By Laurine Brown, PhD
“Most people have not thought of diabetes
as a disease related to environmental
exposure. These studies show that it is.”
— Professor David Carpenter, Director of the Institute for Health
and the Environment at the University of Albany, New York.
Eat right, exercise, and keep your weight in check. This is the conventional advice given to curb the risk of developing diabetes. But research is suggesting that, while very important, adjusting these lifestyle factors might not be enough, especially with a backdrop of environmental pollution. Health officials warn us that the incidence of diabetes (especially type 2, but also type 1) is increasing at an alarming rate; so understanding the causes are critical. Are environmental toxins contributing? What do we know?
What is Diabetes?
Diabetes includes a cluster of diseases resulting in a person having high blood sugar levels. Complications can be serious, including nerve, kidney and eye damage, greater risks of heart disease, stroke, and premature death. Most people with diabetes (90–95 percent) have type 2, which is associated with obesity and increased insulin resistance. It was previously called “adult onset” diabetes, but, disturbingly, now even children as young as 8 years old are being diagnosed with it. Type 1 is an autoimmune disease, which was previously called juvenile diabetes, since it often appears during childhood. Though less common, incidence of type 1 is increasing globally also, especially in children under age 5. Gestational diabetes, a third type, appears during pregnancy, often resolving after childbirth, but it can increase the mother’s risk of type 1 or 2 later in life. Nearly 26 million people in the U.S. have diabetes (with one quarter undiagnosed), ranging from an average of 8.3 percent of the population to a high of 50 percent on several Arizona Native American reservations. The American Diabetes Association puts the current cost of dealing with diabetes at an astounding $174 billion and this is expected to rise as the epidemic continues.
Clues to Environmental Risks – A Disturbing Pattern Emerging
Risk factors like dietary excess, inactivity, and obesity do not completely explain the epidemic levels of diabetes (specifically type 2). The list of other suspect causes, though preliminary, is growing to include everyday environmental pollutants like arsenic and cadmium, some pesticides, bisphenol A (BPA) and phthalates, air pollutants, some persistent organic pollutants (POPs; including dioxin and PCBs), flame retardants, and more. Below are three lines of evidence that offer clues (especially for type 2. See www.diabetesandenvironment.org for type 1).
1. Evidence from animal and human studies shows that everyday chemicals can alter body mechanisms involved in blood sugar control. Mechanisms are not clearly understood, but can include destruction and exhaustion of the insulin-producing pancreatic beta cells, increased insulin resistance, endocrine and metabolic disruption. Examples from lab, animal, and some human studies:
- Low doses of BPA affect glucose tolerance and beta cells and promote insulin resistance. Used in plastic bottles, metal can linings, dental sealants, cash receipts, and more, it may cause “epigenetic” changes, meaning it alters the way genes switch on and off, and genetics that can be passed on to the next generation.
- Though specific mechanisms are unknown, most POPs (dioxins, PCBs, etc.) induce a great number and variety of genes, including several that alter insulin action. Studies with dioxin (which concentrates in our food supply, especially meat and dairy) also show it can over-stimulate or impair insulin secretion from beta cells.
- Chemicals thought to mimic estrogen or other hormones (including BPA, PCBs, dioxin, and arsenic) can cause an excess of insulin signaling and secretion, over-stimulating beta cells. This may provoke insulin resistance and beta cell exhaustion
2. Evidence confirms widespread pollution of many substances suspected of disrupting blood sugar control in people. For over a decade, the U.S. CDC has been monitoring the blood and urine of Americans every two years to measure environmental chemical exposure. Though only several hundred of the 80,000 chemicals currently in use are monitored, the results still confirm our nearly universal exposure to common industrial chemicals (see www.cdc.gov/exposurereport/). Few of these chemicals are ever tested for health effects. Some disturbing findings: a stunning 93 percent of Americans had detectable levels of BPA in their urine, though not surprising, since we make 8 million pounds of it annually; also, of critical concern is the ability of chemicals to cross the placenta and influence fetal development — alarmingly, 99-100 percent of the pregnant women had measurable levels of certain PCBs, organochlorine pesticides, phthalates, polycyclic aromatic hydrocarbons (PAHs) and more in their bodies.
3. A growing body of research links chemical exposures in people to diabetes (and to risk factors driving diabetes, like obesity, insulin resistance, metabolic syndrome). Despite bio-monitoring studies documenting widespread “pollution in people” and evidence that chemicals in everyday products may pose potential risks in the development of diabetes, until very recently, surprisingly little research was done investigating these connections. But scientific evidence is now mounting. A few examples:
- A groundbreaking 2006 study found “striking” associations between various “persistent organic pollutants” and diabetes (mostly type 2, but also type 1). People with high levels of exposure were 38 times more likely to develop diabetes than those with lower exposures. That’s a lot.
- Among studies of occupational exposures, U.S. Air Force personnel in Vietnam who sprayed Agent Orange contaminated with dioxin had elevated rates of diabetes, leading to U.S. government compensation for diabetes in these veterans.
- And a study from a contaminated area in Taiwan found that people with the highest levels of exposure to both mercury and other POPS had 11 times the risk of insulin resistance than those with the lowest exposures. A U.S. study (in 2003-4) found that higher urinary concentrations of BPA were associated with diabetes in adults.
- A growing body of research is linking chemical exposures to obesity, which is associated as a key risk factor for diabetes. However, a 2009 study reviewed the evidence that a variety of endocrine disrupting contaminants can influence fat formation and obesity. And the groundbreaking 2006 study on POPs and diabetes found, remarkably, that obesity did not increase the risk of diabetes if those people had very low levels of POPS pollution in their bodies. In an editorial in The Lancet, Dr. Miquel Porta writes, “This finding would imply that virtually all the risk of diabetes conferred by obesity is attributable to persistent organic pollutants, and that obesity is only a vehicle for such chemicals. This possibility is shocking.”
- An extensive 2011 review by the U.S. National Toxicology Program found “good, qualitative evidence” linking diabetes (and obesity) with POPS, arsenic and maternal smoking, in addition to concerns for other pollutants (like BPA, phthalates, pesticides, and more).
Concluding Thoughts
Diabetes is a costly, dangerous, and debilitating disease, which is creating a serious health threat to a growing number of people. Currently lifestyle factors, thought important, don’t adequately explain the rising incidence. While evidence is not conclusive, studies on environmental factors suggest many pollutants may be yet another important clue to the rise of this disease and deserve attention. Fortunately, if environmental pollutants are contributing to the rise in diabetes, we can clean them up with hopes of turning the tide on this epidemic.
Laurine Brown is a registered dietitian and associate professor of Health and Environmental Studies at Illinois Wesleyan
University. This article is reprinted with permission from Illinois
Wesleyan University’s HealthWise Newsletter. References available at www.iwu.edu/~wellness.
Photo credit: StoykoSabotanov/Thinkstock