A pooled cohort study conducted by McCullough and colleagues found that patients with 25(OH)D levels less than 30 nmol/L had a 31% increased risk of CRC compared with those who had levels between 50 nmol/L to 62.5 nmol/L.6 Patients with levels 75 nmol/L to 87.5 nmol/L had a 19% lower risk, while those with levels 87.5 nmol/L to 100 nmol/L had a 27% lower risk. There was no added benefit seen from obtaining vitamin D levels greater than 100 nmol/L. When broken down by sex, the authors found that for every 25 nmol/L incremental increase in 25(OH)D, there was a 7% decreased risk in men compared with a 19% decreased risk in women. Based on these findings, the authors concluded that higher levels of 25(OH)D in the range of 75 nmol/L to 100 nmol/L were needed, which were levels much higher than were analyzed in many  previous studies.

Although there is evidence to support the role of vitamin D in potentially lowering the risk of CRC, vitamin D supplementation should not be considered a “cure” or a complete prophylactic agent. Despite the aforementioned positive data, there are also studies that show an increased risk of cancer mortality in certain patients with higher 25(OH)D levels — therefore, caution surrounding recommendations on vitamin D should be used in both patients with and without established cancer diagnoses.7


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While the development of CRC involves a number of factors, there is research to support the notion that vitamin D may represent one of them. Patients should be reminded to always consult their physicians when starting vitamin D supplementation in order to avoid toxicity. The typical “normal” recommended adult dosing is 600 to 800 international units (IU) per day, depending on patient age. Individuals who are deficient may require higher doses, which should be administered under the guidance of a physician. Most of the toxicity related to excessive dosing of vitamin D is manifested via hypercalcemia. Symptoms associated with hypercalcemia include abdominal pain, confusion, nephrolithiasis, anorexia, bone pain, and muscle weakness.

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Although much of the recent data regarding vitamin D appear to confirm it has a role in reducing the risk of CRC, additional studies are needed to help further delineate the appropriate levels at which to initiate treatment, the desired target levels, and the appropriate dosing to reach those targets.

References

  1. Klampfer L. Vitamin D and colon cancer. World J Gastrointest Oncol. 2014;6(11):430-437.
  2. World Health Organization. Vitamin D and Cancer. Geneva, Switzerland: WHO Press; International Agency for Research on Cancer; 2008:1-221. http://www.iarc.fr/en/publications/pdfs-online/wrk/wrk5/Report_VitD.pdf. Published on November 24, 2008. Accessed July 31, 2018.
  3. Liu W, Chen Y, Golan MA, et al. Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis. J Clin Invest. 2013;123(9):3983-3996. doi: 10.1172/JCI65842
  4. Chung M, Lee J, Terasawa T, et al. Vitamin D with or without calcium supplementation for prevention of cancer and fractures: an updated meta-analysis for the U.S. Preventive Services Task Force. Ann Inter Med. 2011;155(12):827-838.
  5. Feskanich D, Ma J, Fuchs CS, et al. Plasma vitamin D metabolites and risk of colorectal cancer in women. Cancer Epidemiol Biomarkers Prev. 2004;12(9):1502.
  6. McCullough ML, Zoltick ES, Weinstein SJ, et al. Circulating vitamin D and colorectal cancer risk: an international pooling project of 17 cohorts [published online June 14, 2018]. J Natl Cancer Inst. doi: 10.1093/jnci/djy087
  7. Freedman DM, Looker AC, Abnet CC, et al. Serum 25-hydroxyvitamin D and cancer mortality in the NHANES III study (1988-2006). Cancer Res. 2010;70(21):8587-8597.