Endometriosis is usually discussed in terms of pelvic pain, fertility and reproductive health. A large new study suggests its health implications may extend further.
In a retrospective cohort study published in Diabetologia, researchers followed health records from nearly 3 million women and found that those diagnosed with endometriosis had a 46% higher relative risk of developing type 2 diabetes than women without the condition. The association does not prove that endometriosis causes diabetes, and researchers do not yet know what might connect the two conditions.
“Previous studies largely evaluated endometriosis as a single condition and generally reported little or no overall association with type 2 diabetes,” said lead author Maggie Fuzak Nunziato, a doctoral student in epidemiology at George Mason University. “Our findings add to a growing understanding that endometriosis may affect more than reproductive health alone.”
Endometriosis affects about 1 in 10 women of reproductive age and occurs when tissue similar to the lining of the uterus grows outside the uterus. It can cause chronic pain, infertility and other complications.
For the new study, researchers used the Utah Population Database to examine health records collected between 1996 and 2021. Nearly 100,000 of the women included in the analysis had been diagnosed with endometriosis.
Overall, women with endometriosis were more likely to later develop type 2 diabetes.
The 46% figure represents a relative difference in risk. It does not mean that 46% of women with endometriosis developed diabetes or that an individual woman’s risk increases by exactly that amount.
The association also varied depending on the type of endometriosis and the women researchers examined.
It was stronger among premenopausal women and among women without obesity. That finding is notable because age and obesity are well-established risk factors for type 2 diabetes, yet the relationship with endometriosis was apparent in groups that might not otherwise be viewed as having particularly high diabetes risk.
It does not mean women without obesity are generally at greater risk of diabetes than women with obesity. Rather, within this study, the difference in diabetes risk between women with and without endometriosis was more pronounced in that group.
The researchers also found that the location of endometriosis appeared to matter. The strongest associations were seen among women whose endometriosis had been diagnosed outside the pelvic area.
Those subtype findings require particular caution. Some forms of endometriosis were much less common than others, and differences in diagnosis, medical coding and health care use could influence the size of the associations.
That is one of several reasons the results cannot establish cause and effect.
Women with endometriosis may have more frequent contact with the health care system because of pain, fertility concerns or other symptoms, potentially creating more opportunities for diabetes to be detected. Endometriosis and type 2 diabetes could also share underlying risk factors that were not fully captured in the analysis.
Researchers have proposed chronic inflammation as one possible connection. Endometriosis involves inflammatory processes, and inflammation can also play a role in metabolic disease.
But this study did not establish inflammation as the reason women with endometriosis had higher diabetes risk. Understanding whether there is a shared biological pathway will require additional research.
For now, the findings raise a potentially useful clinical question rather than providing a new screening rule.
If other studies confirm the association, endometriosis could eventually become one more factor clinicians consider when assessing a woman’s long-term metabolic health. That could be particularly relevant for women who do not have some of the more familiar warning signs associated with type 2 diabetes risk.
The research was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health. Additional support for the Utah Population Database and related research infrastructure came from the National Center for Research Resources, the Utah Department of Health, the University of Utah, the National Cancer Institute, the University of Utah’s Program in Personalized Health and the Utah Clinical and Translational Science Institute.