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
