NHANES does not distinguish between type 1 and type 2 diabetes, although it is likely most participants had type 2. As I pointed out in  a letter to the editor, these findings may also have implications for type 1 diabetes (Howard and Howard 2009).

(The above summary is taken from my blog entry for the Collaborative on Health and the Environment: BPA and Type 2 Diabetes: What do the Human Studies Tell Us?)

 

For information on the overlap between type 1 and type 2 diabetes, see the types of diabetes page.

BPA has been shown to affect the immune system of rodents in ways that may be significant for autoimmune diseases. In genetically susceptible mice, BPA enhances the production of autoantibodies. While this study used higher doses than humans are probably exposed to, further studies should be able to determine if these effects also occur at lower doses. The authors conclude that BPA may be a factor in the increased incidence of autoimmune disease in humans (Yurino et al. 2004).

 

Bisphenol A also affects adult rodents' response to infection, and patterns of immune system cells called cytokines. Rodents exposed to bisphenol A in utero showed an increased immune response as adults, with higher levels of certain cytokines. BPA's ability to disturb cytokine production in animals could influence inflammation; cytokines are discussed further on the inflammation page. The effects of BPA on the immune system of rodents depend on the timing of the exposure as well as gender (Richter et al. 2007).

 

In humans, exposure to BPA has been associated with higher levels of cytomegalovirus antibodies in adults, a sign of altered immune system function. In youth, BPA exposure was associated with lower cytomegalovirus antibody levels. It is unclear what could account for these differences. The authors of this study suggest that perhaps the consequences of BPA exposure may vary depending on the timing, quantity, and duration of exposure. Perhaps short exposures stimulate the immune system, and longer exposures result in immune dysfunction (Clayton et al. 2010).

A human study has found an association between BPA exposure and increased insulin resistance, general obesity, and abdominal obesity in Chinese adults (Wang et al. 2011).

Nadal et al. (2009) discusses how BPA targets the insulin-producing beta cells in the pancreas, and causes insulin resistance in animals. By doing so, it may contribute to beta cell exhaustion. More recent research from the same laboratory confirms these effects, in human beta cells as well as mouse beta cells (Soriano et al. 2012). A further study  finds that BPA slows down whole-body metabolism in mice and causes insulin resistance throughout their bodies (Batista et al. 2012).

A number of animal studies have found that BPA can affect beta cells. For example, in mice, very low doses of BPA disrupt beta cell functioning by increasing insulin secretion. The same study found that BPA also increased insulin resistance in these mice (Ropero et al. 2008; Alonso-Magdalena et al. 2006). Exposure to BPA, then, may increase the risk of developing type 2 diabetes. The doses used in these studies were much lower than the "lowest observed adverse effect level (LOAEL)" set by the U.S. Environmental Protection Agency.

A further study found that when pregnant mice were exposed to low and high doses of BPA, their insulin resistance increased, and glucose tolerance decreased during the pregnancy (especially those exposed to the lower doses). Four months after the birth, they had increased insulin resistance and also weighed more than the untreated control mice (without differences in food intake). Interestingly, the effects were not apparent three months after the birth, but reappeared at four months. The exposed male offspring, at 6 months of age, had increased insulin resistance and reduced glucose tolerance as well, in addition to altered insulin secretion (females may have been protected by their higher levels of estrogen). The offspring exposed to the lower doses of bisphenol A in utero had higher birthweights than the controls, while the offspring exposed to the higher doses in utero had lower birthweights. The results suggest that bisphenol A could contribute to the development of diabetes, including gestational diabetes, and predispose male offspring to type 2 diabetes in adulthood (Alonso-Magdalena et al. 2010a).

When researchers exposed mother rats to BPA during pregnancy and lactation, their offspring weighed more and had glucose intolerance as adults. If the offspring were fed a high-fat diet, these effects were accelerated and exacerbated: they were obese and developed severe metabolic syndrome (a cluster of conditions common in people with type 1 and 2 diabetes). Interestingly, these effects showed up at the lowest dose of bisphenol A, but not the higher doses (Wei et al. 2011). Alonso-Magdalena et al. (2010b) review the current scientific evidence linking diabetes to bisphenol A. A number of rodent studies show that low doses of bisphenol A affect glucose metabolism, promote insulin resistance, affect beta cells, and have other effects that may be important in the development of diabetes.

Another study showed that long-term, higher dose exposure to bisphenol A, as well as another chemical, nonylphenol, promotes insulin secretion from the pancreatic islet cells in rats. Nonylphenol is used in some personal care products, pesticides, detergents, and paints. These chemicals, then, could potentially induce exhaustion of the beta cells, and result in diabetes (Adachi et al. 2005).

Some researchers propose that environmental factors that overload beta cells may be a factor in the increasing incidence of type 1 diabetes in children (Dahlquist 2006). Perhaps BPA could be considered one of these factors.

Visit the insulin resistance page for information on the potential role of increased insulin resistance in the development of type 1 diabetes, and the height and weight page for more on those factors and type 1 diabetes.

Exposure to bisphenol A in utero and in early life can affect the body weight of animals, depending on dose and gender (Rubin and Soto 2009). One study, for example, found that exposure to a low dose of bisphenol A during gestation and lactation increased the body weight of rats. The effects varied by age, gender, and diet (Somm et al. 2009). Another study, however, found that exposure to bisphenol A during gestation and lactation led to increased body weight and height after weaning in mice (as compared to controls), but that these difference disappeared by adulthood (Ryan et al. 2010).

 

Ben-Jonathan et al. (2009) reviews some of bisphenol A's effects on fat cells. For example, bisphenol A has been found to affect the transport of glucose in the fat cells of mice, which has implications for the development of diabetes (Sakurai et al. 2004). The combined effects of diet, exercise, genetics, and the environment (including bisphenol A) probably interact to contribute to the development of obesity and metabolic syndrome (Ben-Jonathan et al. 2009).

 

For more information on bisphenol A's ability to increase body weight, or for information on the relationship between type 1 diabetes and increased body weight, please visit the height and weight page.

BPA can affect the endocrine (hormone) system, and is considered an endocrine (hormone) disruptor. Bisphenol A acts is considered an environmental estrogen, because it can act similarly to the hormone estrogen. The mechanism whereby bisphenol A promoted insulin secretion has been shown to involve estrogen receptors (Adachi et al. 2005; Soriano et al. 2012). Bisphenol A can promote insulin secretion and also insulin resistance via its estrogenic effects (Alonso-Magdalena et al. 2006). A cellular analysis shows that bisphenol A may be detrimental to beta cell function by affecting insulin secretion (Makaji et al. 2011). The effects of BPA are similar in mouse and human beta cells, and were significant even at very small doses, the doses that we are exposed to in the environment (Soriano et al. 2012). The mechanisms by which BPA can promote insulin resistance and impaired glucose tolerance are known in mice, and the ability of BPA to have the same effects on human beta cells implies that at least some of these effects are also applicable to humans (Soriano et al. 2012).

Bisphenol A also shows other endocrine disrupting effects besides its estrogenicity (Kruger et al. 2008). For example, bisphenol A can promote the formation of fat cells through mechanisms involving activation of receptors for other hormones, glucocorticoids (Sargis et al. 2009). Different types of bisphenol A (brominated and chlorinated bisphenols, used as flame retardants) have also been found to affect processes involved with endocrine disruption via interacting with certain receptors that are involved in diabetes and obesity (Riu et al. 2011). 

 

Bisphenol A has also been associated with oxidative stress and inflammation in women (Yang et al. 2009). Because exposure can influence the immune system, bisphenol A is considered to be an immunotoxicant (desribed on the autoimmunity page (Dietert and Dietert 2007). Both estradiol, a natural estrogen, and the estrogenic pharmaceutical diethylstilbestrol (DES) showed the same autoimmune-enhancing effects as bisphenol A found by Yurino et al. (2004). 

 

Exposure of human tissues to low doses of bisphenol A inhibits the release of a hormone (adiponectin) that increases insulin sensitivity and reduces tissue inflammation. Any factor that inhibits this hormone's release could lead to insulin resistance (Hugo et al. 2008). Bisphenol A has also been found to affect gene expression in fatty tissue (Somm et al. 2009). BPA affects genes involved metabolic syndrome as well (Marmugi et al. 2011).

 

Bisphenol A may also be able to affect other environmental factors associated with type 1 diabetes, such as the intestine.

Biphenol A exposure has been associated with a number of additional health effects in animals not discussed here. For example, early life exposure of mice to low doses of bisphenol A has been found to impair the fertility of male mice. Disturbingly, these effects were passed down to two subsequent generations (Salian et al. 2009). Whether any potential diabetes-related effects of bisphenol A exposure can also be passed down to subsequent generations in animals or humans has not yet been studied.

There is evidence that bisphenol A shows effects, at low levels of exposure, that could contribute to the development of insulin resistance and type 2 diabetes. BPA has not been evaluated in relation to type 1 diabetes, but should be, due to its clear ability to affect beta cells, and possibly promote autoimmunity as well.