Diabetes and Mercury Poisoning

by Dr. Mark Sircus

Summary

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, but mercury leads the pack in the potency of its toxicity and in the pervasiveness of its 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.

On August 1, 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, Russia [2]

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.

Dr. Mark Sircus Ac. OMD, Director International Medical Veritas Association
International Medical Veritas Association, Copyright 2006 All rights reserved.

References

[1] Ya Wen Chen, Chun Fa Huang, Keh Sung Tsai, Rong Sen Yang, Cheng Chieh Yen, Ching Yao Yang,# Shoei Yn Lin-Shiau, and Shing Hwa Liu. Chem. Res. Toxicol., 19 (8), 1080 -1085, 2006. Institute of Toxicology, Department of Laboratory Medicine, and Department of Orthopaedics, College of Medicine, National Taiwan University, Taipei, Taiwan, and Departments of Traumatology, Surgery, and Emergency Medicine, National Taiwan University Hospital, Taiwan

[2] Trakhtenberg, I.M. From Russian translation. + Chronic Effects of Mercury on Organisms. In Place of a Conclusion

[3] Type I or insulin-dependent diabetes mellitusis the result of a frank deficiency of insulin. The onset of this disease typically is in childhood. It is due to destruction of pancreatic B cells, most frequently believed to be the result of autoimmunity to one or more components of those cells and/or the affects of some environmental cause. Many of the acute effects of this disease can be controlled by insulin replacement therapy. Maintaining tight control of blood glucose concentrations by monitoring, treatment with insulin and dietary management is promoted to minimize the long-term adverse effects of this disorder on blood vessels, nerves and other organ systems,

Type II or non-insulin-dependent diabetes mellitusbegins as a syndrome of insulin resistance. That is, target tissues fail to respond appropriately to insulin. Typically, the onset of this disease is in adulthood, but incidence of type 2 diabetesx is rising in people under 40 and even more alarmingly, in children. Despite monumental research efforts, the nature of the defect has been difficult to ascertain - in some patients, the insulin receptor is abnormal, in others, one or more aspects of insulin signalling is defective, and in others, no defect has been identified. Because there is not, at least initially, an inability to secrete adequate amounts of insulin, insulin injections need not be used for therapy. Rather the disease is controlled through dietary therapy and hypoglycemic agents. Often lifestyle, dietary and nutritional changes can reverse type II diabetes.

[4] In biology, apoptosis (from the Greek words apo=from and ptosis=falling, commonly pronounced ap-a-tow'-sis) is one of the main types of programmed cell death (PCD). Apoptosis can occur, for instance, when a cell is damaged beyond repair, or infected with a virus. The "decision" for apoptosis can come from the cell itself, from its surrounding tissue or from a cell that is part of the immune system.

[5] Over 50 million adults ages 40-74 have pre-diabetes, of which 1 in 4 will develop type 2 diabetes. Based on projected NHANES III data, the number of prediabetic individuals was almost 12 million in 2000 among overweight individuals. Patients with prediabetes have the potential to develop diabetes within a decade if no modifications to their diet and level of physical activity are made. http://www.medscape.com/infosite/hood/article-expanding

[6] Shenker, B. J., Guo, T. L., O, I., and Shapiro, I. M. (1999) Induction of apoptosis in human T-cells by methyl mercury: Temporal relationship between mitochondrial dysfunction and loss of reductive reserve. Toxicol. Appl. Pharmacol. 157, 23-35.

[7] Uchino, M., Tanaka, Y., Ando, Y., Yonehara, T., Hara, A., Mishima, I., Okajima, T., and Ando, M. (1995) Neurologic features of chronic minamata disease (organic mercury poisoning) and incidence of complications with aging. J. Environ. Sci. Health B 30, 699-715.

[8] Takeuchi, T., and Eto, K. (1997) Pathology and pathogenesis of Minamata disease. In Minamata Disease-Methyl Mercury Poisoning in Minamata and Niigata, Japan (Tsubaki, T., and Irukayama, K., Eds.) pp 103-141, Kodansya, Tokyo.

[9] Shigenaga, K. (1976) Pancreatic islet injury induced by methyl mercuric chloride light and electron microscopic studies. Kumamoto Med J. 29, 67-81

[10] ROS (Reactive Oxygen Species) are natural byproducts of oxygen metabolism in the body. Free radicals and other byproducts are formed as a result of this metabolism, and at lower levels can be very beneficial, but when too many of these byproducts are formed the situation of oxidative stress occurs. Reactive oxygen species (ROS) include oxygen ions, free radicals and peroxides both inorganic and organic. They are generally very small molecules and are highly reactive due to the presence of unpaired valence shell electrons. Oxidative stress is a medical term for damage to animal or plant cells (and thereby the organs and tissues composed of those cells) caused by excesses of these reactive oxygen species, which include (but are not limited to) superoxide, singlet oxygen, peroxynitrite or hydrogen peroxide. Superoxide is produced deleteriously by 1-electron transfers in the mitochondrial electron transfer chain. It is defined as an imbalance between pro-oxidants and anti-oxidants, with the former prevailing. The causes of these excesses are many, and include environmental influences of every type. Enzyme activities are sometimes affected negatively, leading to greater production of excess ROS, and heavy metals such as chromium, vanadium, and others are said to be involved, now this new evidence that methylmercury definitely plays a significant role in the pancreas. Cells are normally able to defend themselves against ROS damage through the use of enzymes such as superoxide dismutases and catalases. Small molecule antioxidants such as Ascorbic acid (vitamin-C),uric acid, and glutathione also play important roles as cellular antioxidants. Similarly, Polyphenol antioxidants assist in preventing ROS damage by scavenging free radicals. Studies are conflicting on some antioxidants such as Vit. E. The resulting inflammatory processes are believed to be the result of these ROS excesses and include cardiovascular disease, ALS, neurodegenerative diseases, and many others.

[11] Kajimoto, Y., and Kaneto, H. (2004) Role of oxidative stress in pancreatic beta-cell dysfunction. Ann. N. Y. Acad. Sci. 1011, 168-176.

[12] Tiedge, M., Lortz, S., Drinkgern, J., and Lenzen, S. (1997) Relation between antioxidant enzyme gene expression and antioxidative defense status of insulin-producing cells. Diabetes 46, 1733-1742.

[13] Inoue, M., Sato, E. F., Nishikawa, M., Hiramoto, K., Kashiwagi, A., and Utsumi, K. (2004) Free radical theory of apoptosis and metamorphosis. Redox Rep. 9, 237-247.

[14] Rolo, A. P., and Palmeira, C. M. (2006) Diabetes and mitochondrial function: Role of hyperglycemia and oxidative stress. Toxicol. Appl. Pharmacol. 212, 167-178.