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
reference:
http://www.mpip.org/bb/shtml/372247.shtml
Last month's follow up to the 4th annual discussion: "Is melanoma
simply a vitamin D deficiency cancer?"