Effective Detoxification
for
Infinite Health and Wellness
with
Dr. Garry F. Gordon MD,DO,MD(H)
Gordon Research Institute
April 2011 – Environment/Pollution – by David Kirby
Made in China: Our Toxic, Imported Air Pollution
Mercury, sulfates, ozone, black carbon, flu-laced desert dust. Even as America
tightens emission standards, the fast-growing economies of Asia are filling the
air with hazardous components that circumnavigate the globe.
It is estimated that Asia is churning out 1,400 tons of Mercury
emissions a year, and take as little as four days to reach
North America.
Mercury plumes can wobble in latitude and altitude or park themselves in one
spot for days on end. Emissions from China—and from the United States, and
indeed from every industrial country—feed a network of air currents that, as
equal-opportunity polluters, serve up toxic mercury around the world.
http://au.video.yahoo.com/watch/4414655/11837407
"Ten Americans": We all know pollution and toxins are bad for you. But the
Environmental Working Group has conducted perhaps the deepest analysis of
this issue on the most vulnerable demographic on the planet. One day in 2004,
one blood sample was taken from ten Americans and tested for 413 toxic
chemicals – 287 chemicals were found – including 212 industrial chemicals
banned from the U.S. over 30 years ago.
A Silent Pandemic
• Autism now 1 in every 150 children
• 57% increase in childhood brain
cancer.
• 84% increase in acute lymphocytic
leukemia in children (1975 – 2002)
• About 7.3 million American couples
have trouble becoming pregnant,
or carrying to term, a 20% increase in the last 10 years.
Sperm count decrease one percent every year.
“The combined evidence suggests that neurodevelopmental
disorders caused by industrial chemicals has created a silent
pandemic in modern society.” ~ Lancet, November 8, 2006.
WATCH THE VIDEO: http://video.yahoo.com/watch/6431545/16676271
NO SAFE LEVEL OF LEAD!
Blood lead levels and mortality
Archives of Internal Medicine (AMA Official Journal)
2002 Nov 25;162(21) ):2443-9
Lustberg M, Silbergeld E.
Department of Epidemiology and Preventive Medicine, University of Maryland
Despite declines in blood lead levels during the past 20 years, lead exposure
continues to be a public health concern. Studies have linked lead exposure with
increased risk for diverse health outcomes. Few studies have evaluated the
association of lead exposure and mortality in the general population. METHODS:
To evaluate the association of lead exposure and mortality in the United States,
we used the recently released mortality follow-up data for participants of the
Second National Health and Nutrition Examination Survey, a national crosssectional survey of the general population conducted from 1976 to 1980. Survey
participants aged 30 to 74 years with blood lead measurements were followed up
through December 31, 1992 (n = 4292). RESULTS: After adjustment for potential
confounders, individuals with baseline blood lead levels of 20 to 29 microg/dL
(1.0-1.4 micromol/L) had 46% increased all-cause mortality (RR, 1.46; 95%
confidence interval [CI], 1.14-1.86), 39% increased circulatory mortality (RR, 1.39;
95% CI, 1.01-1.91), and 68% increased cancer mortality (RR, 1.68; 95% CI, 1.022.78) compared with those with blood lead levels of less than 10 microg/dL (<0.5
micromol/L).
(Circulation. 2009;120:1056-1064.)
© 2009 American Heart Association, Inc.
Epidemiology and Prevention
A Prospective Study of Bone Lead Concentration and Death From All
Causes, Cardiovascular Diseases, and Cancer in the Department of
Veterans Affairs Normative Aging Study
Marc G. Weisskopf, PhD; Nitin Jain, MD; Huiling Nie, PhD; David Sparrow, DSc; Pantel Vokonas, MD; Joel
Schwartz, PhD; Howard Hu, MD
DALLAS, Sept. 8, 2009 — Exposure to lead in the environment is associated
with a sharply increased risk of death from cardiovascular disease, according
to research reported in Circulation: Journal of the American Heart Association.
Study highlights:
 New evidence suggests lifetime exposure to environmental lead may be
associated with increased death from cardiovascular disease.
 The risk of death from cardiovascular disease is almost six times higher in
men with the highest levels of bone lead concentrations compared to men
with the lowest levels.
 Environmental exposure to lead is better measured in bone than in blood,
the traditional method.
Volume 105, Number 12, December 1997 * Environmental Health Perspectives
Commentary
Lead Poisoning-One Approach to a Problem That Won't Go Away
John D. Bogden,7 James M. Oleske,2 Donald B. Louria1
1Department of Preventive Medicine and Community Health; and 2Department of Pediatrics, UMDNJ-New Jersey Medical
School, Newark, NJ 07103-2714 USA
Patterson et al. (9) have compared current skeletal lead concentrations with those of
Southwest American Indians who lived 700-1,000 years ago by use of museum samples.
They found that the present concentrations are about 500 to 1,000-fold
greater than those of the museum samples, suggesting that current
body lead burdens are about three orders of magnitude greater than
those of our preindustrial ancestors. Thus, it should not be surprising that
adverse health effects have been associated with modestly increased bone lead stores
in recent studies, including diminished academic achievement and aggressive behavior
in children, and anemia, high blood pressure, and compromised renal function in adults
(10-13).
Because lead is a ubiquitous and widespread contaminant, it will not be possible to
eliminate additional environmental exposure of Americans of all ages. This inevitable
exogenous exposure will be augmented by endogenous exposure as a result of past and
ongoing bone lead accumulation. Dietary Calcium and Lead In the last 25 years, the
blood lead concentration used to define poisoning or excessive exposure has fallen
progressively from 40 to 30 to 25, and finally to 10 pg/dl (3).
Proc. Natl. Acad. Sci. USA
Vol. 90, pp. 2789-2792, April 1993
Medical Sciences
Bone lead content assessed by L-line x-ray fluorescence in
lead-exposed and non-lead-exposed suburban populations in the
United States (blood lead/soil lead/lead-processing factories/pollution)
JOHN F. ROSEN*t, ANNEMARIE F. CROCETTI*, KENNETH BALBI*, JULIE BALBI*, CHERYL BAILEY*,
ISABELLA CLEMENTE*, NANCY REDKEY*, AND SARAH GRAINGER*
*Albert Einstein College of Medicine, Montefiore Medical Center, 111 E. 210th Street, Bronx, NY 10467; and tDepartment of Community
Medicine, New York Medical College, Valhalla, NY 10595
Communicated by Clair Patterson, December 17, 1992
Current evidence linking release of bone Pb to blood is conclusive.
Studies of Pb workers, under conditions when there is a change in exposure,
have demonstrated release of Pb from bone to blood.
Blood Pb concentrations in retired workers are strongly influenced by bone Pb
content; and two distinct kinetic compartments of Pb in bone have been
described. These compartments have half-times of about 1 and 13 years,
respectively. Significant contributions to blood Pb concentrations from bone
stores have been documented.
Accumulated Lead Exposure and Risk of AgeRelated Cataract in Men
Debra A. Schaumberg, ScD, MPH; Flavia Mendes, MD; Mini Balaram, MD; M. Reza Dana, MD, MPH; David Sparrow, DSc;
Howard Hu, MD, MPH, ScD
JAMA. 2004;292:2750-2754.
Context Low-level lead exposure may increase the risk for a number of chronic age-related diseases. Several studies have
documented the presence of lead in lenses with cataract. The intrusion of lead into the lens may alter lens redox status and
cause protein conformational changes that decrease lens transparency.
Objective To determine the relationship of cumulative lead exposure with the development of cataract.
Design, Setting, and Participants Tibial (cortical) and patellar (trabecular) bone lead levels were measured by K x-ray
fluorescence between 1991 and 1999 in a subset of participants in the Normative Aging Study (NAS), a Boston-based
longitudinal study of aging in men. Among the first 795 NAS participants to have bone lead levels measured, we reviewed
eye examination data (collected routinely every 3-5 years) for the period after the bone lead measurements were taken. We
limited the population to men aged 60 years and older who had sufficient eye examination information available (n = 642).
Blood lead levels were also measured.
Main Outcome Measures Cataract assessment was done while masked to the lead level results. A participant was
considered to have cataract if there was documentation for either eye of cataract surgery or a cataract graded clinically as 3+
or higher on a 4-point scale. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated as estimates of the
magnitude and significance of the relationship of lead exposure with cataract, in logistic regression models.
Results The mean age of the study participants was 69 years and cataract was identified in 122 men. The age-adjusted OR
(95% CI) for cataract for men in the highest vs lowest quintile of tibia lead level was 2.68 (1.31-5.50). Further adjustment for
pack-years of cigarette smoking, diabetes, blood lead levels, and intake of vitamin C, vitamin E, and carotenoids resulted in
an OR of 3.19 (95% CI, 1.48-6.90). For patella lead level, there was an increased risk of cataract in the highest vs lowest
quintile (OR, 1.88; 95% CI, 0.88-4.02), but the trend was not significant (P = .16). Blood lead levels, more indicative of shortterm exposure levels, were not significantly associated with cataract (OR, 0.89; 95% CI, 0.46-1.72; P = .73).
Dr. Gordon comments: Finally proof that bone lead
levels are adversely affecting the health of our brain,
as the eye is an extension of the brain. Therefore
immune suppressing is occurring.
Conclusions These epidemiological data suggest that accumulated lead exposure,
such as that commonly experienced by adults in the United States, may be an
important unrecognized risk factor for cataract. This research suggests that reduction
of lead exposure could help decrease the global burden of cataract.
Environ Health Perspect. 2010 Jul;118(7):928-35. Epub 2010 Mar 12.
Low-level mercury can enhance procoagulant activity of
erythrocytes: a new contributing factor for mercury-related
thrombotic disease.
Lim KM, Kim S, Noh JY, Kim K, Jang WH, Bae ON, Chung SM, Chung JH.
Seoul National University, Korea.
Prolonged exposure to low-dose mercuric ion (Hg(2+); 0.25-5 microM for 1-48 hr) induced
erythrocyte shape changes from discocytes to echinocytes to spherocytes, accompanied by
microvesicle (MV) generation. These MVs and remnant erythrocytes expressed
phosphatidylserine (PS), an important mediator of procoagulant activation. Hg(2+) inhibited
flippase, an enzyme that recovers PS into the inner leaflet of the cell membrane, and activated
scramblase, an enzyme that alters lipid asymmetry in the cell membrane. Consistent with
these activity changes, Hg(2+) increased intracellular calcium and depleted ATP and protein
thiol. A thiol supplement reversed Hg(2+)-induced MV generation and PS exposure and
inhibited the increase in calcium ion (Ca(2+)) and depletion of ATP, indicating that free-thiol
depletion was critical to Hg(2+)-mediated procoagulant activity. The procoagulant activity of
Hg(2+)-treated erythrocytes was demonstrated by increased thrombin generation and
endothelial cell adhesion. We further confirmed Hg(2+)-mediated procoagulant activation of
erythrocytes in ex vivo and in vivo rat thrombosis models, where Hg(2+) treatment (0.5-2.5
mg/kg) increased PS exposure and thrombus formation significantly.
CONCLUSION: This study demonstrated that mercury could provoke
procoagulant activity in erythrocytes through protein-thiol depletion-mediated
PS exposure and MV generation, ultimately leading to enhanced thrombosis.
Am J Physiol Heart Circ Physiol. 2008 Sep;295(3):H1033-H1043. Epub 2008 Jul 3.
Low mercury concentrations cause oxidative
stress and endothelial dysfunction in conductance
and resistance arteries.
Wiggers GA, Peçanha FM, Briones AM, Pérez-Girón JV, Miguel M, Vassallo DV, Cachofeiro V, Alonso MJ, Salaices M.
Departamento de Farmacología, Universidad Autónoma de Madrid, Arzobispo Morcillo 4, 28029 Madrid, Spain.
We analyzed the effects of chronic exposure to low mercury concentrations on
endothelium-dependent responses in aorta and mesenteric resistance arteries (MRA).
Wistar rats were treated with mercury chloride (1st dose 4.6 microg/kg, subsequent dose
0.07 microg.kg(-1).day(-1) im, 30 days) or vehicle. Blood levels at the end of treatment
were 7.97 +/- 0.59 ng/ml.
In MRA, SOD did not affect phenylephrine responses; however, when coincubated with lNAME, the l-NAME effect on phenylephrine response was restored in mercury-treated
rats. Both apocynin and SOD restored the impaired acetylcholine-induced vasodilatation
in vessels from treated rats. Endothelial NOS expression did not change in aorta but was
increased in MRA from mercury-treated rats. Vascular O2(-) production, plasmatic
malondialdehyde levels, and total antioxidant status increased with the mercury
treatment.
In conclusion, chronic exposure to low concentrations of mercury promotes
endothelial dysfunction as a result of the decreased NO bioavailability induced
by increases in oxidative stress. These findings offer further evidence that
mercury, even at low concentrations, is an environmental risk factor for
cardiovascular disease.
Neuroendocrinology Letters No.3 June Vol.25, 2004
Copyright © 2004 Neuroendocrinology Letters ISSN 0172–780X www.nel.edu
The beneficial effect of amalgam replacement on health
in patients with autoimmunity
Jarmila Prochazkova, Ivan Sterzl, Hana Kucerova, Jirina Bartova & Vera DM Stejskal
Patients with certain autoimmune and allergic diseases, such as systemic lupus, multiple
sclerosis, autoimmune thyroiditis or atopic eczema, often show increased lymphocyte
stimulation by low doses of inorganic mercury in vitro. The patients often report clinical
metal hypersensitivity, especially to nickel.
In this study we examined the health impact of amalgam replacement in mercury-allergic
patients with autoimmunity. The suitability of MELISA®, an optimized lymphocyte
stimulation test, for the selection of susceptible patients and monitoring of sensitization
was also examined. Amalgam fillings were replaced with composites and ceramic
materials.
Results of lymphocyte reactivity measured with MELISA® indicate that in vitro reactivity
after the replacement of dental amalgam decreased significantly to inorganic mercury,
silver, organic mercury and lead.
Mercury-containing amalgam may be an important risk factor for patients
with autoimmune diseases. MELISA® is a valuable tool for selection of
patients for amalgam replacement and also for monitoring of metal
allergies.
Synergistic effects of toxic metals
(mercury, lead, aluminum) are extreme.
Bernard Windham, M.D.
Mercury and lead are extremely neurotoxic and cytotoxic, but their combined
synergistic effect is much worse. A dose of mercury sufficient to kill 1% of tested
rats, when combined with a dose of lead sufficient to kill less than 1% of rats,
resulted in killing 100% of rats tested(1). Thus with combined exposure the
safe dose is 1/100 as much as the dose individually. Studies in Australia
have confirmed similar relationships hold for people. This means most people in
the U.S. are getting dangerous levels of these metals, enough to cause some
neurologic effects.
(1) Schubert J, Riley EJ, Tyler SA. Combined effects in toxicology. A rapid systematic testing
procedure: cadmium, mercury, and lead. Toxicol Environ Health 1978;4(5/6):763-776.
Diagnosis: Mercury - Money, Politics & Poison
By Jane M. Hightower, MD
Dr. Hightower retraces her investigation
into the modern prevalence of mercury
poisoning, revealing how political
calculations, dubious studies, and
industry lobbyists endanger our health.
While mercury is a naturally occurring
element, she learns there’s much that is
unnatural about this poison’s prevalence
in our seafood.
Mercury is pumped into the air by coalfired power plants and settles in our rivers
and oceans, and has been dumped into
our waterways by industry.
It accumulates in the fish we eat, and
ultimately in our own bodies. Yet
government agencies and lawmakers have
been slow to regulate pollution or even
alert consumers.
We are surrounded by harmful
environmental toxins and poisonous
heavy metals.
Mercury Toxicity
 Emissions from Coal Burning Power Plants
 Mercury Amalgam Dental Fillings
 Vaccines
Biochemist, Rik J.
Deitsch, and physician,
Stewart Lonky, MD,
explore the health
problems associated
with environmental
toxins
The Autoimmune Epidemic is an
investigation into the reasons behind
today’s alarming rise in rates of
autoimmune diseases (multiple
sclerosis, lupus, type 1 diabetes,
rheumatoid arthritis, thyroiditis, and
dozens of other autoimmune
diseases).
Donna Jackson Nakazawa lays out
the mounting evidence showing how
our modern lifestyles, stress levels,
chemical-laden environment and
twenty-first century diet have created
the “perfect storm” (the ripest
possible conditions)
for this epidemic to take
hold. Nakazawa blends
personal stories with
the latest science to
shed light on what we
should know and do to
halt this epidemic.
Autoimmune and Related Diseases (partial list)
(list compiled with the help of Ahmet Hoke, Md, PhD, Director, Neuromuscular Division,
Johns Hopkins Medical Institutions. Last updated March 2008).
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Ankylosing spondylitisis
Autism
Autoimmune Addison’s disease
Autoimmune hepatitis
Autoimmune thyroiditis
Balo disease
Behcet’s disease
Celiac disease – sprue
Chronic fatigue syndrome
Crohn’s disease
Dermatomyositis
Diabetes Type I
Graves’ disease
Guillain-Barre syndrome
Hashimoto’s thyroiditis
Herpes gestationis
Juvenile arthritis
Lupus Nephritis
Lyme’s disease
Meniere’s disease
Multiple Sclerosis
Myasthenia gravis
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Narcolepsy
Parsonnage-Turner syndrome
Pemphigus vulgaris
Pernicious anemia
Primary biliary cirrhosis
Psoriasis Idiopathic pulmonary fibrosis
Raynaud’s phenomenon
Restless leg syndrome
Rheumatic fever
Rheumatoid arthritis
Sarcoidosis
Scleritis
Scleroderma
Sjogren’s syndrome
Systemic lupus erythematosus (SLE)
Testicular autoimmunity
Transverse myelitis
Ulcerative Colitis
Undifferentiated connective tissue disease (UCTD)
Uveitis
Vasculitis
Wegener’s granulomatosis
http://www.donnajacksonnakazawa.com/autoimmune_diseases.htm
Arsenic exposure may be associated
with type 2 diabetes
Published: Tuesday, August 19, 2008
Health & Medicine
http://esciencenews.com/articles/2008/08/19/arsenic.e
xposure.may.be.associated.with.type.2.diabetes
In a study involving a representative sample of U.S. adults, higher levels of arsenic in
the urine appear to be associated with increased prevalence of type 2 diabetes,
according to a report in the August 20 issue of JAMA. Arsenic from inorganic sources
is highly toxic and causes cancer in humans, according to background information in
the article.
Millions of individuals worldwide are exposed to drinking water contaminated with
inorganic arsenic, including 13 million Americans whose public water supply contains
more than the U.S. Environmental Protection Agency standard of 10 micrograms per
liter. Exposure to high concentrations of the element in drinking water and in the
workplace has been shown to be associated with diabetes, but little is known about the
effect of lower levels on diabetes risk. In contrast, arsenobetaine—an organic arsenic
compound derived eating seafood—is considered non-toxic.
"The potential role of arsenic in diabetes development is supported by experimental
and mechanistic evidence," the authors note. Insulin-sensitive cells that are exposed to
insulin and sodium arsenite appear to take in less glucose than cells exposed only to
insulin. Arsenic could also influence genetic factors that interfere with insulin
sensitivity and other processes, or could contribute to oxygen-related cell damage,
inflammation and cell death (which have also been related to diabetes).
Do Environmental Toxins Cause Diabetes?
There's an epidemic of diabetes in America and
scientists now believe they have found out the reason why.
Scientists tested 2,016 Americans for the presence of six
toxins known as POPs (persistent organic pollutants).
The scientists then compared the levels of these 6 toxins
in the participants' bodies to their history of blood sugar
problems and diabetes.
According to the US Centers for Disease Control, from 1980 through
2004, the number of Americans with diabetes more than doubled (from
5.8 million to 14.7 million). The chances that an American child will
become diabetic are now 1 in 3. The odds for a Latinos in the US and
indigenous peoples around the Pacific are even worse, 1 in 2.
Lee, D-H, I-K Lee, K Song, M Steffes, W Toscano, BA Baker, and DR Jacobs. 2006. A Strong
Dose-Response Relation Between Serum Concentrations of Persistent Organic Pollutants
and Diabetes. Results from the National Health and Examination Survey 1999–2002. Diabetes
Care 29:1638-1644.
Medical Mistakes Kill 100,000+ Americans A Year
from The Grisanti Report http://www.drgrisanti.com/dangerous_medicine.htm
If a Jumbo Jet crashed and killed 280 people everyday… 365 days
a year… year after year.. would you be concerned about flying??
Would you question the Federal Aviation Administration? Would you
demand answers?? Think about it .. close to 100,000 people dying every year
from plane crashes. Sounds Ridiculous??!! Well think again…
What if you were told that over 100,000 people are killed and over 2 million
people maimed and disabled
every year... year after year
from modern medicine…
Would you believe it??
Writing in the Journal of the
American Medical Association
(JAMA), Dr. Starfield has
documented the tragedy of the
traditional medical paradigm in
these charted statistics:
Toxic and Heavy Metal Exposure Early
In Life May Promote Disease Later in Life
Via Epigenetics
Metals and Neurotocicology. J. of Nutr. 138,12,2007.
Wright, RO, et al.
Minerals are necessary for normal cellular, metabolic and
neurological function. It is well known that nutrient mineral
deficiency can impair neurological development. Iron
deficiency is a good example. However,It is also known
that iron excess can also impair neurological development.
Heavy metals such as lead, cadmium, mercury, and arsenic are also neurotoxins and
when present early in life can contribute to impaired neurodevelopment and
detrimental health effects later in life and have been called the “fetal origins of
disease.” Suggesting that early environmental metal exposure can program later life
gene expression, or fetal programming.
The mechanism for this phenomenon is termed epigenetics. Epigenetics is the study
of heritable changes in gene expression that occur without changes in DNA
sequence, that unlike mutations, are reversible and responsive to environmental
influences. DNA methylation is the most studied of the epigenetic process that
regulated gene silencing.
Good News In Our DNA: Defects You
Can Fix With Vitamins And Minerals
ScienceDaily (June 3, 2008)
As the cost of sequencing a single human genome
drops rapidly, with one company predicting a price
of $100 per person in five years, soon the only
reason not to look at your "personal genome" will
be fear of what bad news lies in your genes.
University of California, Berkeley, scientists,
however, have found a welcome reason to delve
into your genetic heritage: to find the slight genetic
flaws that can be fixed with remedies as simple as
vitamin or mineral supplements.
Electron microscope image of
budding yeast, Saccharomyces
cerevisiae. UC Berkeley researchers
insert variants of human enzymes
into yeast to see if these enzymes
can be tuned up with vitamins.
"Our studies have convinced us that there is a lot of
variation in the population in these enzymes, and a lot of it affects function,
and a lot of it is responsive to vitamins," Marini said. "I wouldn't be surprised
if everybody is going to require a different optimal dose of vitamins based on
their genetic makeup, based upon the kind of variance they are harboring in
vitamin-dependent enzymes."
The Immortality Edge
by Michael Fossel, MD, PhD, Greta Blackburn, Dave Woynarowski, MD
Realize your longevity potential with a plan
Based on Nobel Prize-winning research. The
Immortality Edge: Realize the Secrets of Your
Telomeres for a Longer, Healthier Life (Wiley,
2011).
http://www.lef.org/VitaminsSupplements/Item33829/TheImmortality-Edge.html
Telomeres play an important role in protecting
our chromosomes from critical damage. The
shortening of the telomere disrupts vital
cellular function and promotes the previously
seemingly inevitable onset of aging and various
diseases, including cancer and Alzheimer’s.
Drawing from the groundbreaking discoveries
about telomeres that won the 2009 Nobel Prize
in Medicine, this book includes a highly
prescriptive program that shows you how to
live longer by slowing telomere shortening and
by rejuvenating your cells through relatively
simple alterations in nutrition and lifestyle.
Microbiol Mol Biol Rev. 2002 Sep;66(3):407-25, table of contents.
Human telomerase and its regulation.
Cong YS, Wright WE, Shay JW.
Department of Cell Biology, University of Texas Southwestern Medical Center Dallas
Abstract
The telomere is a special functional complex at the end of linear eukaryotic
chromosomes, consisting of tandem repeat DNA sequences and associated
proteins. It is essential for maintaining the integrity and stability of linear
eukaryotic genomes. Telomere length regulation and maintenance contribute
to normal human cellular aging and human diseases. The synthesis of
telomeres is mainly achieved by the cellular reverse transcriptase telomerase,
an RNA-dependent DNA polymerase that adds telomeric DNA to telomeres.
Expression of telomerase is usually required for cell immortalization and longterm tumor growth. In humans, telomerase activity is tightly regulated during
development and oncogenesis. The modulation of telomerase activity may
therefore have important implications in antiaging and anticancer therapy.
This review describes the currently known components of the telomerase
complex and attempts to provide an update on the molecular mechanisms of
human telomerase regulation.
PMID: 12208997 [PubMed - indexed for MEDLINE]PMCID: PMC120798
http://www.ncbi.nlm.nih.gov/pubmed/12208997
The Wall Street Journal - Health Industry
U.S. Cell-Aging Researchers Awarded Nobel
Three Scientists Share Prize for Discovery of Enzyme That Has Opened New
Avenue of Research Into Several Serious Diseases
by Gautam Naik – Oct 9, 2009
The scientists discovered the workings of
telomerase, an enzyme that produces tiny units of
DNA that seal off the tips of chromosomes. These
DNA units, known as telomeres, act like the
plastic caps at the ends of a shoelace, keeping
the chromosomes from fraying and the genes
inside them from unraveling.
As we age, though, these caps lose their ability to
protect. One result is that some cells go into a
state known as senescence, where they are alive
but stop dividing. Researchers believe this may
contribute to aging.
Their finding have sparked a new line of
research into possible treatments for agerelated maladies, such as cancer, blindness
and cardiovascular disease.
http://online.wsj.com/article/SB125472880070963893.html
U.S. NEWS - NOVEMBER 28, 2010
– by Gautum Naik
Aging Ills Reversed in Mice
Scientists Tweak a Gene and Rejuvenate Cells, Raising Hopes for Uses in Humans
The research team led by Dr. Ronald DePinho of Dana Farber Cancer Institute made
genetically engineered mice that aged prematurely.
The animals had short, dysfunctional telomeres and suffered a range of age-related
problems, such as:
• atrophied spleens
• intestinal damage
• impaired sense of smell
• shrunken brains
• shrunken testes, depleted sperm count.
"These mice were equivalent to 80-year
old humans and were about to pass away,"
says DePinho. After the experiment, "they
were the physiological equivalent of young
adults."
Their telomeres had lengthened and the
levels of telomerase had increased. This
woke up the dormant brain stem cells,
producing new neurons. The spleen, testes
and brain grew in size.
Two mice involved in an experiment
on age-related degeneration. Mouse
on left, whose telomerase gene was
activated, showed notable
improvements.
How to Turn on Telomerase
Activity and Find the
Fountain of Youth.
By Jeffrey Dach, MD
By now, it is should be obvious to you that activating telomerase, protects the telomeres
from shortening and will slow or reverse the process of aging. On the contrary, knocking
out or inhibiting telomerase activity results in shortened telomeres with acceleration of
the aging process.
What Activates Telomerase ?
Among other things, the bioidentical hormones, 17 beta estradiol (estrogen) and
testosterone activate telomerase. The major mechanism for control and activation of
telomorase is the hTERT promoter gene which stands for the human telomerase reverse
transcriptase (hTERT) gene. When the hTERT gene is sequenced, and the code
reviewed, it turns out there are two estrogen receptor elements in this gene. This
explains why 17-beta estradiol activates telomerase.
The Harvard study used Tamoxifen on genetically modified telomeres. In the real
world, tamoxifen is an estrogen blocker that occupies the cell receptors and turn OFF
telomerase. Androgens were also found to turn on the hTERT gene and activate
telomerase, and as expected, androgen blocker drugs inhibit telomerase.
Bioidentical Hormones are the more logical choice…
http://www.wellsphere.com/genetics-article/bioidentical-hormones-reverse-aging-new-harvard-study-by-jeffrey-dach-md/1295172
Vitamin, Mineral and Herbal
Chelators
and Detoxifiers
Newsweek Publishes Disgraceful Article
on Antioxidants
(Action Alert) February 1, 2011
In their January 25 issue, Newsweek published a scientifically
unsupportable article, entitled “Anti-oxidants Fall From Grace”
claiming that antioxidants “may not be good for your health.”
We asked natural biomedical researcher and physician Jonathan
Wright, MD, to comment—and he didn’t mince words!
Here we go again. Another one-sided “mainstream media” attack on an aspect of natural
healthcare, filled with to-be-expected misinformation, partial information, and—of
course—no attempt at all to present both sides of the manufactured controversy.
[the article] gives us the impression that “antioxidants” cancel “oxidizing agents” in a
straight-line, one-on-one, hand-to-hand-combat manner. If this were true, his conclusion
might make sense. But the truth—as often it is in nature—is more subtle.
Dietary components presently termed “antioxidants” can work on both sides
of the “redox reaction,” sometimes donating electrons, sometimes gaining
them, as needed. To describe their functions more accurately, including both
aspects of electron flow, antioxidants might best be termed “redox reaction
regulators.”
http://www.anh-usa.org/newsweek-publishes-disgraceful-article-on-antioxidants-action-alert/
Anticancer Res. 1997 Sep-Oct;17(5A):3513-20.
Modulating factors of radical intensity
and cytotoxic activity of ascorbate (review).
Sakagami H, Satoh K.
Ascorbate acts both as an antioxidant and as an oxidant, depending
upon the environment in which the molecule is present.
We have reported that millimolar concentrations of ascorbate induced apoptotic cell
death, characterized by cell shrinkage, nuclear fragmentation and internucleosomal
DNA cleavage, in human myelogenous leukemic cell lines. Ascorbate derivatives,
which can induce the apoptosis, produced the radical(s), elevated the oxidation
potential and stimulated the methionine oxidation in the culture medium, whereas
inactive derivatives did not. This suggests that the ascorbate induce the apoptosis
by its prooxidant action. The effects of various factors, such as temperature,
pH, metal, metal antagonist, redox agent, serum protein, polyphenol and
(natural, chemically modified) polysaccharide on the radical intensity and
apoptosis-inducing activity of ascorbate are reviewed. Gallate and
benzo[a]phenothiazine derivatives, which can induce apoptosis or monocytic
differentiation in human myelogenous leukemic cell lines, also produced
radicals. These data suggest the significant role of radicals in the initiation of
diverse biological activities.
PMID: 9413196 [PubMed - indexed for MEDLINE]
This excellent review article will assist in the understanding of how
some forms of oxidative stress could paradoxically be beneficial in
the long run, partly by enhancing antioxidant production, but other
possibilities deserve exploration.
Cardiac mitochondrial bioenergetics, oxidative stress
and aging
Sharon Judge1 and Christiaan Leeuwenburgh2
1Division of Endocrinology, Department of Medicine, College of Medicine; and 2Institute on Aging, Division of Biology of Aging, Department of
Aging and Geriatrics, College of Medicine, University of Florida, Gainesville, Florida
Mitochondria have been a central focus of several theories of aging as a result of
their critical role in bioenergetics, oxidant production, and regulation of cell
death. A decline in cardiac mitochondrial function coupled with the accumulation
of oxidative damage to macromolecules may be causal to the decline in cardiac
performance with age. In contrast, regular physical activity and lifelong caloric
restriction can prevent oxidative stress, delay the onset of morbidity, increase life
span, and reduce the risk of developing several pathological conditions. The
health benefits of life long exercise and caloric restriction may be, at least
partially, due to a reduction in the chronic amount of mitochondrial oxidant
production. In addition, the available data suggest that chronic exercise may
serve to enhance antioxidant enzyme activities, and augment certain
repair/removal pathways, thereby reducing the amount of oxidative tissue
damage.
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Oxidative phosphorylation
(From Wikipedia, the free encyclopedia)
Oxidative phosphorylation is a
metabolic pathway that uses
energy released by the
oxidation of nutrients to
produce adenosine
triphosphate (ATP), the
molecule that supplies energy
to metabolism.
The electron transport chain in
the mitochondrion is the site of
oxidative phosphorylation in
eukaryotes. The NADH and
succinate generated in the
citric acid cycle are oxidized,
releasing energy to power the
ATP synthase.
http://en.wikipedia.org/wiki/Oxidative_phosphorylation
"Vitamin Supplement Use During Breast Cancer
Treatment and Survival: A Prospective Cohort Study“
Xiao-Ou Shu, MD, PhD, MPH
Cancer Epidemiol Biomarkers Prev, 2010 Dec 21
[Epub ahead of print]. 48430 (2/2011)
There is a widespread concern that the use of antioxidant supplements during cancer
treatment may protect tumor cells from the oxidative damage induced by cancer
therapies, thereby reducing the effectiveness of treatment and increasing risk of
mortality.
The epidemiologic data to support this concern is limited, in particular among breast
cancer patients. In fact, to our knowledge, our study is the first large, prospective cohort
study to investigate vitamin supplement use in conjunction with cancer treatment and
subsequent mortality and recurrence risk among breast cancer survivors.
The results of this epidemiological study do not support the current recommendation
that breast cancer patients should avoid use of vitamin supplements.
Instead, our study suggests that vitamin supplement use in the first
six months after breast cancer diagnosis may be associated with
reduced risk of mortality and recurrence.
FDA APROVED VITAMIN C/VITAMIN K3
COMBINATION CANCER DRUG!
Apatone® is an investigational new drug undergoing
clinical trials in the US. First approved for human study
in 2005, the drug includes two vitamin small molecules that target and treat
inflamed cells. (VK3 and VC)
In mid-2007 the drug was granted Orphan drug status by the FDA's
Office of Orphan Products for treatment of late stage urinary bladder
cancer. The mechanism of action relies on inflammatory targeting and
intercellular redox unique to non-vitamin moieties of combined vitamins C
and K3. Apatone selectively targets inflamed cells and inhibits NF-KB, a
nuclear factor kappa-light-chain-enhancer of activated B cells.
Through receptors on the cell surface Apatone targets the same cells that are
illuminated by Positron Emission Tomography (PET). In this way the drug
selectively targets and then treats inflamed cells. The current study is
designed to examine Apatone's effect on specific inflammatory factors
known to degrade bone, a critical part of joint disease, some cancers and
other indications.
http://www.ic-medtech.com/index.php
Altern Med Rev. 2010 Dec;15(4):345-51.
The vitamin C:K3 system - Enhancers and inhibitors
of the anticancer effect.
Lamson DW, Gu YH, Plaza SM, Brignall MS, Brinton CA, Sadlon AE.
Abstract
The oxidizing anticancer system of vitamin C and vitamin K3 (VC:VK3, producing hydrogen peroxide
via superoxide) was combined individually with melatonin, curcumin, quercetin, or cholecalciferol
(VD3) to determine interactions. Substrates were LNCaP and PC-3 prostate cancer cell lines. Three
of the tested antioxidants displayed differences in cell line cytotoxicity. Melatonin combined with
VC:VK3 quenched the oxidizing effect, while VC:VK3 applied 24 hours after melatonin showed no
quenching. With increasing curcumin concentrations, an apparent combined effect of VC:VK3 and
curcumin occurred in LNCaP cells, but not PC-3 cells. Quercetin alone was cytotoxic on both cell
lines, but demonstrated an additional 50-percent cytotoxicity on PC-3 cells when combined with
VC:VK3. VD3 was effective against both cell lines, with more effect on PC-3. This effect was negated
on LNCaP cells with the addition of VC:VK3. In conclusion, a natural antioxidant can enhance or
decrease the cytotoxicity of an oxidizing anticancer system in vitro, but generalizations about
antioxidants cannot be made.
The VC:VK3 combination generates H2O2 efficiently by redox cycling, such that a high
level of VC by the intravenous route may not be necessary for cancer cell death. Since
the VC:VK3 combination increases the cytotoxicity by six- to seven-fold over individual
vitamin use, the oralroute might suffice. Research on this concept proceeded through
the usual route from in vitro, to in vivo, to human trial.
The VC:VK3 system has performed positively in vitro for prostate cancer, breast cancer,
ovarian cancer, bladder cancer, hepatocarcinoma, and some leukemias.
http://www.ncbi.nlm.nih.gov/pubmed/21194250
Vitamins vs. Chemotherapy and Radiation for Cancer Therapy
by Reagan Houston, MS, PE
Townsend Letter – Aug/Sept 2009
Vitamins can strengthen the immune system to
improve regular therapies and safely kill cancer.
Here we compare cancer therapy by
multivitamins with radiation and most
chemotherapies. The late Abram Hoffer, MD,
PhD, prescribed a regimen high in oral vitamin C
plus other vitamins and minerals (Table 1). He
also prescribed a diet low in meat, very low in
sugar, but high in fruits, vegetables, and water.
Most of his patients had failed prior surgery,
radiation, and/or chemotherapy as prescribed by
their oncologists. To all of his cancer patients,
Hoffer offered the vitamin regimen, diet, and
hope based on the results with earlier patients.
Dr. Hoffer's results were
excellent. Those who refused
vitamins lived a median of only
2.6 months. The 101 who
accepted vitamins lived 45
months after seeing Hoffer
(Table 2).
Vitamin C Injections Slow Tumor
Growth in Mice
High-dose injections of vitamin C, also known as ascorbate or
ascorbic acid, reduced tumor weight and growth rate by about
50 percent in mouse models of brain, ovarian, and pancreatic
cancers, researchers from the National Institutes of Health (NIH)
report in the August 5, 2008, issue of the Proceedings of the
National Academy of Sciences.
In their laboratory experiments on 43 cancer and 5 normal cell
lines, the researchers discovered that high concentrations of
ascorbate had anticancer effects in 75 percent of cancer cell
lines tested, while sparing normal cells.
In their paper, the researchers also showed that these high ascorbate concentrations
could be achieved in people.
The team then tested ascorbate injections in immune-deficient mice with rapidly spreading
ovarian, pancreatic, and glioblastoma (brain) tumors. The ascorbate injections reduced tumor
growth and weight by 41 to 53 percent. In 30 percent of glioblastoma controls, the cancer had
spread to other organs, but the ascorbate-treated animals had no signs of disseminated
cancer. "These pre-clinical data provide the first firm basis for advancing pharmacologic
ascorbate in cancer treatment in humans," the researchers conclude.
http://www.nih.gov/news/health/aug2008/niddk-04.htm
Image: Mark Levine
Vitamin C, given at sufficiently high doses,
by itself, can cure life-threatening infections
and neutralize many otherwise fatal toxin
exposures, according to author Thomas E.
Levy, MD, JD in his extensively referenced
new book, Vitamin C, Infectious Diseases,
and Toxins: Curing the Incurable.
Levy's book is unmatched in the medical
literature. According to Dr. E. Cheraskin,
more than 80,000 scientific papers and
reports have been written about vitamin C
since its chemical nature was first
discovered early in the 20th century. The
Vitamin C Foundation credits Levy with
"doing an almost impossible feat of reading,
analyzing and clearly explaining the meaning
of the massive science behind vitamin C."
http://findarticles.com/p/articles/mi_m0ISW/is_2003_May/ai_100767885/
http://www.camltd.co.nz/h1n1.html
High Dose IV Vitamin C
Saves NZ Man with Swine
Flu Damaged Lung
A 56 year old male was referred to Auckland Hospital ICU on 1 July 2009 with total respiratory
failure, for ECMO external oxygenation. The patient had contracted H1N1 Swine flu (confirmed by
tests) while on holiday overseas, and had developed what is known as ‘white out’ pneumonia. This
refers to x-rays showing no air space in the lungs. After 20 days of life-sustaining ECMO treatment
and other critical care, the patient, who was unconscious by induced coma, had not responded. The
ICU team advised the family of the likely outcome and had prepared them for the possibility of the
patient’s death.
At the family’s request, information was provided to ICU doctors including ISO 9001:2008 registered
protocols, safety data, dosages and access to vials of IV vitamin C under CAM's license for
wholesale medicines. The patient received intravenous vitamin C starting on the evening of 21 July,
continuing until 29 July. 25 grams was provided on the first day increasing over the first three days
to 50 grams twice daily which was sustained for a further six days.
By 24 July x-rays indicated increasing lung function and
ECMO external oxygenation was discontinued on 26 July.
After several days of assisted ventilation and critical care
for ongoing secondary conditions, the patient was able to
commence his recovery and rehabilitation. The patient was
discharged from hospital on Friday 18 September, and is
recovering at home on the farm.
Watch the 60 Min News Report:
http://www.3news.co.nz/Living-Proof/tabid/371/articleID/171328/Default.aspx
Anticancer Res. 1996 Jan-Feb;16(1):499-503.
Potentiation of radiotherapy by nontoxic
pretreatment with combined vitamins C and K3
in mice bearing solid transplantable tumor.
Taper HS, Keyeux A, Roberfroid M.
Département des Sciences Pharmaceutiques, Université Catholique de Louvain,
Brussels, Belgium.
Combined vitamins C with K3 most probably constitute a redox-cycling
system producing hydrogen peroxide and other active oxygen species
to which cancer cells are selectively sensitive due to their frequent
deficiency in enzymatic defense system against free oxyradicals
agression.
CONCLUSIONS: A possible introduction of such nontoxic and selective
potentiation procedure into classical protocols of human cancer therapy
appears to be generally accessible and without any additional risk for
patients.
PMID: 8615662 [PubMed - indexed for MEDLINE]
Proposed mechanism for tumoricidal action
of ascorbate acid (AA) Vitamin C.
Pharmacologic concentrations of
ascorbate may engender a
prooxidant cytotoxic state within
tumors.
In initial in vitro experiments, there
was observed hydrogen peroxide
(H2O2)-dependent cytotoxicity after
ascorbate exposure (EC50 4 mM) in
five cancer cell lines, whereas
normal cells were resistant.
PNAS 2008;105:11033-11034
©2008 by National Academy of Sciences
Effects of pharmacologic ascorbic acid concentrations
on cancer and normal cells.
Chen Q et al. PNAS 2005;102:13604-13609
©2005 by National Academy of Sciences
Subsequent Cardiac and Stroke Events in Patients with Known
Vascular Disease Treated with EDTA Chelation Therapy
A Retrospective Study
L. Terry Chappell, Rakesh Shukla, Jun Yang, Rene’ Blaha, Tammy Born, Claus Hancke, William
Mitchell, Efrain Olszewer, Peter van der Schaar and James Ventresco
Context: Myocardial infarction (MI) and strokes are leading causes of death in the US.
Surgical and medical treatments can be helpful, but carry risks of morbidity and
mortality.
Objective: To evaluate whether cardiac events were reduced for patients with known
vascular disease who were treated with intravenous ethylene diamine tetra-acetic acid
(EDTA) chelation therapy.
Results: According to the meta-analysis, expected outcomes in a 3-year
follow-up period for 220 patients with coronary artery disease treated only
with conventional therapies would be 15 MIs and six deaths. There were no
deaths and no MIs in this group of patients who received chelation therapy.
Four patients had strokes but recovered well. There were two angioplasties
and six CABG procedures. Compared with similar patient populations treated
with conventional therapies, patients who also were chelated had a 93.6%
lesser need for angioplasty and a 62.5% reduced need for CABG. Of the
patients that initiated treatment with symptoms, 68.7% had complete
resolution of symptoms.
Books by Lester Morrison, MD, D.SC., F.A.C.P
Morrison, Lester M., M.D., and Schjeide,
O. Arne, Ph.D. Coronary Heart Disease
and the Mucopolysaccharides (Glycosaminoglycans). (1974) Charles C.
Thomas, Publisher. 2600 S. First Street,
Springfield, Illinois 62717. ISBN 0-39802903-2.
Morrison, Lester M., M.D., and Schjeide,
Ole A. Ph.D. Arteriosclerosis. Prevention,
Treatment, and Regression. (1984)
Charles C. Thomas, Publisher. 2600 S.
First Street, Springfield, Illinois 62717.
ISBN 0-398-04919-X.
Morrison, Lester M., M.D., with Nugent,
Nancy. Dr. Morrison’s Heart-Saver
Program. (1982) St. Martin’s Press, 175
Fifth Avenue, New York, N.Y. 10010. ISBN
0-312-21481-2.
Alpha Lipoic Acid (LA)
Alpha-lipoic acid (LA), also known as thioctic acid, is a naturally
occurring compound that is synthesized in small amounts by plants and
animals, including humans. LA contains two thiol (sulfur) groups, which
may be oxidized or reduced. The reduced form is known as dihydrolipoic
acid (DHLA), while the oxidized form is known as LA.
Redox-active metal ions, such as free iron and copper, can induce
oxidative damage by catalyzing reactions that generate highly reactive
free radicals.
Compounds that chelate (bind) free metal ions in a way that prevents
them from generating free radicals offer promise in the treatment of
neurodegenerative and other chronic diseases, in which metal-induced
oxidative damage may play a role. Both LA and DHLA have been found to
inhibit copper- and iron-mediated oxidative damage in the test tube and
to inhibit excess iron and copper accumulation in animal models.
BETA-SITOSTEROL
A substance found in plants. Chemists call it a “plant sterol ester.” It is
found in fruits, vegetables, nuts, and seeds - high levels of Beta Sitosterol
are found in rice bran, wheat germ, corn oils and soybeans.
Beta-sitosterol is used for: heart disease and high cholesterol, boosting
the immune system, preventing colon cancer, gallstones, the common
cold and flu (influenza), HIV/AIDS, rheumatoid arthritis, tuberculosis,
psoriasis, allergies, cervical cancer, fibromyalgia, systemic lupus
erythematosus (SLE), asthma, hair loss, bronchitis, migraine headache,
chronic fatigue syndrome, enlarged prostate (benign prostatic
hyperplasia or BPH), symptoms of menopause, enhancing sexual activity.
Marathon runners sometimes use beta-sitosterol to reduce pain and
swelling after a run.
Some people apply beta-sitosterol to the skin for treating wounds and
burns
Selenium
Selenium is a trace mineral that incorporates itself into proteins to
produce selenoprotein enzymes. These enzymes act as an anti-oxidant
in the body to destroy free radicals and boost both the immune system
and thyroid function. Mercury binds with selenium and reduces
selenoprotein production. This deficiency hampers immune & thyroid
function.
Selenium acts as a mercury magnet with a very strong binding affinity
for the toxic substance. This strong attraction allows selenium to mix
and neutralize their reaction characteristics. This new Hg - Se
substance that is produced is not absorbed by the body and gets
flushed out of the system. This is a very beneficial interaction that
removes mercury from the body before it can lodge in fatty tissue and
cause damage.
Nutr Clin Pract. 2008 Apr-May;23(2):152-60.
The role of selenium in chronic disease.
Boosalis MG.
Division of Clinical Nutrition, University of Kentucky, College of Health
Sciences, Lexington, KY
Selenium functions as a part of proteins known as selenoproteins. Through
these selenoproteins, selenium functions as a defensive mechanism for
oxidative stress, for the regulation of thyroid hormone activity, and for the
redox status of vitamin C and other molecules. In several of its roles,
selenium functions as a dietary antioxidant and thus has been studied for its
possible role in chronic diseases. This article reviews recent studies
regarding selenium status or supplementation in hypertension,
cardiovascular disease, cancer, and diabetes mellitus. A few studies
regarding aging and mortality are also included. What can be ascertained
from this current review is that the maintenance of adequate selenium
nutriture and, at minimum, the prevention of a deficiency in selenium would
be advisable for all individuals. In addition, the indiscriminant use of
selenium supplements should be approached with caution until further
randomized, controlled trials monitor the effects of such supplementation,
especially on a long-term basis.
PMID: 18390782 [PubMed - indexed for MEDLINE]
Mol Biol Rep. 2010 Nov 5. [Epub ahead of print]
Selenium inhibits high glucose-induced
cyclooxygenase-2 and P-selectin expression
in vascular endothelial cells.
Li YB, Han JY, Jiang W, Wang J.
Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, No. 23 Youzheng
Street NanGang District, Harbin City.
Selenium as a component of glutathione peroxidase may be beneficial in
insulin resistance, hence potentially may modify the risk of diabetes and
cardiovascular disease. The aim of our study was to evaluate whether
selenium can also alter high glucose (HG), advanced glycation end products
(AGE), high insulin (HI) and H(2)O(2)-induced expression of cyclooxygenase
(COX)-2 and P-selectin. Human umbilical vein endothelial cells (HUVECs)
were pretreated with selenium and stimulated by HG, AGE, HI and H(2)O(2).
Selenium significantly inhibited HG, AGE, HI and H(2)O(2)-induced expression
of COX-2 and P-selectin. Moreover, selenium also inhibited HG, AGE, HI and
H(2)O(2)-induced activation of p38 mitogen-activated protein kinase (p38
MAPK), which indicated that the preventive effects of selenium on COX-2 and
P-selectin may be associated with p38. Our results indicated that selenium
supplementation can reduce HG, AGE, HI and H(2)O(2)-induced expression of
COX-2 and P-selectin by inhibition of the p38 pathway.
24 – Medical Applications of Zeolite (cont.) from pg 1146
IV. Removal Of Heavy Metals and Organopoisoning
Heavy metals released in wastewater are among the most worrisome
pollution problems due to their cumulative effects along the food chain.
The natural zeolites clinoptilolite, phillipsite, and chabazite are particularly
useful in selectively eliminating ammonia and heavy metals such as Cd2+,
Pb2+, Zn2+, Cu2+, and particularly Cr3+. Generally, clinoptilolite is stable in
an acidic environment and shows high selectivity for many heavy metals.
The preventative effect of zeolites (zeolite tuff containing 61% clinoptilolite)
has been shown to prevent and eliminate organophosphate poisoning. The
organophosphate poison substance XX can strongly inhibit enzyme cholineterase in erythrocytes, and in the stomach, brain and liver. This effect can
be strongly diminished after pretreatment with zeolite ((1 g/kg 5 min before
intoxication).
24 – Medical Applications of Zeolite (cont.) from pg 1147
V. Antimicrobial Effects
Metal exchanged zeolites have been proposed in the last decade for
controlled release of agents against microbial pollution. Zeolites
containing copper ions exhibit good antibacterial activity for both gramnegative and gram-positive bacteria, and the effect developed in a short
period of time.
Tissue conditioners containing silver-exchanged zeolite showed a strong
in-vitro antimicrobial effect on Candida albicans, and also on nasocomial
respiratory infections of S. aureus and P. aeruginosa. All microbes were
killed whether they have been immersed in saliva or not.
A new type of antibacterial temporary filling material in dentistry was
incorporated into urethane acrylate monomer paste. These materials
exhibited prominent in-vitro antibacterial activity against Streptococcus
mutans and Streptococcus mitis.
J Ethnopharmacol. 2001 Oct;77(2-3):203-8.
Preventive effect of Coriandrum sativum (Chinese Parsley)
on localized lead deposition in ICR mice.
Aga M, Iwaki K, Ueda Y, Ushio S, Masaki N, Fukuda S, Kimoto T, Ikeda M, Kurimoto M.
Hayashibara Biochemical Laboratories, Inc., Fujisaki Institute, 675-1 Fujisaki, Okayama 7028006, Japan.
The preventive effect of Coriandrum sativum, Fam. UMBELLIFERAE (Chinese parsley) on lead
deposition was investigated in male ICR mice given lead (1000 ppm) as lead acetate trihydrate
in drinking water for 32 days. Administration of Chinese parsley to mice by gastric intubation
was performed for 25 days from day 7 after the start of lead exposure up to the end of the
experiment. The mice were then sacrificed for comparison of lead distribution. The lead
reached its highest concentration in the femur but localized lead deposition in the femur was
significantly decreased by meso-2,3-dimercaptosuccinic acid (DMSA), a chelating agent used
as a positive control to validate this experimental model. Administration of Chinese parsley
also significantly decreased lead deposition in the femur and severe lead-induced injury in the
kidneys. In addition, urinary excretion of delta-aminolevulinic acid (ALA) which is known to
increase with lead intake was significantly decreased after administration of Chinese parsley.
The MeOH extract of Chinese parsley also reduced lead-induced inhibition of deltaaminolevulinic acid dehydratase (ALAD) activity in vitro.
These results suggest that Chinese parsley has suppressive activity on lead
deposition, probably resulting from the chelation of lead by some substances
contained in Chinese parsley.
PMID: 11535365 [PubMed - indexed for MEDLINE]
Alfalfa Leaf
Alfalfa leaf has an extraordinary ability to alkalize
and detoxify the body. It balances blood sugar
and hormones, and acts as a diuretic
Barley Grass
Containing lots of chlorophyll and other essential
nutrients that act in a way to help detoxify the
body of toxins such as heavy metals and
pollutants.
Cilantro
A perennial herb also known as coriander or
Chinese parsley. It binds to heavy metals and
helps remove them from your body.
Dandelion Leaf
Helps stimulate a sluggish gallbladder and
promotes bile excretion from the liver so the body
can more efficiently process foods and liquids
while also purging harmful toxins.
Garlic
An effective blood purifier and
liver/gastrointestinal detoxifier, garlic has native
organosulfurs that boost levels of enzymes in
the body that detoxify potential carcinogens.
Red Yeast Rice
Used for more than 1,000 years in China as both a
food and a medicinal product. Today it is known as a
nutrient that has been shown in clinical trials to lower
LDL (‘bad’) cholesterol and triglyceride levels, and
raise HDL (‘good’) cholesterol levels.
Carrageenan
A seaweed extract common in the Atlantic Ocean.
A promising microbicide, The laboratory of Cellular
Oncology at the National Cancer Institute reported that
carrageenan is an extremely potent infection inhibitor
for a broad range of sexually transmitted HPVs.
Chlorella
Chlorella is one of the top nutrients for absorption of toxic
metals. Well known in the field of environmental toxicology,
Chlorella readily absorbs toxins such as uranium,
cadmium,and mercury.
Spirulina
Providing more than 12 times more digestible protein than beef,
Spirulina is also known to be good natural bone medicine due
to it's high calcium content. It helps to regulate blood sugar,
helps to detox the body from heavy metals, is good for the
liver and assists with weight loss.
Magnetic Therapy in Eastern Europe: A Review of 30 Years of Research
By Jiri Jerabek, MD, PhD and William Pawluk, MD, MSc
The book presents information summarizing conditions studied, magnetic field strength and type of
field used, frequency and duration of application and summary of actual results. There are detailed
descriptions of many studies on both static (permanent) and frequency (pulsed) fields.
Controlled human studies described include:
· Atherosclerosis
· Brain neurosecretion
· Breast fissures
· Burns
· Carpal tunnel syndrome
· Cervicitis
· Chronic bronchitis
· Controlled Studies Animals
· Corneal trauma
· Edema
· Endometriosis
· Femoral artery surgery
· Fractures
· Increased circulation
· Infected skin wounds
· Ischemic heart disease
· Limb grafts
· Liver function
And more…
THANK YOU
Garry F. Gordon MD, DO, MD(H)