Coordinator of CHE’s Diabetes-Obesity Spectrum Working Group
In a recent review, published in the leading diabetes journal Diabetologia, Hectors et al. (2011) describe how numerous environmental chemicals affect the insulin-producing beta cells of the pancreas. These effects, the authors argue, may be significant in the development of type 2 diabetes. Chemicals like bisphenol A, PCBs, dioxin, organophosphorous pesticides, arsenic, heavy metals, and others, can all affect how the beta cells function, and can interfere with their capacity to secrete insulin.
In type 2 diabetes, both insulin resistance—the body’s inability to respond correctly to insulin—and beta cell malfunction contribute to the disease. The inability of the beta cells to produce enough insulin leads to high blood glucose levels, and eventually diabetes (in many people with type 2, insulin production is higher than normal, to compensate for the insulin resistance—but it is still inadequate to bring blood glucose under control).
But beta cell malfunction is not only significant for type 2 diabetes. Gestational diabetes, diabetes that appears temporarily during pregnancy, is also a disease of inadequate beta cell function. A pregnant woman’s body becomes more and more insulin resistant during the course of the pregnancy, and requires more and more insulin to keep her (and her fetus’s) blood sugar controlled. As in type 2 diabetes, if the beta cells can’t keep up with demand, due to some malfunction, gestational diabetes results, with dangers for both mother and child.
Type 1 diabetes is somewhat different, since it is an autoimmune disease. In type 1, the immune system attacks and destroys the beta cells entirely, leading to no insulin production, resulting in high blood sugar levels, diabetes, and lifelong dependence on pharmaceutical insulin. Researchers are trying to figure out why the beta cells are targeted in type 1 diabetes—why are the beta cells, and only the beta cells, attacked? Some researchers think that various environmental factors that affect beta cells, that can stress them, could make them more sensitive to an autoimmune attack, contributing to type 1 diabetes.
In the 1970s, a rat poison called Vacor was removed from the market after it was found to cause insulin-dependent diabetes in people who were poisoned with it. Vacor acts by destroying the beta cells. Yet some people with Vacor-induced diabetes also developed the same signs of autoimmunity as are seen in type 1 diabetes, the same autoantibodies. In this case, a beta cell toxin seems to have led to beta cell autoimmunity. Can other environmental chemicals, that target beta cells, do the same thing? We don’t know yet, but it is a question that needs to be asked.
Chemicals that affect beta cells should be analyzed as possible contributors to not only type 2 diabetes, but also type 1 and gestational diabetes. Growing research suggests that chemicals may indeed contribute to type 2, but so far, there is very little research on whether chemicals contribute to type 1 or gestational diabetes.
All three of these types of diabetes are increasing in incidence. Type 1 has been increasing in industrialized countries since World War 2, the time that these chemicals came into widespread use. Alarmingly, type 1 is increasing fastest in the youngest children, who, like my son, were diagnosed before they turned 5 years old. No one knows why. I think it is time to consider chemicals as potential contributors to this awful disease. I am not alone.
Three scientists and I wrote a letter to Diabetologia that was published this week, in response to Hectors et al’s review of beta cell disrupting chemicals. In it, we argued that these chemicals—that are in the bodies of children and pregnant women—should be considered in research of type 1 and gestational diabetes.
Here is a link to the letter:
This is about your paragraph starting “In the 1970s,…”
I think it is well known that killing beta cells in the pancreas can cause an autoimmune reaction. I was once reading about research in mice (or rats?) and the abstract said something about “autoimmune diabetes” but the body talked about killing beta cells with a toxin (and the research was not being done in NOD mice or BB rats). That confused me and I asked a researcher about it. His reply was that giving the toxin at a low dose for these types of animals, caused an autoimmune reaction. He did not think it was a good animal model to use, but some researchers did use it.
Your paragraph talks about this in people, but I think there is plenty of animals research which shows this, as well.
I think you are wrong to say that type 1 is increasing most rapidly in the young under 5 years old. It is actually increasing more rapidly among people who are already adults.
The incidence of type 1 has barely been studied in adults. It is likely increasing, although we don’t really know, and it would depend on the population studied. In children, almost all the incidence studies show that 0-4 years olds have the most rapid rate of increase (although it varies by population) as compared to older children. But compared to adults, we don’t know. I am adult onset myself, and you may be right, but the studies aren’t there yet to say one way or another.