Jennifer McPartland, Ph.D., is a Health Scientist.
My colleague Richard Denison at EDF ended his last blog post asking, “The new study [Environmental Chemicals in Pregnant Women in the US: NHANES 2003-2004] leaves me with one question: How many more such wake-up calls do we need before our government enacts policies to ensure the safety of chemicals to which we are exposed?”
Maybe this will help shake us awake! The obesity epidemic in the United States is increasing at alarming rates. So too is an associated disease, type 2 diabetes. Researchers have attributed 70% of the risk associated with developing type 2 diabetes with being overweight or obese, a risk that increases by 4.5% for every 2.2 pounds of weight gained over 10 years.
A healthy diet and hitting the gym should keep these diseases at bay, right? Certainly proper nutrition and exercise are good and important habits for controlling our weight and maintaining overall health. But what if, despite all such efforts, there are contributing factors outside of our control, and even outside of our genetic makeup? And what if those potential factors are found in us, on us, and all around us?
New research suggests that chemicals found in our environment and in everyday products may play a significant role in packing on the pounds.
Major media outlets, including Newsweek and the Washington Post, have profiled the growing concerns about linkages between chemical exposures and obesity and diabetes. These linkages were the focus of an intensive three-day workshop – “Role of Environmental Chemicals in the Development of Obesity and Diabetes” – held last week by the National Institute of Environmental Health Sciences (NIEHS).
The purpose of the workshop was to bring together the collective brainpower of scientists to develop a research agenda that will fill knowledge gaps and allow conclusive results to be drawn on this topic. Researchers representing fields ranging from molecular biology to epidemiology came together to review the evidence linking these diseases to chemicals in six classes: arsenic and other metals, bisphenol A (BPA), organotins and phthalates, nicotine, pesticides, and persistent organic pollutants. These scientists were charged with thoroughly examining the scientific literature for the role these chemicals play in obesity and diabetes.
The emerging science warrants the attention of researchers. Take for example, tributyltin, an endocrine-disrupting compound that has multiple uses, including in pesticides and in certain paints. Recently published work from the lab of Dr. Bruce Blumberg reveals that tributyltin is an “obesogen” – that is, a chemical that disrupts normal biological activity in such a way that “promotes fat accumulation and obesity.”
Quite astonishingly, this effect of tributyltin has been shown to occur in utero before birth in mice. Tributyltin exerts its fat-influencing activity by promoting stem cells (including stem cells derived from humans as well as mice) to preferentially differentiate into adipocytes or fat cells. The Blumberg lab believes that this activity is most likely mediated by tributyltin’s interaction with cellular receptors that activate genes involved in the differentiation of stem cells into fat cells, called adipogenesis. Their studies indicate that tributyltin alters differentiation so that a higher proportion of stem cells become fat cells at the expense of bone cells.
So before we are even born, chemicals like tributyltin may be predisposing us toward obesity by interfering with fetal development.
Given the ubiquity of human exposure to these classes of chemicals and the enormity of the economic and even security impacts that obesity and diabetes have on this country, EDF applauds the efforts of the NIEHS. It is of paramount importance for the U.S. research enterprise to take this issue seriously.
A white paper synthesizing the ideas and recommendations from this workshop will be published in the coming months. In addition, as highlighted during testimony from NIEHS director Dr. Linda Birnbaum before Congress, the agency has already begun funding research on environmental chemical exposures and their potential relationship to metabolic diseases including obesity and diabetes.
As we wait anxiously for the results, a growing segment of the American public is growing increasingly impatient over the failure of the agencies charged with protecting our health to anticipate, develop the data needed to understand, and act to reduce such risks. That failure can in turn be traced to the outmoded and feeble chemical safety policies in this country.
The alarm is sounding and the snooze button should not be an option.