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Individual studies have suggested that some circulating fatty acids are associated with prostate cancer risk, but have not been large enough to provide precise estimates of associations, particularly by stage and grade of disease.Principal investigators of prospective studies on circulating fatty acids and prostate cancer were invited to collaborate. Investigators provided individual participant data on circulating fatty acids (weight percent) and other characteristics of prostate cancer cases and controls. Prostate cancer risk by study-specific fifths of 14 fatty acids was estimated using multivariable-adjusted conditional logistic regression. All statistical tests were two-sided.Five thousand and ninety-eight case patients and 6649 control patients from seven studies with an average follow-up of 5.1 (SD = 3.3) years were included. Stearic acid (18:0) was inversely associated with total prostate cancer (odds ratio [OR] Q5 vs Q1 = 0.88, 95% confidence interval [CI] = 0.78 to 1.00, P trend = .043). Prostate cancer risk was, respectively, 14% and 16% greater in the highest fifth of eicosapentaenoic acid (20:5n-3) (OR = 1.14, 95% CI = 1.01 to 1.29, Ptrend = .001) and docosapentaenoic acid (22:5n-3) (OR = 1.16, 95% CI = 1.02 to 1.33, P trend = .003), but in each case there was heterogeneity between studies (P = .022 and P < .001, respectively). There was heterogeneity in the association between docosapentaenoic acid and prostate cancer by grade of disease (P = .006); the association was statistically significant for low-grade disease but not high-grade disease. The remaining 11 fatty acids were not statistically associated with total prostate cancer risk.There was no strong evidence that circulating fatty acids are important predictors of prostate cancer risk. It is not clear whether the modest associations of stearic, eicosapentaenoic, and docosapentaenoic acid are causal.

Original publication




Journal article


Journal of the National Cancer Institute

Publication Date





Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK (FLC, PNA, RCT, TJK); Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA (MB, GEG, IBK, MLN); Department of Internal Medicine, Division of Cancer Prevention and Control, The Ohio State University College of Medicine, Columbus, OH (TMB); National Institute for Public Health and the Environment - RIVM, Bilthoven, the Netherlands (HBB); Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, the Netherlands (HBB); School of Public Health, Imperial College London, London, UK (HBB); Nutrition and Metabolism Section and the Nutritional Epidemiology Group, International Agency for Research on Cancer, Lyon, France (VC); Departments of Nutrition and Epidemiology, Harvard School of Public Health and Channing Division of Network Medicine, Boston, MA (JEC, MJS); Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (JEC, MJS); Department of Epidemiology, Murcia Regional Health Authority, Spain (MC); CIBER Epidemiology and Public Health CIBERESP, Spain (MC); Cancer Epidemiology Centre, Cancer Council Victoria, Carlton, Victoria, Australia (DRE, GGG, GS); Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, The University of Melbourne, Victoria, Australia (DRE, GGG, GS); FOODplus Research Centre, Waite Campus, The University of Adelaide, Glen Osmond, South Australia, Australia (RAG); Center for Human Nutrition, David Geffen School of Medicine, University of California, Los Angeles, CA (SMH); Department of Cancer Epidemiology, German Cancer Research Center - DKFZ, Heidelberg, Germany (RK); Department of Internal Medicine, University of New Mexico, Albuquerque, NM (IBK); Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI (LNK, SYP, LRW); Cancer Prevention Program, Division of Public Health Sciences, Fred Hu


Endogenous Hormones, Nutritional Biomarkers and Prostate Cancer Collaborative Group, Humans, Prostatic Neoplasms, Eicosapentaenoic Acid, Fatty Acids, Fatty Acids, Unsaturated, Stearic Acids, Logistic Models, Odds Ratio, Risk Assessment, Risk Factors, Case-Control Studies, Prospective Studies, Aged, Middle Aged, Male