Two thirds of American adults are either overweight or obese, and environmental toxins from generations ago may have something to do with it. Scientists from Washington State University may have just uncovered another reason for these skyrocketing obesity rates. While it is true that high-calorie sweeteners have become cheaper and more prevalent, and that sedentary lifestyles are increasingly common, there may also be environmental factors contributing to the obesity epidemic.
In the most recent issue of BMC Medicine, a team of researchers led by Michael K. Skinner demonstrate that exposing pregnant rats to the pesticide dichlorodiphenyltrichloroethane (DDT) caused epigenetic changes (sperm epimutations and differential DNA mutation regions, or DMRs) that led to 50% of the third generation developing obesity. (The first generation is the generation exposed while in utero, not their exposed mothers.) This demonstration of an effect -- albeit on rats -- on the third generation means that current obesity levels may be linked to DDT exposure decades ago. DDT was banned in the United States in 1972.
Although pharmaceutical firms frequently use the terms "familial," "inherited," and "genetics" when marketing treatments for poor health conditions, it is a rare disease, such as Tay-Sachs, that is 100% inherited. It is likely that the bulk of chronic health conditions are influenced heavily by environmental factors, both in the current generation (eating too much and exercising too little leads to obesity for anyone, if the amount of overeating and underexercising is substantial enough) and -- perhaps most insidiously -- in future generations, through epigenetics: the changing of an individual's DNA by the environment. Indeed, recent research has linked DNA methylation and other epigenetic changes to myeloma (a type of cancer), neurodegeneration, and numerous other effects on human health.
Perhaps more troubling than the effect past DDT use may have on the health of current generations of Americans is the fact that pesticides chemically similar to DDT are still in use. Dicofol, an organochlorine pesticide broadly used in agriculture in California and Florida, is structurally very similar to DDT; indeed, DDT is used as an intermediate in its production. It seems likely, if DDT induces epigenetic changes with such startling health effects as third-generation obesity rates of 50%, that the safety of similar substances, such as dicofol, should be re-examined. Animals such as sharks have been shown, through testing, to have high levels of DDT linked to current dicofol use.
In the US, the EPA has not set a maximum contaminant level (MCL) for dicofol in drinking water. Perhaps more troubling, the EPA uses a reference dose (RfD) -- the amount of pesticide consumption believed not to cause harm -- of 0.004 mg per kg of body weight per day (assuming a seventy-year lifespan), which is based solely on "hormonal toxicity seen in both sexes of an oral chronic dog study." The EPA's RfD does not take into account any epigenetic changes induced by dicofol, and limits its concerns to adverse health effects on the current generation -- based on one dog study. (Risks for agricultural workers have been determined separately and are based on rat and rabbit studies, but still do not include any consideration of harms inflicted on future generations via germline mutations.)
Chronic dietary exposure -- via contaminated apples, citrus fruits, strawberries, and other crops -- in children ages one through six is estimated to be 38% of the RfD; unfortunately, this figure has not been evaluated against the amount of dicofol needed to cause epigenetic changes and damage future generations. Indeed, this latter data point may not even be known. Even more disturbing, the EPA states that "the current occupational risk assessment indicates possible unacceptable risk levels [for agricultural workers]," but "EPA has found that it is not appropriate to declare dicofol ineligible at this time [re-registration eligibility decision in 1998]."
Certainly, attention to diet and physical activity levels is important in the fight against obesity. However, it seems inappropriate to ignore the powerful epigenetic effects of environmental factors, both those currently in use and those formerly prevalent.