BACKGROUND - Recent literature suggests that high circulating vitamin D may increase prostate cancer risk. Although the mechanism through which vitamin D may increase risk is unknown, vitamin D concentration could influence circulating sex steroid hormones that may be associated with prostate cancer; an alternate explanation is that it could be associated with prostate-specific antigen (PSA) concentration causing detection bias.
OBJECTIVE - We examined whether serum vitamin D concentration was associated with sex steroid hormone and PSA concentrations in a cross-sectional analysis of men in the National Health and Nutrition Examination Surveys (NHANES).
DESIGN - Testosterone, oestradiol, sex hormone binding globulin (SHBG), androstanediol glucuronide, and 25-hydroxyvitamin D (25(OH)D) were measured in serum from men ages 20 and older participating in NHANES III (n=1,315) and NHANES 2001-2004 (n=318). Hormone concentrations were compared across 25(OH)D quintiles, adjusting for age, race/ethnicity, body fat percentage, and smoking. PSA concentration was estimated by 25(OH)D quintile in 4,013 men from NHANES 2001-2006.
RESULTS - In NHANES III higher testosterone (quintile (Q) 1=17.2, 95% confidence interval (CI)=16.1-18.6; Q5=19.6, 95% CI=18.7-20.6 nmol/L, p-trend=0.0002) and SHBG (Q1=33.8, 95% CI=30.8-37.0; Q5=38.4, 95% CI=35.8-41.2 nmol/L, p-trend=0.0005) were observed with increasing 25(OH)D. Similar results were observed in NHANES 2001-2004. PSA concentration was not associated with serum 25(OH)D (p-trend=0.34).
CONCLUSIONS - Results from these nationally representative studies support a positive association between serum 25(OH)D and testosterone and SHBG. The findings support an indirect mechanism through which vitamin D may increase prostate cancer risk, and suggest the link to prostate cancer is not due to PSA-detection bias. This article is protected by copyright. All rights reserved.
Clinical endocrinology. 2016 Mar 17 [Epub ahead of print]
Gabriella M Anic, Demetrius Albanes, Sabine Rohrmann, Norma Kanarek, William G Nelson, Gary Bradwin, Nader Rifai, Katherine A McGlynn, Elizabeth A Platz, Alison M Mondul
Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD., Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD., Division of Chronic Disease Epidemiology, Epidemiology, Biostatistics and Prevention Institute, University of Zurich, Zurich, Switzerland., Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD., Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD., Department of Laboratory Medicine, Harvard Medical School and Children's Hospital, Boston, MA., Department of Laboratory Medicine, Harvard Medical School and Children's Hospital, Boston, MA., Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD., Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD., Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD.