In a study of Swedish elderly people, researchers found that 3 of 4 types of phthalate metabolites were associated with type 2 diabetes prevalence. The phthalate metabolites linked to diabetes included MMP, MiBP, and MEP, which are breakdown products of phthalates found in body care products. MiBP was related to poor insulin secretion, while MMP and MEP were related to insulin resistance. The phthalate metabolite MEHP, which is a breakdown product of the plasticizer DEHP, was not associated with diabetes in this study (Lind et al. 2012).

Phthalates have also been associated with diabetes in a study of Mexican women. That study found that levels of three types of DEHP metabolites were higher in adult women with diabetes than those without diabetes. The results suggest that phthalate exposures may play a role in diabetes development (Svensson et al. 2011). While the type of diabetes was not specified, it was presumably type 2, since the subjects were older adults and many were overweight.

In animals, rats given the phthalate DEHP developed symptoms of diabetes, including higher blood sugar and lower insulin levels. The changes reversed when the exposure was removed (Gayathri et al. 2004). 

I have written a blog post, "Phthalates and diabetes: Is there a connection?" with more details.

In a series of three studies, researchers examined the effects of phthalates on autoimmunity in mice. They found that after exposure to phthalates, different types of mice developed autoantibodies. But, only the autoimmune-prone mice went on to develop disease. They conclude that phthalates seem to be harmful only to susceptible strains of mice, while other strains are protected (Lim and Ghosh 2003; Lim and Ghosh 2004; Lim and Ghosh 2005).

When pregnant and lactating rats were given DEHP, their offspring developed abnormal beta cells, and alternations of the genes controlling beta cell function at the time of weaning. In adulthood, the female offspring had high blood glucose, impaired glucose tolerance and impaired insulin secretion. The adult males had increased insulin secretion. These results suggest that developmental exposure to phthalates can lead to beta cell dysfunction and glucose abnormalities, and is a potential risk factor for diabetes development (Lin et al. 2011).

In one human study, levels of several phthalate metabolites were associated with increased insulin resistance and abdominal obesity in U.S. men (Stahlhut et al. 2007). In another U.S. study of people aged 6-80, various phthalate metabolites were associated with higher body mass index (BMI) and waist circumference in men aged 20-59. Effects in women were not as consistent. In some ages, exposures was associated with lower BMI (Hatch et al. 2008). In Chinese schoolchildren, levels of certain phthalates were associated with increased BMI or waist circumference (Wang et al. 2013). In a large US population, certain phthalate metabolites were associated with an increased risk of overweight/obesity and BMI in black children, but not children of other ethnic groups (Trasande et al. 2013).

In New York City children, certain phthalate exposures measured at age 6-8 were associated with a higher body mass index and waist circumference one year later (Teitelbaum et al. 2012).  In elderly Swedish women (not men), the phthalate MiBP was related to increased abdominal body fat two years later (Lind et al. 2012). 

 

In laboratory studies, the phthalate MEHP was found to promote the formation of fat cells (DEHP is converted to the metabolite MEHP when ingested) (Feige et al. 2007). The phthalate DCHP has also been shown to promote the formation of fat cells (Sargis et al. 2009).

 

For information on the potential role of increased insulin resistance and increased body weight in the development of type 1 diabetes, please visit the insulin resistance and height and weight pages.

Phthalates are endocrine (hormone) disruptors. Phthalates activate certain hormone receptors called PPARs. PPARs are known to influence blood glucose levels, via insulin resistance, insulin secretion, and fat formation.  Interestingly, pharmaceutical drugs that have the opposite effect on PPARs are used to treat type 2 diabetes, by decreasing insulin resistance (Lind et al. 2012). Desvergne et al. (2009) discuss potential mechanisms of phthalate action on obesity, via what they call "metabolic disruptors." MEHP promotes fat formation through metabolic disruption and by affecting gene expression (Feige et al. 2007; Ellero-Simatos et al. 2011). DCHP promotes fat formation through mechanisms involving the hormone glucocorticoid (Sargis et al. 2009). Disturbed glucocorticoid action is associated with a number of conditions, including type 2 diabetes, obesity, and autoimmune disease (Odermatt et al. 2006).

Various types of phthalates are associated with diabetes, excess weight, and insulin resistance in human studies. These conclusions are supported by animal studies. There is some evidence that exposure to phthalates, and levels in the general population, may contribute to the development of type 2 diabetes. While this "metabolic disruption" is likely more significant for type 2 diabetes than type 1, the ability of phthalates to also promote the development of autoimmunity in animals is cause for concern.