We’re doing what we’re supposed to be doing yet we are getting fatter and fatter
Many of the factors behind the rising rates of obesity are now well-known: diet, exercise and lifestyle.
But one, the environmental chemicals we are exposed to on a daily basis through plastics, food packaging, pesticides and cosmetics, is hardly discussed at all.
Although still an under-researched area, more and more studies are finding that everyday chemicals can cause obesity.
‘When animals are exposed prenatally to these chemicals, their metabolism is reprogrammed so that even if they are never exposed again in their lives, they gain weight,’ says Bruce Blumberg, from the University of California.
Professor Blumberg is one of a growing number of researchers in the US who are looking at how everyday chemicals can trigger increases in body fat.
He has even coined a word ‘obesogens’ to describe the chemicals found to promote dramatic weight gain.
Existing research links obesity to an imbalance between food intake and energy output. But research into obesogens suggests that hormone-altering chemicals may be creating more fat cells in our bodies and allowing existing ones to get larger.
Of particular concern to Blumburg is prenatal exposure, where obesogens may be telling a developing fetus to make more fat cells – creating a lifelong propensity for accumulating fat and obesity.
The Ecologist first reported on the issue back in 2006 and has continued its coverage in recent months but with a new documentary, ‘Programmed to be fat’, being screened in Canada this week the topic may finally be gaining mainstream recognition.
We just keep getting fatter
For some, the question remains, why should we focus attention on the possible impact of obesogens when we’re continuing to eat junk food?
‘The reality is both are happening,’ says Professor Blumberg. ‘We’re being exposed to obesogens and eating bad food. So it’s a double impact. In the US we’re cutting fats yet obesity has doubled. We’re doing what we’re supposed to be doing yet we are getting fatter and fatter.’
In the US, a series of government strategies on obesity over the past two years have all acknowledged the need to do more research into obesogens and over-exposure to chemicals.
A government-sponsored workshop in February of last year brought together more than 135 scientists to evaluate the science linking obesity to exposure to six chemicals; arsenic and other metals, bisphenol A, organotins and phthalates, nicotine, pesticides and pesrsistent organic pollutants.
They found good evidence linking maternal smoking with increased risk of offspring being overweight or obese and enough evidence to suggest the other chemicals, ‘may be contributing to the current epidemics of diabetes and obesity’.
Little research interest in the UK
In the UK the issue has yet to gain acceptance - neither the department of health nor the NHS list it as an obesity factor. A spokesperson for the department of health says evidence for the obesogen theory is 'limited'. The UK’s Health Protection Agency (HPA) does acknowledge it as an ‘emerging’ issue but is not planning any of its own research.
Dr Susan Jebb, from the Medical Research Council Human Nutrition Research unit (HNR) in Cambridge and one of the lead authors of a major government obesity report in 2007, says the idea of contaminants and obesogens were only considered in their report as a ‘wild card’.
‘The evidence in relation to chemical contaminants at the moment is very limited and no more than suggestive, whereas the evidence for some other factors like how much fat you eat or whether you use a bike or car is much stronger and has a clear and measurable effect size,’ says Dr Jebb.
‘I’m not ruling it out but we are right at the beginning of trying to understand it,’ she adds suggesting chemicals may ultimately be found to be linked more to diabetes than obesity.
‘If it does affect our desire to eat then that would be a very plausible mechanism [for obesity] but having more fat cells only gives you the potential to store fat, you still have to eat the extra fat.
‘I’d find it easier to think of plausible mechanims whereby these chemicals might affect your chances of developing diabetes or heart disease, where there are much more specific metabolic processes that could be distrupted. For example, chemical molecules could attach onto the various receptors and affect the uptake of glucose by cells.’
Tom Levitt is deputy editor of the Ecologist
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