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Author Notes:

Correspondence to: Marjorie L. McCullough, ScD, Behavioral and Epidemiology Research Program, American Cancer Society, 250 Williams Street, 6D, Atlanta, GA 30303-1002 (e-mail: marji.mccullough@cancer.org).

Co-first authors: MLM, ESZ, SJW, and VF

Co-senior authors: RGZ and SAS-W

The authors have no conflicts of interest to disclose.

Subjects:

Research Funding:

NCI R01CA152071, R25CA098566, T32CA009001, R03CA212799, and R03CA183016; National Heart, Blood, and Lung Institute T32HL125232; National Cancer Institute Intramural Research Program.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Oncology
  • SERUM 25-HYDROXYVITAMIN D
  • D-BINDING PROTEIN
  • BREAST-CANCER
  • RECTAL-CANCER
  • D SUPPLEMENTATION
  • D-RECEPTOR
  • CALCIUM
  • HEALTH
  • ASSOCIATION
  • METAANALYSIS

Circulating Vitamin D and Colorectal Cancer Risk: An International Pooling Project of 17 Cohorts

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Journal Title:

JNCI: Journal of the National Cancer Institute

Volume:

Volume 111, Number 2

Publisher:

, Pages 158-169

Type of Work:

Article | Final Publisher PDF

Abstract:

Background: Experimental and epidemiological studies suggest a protective role for vitamin D in colorectal carcinogenesis, but evidence is inconclusive. Circulating 25-hydroxyvitamin D (25(OH)D) concentrations that minimize risk are unknown. Current Institute of Medicine (IOM) vitamin D guidance is based solely on bone health. Methods: We pooled participant-level data from 17 cohorts, comprising 5706 colorectal cancer case participants and 7107 control participants with a wide range of circulating 25(OH)D concentrations. For 30.1% of participants, 25(OH)D was newly measured. Previously measured 25(OH)D was calibrated to the same assay to permit estimating risk by absolute concentrations. Study-specific relative risks (RRs) for prediagnostic season-standardized 25(OH)D concentrations were calculated using conditional logistic regression and pooled using random effects models. Results: Compared with the lower range of sufficiency for bone health (50-<62.5 nmol/L), deficient 25(OH)D (<30 nmol/L) was associated with 31% higher colorectal cancer risk (RR = 1.31, 95% confidence interval [CI] = 1.05 to 1.62); 25(OH)D above sufficiency (75-<87.5 and 87.5-<100 nmol/L) was associated with 19% (RR = 0.81, 95% CI = 0.67 to 0.99) and 27% (RR = 0.73, 95% CI = 0.59 to 0.91) lower risk, respectively. At 25(OH)D of 100 nmol/L or greater, risk did not continue to decline and was not statistically significantly reduced (RR = 0.91, 95% CI = 0.67 to 1.24, 3.5% of control participants). Associations were minimally affected when adjusting for body mass index, physical activity, or other risk factors. For each 25 nmol/L increment in circulating 25(OH)D, colorectal cancer risk was 19% lower in women (RR = 0.81, 95% CI = 0.75 to 0.87) and 7% lower in men (RR = 0.93, 95% CI = 0.86 to 1.00) (two-sided Pheterogeneitybysex = .008). Associations were inverse in all subgroups, including colorectal subsite, geographic region, and season of blood collection. Conclusions: Higher circulating 25(OH)D was related to a statistically significant, substantially lower colorectal cancer risk in women and non-statistically significant lower risk in men. Optimal 25(OH)D concentrations for colorectal cancer risk reduction, 75-100 nmol/L, appear higher than current IOM recommendations.

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© 2019 Oxford University Press. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Universal : Public Domain Dedication License (http://creativecommons.org/publicdomain/zero/1.0/).

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