Sugar may not be the only culprit causing diabetes and obesity

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It may no longer be sufficient to limit your intake of sugary snacks or to spend hours in the gym to avoid diabetes and obesity, as the presence of food contaminants known as persistent organic pollutants (POPs) may also be involved in the development of these diseases.

POPs are everywhere…

POPs (such as PCBs (polychlorinated biphenyls) and p,p’-DDE (p,p’-dichlorodiphenyldichloroethylene)) were formerly used in pesticides and produced as byproducts from chemical industrial processes, in power stations, heating stations, or through incineration of preexisting materials. These components are semi-volatile, which allows for transport through the air, and are hydrophobic, resulting in accumulation in animal tissue. POPs are very resistant to biological, chemical and photolytic degradation. Their persistent and volatile nature causes bioaccumulation in the food chain and transboundary transportation far from their original source.

Despite global efforts, such as the Stockholm Convention to ban POPs and other relevant regulations to limit their use and their spread, people are continuously exposed to these compounds through contaminated food such as dairy products, meat, and fish. Not all countries have officially accepted the restriction of POPs and those who have may not be sufficiently monitoring and controlling the spread of these chemicals.

… and seem to be diabetogenic and obesigenic

A group of researchers from the University of Antwerp evaluated the effect of POPs in a study of 151 adult obese individuals and 44 normal weight volunteers used as the control group (1). They found a correlation between the level of POPs – measured in serum and adipose tissue – and abnormal glucose tolerance in obese people. They also found a correlation between the level of POPs and the amount of adipose tissue. Due to the higher affinity of POPs to lipids, individuals with higher body fat levels can accumulate higher amounts of these compounds. Other studies showed similar results, but the exact mechanisms still have to be elucidated (2,3).

Although correlation does not prove causality, the growing consensus nowadays is that exposure to POPs, which are also known to interfere with the function of pancreatic beta-cells, should officially be taken in consideration as an additional risk factor for diabetes and obesity. 


(1) Dirinck, Eveline L., et al. “Exposure to persistent organic pollutants: relationship with abnormal glucose metabolism and visceral adiposity.” Diabetes care 37.7 (2014): 1951-1958.

(2) Taylor, Kyla W., et al. “Evaluation of the association between persistent organic pollutants (POPs) and diabetes in epidemiological studies: a national toxicology program workshop review.” Environmental health perspectives 121.7 (2013): 774-783.

(3) Rylander, Charlotta, et al. “Combining plasma measurements and mechanistic modeling to explore the effect of POPs on type 2 diabetes mellitus in Norwegian women.” Environmental research 142 (2015): 365-373.

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