Can Vitamin D slow the growth of early colon cancer tumors?

Vitamin D written in sand on beach

A study published this past August by cancer researchers from Spain in the journal Colon Cancer, suggests that higher levels of Vitamin D (specifically the amount of Vitamin D receptors) can possibly help in early colon cancer cases by blocking a specific colon cancer progression pathway called Wnt/beta-catenin. Higher levels of Wnt/beta-catenin are thought to be responsible for the initiation of many types of colon cancer in humans. The scientists thought that blocking this pathway might either reduce the progression and growth of colon cancer cells or possibly even prevent the development of colon cancer in the first place.

The study found that while Vitamin D receptors did not have an effect on the number of colon cancer tumors, higher levels of Vitamin D receptors did decrease overall colon cancer tumor load.

It does appear that in more advanced cases of colon cancers, the Vitamin D receptors are already significantly down-regulated and reduced. It’s uncertain on the actual cause of the down-regulation and reduction of the Vitamin D receptors in these more advanced cases of colon cancer.

The authors of the study suggest that Vitamin D receptor concentrations may offer additional treatment options in early colon cancers where the amount of vitamin D receptors have not been significantly reduced.

Vitamin D supplementation may also be a way to reduce or limit the growth of early colon cancer tumors by decreasing the overall tumor load of colon cancer. However, more research needs to be done to determine if Vitamin D supplementation or simply more sun exposure to raise Vitamin D levels in the body would be helpful in either treatment of early-stage colon cancer or possibly prevention of colon cancer by maintaining adequate vitamin D levels.

Larriba MJ, Ordóñez-Morán P, Chicote I, Martín-Fernández G, Puig I, et al. (2011) Vitamin D Receptor Deficiency Enhances Wnt/β-Catenin Signaling and Tumor Burden in Colon Cancer. PLoS ONE 6(8): e23524. doi:10.1371/journal.pone.0023524

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