IMVA - Diabetes and Mercury Poisoning - October 2, 2006

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Diabetes and Mercury Poisoning

International Medical Veritas Association

 

On August 1st of 2006 the American Chemical Society published research that

showed conclusively that Methylmercury Induces Pancreatic Cell Apoptosis and

Dysfunction.[1] Mercury is a well-known toxic agent that produces various types

of cell and tissue damage yet governmental health agencies diminish this fact

exposing billions of people to levels of mercury harmful to pancreatic health.

In the case of diabetes mercury is especially telling for it affects the beta

cells, the insulin itself, and the insulin receptor sites setting off a

myriad of complex disturbances in glucose metabolism.

 

Metals such as iron, arsenic, lead, aluminum, other chemicals and

pharmaceutical drugs are also playing a role in the disruption of glucose

metabolism as

we will examine in another chapter. But mercury leads the pack in the potency

of its toxicity and in the pervasiveness of it presence in the environment,

medicine and dentistry. Doctors who administer mercury laden vaccines and

dentists who plant highly toxic mercury in people’s mouths in the form of

dental

amalgam cannot seem to see the forest from the trees and curb their use of it.

 

Thiol poisons, especially mercury and its compounds, reacting with SH groups

of proteins lead to the lowered activity of various enzymes containing

sulfhydryl groups. This produces a series of disruptions in the functional

activity

of many organs and tissues of the organism.

Professor I.M. Trakhtenberg[2] Russia

 

Enzymes are proteins, and like all proteins they consist of chains of amino

acids. These chains have to be faulted in a specific way to give the enzyme

its activity. In many enzymes, the structure of the enzyme is ensured by

cross-bonding of the amino-acid chains. These cross-bonds consist of double

sulfur

bonds. Sulfur-bridges are covalent S-S bonds between two cysteine amino acids,

which tend to be quite strong. These sulfur bonds are damaged when poisonous

substances that are not naturally present have been added to the local

environment. Mercury binds to the -SH (sulfhydryl) groups, resulting in

inactivation of

sulfur and blocking of enzyme functions while producing sulfur metabolites

with high toxicity that the body has difficulty dealing with. Sulfur is

essential in enzymes, hormones, nerve tissue, and red blood cells. These sulfur

bonds

are crucial to human biology.

 

 

Insulin is synthesized in significant quantities only in Beta cells in the

pancreas and is secreted primarily in response to elevated blood concentrations

of glucose. Each insulin molecule consists of precisely 2 peptide chains (A

and B) bound together by sulfa bonds at the A7-B7 Cysteine site and at the

A20-B19 Cysteine site and there is an additional Cysteine sulfa bond at the

A6-A11. All insulin molecules consist of this two chain structure, with an A

chain

of 21 amino acids and a B chain of 30 amino acids, for a total of 51 amino

acid molecules bound by 3 sulfa bonds. Mercury, in its various forms, has a

great attraction to the sulfhydryls or thiols – these sulfa bonds. A thiol is

any

organic compound containing a univalent radical called a sulfhydryl and

identified by the symbol -SH (sulfur-hydrogen).

 

 

 

 

Various molecules or atoms will affect the rate of an enzyme catalyzed

reaction by binding to the enzyme. Some bind at the same site as the substrate

(the

active site) and prevent the substrate from binding. Others bind at sites on

the enzyme remote from the active site and affect activity by modifying the

shape of the enzyme. Many of these molecules reduce the activity of the enzyme

and are referred to as inhibitors. Mercury is the most potent enzyme inhibitor

that exists; it is in a class of its own and well deserves its title as the

most toxic non-radioactive element. It is because mercury and lead attach

themselves at these highly vulnerable junctures of proteins that they find their

great capacity to provoke biochemical shifts and then morphological changes in

the

body. Transsulfuration pathways in the body are fundamental for life. When

mercury blocks thiol groups cellular proteins lose their reactive properties,

lose their ability to carry out their routine function.

 

Because glycemic regulation is one of the body’s most central homeostatic

mechanisms, mercury’s attack is most problematic,

even at low concentrations, and

indicates that it is playing a great role in the dramatic rise in

diabetes.[3]

 

Insulin has three sulfur-containing cross-linkages and the insulin receptor

has a tyrosine kinase-containing sulfur bond, which are the preferred targets

for binding by both mercury and lead. Should mercury attach to one of these

three sulfur bonds it will interfere with the normal biological function of the

insulin molecule. The average adult inhales thousands of trillions of mercury

atoms a day from a mouth full of amalgam, fish provide trillions more, the air

more, and in children, vaccines provide one day surges of vast trillions of

mercury molecules in the form of ethyl-mercury, which is vastly more toxic than

metallic mercury. Insulin molecules are directly assaulted as are insulin

receptor sites.

 

Insulin - one of the body's most important hormones –

interacts with a cell and is governed

by the shape of the insulin receptor.

 

Equally vulnerable to mercury’s ruin are the receptor tyrosine kinases (RTKs)

which are glycoproteins that transduce insulin’s extracellular signal to the

cytoplasm of the cell. It functions as an enzyme that transfers phosphate

groups from ATP to tyrosine residues on intracellular target proteins. The RTK

insulin receptor is comprised of two extracellular alpha chains disulfide-linked

to two membrane-spanning beta chains. Like the receptors for other protein

hormones, the receptor for insulin is embedded in the plasma membrane. The

effects of insulin are mediated by the insulin receptor (specific RTK for

insulin),

and when insulin binds with its receptor, the receptor activates and recruits

a whole chain of downstream signaling processes.

 

 

 

The insulin receptor is no ordinary protein. It is about 200 times bigger

than insulin itself, it is actually two identical molecules intertwined.

 

The three dimensional crystal structure of insulin-like growth factor 1

(IGF1) receptor provides a clue to the complete vulnerability of humans when it

comes to mercury’s destructive power that can lead to diabetes. The molecular

structure of both IGF1 and the RTK insulin receptor sites are rich in cysteines

and as such we find an array of disulfide-linked modules that mercury

penetrates. Published studies from Northeastern University with thimerosal show

that it

inhibits the ability of insulin-like growth factor-1 (IGF-1) to activate the

enzyme methionine synthase. Decreased activity of IGF-1 signaling is

associated with type 1 diabetes, particularly a failure of signaling in

insulin-secreting beta islet cells.

 

It is these protein's folds, coils, twists, and contours

that govern their interaction with insulin.

Much like the key to your front door fits perfectly with its lock and no

others, an insulin receptor is like the lock and insulin is like the key.

 

A single preliminary experiment at the Joslin Diabetes Clinic showed that

thimerosal (ethyl-mercury) inhibits an early step in the signaling pathway.

Studies at Northeastern also provided evidence that Cu2+ stimulates the IGF-1

signaling pathway, and it appears that thimerosal is also interfering with this

normal activity. Some doctors have speculated about vaccines being responsible

for the increases we are seeing in children’s diabetes but now it is becoming

clearer that children’s systems are under a broad mercury attack with each

source, type of mercury, and mode and timing of contamination setting stages for

different pathologies.

 

The general model of insulin activity indicates that one insulin molecule

engages the cystein-rich domain of the receptor, touching down on both sides of

protein chain that are separated by the disulfide bond. If the geometry of the

receptor has been changed by mercury the message that insulin has arrived to

give glucose to the cell is not received. Mercury is an inhibitor capable of

interfering with PTK catalytic activity exactly because it is

collapsing/damaging these sulfur-containing cross-linkages which changes the

geometry of both

insulin receptor and insulin itself.

 

It is reasonable to assume a direct correlation between rising environmental

mercury levels, mercury exposure through dental amalgam, heavy fish

consumption and exposure to mercury in vaccines with the rapidly expanding

diabetic

pandemic, not to mention the host of drugs and even chemicals put into foods

that

are part of the diabetic equation. The medical establishment is dragging its

collective ass when it comes to understanding the causes of diabetes and thus

is remaining impotent in the face of a steadily worsening human catastrophe. It

is perfectly clear though to health officials that the diabetic epidemic is

expanding rapidly but because they scratch their heads about chemical causes

they remain incapable of arresting the pandemic.

 

Medical and health officials seem to live in an unconscious fog when it comes

to mercury even though Methylmercury (MeHg) induces oxidative stress and cell

cytotoxicity through mitochondrial apoptosis[4] pathways.

 

New information shows that in the United States alone 50 million are pre

diabetic,[5] up from estimates of 41 million only two short years ago and this

could correlate with the rapidly escalating production of mercury pollution

coming from China, which is contributing greatly to increased world wide mercury

exposure. Some say we are all receiving, just through our air, water and food

about a microgram of mercury a day. Sounds like little until you calculate that

a microgram contains 3,000 trillion atoms with each of them holding the

potential to deactivate insulin and the receptor sites crucial to their

function.

 

Mercury can induce apoptosis in human T lymphocytes.

The target organelle was the mitochondrion and that induction of oxidative

stress led to activation of death-signaling pathways.[6]

 

The official position of medical, dental and governmental agencies is that

there have been virtually no cases of mercury poisoning in the United States so

they cannot understand what all the fuss is about from environmentalists and

health activists who are confronting industry and both dentists and doctors’

obscene use of mercury. We hear statements like, " There is a misguided fear out

there, " said Dr. Ed Hewlett of the American Dental Association. " In order to

have even the earliest signs of a problematic effect with mercury fillings, a

person would have to have 500 silver fillings in their mouth, all at the same

time. " Doctors say the same about mercury in vaccines finding no problem

injecting infants with thimerosal containing vaccines. It is apparent that

governments in the United States and China are not interested in investing money

in

reducing the amount of mercury coming out of coal burning smoke stacks or other

point sources of mercury pollution. Instead we have vast propaganda campaigns

diminish the public danger while encouraging fish consumption, flu and other

vaccines containing mercury, and dental amalgam as safe.

 

MeHg triggers ROS production, suppresses insulin secretion,

and induces apoptosis in -cell-derived HIT-T15 cells

and isolated mouse pancreatic islets.

College of Medicine, Taiwan University

 

Mercury has always been known as a toxic metal that induces oxidative stress.

Since it has also been known that pancreatic cells are vulnerable to oxidative

stress it should come as no surprise that researches have found that the

rising tide of mercury in the environment is pushing a worldwide epidemic in

both

type 1 and 2 diabetes. Also of no surprise is that this research showed that

antioxidant N-acetylcysteine effectively is able to reverse MeHg-induced

cellular responses.

 

The Researchers in Taiwan say they have established for the first time that

the mercury compound present as a contaminant in some seafood can damage the

insulin-producing cells in the pancreas. In their experiments, Shing-Hwa Liu and

colleagues exposed cell cultures of insulin-producing beta cells to

methylmercury. They used concentrations of methylmercury at about the same

levels as

people would consume in fish under the U. S. Food and Drug Administration's

recommended limits.

 

It has been shown that an increased incidence of diabetes existed in patients

with documented Minamata disease (MeHg poisoning) in Japan.[7] Takeuchi et

al. reported that the disturbance of pancreatic islet cells was found in autopsy

cases of Minamata disease.[8] In experiments using rats, Shigenaga has found

that pancreatic islets were injured by MeHg and that a high level of blood

glucose was induced by repeated administration of MeHg.[9]

 

It has been suggested in the past that pancreatic beta cells might be rather

sensitive to reactive oxygen species (ROS)[10] attack when they are exposed to

oxidative stress,[11] because of the relatively low expression of antioxidant

enzymes such as catalase and glutathione peroxidase.[12] Diabetes is

typically accompanied by an increased production of free radicals and/or

impaired

antioxidant defense capabilities, indicating a central contribution of reactive

oxygen species. It is a fact that ROS is one of the major factors that induce

oxidative modification of DNA and gene mutation.[13]

 

MeHg significantly increased ROS levels.

 

ROS is involved in the onset, progression, and pathological consequences of

diabetes.[14] The study published by the American Chemical Society showed that

MeHg is capable of suppressing insulin secretion of pancreas cells through a

ROS-triggered pathway. MeHg-induced oxidative stress causes pancreatic beta

cell apoptosis and dysfunction. What this means is that right under doctors and

medical officials noses millions are having their lives ruined.

 

When it comes to mercury vaccines EPA safety levels are exceeded as a vast

number of organic mercury molecules enter the system in one moment but again

health officials step in with what can only be seen as an obscene idea that

suggests that one-day exposures can be averaged out through many months. It’s

like

saying one can take six months of heart medication all in one day. Someday it

will dawn on both dentists and doctors who use mercury that they are actually

poisoning children and people.

 

Because mercury is increasingly becoming elevated in all forms of life, we

can assume that more people will have some defects in pancreatic function.

Pancreatic support is increasingly necessary for optimal health.

Dr. Garry Gordon

 

Most doctors are lost in their force fed concepts when it comes to diabetes

and this blinds them to a tragedy of staggering proportions. The same can be

said of the medical establishment and autism but parents have independently

found out that detoxification and chelation treatments that reduce mercury and

other toxic chemical body burdens helps their children. It is a totally new idea

that reducing mercury exposure and eliminating (chelating) mercury from the

body can reduce, stabilize or even be part of a cure for the diabetic condition.

 

 

Mercury is now part of the human weather with clouds billowing around the

upper atmosphere. The government can doubt all it wants about planetary warming

and the human factor involved in it. They try the same game about mercury

trying to deflect the problem by stating there is and always have been large

scale

natural emissions of mercury. But there is no doubting the rising tonnage

(approximately 20 tons a day) put into the air everyday by human activity.

That’s

a lot of mercury and it’s showing up in the quickly escalating diabetes

statistics.

 

Mark Sircus Ac., OMD International Medical Veritas Association

http://www.imva.info

http://www.magnesiumforlife.com

Email: director

 

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International Medical Veritas Association

Copyright 2006 All rights reserved.

 

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