Mercury and Diabetes
While no human studies have yet linked mercury exposure to diabetes, it could be because no one has looked. Type 2 diabetes is caused by the combination of insulin resistance and dysfunction of the insulin-producing beta cells; mercury has been linked to both of these conditions. Type 1 diabetes is caused by an autoimmune destruction of the beta cells; mercury has been linked to autoimmunity as well (see the "autoimmune" page for information on autoimmunity and mercury).
Let's look at the evidence that mercury can influence beta cells and insulin resistance, and therefore potentially diabetes.
A number of studies have examined the effects of mercury on beta cells in laboratory experiments. One found that inorganic mercury has been found to cause beta cell death, and decrease insulin secretion from beta cells in laboratory experiments (Chen et al. 2010). Another found that methylmercury, at concentrations similar to those found in fish (under the recommended limits), can damage beta cells and lead to beta cell dysfunction (Chen et al. 2006a). A third experiment involved exposing mice to low doses of methylmercury or inorganic mercury. It found that decreased insulin secretion and increased blood glucose levels. Interestingly, insulin and glucose levels gradually returned to normal after mercury exposure ended.
A study from a contaminanted area in Taiwan found that
This study also found that each component of metabolic syndrome (common in people with type 1 or 2 diabetes) that they studied was associated with both mercury and POP exposure levels, including an increased waist circumference (Chang et al. 2010c).
Autoimmune diseases, including type 1 diabetes, are thought to involve chronic inflammation. Inflammation is a general term for the immune system's response to something, such as an infection or injury, and chronic means the response persists over time. At the cellular level, inflammation involves the release and increased activity of various immune system cells (Janeway et al. 1999).
The inflammatory reaction in type 1 diabetes where the beta cells are attacked is called "insulitis." The immune system cells involved in the attack include various types of white blood cells (T-cells and macrophages), and/or the substances they secrete, including cytokines, nitric oxide, and free radicals (Cnop et al. 2005). (See the oxidative stress page for more on free radicals). Certain cytokines and other markers of inflammation may be associated with development of both type 1 and type 2 diabetes (Goldberg 2009). People with type 1 diabetes have higher levels of inflammatory markers than those without diabetes; even patients with good blood sugar control (Snell-Bergeon et al. 2010). A lot of researchers are trying to identifyhow exactly this inflammatory process works in the development of type 1 and type 2 diabetes: what cells are involved, and what their roles are (e.g., Cnop et al. 2005). As for why it happens in the first place, we don't know.
Cytokines are essentially messenger proteins that affect the behavior of other cells. There are various types of cytokines. Some cytokines can reduce inflammation, while other contribute to it: it is the pattern of cytokines that is critical in perpetrating autoimmune disease (Janeway et al. 1999). Cytokines are secreted by immune system cells, and control the duration and strength of the immune response (Duramad et al. 2007). In type 1 diabetes, various cytokines act together in complex ways to induce beta cell death (apoptosis) (Gysemans et al. 2008). Cytokines can affect the expression of genes that are either protective or harmful for beta cell survival (Cnop et al. 2005). A number of environmental contaminants have been found to affect cytokine levels in infants and children, including volatile organic compounds, PCBs, organophosphate pesticides, and persistent organochlorines (summerized in Duramad et al. 2007).
Inflammation can spread from one area of the body to another. This process may be involved in type 1 diabetes, where inflammation in the intestine may spread to the beta cells in the pancreas (Vaarala 2002). Inflammation of the intestine has been found in both children with type 1 diabetes and in animal models of diabetes, and may contribute to the development of type 1 diabetes (see the diet and the gut page) (Vaarala 2008).
Omega-3 fatty acids reduce inflammation, and may be protective against type 1 diabetes (see the nutrition page). Vitamin D can also protect beta cells from cytokines may be able to reduce intestinal inflammation, and also may be protective against type 1 diabetes. Breastfeeding may also reduce inflammation, while stress, wheat, or cow's milk could increase it (see linked pages for sources). Yet interestingly, vaginal delivery, associated with a lower risk of type 1 diabetes in the child, may induce a beneficial form of non-chronic inflammation (see the gestation and birthpage).
Some environmental contaminants have been found to induce inflammation in animals, including some air pollutants, arsenic, trichloroethylene, and nitrosamines. Whether the inflammatory processes induced by these contaminants could contribute to the development of type 1 diabetes is not known-- not all inflammation is created equal. Even closer to home, some contaminants have been found to produce intestinal inflammation in animals, such as some pesticides,bisphenol A, and cadmium (see the diet and the gut page for information and sources). Whether intestinal inflammation produced by these contaminants could contribute to the development of type 1 diabetes is also not known, but the possibility exists, and should be investigated.
The bottom line
Inflammatory processes appear to play a role in the development of type 1 diabetes, although how and why are still being worked out. A number of environmental factors may either protect against or contribute to the development of type 1 diabetes via their ability to protect against or contribute to inflammatory processes.
Oxidative stress means that, at the cellular level, there is an excess of oxidants that overcome the body's antioxidant capabilities to deal with them. These oxidants are often called "free radicals" or "free radical species," because they are chemically unstable and can react with other molecules. Oxidants include both "reactive oxygen species" and "reactive nitrogen species." They can be produced both by the body itself, and as a result of environmental exposures. Scientists have confirmed that oxidative stress is involved in the development of some diseases, but exactly how it is involved is not yet known (Franco and Panayiotidis 2009).
Beta cells are highly sensitive to oxidative stress. Both reactive oxygen species and reactive nitrogen species are likely to be involved in beta cell destruction in type 1 diabetes (Lenzen 2008a). Van Dyke et al. (2010) hypothesize that oxidative/nitrosative stress can trigger type 1 diabetes, and have prevented toxin-induced diabetes in rats with an antioxidant. Alloxan, one of the drugs used to induce insulin-dependent diabetes in lab animals, is thought to cause diabetes via a mechanism that involves reactive oxygen species (Lenzen 2008b). (See the beta cell stresspage for more information on beta cells.)
Treatment with testosterone increases the susceptibility of some types of cells to oxidative stress (Prudova et al. 2007). Unlike other autoimmune diseases, type 1 diabetes is not more common in females than males (see the gender and age page). Perhaps testosterone can increase the susceptibility of beta cells to oxidative stress, contributing to a higher than expected incidence in males.
Environmental factors can not only induce oxidative stress, but can also activate the body's own repair mechanisms to counteract oxidative stress. The resulting cell death or cell survival can depend on the length, intensity, and type of environmental exposure (Franco et al. 2009). In other words, not all oxidative stress may be "bad."
And, not all anti-oxidants may be "good." There is some animal evidence that anti-oxidants can increase insulin resistance. When researchers gave certain mice an anti-oxidant, they were more likely to become insulin resistant (Loh et al. 2009). These findings may help to explain why anti-oxidants have not been found to be protective against type 1 diabetes (see the nutrition page). On the other hand, reactive oxygen species can trigger insulin resistance in animals as well (Houstis et al. 2007).
Many toxic chemicals can generate reactive oxygen and nitrogen species (Lenzen 2008a). A number of environmental contaminants are known to induce oxidative stress as well as apoptosis(programmed cell death). Apoptosis of beta cells is the main cause of beta cell death at the onset of type 1 diabetes (Cnop et al. 2005). Franco et al. (2009) review how many contaminants, including heavy metals, arsenic, some air pollutants, some pesticides, and some persistent organic pollutants, affect apoptosis via oxidative stress.
As an air pollutant, particulate matter carries contaminants that are capable of triggering the production of free radicals, and may affect organs that are sensitive to oxidative stress (MohanKumar et al. 2008). Hathout et al. (2006) propose that the oxidative effects of air pollutants ozone and sulfate (SO4) may contribute to the development of type 1 diabetes.
In genetically susceptible mice, exposure to tricholorethylene at levels found in the environment leads to oxidative and nitrosative stress, and is associated with the induction and exacerbation ofautoimmunity (Wang et al. 2007). High doses of N-nitroso compounds (see the nitrate/nitritepage) can cause diabetes via the generation of free radicals that damage beta cells. The effect of lower levels of exposure is less clear (Kostraba et al. 1992).
The bottom line
Oxidative stress may be involved in the development of type 1 diabetes. Whether the ability of environmental contaminants to produce oxidative stress would lead to the development of type 1 diabetes is not known, but deserves further study.
This information was compiled from the website www.diabetesandenvironment.org - Please visit the site for additional studies and information.
Boyd Haley PhD
It has been said that we are all receiving, just through our air, water and food, about a microgram of mercury a day. Sounds like very 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.
It has been shown that 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. It is a fact that ROS is one of the major factors that induce oxidative modification of DNA and gene mutation.
ROS is involved in the onset, progression, and pathological consequences of diabetes. The study published by the American Chemical Society showed that mercury is capable of suppressing insulin secretion of pancreas cells through a ROS-triggered pathway. Mercury-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.
Dr. Mark Sircus
The information from Dr. Mark Sircus was compiled from the website http://blog.imva.info/medicine/cruel-ignorance-diabetes
 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.
 Kajimoto, Y., and Kaneto, H. (2004) Role of oxidative stress in pancreatic beta-cell dysfunction. Ann. N. Y. Acad. Sci. 1011, 168-176.
 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.
 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.
 Rolo, A. P., and Palmeira, C. M. (2006) Diabetes and mitochondrial function: Role of hyperglycemia and oxidative stress. Toxicol. Appl. Pharmacol. 212, 167-178.
 American Chemical Society (2006, September 29). Mercury Compound Found In Fish Damages Pancreatic Cells. ScienceDaily. Retrieved June 27, 2011