Researchers at McGill University have discovered a molecular basis for the cancer preventive effects of vitamin D, whereby its active form essentially shuts down cancer cells. People with higher blood levels of vitamin D live significantly longer than people who have low blood levels of the vitamin.
The team, led by McGill professors John White and David Goltzman, of the Faculty of Medicine’s Department of Physiology, discovered that the active form of vitamin D acts by several mechanisms to inhibit both the production and function of the protein cMYC.
cMYC drives cell division and is active at elevated levels in more than half of all cancers. Their results are published in the latest edition of Proceedings of the National Academy of Sciences.
For the past several years, there has been considerable interest in the role vitamin D plays in improving health and preventing disease. Previous finding show that low levels of vitamin D have been directly associated with various forms of cancer and cardiovascular disease. Stephen B. Kritchevsky, PhD, Professor of Internal Medicine and Transitional Science at the Wake Forest School of Medicine found a signficant correlation.
“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,” said Kritchevsky. “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 can be obtained from limited dietary sources and directly from exposure to the sun during the spring and summer months, the combination of poor dietary intake and sun avoidance has created vitamin D deficiency or insufficiency in large proportions of many populations worldwide.
It is known that vitamin D has a wide range of physiological effects and that correlations exist between insufficient amounts of vitamin D and an increased incidence of a number of cancers. These correlations are particularly strong for cancers of the digestive tract, including colon cancer, and certain forms 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”.
The team also applied vitamin D to the skin of mice and observed a drop in the level of cMYC and found evidence of a decrease in its function. Moreover, other mice, which lacked the specific receptor for vitamin D, were found to have strongly elevated levels of cMYC in a number of tissues including skin and the lining of the colon. The finding suggests that topical vitamin D may be just as effective as ingested to prevent cancer.