TO: All melanoma researchers, doctors, and patients.


It is high time we filled in details to sharpen the picture and eliminate any remaining doubt that melanoma is a vitamin D deficiency cancer. The 1981 discovery (1) found that the active vitamin D metabolite 1,25D (1,25-dihydroxyvitamin D3) inhibits the growth of human melanoma cells, and although it wasn't yet known for a few years (2), the skin makes this 1,25D from the circulating precursor 25D (25-hydroxyvitamin D3), which is produced in the liver from the inactive vitamin D (cholecalciferol) that is formed in skin exposed to sunlight. Also in the mid-1980's (3), it was found that the 1,25D hormone inhibits the growth of skin cells.

(See (1) Colston K, Colston MJ, Feldman D. "1,25-dihydroxyvitamin D3 and malignant melanoma: the presence of receptors and inhibition of cell growth in culture." Endocrinology. 1981 March;108(3):1083-6. (2) Bikle DD, Nemanic MK, Gee E, Elias P. "1,25-Dihydroxyvitamin D3 production by human keratinocytes. Kinetics and regulation." J Clin Invest. 1986 Aug;78(2):557-66. (3) Smith EL, Walworth NC, Holick MF. "Effect of 1 alpha,25-dihydroxyvitamin D3 on the morphologic and biochemical differentiation of cultured human epidermal keratinocytes grown in serum-free conditions." J Invest Dermatol. 1986 Jun;86(6):709-14.)

Now, every structure or process in the body has a logical purpose for being the way it is. So, why would the body continue sending vitamin D (25D) to the skin if it were faced with a critical shortage? Wouldn't the epidermis be the last place the body would send that precious, remaining vitamin D (25D)? Why would the body suffer a vitamin D (25D) deficiency first inside an organ, gland, or bone, if it didn't have any chance whatsoever of gaining more vitamin D (cholecalciferol) from the internal depletion?

James Semmel
Albuquerque, New Mexico