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Age-specific effects of hormone therapy use on overall mortality and ischemic heart disease mortality among women in the California Teachers Study

Stram, Daniel O. PhD1; Liu, Yuan MS1; Henderson, Katherine D. PhD2; Sullivan-Halley, Jane BS2; Luo, Jianning MS1; Saxena, Tanmai BS1; Reynolds, Peggy PhD3,4; Chang, Ellen T. ScD3,4; Neuhausen, Susan L. PhD2; Horn-Ross, Pamela L. PhD3,4; Bernstein, Leslie PhD2; Ursin, Giske MD, PhD1,5

doi: 10.1097/gme.0b013e3181f0839a
Original Articles

Objective: Although the Women's Health Initiative trial suggested that menopausal hormone therapy (HT) does not reduce coronary heart disease mortality overall, subsequent results have suggested that there may be a benefit in younger women. The California Teachers Study questionnaire and mortality data were used to examine whether age modified the association between HT and the relative risk of overall mortality and ischemic heart disease deaths.

Methods: Participants from the California Teachers Study were 71,237 postmenopausal women (mean age, 63 y; range, 36-94 y) followed prospectively for mortality and other outcomes from 1995-1996 through 2004.

Results: Age at baseline was a much more important modifier of HT effects than was age at start of therapy. Risks for all-cause mortality (n = 8,399) were lower for younger current HT users at baseline than for never users (for women ≤60 y: hazard ratio, 0.54; 95% CI, 0.46-0.62). These risk reductions greatly diminished, in a roughly linear fashion, with increasing baseline age (for women 85-94 y: hazard ratio, 0.94; 95% CI, 0.81-1.10 for all-cause mortality). Similar results were seen for ischemic heart disease deaths (n = 1,464). No additional significant modifying effects of age at first use, duration of use, or formulation were apparent.

Conclusions: These results provide evidence that reduced risks of mortality associated with HT use are observed among younger users but not for older postmenopausal women, even those starting therapy close to their time of menopause.

From the 1Department of Preventive Medicine, University of Southern California, Los Angeles, CA; 2Division of Cancer Etiology, Department of Population Sciences, Beckman Research Institute, City of Hope, Duarte, CA; 3Cancer Prevention Institute of California, Fremont, CA; 4Division of Epidemiology, Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA; and 5Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Norway.

Received April 2, 2010; revised and accepted July 6, 2010.

Funding/support: This study was supported by grants R01 CA77398 and P01 CA017054 from the National Institutes of Health and by the California Breast Cancer Act of 1993, California Department of Health Services. The collection of cancer incidence data used to define one of the variables in this study was supported by the California Department of Health Services as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885; the National Cancer Institute's Surveillance, Epidemiology, and End Results Program under contract N01-PC-35139 awarded to the University of Southern California, contract N01-PC-35136 awarded to the Northern California Cancer Center, and contract N02-PC-15105 awarded to the Public Health Institute; and the Centers for Disease Control and Prevention's National Program of Cancer Registries, under agreement U55/CCR921930-02 awarded to the Public Health Institute.

The ideas and opinions expressed herein are those of the authors, and endorsement by the State of California, Department of Health Services, the National Cancer Institute, and the Centers for Disease Control and Prevention or their contractors and subcontractors is not intended nor should be inferred.

Financial disclosure/conflicts of interest: None reported.

Address correspondence to: Daniel O. Stram, PhD, Division of Biostatistics, Keck School of Medicine, 1540 Alcazar Street, Room 220G, Los Angeles, CA 90033. E-mail:

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