Researchers from McGill University have found a cellular explanation for the cancer-protective properties of vitamin D, demonstrating that its active form can stop the growth of cancer cells. The study indicates that people who have higher concentrations of vitamin D in their blood appear to live considerably longer than those with lower levels.
The researcher, led by John White and David Goltzman, both professors in the Department of Physiology, found that active vitamin D reduces production and function of the cancer promoting protein cMYC by multiple mechanisms. cMYC promotes cell proliferation and is deregulated in over half of all cancers. The results were published in the journal Proceedings of the National Academy of Sciences (updated April 10, 2024).
Recently, there is a tendency toward the expansion of interest in the possible role of vitamin D in health promotion and disease prevention. Earlier reports have associated vitamin D deficiency with an increased risk of a number of malignancies and cardiovascular disease.
Stephen B. Kritchevsky, PhD, professor of medicine and translational science at Wake Forest School of Medicine, identified a strong link between vitamin D deficiency and these two outcomes.
“We observed vitamin D insufficiency (defined as blood levels <20 ng/ml), in one third of our study participants. This was associated with nearly a 50 percent increase in the mortality rate in older adults,” Kritchevsky said. “Our findings suggest that low levels of vitamin D may be a substantial public health concern for our nation’s older adults.”
Although vitamin D is synthesised in the skin through sun exposure, and is also acquired via a few dietary sources, insufficient sun exposure and low intake of dietary sources of vitamin D have led to global widespread vitamin D deficiency, linked to an elevated risk of various cancers, mainly those of the digestive system and some types of leukemia.
“For years, my lab has been dedicated to studying the molecular mechanisms of vitamin D in human cancer cells, particularly its role in stopping their proliferation,” said Prof. White. “We discovered that vitamin D controls both the rate of production and the degradation of cMYC. More importantly, we found that vitamin D strongly stimulates the production of a natural antagonist of cMYC called MXD1, essentially shutting down cMYC function.”
In an animal study, scientists found that vitamin D applied to mouse skin decreased cMYC levels and activity, and that mice lacking the vitamin D receptor had significantly elevated cMYC, suggesting that topical vitamin D may be as effective as oral forms in preventing cancer-related processes.
These results emphasize the considerable promise of vitamin D as a cancer prevention agent, and highlight its general importance in health and disease prevention.
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