Journal
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Volume 97, Issue 10, Pages E1948-E1952Publisher
ENDOCRINE SOC
DOI: 10.1210/jc.2012-1972
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Funding
- National Institutes of Health (NIH)/Eunice Kennedy Shriver National Institute of Child Health and Human Development
- NIH/National Institute on Aging (NIA) [R01 HD044876, K08 AG03575]
- NIH/University of California San Francisco Clinical and Translational Science Institute [UL1 RR024131]
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Context: Individuals with metabolically healthy or benign obesity vs. unhealthy or at risk obesity have been distinguished; however, the predisposing factors for developing these phenotypes are poorly understood. Objective: Our objective was to examine pubertal timing marked by menarcheal age in relation to at-risk obese, benign obese, and healthy normal-weight phenotypes at midlife and to characterize the potential role of androgens, marked by the free androgen index (FAI), in accounting for any associations between menarcheal age and obesity phenotype. Design: The study was cross-sectional. Setting and Participants: Participants included a multiethnic community sample of 989 premenopausal women ages 25-45 yr (mean = 35.2 yr; SD = 5.5 yr). Main Outcome Measure: Membership in at-risk obese, benign obese, and healthy normal-weight groups was defined by body mass index and number of metabolic syndrome components. Results: With each 1-yr increase in menarcheal age, the probability of having the at-risk obese compared with the healthy normal-weight phenotype decreased by 22%. This association attenuated when FAI was covaried, suggesting androgen levels may account for this association. In addition, higher FAI was independently related to having the at-risk obese compared with the healthy normal-weight phenotype as well as having the at-risk compared with the benign obese phenotype (all P < 0.05). Conclusions: Younger menarcheal age is associated with having the metabolically unhealthy obesity phenotype compared with the healthy normal-weight phenotype at midlife. This relation may be driven by levels of bioavailable androgens, which were especially elevated among women with the at-risk obesity phenotype. (J Clin Endocrinol Metab 97: E1948-E1952, 2012)
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