drugs mimic the effects of
transmitter substances of the sympathetic nervous system. Amines are
organic compounds and functional groups that contain a basic nitrogen
atom with a lone pair. Amines are derivatives of ammonia, wherein one or
more hydrogen atoms have been replaced by a substituent such as an
alkyl or aryl group.
FAQ
Q: Can Nolvadex (Tamoxifene) and Arimidex
(Anastrozole) be used together?
There is a lot of confusing information on wether or not these two
compounds can be ran together. Looking at drug interaction charts,
Medscape has the following:
tamoxifen + anastrozole
tamoxifen decreases levels of anastrozole by unspeci ed interaction
mechanism. High likelihood serious or life-threatening interaction.
Contraindicated unless bene ts outweigh risks and no alternatives
available. Never use combination. Anastrozole and tamoxifen should not
be administered together.
This information has been contradited by a few studies.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2362190/
In conclusion, the results of this study con rm that anastrozole does not
affect the pharmacokinetics of tamoxifen when the two drugs are given
in combination to post-menopausal women with early breast cancer. In
addition, the oestradiol suppressant effects of anastrozole appear
unaffected by tamoxifen.
http://publications.icr.ac.uk/629/
As a result of (a) the lack of effect of anastrozole on tamoxifen and DMT
levels and (b) the observed fall in blood anastrozole levels having no
signi cant effect on oestradiol suppression by anastrozole, we conclude
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that the observed reduction in anastrozole levels by tamoxifen is unlikely
to be of clinical signi cance when anastrozole and tamoxifen are
administered together.
The actual ATAC trial that this information comes from. Pharmacokinetic
details can be found here
http://www.nature.com/bjc/journal/v85/n3/pdf/6691925a.pdf
"...the observed fall in blood anastrozole levels having no signi cant effect
on oestradiol suppression by anastrozole, we conclude that the observed
reduction in anastrozole levels by tamoxifen is unlikely to be of clinical
signi cance when anastrozole and tamoxifen are administered together."*
A: Taking arimidex with tamoxifen decreases the serum concentration of
anastrozole by 27%, but has no effect on the pharmacodynamics of
either
Q: Does Aromasin need to be taken with fat?
A: It works better when taken with a high fatty meal, yes.
http://www.rxlist.com/aromasin-drug.htm
Exemestane is freely soluble in N, N-dimethylformamide, soluble in
methanol, and practically insoluble in water
http://www.rxlist.com/aromasin-drug/indications-dosage.htm
the recommended dose of AROMASIN is 50 mg once daily after a meal.
http://www.drugs.com/monograph/aromasin.html
High-fat meal increases plasma exemestane concentrations by
approximately 40%.
http://labeling.p zer.com/showlabeling.aspx?id=523
Absorption: Following oral administration of radiolabeled exemestane, at
least 42% of radioactivity was absorbed from the gastrointestinal tract.
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Exemestane plasma levels increased by approximately 40% after a
high-fat breakfast.
http://www.drugs.com/monograph/aromasin.html
Dosages >25 mg daily not shown to provide substantially greater
suppression of plasma estrogens but may increase adverse effects
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Esters
A Primer On Esters And How They Work
One of the most misunderstood subjects in the world of steroids is the
ester--the mechanism by which injectable esteri ed steroids like
testosterone cypionate, testosterone enanthate, and Sustanon work. If you
take a quick look around the Internet you will probably nd countless
articles that consider one form of a steroid far more effective than another.
Arguments over the superiority of cypionate to enanthate, or Sustanon to
all other testosterones are of course very common. Such arguments are in
all practicality, baseless. In this report we'll take an authoritative look at the
ester and what speci cally it does to a steroid.
I'm sure that if you have taken an interest in anabolic steroids you have
noticed the similarities on the labeling of many drugs. Let's look at
testosterone for example. One can nd compounds like testosterone
cypionate, enanthate, propionate, heptylate; caproate, phenylpropionate,
isocaproate, decanoate, acetate, the list goes on and on. In all such cases
the parent hormone is testosterone, which had been modi ed by adding an
ester (enanthate, propionate etc.) to its structure. The following question
arises: What is the difference between the various esteri ed versions of
testosterone in regards to their use in bodybuilding?
An ester is a chain composed primarily of carbon and hydrogen atoms.
This chain is typically attached to the parent steroid hormone at the 17th
carbon position (beta orientation), although some compounds do carry
esters at position 3 (for the purposes of this article it is not crucial to
understand the exact position of the ester). Esteri cation of an injectable
anabolic/androgenic steroid basically accomplishes one thing, it slows the
release of the parent steroid from the site of injection. This happens
because the ester will notably lower the water solubility of the steroid, and
increase its lipid (fat) solubility. This will cause the drug to form a deposit in
the muscle tissue, from which it will slowly enter into circulation as it is
picked up in small quantities by the blood. Generally, the longer the ester
chain, the lower the water solubility of the compound, and the longer it will
take to for the full dosage to reach general circulation.
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Slowing the release of the parent steroid is a great bene t in steroid
medicine, as free testosterone (or other steroid hormones) previously
would remain active in the body for a very short period of time (typically
hours). This would necessitate an unpleasant daily injection schedule if one
wished to maintain a continuous elevation of testosterone (the goal of
testosterone replacement therapy). By adding an ester, the patient can visit
the doctor as infrequently as once per month for his injection, instead of
having to constantly re-administer the drug to achieve a therapeutic effect.
Clearly without the use of an ester, therapy with an injectable anabolic/
androgen would be much more dif cult.
Esteri cation temporarily deactivates the steroid molecule. With a chain
blocking the 17th beta position, binding to the androgen receptor is not
possible (it can exert no activity in the body). In order for the compound to
become active the ester must therefore rst be removed. This automatically
occurs once the compound has ltered into blood circulation, where
esterase enzymes quickly cleave off (hydrolyze) the ester chain. This will
restore the necessary hydroxyl (OH) group at the 17th beta position,
enabling the drug to attach to the appropriate receptor. Now and only now
will the steroid be able to have an effect on skeletal muscle tissue. You can
start to see why considering testosterone cypionate much more potent than
enanthate makes little sense, as your muscles are seeing only free
testosterone no matter what ester was used to deploy it.
Actions Of Di erent Esters
There are many different esters that are used with anabolic/androgenic
steroids, but again, they all do basically the same thing. Esters vary only in
their ability to reduce a steroid's water solubility. An ester like propionate for
example will slow the release of a steroid for a few days, while the duration
will be weeks with a decanoate ester. Esters have no effect on the
tendency for the parent steroid to convert to estrogen or DHT
(dihydrotestosterone: a more potent metabolite) nor will it effect the overall
muscle-building potency of the compound. Any differences in results and
side effects that may be noted by bodybuilders who have used various
esteri ed versions of the same base steroid are just issues of timing.
Testosterone enanthate causes estrogen related problems more readily
than Sustanon, simply because with enanthate testosterone levels will peak
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and trough much sooner (1-2 week release duration as opposed to 3 or 4).
Likewise testosterone suspension is the worst in regards to gyno and water
bloat because blood hormone levels peak so quickly with this drug. Instead
of waiting weeks for testosterone levels to rise to their highest point, here
we are at most looking at a couple of days. Given an equal blood level of
testosterone, there would be no difference in the rate of aromatization or
DHT conversion between different esters. There is simply no mechanism
for this to be possible.
There is however one way that we can say an ester does technically effect
potency; it is calculated in the steroid weight. The heavier the ester chain,
the greater is its percentage of the total weight. In the case of testosterone
enanthate for example, 250mg of esteri ed steroid (testosterone
enanthate) is equal to only 175mg of actual testosterone. 75mg out of each
250mg injection is the weight of the ester. If we wanted to be really picky,
we could consider enanthate slightly MORE potent than cypionate (I know
this goes against popular thinking) as its ester chain contains one less
carbon atom (therefore taking up a slightly smaller percentage of total
weight). Propionate would of course come out on top of the three, releasing
a measurable (but not signi cant) amount more testosterone per injection
than cypionate or enanthate. [See
Esters Active Half-Life Table
Different esters exist for various compounds. Different esters give
compounds different clearance times in the blood. All over the internet, you
will nd different (unreferenced) information on the half-life of compounds.
A lot of the confusion comes from a lack of understanding on a compound's
half-life versus it's biological or terminal half-life. For our purposes, we
really only care about the terminal half-life, de ned as:
The biological half-life or elimination half-life of a substance is the time it
takes for a substance (for example a metabolite, drug, signaling molecule,
radioactive nuclide, or other substance) to lose half of its pharmacologic,
physiologic, or radiologic activity, as per the MeSH de nition.
Reference study.
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Ester
Half-life
Terminal Half-life
Suspension
within 1 hour
Acetate
3 days
1 day
Propionate
2 days
0.8 days
Phenylpropionate
4.5 days
1.5 days
Butyrate
2-3 days
Valerate
3 days
Hexanoate
3 days
Caproate
4-5 days
Isocaproate
9 days
Heptanoate
5-6 days
Enanthate
10.5 days
4.5 days
Cypionate
6-7 days
5 days
Octanoate
6-7 days
Nonanoate
7 days
Decanoate
15 days
7.5 days
Undecylenate
8-9 days
14 days
Undecanoate
16.5 days
20.9 days
4 days
IMPORTANT NOTE: These half-lives are approximations, and may vary
slightly depending on injection site, carrier oil, and other factors. There isn't
any pharmacokinetics studies done on the majority of AAS. Most of the
above is the theoretical half-lives when we are not presented with real
data.
Esters And The Active Dose
It is important for every person to understand that the ester which is
attached to any injectable anabolic steroid possesses a certain percentage
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amount of the total molecular weight of the molecule. Therefore, for
example, 100mg of Testosterone Enanthate is not 100mg of pure
Testosterone. The reality is that you are receiving less Testosterone than
most of you think, and once the ester has been removed through the
esterase enzyme, the amount of pure un-esteri ed Testosterone left over is
very different depending on the ester in question that was previously
attached to the hormone.
Long chain esters, such as Cypionate, Decanoate, Enanthate, etc. possess
a much heavier molecular weight than short chain esters. Consequently, on
a mg for mg basis, you are receiving far extra mg of steroid in a short
estered compound as opposed to a large estered compound. As an
example, there exists a larger amount of mg of Testosterone in 100mg of
Testosterone Propionate than 100mg of Testosterone Enanthate. This is
due to the shorter, and therefore lighter weight of the Propionate ester in
comparison to the larger and therefore much heavier Enanthate ester.
Many individuals just do not realize this, and should always consider this
factor as one of the factors involved in the decision making process
concerning which ester variant of any given compound to use during a
cycle.
Listed below is the percentages of the actual hormones for each
ester:
Testosterone Ester
% Of The Actual Hormone
Acetate
87%
Propionate
80%
Phenylpropionate
66-67%
Isocaproate
72%
Enanthate
70%
Cypionate
69%
Decanoate
62%
Undecylenate
61%
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Undecanoate
61%
Milligrams below are the estimated amount of active hormone per 100 mg
of compound.
Compound Ester
Pure Hormone
Boldenone (EQ) base
100 mg
Boldenone (EQ) acetate
83 mg
Boldenone (EQ) Propionate
80 mg
Boldenone (EQ) Cypionate
69 mg
Boldenone (EQ) Undecylenate
61 mg
Clostebol Base
100 mg
Clostebol Acetate
84 mg
Clostebol Enanthate
72 mg
Drostanolone (Masteron)
Base
100 mg
Drostanolone (Masteron)
Propionate
80 mg
Drostanolone (Masteron)
Enanthate
71 mg
Methenolone (Primobolan)
Base
100 mg
Methenolone (Primobolan)
Acetate
82 mg
Methenolone (Primobolan)
Enanthate
71 mg
Nandrolone Base
100 mg
Nandrolone Cypionate
69 mg
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Nandrolone (NPP)
Phenylpropionate
63 mg
Nandrolone (Deca) Decanoate
62 mg
Nandrolone Undecylenate
60 mg
Nandrolone Laurate
56 mg
Stenbolone Base
100 mg
Stenbolone Acetate
84 mg
Testosterone Base
100 mg
Testosterone Acetate
83 mg
Testosterone Propionate
80 mg
Testosterone Isocaproate
72 mg
Testosterone Enanthate
70 mg
Testosterone Cypionate
69 mg
Testosterone Phenylpropionate
67 mg
Testosterone Decanoate
62 mg
Testosterone Undecanoate
61 mg
Trenbolone Base
100 mg
Trenbolone Acetate
83 mg
Trenbolone Enanthate
68 mg
Trenbolone Hexahydrobenzyl
Carbonate
65 mg
Trenbolone
Cyclohexylmethylcarbonate
65 mg
Sustanon: The "King" Of Testosterone Blends
The four different testosterone esters in this product certainly look
appealing to the consumer, there is no denying that. But for the athlete I
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think it is all just a matter of marketing (Hell, why buy one ester when you
can get four?). In clinical situations I can see some strong uses for it. If you
were undergoing testosterone replacement therapy for example, you would
probably nd Sustanon a much more comfortable option than testosterone
enanthate. You would need to visit the doctor less frequently for an
injection, and blood levels should be more steadily maintained between
treatments. But for the bodybuilder who is injecting 4 ampules of Sustanon
per week, there is no advantage over other testosterone products. In fact,
the high price tag for Sustanon usually makes it a very poor buy in the face
of cheaper testosterone enanthate/cypionate. Bodybuilders should
probably stop looking at the four ester issue, and stick with totals (Sustanon
is just a 250mg testosterone ampule). Were enanthate to be available for
say $10 per amp of 250mg, and Sustanon priced nearly double that, buying
the Sustanon would be like throwing money away. If you could get nearly
double the milligram amount for the same price with enanthate, this is the
better product to go with hands down. Leave the high priced stuff for the
guys who don't know any better.
Ester Pro les
Acetate ( C2 H4 O2 )
Also referred to as Acetic Acid; Ethylic acid; Vinegar acid; vinegar;
Methanecarboxylic acid. Acetate esters delay the release of a steroid for
only a couple of days. Contrary to what you may have read, acetate esters
do not increase the tendency for fat removal. Again, there is no known
mechanism for it to do so. This ester is used on oral primobolan tablets
(metenolone acetate), Finaplix (trenbolone acetate) implant pellets, and
occasionally testosterone.
Propionate ( C3 H6 O2 )
Also referred to as Carboxyethane; hydroacrylic acid; Methylacetic acid;
Ethylformic acid; Ethanecarboxylic acid; metacetonic acid; pseudoacetic
acid; Propionic Acid. Propionate esters will slow the release of a steroid for
several days. To keep blood levels from uctuating greatly, propionate
compounds are usually injected two to three times weekly. Testosterone
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propionate and methandriol dipropionate (two separate propionate esters
attached to the parent steroid methandriol) are popular items.
Phenylpropionate ( C9 H10 O2 )
Also referred to as Propionic Acid Phenyl Ester. Phenylpropionate will
extend the release of active steroid a few days longer than propionate. To
keep blood levels even, injections are given at least twice weekly.
Durabolin is the drug most commonly seen with a phenylpropionate ester
(nandrolone phenylpropionate), although it is also used with testosterone in
Sustanon and Omnadren.
Isocarpoate ( C6 H12 O2 )
Also referred to as Isocaproic Acid; isohexanoate; 4-methylvaleric acid.
Isocaproate begins to near enanthate in terms of release. The duration is
still shorter, with a notable hormone level being sustained for approximately
one week. This ester is used with testosterone in the blended products
Sustanon and Omnadren.
Caproate ( C6 H12 O2 )
Also referred to as Hexanoic acid; hexanoate; n-Caproic Acid; n-Hexoic
acid; butylacetic acid; pentiformic acid; pentylformic acid; n-hexylic acid; 1pentanecarboxylic acid; hexoic acid; 1-hexanoic acid; Hexylic acid; Caproic
acid. This ester is identical to isocarpoate in terms of atom count and
weight, but is laid out slightly different (Isocaproate has a split
con guration, dif cult to explain here but easy to see on paper). Release
duration would be very similar to isocaproate (levels sustained for
approximately one weak), perhaps coming slightly closer to enanthate due
to its straight chain. Caproate is the slowest releasing ester used in
Omnadren, which is why most athletes notice more water retention with this
compound.
Enanthate ( C7 H14 O2 )
Also referred to as heptanoic acid; enanthic acid; enanthylic acid; heptylic
acid; heptoic acid; Oenanthylic acid; Oenanthic acid. Enanthate is one of
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the most prominent esters used in steroid manufacture (most commonly
seen with testosterone but is also used in other compounds like Primobolan
Depot). Enanthate will release a steady (yet uctuating as all esters are)
level of hormone due to the length of the ester. Although in medicine
enanthate compounds are often injected on a bi-weekly or monthly basis,
athletes will inject at least weekly to help maintain a uniform blood level.
Cypionate ( C8 H14 O2 )
Also referred to as Cyclopentylpropionic acid, cyclopentylpropionate.
Cypionate is a very popular ester here in the U.S., although it is scarcely
found outside this region. Its release duration is almost identical to
enanthate, and the two are likewise thought to be interchangeable in U.S.
medicine. Althletes commonly hold the belief than cypionate is more
powerful than enanthate, although realistically there is little difference
between the two. The enanthate ester is in fact slightly smaller than
cypionate, and it therefore releases a small (perhaps a few milligrams)
amount of steroid more in comparison.
Decanoate ( C10 H20 O2 )
Also referred to as decanoic acid; capric acid; caprinic acid; decylic acid,
Nonanecarboxylic acid. The Decanoate ester is most commonly used with
the hormone nandrolone (as in Deca-Durabolin) and is found in virtually all
corners of the world. Testosterone decanoate is also the longest acting
constituent in Sustanon, greatly extending its release duration. The release
time with Decanoate compounds is listed to be as long as one month,
although most recently we are nding that levels seem to drop signi cantly
after two weeks. To keep blood levels more uniform, athletes (as they have
always known to do) will follow a weekly injection schedule.
Undecylenate ( C11 H20 O2 )
Also referred to as Undecylenic acid; Hendecenoic acid; Undecenoic acid.
This ester is very similar to decanoate, containing only one carbon atom
more. Its release duration is likewise very similar (approximately 2-3
weeks), perhaps extending a day or so past that seen with decanoate.
Undecylenate seems to be exclusive to the veterinary preparation
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Equipoise (boldenone undecylenate), although there is no reason it would
not work well in human-use preparations (Equipoise certainly works ne for
athletes). Again, weekly injections are most common.
Undecanoate ( C11 H22 O2 )
Also referred to as Undecanoic Acid; 1-Decanecarboxylic acid;
Hendecanoic acid; Undecylic acid. Undecanoate is not a commonly found
ester, and only appears to be used in the nandrolone preparation
Dynabolan, and oral testosterone undecanoate (Andriol). Since this ester is
chemically very similar to undecylenate (it is only 2 hydrogen atoms larger),
it has a similar release duration (approximately 2-3 weeks). Although this
ester is used in the oral preparation Andriol, there is no reason to believe it
carries any properties unique of other esters. Andriol in fact works very
poorly at delivering testosterone, bolstering the idea that oral administration
is not the idea use of esteri ed androgens.
Laurate ( C12 H24 O2 )
Also referred to as Dodecanoic acid, laurostearic acid, duodecyclic acid, 1undecanecarboxylic acid, and dodecoic acid. Laurate is the longest
releasing ester used in commercial steroid production, although longer
acting esters do exist. Its release duration would be closer to one month
than the other esters listed above, although realistically we are probably to
expect a notable drop in hormone level after the third week. Laurate is
exclusively found in the veterinary nandrolone preparation Laurabolin,
perhaps seen as slightly advantageous over a decanoate ester due to a
less frequent injection schedule. Again athletes will most commonly inject
this drug weekly, no doubt in part due to its low strength (25mg/ml or 50mg/
ml).
Conclusion
While the advent of esters certainly constitutes an invaluable advance in
the eld of anabolic steroid medicine, clearly you can see that there is no
magic involved here. Esters work in a well-understood and predictable
manner, and do not alter the activity of the parent steroid in any way other
than to delay its release. Although the lure surrounding various steroid
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products like testosterone cypionate, Sustanon, Omnadren etc. certainly
makes for interesting conversation, realistically it just amounts to
misinformation that the athlete would be better off ignoring. Testosterone is
testosterone and anyone who is going to tell you one ester form of this (or
any) hormone is much better than another one should do a little more
research, and a lot less talking.
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Human Growth Hormone (Somatotropin)
Drug Class: Growth Hormone/IGF-1 Precursor
Active Life: Varies by injection method
Human Growth Hormone is a proteinaceous hormone made up of a chain
of 191 amino acids and is produced by the pituitary gland. It is responsible
for the protein deposition, growth of tissues, and the breakdown of
subcutaneous fat stores. Human growth hormone is produced in its highest
levels during adolescence, as should be no surprise since this is when the
majority of a person's body growth occurs. In adulthood, growth hormone
still circulates in the body but at much lower levels. The primary medical
purpose for administration of human growth hormone is for those that suffer
from a de ciency of the hormone during their adolescence so that normal
growth can occur. However in recent years the popularity of human growth
hormone has surged as a means to treat age-related degenerative
conditions, as well as other so-called "anti-aging" therapies.
Human growth hormone rst became available in the 1980's. At rst it was
extracted from the pituitary glands of cadavers. This practice was
discontinued however when it was determined that administration of the
hormone that was collected this way was linked to the spread of a fatal
brain disease. All of the human growth hormone that is now produced is
synthetic.
In terms of the use of human growth hormone for strength athletes and
bodybuilders, the effects are two fold. First, it has been demonstrated that
consistent administration of human growth hormone can help to promote
loss of body fat. In part this is due to the ability of the compound to cause
cells in the body to increase the rate with which they utilize fats while also
decreasing the rate that carbohydrates are used. This fat loss is achieved
because of the ability of growth hormone to stimulate triglyceride hydrolysis
in adipose tissue as well2 .
In conjunction with this, human growth hormone helps to promote the
movement of amino acids through cell membranes. This, along with the
fact that growth hormone promotes the growth of the cells in the body and
increases the rate at which these cells divide and multiple, obviously
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indicates that it is also capable of enhancing anabolism if used at
appropriate doses.
Many users also have an interest in using human growth hormone for the
ability of the compound to help heal existing injuries and prevent new ones
from occurring. There is some evidence that growth hormone can help to
promote the production of new and regeneration of damaged cartilage
when used in conjunction with insulin-like growth factor. It is actually the
insulin-like growth factor that stimulates the production of cartilage. Insulinlike growth factor is released from the liver in response to circulating growth
hormone3 .
It has also been demonstrated that human growth hormone has positive
effects on erythropoeisis, i.e. the manufacture of red blood cells4 . This
effect should help to improve the endurance of an athlete and may also
help to promote anabolism. To the degree with which this effect will occur in
users varies quite widely, but all users should show some improvement.
Use/Dosing
Human growth hormone is primarily secreted in rhythmic pulses during
sleep. This occurs by the mechanism of Growth Hormone Releasing
Hormone and Somatostatin being released in an alternating fashion. For
the most part users will want to mimic the natural release of growth
hormone, while also not disrupting the body's natural production of the
hormone. This is often a delicate balance.
Dosing Schedule
In terms of a dosing schedule for the compound, there is some controversy
as to the best method for fat loss/anabolism. It is thought by many that daily
dosing is of primary importance when using human growth hormone due to
the extremely short active life of the drug. Blood concentrations of the
hormone reach their peak within two to six hours of the injection, with the
half life being only twenty to thirty minutes3 . This of course makes it
impossible to maintain stable blood levels of the compound.
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However a stable level of the hormone is seemingly unnecessary as this
does not occur naturally when the body produces the hormone. In fact
there is some research that indicates that administration of the hormone
every other day, instead of injections every day, may result in a more
ef cient use of the hormone. In a study using children ranging in ages of
two to four, it was demonstrated that administration of the compound every
other day, as opposed to every day, resulted in more growth in the children
giving this dosing schedule5 . One theory as to why this may occur is that
injections every other day may simulate the natural pulsile frequency of
growth hormone secretion. This would also allow the growth hormone
receptors in the body recover from the surge of growth hormone that would
be circulating and then be better able to make use of the next dose that is
administered the next day.
The only problem with the above theory is that it has never been tested in
terms of its effect on muscle growth and/or fat loss, only in the height
growth in extremely young children. For the most part strength athletes and
bodybuilders have administered growth hormone every day and have
achieved good results. This method would seemingly provide a user with a
consistent wave of growth hormone throughout their cycle and allow the
body to utilize it rather ef ciently.
Another common practice among users is to run growth hormone for ve
days and then take one or two days off, or some other similar schedule.
This would seemingly be "splitting the difference" between the two dosing
schedules outlined above (as well as save money), but there is no research
to indicate that it is of any signi cant bene t either way.
As for the time of day a user should inject human growth hormone, it would
be least disruptive to the natural release of the hormone to administer it
sometime early in the day. If a user were to inject it close to when they
were going to sleep, this would surely negate any natural release of growth
hormone, something that a user would obviously want to avoid. There is no
standard to which most adhere to when deciding how close to going to
sleep that they will administer growth hormone, however mid-afternoon
should be early enough that it does not interfere with the natural release of
the hormone during sleep.
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In terms of dosages needed to see speci c results, there is primarily only
anecdotal evidence to be relied upon when it comes to fat loss and an
anabolic response. The relevant research does not discuss these effects in
any great scope. However, most users have indicated that doses of
approximately two to four international units (2-4 iu) per day in men will
usually produce a noticeable loss of body fat in most users. In terms of
getting an anabolic response, the experience of users vary considerably.
For the most part it can be concluded that most users will need to
administer larger doses than needed to experience fat loss if they wish to
see a noticeable anabolic response from human growth hormone. How
much more varies from individual to individual. There are some users who
have indicated that using extremely large doses of the hormone has
resulted in dramatic gains in muscle mass, but often these doses are cost
prohibitive for most. Individuals will likely have to experiment themselves to
nd a level that they are comfortable with, as well as what they can afford.
Ramping
As a general rule the best way to start an HGH program is to start with a
low dose and ease the administration into the higher doses. This will avoid,
or at least minimize, many of the common side effects of HGH such as
bloating, joint pain and swelling. Most people can tolerate approximately 2
i.u.'s with few side effects, so that would be the recommended starting
dose. A scheduled program would look like this:
• Week 1-4: HGH 2i.u.'s one injection
• Week 5: HGH 2.5 i.u.'s one injection
• Week 6: HGH 3 i.u.'s split into two injections of 1.5 i.u.'s each
• Week 7: HGH 3.5 i.u.'s split into two injections of 1.75 i.u's each
• And so forth until you reach your desired dose.
If at any point in this progression unbearable bloating or joint pain becomes
an issue, the dose must be reduced by 25% and held at a lower dosage for
a couple of weeks. If the side effects subside, progression may resume
back up towards desired level. If the side effects remain, the dose must be
reduced again and held at a lower level for two weeks before beginning
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upward progression. This method will keep the HGH experience a good
one with minimal side effects.
Duration
As for the duration of a cycle of growth hormone, it is believed by many that
the compound must be administered for a minimum of 20 to 30 weeks to
see results. The action of the compound is slow acting and therefore
lengthy cycles are needed. However due to its relative safety it can be run
for several months, and even years, with little to no negative results. Of
course this is dependent on the user and his or her individual reaction to
the compound, along with the doses that they are using.
Administration
Human growth hormone can be administered using either intra-muscular or
subcutaneous injections. There is no difference in the absorption of the
compound.
Post Cycle Therapy
No type of post-cycle therapy is necessary when discontinuing growth
hormone as it should continue to be produced naturally by the body of the
user. The negative feedback loop that indicates to the body that there is
enough of the hormone circulating is related to insulin-like growth factor.
Speci cally, when insulin-like growth factor is secreted by the liver a signal
is sent to the pituitary gland and hypothalamus to cease the production of
growth hormone6 .
Although not necessary, some opt to use growth hormone peptides to help
promote their release of natural growth hormone.
Side E ects and Risks
For the most part, human growth hormone is a relatively mild compound
with little in the way of side effects when compared to anabolic steroids.
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The most common side effects experienced by users are sleepiness,
bloating and/or joint pain. hGH improves sleep quality by a large margin,
but when rst taking it, it's not uncommon to feel intermittent sleepiness
throughout the day like you want to take a nap.
The majority of users anecdotally report that any joint pain they experience
most often ceases after a few weeks of administration of the drug2 .
In addition, at extreme high doses and long durations, it's possible to
induce enlarged organs, carpal tunnel syndrome and acromegaly, which is
a thickening of or abnormal growth of the bones7 . Think of Andre the Giant.
For this reason, it would be advisable for users that are in their mid-to-late
20's or younger to consult with a physician if they're planning on
administering growth hormone. This is due to the fact that if the growth
plates of a user aren't yet fused, there's a potential for disproportionate
bone growth. If there's a chance that a user has cancer or other tumours,
it's imperative they ensure that they don't begin administering growth
hormone prior to getting medically cleared. This is due to the fact that hGH
can accelerate tumor growth rates.
Some users may also experience some other conditions related to use of
growth hormone. Thyroid suppression, insulin resistance, and prostate
growth are all possible side effects that could be experienced. There are
various methods to help deal with these occurrences, ranging from the mild
to the very aggressive. This pro le will not go into great detail about these
therapies, however it should be noted that most users are unlikely to have
major dif culties with these side effects if their doses remain relatively
moderate.
Human growth hormone has also been shown to cause gynocomastia in
some users. The exact mechanism that this occurs is not know, however it
is believed to be related to either the a rise in prolactin levels or else the
growth hormone causes breast tissue growth when coupled with a high
level of estrogen in the body. To combat this, the usual protocol can be
used, i.e. use of aromatase inhibitors, selective estrogen receptor
modulator and/or compounds that help to reduce prolactin levels.
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Does using HGH shut down natural HGH production?
Answer:
The mechanism by which chronic exposure to hGH leads to tolerance,
dependence, and a withdrawal syndrome is unclear and does not
involve the suppression of hormone secretion. During the nadir of
growth velocity, which follows the withdrawal of prolonged drug therapy,
serum GH levels remain normal, as do serum IGF-I and IGF-binding
protein-3 levels (4). Moreover, endogenous pulsatile secretion of GH
resumes within days even after long-term hGH therapy (7).
http://press.endocrine.org/doi/full/10.1210/jcem.87.8.8721
HGH Brands List
Only brands listed here are the only HGH brands that are the exception to
our "No Source Talk" rule. If your brand isn't listed there just refer to it as
"generic HGH."
Brand
Ansomo
ne
Fitropin
Amino
Acid
191
Purity
Manufacturer (Country)
192
medi
um
low
Genotro
pin
Humatro
pe
Hygetro
pin
Hypertro
pin
Jintropin
191
high
2008 2010
1996
191
high
1998
Eli Lilly (USA)
191
2008
191
medi
um
high
191
high
1997
Norditro
pin
Nutropin
191
high
1997
Zhongshan Hygene
Biopharm (China)
Neogenica Bioscience
(China)
GeneScience
Pharmaceuticals (China)
Novo Nordisk (USA)
191
high
1997
Genentech (USA)
Scitropin
191
2005
SciGen (Singapore)
Saizen
191
medi
um
high
1997
Merck Serono (Switzerland)
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fi
Available
Since
2005
2007
Vol. 1
Anke Biotechnology (China)
Kexing Biotech (China)
P zer (USA)
385
Serosti
m
TevTropin
Zomacto
n
Zorbtive
191
high
2002
EMD Serono (USA)
191
medi
um
medi
um
high
2001
Teva Pharmaceuticals
(USA)
Ferring Pharmaceuticals
(Australia)
EMD Serono (USA)
191
191
2002
2003
References
• Viganò et al. Effects of Recombinant Growth Hormone on
Visceral Fat Accumulation: Pilot Study in HIV-Infected
Adolescents.J Clin Endocrinol Metab. 2005 Apr 19; [Epub ahead
of print]
• Llewellyn, William, Anabolics 2004, 2003-4, Molecular Nutrition,
pp. 236-8
• Identi cation of an insulin-responsive element in the promoter of
the human gene for insulin-like growth factor binding protein-1. J
Biol Chem 268:17063-8, 1995
• Christ ER, Cummings MH, Westwood NB, Sawyer BM, Pearson
TC, Sonksen PH, Russell-Jones DL. The importance of growth
hormone in the regulation of erythropoiesis, red cell mass, and
plasma volume in adults with growth hormone de ciency., J Clin
Endocrinol Metab 1997 Sep;82(9):2985-90
• Lampit, M. Hochberg, Z. Testosterone blunts feedback inhibition
of growth hormone secretion by experimentally elevated insulinlike growth factor-I concentrations.J Clin Endocrinol Metab. 2005
Mar;90(3):1613-7
• Yarasheski KE. Growth hormone effects on metabolism, body
composition, muscle mass, and strength. Exerc Sport Sci Rev
1994;22:285-312
• Growth hormone induced increase in serum IGFBP-3 level is
reversed by anabolic steroids in substance abusing power
athletes. Clin Endocrinol (Oxf) 49:459-63, 1998
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Peptides
A peptide is a compound consisting of two or more amino acids linked in a
chain, the carboxyl group of each acid being joined to the amino group of
the next by a bond.
Datbtrue Archive HERE
Peptide Guide
BPC 157
BPC 157 is a peptide of a sequence of amino acids with a molecular
formula of 62 carbons, 98 hydrogens, 16 nitrogens, and 22 oxygen atoms
(C62-H98-N16-O22). BPC stands for “Body Protecting Compound”.
BPC-157 accelerates wound healing, and, via interaction with the Nitric
Oxide (NO) system, causes protection of endothelial tissue and an
“angiogenic” (blood vessel building) wound healing effect. BPC 157 is
surprisingly free of side effects, and has been shown in research that’s
been happening since 1991 to repair tendon, muscle, intestines, teeth,
bone and more, both in in-vitro laboratory “test-tube” studies, in in-vivo
human and rodent studies, and when used orally or inject subcutaneously
(under your skin) or intramuscularly (into your muscle). BPC-157 is also
known as a “stable gastric pentadecapeptide”, primarily because it is stable
in human gastric juice, can cause an anabolic healing effect in both the
upper and lower GI tract, has an antiulcer effect, and produces a
therapeutic effect on in ammatory bowel disease (IBD) – all again
surprisingly free of side effects.
More On This Peptide Below
CJC-1295 with DAC
CJC-1295 is a tetra substituted peptide made up of thirty amino acids. It
has been shown through scienti c research studies to bio-conjugate to the
protein serum albumin which provides an advanced level of homeostasis in
animals being tested. The use of CJC-1295 with DAC prevents the
production of DPP-IV from occurring as determined in scienti c studies with
the animal test subjects. This results in the GHRH1-29 experiencing an
extended half-life, one which can last over seven days. With the increased
stabilization of GHRH1-29, growth hormones are able to function at greater
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levels and test subjects are then able to experience an increased level of
stability in the growth hormones. CJC-1295 with DAC is the preferred and
more powerful GHRH component in a peptide protocol. Throughout
scienti c studies, it has been understood the presence of CJC-1295 with
DAC allows for a few elevated processes test subjects experience. This
includes Muscular Tissue Growth, Increased Bone Density and Body Fat
Reduction.
CJC-1295 w/o DAC
CJC-1295 without DAC is a 30 amino acid peptide hormone, better known
in the community as a GHRH (growth hormone releasing hormone).
Essentially, what this means is this peptide will release a series of pulses
over a long period of time which usually equates to fewer injections. Even
though CJC-1295’s main function upon creation was found to boost protein
synthesis, increased growth of muscle tissue and many other bene ts
come with it as well. CJC-1295 also helps injury recovery times, reduce
body fat, boost immune system and bone density and cellular repair (skin
and organs). The term CJC 1295 without DAC this is really means that they
are looking at MOD GRF 1-29. And this modi cation had resulted in a
greater peptide bond, the average user will still likely need to inject two to
three times a day with a GHRP to get the maximum effectiveness for
releasing endogenous growth hormone. If you prefer to use shorter spikes
of GH release then the use of the MOD GRF 1-29 (CJC 1295 without DAC)
is optimal.
DSIP
DSIP stands for Delta sleep-inducing peptide. This type of peptide is
classi ed as a neuropeptide and it works by inducing spindle and delta
EEG activity and by reducing motor activity. This peptide is utilized in order
to help people fall asleep and stay asleep. This peptide is popular with
bodybuilders who have learned about the power and potential of peptides
through their training and supplementation regimens. DSIP lowers basal
corticotropin levels and blocks their release. It also makes it easier for the
body to release LH (luteinizing hormone). In addition, it makes it simpler for
the body to release somatotrophin (and somatoliberin secretions) and to
block the production of somatostatin. This peptide may help people to
manage stress. In addition, it may have the power to alleviate the
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symptoms of hypothermia. It’s also known as an effective means of
normalizing blood pressure and contractions which are myocardial. As well,
it may offer anti-oxidant bene ts (slow down cell damage).
Epitalon
Epitalon (a.k.a. epithalon or epithalone) is a synthetically-derived
tetrapeptide, meaning that it consists of four amino acid chains. It was
discovered by the Russian scientist Professor Vladimir Khavinson, who
then conducted epitalon-related research for the next 35 years in both
animal and human clinical trials. Epitalon’s primary role is to increase the
natural production of telomerase, a natural enzyme that helps cells
reproduce telomeres, which are the protective parts of our DNA. This
allows the replication of our DNA so the body can grow new cells and
rejuvenate old ones. Furthermore, Epitalon has been shown to inhibit the
growth of cancerous tumors, enabling a longer and healthier life in the
future. And research has shown that epitalon is a powerful antioxidant that
eliminates oxygen-free radicals responsible for damaging and killing cells.
As a result of epitalon’s effect on telomerase production, the bene ts are
unique and far-reaching. Bene ts of epitalon include: Increase of human
lifespan Signi cant boosting of energy levels Promotion of deeper sleep
Delay and prevention of age-related diseases such as cancer, heart
disease and dementia Improvement of skin health and appearance Healing
of injured and deteriorating muscle cells
Follistatin
Follistatin is an inhibitor of TGF-β superfamily ligands that repress skeletal
muscle growth and promote muscle wasting. Accordingly, follistatin has
emerged as a potential therapeutic to ameliorate the deleterious effects of
muscle atrophy. In the setting of disease, increasing follistatin expression in
musculature has proven bene cial for improving aspects of pathology in
dystrophin-de cient mdx mice that model Duchenne and Becker muscular
dystrophy (DMD, BMD). Administration of recombinant follistatin has also
been shown to promote muscle hypertrophy in wild-type mice, and
ameliorate the progression of a mouse model of spinal muscular atrophy
(SMA).
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GHRP-2
GHRP-2 is a synthetic agonist of ghrelin, the newly-discovered gut peptide
which binds to the growth hormone (GH) secretagogue receptor. Ghrelin
has been shown to have two major effects, stimulating both GH secretion
and appetite/meal initiation. GHRP-2 has been extensively studied for its
utility as a growth hormone secretagogue (GHS). Animal studies have
shown its effect on food intake. However, whether GHRP-2 can also
stimulate appetite in humans when administered acutely is not known.
When administered either centrally or peripherally to rodents, ghrelin
increases food intake and body weight. Interestingly, its effects on food
intake are independent of GH secretion and appear to be mediated via the
NPY/Agouti gene-related protein (AGRP) neurons in the hypothalamic
arcuate nucleus. Peripheral ghrelin administration has recently been shown
to stimulate food intake in lean, healthy men and women and in cancer
patients.
Data suggest that circulating ghrelin is also implicated in meal to meal
regulation. Ghrelin levels increase in anticipation of a meal and are
suppressed by food ingestion, but the underlying mechanisms are not
known. The meal-related suppression of ghrelin is proportional to the
carbohydrate (CHO) content of the meal but does not appear to be directly
related to glucose or insulin, although insulin administration decreases
ghrelin.
GHRP-6
GHRP-6 is an injectable peptide in the category of growth hormone
releasing peptides, or GHRP’s. The most common use of these peptides is
to increase GH production. Other peptides in this category include
GHRP-2, hexarelin, and ipamorelin. With regard to increasing GH, all of
these work similarly, and there is no need or advantage to combining them.
Instead, the one most suited for the particular case is chosen. The principal
use of GHRP-6 is to provide increased GH levels, which also results in
increased IGF-1 levels. This aids fat loss and in some instances aids
muscle gain as well. Generally, GHRP use is chosen as an alternate to GH
use, and only rarely is combined with GH. GHRP-6 is most generally used
for the same purposes that GH might be used, but may be chosen where a
cost advantage exists favoring GHRP-6, GH is not available, or the
individual prefers the idea of stimulating his own GH production to injecting
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GH. These purposes can include increased fat loss, improved muscle gain
when used in combination with anabolic steroids, cosmetic improvement of
the skin, and improved healing from injury.
Hexarelin
Hexarelin is a peptide that can promote the secretion of certain hormones.
It is a hexipeptide that consists of six amino acids that can release certain
hormones as they are needed. It has a half-life of about 70 minutes. Some
studies have derived several different effects linked to its use, including
elevated levels of fat loss, connective tissues, density of bone minerals,
meiosis, mitosis, and elasticity. In turn, these effects have led to animal test
subjects experiencing improved endurance, joint rehabilitation, wound
healing, and improved muscle strength. Studies also conclude that
Hexarelin’s functionality can last a long stretch of time. Furthermore,
scienti c studies on animal test subjects have determined that Hexarelin
does not induce an increased desire for food consumption. The peptide
achieves this because it does not increase the levels of ghrelin; the amino
acid peptide that clears out the gastric system and induces hunger. Further
scienti c studies have also determined that the peptide promotes an
increase in the secretion of IGF-1 from the liver of animal test subjects.
This additional secretion plays a key role in breaking down fat and
improving strength.
HGH Fragment 176-191
HGH Fragment 176-191 is a fragment of the HGH peptide. Scientists found
that if they truncated the peptide at the C terminal region they could isolate
the fat loss attributes associated with HGH. Taking this fragment from HGH,
including the peptide bonds from 176-191, they found they had developed
a peptide that regulated fat loss 12.5 times better than regular HGH. It has
an incredibly ability to regulate fat metabolism without the adverse side
effects on insulin sensitivity. By isolating the tail end of the GH molecule,
scientists have found that HGH Frag 176-191 works even better than HGH
to stimulate lipolysis (breaking down of fat). In fact, it actually inhibits
lipogenesis; meaning, it stops formation of fatty acids and other lipids. Also,
unlike other fat burning compounds out there, users will not experience
hunger suppressing qualities or the jittery feelings that can be associated
with ephedrine like compounds. Since it does not compete for HGH
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receptors, multiple studies have shown that HGH Frag 176-191 will not
cause hyperglycemia. In addition, it will promote lean body mass, protein
synthesis, increase bone mineral density, and better sleep.
IGF1-DES
IGF-1 DES is a peptide secreted by the liver and consists of 67 amino
acids. IGF-1 DES stimulates hormones as it is a highly anabolic structure.
In living organisms, IGF-1 DES offers a number of bene ts and is
responsible for creating hyperplasia (or hypergensis), which is a process
that regulates the growth of cells. Scienti c research involving IGF-1 DES
indicates the peptide is also capable of in uencing neurological growth,
maintain nerve cell function, and promote nerve growth. Its ability to create
hyperplasia leads scientists to use animals for researching the ability of
IGF-1 DES in relation to growing cells and the development of tissue.
Studies show that IGF-1 DES has the capability to in uence the neuronal
structure and functions of the brain, and continuing animal studies are
watching the peptide’s effects on muscular and skeletal growth.
IGF1-LR3
The polypeptide IGF-1 LR3, also known as Long R3 IGF-1, is a peptide
chain consisting of 83 amino acids. It contains a molecular weight of 9200,
and its molecular structure of C990H1528N262O300S7. Speci cally,
scienti c studies have determined that IGF-LR3’s relationship with the
pancreas and liver can be traced down to speci c secretions. In the case of
the pancreas, it has been determined that the peptide can be linked to the
secretion of insulin. This secretion guides the cells that are found within the
skeletal muscles, fatty tissues, and liver to absorb glucose from an animal
test subject’s bloodstream. In the case of the liver, it has been determined
that the peptide can be linked to the secretion of IGF-1, also known as
Insulin-like Growth Factor-1 or Somatomedin C. This secretion has been
shown to possess highly anabolic properties. What this means is, the
secretion has been determined to play a vital role in muscle and tissue
growth as it relates to muscular and skeletal tissue growth and repair.
Insulin
Insulin (/ˈɪn.sjʊ.lɪn/ from Latin insula, 'island') is a peptide hormone
produced by beta cells of the pancreatic islets; it is considered to be the
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main anabolic hormone of the body. It regulates the metabolism of
carbohydrates, fats and protein by promoting the absorption of glucose
from the blood into liver, fat and skeletal muscle cells. In these tissues the
absorbed glucose is converted into either glycogen via glycogenesis or fats
(triglycerides) via lipogenesis, or, in the case of the liver, into both. Glucose
production and secretion by the liver is strongly inhibited by high
concentrations of insulin in the blood.
Circulating insulin affects the synthesis of proteins in a wide variety of
tissues. It is therefore an anabolic hormone, promoting the conversion of
small molecules in the blood into large molecules inside the cells. Low
insulin levels in the blood have the opposite effect by promoting
widespread catabolism, especially of reserve body fat. The secretion of
insulin and glucagon into the blood in response to the blood glucose
concentration is the primary mechanism of glucose homeostasis.
Ipamorelin
Ipamorelin is a pentipeptide, meaning that its structure is comprised of ve
amino acids. It contains a molecular mass of 711.85296, and its molecular
formula is C38H49N9O5. It can sometimes go by the alternate names
Ipamorelin Acetate, IPAM, and NNC-26-0161. It is a secretogogue, and is
considered to be an agonist, meaning that it possesses the ability to bind
certain receptors of a cell and provokes a cellular response. Ipamorelin’s
operational mechanics enables the peptide to stimulate the production of
pituitary gland-based expression of secretions related to growth amongst
animal test subjects. At the same time, the presence of the peptide has
been shown to inhibit the production of a secretion known as somatostatin.
In essence, this peptide is primarily responsible for inhibiting the production
of growth secretions. Additionally, it has been determined that Ipamorelin
has the ability to boost the production of IGF-1, or Insulin-like Growth
Factor 1. This particular peptide, which is secreted by the liver, has been
shown to be highly anabolic in its nature. What this means is, its presence
plays a key role in the overall growth and repair of muscular and skeletal
tissue.
MGF (Mechano Growth Factor)
Mechano Growth Factor (MGF) also known as IGF-1Ec is a growth factor/
repair factor that is derived from exercised or damaged muscle tissue.
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What makes MGF special is its unique role in muscle growth. MGF has the
ability to cause wasted tissue to grow and improve by activating muscle
stem cells and increasing the up-regulation of protein synthesis, this unique
ability can rapidly improve recovery and speed up muscle growth. MGF can
initiate muscle satellite (stem) cell activation in addition to its IGF-1 receptor
domain which, in turn, increases protein synthesis turnover; therefore, if
used correctly it can improve muscle mass over time. MGF is like a highly
anabolic variant of IGF. After you have trained, the IGF-I gene is spliced
towards MGF then that causes hypertrophy and repair of local muscle
damage by activating the muscle stem cells as well as other important
anabolic processes, including the above mentioned protein synthesis, and
increased nitrogen retention.
PEG-MGF
PEG-MGF is pegylated mechanic growth factor, which is a research
peptide used in a variety of scienti c research conducted throughout the
world. The peptide has proved useful with the MGF being a variant of IGF
(insulin-like growth factor), which is responsible for increasing the stem cell
count in muscles. This enables the muscles bers to mature and fuse. The
peptide is being thoroughly tested in patients where muscle bers are
broken down and need assistance with muscle growth. The PEG-MGF
peptide creates new bers, promotes protein synthesis and helps with
nitrogen retention; this makes it ideal for those who do hard workouts or
suffer from muscular diseases.
PT-141 Bremelanotide
PT-141, also known as Bremelanotide, is a research peptide that has
shown promise in scienti c studies, on animal test subjects, to regulate
blood ow restriction, in ammation, and helping improve sexual
dysfunction. PT-141 was developed from the Melanotan 2 Peptide, which
underwent studies in a laboratory setting as a sunless tanning agent. It is
from this scienti c testing that the potential bene ts of PT-141 were
discovered. Scientists have determined through rigorous testing on animal
test subjects, because of the ability to regulate blood ow restriction and
in ammation by PT-141, it very well may be instrumental in managing the
onset of hemorrhagic shock and reperfusion injury. What this means is it
could potentially reduce, or outright prevent in ammation that may be
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triggered by a variety of irritants or diseases. This, in turn, could also help
reduce any damage that could potentially occur within blood vessels and
surrounding tissue. Additional studies have determined PT-141 is a
potential remedy for the treatment of sexual dysfunction. Results from early
research studies has shown PT-141 does not act on the vascular system
like former compounds, but works by activating the melanocortin receptors
in the brain.
Selank
Selank is a peptide that has a molecular mass of 751.9 and a molecular
formula of C33H57N11O9. It is considered to be a heptapeptide, meaning
that it is a peptide chain made up of seven amino acids. Its sequence is
Thr-Lys-Pro-Arg-Pro-Gly-Pro. According to scienti c study that has been
based on animal test subjects, it has been determined that the functional
mechanics of Selank gives it the capacity to increase the secretion of
serotonin. This neurotransmitter is noted for its ties to mood regulation, and
it has also been noted to contain links to sleep and appetite regulation. The
presence of the peptide and its ability to cause an uptick in the release of
serotonin means that the animal test subject can experience a more
ef cient means of homeostasis in terms of mood, hunger, and sleep. In
addition to inducing a greater metabolic rate of serotonin, it has also been
determined that Selank has the capacity to modulate the expression of
interleukin 6, a white blood cell-secretion that can act as both a proin ammatory cytokine and an anti-in ammatory myokine. This secretion
plays a key role in stimulating the immune response during infection and
after trauma, particularly during instances of tissue damage leading to
in ammation.
Sermorelin (GRF 1-29)
Sermorelin or GRF 1-29 is a growth hormone secretagogue, which means
that it stimulates the pituitary gland to produce and secrete HGH. It is a
form of GRF that contains only the rst 29 amino acids. GRF that is
produced by neurosecretory neurons in the brain contains 44 amino acids.
Only the rst 29 amino acids are responsible for stimulating pituitary
production and secretion of HGH. Sermorelin has highly speci c receptors
on pituitary somatotrophs. So it binds to the cells that produce and release
HGH. Upon binding, Sermorelin acts through a cylicAMP second
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messenger system exactly the same as that used by naturally occurring
growth hormone releasing hormone. Furthermore, it has an excellent safety
pro le. Its effects are regulated at the level of the pituitary gland by
negative feedback and by release of somatostatin so there are less safety
concerns such as those associated with HGH overdosing. Tissue exposure
to HGH released by the pituitary in uence of Sermorelin mimics normal
physiology, By stimulating the pituitary it preserves more of the growth
hormone neuroendocrine axis that fails with aging, Semorelin in a complex
way, helps preserve not only youthful anatomy but also youthful physiology,
it gives all of the bene ts of HGH and more. Another big advantage of
semorelin is that it causes the pituitary gland to up-regulate. This stimulates
the gland to rejuvenate. There are many reports in peer-reviewed medical
and scienti c literature showing that GRF/Sermorelin also has a direct
effect on the brain to promote non-REM slow wave sleep.
Thymosin Beta 4 (TB-500)
Thymosin Beta 4 or TB-500, as it is called, is an exploration peptide that is
tested primarily for its abilities to increase strength, endurance and
restoration in subjects. It is known to have many of the same effects of
growth hormone in animals equating to results in humans that would be
related to an increase in testosterone. It has been shown to inhibit tumor
growth making TB-500 an amazing product for research studies and with
further testing, something that may become widely accepted in the minds of
many. TB-500 has been proven to speed up the therapeutic process in
wounds as well as being used clinically for anti-in ammatory purposes.
This is extremely important when it comes to competitive competitions or
events as well as simple body maintenance. Recovery times and pain relief
occur much faster for the duration of use allowing for peak performance as
well as a healthier well being. Subjects have also proven a slight increase
in hair growth which is a positive side effect of TB-500 use. As you can see,
research in animals has shown superior and appealing results in existing
studies when it comes to its use. In inclusion to the restoration aspects of
using TB-500 as an exploration peptide, there are several other notable
facts that are being discovered. Subjects have proven a signi cant increase
in muscle growth which clearly improves strength and endurance as well as
a huge enhancement in muscle tone itself. The improvement in exibility
due to its anti- in ammation components and known abilities to be able to
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stretch tissue safely have made this a favorite of those performing
investigation in the area of performance and physical enhancements.
Exploration of this peptide on subjects is simply producing astonishing
results in most cases.
The Body's Growth Hormone System & Peptides
Besides Growth hormone (GH) itself, your body utilizes three basic
hormones:
• Growth Hormone Releasing Hormone (GHRH)- Released by the brain
to tell your bodies growth hormone storage cells (somatotrophs) to
release growth hormone.
• Somatostatin- Acts as the "off switch" and tells your cells
(somatotrophs) to cease growth hormone release.
• Ghrelin- Created in the stomach, this hunger derived hormone reduces
Somatostatins "off switch" effect and encourages the brain to release
more GHRH.
If GHRH is always around the somatotrophs (GH storing cells) are
constantly releasing and unable to store GH. This results in a constant
dribble or "bleed" of GH rather than a big pulse. Growing, development,
and maturity requires GH to be released in a pulsatile manner.
This is where Somatostatin comes into play. It instructs your somatotrophs
to cease the GH release allowing them to begin storing and stockpiling GH.
However if Somatostatin is always present the body would never release
enough GH to function. What if GHRH and Somatostatin are trying to work
at the same time? For the most part Somatostatin is stronger and no GH
will be released.
Further bene ting this hormonal seesaw is Ghrelin. When Ghrelin makes
its way up to the brain it makes it easier for GHRH to do it's job by
suppressing Somatostatins effects. It is possible for Ghrelin on its own to
cause a GH release even with a high Somatostatin presence. However,
GHRH and Ghrelin together have a synergistic GH effect, meaning that the
spike of GH released is larger than could have been produced by each on
their own.
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Growth Hormone Releasing Hormones (GHRH):
•
•
•
•
•
CJC-1295
CJC-1293
GRF(1-29)
Sermorelin
Modi ed GRF(1-29)
Which GHRH?
GRF(1-29) and Sermorelin are essentially the same thing. Sermorelin just
being the name of a FDA-approved version of GRF(1-29). The issue here
is that these are easily rendered ineffective within minutes of injecting due
to destruction by blood enzymes (unless you could pin directly into your
pituitary gland). What remains of the list are analogs, or altered versions, of
the original GRF(1-29).
Using an anolog that is able to survive blood enzymes for around 30
minutes is ideal
CJC-1293 is GRF(1-29) with 1 amino acid swap plus the Drug Af nity
Complex (DAC). DAC acts as a velcro holding the amino acids together for
a longer period of time. The single amino acid swap makes the analog
peptide stronger but not by enough. The half-life is maybe double
GRF(1-29) in humans. So 5 minutes of half-life.
CJC-1295 is GRF(1-29) with 4 amino acid alterations and the Drug Af nity
Complex (DAC). This version is extra strong and will last more than 30
minutes and the DAC increases the half-life even more by preventing
breakdown by blood enzymes.
Here is the interesting part: You do not want to use any of the CJC's. The
rst (CJC-1293) does not survive long enough after injection and the
second (CJC-1295) survives for too long and is always around preventing
Somatostatin from stopping GH release resulting in a GH bleed.
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Synthetic forms of Ghrelin exist known as Growth Hormone Releasing
Peptides (GHRP's) and act in the same way that natural Ghrelin does.
What do you want to use? You want an analog that utilizes those 4 amino
acid swaps and mantains the ability to still be broken down after those 30
or so minutes. This is known as Mod ed GRF(1-29).
**There is debate as to whether or not CJC-1295 without DAC is the same
as Mod GRF(1-29)
Growth Hormone Releasing Peptides, Ghrelinmimetics (GHRP):
•
•
•
•
GHRP-6
GHRP-2
Ipamorelin
Hexarelin
Which GHRP?
Hexarelin is the strongest in the family known to give the biggest pulse of
all. Will create prolactin and cortisol side effects. Desensitization will
happen regardless of the dose.
GHRP-2 has the second strongest GH release, lower hunger effect, and no
gastric motility. GHRP-2 will result in the most bang for your buck. This is a
second generation GHRP. Usage of this peptide can also come with
elevated levels of cortisol and prolactin. Desensitization is unclear if used
beyond saturation dose.
GHRP-6 has the second strongest GH release. It can cause an intense
hunger effect and gastric motility. This is a rst generation GHRP. Slightly
creates prolactin and cortisol issues. Desensitization does not occur.
Ipamorelin does not release as much GH as other GHRPs, but at very
large doses was shown to give a large release of GH without
desensitization. Has no almost no hunger effect. This mildest in the bunch,
but does not create prolactin or cortisol.
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Dosing Schedules
Injecting a GHRH on its own is not very effective since you are unable to
know when your bodies somatostatin is active. Because of this you'll need
to pick a GHRP to be paired with your GHRH of choice. This ensures that
Somatostatin, if present, will be suppressed and the two peptides will
synergistically amplify the natural GH pulse.
Dosing is going to be mostly dependent on your goals and it is generally
recommended to asses your tolerance before diving right into multiple
doses per day. Starting slow and gradually increasing to multiple doses per
day may alleviate some side effects
Note: a saturation dose is de ned as 1mcg/kg of bodyweight or 100mcg,
the latter being the most commonly used (except in Hexarelin in which
200mcg is considered the saturation dose). Some minority of people have
sleep interruption rather than better sleep from pre-bed dosing. Often a
move from GHRP-6, GHRP-2, or Hexarelin to the smoother Ipamorelin will
remedy this. If not moving the pre-bed dose to the morning often does.
• Minimalist- Dosing below saturation levels pre-bed i.e.: ~50mcg each of
a GHRP and GHRH
• Pre-bed Saturation- 100mcg of each GHRP (except Hexarelin) and
GHRH. Results in better overall health, recovery and well being. This is
a solid general anti- aging protocol.
• Pre-bed & Post Workout Saturation Dose- PWO serves protein
metabolism well and increases protein synthesis. Twice a day saturation
doses has increased recovery, contribution to anabolism, injury healing,
better well being and serious anti-aging properties.
• Pre-bed, PWO, and Morning Saturation Doses- The morning dose,
when fasted, engages the release of fatty acids which can be burned off
for energy during activity. Three saturation doses per day further
increases anabolism and decreases catabolism. Local growth factors
will rise including systemic IGF-1, but within physiological levels,
resulting in no enhanced health dangers, no abnormal organ or
structural growth.
There are more advanced dosing protocols but for simplicity they have
been left out of this text.
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Administration
For best results doses should be administered on an empty stomach (2 or
so hours after eating) or with only protein in the stomach. Fats and Carbs
blunt the bodies GH release. So, administer your dose, wait 20 minutes for
the GH pulse to reach its peak and then you can eat Carbs or fats without
having to worry about blunting the GH pulse. If dosing multiple times per
day allow at least 3 hours between administrations.
BPC 157 & Healing Your Body
What is BPC 157?
BPC 157 is a sequence of amino acids with a molecular formula of 62
carbons, 98 hydrogens, 16 nitrogens, and 22 oxygen atoms (C62-H98N16-O22).
Should you care to know the nitty-gritty speci cs, that comes out to a fteen
amino acid sequence of the following:
L-Valine, glycyl-L-alpha-glutamyl-L-prolyl-L-prolyl-L-prolylglycyl-L-lysyl-Lprolyl-L-alanyl-L-alpha-aspartyl-L-alpha-aspartyl-L-alanylglycyl-L-leucyl-;
glycyl-L-alpha-glutamyl-L-prolyl-L-prolyl-L-prolylglycyllysyl-L-prolyl-L-alanylL-alpha-aspartyl-L-alpha-aspartyl-L-alanylglycyl-L-leucyl-L-valine.
That's the long, fancy name for BPC 157.
BPC, for reasons you're about to discover, stands for “Body Protecting
Compound”. Your body already makes it in your own gastric juices in very
small amounts, where it serves to protect and heal your gut. But if you can
get the super concentrated version and get it into your system, it has an
extremely high level of biological healing activity just about anywhere you
put it.
What Does BPC 157 Do?
BPC 157 is surprisingly free of side effects, and has been shown in
research that's been happening since 1991 to repair tendon, muscle,
intestines, teeth, bone and more, both in in-vitro laboratory “test-tube”
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studies, in in-vivo human and rodent studies, and when used orally or inject
subcutaneously (under your skin) or intramuscularly (into your muscle).
Just take a look at the following, all of which was hunted down and
identi ed by Suppversity in their article on BPC 157. BPC-157 has been
shown to:
• Promote tendon and ligament healing by tendon outgrowth, cell
survival, and cell migration in a rodent model of Achilles tendon rupture,
and also when administered in drinking water to rats with damaged
medial collateral ligaments.
• Tendon-to-bone healing effective enough that they may actually
“successfully exchange the present reconstructive surgical
methods.”
• Counter the damaging effects of NSAIDs like ibuprofen or advil on
the gut lining so effectively that scientists termed BPC 157 “a NSAIDs
antidote” one of which they say that “no other single agent has
portrayed a similar array of effects."
• Repair the damage from in ammatory bowel disease (IBD) within
just days of oral administration in a rodent model of IBD.
• Help cure perdidontitis when administered in a rodent model of
periodontitis, signi cantly enough to have scientists conclude that “BPC
157 may represent a new peptide candidate in the treatment of
periodontal disease.“
• Reverse systemic corticosteroid-impaired muscle healing, in a
rodent models where BPC 157 was administered orally once daily for 14
days to rats with crushed gastrocnemius muscle. Similar bene ts were
demonstrated in a rodent study by Novinscak et al.
• Accelerate bone healing in rabbits who suffered segmental bone
defect before being treated with BPC 157.
BPC-157 is also known as a “stable gastric pentadecapeptide”, primarily
because it is stable in human gastric juice, can cause an anabolic healing
effect in both the upper and lower GI tract, has an antiulcer effect, and
produces a therapeutic effect on in ammatory bowel disease (IBD) – all
again surprisingly free of side effects.
As demonstrated in the research studies cited above, BPC 157 also
accelerates wound healing, and, via interaction with the Nitric Oxide (NO)
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system, causes protection of endothelial tissue and an “angiogenic” (blood
vessel building) wound healing effect. This occurs even in severely
impaired conditions, such as in advanced and poorly controlled irritable
bowel disease, in which it stimulates expression of genes responsible for
cytokine and growth factor generation and also extracellular matrix
(collagen) formation, along with intestinal anastomosis healing, reversal of
short bowel syndrome and stula healing – all of which can extremely
frustrating issues in people who have gut pain, constipation, diarrhea and
bowel in ammation.
So if you have frustrating joint pain that won't go away, some kind of
muscle tear, sprain or strain, or gut “issues”, you should potentially
consider using BPC 157.
How Much BPC 157 To Take
There is an abundance of research on BPC-157 and it has been shown to
be effective systematically when injected once daily at anywhere from
1-10mcg per kg of body weight. In most cases, this comes out to a dose of
anywhere from 200mcg up to 800mcg. Some report the most success
dosing twice per day with 250-350mcg for a total of 500-700mcg per day.
So as you can see, there's quite a bit of variability in dosage
recommendations.
How To Inject BPC 157 Or Take BPC 157 Orally
BPC 157 acts systemically.
• This means that whether you inject it subcutaneously – an easier and
more-pain free under-the-skin method that you should do as close to the
area of pain as possible…
• ….or you inject it intramuscularly – the more painful and teeth-gritting
version of essentially “stabbing” the needle into the muscle as close to
the injury as possible…
• …or you simply spray it into your mouth orally…
• …the BPC 157 going to render some amount of bene t in whichever
part of your body needs healing. To what extent is still unknown.
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Side Note: Datbtrue believed the best way of administration was to inject as
close to the injury as possible.
Subcutaneous injections are also relatively simple. You can either pinch an
area of skin near the injury site and thrust the needle into that pinched area
of skin.
Intramuscular injections will be the more painful option depending on the
location of the injury, but again, you will inject as close to the injury as
possible.
Oral administration of BPC 157 is quite straightforward. Just spray it into
your mouth (remember: very slowly to not damage the peptide), hold it in
your mouth for 90-120 seconds, then swallow.
How Long To Take BPC 157
Based on the current human studies to date, BPC 157 can be safely
administered for four weeks, followed by a two week rest. Again, this is just
using the data we have, some have used longer and not reported any ill
effects, but that doesn't mean there wasn't any.
Use In The Medical Field
Ok, so you may be now wondering why in the heck your physician,
physical therapist, surgeon, gastroenterologist, etc. hasn't told you
about this stuff.
Here's the deal: since BPC 157 is a completely natural gastric juice
peptides, it's technically not patentable, period. That means big pharma
can't make money off BPC 157, and that means it's not getting marketed to
your local doctor or hospital or anywhere else in the health care system. It's
also not available as an FDA regulated drug, or even considered to be
“sellable” for human use.
Studies and Other Links
• GHRP-2 GHRP-2 increases GH levels
• Human Growth Hormone
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• Insulin-like Growth Factor 1
• Melanotan II
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Side E ects
General
• Acne
• Erectile Dysfunction
• Estrogen Imbalance
• Gonad Atrophy
• Gynecomastia
• Hair Loss
• Hematocrit Increase
• Hypothalamic–pituitary–gonadal axis (HPTA) Shutdown
• Hypertrophic Cardiomyopathy
• Hypogonadism
• Hypothyroidism
• Increased Hematocrit
• Joint Pain
• Lactation (Galactorrhea) - caused by Hyperprolactinemia
• Liver Stress - caused by Hepatotoxic compounds
• Painful Back / Shin / Calf / etc. Pumps
• Lipid (HDL / LDL) Increases
• Spermatogenesis Changes
• "Test Flu" (See Below)
Trenbolone
• Decreased Respiratory Capacity and Treatment
• Insomnia
• Gynecomastia (caused by Hyperprolactinemia)
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Acne
Without Accutane
Why without Accutane?
Accutane has been connected not only to the short term side effects that
we all know of (stomach discomfort, dry skin/eyes/lips, liver effects, joint
pain) but also to severe, potentially permanent side effects such as: joint
pain, Crohn's Disease, Irritable Bowel Syndrome, depression, sexual side
effects, dry skin, nosebleeds, reduced healing ability, etc. Accutane is
structurally similar to Vitamin A, and most of these effects are related to
Vitamin A toxicity. Research Accutane side effects, and Vitamin A toxicity
before getting on Accutane. Accutane should be the complete last resort for
acne.
Steroids and Acne
Unfortunately, any amount of steroids is most likely going to increase acne
especially if you are predisposed to it. Some hormones will affect people
differently, some get more acne on tren, some test, some NPP, etc.
Regardless of E2, you will get acne from steroids.
Estrogen (E2) high or low can both cause acne (usually high, but large
uctuations are no good), and acne may result even from having normal
estrogen levels just due to the androgens in your system. Aim for
consistent E2 levels, this will lower your chance of acne the most.
DHT and Acne
Nizoral and Head & Shoulders are supposedly good for fungal acne,
although it may be hard to identify it as such though.
Ketoconazole or Nizoral are typical anti androgens. Get the bene ts of
stopping DHT from binding to the sebaceous gland without ingesting an
anti-androgen.
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Solutions
Lifestyle Habits & Washing Habits
Firstly, a great resource is acne.org and it's subsequent forums and this
includes much general consensus from acne groups.
Refrain from using harsh washes or activities that will increase
in ammation of the skin (#1 reason for acne). This means:
• Do not use alcohol, sulfates (soap), acne bead scrubs, overly drying
washes. instead use gentle cleansers, (acne.org has one), sulfate
free, and wash your face very lightly and splash water to wash it
off. PAT to dry DO NOT scrub.
• Do not touch, scrape, or pop your acne. Don't run your dirty ngers over
your acne. Do not spend time pushing out plugged comedones, black
heads, white heads. Do not excessively press and pop pimples that are
not popping, even if the end result it pops. If it takes more than 15
seconds for it to pop, leave it alone until its ready instead: if you must,
only pop pimples that are easily popped and ready with clean
hands right before you wash it. A warm shower can make it easier
to pop but scalding hot water may be negative to skin moisture.
However it is more ideal to never pop pimples
• Do not sleep on dirty bedsheets or pillow cases. Do not re wear dirty
shirts, or continue wearing a gym shirt that you just worked out in.
instead, shower/rinse immediately after gym and put on a clean
shirt. If you go home after gym and shower that is usually ne too.
Replace bedsheets 2x a week and pillow cases EOD ( ipping the
pillow after the day to get double use)
• Do not excessively wash your skin, it leads to over-drying. If possible,
wash your back/face with a gentle wash 1x a day at the max. If you
need to take a second shower before bed due to general day sweat,
rinsing with water and wiping with hands is completely ne.
Washing
• As counterintuitive as it sounds, over washing can lead to acne. Your
aim should be to maintain a certain level of stability with your skin. This
means over-washing will dry out your skin and cause acne. You must
completely avoid normal soap and sulfates.
• Consider a salicylic acid wash or benzoyl peroxide wash (the OG
proactive uses this) and using 1x a day max. If they dry out your skin
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stop for a couple days. Some people nd success with a benzoyl
peroxide wash, but I think salicylic acid is better as benzoyl peroxide is a
generally better treatment for leaving on skin. Others have the opposite
opinion.
• Consider washing your back with no soap at all if you haven't gotten
extremely dirty. Your body maintains a natural ph and good bacteria that
lessen the ability for bad bacteria to colonize and from acne. Simply
rinsing off and not washing at all can do wonders due to the reduced
in ammation on your skin.
• Wash lightly, do not scrub, do not rub hard. Your objective is to clear the
previous medicine from your skin and remove any layer of acne
promoting containment on your skin. (Bacteria from sweat, pollution,
clogged pores, etc.)
Treatment
This is where it gets to the good stuff.
Test all medications rst in a small part of skin before dousing
yourself with it. Benzoyl Peroxide and Azaelic Acid tend to be the
biggest culprits of redness, as well as Differin to a lesser extent.
• Adapalene (brand name Differin) is a 3rd generation retinoid that
speci cally targets the mechanisms that produce acne. It prevents the
formation of comedones by 50-60% according to studies. Retinoids are
structurally related to Vitamin A - and Accutane is a retinoid. Adapalene
(Differin) is a topical retinoid and since being applied to the skin it does
not absorb through the blood stream (as shown by studies signi cantly
insigni cant amounts get through). So, you're basically taking topical
Accutane. Adapalene (Differin) has always been the most effective acne
medication for me in permanently reducing the amount of acne I get,
and after a year of diligent use in my teens I never got pimples anymore.
Additionally, Adapalene (Differin) increases the ef cacy of other popular
acne treatments such as topical Clindamycin and Benzoyl Peroxide.
• Benzoyl Peroxide 2.5% (gel version is best) - there is no evidence
that stronger concentrations are better, and they generally just dry out
the skin more. Benzoyl Peroxide is the holy grail of treatment because
bacteria never get resistant to it. It provides an oxygen rich environment
that is impossible for bacteria to live in. Issues with BP = sensitivity to
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•
•
•
•
•
sunlight, redness on skin, allergic reaction (under 5% have this) so
take away = start slow when using benzoyl peroxide, EOD at rst, then
ED. 2x a day if your body can handle it. It also bleaches clothes, so if
you put it on before putting on clothes you need to let it dry, and
probably have a white t shirt/white sheets.
Topical Clindamycin: Clindamycin is a popular antibiotic, but when
used topically for acne treatment it signi cantly boosts the ef cacy of
Adapalene and Benzoyl Peroxide. However, tolerance increases pretty
quickly, and I only recommend using it when a breakout occurs, or for
spot treatment of speci c pimples. It's useful l usually sold in
combination with Benzoyl Peroxide 5% but it's in your interest to get it
separately because 5% Benzoyl Peroxide is over drying and this way
you can regulate your tolerance to it
Curology (prescription) 4% Azelaic Acid. (precursor to Salicylic Acid)
1% Clindamycin, 4% Nicotinamide. I've read good things about this
from skin care addiction but have not used myself. Studies show
Nicotinamide being as effective as 1% Clindamycin without resistance.
Salicylic Acid option: a slightly weaker option than Benzoyl Peroxide,
but still effective. Be sure the lotion it's mixed with is quality and you
might nd something useful. You might be better off nding it in pure gel.
However Benzoyl Peroxide has shown in studies be more effective and
the combo treatment with Differin is promising.
Jojoba Oil: widely considered the best type of oil to moisturize your skin
because it is very similar to the natural oils that we produce. It's a
favorite on /r/skincareaddiction
Zinc 20-50mg for 3 days after breakout you can't stay on high zinc
forever, but doing this has been found to be effective. Lots of anti
in ammatory properties in Zinc. 10-20mg is about a maintenance dose.
It's good to use Zinc-Carnosine complex, because it has the added
bene t of restoring stomach lining and reversing damage from spicy
food etc. No heartburn for some.
Side Notes
Adapalene (Differin) used to be prescription only, but is now available over
the counter. It also comes in a mixture formula with Benzoyl Peroxide
called Epiduo, but it is still prescription only.
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Clindamycin is prescription only. Benzoyl peroxide can be found anywhere.
For all of these drugs you should be aiming to get the gel versions. If you
go to your dermatologist and ask for them, you should probably be able to
get everything that you want.
Adapalene (used rst) followed by Clindamycin, and Benzoyl Peroxide, is
the holy trinity of destroying acne. If using these 3 medications is causing
you to get overly dry skin, you probably want to drop everything but always
continue Adapalene usage as it improves your skin over time and reduces
your ability to create new comedones. If you can only take Adapalene 1x a
day is ne. 2x is better. It's better to use a thin layer of it everywhere (more
just over-dries) if your skin is sensitive from overuse, just spot treat with it
for a while but you really want to throw it on everywhere
Moisturizing
Use a non-comodegenic moisturizer. The oil you should be using on your
face is Jojoba Oil. Cetaphil and CeraVe make great facial moisturizers. Use
these after treatment in combination with Jojoba Oil, if Jojoba Oil is not
enough.
Dietary Factors
• Many people swear that cutting out Dairy reduced their acne.
Considering the amount of hormone derivatives pumped into cows, it is
a reasonable assumption. Since many of us are putting hormones into
our body anyways, it might not matter, but most people get reduced
acne from cutting out Dairy.
• Cutting out Sugar & Fructose can reduce acne. Inconsistent blood sugar
levels are related to acne, and high amounts of sugar provide a good
environment for bacteria to proliferate. Try it out.
• Eating more veggies. Try it out, it might help.
Generally diet cannot cure acne on its own, but if it helps, it's worth it. If
something you're eating is creating acne, it's probably not something you
want in your body anyway.
Summary
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In summary, if you get anything out of it: GET ADAPALENE (DIFFERIN)!
it's the most effective treatment for preventing further acne (and reducing
current). It's basically topical accutane.
With Accutane
Introduction
Isotretinoin (Accutane) is primarily used to treat bad cases of cystic acne,
and to help the skin more rapidly renew itself. In addition, it is used in rare
cases for certain skin cancers and skin diseases. It is a type of retinoid,
which is naturally found in the body in small amounts. In the USA, it’s a
prescription drug, but it is sold over the counter without a prescription in
many countries.
Bodybuilders who use anabolic steroids have utilized Accutane to
counteract the negative effects of steroids on their skin; especially, the acne
related side effects.
When other treatments fail, Accutane becomes the last resort to help
combat acne issues
How it Works
Accutane works as an isomer of Vitamin A, which reduces the amount of oil
released by the oil glands in the skin; this will make it dif cult for acne to
form and reduce it signi cantly. Nearly all patients achieve clearing of acne
during a course, with 90% reporting ‘excellent’ results with higher dosages.
Those that choose to dose low will have results with diminished side
effects, but run the risk of recurrence.
Bodybuilding
Since chances of acne are increased with anabolic steroid use, and
bodybuilding requires looking good (especially physique competitors),
many athletes who have failed to conquer their acne with natural remedies
will turn to Accutane.
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It is the androgenic increases associated with steroids that will trigger
increased acne. This is especially true for those genetically prone to the
condition. Also, the hormonal changes can trigger acne as well, such as
increased testosterone levels.
Side Effects
High doses of Accutane will result in vitamin A toxicity, which will result in
both permanent and temporary side effects.
Permanent and temporary side effects such as :
•
Stunted growth: The FDA, in 2010, stated the drug may stop bone
growth in teenagers still growing
•
In ammatory bowel disease: Some studies have linked this drug to
causing Crohn’s disease
•
Eye changes: Decreased night vision and dry eyes have been
reported
•
Other issues like skin problems, hyperostosis, and birth defects (in
pregnant women) have been reported
•
Psychological effects, particularly depression, seems to be a
common, but that has yet to be proven in studies
Dosage
Among bodybuilders, the dosage should be conservative. Once a day dose
of 10-20mg for 6-8 weeks (some need more, some need less), depending
on severity, should work ne, but you can extend it necessary. Some users
suggest using Accutane 10-20mg 2-3 times per week when coming off
cycle or dropping to a cruise dose of Test; to prevent acne sides if you're
susceptible to it. Among the general public ghting acne, a dosage of
50-150mg per day may be prescribed by their physician. It is a good idea to
take the drug with a large meal.
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Blood Pressure
Jcaesar369's Original Blood Pressure Medication Post: Here
TL;DR Version
• Blood Pressure (BP) is a complex vital sign, and cannot be easily taught
and all encompassed within even several pages of text. You could take
an entire semester long course in college learning the physiology of
blood pressure and still not know everything about it. The point of my
post and this section of the wiki is NOT to completely educate anyone
about BP, but to teach anyone willing to learn how to (fairly) easily
manage their BP on their own without a doctor (although if you feel
comfortable going to your doctor to get BP medication while on AAS,
then by all means please do) and know a thing or two about what they
are doing.
• Different steroids WILL require different BP medications
• Trenbolone: This is where you will want Nebivolol 5 or 10 mg every day
(or higher if need be, 20 mg being the highest you should ever go).
Nebivolol is a selective (the most) beta blocker that will slow down the
increased Heart Rate (HR) you experience on tren. As a beta blocker,
Nebivolol is a bit more dif cult to use than other BP medications, as it
will require a taper off period.
The taper is SIMPLE.
Example: You are on 10 mg Nebivolol every day.
Week 1 of the taper you will take 10 mg Nebivolol for 4 days, then 7.5 mg
for 3 days
Week 2 you will take 7.5 mg every day
Week 3 you will take 5 mg every day
Week 4 you will take 2.5 mg every day
Week 5 you will take 2.5 mg every OTHER day
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This taper guideline is a GENERAL EXAMPLE and can be customized to
t your own needs, but every taper should look fairly similar to this. Larger
dosages will take longer to taper off of.
• All other steroids: Use a simple ACE I such as Lisinopril or an ARB such
as Losartan every day to manage BP. These drugs help the kidneys and
liver function better as well. If this does not cut it, you must read my
above post to consider duplicate (2 drugs) or triple therapy to manage
your BP.
• Disclaimer: all of the above from me are just RECOMMENDATIONS and
ADVICE. I am not a doctor nor a medical professional, and you should
trust their judgment (but also use your own) when managing your life
and BP. If you do not feel con dent that you know how to take BP meds
after all your research, ask in the Ask anything threads for help, or go to
a real doctor. Do not take them blindly.
More on Blood Pressure
• Taking your BP once a day is not enough, as this is only a time snapshot
of what is occurring in your body. You want to take your BP 2-4 times per
day. Ideally once in the morning, once in the afternoon, once before bed.
The more the better.
• When you take your BP, the rst reading doesn't count. You could be
anxious, nervous, what have you. Take your BP a total of 3-4 times, with
the rst time not counting. Write down each reading, and average them.
This is your current BP at that time.
• Take your BP after 5 minutes of sitting and relaxing, doing something
that calms you down. Watch a funny TV show, read a book, meditate,
sudoku, whatever tiny little hobby you like. Heck read some reddit. You
want to be seated, straight up, back against support like a good chair,
both feet planted at on the oor. Your arm should be rested on a table
of appropriate height, with your elbow 100% supported and you are
giving no though or energy to keeping your arm up. Use a BP machine
on your upper arm (no wrist ones) to take the readings. Make sure the
cuff you are using is large enough.
• BP should be managed FIRST with cardio done 5-7 days per week (the
more the better) and an active healthy lifestyle and diet low in sodium
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and caffeine and ZERO other drugs of abuse. BP can then be
attempted at management with supplements, such as CoQ10, hibiscus
tea, Garlic extract, etc etc the list goes on. These supplements do very
little/basically nothing for MOST people who are natural. Imagine how
much they actually do for people on steroids, with AAS induced HTN.
Most people on AAS are likely to encounter some time period that they
need or should be on legitimate BP medications. Do not feel like you are
a loser because you need real BP meds while on AAS. However,
de nitely try cardio and adding 1-2 supplements to your daily regimen to
see if they help you before admitting defeat and taking real BP meds.
• Hypertension (HTN or high blood pressure) is known as the silent killer,
because you may never know you have it but it is very bad for your heart
and body and organs. There is a way to possibly be able to tell your BP
is high without taking it: when you lay down at night and everything is
dark and calm and you are rested, and you can feel your veins pulsing
and beating in your head or ears when you're on the pillow, this is a
plausible indicative sign your BP is too high, and you should start using
a real machine to monitor it.
Cialis For Blood Pressure
Cialis (Tadala l) DOES NOT lower BP. AT ALL, EVER. Anyone who tells
you otherwise is lying, right to your face, or otherwise ill informed. Read my
submitted post above for a full explanation on this.
Package insert for Cialis, FDA approved.
Taken directly from page 7:
Effects on Blood Pressure
Tadala l 20 mg administered to healthy male subjects produced no
signi cant difference compared to placebo in supine systolic and
diastolic blood pressure (difference in the mean maximal decrease of
1.6/0.8 mm Hg, respectively) and in standing systolic and diastolic blood
pressure"
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Until someone shows you scienti c data done on many people showing
proof that Cialis lowers blood pressure, don't believe it. Do not attempt to
use Cialis to control BP.
Gynecomastia
See The Estrogen Handbook
Lactation (Galactorrhea)
Preventing
When you're wanting to preventatively take action against prolactin, a
Dopamine Agonist may not be the best choice to start with as they come
with many unwanted sides and can be harsh drugs. You should always
have a Dopamine Agonist on hand if you wish to take a 19-Nor, but if you
wish to run something preventatively, you should start with some
supplements.
Supplements To Help Control Prolactin:
PLEASE READ: Prolactin-Inhibiting Supplements Wiki Page
• Vitamin B6 (Pyridoxine Hydrochloride & P-5-P) - To lower prolactin
levels it's recommend you take 50-200mg of P-5-P a day, in divided
doses. If you want to take regular B6, which can sometimes cause
minor side effects, take 300-1000 mg per day in divided doses.
Read the label before you buy B6 (if you choose not to get P-5-P),
because the Pyridoxine Hydrochloride type of B6 (in most
supplements) has been shown to be a prolactin inhibitor, but
Pyridoxal Hydrochloride has been shown to be ineffective at
lowering prolactin – make sure you buy the right type!
• Vitamin B6 - Examine Page
• Vitamin E - When using Vitamin E as a prolactin inhibitor, it's
recommended that you take 300-400 IU per day of natural Vitamin E –
this can be raised up to dosages such as 1000 IU for greater prolactin
control, but be aware of the possible side effects outline here
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Natural Vitamin E is labelled D-Alpha Tocopherol whereas synthetic
is labeled DL-Alpha Tocopherol – the natural form works best. DAlpha Tocopherol with mixed natural tocopherols or D-Alpha
Tocopherol with mixed natural tocotrienols are the absolute best
forms to take.
• Vitamin E - Examine Page
• SAM-e - Take 400-1200 mg a day of SAM-e along with Vitamin B6 and
Vitamin E. An added bonus is SAM-E's ability to detoxify the liver.
• SAM-e - Examine Page
• Other Effective Prolactin-Inhibiting Supplements
Remember, only use your Dopamine Agonist if blood work shows elevated
levels or if your nipple(s) leak ON THEIR OWN. Do NOT squeeze your nips
and force liquid out, even natural guys can do this, by doing this you will
stimulate and cause an increase in prolactin.
DO NOT TOUCH YOUR NIPS.
Stopping Lactation
See Estrogen Handbook
Liver Stress
Here are some of the most common signs indicating you may have a
serious liver issue. Warning signs usually appear in the following order, with
the later signs being the most serious:
• Reduced appetite
• Nausea and fever
• Excessive Itchiness
• Yellow eyes or skin (jaundice)
• Very dark urine (dark amber colored)
• Bloody stools
Waiting for all these signs to appear means you have waited too long. You
want to take action BEFORE these signs appear.
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Preventing
See Liver Protection
Painful Pumps
Sometimes when you use AAS (especially some orals) you can get painful
back / shin / calf / etc. pumps.
The rst line of action should be:
• Taurine (3-10g pre-workout, you may also add 3-5g AM/PM depending
on when you workout)
• Magnesium (200-500mg pre-workout, you may also add 200-500mg AM/
PM depending on when you workout)
• Potassium (200-300mg pre-workout, you may also add 200-300mg AM/
PM depending on when you workout)
• Upping your water intake (1-2 gallons ED)
If none of this helps, anecdotally, Cialis (10-15mg ED) has been known to
help.
"Test Flu"
First, what is “Test Flu”? It is not an of cial diagnosis that a physician would
label, but a term that is associated with the u because of the similarity of
symptoms. The symptoms have a rapid onset. Often starts with the onset
of low grade fever, headache, fatigue, and body aches. Not in that exact
order or even all the symptoms listed may occur. Listed below are a few
symptoms you may be experiencing:
• Fever (low grade)
• Severe aches and pains in the joints and muscles
• Generalized weakness
• Fatigue
• Headache
• Dry cough
• Sore throat and watery discharge from your nose
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“Test Flu” varies from individual to individual based on their immune
system. It’s the inter-correlation between your immune system and your
endocrine. If you overload one then the other responds unfavorably. It’s
your body’s auto immune response to the foreign substance that has
entered your body and caused and in ux of hormones. Your body sees the
large increase as foreign and tries to get rid of it. Triggering an
in ammatory response and raising you metabolism. Once your body builds
its resistance to it, the symptoms relieve or even resolve. This usually takes
a week or so.
Really there isn't much you can do besides wait it out, but here is an OTC
remedy:
• Emergen-C (or just Vitamin C) - 4000mg split the dose ½ in the AM, ½
in the PM
AND
• Zinc - 100mg - split the dose ½ in the AM, ½ in the PM
Do this for a week and drop the dosages in half until symptoms
subside.
Drink plenty of water to ensure hydration which will also aid in
recovery.
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Bloodwork
If you're going to use anabolic steroids—or any type of performance
enhancing compounds—it's important to run bloodwork at least three to
four times per year. It's like getting your pool water checked to make sure
there is the right amount of chemicals for it to stay clear and problem free,
or checking the air pressure in your car's tires to ensure you don't have a
blowout at high speed on the freeway.
What's more, it would be a good idea to get bloodwork before cycling, so
you can know where your baseline is and ag any problems ahead of time.
For example, you might have elevated liver values from some other
medication or health issue. You could have elevated blood glucose levels,
indicating you're pre-diabetic.
It's far better to know these things in advance and get them treated as soon
as possible. If you know about any red ags beforehand it will help prevent
even bigger issues, such as when you have elevated liver values when
running a harsh oral steroid. Or you may have high estrogen going into a
cycle, so you may want to reduce your levels, or avoid using excessive
aromatizing compounds.
When you use anabolic steroids, the pituitary glands of the HPTA axis react
to exogenous hormones by going dormant. As a result, your LH and FSH
levels will quickly drop to near zero, and your body will no longer produce
Testosterone on its own.
Further examples of effects on bloodwork include:
• Testosterone, Dianabol, Nandrolone can increase Estrogen (E2) levels.
• Trenbolone can quickly strain your lipids and cortisol levels.
• Equipoise (EQ, Boldenone) is known to cause elevated RBC (red blood
cell) counts.
If you want to use AAS safely, bloodwork is essential.
• A pre-cycle check will warn of any potential reason not to use AAS and
give a baseline for comparison later on.
• A mid-cycle check will show things at their worst from a health
perspective.
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It's good to have a baseline knowledge of individual health markers, so be
sure to check out our Health Markers page.
How Do I Get Bloodwork?
There are two principal ways to get bloodwork done.
1. The most common is to request bloodwork from your doctor, give him/
her a list of things you want to get done, and s/he will send you to the
lab. Some hesitate to do this, as they're afraid of potentially being
agged as a steroid or drug abuser, and they don't want it to potentially
affect their health insurance or employment options.
2. A popular second method of getting bloodwork is ordering it online. This
way you independently pay for what you want done, and then take the
printed request forms to a private lab.
What Bloodwork do you need before Your First
Cycle?
When ordering online, you can usually nd a Standard Male Hormone
Panel.
This typically includes:
Androgens — You'll need a baseline for your HPTA axis to know if you're
already hypogonadal (low T levels), as well as if you've recovered fully after
your PCT.
• LH/FSH: These gonadotropins stimulate the testes to produce
testosterone.
• Testosterone, Free Testosterone: Free testosterone should be
measured directly, not calculated.
• SHBG (Sex Hormone Binding Globulin): binds to Testosterone in the
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• A test after completing PCT can ensure things have returned to normal.
• For those that Blast & Cruise (B&C), it's important to run bloodwork at
least 3-4 times per year to ensure health levels are stable and not
declining or anomalous for any reason.
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• Estradiol: E2 is affected by aromatizing hormones. It's good to know if
it's high when going in, and when dialing in AI mid-cycle.
Basic Health Markers — These are important to know that you're
generally healthy going into the cycle.
• CBC (Complete blood count)
• Lipids (LDL/HDL): AAS aren't good for cholesterol levels. You'll need a
baseline to ensure you're healthy going in.
• Liver function (AST/ALT/GGT/Bilirubin): These are mainly important if
you're planning on orals. You want to be sure your liver is healthy going
into the cycle.
• PSA (Prostate Speci c Antigen): If this is elevated you could have
prostate cancer. If you have prostate cancer and take androgens, it's like
throwing gasoline on a re. Ensure levels are normal prior to starting any
AAS.
• Insulin, Glucose: you'll want to ensure you're not pre-diabetic.
Not too complicated, right?
Where To Get Private bloodwork
There are many services through out the world that provide individuals the
capability to get private paid bloodwork. These services are invaluable to
AAS users to monitor health and safety.
In the USA
There are several providers in the USA to choose from.
Note: Unfortunately, testing is unavailable in NY, NJ, MA, MD, and RI. If
you're a resident of one of these states you'll have to drive Out-of-State to
use Private MD Labs, LabsMD, or any other private lab. Instructions Below.
MA & MD residents only: You can use Health Tests Direct.
Private MD Labs
Private MD Labs — A good and trusted lab with many locations.
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• Hormone Panel with Estradiol Sensitive and Testosterone LC/MSMS Same as above, but with LC/MS estrogen test. Use this to get an
accurate estrogen reading while running Trenbolone. DO NOT use this
to test whether your tren is counterfeit, as it will not count it in the
estrogen test.
• Anything with Test 070195 will show the actual value for testosterone,
rather than “high” or “greater than 1500.”
• Thyroid TSH, T4 and T3 Panel optional, check thyroid levels if you
suspect anything wrong with them.
• Liver Panel This test is important if using oral steroids. This is included
in the Hormone Panel for Females. You do not need to order it
separately.
• Lipid Test to check cholesterol levels
• Anything with Test 303756 contains a lipid panel.
ULTA Labs
• ULTA Labs offers affordable bloodwork nationwide. Secure and
con dential lab testing, most results available in 1-2 business
days. Licensed Medical Director in every state that reviews each
order.
Synergistic Labs
• Synergistic Labs started November 2021 and is growing
quickly in the tness community. They provide fully customizable
lab orders through their site. They service every state except
NY, NJ, and RI.
LabsMD
• Hormone Panel for Females will provide the actual number for
testosterone rather than "> 1500". The assay used for testing
estradiol will not give a false reading when using tren.
Walgreens
• Cholesterol tests are available at most locations.
Bloodwork for residents of NY, NJ, MA, MD, & RI
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1. Add the tests needed to cart.
2. At checkout, select a LabCorp / Quest location to go to that is outside of
your state.
3. If applicable, apply coupon code (Google search for a 15% coupon
code for Private MD Labs) This should give the price needed to pay for
the tests.
4. In a new browser tab, buy a gift certi cate of that amount on the Private
MD Labs or Labs MD website. Using a credit/debit card with a NY, NJ,
MA, MD, or RI billing address should work here.
5. Use that gift certi cate code to pay for the test. NOTE: Some report
being able to skip Step 4 and just pay using their credit card, even if the
billing information is a NY, NJ, MA, MD, & RI address.
6. Leave credit card info blank. Put in both Billing Information and Patient
Information with your own name, but with an address outside of your
state. Others put a out-of-state relative's address (with their permission)
with no issues. Nothing should be physically mailed to that address
either . . . Billing address shouldn't matter since you didn't put in credit
card info, but they ask for it anyway.
7. Print requisition papers. You may optionally (but recommended) set up
an appointment for your desired out-of-state LabCorp / Quest location.
8. Show up to the LabCorp/Quest location. If asked for ID it's reportedly
ne to show your NY, NJ, MA, MD, & RI Drivers License. Alternatively,
others have used Passports, Work or School IDs, etc.
9. Wait to be emailed the lab results.
For Discounted Labs
1. Make an account and order desired labs on discountedlabs.com
2. Print requisition papers. You may optionally (but recommended) set up
an appointment for your desired out-of-state LabCorp / Quest location.
3. Show up to the LabCorp / Quest location. If asked for ID it's reportedly
ne to show your NY, NJ, MA, MD, & RI Drivers License. Alternatively,
others have used Passports, Work or School IDs, etc.
4. Wait to be emailed the lab results.
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Australia, New Zealand
Bloodworks.info — Regardless of whether you get your bloods done by
your local doctor or by an online service, you can get expert interpretation
of blood tests at Bloodworks.info.
United Kingdom (UK)
Medichecks
Medichecks
Blue Horizon
Blue Horizon Medical
Canada
Ontario
If you live in Ontario you can use GetMaple.ca to easily talk to a doctor and
get a requisition form for bloodwork. It's $50 to talk to a doctor online. You
show your health card, tell them you're on steroids, answer their questions
and tell them what you want to have checked. They email you a requisition
form in a few minutes that you can take to a life labs or similar.
Info Taken From This Post
The Following are all anecdotes taken from the thread linked above:
• In Ontario? Go to an Appletree clinic and say you want bloodwork. That
easy. They also run acne clinics and oversee and prescribe Accutane.
Dudes take good care of us.
• Worth saying, just go to a walk-in. Say you're on steroids, don't be
embarrassed, literally no one cares. Is there a chance you encounter a
doctor who says SHAME and refuses to give you healthcare? Sure.
Less likely than them just covering their asses and checking your shit.
Maybe you won't get uncapped Test levels, but you'll get your lipids and
liver enzymes checked.
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New Brunswick
• In New Brunswick. I don't have a family doctor, so I went to a
walk in clinic and told the doctor I was planning to go on
steroids, and wanted bloodwork done. He lled out a bloodwork
order form that I could take to the hospital, or to a walk-in blood
clinic. After a couple visits, I asked for the order to be made a
recurring one. So now I can just stop in at the walk-in blood
clinic (they charge $14 to draw) and they'll use the order they
have on le and send it to the hospital lab. Lab results get sent
to the doctor that ordered them. I generally don't go to the clinic
to review results, I go to the personal health records of ce at the
hospital and request a hard copy of the results. They print it out
and hand it over to me.
British Columbia
• In BC but this should go for anywhere in Canada (Naturopaths
cannot order blood tests in New Brunswick). Go to a
naturopathic doctor, they can request blood tests. Most bene ts
packages include visits to naturopaths, so it's in a way almost
free.
Montreal
• I'm in Montreal, and i just went to a doctor, walk-in clinic and
asked for blood test, the reason if I remember was test booster,
feeling moody. He gave me a paper with the test he wanted
checked, i checked the rest, didn't get in trouble.
Quebec
• In Quebec. I went to my doctor and basically told her I was on
and explained why bloodwork was important for me to stay safe.
If the doc is reasonable they will hook you up, if the doc is hardheaded (the rst doc I tried was like this) then just go to another
doc. The thing that sucks is that you can't get bloods as often as
you'd like because the doc probably won't think its necessary.
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• I go to a medical clinic in Ottawa (Sandy Hill Clinic) that has
large numbers of drug users. Every big town or city has one.
Just look up HIV Prevention on your cities web site. There they
practice "Harm Reduction" so when you ask a doc for any test in
order to reduce harm, they will do it eagerly.
Alberta
• Honestly I just kept asking ... This is in Alberta btw. Ended up nding
someone at a walk in clinic (Calgary) willing to write me up for what I
wanted.
• In Alberta i went to a walk in with the whole im tired etc thing to get my
rst bloods. Eventually i got sick of making excuses so i just told him
what im going to be taking and that i wanted regular bloodwork to
monitor health. Very understanding no lecture nothing he just said ok
whatever you need on the panel let me know and i will give you req
sheets for it. When you want more bloodwork just make an appointment.
Now i just go to him when i need bloodwork and he's also my family doc
now as well.
• I went to a walk-in clinic. Told the doctor I want a sheet for SELF PAID
bloodwork. Tell them your interested in having your hormones check
because you feel rundown and you just want to see for your piece of
mind. Photo copy it and keep re using it. The costs for self paid test vary
place to place and Provence to Provence. In BC a testosterone test from
a lab cost $80. In Alberta labs charge $45 and the universities charge
$22. Shop around and check your local university for pricing . There is
single collection fee aswell each time you go, in Alberta it's $25. If the
doctor puts their info on the sheet get a new slip from another doctor or
they'll keep being sent your bloodwork and your history will show up. If
your tight with your doctor they won't mind. Be aware your bloodwork is
not private and will be sent to provincial data bases for physicians to
access. It may be possible for self paid bloodwork to be request not to
appear in databases. However my self Paid blood has.
• AB here. I go to a Naturopath to avoid getting labeled a drug user on my
medical le. Work bene ts cover 2 blood tests /yr.
• Related top-level thread on Canadian bloodwork
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Ottawa
Potential Route: Go to a walk-in clinic. When the doc comes in, say you
are taking a Test booster, you feel moody, and your nipples are sensitive. S/
he will send you for a blood test. Make sure you say your nipples are
sensitive or s/he wont check the E2 boxes on the form. These forms are
good for a year, so once you have them, just give blood when you want.
Additional Notes
If running Trenbolone ...
When running Tren, if you get your Estrogen (E2) levels checked, make
sure to get the LC/MS sensitive estrogen reading. Why? Most estrogen
tests are ECLIA or RIA. These will count tren as estrogen. This will give you
a false estrogen reading if you are trying to dial your AI in. The only time
you may want the ECLIA or RIA method is when you wish to see if there
actually is Trenbolone in a vial that you believe to be Trenbolone—but this
shouldn't be necessary, right? You wouldn't work with a source you don't
trust, would you?
Tren has negative impact on the following that you should check if running
it: Liver Function Tests (LFTs); fractionated cholesterol (HDL/LDL), AST/
ALT/GGT/Bilrubin (liver hormones that show how well things are
functioning).
Haematology: Measures haemoglobin, red blood cell numbers and size,
as well as distribution of white blood cell types.
Electrolytes and LFT's: gives information on liver and kidney function.
Fractionated cholesterol: HDL/LDL ratio and triglycerides.
Iron studies: Total serum iron, transferrin levels (the carrier protein) and
ferritin (the tissue storage protein).
Thyroid Function Tests: T3, T4, Thyroid Stimulating Hormone (TSH) will
tell you if there are any problems with your thyroid.
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Cortisol: If your stress hormones are elevated it could point to other as-yet
undiagnosed preexisting disorders or conditions. Tren has a tendency to
elevate cortisol levels.
hGH, IGF-I: Only necessary if using hGH or hGH releasing peptides to
measure effectiveness. A moderate rise will be seen with AAS use alone.
hGH stands for human Growth Hormone, a 171 amino acid polypeptide
hormone released from the Anterior Pituitary gland in the brain. Its release
is controlled by at least two hormones from the Hypothalamus...GH
Releasing Factor and Somatostatin. GHRF stimulates GH in a pulsitile
manner, while Somatostatin inhibits it's release. IGF-I, which is released
from the liver into the circulation in response to GH release, is also thought
to inhibit GH release in a negative feedback loop.
IGF-I is thought to mediate many of the effects of hGH. In response to
hGH, muscle and many other tissues, can make their own IGF-I inside the
cells. The resultant IGF-I synthesis effects both neighboring cells, and the
cell itself via the Akt pathway (autocrine/paracrine secretion). Some of
those neighboring cells in muscle are satellite cells, which are stem cells
present inside the muscle sarcolemma, but outside of the actual muscle
cells. IGF-I has the effect of increasing their number, and to differentiate
(change them) into muscle cells. The satellite cell changes into a myoblast
(primitive muscle cell) which then fuses into an existing bre (particularly an
inured one) and donates its nucleus.
When a muscle has to grow or repair, it requires more DNA which is
donated by the satellite cells. This is to keep the protein/DNA ratio constant
as a cell grows. Skeletal muscle is unusual in that it is a multi-nucleated
cell. This is thought necessary as skeletal muscle cells are so relatively
large that one nucleus could not adequately serve the whole cell.
The effects of IGF-I administration for bodybuilding purposes are
controversial in terms of ef cacy of low (microgram) dosages. In clinical
trials it has been used in the range of 8-10 milligrams per day. There seems
to be a great disparity here between anecdotal reports and published
studies.
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Related Posts
Reddit thread: So you got your bloodwork, but what does it all mean?
If you run Tren, you should include bilirubin on your bloodwork.
Blood Values Sorted By Mass and Molar
Concentration
View Full Size
Research topics (to be moved)
GHRP's: GHRP's are peptide hormones (short chain of amino acids) that
stimulate either directly or indirectly hGH release in humans. GRP6 or
GHRP2 are relatively short acting, while CJC1295 is longer acting. GHRP6
stimulates Gherelin release, resulting in hunger. GHRP2 does not have the
same effect on Gherelin, but like GHRP6, it elevates cortisol. Ipamorelin
stimulates GH release without the increases in Gherelin and cortisol seen
with the others.
Myostatin Inhibitors: Myostatin is a protein hormone that stops muscle
growing too big. It is thought that most organs, including skeltal muscle,
have a speci c growth regulating protein. In Skeletal muscle, that is
myostatin or GDF8, Growth and Development Factor 8. So if myostatin
stops muscles from growing too big, why not suppress or inhibit it? There is
much research to try and accomplish this in humans without side effects.
There are three viable methods for myostatin inhibition.
• First, there is the antibody approach. This entails injecting a monoclonal
(very speci c) antibody into a subject, which will bind to, and tie up
circulating myostatin levels. See MYO-029: Stamulumab).
• Second, there is the “small molecule approach” that use inhibitors of the
myostain receptor, such as SB 431 542 and GW 788 388. These
receptor inhibitors act in a similar manner to Nolvadex as a blocker of
the estrogen receptor. It won't reduce the amount of myostatin, but it will
block its effects at the receptor level.
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• Third, there is the use of a soluble portion of the receptor (ActIIb
receptor), which mops up myostatin in the blood and acts essentially as
a binding protein for myostatin. Analogous to SHBG, which we are all
familiar with, which mops up (binds) testosterone and its analogues in
the blood. ActIIb receptor binds too and deactivates myostatin. The
Activin receptor and the Myostatin receptor are essentially the same
thing.
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Health Markers
Individual Heath Markers De ned
Alanine amino-transferase (ALT)
An enzyme produced primarily in the liver but also in other tissues. ALT is
involved in amino acid and protein metabolism. Used as a primary marker
of hepatic strain. Also called Serum Glutamic Pyruvic Transaminase
(SGPT).
Albumin
The main protein that circulates in the blood. Produced in the liver and has
antioxidant properties. Transports certain hormones, vitamins, and
minerals, and plays a role in water balance. Used as an indicator of liver
health. Higher levels are optimal.
Alkaline Phosphatase (ALP)
A family of cholestatic enzymes produced mainly in the liver, but also in the
intestines, kidneys, and bone. Used as a marker of hepatic strain, often
relating to disease of the bile ducts.
Apolipoprotein A-I (apoA-I)
A constituent of HDL (good) cholesterol, apoA-I is responsible for initiating
bene cial reverse cholesterol transport. This process pulls cholesterol
particles from the artery walls and transport them back to the liver. Higher
levels are optimal.
Apolipoprotein B (apoB)
A constituent of LDL (bad) cholesterol, apoB is responsible for attaching
these lipoproteins to artery walls. ApoB is a promoter of fatty plaque
deposits in the arteries. Lower levels are optimal.
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Aspartate amino-transferase (AST)
An enzyme produced primarily in the liver but also in muscle tissue. AST is
involved in amino acid and protein metabolism. Used as a marker of
hepatic strain, although it is considered less speci c than ALT testing. Also
called Serum Glutamic-Oxalocetic Transaminase (SGOT).
Basophils
A type of white blood cell. Action not fully understood, but cells are known
to carry histamine, heparin, and serotonin. Levels are elevated with allergic
reaction and parasitic infection.
Bicarbonate
A measure of carbon dioxide content in the blood, and a common marker of
the acid-base balance.
Bilirubin
A waste product made from the breakdown of red blood cells. Excreted into
the bile. Regarded as an important indicator of liver health. Elevated levels
in the blood indicate liver toxicity.
Blood Urea Nitrogen (BUN)
A waste product from the breakdown of proteins, ltered and excreted
through the kidneys. Elevated levels may indicate a number of problems
including excessive protein intake, kidney damage, dehydration, heart
failure, or reduced production of digestive enzymes. Low levels may be
indicative of many things including malnutrition or liver damage.
BUN/Creatinine Ratio
The ratio of Blood Urea Nitrogen to Creatinine, used as a marker of kidney
and liver health.
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C-reactive Protein (CRP)
A key marker of in ammation in the body. Elevated levels may indicate
increased risk of cardiovascular disease or stroke.
Carbon Dioxide (CO2)
Byproduct of respiration, and a common marker of the acid-base balance.
See also Bicarbonate.
Calcium
Electrolyte involved in a myriad of body functions including bone
metabolism, protein utilization, muscle and nervous system functioning,
cardiovascular functioning, blood clotting, and nutrient transport.
Chloride
Electrolyte involved in the regulation of water balance. Elevated levels may
indicate a number of things including anemia, dehydration, excess salt
consumption, and hyperthyroid. Low levels may indicate heart or kidney
failure, severe vomiting, or a number of other health conditions.
Cholesterol, Total
A measure of all fractions of cholesterol in the blood (LDL, VLDL, and
HDL). High total cholesterol is regarded as a risk factor for cardiovascular
disease.
Cholesterol, HDL
A measure of the bene cial high-density lipoprotein (HDL) fraction of
cholesterol, which helps remove plaque deposits from arteries. High levels
are optimal. Low levels may be found in cardiovascular disease.
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Cholesterol, LDL
A measure of the low-density lipoprotein (LDL) fraction of cholesterol. This
is the primary atherogenic particle, meaning it tends to promote the
formation of plaque deposits in the arteries. Low levels are optimal.
Cholesterol, VLDL
A measure of the very low-density lipoprotein (LDL) fraction of cholesterol.
VLDL contains the highest amount of triglycerides. Considered an
atherogenic (“bad”) cholesterol particle. Lower levels are optimal.
Cholesterol, LDL/HDL Ratio
A measure of the primary atherogenic particle (LDL) in relation to the
primary antiatherogenic particle (HDL). This ratio is generally considered
the most important cholesterol test value for assessing cardiovascular
disease risk. A low ratio is desirable.
Creatine Kinase
An enzyme found largely in the heart and muscle, and responsible for
converting creatine to phosphocreatine. Elevated levels may be linked to a
number of things including heart attack, kidney failure, or sever muscle
damage.
Creatinine
A waste product of muscle metabolism. Low levels may indicate kidney
disease, malnutrition, or liver disease. High levels may indicate a number of
things including reduced kidney function or muscle degeneration. Creatine
supplementation may also elevate creatinine levels.
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Eosinophils
A type of white blood cell. Similar to basophils, eosinophils are used by the
body to protect against allergy and parasites. Levels are elevated with
infection, and are low with good health.
Estradiol
The principle active form of estrogen. High levels can be associated with
water retention, fat buildup, and gynecomastia (men). Also plays a role in
prostate hypertrophy. Low levels of estradiol may be associated with
increased heart disease risk.
Follicle Stimulating Hormone (FSH)
A pituitary hormone involved in reproduction. In men, FSH is mainly
responsible for supporting spermatogenesis. In women it supports
ovulation.
Gamma-Glutamyl Transpeptidase (GGT)
A cholestatic enzyme produced in the bile ducts. GGT is involved in
glutathione metabolism and the transport of amino acids and peptides.
Used as a marker of hepatic strain.
Globulin
A blood protein similar to albumin. Globulin is responsible for transporting
certain hormones, lipids, metals, and antibodies. Levels may be elevated in
many conditions including chronic infections, liver disease, arthritis, cancer,
or lupus. Lower levels may be found with a number of conditions including
suppressed immune system, malnutrition, malabsorption, and liver or
kidney disease.
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Glucose (fasting)
Glucose is the product of carbohydrate metabolism and the primary source
of energy for most cells in the body. Fasting glucose levels are elevated in
a number of conditions including diabetes, liver disease, metabolic
syndrome, pancreatitis, dieting, and stress. Low fasted glucose levels may
indicate liver disease, overproduction of insulin, hypothyroidism, or other
diseases.
Hematocrit
A measure of the percentage of red cells in the blood. Low levels indicate
an anemic condition. High levels may indicate a number of things including
dehydration, increased red cell breakdown in the spleen, cardiovascular
disease, or respiratory disease. Anabolic steroids may also increase
hematocrit.
Hemoglobin
A constituent of red blood cells, and the main carrier of oxygen and carbon
dioxide in the blood. Levels may be suppressed with a number of
conditions including malnutrition, malabsorption, and anemia. High levels
may indicate many things including dehydration, cardiovascular disease, or
respiratory disease. Anabolic steroids may also increase hemoglobin
levels.
Homocysteine
A compound formed from the metabolism of the amino acid methionine.
Involved in blood clotting and LDL cholesterol oxidation. Elevated levels of
homocysteine indicate an increased risk of cardiovascular disease and
stroke.
Iron
Mineral necessary for many functions including the formation of
hemoglobin and certain proteins, and the transport of oxygen. Elevated
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levels may be caused by many conditions including certain forms of
anemia, liver damage, hepatitis, iron poisoning, or vitamin B6 or B12
de ciency. Low levels can indicate a number of things including
gastrointestinal blood loss, heavy menstrual bleeding, iron malabsorption,
or dietary iron de ciency.
Lactic Acid Dehydrogenase (LDH)
An intracellular enzyme found in many tissues including the kidney, heart,
skeletal muscle, brain, liver, and lungs. Used as a marker of tissue
damage. High levels are found in many conditions including heart attack,
anemia, low blood pressure, stroke, liver disease, muscle injury, muscular
dystrophy, and pancreatitis.
Luteinizing Hormone (LH)
A pituitary hormone responsible for the stimulation of testosterone
production in the testes (men). LH primarily supports ovulation in women.
Lymphocytes
A type of white blood cell. Primary role is to ght viral infection. Levels are
elevated with active infection. Low levels are associated with suppressed
immune system or active bacterial infection (noted by elevated neutrophils).
Mean Corpuscular Volume (MCV)
A measure of the size of red blood cells, determined by measuring the
volume of a single red blood cell. Useful in determining the cause of
anemia. Elevated levels may re ect a number of things including a
de ciency of vitamin B6 or folic acid. Low levels may re ect iron de ciency,
or other causes.
Mean Corpuscular Hemoglobin (MCH)
A measure of the average weight of the hemoglobin in red blood cells.
Useful in determining the cause of anemia.
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Mean Corpuscular Hemoglobin Concentration (MCHC)
A measure of the average concentration of hemoglobin in red blood cells.
Useful in evaluating the cause of, and therapy for, anemia. Low levels may
indicate blood loss, B6 or iron de ciency, or other causes.
Monocytes
A type of white blood cell. Primary role is to ght severe infection not
suf ciently countered by lymphocytes and neutrophils. Levels can be
elevated with a number of things including chronic infection and certain
cancers. Low levels indicate good health.
Neutrophils
A type of white blood cell, also known as granulocytes. The primary white
cell used by the body to ght bacterial infection. Levels are elevated with
infection. May be suppressed with compromised immune system or bone
marrow.
Phosphorous
An abundant electrolyte involved in a number of body functions including
the utilization of carbohydrates, fats, and proteins for cellular maintenance,
repair, and growth, the production ATP for the storage of cellular energy,
the transport of calcium, the maintenance of osmotic pressure, and the
maintenance of heartbeat regularity.
Platelet Count
A measure of the concentration of platelets (also known as thrombocytes)
in the blood. Platelets are involved in blood clotting, and protect against
excessive bleeding. Elevated levels may be linked with a number of things
including dehydration. Low levels are found in suppressed immune system
functioning, drug reactions, or de ciencies of vitamin B12 or folic acid, or
may have other causes.
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Potassium
A key electrolyte necessary for nerve and muscle function, and the
transport of nutrients and waste products in and out of cells. Along with
sodium it helps maintain the acid base balance and osmotic pressure. High
levels may be caused by a number of things including kidney failure,
metabolic or respiratory acidosis, and red blood cell destruction.
Prolactin
A reproductive hormone involved speci cally in lactation. Prolactin is
sometimes (but not commonly) elevated in steroid abusers, and may be
linked to estrogen excess or hormone imbalance. Elevated prolactin may
also indicate other issues with the pituitary.
Prostate-speci c antigen (PSA)
A protein found in prostate cells. Used as a screening for prostate cancer
risk. Elevated levels re ect an increased risk of developing prostate cancer.
Low levels are desirable, although do not assure against prostate cancer.
Red Blood Cell Count
A measure of the total concentration of red blood cells, responsible for
transporting oxygen and carbon dioxide in the body. High red cell counts
are seen with a number of conditions including heart disease, dehydration,
or pulmonary brosis. Low levels may be linked to many things including
anemia, bone marrow failure, red blood cell destruction, bleeding,
leukemia, and malnutrition.
Red Cell Distribution Width (RDW)
A measure of the variation in size between red blood cells. Useful in
evaluating the cause of, and therapy for, anemia. Increased values may
indicate a number of things including vitamin B12, folic acid, or iron
de ciency.
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Sodium
An abundant electrolyte necessary for many functions including the
maintenance of osmotic pressure, acid-base balance, and nerve impulse
activity. Disturbances in the sodium level may be caused by minor things
including excessive sweating, vomiting, diarrhea, water intake, or very
serious conditions including heart, kidney, or liver disease.
T3 Uptake
This test measures the level of unsaturated thyroxine binding globulin (a
carrier of thyroid hormones) in the blood. Increased levels may indicate a
number of things including hyperthyroidism (overactive thyroid), liver
disease, cancer, and decreased lung function. Low levels may be indicative
of hypothyroidism (under active thyroid), excess estrogen levels,
pregnancy, or other causes.
Testosterone, Total
The measure of both unbound (active) and bound (inactive) portions of
testosterone in the blood.
Testosterone, Free
The measure of free (unbound) testosterone in the blood. This represents
the total amount of testosterone immediately available to tissues.
Thyroid-Stimulating Hormone (TSH)
A pituitary hormone responsible for stimulating the release of thyroid
hormones.
Thyroxine (T4)
The more abundant of the two major thyroid hormones (T3 and T4). T4
serves mainly as a reservoir for the more active thyroid hormone (T3),
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which helps to stabilize and regulate thyroid supply. This is a key marker of
the state of thyroid health (low, normal, or overactive).
Thyroxine, Free Index
This measure is a calculation of the amount of unbound (free) T4 in the
blood. This is a key marker of the state of thyroid activity (low, normal, or
overactive).
Total Protein
A measure of the total serum protein concentration, mainly albumin and
globulin. Serum proteins are important to the function and supply of
enzymes, hormones, nutrients, and antibodies, and also play a role in
maintaining the water and pH balance. Low levels may indicate a number
of things including malnutrition, liver disease, malabsorption, diarrhea, or
severe burn injury. Elevated levels may indicate infection, liver damage, or
other disease.
Triglycerides
The main storage form of fatty acids in the body. May be metabolized and
used for energy. Elevated triglyceride levels may contribute to hardening of
the arteries (atherosclerosis), and increase the risk of heart disease or
stroke. Low levels are optimal.
Urea
see Blood Urea Nitrogen (BUN)
Uric Acid
The waste product of purine metabolism, which is ltered and excreted
through the kidneys. Elevated levels may indicate a number of things
including gout, infection, kidney damage, and excessive protein intake. Low
levels may indicate kidney damage, malnutrition, liver damage, or other
causes.
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White Blood Cell Count
A measure of the total concentration of white blood cells (also known as
leukocytes), responsible for ghting infection and protecting the body from
pathogens. A differential measure of white blood cells is usually also taken
including neutrophils, eosinophils, basophils, lymphocytes, and monocytes.
Levels may be elevated with certain infections or allergic conditions.
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