Sarah Howard
Coordinator of CHE’s Diabetes-Obesity Spectrum Working Group
In the past couple of months, three new analyses have asked the question: Is exposure to the widespread environmental chemical bisphenol A (BPA) associated with type 2 diabetes in humans? These three add to two previous studies on the same topic, for a grand total of five. It is a good question to ask, since laboratory evidence shows that exposure to BPA can cause insulin resistance in animals, as well as disrupt the functioning of the insulin-producing beta cells in the pancreas, essentially a recipe for type 2 diabetes (Alonso-Magdalena et al).
As we might expect, the new evidence does not provide a clear-cut answer to that question.
Four of the five human studies on BPA and diabetes used the same dataset, the National Health and Examination Survey (NHANES), which is the Center for Disease Control and Prevention’s biennial biomonitoring survey of a large sample of US residents. Using NHANES data from 2003/04, Lang et al found that higher BPA concentrations in urine were associated with diabetes and cardiovascular diagnoses, but not with other common diseases. Melzer et al then analyzed NHANES data from a subsequent survey, from 2005/06, and found that in those years, BPA levels were lower than they had been in 2003/04. The association between heart disease and BPA remained significant in 2005/06. The associaton between BPA and diabetes was significant in pooled data (2003-06), but did not reach significance in 2005/06 alone.
That brings us to the three more recent analyses. Shankar et al also analyzed NHANES data, and found that pooled data from 2003-08 show a positive association between BPA and diabetes. Silver et al took a slightly different view of the 2003-08 NHANES data, defining diabetes by whether or not participants took a diabetes medication, or had high long-term blood glucose levels (instead of using self-reported diabetes, as in the previous analyses). These authors also found an overall positive association between BPA and diabetes in 2003-08 pooled data, although breaking down by year, the association was only significant in 2003/04, not 2005/06 or 2007/08. Curiously, average BPA levels in 2007/08 were up again slightly, after falling between 2003/04 and 2005/06.
The fifth study on BPA and diabetes analyzed a group of Chinese adults, whose average urinary BPA level was lower than in the US. Dividing participants into quartiles of BPA exposure, the data shows that risk of diabetes was higher in people in the second and fourth quartiles of exposure, but not the third. The overall trend was not significant (Ning et al).
As a whole, the human studies sometimes find significant associations between BPA and diabetes, especially in NHANES data from 2003/04, but not always, not in other years or in other surveys. All of these studies have the same main weakness: a cross-sectional design that only considers one snapshot in time, and does not include multiple exposure measurements or disease development over time. No human studies have yet looked to see whether developmental exposures to BPA increase the later risk of diabetes, despite animal evidence that in utero exposures can cause insulin resistance and reduce glucose tolerance in male mice, predisposing them to diabetes later in life. Considering that there is widespread exposure to BPA, including in pregnant women, aminiotic fluid, and umbilical cord blood, such studies are urgently needed.
References
Alonso-Magdalena P, Quesada I, Nadal A. 2011. Endocrine disruptors in the etiology of type 2 diabetes mellitus. Nat.Rev.Endocrinol. 7(6):346-353. http://www.ncbi.nlm.nih.gov/pubmed/21467970
Lang IA, Galloway TS, Scarlett A, Henley WE, Depledge M, Wallace RB, Melzer D. 2008. Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults. JAMA 300(11):1303-1310. http://www.ncbi.nlm.nih.gov/pubmed/18799442.
Melzer D, Rice NE, Lewis C, Henley WE, Galloway TS. 2010. Association of urinary bisphenol a concentration with heart disease: evidence from NHANES 2003/06. PLoS.One. 5(1):e8673. http://www.ncbi.nlm.nih.gov/pubmed/20084273.
Ning G, Bi Y, Wang T, Xu M, Xu Y, Huang Y, Li M, Li X, Wang W, Chen Y, et al. 2011. Relationship of Urinary Bisphenol A Concentration to Risk for Prevalent Type 2 Diabetes in Chinese Adults: A Cross-sectional Analysis. Ann.Intern.Med. 155(6):368-374. http://www.ncbi.nlm.nih.gov/pubmed/21930854
Shankar A, Teppala S. 2011. Relationship between Urinary Bisphenol A Levels and Diabetes Mellitus. J.Clin.Endocrinol.Metab http://www.ncbi.nlm.nih.gov/pubmed/21956417
Silver MK, O’Neill MS, Sowers MR, Park SK. 2011. Urinary Bisphenol A and Type-2 Diabetes in U.S.Adults: Data from NHANES 2003-2008. PLoS.One. 6(10):e26868. http://www.ncbi.nlm.nih.gov/pubmed/22046388
Our Health and Environment Blog 
Another study came out two days after I wrote this. It found BPA levels were associated with an increased risk of obesity and insulin resistance in Chinese adults:
http://www.ncbi.nlm.nih.gov/pubmed?term=22090277
Wang T, Li M, Chen B, Xu M, Xu Y, Huang Y, Lu J, Chen Y, Wang W, Li X, Liu Y, Bi Y, Lai S, Ning G. 2011. Urinary Bisphenol A (BPA) Concentration Associates with Obesity and Insulin Resistance. J.Clin.Endocrinol.Metab [epub ahead of print].
According to Jenny Ruhl’s blog ( google Blood Sugar 101 ),. there is a substantial body of evidence that rodents are an inappropriate model for human diabetes. She cites drugs that benefit rodents with diabetes are harmful to humans. She also states that the research industry has such a vested interested in rodent diabetes studies that there is no likely end to this scientific misadventure. That is good news for the diabetic rats though ! So its a good idea to avoid BPA for many reasons, but be very wary of conclusions from rodent diabetes.