It is unclear whether obesity phenotypes measured by different anthropometric indices are associated with a risk of colorectal adenocarcinoma by anatomical location.
We compiled harmonized population-based cohort studies (Cohort of Norway, CONOR) with 143,477 participants that were conducted between 1994 and 2010. General, abdominal, and gluteofemoral obesity were assessed by body mass index (BMI, kg/m2), waist circumference (cm), and hip circumference (cm). Other measures examined were waist to hip ratio, waist to height ratio, and body adiposity index. We performed Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) of obesity relative to a risk of colorectal adenocarcinoma.
In total, 2,044 incident cases of colorectal adenocarcinoma were identified. We observed a positive association between waist circumference (high versus low) and adenocarcinoma in the proximal colon (HR = 1.9, 95% CI = 1.5, 2.5) and distal colon (HR = 1.7, 95% CI = 1.3, 2.3) when adjusted for BMI. The association with waist circumference was especially strong in men. BMI was not associated with adenocarcinoma in the colon or rectum after adjusting for waist circumference. We found no association between hip circumference and colorectal adenocarcinoma. When adjusted for BMI plus waist circumference, body adiposity index was negatively associated with adenocarcinoma in the proximal or distal colon.
Abdominal obesity, but not general or gluteofemoral obesity, was associated with an increased risk of adenocarcinoma in the proximal and the distal colon, especially in men. Muscularity may be negatively associated with risk of colon adenocarcinoma.
From the aDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; bDepartment of Epidemiology and Biostatistics, Imperial College London, London, United Kingdom; and cHUNT Research Centre, Department of Public Healthand General Practice, Norwegian University of Science and Technology, Levanger, Norway.
Submitted 30 April 2015; accepted 19 January 2016.
Yunxia Lu and Kristian Hveem contributed for conceptualization and design; Eivind Ness-Jensen and Kristian Hveem for data collection; Yunxia Lu for data analysis; all for reporting of results and interpretation of data; Yunxia Lu for drafting of manuscript; all for contribution to critical comments and revisions; all for final approval of the version to be published.
The authors report no conflicts of interest.
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Correspondence: Yunxia Lu, Department of Molecular Medicine and Surgery, Karolinska Institutet, SE-171, 76 Stockholm, Sweden. E-mail: email@example.com.