Oral Contraceptives in Polycystic Ovary Syndrome: Risk-Benefit Assessment

Bulent O. Yildiz, M.D.

Disclosures

Semin Reprod Med. 2008;26(1):111-120. 

In This Article

OCP Use and the Risk of Diabetes

The influence of OCPs on glucose/insulin homeostasis will depend on various factors including the dose of estrogen, the dose and type of the progestin, the mode of administration, and other confounding factors including age, body weight, ethnicity, medical problems, family history of diabetes, and smoking.[23] Earlier cross-sectional studies reported that, depending on the type of the progestin, OCPs decrease insulin sensitivity and increase glucose, insulin, and C-peptide levels during oral and intravenous glucose tolerance test.[24,25,26] It was suggested that estrogen component of the OCP causes insulin resistance, and progestins modify the response.[25]

A few large epidemiologic studies addressed the question of whether OCP use increases the risk of developing diabetes.[27,28,29,30] Cross-sectional data including fasting glucose, insulin, and C peptide from more than 3000 women in the Third National Health and Nutrition Examination Survey (1988-1994); showed that, after adjustment for confounding factors, current OCP users, never-users, and past users have similar values.[27] Another prospective observational study of 1940 women in the Coronary Artery Risk Development in Young Adults (CARDIA); analyzing associations between current use of OCPs and fasting glucose and insulin and presence of diabetes reported that current OCP use is not associated with impaired carbohydrate metabolism or increased risk of diabetes in young women. On the contrary, OCPs were found to be associated with lower glucose levels and lower odds of diabetes in this study.[28]

The association between OCP use and incidence of type 2 diabetes was evaluated among 115,117 female nurses free of diabetes, CVD, and cancer in 1976 followed for 12 years. During 1,237,440 person-years of follow-up, 2276 women who provided information on OCP use were diagnosed with type 2 diabetes. Women who used OCPs in the past had marginally increased relative risk of 1.10 (95% CI, 1.01 to 1.21);, whereas current users of OCP had a relative risk of 0.86 (95% CI, 0.46 to 1.61).[29] Another study by the same investigators reexamined the potential association between OCP use and subsequent incidence of type 2 diabetes in a prospective cohort of 98,590 female nurses aged 25 to 42 years and free of diabetes, CVD, and cancer at baseline in 1989 followed for 4 years. During 352,067 person-years follow-up, 185 incident cases of type 2 diabetes were diagnosed indicating an already low absolute risk of type 2 diabetes in this group of women.[30] After adjusting for age, body mass index (BMI);, cigarette smoking, family history of diabetes, parity, physical activity, alcohol intake, ethnicity, history of diagnosis of infertility, dyslipidemia, and hypertension, the relative risk for current users was 1.6 (95% CI, 0.9 to 3.1);, and the relative risk for past users was 1.2 (95% CI, 0.8 to 1.8).[30] Finally, in a retrospective cohort of 904 women with recent gestational diabetes that were followed over 7 years, the risk of type 2 diabetes did not differ between the long-term low-dose OCP (ethinyl estradiol/norethindrone or ethinyl estradiol/levonorgestrel); users and nonhormonal contraceptive users.[31] Overall, these data suggest that the long-term use of OCPs does not significantly influence the risk of type 2 diabetes in reproductive-aged women.

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