The aim of this study was to estimate associations of obesity with reproductive hormone levels as women progress from premenopausal to postmenopausal status.
This was a longitudinal study conducted in the population-based Penn Ovarian Aging Cohort (N = 436). At cohort enrollment, the women were premenopausal, ages 35 to 47 years, with equal numbers of African Americans and whites. Anthropometric measures, menopause status, and reproductive hormone measures were evaluated for 12 years. Associations of the anthropometric measures with estradiol, follicle-stimulating hormone, and inhibin B in the menopausal transition were estimated using generalized linear regression models for repeated measures.
Associations between obesity and hormone levels differed by menopause status as indicated by significant interactions between each hormone and menopausal stage. Premenopausal obese and overweight women had significantly lower estradiol levels compared with nonobese women, independent of age, race, and smoking (obese: 32.8 pg/mL [95% CI, 30.6-35.2] vs nonobese: 39.8 pg/mL [95% CI, 37.0-42.8], P < 0.001). The associations reversed postmenopause, with obese women having the highest estradiol levels (obese: 20.6 pg/mL [95% CI, 17.2-24.7] vs nonobese: 12.2 pg/mL [95% CI, 10.1-14.8], P < 0.001). Inhibin B levels were significantly lower in premenopausal obese compared with nonobese women but reversed in the late transition stage. Follicle-stimulating hormone levels were lowest in postmenopausal obese compared with nonobese women (P < 0.001). Measures of waist circumference (central adiposity) and waist-to-hip ratio paralleled the body mass index results.
Obesity is an important factor in hormone dynamics independent of age, race, and smoking in midlife women, although the mechanisms remain unclear.
Obesity is an important factor in hormone changes of the menopausal transition, independent of age, race, and smoking. Premenopausal associations between obesity and reproductive hormones reversed after menopause.
From the Departments of 1Obstetrics/Gynecology and 2Psychiatry, University of Pennsylvania, Philadelphia, PA; 3Center for Clinical Epidemiology and Statistics, University of Pennsylvania, Philadelphia, PA; and 4Center for Research in Reproduction and Women's Health, University of Pennsylvania, Philadelphia, PA.
Received October 23, 2009; revised and accepted December 8, 2009.
Funding/support: This work was supported by grants from the National Institutes of Health: R01-AG-12745 (Dr. Freeman, Principal Investigator) and RR024134 (Clinical and Translational Research Center).
Financial disclosure/conflicts of interest: None reported.
Address correspondence to: Ellen W. Freeman, PhD, Department of Obstetrics/Gynecology, 3701 Market Street, Suite 820 (Mudd), Philadelphia, PA 19104. E-mail: email@example.com