한빛사 논문
Abstract
NaNa Keum, Darren C. Greenwood, Dong Hoon Lee, Rockli Kim, Dagfinn Aune, Woong Ju, Frank B. Hu and Edward L. Giovannucci
Affiliations of authors: Departments of Nutrition and Epidemiology (NK, DHL, FBH, ELG) and Department of Social and Behavioral Sciences (RK), Harvard School of Public Health, Boston, MA; Division of Biostatistics, University of Leeds, Leeds, UK (DCG); Department of Public Health and General Practice, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway (DA); Department of Epidemiology and Biostatistics, Imperial College London, London, UK (DA); Department of Obstetrics and Gynecology, Ewha Womans University, Seoul, Republic of Korea (WJ); Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA (FBH, ELG).
*Correspondence to: NaNa Keum, MS, Departments of Nutrition and Epidemiology, Harvard School of Public Health, Building 2, 3rd Floor, 655 Huntington Avenue, Boston, MA, 02115
Abstract
Background: Adiposity, measured by body mass index, is implicated in carcinogenesis. While adult weight gain has diverse advantages over body mass index in measuring adiposity, systematic reviews on adult weight gain in relation to adiposity-related cancers are lacking.
Methods: PubMed and Embase were searched through September 2014 for prospective observational studies investigating the relationship between adult weight gain and the risk of 10 adiposity-related cancers. Dose-response meta-analyses were performed using a random-effects model to estimate summary relative risk (RR) and 95% confidence interval (CI) for each cancer type. All statistical tests were two-sided.
Results: A total of 50 studies were included. For each 5kg increase in adult weight gain, the summary relative risk was 1.11 (95% CI = 1.08 to 1.13) for postmenopausal breast cancer among no- or low-hormone replacement therapy (HRT) users, 1.39 (95% CI = 1.29 to 1.49) and 1.09 (95% CI = 1.02 to 1.16) for postmenopausal endometrial cancer among HRT nonusers and users, respectively, 1.13 (95% CI = 1.03 to 1.23) for postmenopausal ovarian cancer among no or low HRT users, 1.09 (95% CI = 1.04 to 1.13) for colon cancer in men. The relative risk of kidney cancer comparing highest and lowest level of adult weight gain was 1.42 (95% CI = 1.11 to 1.81). Adult weight gain was unrelated to cancers of the breast (premenopausal women, postmenopausal HRT users), prostate, colon (women), pancreas, and thyroid. An increase in risk associated with adult weight gain for breast cancer was statistically significantly greater among postmenopausal women (P heterogeneity = .001) and HRT nonusers (P heterogeneity = .001); that for endometrial cancer was alike among HRT nonusers (P heterogeneity = .04).
Conclusions: Avoiding adult weight gain itself may confer protection against certain types of cancers, particularly among HRT nonusers.
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