Verdant Nation: Pervasiveness of environmental contaminants: what does this mean for obesity?

Everybody knows that obesity results from energy in being greater than energy out, right? Okay, we know that it's a lot more complex than that, but what if obesity could arise separate from this? We're pretty wedded to the idea that diet and physical activity are major risk factors, so it may be a little disconcerting to learn that a new body of research suggests that being exposed to "obesogens," chemicals in the environment (usually man-made), may program us to be fat. In this first post, I will provide a very basic overview of obesogens, leaning heavily on two reports. In the second post of this two-part series, I will discuss what this means in terms of the precautionary principal versus level of evidence.

CBC (the Canadian Broadcasting Company) aired a documentary earlier this year that discussed the puzzling results of scientists researching endocrine-disrupting chemicals. Their original projects were not about fat, but their lab animals turned out to be unusually heavy after being exposed to these chemicals. The documentary can be accessed here. You can have a sneak-peek by viewing the trailer below.

We know that fat tissue acts like an endocrine organ. Since endocrine-disrupting chemicals include a wide variety of substances it is difficult to generalize mechanisms of actions. The Endocrine Society gives the following broad definition (Diamanti-Kandarakis et al, 2009):

"An endocrine-disrupting substance is a compound, either natural or synthetic, which through environmental or inappropriate developmental exposures alters the hormonal and homeostatic systems that enable the organism to communicate with and respond to its environment."

In general though, it is thought that obesogens mimic hormones, which can increase the size of fat cells, increase the number of fat cells or negatively affect appetite, metabolism, and/or food preferences (Holtcamp, 2012). Much of the evidence to date has been from animal studies, but there are many epidemiological studies linking exposures of 15-20 chemicals during fetal and infant development to infant and child weight status (Holtcamp, 2012). Take for instance, smoking during pregnancy - there is fairly persuasive epidemiological evidence linking this to obesity in children (Oken et al, 2008). There is also some evidence for an effect of endocrine-disrupting chemicals on adult weight status; however this is a burgeoning area of research that is need of more studies (Tang-Péronard et al, 2011).

Obesogens (those in addition to the byproducts of smoking) are found everywhere - in industrial solvents/s and their byproducts (PCBs), plastics (BPA), plasticizers (phthalates) in PVC, organotins, pesticides (atrazine, DDE), surfactants used to reduce friction (PFOA), and pharmaceutical agents (DES) (Diamanti-Kandarakis et al, 2009)(Holtcamp, 2012). We are exposed to these chemicals by drinking contaminated water, eating contaminated food, breathing contaminated air, or coming into contact with contaminated soil. In industrial areas, chemicals can leach into the soil and contaminate the ground water, and may bio accumulate in both humans and animals. The web of contamination is so complex that areas considered "prestine"and remote from the original site that produced the chemical, have been found with levels of the chemical (Diamanti-Kandarakis et al, 2009). Many of these obesogens are also found in items we may or may not use every day. Examples include: medical devices, some canned foods, cash register receipts, designer handbags, items made of Gore-tex(TM), wallpaper, vinyl blinds, tile, and vacuum cleaner dust, air fresheners, laundry products, personal care products, items with Scotchgard(TM) (e.g. carpets, furniture, and mattresses), non-stick cook-ware, and microwaveable food items. There are also potential dietary obesogens including phytoestrogens (soy) (Diamanti-Kandarakis et al, 2009) and MSG (monosodium glutamate) (Holtcamp, 2012).

Many endocrine-disruptors demonstrate an inverted U-shaped dose-response association. This means that with medium "doses" of the chemical, obesity risk increases. But at low and high doses, the risk decreases. This likely depends on the chemical and other factors as some endocrine-disruptors have been found to increase risk at very low or very high levels. Estimating the level of exposure that leads to a negative outcome is complex in a living, human population. It depends on sex, age at exposure, length of exposure, the mix of chemicals one is exposed to, and innate lag between exposure and effect (Diamanti-Kandarakis et al, 2009), to name a few.

The link between these chemicals and obesity can only be considered exploratory and hypothesis-generating at this point. Nonetheless, endocrine-disruptors can be detected in all animals and humans (Diamanti-Kandarakis et al, 2009). Some researchers link this to the fact that even individuals on the low end of the BMI distribution are increasing in weight (hinting that obesogens may be the cause of everyone increasing weight on a population scale). I'm not so sure that this link can be made given the drastic change in our food system and our increasingly sedentary lifestyle. I'll delve more into what this may mean in the next post.