To determine whether women with vasomotor symptoms (VMS) have lower bone mineral density (BMD) than do women without VMS.
We analyzed data from baseline to annual follow-up visit 5 for 2,213 participants in the bone substudy of the Study of Women's Health Across the Nation. At baseline, women were aged 42 to 52 years, had an intact uterus and one or more ovaries, were not using exogenous hormones, were not pregnant or lactating, and were premenopausal or early perimenopausal. Menopausal stage and VMS were assessed by annual questionnaire. Menopausal stages were premenopausal, early perimenopausal, late perimenopausal, and postmenopausal. Using repeated-measures mixed models, we determined the association between VMS (any vs none) and BMD (by dual x-ray absorptiometry) within each menopause status category.
After controlling for age, time within each menopausal stage, race/ethnicity, study site, and baseline menopausal stage, postmenopausal women with any VMS had lower lumbar (0.008 g/cm2 lower, P = 0.001) and lower total hip (0.005 g/cm2 lower, P = 0.04) BMD than did postmenopausal women without VMS. Compared with early perimenopausal women without VMS, early perimenopausal women with any VMS had lower femoral neck BMD (0.003 g/cm2 lower, P = 0.0001). Premenopausal women with any VMS had lower femoral neck BMD (0.003 g/cm2 lower, P = 0.03) compared with premenopausal women without VMS.
Even in the earliest menopausal transition stages, women with VMS had lower BMD than did women without VMS. Effects varied by anatomical site, being most evident at the lumbar spine and total hip in postmenopausal women and at the femoral neck among premenopausal and early perimenopausal women.
To determine the association between vasomotor symptoms and bone mineral density, data were analyzed from 2213 participants of the Study of Women's Health Across the Nation. Even in the earliest menopause transition stages, women with vasomotor symptoms had lower bone mineral density on average compared to women without vasomotor symptoms.
From the 1Department of Internal Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA; 2Division of Preventive and Behavioral Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA; 3Department of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh, PA; 4Department of Public Health Sciences, University of California, Davis, CA; and 5Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA.
Received February 14, 2008; revised and accepted July 1, 2008.
Funding/support: Dr Crandall's work was supported by National Institutes of Health (NIH) research grant 5K12 AG01004-08 from the National Institute on Aging. The SWAN has received grant support from the NIH Department of Health and Human Services, through the National Institute on Aging, the National Institute of Nursing Research, and the NIH Office of Research on Women's Health (grants NR004061, AG012505, AG012535, AG012531, AG012539, AG012546, AG012553, AG012554, and AG012495).
Financial disclosure: None reported.
Address correspondence to: Carolyn J. Crandall, MD, MS, David Geffen School of Medicine/GIM, University of California, Los Angeles, 1st Floor, 911 Broxton Avenue, Los Angeles, CA 90024. E-mail: email@example.com