Can Preventing Pollution Also Prevent Diabetes?
(Guest blogger Sarah Howard is a CEH supporter and an environmental health advocate.)
Diabetes is the quintessential “lifestyle” disease – or is it?
There is growing scientific evidence that exposure to environmental contaminants may contribute to the development of diabetes. A provocative study of U.S. residents found that people who were obese but had very low levels of contaminants in their bodies did not have increased rates of diabetes. Only in people with certain levels of contaminants was obesity associated with diabetes. Not only that, but exposure to some contaminants may also lead to weight gain. Obesity alone may not be the whole story in diabetes, although it does play a role; obesity may even increase the toxicity of contaminants. We may need to rethink our preconceptions about diabetes.
Diabetes is big business. An estimated $376 billion are spent on diabetes-related health care costs worldwide, constituting 12% of total health expenditures. What if we can reduce those costs by reducing toxic exposures?
The National Institute of Environmental Health Sciences is conducting a “state of the science” evaluation of environmental contaminants and both diabetes and obesity. Scientists are raising the issue of diabetes and contaminants; dozens of studies have found associations between various contaminants and diabetes in humans. These contaminants include a number of persistent organic pollutants (POPs) such as PCBs and dioxin, bisphenol A, air pollutants, arsenic, cadmium, some PBDEs, and some pesticides.
Other scientists, of course, have questioned these findings (that’s what scientists do, after all). They wonder if perhaps diabetes somehow causes people to have higher levels of contaminants in their bodies? So far, a few studies have addressed this question, and found that actually, diabetes does not appear to affect the body’s processing or excretion of contaminants. Studies are also finding contaminants to be associated with insulin resistance and metabolic syndrome, precursors to diabetes. Thus far, then, the evidence suggests that the contaminants are contributing to the diabetes, and not the other way around.
Interestingly, some endocrine disrupting compounds may be able to interfere with the body’s weight control mechanisms, and increase fat formation and obesity. Wait a minute, so people exposed to contaminants might gain more weight even if they eat the same amount as someone not exposed? That’s right—it’s not just metabolism anymore.
Scientists had already found that high doses of some contaminants can contribute to diabetes, such as arsenic and dioxin—even the U.S. government recognizes diabetes as associated with vets’ exposure to Agent Orange during the Vietnam War. But newer studies are finding that lower exposure levels, as are found in the general population, may also contribute to diabetes.
It’s not just the dose that makes the poison, it’s also the timing. Exposures in the womb or during early childhood may have health effects later in life, especially in the case of endocrine disrupting compounds. These early exposures may also be able to detrimentally affect the immune system in ways that could contribute to autoimmune disease; type 1 (juvenile) diabetes is an autoimmune disease. Early contaminant exposures have also been linked to weight gain later in life, in animals and humans.
I’ve created a website that summarizes the peer-reviewed, scientific evidence relating to the various environmental factors that may affect the development of diabetes. I focused on type 1 diabetes, but the environmental contaminant sections includes information on type 2 as well, including citations for all of the studies described above.
Please visit www.diabetesandenvironment.org to find out more!