Scientists at McGill University have uncovered a molecular mechanism explaining vitamin D’s potential role in protecting against cancer. Their research shows that the active form of vitamin D inhibits the growth of cancer cells. Additionally, individuals with higher blood levels of vitamin D tend to have significantly longer lifespans compared to those with lower levels.
Led by Professors John White and David Goltzman from the Department of Physiology, the team discovered that active vitamin D suppresses both the production and activity of the cancer-promoting protein cMYC through various pathways. This protein drives excessive cell division and is overexpressed in more than half of all human cancers. The findings were published in the Proceedings of the National Academy of Sciences.
In recent years, growing attention has focused on vitamin D’s potential benefits for overall health and preventing diseases. Previous studies have linked vitamin D deficiency to higher risks of various cancers and cardiovascular conditions. Stephen B. Kritchevsky, PhD, a professor at Wake Forest School of Medicine, highlighted a clear association between low vitamin D levels and increased mortality.
“We found vitamin D insufficiency (blood levels below 20 ng/ml) in about one-third of our participants, which correlated with a nearly 50% higher death rate among older adults,” Kritchevsky noted. “This suggests that inadequate vitamin D could pose a major public health issue for the elderly population.”
Although the body produces vitamin D through sunlight exposure on the skin and obtains small amounts from certain foods, limited sun exposure and poor dietary intake have contributed to widespread deficiency worldwide. This has been associated with greater risks of several cancers, particularly those affecting the digestive tract and certain leukemias.
“For years, my laboratory has explored the molecular actions of vitamin D in human cancer cells, especially how it halts their uncontrolled growth,” explained Professor White. “We learned that vitamin D regulates both the synthesis and breakdown of cMYC. Even more crucially, it dramatically boosts the production of MXD1, a natural opponent of cMYC that effectively blocks its activity.”
In experiments with mice, applying vitamin D to the skin reduced cMYC levels and function. Conversely, animals without the vitamin D receptor showed markedly higher cMYC expression, indicating that topical vitamin D might offer similar protective effects against cancer processes as oral intake.
These discoveries underscore vitamin D’s strong potential as an agent for cancer prevention and emphasize its broader significance in promoting health and reducing disease risk.
