Are Plastics Making America Fatter?
By Sarah (Steve) Mosko
Still disappointingly chubby after cutting back on junk foods and exercising regularly?
Two-thirds of U.S. adults are now either overweight or down right obese. And while an unhealthy diet and sedentary lifestyle can contribute to an expanding waistline, evidence is accumulating that exposure to substances in everyday plastics and other industrial chemicals can fatten you up too.
Doctors gauge fatness by the Body Mass Index (BMI), based on a person’s height and weight. For adults, the cutoffs are 25 for overweight and 30 for obesity.
The average U.S. man or woman now has a BMI of 28.7, according to the Centers for Disease Control. One-third of adults are overweight, and another third are obese. Even those at the lower end of normal are showing an upward trend.
And not just adults are tipping the scales. A national survey of children and teens found that 32 percent are overweight or obese. Even animals seem to be gaining weight, including domestic pets and feral rodents. The ubiquity of the problem has led scientists to suspect environmental influences.
The term “obesogen” was coined in 2006 to denote environmental chemicals that promote fat. Bruce Blumberg, a biology professor at the University of California, Irvine, discovered that the hormone-disruptor tributyltin (TBT), known to cause sex reversal in fishes, makes mice grow up fatter even though they were only exposed in utero and ate a normal diet. TBT activates receptors within a cell’s nucleus called PPAR-gamma which regulate the number and size of fat cells by instructing stem cells that give rise to fat cells.
Among its uses, TBT prevents yellowing of clear plastics and catalyses the synthesis of polyvinyl chloride plastics, though a related compound, dibutyltin, is more commonly used nowadays. Research ethics prevent intentional human exposure to toxic chemicals, but Blumberg says there is no doubt these tin compounds would promote obesity in humans because we already have medications for diabetes which activate the very same receptors and cause weight gain – Actos and Avandia.
Blumberg thinks there is already good evidence for about 20 obesogens. Given the tens of thousands of industrial chemicals in use today, many more could be lurking about. Although research on obesogens is still in its infancy, among the known obesogens are two others associated with common plastics: phthalates and BPA (bisphenol-A).
Phthalates are a family of plasticizers (softeners) used in polyvinyl chloride plastics. Human studies have documented bigger waistlines and higher BMIs in adults whose urine shows higher levels of the breakdown products of phthalates. Though how phthalates (or their metabolites) promote fatness is not well understood, there is evidence from animal studies that PPAR-gamma receptors are sometimes involved.
While TBT is thought to have greater potency as an obesogen, human exposure to phthalates is conceivably greater because phthalates are used in a myriad of personal care products and consumer plastics – everything from shower curtains and medical IV bags to children’s toys. Phthalates can migrate out of plastics, explaining in part why over 90 percent of Americans test positive for phthalates.
BPA is a building block of polycarbonate plastics and also found in the epoxy lining of canned foods and beverages and on cash register receipts. It too leaches out of products, and ingestion contributes to its widespread presence in human tissues, including breast milk.
Most of the obesogen research on BPA has been done in cell cultures or lab rodents exposed early in development, though higher BPA exposure has been documented in obese women too. BPA actually reduces the number of fat cells, but instead makes them grow much larger, according to Frederick vom Saal of the University of Missouri. Though how BPA does this is unclear, Blumberg has shown that the PPAR-gamma receptor is not involved. He speculates that BPA’s proven mimicry of the hormone estrogen might be.
Blumberg’s latest research reveals that a chemical cousin of BPA (called BADGE for short), used in the epoxy lining of milk cartons and other cardboard beverage containers, pushes human stem cells to morph into fat cells by an unknown mechanism. Like BPA, BADGE also leaches into a container’s contents.
A 2011 National Toxicology Program workshop on obesogens also identified several pesticide obesogens, and prenatal nicotine exposure through maternal smoking during pregnancy is the obesogen with the strongest support from human studies. The hypothesis driving current research is that early developmental exposure to obesogens programs fat cells and the neural circuits controlling feeding behaviors which, combined with a less healthy lifestyle, set the stage for obesity.
Though adult exposure to some obesogens might also add to weight struggles, scientists are most interested in the prenatal period through puberty when a person’s fat cell makeup and metabolic set point for weight gain are established. Blumberg says to expect investigations in the near future revealing transgenerational effects where prenatal exposure affects subsequent generations too.
Blumberg does not, however, think that early obesogen exposure necessarily destines a person to becoming fat, but it could make weight control tougher.
It will be a while before scientists sort out how environmental obesogens figure into America’s obesity epidemic. However, given that obesity increases risk for serious medical conditions, including diabetes, cardiovascular disease and cancer, minimizing unnecessary exposures seems wise.
Blumberg recommends avoiding plastics and tobacco smoke, filtering water, and eating fresh organic foods in lieu of canned/prepackaged items.