Nutrigenomics, vitamin D and cancer prevention

Abstract

Although there is growing epidemiological, preclinical and clinical evidence suggesting that low vitamin D intake, exposure and/or status is associated with an increased risk of various types of cancer, the optimum amount needed remains controversial. Furthermore, there is evidence that a U- or J-shaped response curve exist between 25(OH)D and certain cancers. Increasing information about the impact of genetic variation, especially polymorphisms that influence absorption, transport, metabolism and associated molecular targets, should help clarify inconsistencies in the data regarding vitamin D's effect on cancer risk. Rather than focusing on the main effects of a few variants of these genes alone, future studies need to consider gene-nutrient or environmental interactions. Nutrigenomics should clarify who might benefit and be placed at risk because of vitamin D exposure.

Fig. 1

Proposed mechanism of action of 1,25(OH)₂D in target cells. 1,25(OH)₂D binds to the vitamin D receptor (VDR) and forms a heterodimer with the retinoid X receptor (RXR). This complex binds to the vitamin D response element (VDRE) to induce or repress expression of target genes. Examples of genes with VDREs related to carcinogenesis include those involved in regulating apoptosis, proliferation, differentiation, inflammation and immunomodulation. Modified from McCullough et al. [39].