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Welcome to PSR's Environmental Health Policy Institute, where we ask questions -- then we ask the experts to answer them. Join us as physicians, health professionals, and environmental health experts share their ideas, inspiration, and analysis about toxic chemicals and environmental health policy.

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Environmental Chemicals in Diabetes and Obesity: Unexplored Territory

By Sarah Howard

Diabetes and obesity are caused by poor diet and lack of exercise, right? Not so fast. New research is shedding light on additional factors that may play a role in the development of these conditions, including exposure to environmental chemicals. First, let’s clarify what we mean by “diabetes.” There are numerous types of diabetes, all characterized by high blood glucose levels.  Diabetes can lead to other serious problems:  compromised vision, light sensitivity and blindness; painful sores and infections in the feet and skin, sometimes resulting in the need for the foot or leg to be amputated; damage to nerves, causing pain, tingling, loss of feeling, and problems digesting food.

The most common types of diabetes are type 2, type 1, and gestational diabetes. Perhaps 90% of people with diabetes have type 2, which is associated with obesity and insulin resistance; about 80% of U.S. adults with diabetes are overweight or obese.(1) The diagnosis of type 2 diabetes is commonly made at older ages—although alarmingly, even children are now developing type 2.

Type 1 diabetes is an autoimmune disease in which the body makes little or no insulin. Daily injections of insulin are needed.  Type 1 diabetes is often diagnosed during childhood, although it can appear at any age. U.S. youth with type 1 diabetes are less likely to be obese than youth without diabetes, but somewhat more likely to be overweight. Youth with type 2 diabetes are more likely to be obese than youth with either type 1 or no diabetes.(2) Pregnant women can develop gestational diabetes, which resolves after the baby is born, although it increases the subsequent risk of diabetes, obesity, and metabolic syndrome in both mother and child. Obesity increases the risk of developing gestational diabetes.(3)

Worldwide increases

Worldwide, the number of adults living with diabetes more than doubled between 1980 and 2008, with increasing prevalence in both men and women. While population growth and aging contribute to this trend, there is also an important epidemiological component, since average fasting blood glucose levels have risen as well.(4) In children, there has been a well-documented worldwide increase in type 1 diabetes incidence over recent decades, with an especially alarming increase in incidence that reaches 5.4% per year in European children under age 5.(5, 6) Even gestational diabetes may be becoming more common as well.(7)

Can diet and exercise fully explain these increases? No environmental factor has been able to explain the increase in type 1 diabetes incidence, while changes in diet and exercise are unlikely to explain the worldwide trend in type 2 diabetes. There may be lesser-known factors that are playing a role in diabetes development.

Environmental exposures

In 2006, Dr. Duk-Hee Lee and colleagues published a groundbreaking study, “A strong dose-response relation between serum concentrations of persistent organic pollutants and diabetes: results from the National Health and Examination Survey 1999-2002.”(8) In it, the authors found that body burden levels of persistent organic pollutants (POPs) were very strongly associated with diabetes. (POPS are a class of pollutants that are organic (carbon-based) and long-lasting in the environment. They include industrial chemicals like PCBs, pesticides like DDT, and by-products of industry like dioxin.) Surprisingly, in people with low levels of POPs, obesity did not increase the risk of diabetes. In other words, exposure to POPs could explain diabetes even better than obesity did.

These surprising findings triggered a flurry of research into type 2 diabetes and environmental chemicalsSubsequent longitudinal studies, animal studies, and cross-sectional studies confirmed associations between various chemicals and type 2 diabetes, insulin resistance, obesity, and metabolic syndrome. In fact, exposure to environmental chemicals may help to explain why many overweight or obese people never develop diabetes, and why some thin people do develop type 2 diabetes.

In 2011, the National Institute of Environmental Health Sciences (NIEHS) brought together experts to evaluate the evidence linking chemical exposures to diabetes and obesity. With analyses of a variety of different chemicals, including POPs, arsenic, BPA, phthalates, and pesticides, they concluded that, “Overall, the review of the existing literature identified linkages between several of the environmental exposures and type 2 diabetes,” especially arsenic and POPs. Meanwhile, “Research on environmental chemical exposures and type 1 diabetes was very limited. This lack of research was considered a critical data gap.”(9)

The NIEHS workshop also found support for the “developmental obesogen hypothesis,” suggesting that chemical exposures may increase the risk of obesity. The effects may be most apparent when chemical exposure during development is combined with a high-fat, high-carbohydrate, or high-calorie diet later in life.(9) Alarming new research shows that developmental exposure to the endocrine-disrupting chemical tributyltin can lead to increased number of fat cells, larger fat cells, and reprogramming of stem cells to develop into fat cells instead of bone cells, in three subsequent generations of mice.(10)

Many questions remain

The evidence is growing, but many questions remain. We still do not know how important environmental chemical exposures are in relation to other factors like diet and obesity in type 2 diabetes development. We still have very little research on type 1 diabetes or gestational diabetes and environmental chemicals, although there are a few preliminary studies.(11) We still do not fully understand the mechanisms by which these chemicals may influence diabetes or obesity risk. We do not know how the various environmental factors linked to diabetes and obesity, such as the microbiome, vitamin D levels, nutrition, viruses, and chemicals, may all interact with one another in people of various genetic backgrounds to influence diabetes and obesity risk. We do not know the risk of weight loss, which can result in the release of chemicals stored in fat.(12) We still do not know how environmental chemicals may affect blood glucose control or the risk of complications in people who already have diabetes—and a few preliminary studies suggest that they may.(13)

And most importantly, we still do not know if reducing chemical exposures will prevent diabetes or obesity—but it is critical that we find out.

Reference List

1. Nguyen NT, Nguyen XM, Lane J, Wang P (2011) Relationship between obesity and diabetes in a US adult population: findings from the National Health and Nutrition Examination Survey, 1999-2006.  Obes.Surg. 21: 351-355

2. Liu LL, Lawrence JM, Davis C, et al (2010) Prevalence of overweight and obesity in youth with diabetes in USA: the SEARCH for Diabetes in Youth study.  Pediatr.Diabetes 11: 4-11

3. Reece EA, Leguizamon G, Wiznitzer A (2009) Gestational diabetes: the need for a common ground.  Lancet 373: 1789-1797

4. Danaei G, Finucane MM, Lu Y, et al (2011) National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants.  Lancet 378: 31-40

5. DIAMOND Project Group (2006) Incidence and trends of childhood Type 1 diabetes worldwide 1990-1999.  Diabet.Med. 23: 857-866

6. Patterson CC, Dahlquist GG, Gyurus E, Green A, Soltesz G (2009) Incidence trends for childhood type 1 diabetes in Europe during 1989-2003 and predicted new cases 2005-20: a multicentre prospective registration study.  Lancet 373: 2027-2033

7. Ferrara A (2007) Increasing prevalence of gestational diabetes mellitus: a public health perspective.  Diabetes Care 30 Suppl 2: S141-S146

8. Lee DH, Lee IK, Song K, et al (2006) 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 29: 1638-1644

9. Thayer KA, Heindel JJ, Bucher JR, Gallo MA (2012) Role of environmental chemicals in diabetes and obesity: a national toxicology program workshop review.  Environ.Health Perspect. 120: 779-789

10. Chamorro-Garcia R, Sahu M, Abbey RJ, Laude J, Pham N, Blumberg B (2013) Transgenerational Inheritance of Increased Fat Depot Size, Stem Cell Reprogramming, and Hepatic Steatosis Elicited by Prenatal Obesogen Tributyltin in Mice.  Environ.Health Perspect.

11. Howard SG, Lee DH (2012) What is the role of human contamination by environmental chemicals in the development of type 1 diabetes?  J.Epidemiol.Community Health 66: 479-481

12. Hong NS, Kim KS, Lee IK, et al (2011) The association between obesity and mortality in the elderly differs by serum concentrations of persistent organic pollutants: a possible explanation for the obesity paradox.  Int.J.Obes.(Lond)

13. Lee DH, Jacobs DR, Jr., Steffes M (2008) Association of organochlorine pesticides with peripheral neuropathy in patients with diabetes or impaired fasting glucose.  Diabetes 57: 3108-3111

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