In their book Infectious Diabetes Doug Kaufman and Dr. David Holland describe a significant link between diabetes and cancer, pointing out that when our immune system is compromised and unable to fight off fungal invasions that we succumb to cancer more easily. Diabetics are predisposed to cancer at much higher rates than non-diabetics.
People with type 2 diabetes (the most common form) are twice as likely to develop liver or pancreatic cancer. They also run a higher-than-normal risk of developing colon, bladder and breast cancer. Diabetes doubles the risk of liver, pancreas, and endometrial cancer. It increases the risk of colorectal, breast, and bladder cancer by 20% to 50%.
Patients with type 2 diabetes also have a 20 percent increased risk of developing blood cancers, such as non-Hodgkin lymphoma, leukemia and myeloma, according to a new meta-analysis led by researchers at The Miriam Hospital.
Though the mainstream of medicine says, “Though type 2 diabetes and cancer share many risk factors, the potential biologic links between the two diseases are incompletely understood.”
However, we can easily identify some of the common denominators of diabetes and cancer. Sugar and the inflammation it causes is common to both diseases. Another common denominator are acid conditions that strike the pancreas, which is the organ in our body most sensitive to lowered pH. Acid conditions are synonymous with low oxygen conditions and higher levels of oxidative stress.
Pancreatic beta cells are sensitive to reactive oxygen species (ROS) attack when they are exposed to oxidative stress, because of the relatively low expression of antioxidant enzymes such as catalase and glutathione peroxidase. Diabetes is typically accompanied by increased production of free radicals and/or impaired antioxidant defense capabilities, indicating a central contribution of reactive oxygen species.
What we will concentrate on in this chapter is mercury toxicity and in the next one we will look at how magnesium deficiencies underlie most diabetic conditions. What we have in diabetes is mercury toxicity slamming into widespread magnesium deficiencies.
Insulin resistance results from functional and structural abnormalities
of insulin receptors caused by oxidative cell membrane injury.
Dr. Majid Ali
One of the strongest hypothesis to explain why diabetes might increase the risk for certain cancers revolves around hyperinsulinemia, the high blood levels of insulin characteristic of diabetes. "From animal studies we know that high insulin levels can directly promote tumor growth," said Dr. Frank Hu, M.D., assistant professor of nutrition at the Harvard University School of Public Health, Boston.
Low serum and intracellular magnesium concentrations are associated with insulin resistance, impaired glucose tolerance, and decreased insulin secretion. Magnesium improve insulin sensitivity thus lowering insulin resistance. Magnesium and insulin need each other. Without magnesium, our pancreas won’t secrete enough insulin–or the insulin it secretes won’t be efficient enough–to control our blood sugar.
Signs of severe magnesium deficiency include:
Sores or bruises that heal slowly
Dry, itchy skin
Unexplained weight loss
Blurry vision that changes from day to day
Unusual tiredness or drowsiness
Tingling or numbness in the hands or feet
Frequent or recurring skin, gum, bladder or vaginal yeast infections
But wait a minute, aren’t those the same symptoms for diabetes? Many people have diabetes for about 5 years before they show strong symptoms. By that time, some people already have eye, kidney, gum or nerve damage caused by the deteriorating condition of their cells due to insulin resistance and magnesium deficiency. Dump some mercury and arsenic on the mixture of etiologies and pronto we have the disease condition we call diabetes.
Though diabetes has multiple etiologies, nothing explains the epic rise in diabetes as does the relationship between the rising tide of mercury and the decreasing tide of magnesium sufficiency. Mercury toxicity and magnesium deficiency are common causes of cancer and diabetes.
In this chapter we concentrate on the Hun Hordes of Mercury and in the next we will begin to review magnesium, first in its relationship to diabetes and then in another following chapter, how magnesium deficiencies lead to cancer and thus why magnesium medicine must be included in all cancer protocols.
The CDC says that diabetes is disabling, deadly and on the rise. The incidence of diabetes is skyrocketing not only in adults but in the juvenile population as well. Health care experts have called the alarming rise in diabetes and its related complications “an epidemic” that threatens to spiral out of control. In 1997 15.7 millions adults in the United States were reported to have diabetes.  By the year 2002, this number had already swelled to 18.0 million or 8.7% of all adults.
Diabetes is a fundamental disease that affects the entire colony of cells in a person because it has to do with energy metabolism and the vastly important hormone insulin and its receptor sites. All life is dependent upon basic metabolism, the input of nutrients and removal of wastes. Insulin allows blood sugar (glucose) to be transported into cells so that they can produce energy or store the glucose until it is needed. Insulin binds with receptors on cells like a key would fit into a lock.
 American Diabetes Association: Diabetes Facts and Figures [factsheet online] 1997 [cited August 1999][16 screens]. Available from: URL: http://www.diabetes.org/ada/c20f.asp
 CDC. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2003.pdf
Diabetes is often conceptualized as a severe imbalance of part of endocrine system that destroys our ability to metabolize food. The unbalance results in elevated levels of insulin, a lack of insulin, or the cell insulin receptor sites becoming insensitive to insulin. It has long been thought that a diet rich in “empty” sugars will catch our pancreas and adrenal glands in a biochemical see-saw, overworking them and this could weaken the pancreas and result in diabetes yet the medical establishment insists that there is absolutely no link between sugar consumption and diabetes.
Sugars increase our body's production of adrenaline which puts the body into a state of ’fight or flight' stress, without anything to fight or flee from, except the consumption of sugar. This stress reaction increases the production of both cholesterol and cortisone. White sugar lacks the vitamins and minerals required for its own metabolism. To be metabolized, “empty” sugars must draw on our body's stores of vital nutrients. The more sugars you eat, the more vitamins and minerals you need. It can leach B, C, D vitamins, and the following important minerals: calcium, phosphorous, iron, zinc, selenium, magnesium and chromium from body tissues.
As these are depleted, our body becomes less able to carry out other functions that require minerals and vitamins to be present. Chromium is important here for it is thought to enhance the activity of the hormone insulin. And selenium is useful as a controlling agent for mercury which attacks insulin and its binding sites.
White sugar and all the foods that use it can be considered poison simply because they strip the body of crucial minerals and vitamins that allow other vastly more toxic poisons to defeat the body’s defenses.
In 2000-2001, about 82,000 lower-limb amputations
were performed annually among people with diabetes.
In fact, statistics show that every hour, nine people with diabetes
must have a toe, foot or leg amputated to save their lives CDC
This is just one cruel-some aspect of diabetes, of which there are many. According to the researchers, 25-44 pct of heart-suffering people are also diabetic. The nexus between type II diabetes, insulin and heart diseases is renowned. Insulin is a high alert drug because of its ability to throw people into dangerously low blood sugars.
Few in the world of medicine see that diabetes actually results from poisoning. In volume 18 of Clinical Toxicology in 1981 there was a write up about cases of suicide attempts using rat poisoning where all four cases showed hyperglycemia and ketosis. The authors concluded that ingestion of rodenticide can cause diabetes mellitus after they noticed that the onset of diabetes mellitus varied within a very short period of time after swallowing of the poison – only 4 to 7 days.
Medical science avoids telling doctors how sensitive the insulin receptor sites are to chemical poisoning. Patients treated with the atypical anti-psychotic agents clozapine and olanzapine are showing increased risk for insulin resistance according to a study published in the January 2005 issue of The Archives of General Psychiatry, one of the JAMA/Archives journals. The American Diabetes Association made an announcement warning people to be careful to watch for signs they are developing diabetes, obesity or high cholesterol if they are taking Abilify, Clozaril, Geodon, Risperdal, Seroquel or Zyprexa.
Below we offer demographic maps of diabetes prevalence by state and then compare with maps of mercury concentrations.
Source: CDC, Behavioral Risk Factor Surveillance System.
The first thing one should notice about these charts is that there is no significant difference in diet and exercise patterns from state to state to explain the different rates of diabetes we see in the CDC map. What the maps below suggest is massive poisoning with mercury is influencing much of the in diabetic epidemic.
 Gallanosa, AG, Spyker DA, Curnow, RT. Clinical Toxicology, Vol 18. No.4, pages 441-449, 20 references, 1981 Diabetes Mellitus Associated with Autonomic and Peripheral Neuropathy After Vacor Rodenticide Poisoning: A review
 Arch Gen Psychiatry. 2005; 62: 19 – 28.
 Journal Diabetes Care. February 2004
Researchers were baffled by the increased incidence of diabetes in Appalachia. In West Virginia, the only state entirely in Appalachia, 1 in 10 people aged 18 and older was told by a doctor that he or she had diabetes in 2002. Dr. Robert B. Walker of Marshall, noting that West Virginia's incidence of diabetes is 41 percent above the national average said, "No disease stresses rural West Virginia families and health providers more than diabetes."
Up and down the eastern part of the United States we find high levels of mercury. The above maps and demographics set the stage for a serious proposal that mercury poisoning is at the heart of the modern plague of diabetes, and thus also of heart and kidney disease, strokes, blindness, and other common complications of diabetes.
No one in mainstream medicine is taking into account the intensifying increase in background mercury contamination of fish, water, air, soil and foods or calculating the hundreds of trillions of mercury atoms and molecules being absorbed directly each day, day after day, year after year through having gram weight quantities placed directly in the mouth. Also, almost unbelievably, mercury is injected directly into children’s blood streams via vaccines.
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 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.
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
Mercury, in its various forms, has a great attraction to the sulfhydryls or thiols. 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.
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 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.
Adult onset (type 2) diabetes develops when glucose homeostatic regulation breaks down. Most type-2 diabetics produce enough insulin but have developed resistance to normal insulin action in target tissues and now we have an explanation why. When we look at the fact that peripheral cells each have approximately 3,500 receptor sites, (other cells have less) that there are 70 trillion cells in the body; and thousands of trillions of atoms an average person with a mouth full a amalgam might ingest each day, we can see why diabetes tends under most conditions, even with mercury directly assaulting these sulfur bonds, to be a slow onset disease and that’s why the prevalence increases with age.
When the available sites on the cells drop into the 1,200 to 1,500 ranges the cell and entire insulin hormone system run into serious trouble. When it comes to children and early onset diabetes thimerosal is one likely villain. Thimerosal is ethyl-mercury mixed with aluminum in the vaccine and if anyone ever wanted to discover the ultimate elixir of death, they probably found it. Injecting millions of children with 150,000 trillion atoms of supercharged death particles (50 micrograms in two thimerosal containing vaccines before this preservative was removing from most vaccines in 1999) was surely the ultimate treason against a generation of children.
Vaccines are the largest cause of
insulin dependent diabetes in children.
Dr. J. Barthelow Classen
Dr. J. Barthelow Classen, in the Journal of Pediatric Endocrinology and Metabolism (2003), published research into the links between vaccine and insulin-dependent diabetes. Classen's research indicates that vaccinations can cause autoimmune diseases and he cites research from New Zealand indicating that the incidence of diabetes there has increased by 50 percent since 1988 when hepatitis B was given to New Zealand children under 16.
He also cited a rapid rise in the incidence of childhood diabetes since the introduction of the HiB vaccine--50 cases of diabetes per 100,000 vaccinated children. According to Classen vaccines in general can cause interferon release, which can in turn induce human diabetes. “Our results conclusively prove there is a causal relationship between immunization schedules and diabetes,” states Dr. Classen. The Hep B vaccine was notorious for its heavy concentration of mercury. Though thimerosal (fifty percent mercury by weight) has been taken out of Hep B vaccines in the United States that is not the case in the third world.
Mercury interacts with sulfhydryl groups and disulfide bonds,
as a result of which specific membrane transport is blocked
and selective permeability of the membrane is altered.
Thus insulin's ability to lower blood sugar is compromised. Mercury is causing chronic hyperinsulinemia because insulin resistance causes serum hyperglycemia and intra-cellular hypoglycemia (since glucose cannot get into cells) and the cells perceive this state as starvation. As a consequence, blood glucose levels become so elevated that the glucose "spills over" into the urine, and is converted into triglycerides (fat), which contribute to cardiovascular illness. Despite these high blood glucose levels, cells "starve" since insulin-stimulated glucose entry into cells is impaired, which leads to an acid condition ketosis. To compensate the body releases glugcagon, cortisol, and catecholamines which further raise blood sugar levels. More insulin is pumped out resulting in hyperinsulinemia and this creates a cascading biological disaster of triglyceride and cholesterol excess, hypertension, inflammatory cytokine release and further endocrine dysfunction. 
Peripheral neuropathy is a common condition that can cause
numbness and tingling. It can be caused by diabetes or
overexposure to toxic chemicals, such as mercury or lead.
Park Nicollet Institute
It is through mercury’s attack on these sulfide bonds that mercury is able to change the biological properties of proteins and change important physiological functions. Full recognition of the poisonous strength of mercury comes through a focused study of the series of physiological processes that are affected when SH groups are disturbed.
Mercury is acting in the place of first cause creating the high levels of glucose through its interference in insulin and insulin receptor sites. All these glycated proteins are creating 50 times the amount of free radicals than non-glycated proteins.
Though mercury has other toxic routes creating havoc in cardiovascular tissues and even in nuclear cell processes, advanced glycosylation will normally accelerate mitochondrial damage, encourage expression of defective cancer genes, and cause protein damage underlying skin aging and wrinkling as well as providing for stiffer joints.
The beginning symptoms of diabetes are so mild that most who exhibit them do not realize that they are under a sentence of premature death and disability. The same could be said about the beginning symptoms of mercury poisoning.
 Trakhtenberg, I.M. From Russian translation. Chronic Effects of Mercury on Organisms. In Place of a Conclusion
 Metabolic Dysglycemia Profile. Laboratory Assessments. http://www.gsdl.com/assessments/dysglycemia/appguide/index.html
 Feener EP, Kin GL. Vascular dysfunction in dia-betes mellitus. Lancet 1997(suppl):9-13.
 Lempiainen P, Meykkanen L, Pyorala K, Laakso M, Kuusisto J. Insulin resistance syndrome predicts coronary heart disease events in elderly nondiabetic men. Circulation 1999;100:123- 128.
In the beginning of the last section we stated that diabetes actually results from poisoning. Pancreatic beta cells are sensitive to reactive oxygen species (ROS)  and oxidative stress caused by radiation exposure. Radiation of course is another form of poison.
Incidence of type 1 diabetes mellitus, a disorder involving the immune system, was observed within the residential population of Hiroshima among survivors of the atom bomb detonation. Studies have also shown that thymectomy and a sub-lethal dose of gamma radiation induces type 1 diabetes in rats. Mass screening for diabetes mellitus has been conducted on 64,000-113,000 atomic bomb survivors residing in Hiroshima City since 1961. From 1971 to 1992 a 2.7-fold increase in the prevalence of diabetes mellitus was observed in males and a 3.2-fold increase in females.
Researchers at the Pediatric Hospital A. Meyer, Florence, Italy studied children in Gomel, Belarus in the years subsequent to the Chernobyl disaster. The results of the study confirmed the hypothesis that environmental pollution such as that subsequent to the Chernobyl accident can cause diabetes.