Although the topic of body weight has always been present in the media, lately the subject of weight loss and gain has received substantial news coverage. The public has been subjected to overwhelming amounts of information ranging from body image issues such as anorexia and bulimia, to the health hazards of obesity. With approximately one-third of the adult population in the United States overweight and another third obese in 2008, many researchers are working hard to find sources of obesity and halt the epidemic (1).
Historically, risk factors for obesity have included a sedentary lifestyle and a high-calorie diet. However, recently scientists have been exploring the roles of several environmental factors in health-threatening weight gain.
Many common plastic containers have been found to be a source of BPA.
History of BPA
One environmental factor in particular, Bisphenol A (BPA), has recently been implicated as a potential trigger of obesity and other health risks. A compound that was originally synthesized as a chemical estrogen, BPA is a small molecule used as a monomer in the polymerization reaction used to produce polycarbonate plastics and epoxy resins. These substances are in turn used in baby bottles, food and drink containers, and dental fillings (2, 3). The compound is used in a wide range of items because it forms a clear plastic that is both durable and lightweight. However, when subjected to heat or changes in pH, trace amounts of BPA can migrate from their polymer framework into the food or water they are designed to contain (3). Studies have suggested that consumption of these leached BPA molecules can inhibit adiponectin release from human adipose tissue and adipocytes (1).
The Effects of BPA upon Metabolic Syndrome
In the human body, the protein adiponectin is an adipocyte-specific hormone that both regulates the metabolism, and signals the body to breakdown fatty acids. This process protects against serious dietary health concerns such as metabolic syndrome and obesity (4).
Metabolic syndrome is defined by many conditions including abdominal obesity, glucose intolerance, hyperinsulinemia, hypertriglyceremia, and hypertension. The syndrome is also associated with complications such as type II diabetes and cardiovascular disease. The protein adiponectin, which is inhibited by BPAs, increases fatty acid oxidation and glucose metabolism in muscle while simultaneously reducing glucose output and enhancing insulin sensitivity in the liver. All of these biological processes counteract metabolic syndrome (3). Consequently, any factor that suppresses adiponectin release could promote insulin resistance and increase the risk of developing metabolic syndrome.
Clinical Testing in Mice
The link between BPA and obesity was first investigated using pregnant mice. Scientists fed the mice doses of BPA that were up to ten times lower than the concentrations found in the average human, which range from 0.3 to 5 ng/mL in adult and fetal human plasma, urine, and breast milk (1). The offspring of the pregnant mice exhibited increased rates of cancer in the prostate and mammary glands, which was expected. However, they also displayed abnormal growth later in life, which was unusual.
Intrigued by this study, researchers conducted another experiment on pregnant rats that were exposed to BPA though drinking water. The rats were either given a low dose of BPA at 0.1 mg BPA/kg or a high dose at 1.2 mg BPA/kg (2). They were fed this amount of BPA from day 6 of pregnancy until the end of lactation so that the offspring were exposed to BPA only through their mother via the placenta and breast milk. When the weight of the offspring was measured, both male and female pups showed an increase in body weight compared to the control group (2). However, the increase was more prominent in female offspring than in male offspring. Interestingly, the effect was dose-dependent only in females, and did not increase steadily with dose as scientists expected. The researchers found that if the mothers were exposed to the lower dose of BPA, the female offspring experienced increased weight gain. However, females whose mothers were exposed to the higher dose of BPA did not gain weight. As adults, the females exposed to the low doses typically remained heavier than those exposed to high doses. When measured at 18 months of age, the low-dosed females were approximately 11 percent heavier than the high-dosed females (2).
Further Testing in Human Breast Tissue
Consumption of materials contained in certain plastics often leads to BPA exposure.
Another study was conducted on female human adipose tissue samples not long after the rat experiment. Samples of adipose tissue from the breast, subcutaneous abdominal tissue, and visceral adipose explants (fat associated with internal organs) were taken and exposed to different amounts of BPA in vitro. The effect upon adiponectin levels was observed. As a positive control, they compared BPA’s effect to that of E2, a form of naturally occurring human estrogen (4). Although background rates of adiponectin in the separate patients varied greatly, when the tissues were treated with BPA and E2, almost every patient’s tissues had reduced adiponectin secretion levels. The experiment was repeated with tissue samples from women classified as morbidly obese. Because most of the women who gave tissues did so because they were undergoing some type of surgery to reduce their overall body weight (such as gastric bypass surgery), the researchers wanted to make sure that high body weight was not skewing the results of the experiment (4). Thus, the second experiment was done to observe whether the adiponectin responsiveness to BPA or E2 was affected by obesity (4). The researchers found that the suppressive effect was greater on subcutaneous tissue than on visceral fat tissue, which was not exactly consistent with previous findings. However, both BPA and E2 inhibited release of adiponectin in all fatty tissue by 50 percent after 6 hours, and 65 percent after 24 hours (4). This study concluded that BPA was equally effective as, and at times even better than E2 at suppressing adiponectin secretion (4). It also showed that BPA inhibited adiponectin release from samples of human adipose tissue, which, as previously stated, could lead to health risks such as heart disease and type II diabetes (3).
In addition, the researchers found the same kind of non-monotonic dose-dependency as in the rat experiment, in which the lower dosages suppressed adiponectin production more than the higher dosages did. The increased efficacy of low levels of BPA is significant because humans do not usually come into contact with extremely high doses of BPA. The BPA that they are exposed to is from the slow leaching of the compound from plastics, which only provides a miniscule amount at a time. Thus, when humans do consume BPA, they seem to ingest an amount at which the chemical can do the most damage.
Other Risks of BPAs
Studies have also suggested that BPA is linked to other health hazards including increased cancer incidence and premature puberty in children (1). Unfortunately, because of its usefulness, BPA remains as a component in plastic manufacturing. This is especially true in third world countries, where the use of BPA makes plastics production fast and efficient. Thankfully, measures are being taken to curb BPA use. Canada has recently named it a “toxic chemical” and does not allow its use in manufacturing (1). Although its use is being mediated, the vigilant consumer would do well to take heed of labels and ingredient lists to make sure that they are not accidentally consuming this detrimental compound.
References
1. G. Stemp-Morlock, Environ. Health. Persp. 115, 242 (2007).
2) B. Rubin, A. Soto, Mol. Cell. Endocrinol. 304, 55-62 (2009).
3) N. Ben-Jonathon et al., Mol. Cell. Endocrinol. 304, 49-54 (2009).
4) E. Huge et al., Envrion. Health Persp. 116, 1642-1647 (2008).