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The Connection Between POPs and Metabolic Syndrome

Metabolic syndrome and diabetes continue to trend upward worldwide. More than one third of Americans meet the criteria for metabolic syndrome, and rates of diagnosis have increased from 1988 to 2012.1 This increase is especially prevalent in lower socioeconomic groups, and it is not solely driven by the rise in obesity.1

What can account for this increase? In the following video, IFM educator Robert Rountree, MD, talks about the rise in incidence of diabetes and metabolic syndrome:

Persistent Organic Pollutants

A growing line of research points to persistent organic pollutants (POPs) as a contributing factor in the increased rates of metabolic syndrome.2 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 agricultural or industrial applications, and they can also be byproducts of industrial processes and of incineration of certain 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 homeostasis4 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.11 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 may aggravate clinically relevant complications of obesity.4

Another study found that POPs are not only implicated in the complications of overweight or obese individuals, but may also impair the metabolic functioning of those who are considered “normal weight.”12 Published in Diabetes & Metabolism, a small study found that increased serum POP concentrations may play an important role in the development of unhealthy metabolic phenotypes in lean people.12 Another study with over 1,300 patients lends credence to 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.13

Evidence suggests that even prenatal exposure to POPs may have long-term consequences.14,15 POP exposure is widespread and can even happen with healthy dietary sources like fruits and vegetables.16 High seafood consumption, living in a home with carpeted floors, and consuming preheated packaged foods also increase exposure to certain types of POPs (perfluoroalkyl and polyfluoroalkyl substances—PFASs).17 The breadth of potential exposures to POPs like PFASs make it difficult to completely avoid them.18

Potential Mechanism

Although epidemiological studies have demonstrated that POPs could lead to metabolic syndrome, the mechanism has remained unclear until recently.11 In 2020, researchers put forward the hypothesis that the dysbiosis of gut microbiota and the lipid metabolome may be involved in the pathophysiology of metabolic syndrome. A study published in Chemosphere suggests that dichlorodiphenyldichloroethylene (DDE) exposure increases body weight and fat content and impairs glucose homeostasis, increases gut dysbiosis as indicated by an increased Firmicutes-to-Bacteroidetes ratio, and causes alterations to the plasma lipid metabolome. The study provides novel insight into the underlying mechanisms of POP-induced obesity and diabetes, suggesting that the gut microbiota may be one of the targets.11

Risks When Dealing With POPs

Detoxifying the body of POPs, many of which are fat-soluble and collect in adipose tissue,19 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 contaminants from fat and bypassing enterohepatic recirculation.20

In some patients, there may be adverse health risks when POPs are released from adipose tissue. For instance, a 2019 paper on organochlorine pesticides, or OCPs (a type of POP), states that “Weight gain may help sequester circulating OCPs in adipose tissue. As obesity is the most common reason that adipocytes become dysfunctional, midlife obesity can increase dementia risk through the chronic release of OCPs into circulation.”20 Whether weight loss is intentional or unintentional, the release of OCPs may negatively affect the brain.20

When the exposure history indicates potentially long-term or high exposure to POPs, consider supporting biotransformation and excretion of these compounds. Caution is warranted, and the patient’s safety needs to be carefully evaluated to avoid neurologic and other potential consequences of increased serum levels of POPs.

Conclusion

Many factors likely contribute to the increase in metabolic syndrome, including changes to the food supply, food processing, sedentary lifestyles, and more. However, a 2019 meta-analysis concluded that there is “compelling evidence indicating that exposure to POPs increases the risk of developing insulin resistance and metabolic disorders.”21

As the evidence continues to accumulate, understanding the triggering and mediating roles that toxins may play in metabolic disorders and diabetes becomes increasingly relevant. For patients with diabetes or insulin resistance, evaluating their exposure history to POPs may provide important clues.

Learn More About Biotransformation Pathways and Toxic Exposures

For more information about how toxin exposures might affect the health of your patients, please read the following IFM-authored articles:

Toxin exposures at home

Talking to patients about toxins

Sleep and biotransformation

References
  1. Moore JX, Chaudhary N, Akinyemiju T. Metabolic syndrome prevalence by race/ethnicity and sex in the United States, National Health and Nutrition Examination Survey, 1988-2012. Prev Chronic Dis. 2017;14:E24. doi:5888/pcd14.160287
  2. Yang C, Kong APS, Cai Z, Chung ACK. Persistent organic pollutants as risk factors for obesity and diabetes. Curr Diab Rep. 2017;17(12):132. doi:10.1007/s11892-017-0966-0
  3. Persistent organic pollutants: a global issue, a global response. United States Environmental Protection Agency. Updated December 2009. Accessed August 1, 2019. https://www.epa.gov/international-cooperation/persistent-organic-pollutants-global-issue-global-response
  4. 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
  5. 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
  6. 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
  7. 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
  8. 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
  9. Codru 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
  10. 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
  11. 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
  12. 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
  13. Aris IM, Fleisch AF, Oken E. Developmental origins of disease: emerging prenatal risk factors and future disease risk. Curr Epidemiol Rep. 2018;5(3):293-302. doi:1007/s40471-018-0161-0
  14. Lauritzen HB, Larose TL, Øien T, et al. Prenatal exposure to persistent organic pollutants and child overweight/obesity at 5-year follow-up: a prospective cohort study. Environ Health. 2018;17(1):9. doi:1186/s12940-017-0338-x
  15. Arrebola JP, Castaño A, Esteban M, et al. Differential contribution of animal and vegetable food items on persistent organic pollutant serum concentrations in Spanish adults. Data from BIOAMBIENT.ES project. Sci Total Environ. 2018;634:235-242. doi:1016/j.scitotenv.2018.03.283
  16. Hu XC, Dassuncao C, Zhang X, et al. Can profiles of poly- and perfluoroalkyl substances (PFASs) in human serum provide information on major exposure sources? Environ Health. 2018;17(1):11. doi:1186/s12940-018-0355-4
  17. Sunderland EM, Hu XC, Dassuncao C, Tokranov AK, Wagner CC, Allen JG. A review of the pathways of human exposure to poly- and perfluoroalkyl substances (PFASs) and present understanding of health effects. J Expo Sci Environ Epidemiol. 2019;29(2):131-147. doi:1038/s41370-018-0094-1
  18. Jackson E, Shoemaker R, Larian N, Cassis L. Adipose tissue as a site of toxin accumulation [published correction appears in Compr Physiol. 2018;8(3):1251]. Compr Physiol. 2017;7(4):1085-1135. doi:1002/cphy.c160038
  19. Genuis SJ. Elimination of persistent toxicants from the human body. Hum Exp Toxicol. 2011;30(1):3- doi:10.1177/0960327110368417
  20. Lee DH, Porta M, Lind L, Lind PM, Jacobs DR Jr. Neurotoxic chemicals in adipose tissue: a role in puzzling findings on obesity and dementia. Neurology. 2018;90(4):176-182. doi:1212/WNL.0000000000004851
  21. Kim YA, Park JB, Woo MS, Lee SY, Kim HY, Yoo YH. Persistent organic pollutant-mediated insulin resistance. Int J Environ Res Public Health. 2019;16(3):E448. doi:3390/ijerph16030448

 

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