TO: All melanoma researchers, doctors, and patients.

Last month's post recalled three landmark studies from the 1980's that
found the 1,25D hormone is made in the skin and inhibits both the
growth of melanoma and the growth of skin; this active form of vitamin
D is produced from the circulating precursor 25D produced in the liver
from the inactive vitamin D, cholecalciferol, photosynthesized in the
skin.

So, sending more vitamin D (25D) to the skin would inhibit skin cell
growth, which would reduce the synthesis of more vitamin D
(cholecalciferol).  A vitamin D (25D) deficiency in an internal
tissue, say breast or prostate, would not benefit the body like it
would in the skin, which is the body's chief provider of vitamin D
(cholecalciferol).  In the skin, a vitamin D (25D) deficiency has a
chance at producing more vitamin D (cholecalciferol), via the
increased skin cell production, but it carries the risk of melanoma,
which the 1981 study observed grows uncontrollably without that
vitamin D (1,25D from circulating 25D).

The exact site of melanoma therefore depends both on sun exposure and
on circulation, because the spots with weakest blood flow in the
regions contributing least to D3 production--whether from too little
sunlight (pale skin) or too much sunlight (tan skin)--will thus become
deficient first.

James Semmel
Albuquerque, New Mexico

reference:
http://www.mpip.org/bb/shtml/377039.shtml
Last month's follow up to the 4th annual discussion: "Is melanoma
simply a vitamin D deficiency cancer?"