Endocrine Disrupting Chemicals: The Obesity Link

It is clear that genetic factors cannot explain the increase in the prevalence of obesity seen in the last few decades. Mounting evidence suggests that exposure to new environmental factors have played by far the largest part in this obesity epidemic. Western food is undoubtedly to blame because its composition is obesogenic in nature. In this regard Western food is highly refined, and this processing removes most of the micronutrient content, and these micronutrients are required as cofactors for enzymes in key metabolic pathways. Western food also contains metabolic poisons such as trans fats and refined crystalline fructose that can further disrupt metabolic pathways. The lack of fibre in Western food is also problematic because it causes a loss of postprandial glycaemia through a disruption to normal digestive processes. The result of consumption of Western foods is a slow deteriorating metabolic regulation that ultimately leads to widespread hormonal and endocrine disruption, particularly insulin and leptin resistance.

However, the roots of obesity may be sewn far before any proper exposure to Western food begins. It has been suggested for example that exposure of the foetus to endocrine disrupting chemicals may cause changes to the normal foetal growth and development period due to widespread disruption to the normal chemical milieu. Many chemicals in the environment for example are oestrogenic in nature, and can accumulate in adipose tissue where they can be stored almost indefinitely. Exposure to such oestrogenic chemicals in the womb is highly problematic because available evidence suggests that they may cause hormonal disruption. This can lead to permanent physiological and metabolic changes that programme homeostatic control set points and this may increase the risk of obesity when subsequently exposed to obesogenic foods. Chemicals suspected of causing hormonal disruption in humans include polychlorinated biphenyls (PCBs) and p,p’-dichlorodiphenyldichloroethylene (DDE).

Researchers have investigated the association between exposure to hormone disrupting chemicals and the subsequent development of obesity in long-term prospective studies. For example, in one study1 researchers assessed the exposure of mothers to PCBs and DDEs using samples of blood and milk taken before and after birth. They then took anthropometric measurements of their children at between ages 5 and 7. Girls born to overweight mothers had body mass indices that were associated with the PCB exposure of their mothers. In addition these girls had changes in body mass indices between the ages of 5 and 7 that were associated with maternal PCB and DDE exposure. PCB exposure was also associated with an increased waist circumference in girls born to overweight and normal weight mothers, but DDE was associated with an increased waist circumference only in girls born to overweight mothers. There was no observed association between PCB or DDE exposure and body weight in boys.

Dr Robert Barrington’s Nutritional Recommendation: These results show that girls born to overweight mothers may have an increased risk of obesity in later life if exposed to PCBs or DDEs in the womb. However, studies have shown that the picture is incredibly complicated and that exposure level is an important determinant of the outcome. For example studies observing a low exposure to endocrine disrupting chemicals during foetal growth (such as the one cited here) have observed increases in body mass indices in later life. However, those observing high exposures have observed low body mass indices in later life. The association also appears to be sex dependent. Because hormone disrupting chemicals are stored in adipose tissue, it might be that overweight mothers are able to build up larger stores of these chemicals compared to lean counterparts. Of course it should not be forgotten that exposure to obesogenic foods may be a requirement of the development of obesity irrespective of the subsequent PCB or DDE exposure. Therefore the individual may still have the final say on obesity development through what they ultimately put in their mouths.

RdB

1Tang-Peronard, J. L., Heitmann, B. L., Andersen, H. R., Steuerwald, U., Grandjean, P., Weihe, P. and Jensen, T. K. 2014. Association between prenatal polychlorinated biphenyl exposure and obesity development at ages 5 and 7 y: a prospective cohort study of 656 children from the Faroe Islands. American Journal of Clinical Nutrition. 99: 5-13

About Robert Barrington

Robert Barrington is a writer, nutritionist, lecturer and philosopher.
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