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      Central body fatness is a stronger predictor of cancer risk than overall body size

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          Abstract

          The importance of body size versus weight distribution for cancer risk is unclear. We investigated associations between measures of body size and shape and the risk of developing cancer. The study population consisted of 26,607 participants from the Alberta’s Tomorrow Project cohort. Two main measures of body shape and size were examined: i) body mass index (BMI) and ii) waist circumference (WC). Incident cancers were identified via linkage to the Alberta Cancer Registry. Cox proportional hazards models were used. Males and females classified as obese (BMI ≥ 30 kg /m −2) have a 33% and 22% increased risk of all-cancer, respectively, than their normal weight counterparts. Similar all-cancer risk increases are observed for those above sex-specific WC guidelines. Mutual adjustment for WC attenuates the association between BMI and all-cancer risk, especially among females. Central adiposity appears to be a stronger predictor of all-cancer risk than body size.

          Abstract

          Obesity is linked to increased cancer risk but the impact of body size versus weight distribution in determining the increased risk is unclear. Here the authors examined body mass index, waist circumference, and waist to hip ratio in relation to all-cancer incidence and incidence of seven individual cancers in a population of approximately 26,000 individual and conclude that central adiposity appears to be a stronger predictor of all-cancer risk than body size.

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          Waist circumference and not body mass index explains obesity-related health risk.

          The addition of waist circumference (WC) to body mass index (BMI; in kg/m(2)) predicts a greater variance in health risk than does BMI alone; however, whether the reverse is true is not known. We evaluated whether BMI adds to the predictive power of WC in assessing obesity-related comorbidity. Subjects were 14 924 adult participants in the third National Health and Nutrition Examination Survey, grouped into categories of BMI and WC in accordance with the National Institutes of Health cutoffs. Odds ratios for hypertension, dyslipidemia, and the metabolic syndrome were compared for overweight and class I obese BMI categories and the normal-weight category before and after adjustment for WC. BMI and WC were also included in the same regression model as continuous variables for prediction of the metabolic disorders. With few exceptions, overweight and obese subjects were more likely to have hypertension, dyslipidemia, and the metabolic syndrome than were normal-weight subjects. After adjustment for WC category (normal or high), the odds of comorbidity, although attenuated, remained higher in overweight and obese subjects than in normal-weight subjects. However, after adjustment for WC as a continuous variable, the likelihood of hypertension, dyslipidemia, and the metabolic syndrome was similar in all groups. When WC and BMI were used as continuous variables in the same regression model, WC alone was a significant predictor of comorbidity. WC, and not BMI, explains obesity-related health risk. Thus, for a given WC value, overweight and obese persons and normal-weight persons have comparable health risks. However, when WC is dichotomized as normal or high, BMI remains a significant predictor of health risk.
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            Obesity as a Major Risk Factor for Cancer

            The number of cancer cases caused by being obese is estimated to be 20% with the increased risk of malignancies being influenced by diet, weight change, and body fat distribution together with physical activity. Reports from the International Agency for Research into Cancer and the World Cancer Research Fund (WCRF) have shown that the strongest evidence exists for an association of obesity with the following cancer types: endometrial, esophageal adenocarcinoma, colorectal, postmenopausal breast, prostate, and renal, whereas the less common malignancies are leukemia, non-Hodgkin's lymphoma, multiple myeloma, malignant melanoma, and thyroid tumours. To be able to develop novel methods in prevention and treatment, we first must understand the underlying processes which link cancer to obesity. Four main systems have been identified as potential producers of cancer in obesity: insulin, insulin-like growth factor-I, sex steroids, and adipokines. Various novel candidate mechanisms have been proposed: chronic inflammation, oxidative stress, crosstalk between tumour cells and surrounding adipocytes, migrating adipose stromal cells, obesity-induced hypoxia, shared genetic susceptibility, and the functional defeat of immune function. Herein, we review the major pathogenic links between obesity and susceptibility to cancer.
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              BRCA1 and BRCA2: 1994 and beyond.

              The discovery of the first gene associated with hereditary breast cancer, BRCA1, was anticipated to greatly increase our understanding of both hereditary and sporadic forms of breast cancer, and to lead to therapeutic and preventive breakthroughs. Much has been learned during the past decade about the genetic epidemiology of breast cancer, the ethnic distribution and clinical consequences of BRCA1 and BRCA2 mutations, and the central role of DNA repair in breast cancer susceptibility. The ability to translate this knowledge into novel treatments, however, remains elusive.
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                Author and article information

                Contributors
                darren.brenner@ucalgary.ca
                Journal
                Nat Commun
                Nat Commun
                Nature Communications
                Nature Publishing Group UK (London )
                2041-1723
                22 January 2019
                22 January 2019
                2019
                : 10
                : 383
                Affiliations
                [1 ]ISNI 0000 0001 0693 8815, GRID grid.413574.0, Department of Cancer Epidemiology and Prevention Research, CancerControl Alberta, , Alberta Health Services, ; Calgary, T2S 3C3 AB Canada
                [2 ]ISNI 0000 0004 1936 7697, GRID grid.22072.35, Bachelor of Health Sciences, Cumming School of Medicine, , University of Calgary, ; Calgary, T2N 4N1 AB Canada
                [3 ]ISNI 0000 0001 0693 8815, GRID grid.413574.0, Alberta’s Tomorrow Project, CancerControl Alberta, , Alberta Health Services, ; Calgary, T2T 0J6 AB Canada
                [4 ]ISNI 0000 0001 2157 2938, GRID grid.17063.33, Dalla Lana School of Public Health, , University of Toronto, ; Toronto, M5T 3M7 ON Canada
                [5 ]ISNI 0000 0004 1936 7697, GRID grid.22072.35, Departments of Oncology and Community Health Sciences, Cumming School of Medicine, , University of Calgary, ; Calgary, T2N 4Z6 AB Canada
                Author information
                http://orcid.org/0000-0002-4783-1966
                Article
                8159
                10.1038/s41467-018-08159-w
                6342989
                30670692
                292b160c-b723-4a1a-8bb0-fdb80e6bff9d
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 23 April 2018
                : 19 December 2018
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