Exposure to “obesogenic” chemicals has an important role in the obesity and diabetes pandemic. Studies dating back to the 1970s have shown that low-dose chemical exposures were associated with weight gain in experimental animals. Since then, a growing number of studies show links between toxins and weight gain, obesity and diabetes. Known or suspected culprits behind negative epigenetic changes include toxins such as heavy metals, pesticides, plastic compounds including BPA, diesel exhaust, tobacco smoke, polycyclic aromatic hydrocarbons, hormones, radioactivity, viruses, bacteria and endocrine disrupting chemicals.
The main role of fat cells is to store energy and release it when needed. Scientists now know that fat tissue acts as an endocrine (hormone) organ, releasing hormones related to appetite and metabolism. Research to date suggests that different obesogenic compounds may have different mechanisms of action, some affecting the number of fat cells, others the size of fat cells, and still others the hormones that influence appetite, satiety, food preferences, and energy metabolism. Another mechanism through which these chemical obesogens can contribute to weight gain is through their impact on the gut microbiome, linking gut ecology and environmental chemicals to obesity and diabetes.
BPA, or bisphenol-A, a chemical found in everything from plastic bottles to metal food containers, may be partly to blame for our excess weight. BPA has been shown to alter the body’s metabolism, increasing weight gain and making it difficult to lose weight. In a study of 1,326 children, girls between ages 9 and 12 with high BPA levels had double the risk of being obese than girls with low BPA levels, validating previous animal and human studies. The chemical can alter the body’s metabolism and make it harder to lose weight. Girls with high levels of BPA, two micrograms per litre or more, were twice as likely to be obese as girls with lower levels of BPA in the same age group. Girls with very high levels of BPA, more than 10 micrograms per litre, were five times more likely to be obese, the study showed. In animal experiments, a mother’s exposure to BPA is producing the same outcomes that we see in humans born light at birth: an increase in abdominal fat and glucose intolerance. BPA affected rodent fat cells at very low doses, 1,000 times below the dose that regulatory agencies presume causes no effect in humans.
A growing body of evidence shows that the use of certain pesticides may also be associated with weight gain and diabetes risk. In animal experiments, mice fed high-fat diets gained about 30% more weight and had higher blood sugar than other mice eating the same high-fat diets when they also ingested doses of a brominated flame retardant, hexabromocyclododecane (HBCD), which is used in building materials and insulation. Perfluorooctanoic acid (PFOA) is a ubiquitous chemical, used in non-stick cookware, Gore-Tex™ waterproof clothing, Scotchgard™ stain repellent on carpeting and mattresses and is a potential endocrine disruptor. Researchers gave pregnant mice PFOA during pregnancy and when the offspring reached adulthood, they became obese, reaching significantly higher weight levels than controls. Phthalates are plasticizers that have been related to obesity in humans and occur in many PVC items as well as in scented items such as air fresheners, laundry products, and personal care products, and many plastics.
