Vitamin D has been identified as a potential protective factor in the development of colorectal cancer (CRC).
We expect to see a stronger association of ultraviolet B (UVB) exposure and CRC with increasing age since chronic vitamin D deficiency leads to sustained molecular changes that increase cancer risk.
The DINOMIT (disjunction, initiation, natural selection, overgrowth, metastasis, involution, and transition) model postulates various stages of cancer development due to vitamin D deficiency and the associated latency period.
Some of the risk factors linked to increased risk of developing CRC include obesity, sedentary lifestyle, consumption of high-fat, high-meat diets and calorie rich and fiber deficient food . Apart from these known risk factors, inadequate vitamin D status as assessed by serum 25-hydroxyvitamin D (25(OH)D) concentration has also been identified as a potential risk factor in the pathogenesis of CRC.
Vitamin D has been identified as a potential protective factor in the risk of developing CRC. Intake of 1000IU/day of vitamin D is shown to be associated with 50% lower risk.
A meta-analysis using random effects model showed that the hazard ratio for mortality was lower with higher serum vitamin D status. The results of this study suggested regular testing and restoration of vitamin D status to adequacy for lowering the mortality in colorectal cancer.
Vitamin D is a fat-soluble vitamin which has limited dietary sources and is predominantly obtained when exposed to ultraviolet B (UVB) radiation in sunlight .
Previtamin D3 is an intermediate product in the production of cholecalciferol. It is formed when UVB light of wavelengths between 280 and 315nm from sunlight acts on 7-dehydrocholesterol present in the epidermal layers of the skin. It then converts by spontaneous isomerization into cholecalciferol which is converted into the active form of vitamin D through two-step hydroxylation [6]. Availability and exposure to UVB in sunlight is strongly correlated to the concentration of calcidiol and calcitriol levels in blood. UVB exposure and supplemental vitamin D both increase calcitriol in a dose-dependent fashion, and increases in calcitriol have been shown to depend on baseline vitamin D status. In addition, a number of molecular factors may influence levels of serum 25(OH) D, including expression of the APOE4 allele.
This study supports the need for adequate public health programs to avoid vitamin D inadequacy at national and global levels, whether through screening those at risk, through selective supplementation, or through population-based measures such as food fortification.
Future studies can aim at identifying the cancer types which show significant improvement with vitamin D supplementation.
Studying the association between chronic vitamin D deficiency and CRC incidence will help in understanding the necessity for population-wide screening programs for vitamin D deficiency, especially in regions with inadequate UVB exposure.
These programs may help decrease risk of CRC, as well as other cancers whose risk is associated with vitamin D deficiency, for high-risk populations whose vitamin D deficiency has been especially chronic.
Refences:
Colorectal cancer incidence rates: Cancer Today, Ferlay J, Ervik M, Lam F, Colombet M, Mery L, Piñeros M, Znaor A, Soerjomataram I, Bray F (2018). Global Cancer Observatory: Cancer Today. Lyon, France: International Agency for Research on Cancer. Available from: https://gco.iarc.fr/today
2. Estimates for UVB (280315nm), adjusted for cloud cover and aerosols: Beckmann M, Václavík T, Manceur AM, prtová L, von Wehrden H, Welk E, et al. glUV: a global UV-B radiation data set for macroecological studies. Tatem A, editor. Methods Ecol Evol [Internet]. 2014 Apr 1 [cited 2020 Apr 1];5 (4):37283. Available from: http://doi.wiley.com/10.1111/2041-210X.12168
