Are chemicals preventing you from losing weight?
There's good reason to believe that early exposure to "obesogens"—chemicals that can affect our fat cells—set some people up for lifelong weight struggles
When a friend complains, “I just can’t lose weight,” you might assume that she’s not trying hard enough. After all, weight gain is the result of eating more calories than you burn, right?
Not always. Science has shown that obesity is often caused by multiple factors, such as genetic predisposition, differences in metabolism and lifestyle triggers such as stress and poor sleep. Now, the medical community is confirming a new factor: obesogens—hormone-disrupting chemicals lingering in the air we breathe and in the food we eat. The studies are showing that exposure to any one of a few nasty chemicals (also linked to male reproductive disorders and cancers), either as a fetus or as an adult, can do at least some of the following:
• reset fat cells to grow faster,
• increase the number of fat cells,
• mess with appetite regulation, and
• set off metabolic changes that make dieting and exercise weak weight-loss tools.
Earlier this year, the American National Institutes of Health announced millions of dollars in research funding to find out which chemicals in our environment might be partly responsible for the growing obesity epidemic. The concern: Scientists have already shown precisely how we are being exposed to one chemical that directly triggers the production of more fat cells (more on that later).
Dr. Arya Sharma, a professor of medicine and the chair in obesity research and management at the University of Alberta, says it is important to gain a better understanding of how hormone-disrupting chemicals play a role in the cause of obesity for future management and treatment. “But it is also important for everyone to understand that the causes of obesity vary greatly among individuals—as do the solutions.”
In other words, attempting to limit exposure to these chemicals won’t solve a sudden or lifelong struggle with obesity. That said, until researchers determine how significant a role obesogens play in weight gain, Sharma and others suggest it is prudent for pregnant women to safeguard against exposure. As for the rest of us, it can’t hurt to know what we might be up against, and to take similar precautions where reasonable.
How do obesogens work?
The word obesogen—any natural or man-made substance that makes you gain weight—was coined by Bruce Blumberg, a professor in the department of developmental and cell biology at the University of California in Irvine. “It seemed like an obvious word,” he says. In 2003, he fell upon the direct causal connection between tributyltin—a wood preservative that used to be applied to the hulls of ships and is still floating around in the oceans—and weight gain. While his research group was studying how endocrine disruptors including tributyltin trigger sex reversal in fish, they discovered that this chemical activated a hormone receptor called PPARgamma, which is the master regulator of fat cell development. It can regulate the fate of multipotent stromal stem cells (MSCs) to predispose them to form fat instead of bone. (The paper was published in 2006.)
“We showed that exposure to tributyltin prenatally in mice predisposes more of their MSCs to become fat cells. No matter what we did to change those into bone cells, they formed fat cells instead,” says Blumberg. While scientists can’t be absolutely certain this finding occurs in humans (and obviously it can’t be tested for safety reasons), he says, “we do know that activating the PPARgamma with the diabetes drugs Actos and Avandia causes weight gain in humans.”
As far as researchers know, the number of fat cells each person has is programmed in early life. Once set, the body defends that number vigorously. So far, tributyltin offers the only fully understood causal explanation between weight gain and an endocrine disruptor. “However, we know other chemicals also make more fat cells; we just don’t know the mechanisms yet,” says Blumberg. Researchers are working furiously to find them.
The main (potential) culprits
The strongest evidence showing a connection between prenatal exposure to low doses of some endocrine disrupters and later development of obesity is in animal studies. A growing pool of studies show significant patterns between human exposure to certain chemicals and weight gain. In addition to tributyltin, here are the chemicals there is concern about:
Bisphenol A (BPA) and phthalates We ingest BPA when it leaches from polycarbonate plastic and epoxy resins—used in plastic food containers as well as canned-food linings and beverage bottles—into our beverages and food. In 2009, Health Canada banned BPA in plastic baby bottles because of a concern that exposure would harm infants and newborns. It has since concluded that the levels of BPA we are exposed to via other packaged food—namely water bottles, cans and infant formula—is safe.
While BPA has a relatively short chemical life, research is readily performed on it because of our constant exposure. Two Japanese studies, published in 2002 and 2007, showed that BPA not only triggers the conversion of cells to fat cells but also increases the quantity of stored fat in those cells in mice.
Furthermore, a study published in Biotechnology Letters in 2010 suggests that both BPA and benzyl butyl phthalate (used in vinyl products such as kids’ toys to make them soft) may trigger obesity the same way as tributyltin: by activating the PPARgamma receptor and inducing more fat cells. According to Health Canada, simply touching or licking these toys does not constitute a health risk (however, prolonged sucking by an infant may, depending on how much phthalate leaches out). In January of this year, Health Canada announced regulations to limit concentrations of phthalates in children’s toys and products.
There is also increasing evidence that other phthalates may influence metabolism. Specifically, a study published in 2008 in Toxicology examined fetal exposure in rats to the phthalates diisobutyl phthalate (DiBP, used in some plastics and nail polish), butylparaben (an antifungal used in certain cosmetics absorbed through the skin) and perfluorooctanoate (found in a variety of sources from industrial waste to stain-resistant carpets). It found that these compounds altered insulin and leptin levels, which play a role in the programming of the body’s metabolic system.
A study of human exposure, published earlier this year in Environmental Health Perspectives, showed that higher phthalate and BPA blood level concentrations in humans are associated with altered thyroid function, which regulates metabolism.
Polybrominated diphenyl ethers (PBDEs) These flame retardants are used in a wide range of products, including furniture foam, plastics for TV cabinets, consumer electronics, wire insulation and coatings for draperies and upholsteries (how PBDEs get into our body is not understood). An animal study published in Obesity in 2007 showed that PBDEs, fat-soluble chemicals (which tend to congregate and remain in fat cells), significantly disrupt insulin production and alter fat cells to trigger metabolic obesity in rats—meaning their metabolism slowed to a rate that caused them to become obese.
Dichlorodiphenyldichloroethylene (DDE) This breakdown product of the banned pesticide DDT persists in the environment because both are slow to degrade. Most exposure is thought to come from the diet (via the soil), and small amounts are present in water and air. The first-ever review of research, published in Obesity Reviews in 2011, showed that women with higher blood level concentrations of the pesticide near the start of pregnancy had infants who were much more likely to experience rapid weight gain. “They were twice as likely to grow rapidly during their first six months and 60 percent more likely to have high BMI scores at 14 months,” says Michelle Mendez, co-author of the study and a staff scientist at the Centre for Research in Environmental Epidemiology in Barcelona, Spain. “A substantial number of studies have shown that rapid growth in the first months of life is associated with an increased risk of obesity later on in childhood and even in adulthood.”
Who is vulnerable?
Researchers are focusing on prenatal exposure, as this is when stem cells are programming fat cells to develop. However, Blumberg points out that we know adult stem cells can convert to fat cells as a result of chemical exposures, too. For example, as mentioned, the diabetes drugs Avandia and Actos trigger the production of more fat cells. Studies have also shown that a natural obesogen, fructose, tricks the body into thinking it is hungry by acting on the hormones ghrelin and leptin, which control satiation. The concern is that people who eat a diet high in fructose have a higher risk of being overweight or obese (even excluding the fact that the food tends to be higher in calories).
Since many of the chemicals under investigation are widespread, it begs the question: Why isn’t everyone obese? “Because nothing affects someone the same as everyone else,” says Blumberg. “If I give a thousand people the same drug, there will be a range of responses. Many will respond the same way, but some will experience adverse effects while others will experience no effects at all. The challenge for us is to figure out which part of the population is more at risk to obesogens.”
Until then, says Blumberg, it is probably reasonable to conclude that because plastics and pesticides have become more widely used, people born after 1970 are much more likely to have been exposed to obesogens prenatally and throughout their lives.
So, can you attribute sudden weight gain under age 40 to obesogens as you may have been exposed consistently and cumulatively as a fetus or at a young age? No, insist Sharma and others, reminding us that there is never one single reason for obesity. As for whether obesogens are to blame for lifelong weight troubles if you are under 40, Blumberg is more tentative: “I wouldn’t rule it out as one possible cause.”
The budding field of “metabolomics” (the analysis of molecules generated during metabolism) holds promise for the eventual development of a simple test that could gauge a person’s chemical exposure and its impact on body weight. Sharma says this is not tremendously valuable from a clinical perspective because the exposure has already occurred. “We still have to fall back on basic weight-management strategies, which include evaluating diets and eating triggers, as well as getting plenty of exercise. But these still do not work for everyone.”
According to Blumberg, however, it might be helpful for people to know if chemicals play a role in their weight, so they will understand that they have to work harder than others to maintain a healthy weight.
What can you do?
There isn’t a whole lot you can do to avoid certain obesogens—namely pesticides and fire retardants—because products made with them are still on our planet and chemical residues are extremely slow to degrade. “What we hope to examine in future work [with DDE] is the extent to which efforts to ensure a healthy, balanced diet and adequate levels of physical activity reduce the risk that children with rapid weight gain early in life remain overweight in the long term. These types of practices are the best advice for pregnant women,” says Mendez.
Blumberg adds, “I would say it is good for everyone to eat healthier foods, and to aim to have less chemicals in their diet. We can benefit from this at any age, but it is particularly true for pregnant women and young children.”
This article was originally titled "Are chemicals making us fat?" in the October 2011 issue of Best Health. Subscribe today to get the full Best Health experience–and never miss an issue!