PORTLAND, OR—Few people think of type 2 diabetes as being an “environmental” disease. But new data, recently published in prominent diabetes journals, point to an etiologic connection between exposure to “persistent organic pollutants (POPs)” and risk of diabetes, said John Peterson “Pete” Myers, at the annual meeting of the American Holistic Medical Association.
Three recent papers from researchers at the Kyungpook University Department of Preventive Medicine, Daegu, Korea, paint a disturbing picture that should prompt a reassessment of our assumptions about diabetes, said Dr. Myers, director of Environmental Health Sciences, a non-profit organization to advance public understanding of environmental influences on health and illness.
Dr. Duk Hee Lee and colleagues analyzed NHANES data from over 2,000 American subjects. They found that the odds ratio for having type 2 diabetes was strongly associated with lipid-adjusted serum levels of six persistent organic pollutants (POPs), mainly organochlorine pesticides and non-dioxin-like polychlorinated biphenyls (PCBs).
The six POPs they studied all showed some degree of correlation with diabetes; individuals with measurable serum levels were consistently more likely to be diabetic compared with people who had no detectable levels of these compounds. The authors noted “striking dose-response relationships between serum concentrations of the six selected POPs and the prevalence of diabetes” (Lee DH, et al. Diabetes Care. 2006; 29(7): 1638–1644).
After controlling for age, BMI, socioeconomic status, race and ethnicity, they still saw strong correlations between serum levels of the POPs and diabetes; the link was strongest among younger people, Mexican-Americans and obese people.
In a separate paper, they described an equally clear correlation between organochlorine levels and insulin resistance in a sub-cohort of 749 non-diabetic individuals from the NHANES cohort (Lee DH, et al. Diabetes Care. 2007; 30(3): 622–628).
The third paper details a correlation between certain POPs and metabolic syndrome (Lee DH, et al. Diabetologia. 2007; 50(9): 1841–1851). In other words, elevated serum levels of various environmental pollutants seem to be linked with the core endocrine dysregulations underlying type 2 diabetes and its precursor conditions.
This is not to say that environmental toxins cause diabetes, Dr. Myers stressed. Like many epidemiological analyses, Lee’s data show associations, not direct causal relationships. Still, they cannot be ignored.
Isolated exposure to POPs, in and of itself, may not cause diabetes. But in the context of a poor diet high in refined carbs, lack of exercise, and genetic predisposition toward insulin resistance, chronic exposure could certainly be a contributory factor, another physiological challenge to an already stressed endocrine system.
