Metabolic syndrome and diabetes continue to trend upward worldwide. The International Diabetes Federation estimates that one quarter of the world’s adults have metabolic syndrome;1 likewise, the prevalence in the US ranged from 23-27% from 1999-2010.2
What can account for this increase? In the following video, IFM educator Tom Malterre, MS, CN, talks about the possible connection between the increase of persistent organic pollutants (POPs) in the environment and the rise in incidents of diabetes and metabolic syndrome:
One line of research points to POPs. POPs are a class of toxins present in water and transportable by wind. The name is apt, as they persist for years and can accumulate throughout the food chain. POPs are produced intentionally for agriculture or industrial applications, and they can also be byproducts of industrial processes or incineration of particular items. Wind patterns, currents, and contaminated rain spread these pollutants far and wide. POPs can also be absorbed when consumed, which is especially dangerous for people who consume large amounts of fish and/or other animals high on the food chain.3
Studies suggest that POPs may impair metabolic homeostasis,4 and may be correlated with insulin resistance and type 2 diabetes.5-10 For example, populations who eat more marine mammals have higher serum levels of POPs and higher rates of metabolic syndrome and diabetes.5
A 2018 study suggests that in morbidly obese individuals, metabolic syndrome is related to circulating levels of organochlorine pesticides and PCBs, and the authors propose that these compounds aggravate clinically relevant complications of obesity.4 Another recent study found that the effects of POPs are not only implicated in overweight or obese individuals, but can also impair the metabolic functioning of those who are considered “normal weight.” Published in Diabetes & Metabolism, the small study found that increased serum POP concentrations may play an important role in the development of unhealthy metabolic phenotypes in lean people.11 Another study confirms these results, supporting the hypothesis that POP concentrations are associated with unhealthy metabolic phenotypes, not only in obese and overweight individuals, but also “and probably more strongly” in normal-weight individuals.12
Moreover, elevated levels of POPs have been linked to insulin resistance, as well as to impaired mitochondrial function.5 Treatment of cells with dioxins have also been found to induce mitochondrial abnormalities and insulin secretion impairment.6
Detoxifying the body of POPs, many of which are fat-soluble, can be challenging. Weight loss can liberate toxins from fatty tissue, increasing blood levels and leading to a host of symptoms and eventual reabsorption of POPs. Therefore, eliminating these pollutants requires excreting the contaminated fat and bypassing enterohepatic recirculation.13
At IFM’s Detox Advanced Practice Module (APM), practitioners will learn more about the complexities of biotransformation and gain the tools necessary to diagnose and treat the toxic component of their patients’ total health pictures.
- Alberti G, Zimmet P, Shaw J, Grundy SM. The IDF Consensus Worldwide Definition of the Metabolic Syndrome. Brussels, Belgium: International Diabetes Federation; 2006. https://www.idf.org/e-library/consensus-statements/60-idfconsensus-worldwide-definitionof-the-metabolic-syndrome.html. Accessed May 5, 2017.
- Beltrán-Sánchez H, Harhay MO, Harhay MM, McElligott S. Prevalence and trends of metabolic syndrome in the adult U.S. population, 1999-2010. J Am Coll Cardiol. 2013;62(8):697-703. doi:1016/j.jacc.2013.05.064.
- Persistent organic pollutants: a global issue, a global response. United States Environmental Protection Agency. https://www.epa.gov/international-cooperation/persistent-organic-pollutants-global-issue-global-response. Updated December 2009. Accessed May 5, 2017.
- Dusanov S, Ruzzin J, Kiviranta H, et al. Associations between persistent organic pollutants and metabolic syndrome in morbidly obese individuals. Nutr Metab Cardiovasc Dis. 2018;28(7):735-742. doi:1016/j.numecd.2018.03.004.
- Lim S, Cho YM, Park KS, Lee HK. Persistent organic pollutants, mitochondrial dysfunction, and metabolic syndrome. Ann N Y Acad Sci. 2010;1201:166-176. doi:1111/j.1749-6632.2010.05622.x.
- De Tata V. Association of dioxin and other persistent organic pollutants (POPs) with diabetes: epidemiological evidence and new mechanisms of beta cell dysfunction. Int J Mol Sci. 2014;15(5):7787-7811. doi:3390/ijms15057787.
- Chang J-W, Chen H-L, Su H-J, Lee C-C. Abdominal obesity and insulin resistance in people exposed to moderate-to-high levels of dioxin. PLoS One. 2016;11(1):e0145818. doi:1371/journal.pone.0145818.
- Aminov Z, Haase R, Rej R, et al. Diabetes prevalence in relation to serum concentrations of polychlorinated biphenyl (PCB) congener groups and three chlorinated pesticides in a Native American population. Environ Health Perspect. 2016;124(9):1376-1383. doi:1289/ehp.1509902.
- Cordu N, Schymura MJ, Negoita S; Akwesasne Task Force on Environment, Rej R, Carpenter DO. Diabetes in relation to serum levels of polychlorinated biphenyls and chlorinated pesticides in adult Native Americans. Environ Health Perspect. 2007;115(10):1442-1447. doi:1289/ehp.10315.
- Lee D-H, Lee I-K, Song K, et al. A strong dose-response relation between serum concentrations of persistent organic pollutants and diabetes: results from the National Health and Examination Survey 1999-2002. Diabetes Care. 2006;29(7):1638-1644. doi:2337/dc06-0543.
- Ha KH, Kim SA, Lee YM, Kim DJ, Lee DH. Can persistent organic pollutants distinguish between two opposite metabolic phenotypes in lean Koreans? Diabetes Metab. 2018;44(2):168-171. doi:1016/j.diabet.2017.12.008.
- Gasull M, Castell C, Pallarès N, et al. Blood concentrations of persistent organic pollutants and unhealthy metabolic phenotypes in normal-weight, overweight, and obese individuals. Am J Epidemiol. 2018;187(3):494-506. doi:1093/aje/kwx267.
- Genuis SJ. Elimination of persistent toxicants from the human body. Hum Exp Toxicol. 2011;30(1):3- doi:10.1177/0960327110368417.
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