Phthalates and Obesity

Awhile back, the news cycle was all atwitter about this paper published in the International Journal of Obesity. I had posted about it over on Daily Kos last year, to a lukewarm response (political blogs aren’t really in to environmental health, I guess).

The investigators begin by observing that the relationship between obesity and The Big Two, their term for inactivity and inbalanced diet is based on presumed mechanisms and "ecological studies". An ecological study is a type of epidemiological study that examines broad trends in environmental factors and disease; it is not designed to examine specific relationships between exposure and disease, and is considered more useful for generating rather than testing scientific hypotheses. Food industry apologists use this fact to cast doubt on the relationship between diet, exercise and obesity. The investigators argue this doesn't disprove that relationship, but points to the need to look for other factors to help explain the obesity epidemic.

One of the arguments they explored is the relationship between exposure to endocrine disruptors and increased adiposity. The relationship between endocrine disruptor exposure and obesity is an active area of environmental health research. Last year, I posted about a paper exploring the relationship between exposure to the plasticizer bisphenol-A and insulin resistance in mice, occurring at fairly low levels. More recently, a paper has been published describing the relationship between phthalate exposure, girth in males and insulin resistance.

A bit about insulin resistance. Insulin is a hormone that is released from the pancreas after eating. It signals insulin-sensitive tissues, principally muscle, to absorb glucose, which correspondingly reduces blood glucose levels. In an insulin-resistant individual, the normal levels of insulin secreted do not signal cells to absorb glucose. Years of hyperglycemia, from excess carbohydrates in the diet, are thought to disrupt the release of insulin, resulting in glucose intolerance and subsequently Type-2 diabetes. The mechanism for this phenomenon is not entirely clear, and it has not been fully resolved If this loss of pancreatic function results primarily from excessive secretion of insulin (exhaustion of beta-cells in the pancreas) or toxicity to beta-cells (hyperglycemia or other causes). More recent research seems to point to the latter.

Insulin resistance is part of the metabolic syndrome that includes central obesity, elevated insulin secretion, and elevated fatty acids in the bloodstream. Central (visceral) obesity elevates levels of free fatty acids in serum, which might provoke insulin resistance and disrupt lipid metabolism. Testosterone can reduce body fat and increase insulin sensitivity in men, which is where phthalates come in to the picture. Phthalates have been shown to be antiandrogenic agents in male laboratory animals, disrupting testicular steroid hormone synthesis and reproductive function. Some observations suggest that anti-androgenic effects also occur in humans. These investigators were evaluating the hypothesis that increased phthalate exposure would be associated with increased abdominal obesity and insulin resistance, which correspondingly could be precursors to Type-2 diabetes and cardiovascular disease.

The short answer from the study was that concentrations of several prevalent phthalate metabolites showed statistically significant correlations with abdominal obesity and insulin resistance. The authors caution that phthalate exposure only explains some of the variability in measurements of girth and insulin resistance, which they chalk up to obesity being a complex, multi-factorial syndrome (critics may conclude this means there’s no meaningful relationship between phthalate exposure and obesity. . . ). The authors also caution this is a snapshot in time (i.e. a cross-sectional study), and that longitudinal studies (which follow trends over time) are needed to better understand the possible relationship between phthalates and insulin resistance. Other factors to consider in judging the significance of phthalate exposure in metabolic diseases such as diabetes include cumulative exposures to multiple phthalates and exposures to other common contaminants including bisphenol-A, PCBs, dioxins and organochlorine pesticides.

The Washington Post has a reasonably carefully worded article about this issue. Sadly, most other newspapers are mangling what is actually a fairly carefully worded study.

Phthalate exposure isn’t going away any time soon (that’s a story for another day), so what do you do about this? Well, we still have control over the Big Two – diet and activity level.