Body Mass Index Positively Associated With Many Cancers in UK Study
In a UK population-based cohort study of associations between body mass index (BMI) and 22 specific cancers reported in The Lancet by Bhaskaran et al, positive associations were found for most cancers and were strongest for uterine, gallbladder, kidney, cervix, thyroid, liver, colon, ovarian, and postmenopausal breast cancers and leukemia. Inverse associations were observed for prostate and premenopausal breast cancers.
Study Details
The study involved primary care data from individuals in the Clinical Practice Research Datalink with BMI data for 5.24 million persons. Relationships with BMI were assessed for the following cancers: female breast, prostate, colon, rectum, lung, malignant melanoma, bladder, stomach, esophageal, non-Hodgkin lymphoma, leukemia, ovary, pancreas, multiple myeloma, uterus body, brain and CNS, liver, kidney, cervix, oral cavity, thyroid, and gallbladder. Cox models were used to analyze associations adjusting for potential confounders. Hazard ratios (HRs) were estimated using a separate model for each cancer with a linear BMI term, adjusted for age, diabetes status, smoking, alcohol use, socioeconomic status, and calendar year and stratified by sex
Follow-up ended a mean of 7.5 years after the first eligible BMI measurement. Cancer developed in 201,504 persons (3.8%), with the study cancers developing in 166,955 (3.2%).
Positive Associations
Each 5 kg/m2 increase in BMI was approximately linearly associated with increased risk of uterine cancer (HR = 1.62, P < .0001; 1.63, P < .0001 in never-smokers only), gallbladder cancer (1.31, P < .0001; 1.50, P <.001, in never-smokers), kidney cancer (1.25, P < .0001; 1.25, P < .0001, in never-smokers), cervical cancer (1.10, P = .00035; 1.14, P = .0010, in never-smokers), thyroid cancer (1.09, P = .0088; 1.11, P = .017, in never-smokers), and leukemia (1.09, P < .0001; 1.07, P = .0011, in never-smokers).
Each 5 kg/m2 increase in BMI was also positively associated (all P < .0001) with liver cancer (HR = 1.19; 1.26, P < .0001, for never-smokers), colon cancer (1.10; 1.11, P < .0001, for never-smokers), ovarian cancer (1.09; 1.08, P = .00036, in never-smokers), and postmenopausal breast cancer (1.05; 1.05, P < .0001, in never-smokers), but these effects varied by underlying BMI or individual-level characteristics.
Positive associations were also observed for rectal cancer (HR = 1.04, P = .017; 1.05, P = .0024, in never-smokers) and pancreas cancer (1.05, P = .012; 1.11, P = .00024, in never-smokers). There was no significant positive association for esophageal cancer (1.03, P = .056), gastric cancer (1.03, P = .16), or bladder cancer overall (1.03, P = .062), but a significant association in patients with these cancers who were never-smokers (1.16, P < .0001; 1.08, P = .013; and 1.05, P = .033).
Inverse Associations
Each 5 kg/m2 increase in BMI was associated with reduced risk for prostate cancer (HR = 0.98, P = .0042; 0.96, P = .0021, in never-smokers) and premenopausal breast cancer (0.89, P < .0001; 0.89, P < .0001, in never-smokers). A significant inverse association was observed among all patients with lung cancer (0.82, P < .0001) and oral cavity cancer (0.81, P < .001), but not among never-smokers with these cancers (0.99, P = .55; and 1.07, P = .26). An inverse association was observed among patients with malignant melanoma who were never-smokers (0.96, P = .013) but not among all patients (0.99, P = .39).
No significant associations with BMI among all patients or among never-smokers were observed for brain and CNS cancers, non-Hodgkin lymphoma, or multiple myeloma.
The investigators estimated that, assuming causality, 41% of uterine caners and ≥ 10% of gallbladder, kidney, liver, and colon cancers could be attributable to excess weight and that a 1 kg/m2 population-wide increase in BMI would result in development of 1 of the 10 cancers most positively associated with BMI in an additional 3,790 UK persons each year.
The investigators concluded: “BMI is associated with cancer risk, with substantial population-level effects. The heterogeneity in the effects suggests that different mechanisms are associated with different cancer sites and different patient subgroups.”
Krishnan Bhaskaran, PhD, of London School of Hygiene and Tropical Medicine, is the corresponding author for The Lancet article.
The study was funded by the National Institute for Health Research, Wellcome Trust, and Medical Research Council. The study authors reported no potential conflicts of interest.
The content in this post has not been reviewed by the American Society of Clinical Oncology, Inc. (ASCO®) and does not necessarily reflect the ideas and opinions of ASCO®.
