This year, kiss the flu goodbye!
Vitamin D boosts the immune system and enhances the body’s ability to kill bacteria or viruses—intercellular invaders—that make their way into body cells. When a mechanism known as a toll-like receptor (TLR) recognizes the invaders, it causes direct anti-germ activity by stimulating the action of peptide proteins that bind to and kill viruses, bacteria and fungi.[i] [ii] [iii]
The peptides are called cathelicidins, and they do their work by breaking down the cell walls of viruses and bacteria.[iv] The gene that turns on cathelicidin is a direct target of vitamin D. Therefore, it is vitamin D that triggers the action of cathelicidins against all of these “invaders, [v] including the viruses that cause flu and colds.
It is important to understand that ultraviolet B light (UVB) is the wave length of sunlight that, when it contacts the skin, stimulates the skin to produce vitamin D. The skin does not produce any vitamin D unless UVB is available. UVB, plentiful in summer sunshine, is filtered out in winter at high latitudes because of the sun’s position in the southern sky (northern sky in the southern hemisphere). This is called “vitamin D winter.” Blood vitamin D levels, therefore, become very low in winter unless some other method is used to keep them at desirable levels. So what does all this have to do with flu and colds? I will post the answer in my next blog.
[i] Zhang, L. et al. Contribution of Human -Defensin 1, 2, and 3 to the Anti-HIV-1 Activity of CD8 Antiviral Factor. Science 2002;298:995-1,000.
[ii] Wang, T. et al. Cutting edge: 1,25-dihydroxyvitamin D3 is a direct inducer of antimicrobial peptide gene expression. J Immunol 2004;173:2909-12.
[iii] Herr, C. et al. The role of cathelicidin and defensins in pulmonary and inflammatory diseases. Expert Opin Biol Ther 2007;7:1449-61.
[iv] Liu, P. et al. Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. Science 2006;311:1770-73.
[v] Gombart, A. et al. Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. FASEB J 2005;19:1067-77.