Obesity's helper in triggering diabetes
12 April 2007
New Scientist
Aria Pearson
If true, it could turn the conventional wisdom of how obesity causes diabetes on its head. Emerging evidence suggests that pollutants stored in body fat may be contributing to the ongoing rise of type 2 diabetes.
While obesity is still thought to be a major cause, there is more and more evidence to suggest that persistent organic pollutants (POPs) also play a key role.
POPs are synthetic chemicals that can accumulate in the fatty tissue of animals. Many POPs - such as polychlorinated biphenyls (PCBs), which were used as coolants in electrical equipment, and pesticides such as DDT - have been banned in developed countries, but they remain in the food chain and often end up in people.
Last year, Duk-Hee Lee at Kyungpook National University in Daegu, South Korea, and her colleagues reported that people with higher levels of six different POPs were more likely to have diabetes than people with low levels of POPs (New Scientist, 30 September 2006, p 18).
Now, a follow-up study published last month suggests an association in non-diabetic people between certain pesticides, PCBs and insulin resistance - a precursor to diabetes (Diabetes Care, vol 30, p 622). Fat people with POPs in their blood were more likely to develop insulin resistance than thin people with POPs, but the expected association between obesity and insulin resistance disappeared in people with no POPs. "This suggests the possibility that POPs stored in fat tissue, not obesity itself, may be a key factor for the development of type 2 diabetes," says Lee.
The information used by the researchers was designed to be representative of the general population in the US. "That's the somewhat shocking implication," says David Jacobs at the University of Minnesota, Minneapolis, who supervised Lee's research. "The association exists at everyday background levels of POPs."
The precise mechanism by which POPs could contribute to diabetes remains a mystery. Some PCBs, such as dioxin, are known to interfere with genes that control insulin sensitivity, says Lee, although dioxin was not studied by her group.
However, it could also be the other way around, says Matthew Longnecker, an epidemiologist at the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina. "People with diabetes or a pre-diabetic condition may clear POPs from their system at a slower rate," he says. This would lead to increased concentrations of POPs over time.
Lee acknowledges that this is a possibility but thinks it is unlikely. Long-term studies will be needed to pin down the sequence of events, but previous studies have also shown a causal link between POPs and diabetes, she says. For example, US air force pilots who sprayed Agent Orange - which contains dioxin - during the Vietnam war are more likely to develop diabetes, as are people who live near waste sites contaminated with POPs.
Robert Lustig, a paediatric endocrinologist at the University of California, San Francisco, agrees, but warns that the relationship could be more complicated yet, as animal studies have shown that environmental toxins in the womb may cause obesity in later life, which could then lead to diabetes. "We just don't know," he says. "But is there reason to be concerned? You bet."