Looking Inside the Black Box:
Understanding Analytical Approaches,
Diagnostic Tools, and Detoxification Strategies
for Mercury Intoxication
Christopher W. Shade, Ph.D.
chris@quicksilverscientific.com
Quicksilver Scientific, LLC
Lafayette, CO 80026
(303)263-6903
Mercury and The Human
Detoxification System
1. What the key forms of Hg are
2. How the Natural Detoxification System Works
3. How the Detox System gets subverted leading
to biochemical stress
4. Mercury Analysis (Blood is not a dirty word)
5. Intestinal Metals Detox System to repair and
amplify the bodies Detoxification System and
safely remove mercury
Forms of mercury
• Hg0 – Elemental Mercury
– The metal form; both liquid and gas forms
• HgII – Inorganic Mercury
– The salt, formed by oxidation of Hg0
• MeHg - Methylmercury
– Organomercurial, formed by bacterial
synthesis
• EtHg - Ethylmercury
– Synthetic organomercurial; antimicrobial
Transport of mercury
• Hg0
– 80% uptake in lungs, crossed BBB, diffuses in to
tissues; moderate uptake from intestines
• HgII
– Very poor uptakes in intestines; poor mobility; does
not cross BBB
• MeHg
– 95% uptake from intestines, good mobility, crosses
BBB
• EtHg
– 100% absorbtion (inj), good mobility, crosses BBB
Targets of mercury forms
•
•
•
•
•
Brain/CNS
Kidney
Liver
Heart
Pituitary/Thyroid
– And thus all glandular
The Heart of the Toxicity
1. Inappropriate Binding – enzymes, redox
proteins, membranes
2. Oxidative Damage and related Inflammation,
including membrane damage (Parinanada)
and apoptosis (cell death)
The Heart of the Toxicity
• Thiol Binding and Redox Reaction
– Reduced sulfur groups, R-SH,
– Hg replaces proton and binds to sulfur
• R-SH + Hg2+ = R-SHg+ + H+
– Enzymes use thiols to anchor functional metals (Zn,
Ni, Cu, Fe)
– Bind and alter membrane or trigger membrane
reorganization and consequent auto-oxidation
– Oxidize Thioredoxin (protein repair molecule)
– Deplete Glutathione system
Inorganic Hg and Poisoning of
the Extracellular Matrix
Mercury and The Human
Detoxification System
1. What the key forms of Hg are
2. How the Natural Detoxification System Works
3. How the Detox System gets subverted leading
to biochemical stress
4. Mercury Analysis (Blood is not a dirty word)
5. Intestinal Metals Detox System to repair and
amplify the bodies Detoxification System and
safely remove mercury
Defense – Glutathione System
Antioxidant, Detoxification, Protein Repair
• Glutathione (GSH) - A thiolic tripeptide
composed of glutamate, cysteine, and glycine
Defense – Glutathione System
Antioxidant, Detoxification, Protein Repair
•
•
•
•
•
•
Synthetases (synthesize GSH from precursors)
Transpeptidases (take apart and reassemble)
Transferases (Phase II conjugation)
Peroxidases (radical quenching)
Reductases (repair after quenching)
Redoxins (using GSH as reducing equivalent for
protein repair)
• Glutathionylation – protection of Proteins
– What to do? Quench the fire or protect the children?
The Human Detoxification
System
• Detoxification Phases I, II, III
– Phase I is an activation,
– Phase II is conjugation
– Phase III is transport (recently
delineated; control point)
The Human Detoxification
System
• Phase I - an oxidative activation, usually
the Cytochrome P450 system
– Prepares toxin for conjugation in Phase II with
GSH, Glucuronic acid, Sulfate, Gycine or
other amino acid, Taurine, Methyl group
– Not needed for metals, but very important to
have coupled to Phase II
• Creates Essentially Free-Radicals
The Human Detoxification
System
• Phase II – conjugation makes toxin more
water soluble and recognizable by
transporters
– Glutathione S-Transferases (GST)
responsible for GSH conjugation
– Low expression in people with high MeHg and
with sensitivity (allergy) to Thimerosal
(EthylHg)
The Human Detoxification
System
• Phase III is the transport out!
– Several transport proteins (cMOAT, OAT,
MRP1, MRP2, GS-X)
• Organic Anion Transporters
– Same transporters for many pathways
(glucuronide, sulfate, glycinate, GSH)
– In cells, liver, intestines, kidneys – biggest in
liver then intestines
Mercury and The Human
Detoxification System
1. What the key forms of Hg are
2. How the Natural Detoxification System Works
3. How the Detox System gets subverted leading
to biochemical stress
4. Mercury Analysis (Blood is not a dirty word)
5. Intestinal Metals Detox System to repair and
amplify the bodies Detoxification System and
safely remove mercury
Breakdown of the defense
system
• GSH deficiency –
– Genetic (GCS polymorphisms, epigenetic dysfunction)
– Environmental (oxidative consumption or inflammation)
• GST problems –
– Genetic (GST polymorphisms, epigenetic dysfunction)
– Environmental (Inflammatory cascade/ARE dysfunction)
Disease and Gen Polymorphisms
of GSH genes
• Hemolytic Anemia – GST (Beutler et al 1988)
• Sensitivity to DDT – GCS and GST (Hung et al.
2004)
• Bladder Cancer (Hung et al. 2004)
– O.R. GSTM1 = 1.69
– O.R. GSTT1 = 1.74
– O.R. GSTM1 + Env Exposure = 2.77
• Acute leukemia – GST
Breakdown of the defense
system
• GSH deficiency –
– Genetic (GCS polymorphisms, epigenetic dysfunction)
– Environmental (oxidative consumption or inflammation)
• GST problems –
– Genetic (GST polymorphisms, epigenetic dysfunction)
– Environmental (Inflammatory cascade/ARE dysfunction)
• Phase III can get blocked and then
downregulates Phase II enzymes
– Can stop multiple detoxification pathways!
Biggest Reason for Phase III
Dysfunction
Inflammation!
Especially in Gut!
-Hallmark of Autism cases
-Easily caused by heavy metal induced
oxidative damage
Coordinated Expression of Phase II
and III
MRP2 and GSTπ
coregulated
Oxidative Activation
Phase I
Phase II
Glutathione
Conjugation
Sulfation
Blood
Cellular MRP1
Phase III
OATP
LIVER
MRP2
Normal Small Intestine
Glucuronidation
Oxidative Activation
Phase I
Phase II
Glutathione
Conjugation
Sulfation
Glucuronidation
Blood
Cellular MRP1
Phase III
OATP
LIVER
MRP2
Inflamed Small Intestine
Oxidative Activation
Phase I
Phase II
Glutathione
Conjugation
Sulfation
Glucuronidation
Blood
Cellular MRP1
Phase III
Inflammation
causes
Downregulation
of MRP2
OATP
LIVER
MRP2
Inflamed Small Intestine
Negative
Feedback –
Inhibition of
Phase II
Oxidative Activation
Oxidative Stress From
Phase I/Phase II mismatch
Phase I
Build-up of both
cellular and
blood-borne
toxins
Phase III
Inflammation
causes
Downregulation
of MRP2
Sulfation
Glucuronidation
Cellular MRP1
Blood
Phase II
Glutathione
Conjugation
OATP
LIVER
MRP2
Inflamed Small Intestine
Negative
Feedback –
Inhibition of
Phase II
Amalgam as Cause for Inflammation
Cysteine Mouth Rinse
HgII
[V]
[V]
C:\Clarity\WORK1\20090224_Chrom _200908_0023 ARDL Waters
54
667.730
56
57
699.743
702.963
58
685.300
680.447
55
663.460
627.340
48
614.810
110
109
1575.140
0.0
1589.303
108
1570.753
1553.067
107
1557.593
105
1539.837
0.0
52
0.5
106
Voltage
HgII
0.5
53
HgII
49
MeHg
630.537
MeHg
648.993
1.0
MeHg
Voltage
50
1.0
644.467
51
C:\Clarity\WORK1\20090224_Chrom _200908_0023 ARDL Waters
-0.5
1540
1580
1560
Time
No Amalgam
25ppt MeHg,
5ppt HgII
1600
1620
[min.]
620
640
660
680
Time
700
[min.]
Amalgam – 10ppb
Amalgam (2nd Rinse) – 16ppb
MeHg Mitochondrial Inferno – Breakdown
of the Thiolic Protection System
Mitochondrial Stress – The
MeHg-induced Blaze
1) Covering Exposed Thiols
Leaking ROS and cyt c
Decay in GSH
2) Mopping up ROS
3) Binding Hg
Insufficient
Protection
from GSH
ROS and Hg Oxidize TrX
TrX releases ASK1
Apoptosis – Cell Death
Mercury and The Human
Detoxification System
1. What the key forms of Hg are
2. How the Natural Detoxification System Works
3. How the Detox System gets subverted leading
to biochemical stress
4. Mercury Analysis (Blood is not a dirty word)
5. Intestinal Metals Detox System to repair and
amplify the bodies Detoxification System and
safely remove mercury
Testing for Hg
1.
Ambient Measures
1. Blood
2. Hair
3. Urine
4. Stool
2.
Provoked Measure
1. Urine
Testing for Hg
H
H
Hg
H
1.
Ambient
1. Blood – MeHg + HgII (MeHg larger)
2. Hair – MeHg only
3. Urine – HgII (little bit of MeHg)
4. Stool – MeHg + HgII
2.
Provoked
1. Urine – MeHg + HgII
Challenge Tests – What do they mean?
Are They Necessary?
Mercury Industry Workers
Dentists
Controls (Amalgam)
Amalgam-free Referents
Mercury Industry Workers
Dentists
Controls (Amalgam)
Amalgam-free Referents
Chelation therapy – Dump from blood
followed by reloading from cellular
burden
Mercury Speciation Testing
• Separates the two main forms of mercury
in the human body
– Once separately measured, ambient
measurements reveal A LOT without
challenge tests
Whole Blood vs. RBC
• Partitioning between RBC and plasma different
for MeHg and HgII
– MeHg 90% RBC/10% Plasma
• Access to brain, intracellular, metabolic-heme
– HgII 50%/50%
• Lymph an extension of plasma: ~5X the volume of blood
• Extracellular Matrix, also concept of terrain
– Look at both forms with whole blood
Inorganic Hg and Poisoning of
the Extracellular Matrix
…Uhhh, What Matrix?
MethylMercury
H
H
Hg
The Unsuspected Factor
H
1. Direct toxicity not as high as Hg(II)
1. One binding site vs. 2 major and 2 minor
2. BUT…has many insidious properties
3. Is slow to excrete bank of mercury
1. Constant source of inorganic mercury from breakdown
1. Can continue symptoms of hypersensitivity from amalgam
after amalgams removed
4. Has “all-access pass”
1. Intracellular, BBB, placental barrier
5. Can form allergy that will persist till all gone
6. If phase II enzymes weak, can stay for long, long time
Accumulation
H
H
Hg
H
Enterohepatic
Circulation of MeHg
Blood Testing
H
H
Hg
• Old Dictum – blood is only recent exposure, 3-days
H
• Reality
– 3-day residence only the quick decay after a large
dose
– For MeHg, Steady state develops after initial decay;
Then blood reflects body burden!
• Real Problem
– Most labs detection limits too high to see dynamics
– Need sensitive equipment!
Blood Testing: The Great Tuna
Experiment
• 2 cans of Albacore Tuna in one sitting
2.50
24 hours later
Blood MeHg (ng/mL)
2.00
24 hours later
1.50
1.00
0.50
2 hours later
Pre-Tuna
2 hours later
0.00
10/26/2008 10/27/2008 10/28/2008 10/29/2008 10/30/2008 10/31/2008
Initial Decay – Redistribution to Tissues
The Great(er) Walleye Experiment
*Nothing is new under the sun*
Clarkson et al., Arch. Env. Health, 1980
Walleye Experiment – Decay and
Body Burden
After initial peak and decay, Blood reflects Body Burden!
Mercury Speciation Testing
H
H
Hg
H
Testing for MeHg
H
[mV]
200
My GC - 6 (05.August 2008)
H
343
Hg
H
4037.647
MeHg
HgII
-200
MeHg
4020
4030
4040
Time
4050
346
4059.930
4055.427
4024.440
4042.010
342
344
341
-600
345
HgII
-400
4019.867
Voltage
0
4060
[min.]
Mercury Speciation Testing and
Compartment Ratio Testing
Ambient Measurement Suite
1. Blood – MeHg + HgII
2. Hair – MeHg only
-Compare to blood MeHg for excretion
measurement
3. Urine – HgII
-Compare to blood inorganic mercury for
excretion measurement
Dentist Levels - Healthy
Dentist Levels – Chronic Inflammation
Dentist Levels – Kidney Problem
Blood Mercury
MeHg
Patient Blood
QS Average
Hg(II)
HgT
0.5
1
1.5
2
2.5
Concentration of Mercury (ng/m L or ug/L)
Indication of Kidney Mercury Excretion
Ability
G o o d H g( II) E xc re t io n Line
5.00
Urine Hg(II)
(ng/mL)
0
( 7 :1)
4.50
4.00
3.50
3.00
2.50
2.00
1.50
1.00
0.50
0.00
0
0.5
1
Blood Hg(II) (ng/m L)
1.5
Patient – MeHg: Detox Enzyme
Defficiency
Hg Retention – Hair:Blood
Normal Excretion
700
1200
600
Hair:Blood MeHg ratio
Hair MeHg (ng/g)
1000
800
600
400
500
400
300
200
100
200
0
0
0.000
1.000
2.000
3.000
Blood MeHg (ng/m L)
4.000
5.000
0.000
1.000
2.000
3.000
Blood MeHg (ng/mL)
4.000
5.000
Problem of Toxicity Diagnosis
• Levels can not show toxic response
• Toxic response from
– Abilities of your defense systems
– Hyper-sensitivities/Allergies developed during
exposure
• Must be Diagnosed from combination of:
– Clinical Symptomology, and
– Auxiliary Testing
Auxiliary Testing
•
•
•
•
•
•
Allergy Testing – MELISA, ELISA
Porphyrins – stress to ATP cycle and to kidneys
GSH Levels – antioxidant/detoxifier defense
GST Activity
Trx and TrxR
Genetic Susceptibilities
– GCL, GSTm, GSTp, ApoE, CPox
Mercury and The Human
Detoxification System
1. What the key forms of Hg are
2. How the Natural Detoxification System Works
3. How the Detox System gets subverted leading
to biochemical stress
4. Mercury Analysis (Blood is not a dirty word)
5. Intestinal Metals Detox System to repair and
amplify the bodies Detoxification System and
safely remove mercury
Removal of Hg
Amplifying and Augmenting Natural
Systems
Biochemical Hg Removal
Requirements
1. Intracellular Glutathione Sufficiency
-Liposomal gets in some cells
-Transpeptidases dissemble/reassemble
2. Effective GST Activity (Phase II mobilization)
3. Effective Phase III Clearance including
intestinal binding
Product/System for Intestinal
Detoxification
1. Intestinal Metals Detox (IMD)
-Phase III opener (dietary supplement)
2. Phytonutrients – Antioxidant Response Element
- Upregulate Transcription of Phase II,
GSH, SOD via ARE
3. Source of GSH
-ReadiSorb Liposomal GSH; Livon Labs
-Nutritional Therapy; OSR
Product/System for Intestinal
Detoxification
• Intestinal Metals Detox (IMD)
– Use Intestines NOT Kidneys for Metal Removal
– Insoluble (NON-ABSORBED) silica particles
saturated with strong (thiol) binding groups
– Binds Mercury in Intestines and moves out of Body
• Interrupts Enterohepatic Circulation
• Opens Phase III transporters
– Bilirubin levels fall dramatically too!
• Then relies on the Natural Detox System (GSH)
Oxidative Activation
Oxidative Stress From
Phase I/Phase II mismatch
Phase I
Build-up of both
cellular and
blood-borne
toxins
Phase III
Inflammation
causes
Downregulation
of MRP2
Sulfation
Glucuronidation
Cellular MRP1
Blood
Phase II
Glutathione
Conjugation
OATP
LIVER
MRP2
Inflamed Small Intestine
Negative
Feedback –
Inhibition of
Phase II
Oxidative Activation
Phase I
Phase II
Glutathione
Conjugation
Sulfation
Blood
Cellular MRP1
Phase III
OATP
LIVER
MRP2
Normal Small Intestine
Glucuronidation
Phase III Enhancement
Bilirubin (unrelated to GSH) falls too
Oxidative Activation
Phase I
Phase II
Glutathione
Conjugation
Sulfation
Glucuronidation
Table 2. Bilirubin Levels on Select Patients with
Elevated Blood Bilirubin (From Clinics 1 & 2, 710 interventions)
Before
After
% Change
2
1.1
-45
1.7
0.9
-47.1
1.4
1.3
-7.1
1.2
0.9
-25.0
3.4
2.6
-23.5
1.7
1.2
-29.4
Blood
Cellular MRP1
Phase III
OATP
LIVER
MRP2
Normal Small Intestine
A Look at Natural Attenuation PostRevision
Halbach et al., 2008, Environ Research 107:69-78
Changes in RBC Hg after Dental
Revision
RevisionMeHg
No Revision MeHg
No Revision HgII
RevisionRevision
HgII
Halbach et al., 2008, Environ Research 107:69-78
MeHg Moving from tissues to
Bloodstream… But NOT Out!
Modeled Trend Revision
Modeled Trend No Revision
Halbach et al., 2008, Environ Research 107:69-78
Blood Stream Decrease with
Quicksilver IMD
1.4
0.5
MeHg
HgII
0.45
1.2
0.4
0.35
0.3
0.8
0.25
0.6
0.2
0.15
0.4
0.1
0.2
0.05
0
11/24/2007
1/13/2008
3/3/2008
4/22/2008
6/11/2008
7/31/2008
Depressed Phase II Transferases keep MeHg in
cells; Once they kick in again, enterohepatic
circulation retards excretion from body
9/19/2008
0
11/8/2008
Blood HgII (ng/mL)
Blood MeHg (ng/mL)
1
IMD Decreases Half-Life in Blood
1.4
0.350
blood MeHg
0.300
Fecal MeHg Excretion
1
0.250
0.8
0.200
0.6
0.150
0.4
0.100
0.2
0.050
Fecal MeHg (ng/g-ww)
Blood MeHg (ng/mL)
1.2
0
0.000
08/10/08 08/20/08 08/30/08 09/09/08 09/19/08 09/29/08 10/09/08 10/19/08 10/29/08
With IMD
No Treatment (Walleye)
½-Life ~ 17 days
½-Life = 46-66 days
To Baseline = 40 days
To Baseline = 160+ days
Small Clinical Trial Results
Table 3.1 Changes in blood mercury levels during 7-10 day intervention with amalgam revision
and nutritional support.
Clinic 1
%Decr HgT
%Decr MeHg
%Decr HgII
IMD (n=8)
23.9
22.9
12.4
Clinic 2
No Treatment (n=4)
0.4
5.1
-4.1
IMD only (n=5)
16.3
15.9
7.1
IMD+OSR (n=7)
17.5
32.3
-15.0
Individual Trial Results
Before Blood Mercury Comparison
MeHg
3/14/2009
12/10/2008
QS Average
Hg(II)
3 months, stopped
fish consumption
HgT
0
0.5
1
1.5
2 2.5
3
3.5
4 4.5
5
5.5
6 6.5
7
7.5
8
8.5
9
9.5 10 10.5
Concentration of Mercury (ng/m L or ug/L)
Before Blood Mercury Comparison
MeHg
8/8/2008
1/23/2009
QS Average
Hg(II)
7 months while
continuing to eat fish
HgT
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
5
Concentration of Mercury (ng/m L or ug/L)
5.5
6
6.5
7
Patient – MeHg: Detox Enzyme
Deficiency
Patient – MeHg: Detox Enzyme
Deficiency
2
2/12/209
4/16/2009
5/7/2009
7/8/2009
8/25/2009
1
0
2
4
6
8
10
12
14
Amalgam Removal and 5 months
IMD w/ phytonutrients and
nutritional therapy
16
18
20
Huggins Protocol
Includes Ancestral Diet, Matrix Supplements, IMD, and OSR
Blood Mercury Comparison
MeHg
2/23/2009
7/6/2009
QS Average
Hg(II)
HgT
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
Concentration of Mercury (ng/m L or ug/L)
5
5.5
6
Product/System for Intestinal
Detoxification
1. Intestinal Metals Detox (IMD)
-Phase III opener
2. Phytonutrients – Antioxidant Response Element
- Upregulate Transcription of Phase II,
GSH, SOD
3. Source of GSH
-ReadiSorb Liposomal GSH
-Nutritional Therapy
“Phytogenomics”
• Certain Phytochemicals upregulate Phase
II enzymes as well as GSH, SOD
• The Anti-Inflammatory Cascade
• Polyphenols
• Sulfur compounds
– Crucifers
– Garlic oil
– NOT CHELATORS!!!
Also Progesterone and
Pregnenolone very
strong in this regard.
Chemoprevention by Keap1-Nrf2 Signaling
pathway by Phase II Inducers
Kwak et al., 2004, Mutation Research, 555:133-148
Putting it All Together
Mitochondrial
Decrease Exposure/
Stress – The
Hg-induced
Increase Export
Blaze
Leaking ROS and cyt c
Decay in GSH
Increase GSH synthesis and
Recycling
Insufficient
1) Covering Exposed Thiols
Increase GSH Enzyme
2) Mopping
up ROS
Activity
3) Binding Hg
Protection
from GSH
ROS
andTrx
Hg and
Oxidize
Increase
TrxRTrX
TrX releases ASK1
Put out the Fires –
Apoptosis
– Cell cells
Death
Save the
Polyphenolics
• Anti-inflammatory cascade
• Upregulate Phase II enzymes through
binding to membrane and nuclear receptors
(transcription factors)
• Vascular protective effects (strengthen
capillaries and improve oxygen delivery)
• Anti-cancer
• Cross BBB
Flavanols (Polyphenolics)
Ellagic Acid
Epicatechin – in tea, cocoa;
monomer for OPC’s from Pine
Bark, Grape seeds,
Quercetin
Haritaki –
Terminalia Chebula
Haritaki –
Terminalia Chebula
1. Aged rates had higher markers of mitochondrial free-radical damage
2. Also Uptick of CAT and GPx, downturn of MnSOD, GR, GST, GSH. Vit C,
Vit E
- normal defenses and export system can’t keep up wit the load,
resulting in more accumulation of free-radical generating molecules
and more reliance on downstream protections
-further depleting GSH
3. ALL MARKERS REVERSED TO YOUNG LEVELS WITH HARITAKI
The Clearing, The Clearing. The Great Clearing
This is the path to fulfillment.
So be it!
Sulfur Compounds
• Anti-inflammatory cascade
• Upregulate Phase II (and Phase III)
enzymes through binding to membrane
and nuclear receptors (transcription
factors)
• Vascular protective effects
• Anti-carcinogenic
Sulfur Compounds
Sulforaphane – the famous crucifer
compound
Erucin – from crucifers; not as
strong as SF
Allyl-isothiocyanate – “Oil of
mustard”, horseradish
Allicin – from garlic
Product/System for Intestinal
Detoxification
1. Intestinal Metals Detox (IMD)
-Phase III opener
2. Phytonutrients – Antioxidant Response Element
- Upregulate Transcription of Phase II,
GSH, SOD
3. Source of GSH
-ReadiSorb Liposomal GSH or Livon Labs
-Nutritional Therapy
Liposomal Glutathione
Liposomal Encapsulation
•Phospholipid bilayer
•Bypasses peptidases that break down
glutahione
•Direct absorption in upper intestine
•Some evidence that they enter cells
•Macrophage oxidative damage
protection
Unilamellar liposomes
Nutritional GSH Augmentation
•
Vitamin C
• Antioxidant Phytonutrients
• Glutathione Precursors
• NAC, glutamate, glycine
• NAC and Vit C
• Whey powder
• GGC – gamma glutamyl cysteine (product in
development from Australia)
Summary
• Retention Toxicity Related to Dysfunction of
Natural Glutathione Detox System, BUT Affects
other detox systems
• Inflammation as major impediment to detox
• MeHg a hidden danger with amalgam
• Hg speciation testing and Compartment
Ratio Analysis to monitor detox
• Opening channels and upregulating natural
system a safe and effective detox strategy
Thank You Huggins
Alliance!
Organic Anion Transporters: GSH
Ionization in Aqueous Solutions
H2O
_
Mercuric DiGlutathione DiAnion
Hg(GSH)2-2 - Soluble, mobile, recognizable
-2
Hg
MethylMercuric Glutathione
MonoAnion
CH3Hg(GSH)-1 - Soluble, mobile, recognizable
CH3
Hg
-1
Cruciferous Compounds
Sulforaphane – the famous crucifer
compound
Glucosinolate
Glucobrassicin
Indole-3-Carbinol
Transformations of mercury
•
•
•
•
•
Hg0  HgII (saliva, blood and tissues)
HgII  Hg0 (intestines)
HgII  MeHg (intestines)
MeHg  HgII (intestines, tissues)
EtHg  HgII (tissues, blood)
Small Clinical Trial Results
Table 3.1 Changes in blood mercury levels during 7-10 day intervention with amalgam revision
and nutritional support.
Clinic 1
%Decr HgT
%Decr MeHg
%Decr HgII
IMD (n=8)
23.9
22.9
12.4
Clinic 2
No Treatment (n=4)
0.4
5.1
-4.1
IMD only (n=5)
16.3
15.9
7.1
IMD+OSR (n=7)
17.5
32.3
-15.0
Individual Trial Results
Before Blood Mercury Comparison
MeHg
3/14/2009
12/10/2008
QS Average
Hg(II)
HgT
0
0.5
1
1.5
2 2.5
3
3.5
4 4.5
5
5.5
6 6.5
7
7.5
8
8.5
9
9.5 10 10.5
Concentration of Mercury (ng/m L or ug/L)
Before Blood Mercury Comparison
MeHg
8/8/2008
1/23/2009
QS Average
Hg(II)
HgT
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
5
Concentration of Mercury (ng/m L or ug/L)
5.5
6
6.5
7