Affiliations 

  • 1 Affiliations of authors: Clinical Trial Service Unit and Epidemiological Studies Unit (NEA) and Cancer Epidemiology Unit (RCT, PNA, TJK), Nuffield Department of Population Health, University of Oxford, Oxford, UK; Division of Cancer Epidemiology and Genetics, US National Cancer Institute, Bethesda, MD (DA, AB); Division of Public Health Science (MJB, GEG, MLN), SWOG (formerly the Southwest Oncology Group) Statistical Center (PJG, CMT), and Cancer Prevention Program (JMS), Fred Hutchinson Cancer Research Center, Seattle, WA; Department of Epidemiology (JMS) and Department of Biostatistics (CMT), University of Washington, Seattle, WA; Department for Determinants of Chronic Diseases, National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands (HBBdM); Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, the Netherlands (HBBdM); Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK (HBBdM, MJG); Department of Social & Preventive Medicine, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia (HBBdM); Sorbonne Paris Cité Epidemiology and Biostatistics Research Center, Nutritional Epidemiology Research Team, Inserm U1153, Inra U1125, Cnam, University Paris 13, University Paris 5, University Paris 7, Bobigny, France (MD, PG, SH, MT); National Institute for Health and Welfare, Helsinki, Finland (MH, PK, HR); The Prevention and Research Center Mercy Medical Center, Baltimore, MD (KJH); Department of Preventive Medicine, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA (BEH); University of Hawaii Cancer Center, Honolulu, HI (LNK); Department of Functional Biology, Faculty of Medicine, University of Oviedo, Asturias, Spain (CL); Institute of Epidemiology II, Helmholtz-Zentrum München, Neuherberg, Germany (formerly of Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany) (JL); Intramural Research Program, National Institute on Aging, Department of Neurology, University of Tennessee Health Science Center, Memphis, TN (EJM); Danish Cancer Society Research Center, Copenhagen, Denmark (AO); Epidemiology and Prevention Unit, Fondazione IRCCS Istituto Nazionale dei Tumori, 20133 Milan, Italy (VP); Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (EAP); Roswell Park Cancer Institute, New York, NY (MER); Department of Epidemiology, Harvard School of Public Health, Boston, MA (MJS); Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (MJS); Department of Surgery and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden (PS); Hellenic Health Foundation, Athens, Greece (AT); Department of Epidemiology, GROW School for Oncology and Developmental Biology, Maastricht University, the Netherlands (PAvdB)
J Natl Cancer Inst, 2016 11;108(11).
PMID: 27385803 DOI: 10.1093/jnci/djw153

Abstract

BACKGROUND: Some observational studies suggest that a higher selenium status is associated with a lower risk of prostate cancer but have been generally too small to provide precise estimates of associations, particularly by disease stage and grade.

METHODS: Collaborating investigators from 15 prospective studies provided individual-participant records (from predominantly men of white European ancestry) on blood or toenail selenium concentrations and prostate cancer risk. Odds ratios of prostate cancer by selenium concentration were estimated using multivariable-adjusted conditional logistic regression. All statistical tests were two-sided.

RESULTS: Blood selenium was not associated with the risk of total prostate cancer (multivariable-adjusted odds ratio [OR] per 80 percentile increase = 1.01, 95% confidence interval [CI] = 0.83 to 1.23, based on 4527 case patients and 6021 control subjects). However, there was heterogeneity by disease aggressiveness (ie, advanced stage and/or prostate cancer death, Pheterogeneity = .01), with high blood selenium associated with a lower risk of aggressive disease (OR = 0.43, 95% CI = 0.21 to 0.87) but not with nonaggressive disease. Nail selenium was inversely associated with total prostate cancer (OR = 0.29, 95% CI = 0.22 to 0.40, Ptrend < .001, based on 1970 case patients and 2086 control subjects), including both nonaggressive (OR = 0.33, 95% CI = 0.22 to 0.50) and aggressive disease (OR = 0.18, 95% CI = 0.11 to 0.31, Pheterogeneity = .08).

CONCLUSIONS: Nail, but not blood, selenium concentration is inversely associated with risk of total prostate cancer, possibly because nails are a more reliable marker of long-term selenium exposure. Both blood and nail selenium concentrations are associated with a reduced risk of aggressive disease, which warrants further investigation.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.