(NaturalNews) It is an undisputed, scientifically validated fact that vitamin D helps to prevent many chronic conditions ranging from heart disease to diabetes, stroke and dementia. Some of the most compelling work has shown that the prohormone can cut the risk associated with certain forms of cancer by as much as 78 percent. To date, the precise mechanism by which the sunshine vitamin works its magic have not been fully understood, though many scientists believe there is a relationship between saturation of the vitamin and cellular replication that increases cancer risk.
A research team from McGill University
in Canada has published new findings in the Proceedings of the National Academy of Sciences
journal that explains the molecular basis for the potential cancer preventive effects of vitamin D. The team discovered that the active form of vitamin D (D3) acts through multiple mechanisms to inhibit both the production and function of a special protein identified as 'cMYC.' cMYC is known to drive cell division and is active at elevated levels in more than half of all cancers.
Vitamin D deficiency is running at epidemic levels, as millions of unsuspecting children and adults are at significantly increased risk of illness and early death. As we age, the normal conversion of ultraviolet rays in the skin from sun exposure becomes limited, and coupled with a never ending barrage of senseless warnings to avoid sun contact, many individuals sustain dangerously low vitamin D blood levels throughout the year.
Vitamin D inhibits a protein mechanism used by tumor cells to drive cancer growth
Researchers worked to gain a better understanding of how vitamin D squelches the activity of the cMYC protein to halt tumor growth and metastatic progression. Lead study author, Dr. John White commented "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."
Working with a special strain of mice that exhibit similar metabolic similarities with humans, the team applied vitamin D to the skin to assess cMYC activity.
observed a drop in the level of cMYC and found evidence of a decrease in its function. In addition, certain mice lacked specific receptors for vitamin D due to genetic susceptibility and had highly elevated levels of cMYC in a number of tissues including skin and the lining of the colon. This inherited predisposition to certain forms of cancer
is also believed to exist in humans. Those individuals would benefit from vitamin D supplementation to lower the cMYC protein activity and lower cancer risk.
Dr. White concluded "Taken together, our results show that vitamin D puts the brakes on cMYC function, suggesting that it may slow the progression of cells from premalignant to malignant states and keep their proliferation in check."
Most nutritionists and alternative health practitioners now understand that maintaining a blood saturation level of 50 to 70 ng/mL (using the standard 25(OH)D test) provides optimal protection against many chronic conditions including cancer, as it blocks a specific protein that encourages cellular proliferation.Sources for this article include:http://www.mcgill.cahttp://www.medicalnewstoday.com/releases/253198.phphttp://www.medicalnewstoday.com/releases/253177.phphttp://www.eurekalert.org/pub_releases/2012-11/mu-nde112212.phpAbout the author:
John Phillip is a Certified Nutritional Consultant and Health Researcher and Author who writes regularly on the cutting edge use of diet, lifestyle modifications and targeted supplementation to enhance and improve the quality and length of life. John is the author of 'Your Healthy Weight Loss Plan', a comprehensive EBook explaining how to use Diet, Exercise, Mind and Targeted Supplementation to achieve your weight loss goal. Visit My Optimal Health Resource
to continue reading the latest health news updates, and to download your Free 48 page copy of 'Your Healthy Weight Loss Plan'.
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