Objective: Physical inactivity increases postmenopausal and possibly premenopausal breast cancer risk, although different biologic mechanisms are proposed. Our primary objective was to estimate breast cancer risk associated with high versus low levels of moderate-vigorous recreational activity, separately for premenopausal and postmenopausal women.
Methods: We conducted a systematic review of literature published to July 2015. Included reports were cohort or case-control studies relating moderate-vigorous recreational physical activity (metabolic equivalent ≥3.0) to breast cancer incidence, exclusively (≥90%) in premenopausal or postmenopausal women. We appraised study quality and performed meta-analyses using random effects modeling. Subgroup meta-analyses were based on tumor subtype, race, body mass index, parity, hormone therapy use, family history of cancer, and statistical adjustment for body fatness. Dose-response relations were examined.
Results: Pooled relative risks (RRs, 95% CI) for women with higher versus lower levels of moderate-vigorous recreational activity were RR = 0.80 (0.74-0.87) and RR = 0.79 (0.74-0.84) for premenopausal (43 studies) and postmenopausal (58 studies) breast cancer, respectively, with high heterogeneity. Inverse associations were weaker among postmenopausal cohort studies (RR = 0.90 [0.85-0.95]) and studies that statistically adjusted for nonrecreational (eg, occupational, household) activity (RR = 0.91 [0.77-1.06] premenopausal, RR = 0.96 [0.86-1.08] postmenopausal). Risk estimates with versus without body fatness adjustment did not vary by menopause status, although other subgroup effects were menopause-dependent. Among studies of overweight/obese women, there was an inverse association with postmenopausal but not premenopausal breast cancer (RR = 0.88 [0.82-0.95] and RR = 0.99 [0.98-1.00], respectively). Dose-response curves were generally nonlinear.
Conclusions: Although risk estimates may be similar for premenopausal and postmenopausal breast cancer, subgroup effects may be menopause-dependent.
1Department of Cancer Epidemiology and Prevention Research, CancerControl Alberta, Alberta Health Services, Calgary, Alberta, Canada
2Department of Community Health Sciences, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada
3Knowledge Resource Service, Alberta Health Services, Calgary, Alberta, Canada
4Department of Oncology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Address correspondence to: Heather K. Neilson, MSc, Department of Cancer Epidemiology and Prevention Research, CancerControl Alberta, Alberta Health Services, Holy Cross Centre, Room 514, Box ACB, 2210 2nd Street S.W., Calgary, Alberta, Canada T2S 3C3. E-mail: email@example.com
Received 22 April, 2016
Revised 24 July, 2016
Accepted 24 July, 2016
Funding/support: This work was supported by a Health Senior Scholar Award from Alberta Innovates-Health Solutions and the Alberta Cancer Foundation Weekend to End Women's Cancers Breast Cancer Chair held by Christine Friedenreich. This work was also supported by a Career Development Award in Prevention from the Canadian Cancer Society held by Darren Brenner.
Financial disclosure/conflicts of interest: None reported.
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