Exposure to a group of chemicals known as obesogens has been linked to weight gain and researchers continue to uncover more information about these chemicals.
Studies have found that consuming obesogens such as the chemical tributyltin increases risk of obesity in those exposed, as well as in their children, grandchildren and great-grandchildren.
Until recently, if you were trying to keep off excess pounds the conventional wisdom was relatively simple. Sure, you could name a number of diet and exercise philosophies, but the basic advice was the same: Eat less, exercise more! However, in the last few years, new research has shown that the issues involved in weight gain and loss are more complex than we once believed. While diet and exercise are essential to maintaining a healthy weight, other factors also seem to influence how likely our bodies are to put on and store excess pounds—one of which is exposure to a group of chemicals known as obesogens.
For tips on lessening your exposure to obesogens see 14 Ways to Reduce Your Obesogen Intake.
The term “obesogen” was coined in 2006 by Bruce Blumberg, professor of developmental and cell biology at the University of California, Irvine. It’s now being used everywhere from The Dr. Oz Show to the White House Task Force on Childhood Obesity Report, which recently recommended prioritizing new research on these chemicals.
While we still have a lot to learn, research is uncovering many interesting things about obesogens. About 20 chemicals are currently believed to be obesogens, and many of them are substances to which we’re all widely exposed, including several common pesticides and bisphenol-A (BPA), a chemical found in some plastics.
Blumberg has been active in communicating with the general public about this research and its implications for our health. I spoke with him to learn more about this class of chemicals, particularly his research on mice and a chemical called tributyltin.
The definition of an obesogen is simple: “An obesogen is a chemical that makes an animal or a human fat,” Blumberg says. As he points out, that’s a functional definition—it’s not limited to any one class of chemicals—and any substance that causes weight gain could be considered an obesogen. (You could make a case for donuts, he jokes. They certainly can cause weight gain.)
Different obesogens can work on our bodies in different ways, Blumberg says. “One way is that it works on the fat cells directly—it makes more or larger fat cells. Or it can do that indirectly by altering appetite and satiety, making an animal hungry, or reducing the sensation of satiety. Or it can change metabolism, perhaps slow metabolism. There’s evidence for all those methods for one or another obesogen.”
Most obesogens are also endocrine disruptors. Our endocrine systems produce hormones that regulate growth, metabolism and sexual function, and endocrine-disrupting chemicals interfere with this system. Along with an increased likelihood of acting as obesogens, endocrine disruptors are associated with a range of issues for humans and wildlife, including reproductive and developmental issues, and an increased risk of some types of cancer.
Some of Blumberg’s most interesting work on obesogens has centered on mice exposed to the chemical tributyltin. A highly persistent organic pollutant, tributyltin has been used as an antifouling agent in marine paints, where it has caused damage to marine life. Also used in a range of household products such as building materials and textiles (including carpet), tributyltin is widespread in the environment—the chemical is often found in samples of household dust. Blumberg first decided to study the effects of tributyltin on hormone receptors after attending a conference in Japan and learning that it had been shown to cause sex reversal in some fish.
Studies show that tributyltin not only causes mice to gain weight, but that the effects are long-lasting. One recent study published in the journal Environmental Health Perspectives in March 2013 found that exposure to this chemical had an effect on multiple generations of mice. “We found that when we expose pregnant mice to low levels of tributyltin in the drinking water throughout pregnancy that the babies—the F1—that were exposed in utero got fatter. Our mice that were exposed to tributyltin live in the same environment, eat the same food, have the same access to exercise that the unexposed mice do, yet they get fatter,” Blumberg says.
However it wasn’t just the next generation of mice that were affected; it was also the F2 and F3—the next two generations of mice. Blumberg is clear about what this means: “We need to reconsider how we think about such chemicals. These data, and data from other researchers with different chemicals and different exposure paradigms, say that there can be such a thing as transgenerational effects—permanent effects that will affect our descendants.”
Although Blumberg’s studies were done on mice, there’s good reason to think they might also apply to humans: Prescription drugs such as Actos and Avandia act on the same hormone receptors that tributyltin works on, and these drugs are also associated with weight gain in humans. It’s also interesting to note that research shows we may be especially sensitive to exposure to obesogens in the womb and in early life, although evidence suggests that obesogens can affect adults as well.
Quite a number of journal articles have been published about obesogens, and the issue is being taken seriously within the scientific community, including federal institutions such as the National Toxicology Program. This organization held a workshop in 2011 to review the current literature on environmental chemicals and their potential role in obesity and diabetes.
Kristina Thayer, director of the National Toxicology Program’s Office of Health Assessment and Translation, explains that the purpose of this workshop was to assess the current state of the science on obesogens, and to identify areas where more research might be warranted. “This is an emerging area of science and we weren’t sure exactly what we were going to find,” Thayer says. “But there were certain examples of environmental chemicals that seemed to be linked to either diabetes or obesity.” The particular categories of potential obesogens they looked at included arsenic, persistent organic pollutants, maternal smoking/nicotine, organotins, phthalates, BPA and pesticides.
“In some cases they were very strong associations, in some cases they were more suggestive associations, but collectively it suggested to us that these areas need to be explored,” Thayer says. (Find the full report in Role of Environmental Chemicals in Diabetes and Obesity: A National Toxicology Program Workshop Review.)
Public health advocates are concerned about obesogens because the related problems of obesity and diabetes are serious public health concerns. Rates of diabetes have risen steadily for the past few decades. According to statistics from the Centers for Disease Control and Prevention (CDC), before 1960 just 1 percent of the U.S. population had been diagnosed with diabetes; that’s now almost 7 percent. And the risk of developing diabetes continues to rise. For an American born in the year 2000, the chances of developing diabetes at some point in life are approximately one in three.
The numbers for obesity are even higher. Currently, one-third of U.S. adults are classified as obese while another third are overweight. Overweight and obesity are leading risk factors for developing type 2 diabetes, and also increase risk of stroke, coronary heart disease and some types of cancer.
But obesity isn’t a problem in the U.S. alone. Rates of obesity are rising globally. While only about 10 percent of the worldwide population is considered obese, that number has nearly doubled since 1980. Intriguingly, evidence shows that animals are also gaining weight. According to research from the University of Alabama at Birmingham published in 2010, the average weights of animals living near human environments, including lab animals, household pets and even wild rodents, have risen in the past few decades.
There’s no doubt that obesity is a complicated subject, and public health programs trying to combat it are looking at a whole range of issues. But there is strong evidence that obesogens are contributing to the problem. In a recent issue of the journal Obesity, Jerrold J. Heindel and Thaddeus T. Schug described it this way: “We propose that the confluence of these factors during development…in association with overnutrition and decreased activity along with additional environmental exposures throughout life creates the ‘perfect storm’ that is driving the obesity epidemic throughout the world.”
Exposure to obesogens doesn’t make us destined to become overweight. But it does mean we have to work harder to keep off excess pounds, Blumberg says. “If my mom had unwittingly exposed me to obesogens when she was pregnant—which she may have done, because [the chemical pesticide] DDT was very prevalent back in those days—this means I’m going to store calories more efficiently and therefore I need to be more vigilant about diet and exercise in order not to become heavier than someone who wasn’t exposed.”
That’s good to know, because it turns out most of us have already been exposed to chemicals widely believed to be obesogens. For example, the CDC highlighted BPA and PFOA (perfluorooctanoic acid) in its Fourth National Report on Human Exposure to Environmental Chemicals as being particularly widespread—that is, they were found in the blood or urine of most people studied. BPA is found in many plastics, but especially in those used for food storage including in the linings of food and beverage cans. PFOA is a byproduct of a chemical commonly used in nonstick cookware, the lining of microwave popcorn bags, and many commercial products treated for stain- and water-resistance. Both are generally categorized as endocrine disruptors and obesogens, and both are frustratingly difficult to avoid.
Blumberg is realistic about these issues. “It’s virtually impossible to eliminate exposure to endocrine disruptors,” he says. “The best you can do is reduce exposure as much as you can.” We offer some practical tips on where to start, particularly in weeding out chemicals we consume along with our food, in our article 14 Ways to Reduce Your Obesogen Intake.
While lifestyle changes can help reduce our exposure to obesogens, it would also make sense to strengthen chemical laws in this country, Blumberg says. Under current laws, it’s incredibly difficult to prove that a chemical that’s already on the market is harmful and needs to be regulated. “Chemical law is very bizarre in this country,” Blumberg says. “You probably know that in civil law you find or don’t find something by preponderance of the evidence. In criminal law we have ‘beyond a reasonable doubt.’ But in chemical law, it seems to be ‘beyond the remotest shadow of a doubt.’ I don’t know where that came from. There’s just no justification for that.”
He says a good start would be considering the precautionary principle: The idea that regulation should err on the side of caution, taking precautionary measures if there is reason to believe a chemical might negatively affect human health. That idea seems especially justified in the case of chemicals we believe may have permanent effects on future generations.
“It’s one thing to do something that affects ourselves,” Blumberg says. “But it’s a whole other level of concern to say something that we do affects our descendants forevermore. And I think that means we need to be more cautious.”
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