There is a well-documented and unexplained increase in the incidence of type 1 diabetes in children around the world, and alarmingly, this increase is most rapid in children under age 5. Type 2 diabetes shows a parallel increase, and is also now appearing even in children. About 6.4% of the world’s adults have diabetes – that’s 285 million people. Health expenditures due to diabetes are estimated to be $376-672 billion US dollars in 2010 worldwide, about 12% of total health expenditures, and this figure does not include expenditures on children with diabetes.
Type 2 is the most common type of diabetes, and the type normally associated with obesity and insulin resistance. Type 1, formerly called juvenile diabetes, is an autoimmune disease where the insulin-producing beta cells of the pancreas are destroyed. There are a number of similarities between type 1 and 2 diabetes, and intermediate types exist as well (such as Latent Autoimmune Diabetes in Adults (LADA), also known as “type 1.5”). For example, dysfunctional beta cells are present in both type 1 and type 2 diabetes, and about 10% of people with type 2 test positive for the autoantibodies characteristic of type 1. Excess weight gain and increased insulin resistance have been associated not only with the development of type 2 diabetes but also with type 1. Women who develop gestational diabetes, meanwhile, are at risk to develop either type 1 or type 2 after pregnancy. Many authors propose that type 1 and type 2 can be thought of as two ends of a “diabetes spectrum,” an idea consistent with findings of genetic susceptibility to these diseases.
Most people think of diabetes as a “lifestyle” disease, and do not consider the possibility that environmental contaminants may play a role in its pathogenesis. In 2006, Dr. Duk-Hee Lee and colleagues published a provocative study that found very strong associations between diabetes and low-dose exposure to various persistent organic pollutants (POPs). In fact, the study found that people who were obese but who had very low concentrations of POPs did not have an increased prevalence of diabetes. On the other hand, the association between POPs and diabetes was stronger in obese individuals than in people who were lean, implying that obesity may increase the toxicity of POPs. While previous studies had found some associations between diabetes and high levels of POP exposures (to dioxin, for example), few had looked at low-level exposures.
A growing number of subsequent studies have found associations between diabetes and exposure to a variety of environmental contaminants, not only POPs, but also bisphenol A, some pesticides, and some air pollutants. In fact, type 1, type 2, and even gestational diabetes have all been associated with exposures to contaminants, although thus far the strongest evidence is for type 2. Unfortunately, many studies on contaminant exposures do not distinguish between the various types of diabetes, and very few have focused on type 1 or gestational diabetes.
Associations, however, do not necessarily imply causation. Does diabetes affect the body’s processing or excretion of contaminants, resulting in higher levels of contaminants in the body, or might contaminants contribute to disease development? Two prospective studies have found associations between diabetes and DDE levels, and some studies have found that diabetes does not seem to affect the body’s processing or elimination of POPs. A number of studies have found contaminant exposures to be associated with various precursors to diabetes, including high blood glucose levels, increased body mass index (BMI), increased insulin resistance, and metabolic syndrome. Toxicological studies, meanwhile, are identifying biological mechanisms that may be at work, showing, for example, that some contaminants may be able to affect the beta cells and insulin secretion, induce weight gain, affect metabolism, increase insulin resistance, and exacerbate or accelerate autoimmunity.
In sum, current evidence suggests that some environmental contaminants may in fact contribute to the development of diabetes. Could these contaminants be in part responsible for the increasing incidence of diabetes worldwide? If environmental contaminants can contribute to the development of diabetes, then preventing pollution, reducing the use of toxic substances and reducing exposures may be a novel way to decrease the incidence of diabetes and its related human and economic costs.
I have summarized the many studies on diabetes and contaminants on a website, www.diabetesandenvironment.org, and I add new studies as they become available. This website focuses on type 1 diabetes and the various environmental factors that may contribute to the disease, emphasizing how both contaminant and lifestyle factors may interact with each other. I focused on type 1 since my young son and I both now have this disease, but I also included type 2 and gestational diabetes because of the overlap among all of these types of diabetes.
Additional sources not included here are available on the website www.diabetesandenvironment.org.
Lee DH, Lee IK, Song K, Steffes M, Toscano W, Baker BA, Jacobs DR, Jr. 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(7):1638-1644. PubMed ID: 16801591.
Longnecker MP, Klebanoff MA, Brock JW, Zhou H. 2001. Polychlorinated biphenyl serum levels in pregnant subjects with diabetes. Diabetes Care 24(6):1099-1101. PubMed ID: 11375377.
Rignell-Hydbom A, Lidfeldt J, Kiviranta H, Rantakokko P, Samsioe G, Agardh CD, Rylander L. 2009. Exposure to p,p’-DDE: a risk factor for type 2 diabetes. PLoS.One. 4(10):e7503. PubMed ID:19838294.
Shaw JE, Sicree RA, Zimmet PZ. 2010. Global estimates of the prevalence of diabetes for 2010 and 2030. Diabetes Res.Clin.Pract. 87(1):4-14. PubMed ID: 19896746.
Turyk M, Anderson H, Knobeloch L, Imm P, Persky V. 2009. Organochlorine exposure and incidence of diabetes in a cohort of Great Lakes sport fish consumers. Environ.Health Perspect. 117(7):1076-1082. PubMed ID:19654916.
Zhang P, Zhang X, Brown J, Vistisen D, Sicree R, Shaw J, Nichols G. 2010. Global healthcare expenditure on diabetes for 2010 and 2030. Diabetes Res.Clin.Pract. 87(3):293-301. PubMed ID: 20171754.
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