[ginko]

I never claimed vitamin D was a cure for cancer. I did quote an article that was talking about a study that showed a link between blood levels of calcitriol and progression of cancer.

You don't find it interesting that they report lower levels of blood vitamin D correlated with increased spreading of tumors?

If vitamin D can slow or stop the spreading of tumors in colon cancer(they concluded it might), don't you think it might prove useful for other forms of cancer?

I mean, what else are you expecting from me or anyone else? If there was a supplement or drug that cured cancer, we wouldn't even be having this conversation.

We need to be making educated guesses when we have no other options, especially when there is no downside to the "treatment" in question.

Vitamin D is paramount to health, more so than you realize. We should all be supplementing with a couple thousand IU's of vitamin D daily if we aren't getting sunlight(which studies show we aren't, glass and pollution block UV-B which is what our skin converts to vitamin D).

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"Am J Clin Nutr. 2006 Jul;84(1):18-28. Links
Estimation of optimal serum concentrations of 25-hydroxyvitamin D for
multiple health outcomes.Bischoff-Ferrari HA, Giovannucci E, Willett
WC, Dietrich T, Dawson-Hughes B.
Department of Nutrition, Harvard School of Public Health, Boston, MA.

Recent evidence suggests that vitamin D intakes above current
recommendations may be associated with better health outcomes. However,
optimal serum concentrations of 25-hydroxyvitamin D [25(OH)D] have not
been defined. This review summarizes evidence from studies that
evaluated thresholds for serum 25(OH)D concentrations in relation to
bone mineral density (BMD), lower-extremity function, dental health,
and risk of falls, fractures, and colorectal cancer. For all endpoints,
the most advantageous serum concentrations of 25(OH)D begin at 75
nmol/L (30 ng/mL), and the best are between 90 and 100 nmol/L (36-40
ng/mL). In most persons, these concentrations could not be reached with
the currently recommended intakes of 200 and 600 IU vitamin D/d for
younger and older adults, respectively. A comparison of vitamin D
intakes with achieved serum concentrations of 25(OH)D for the purpose
of estimating optimal intakes led us to suggest that, for bone health
in younger adults and all studied outcomes in older adults, an increase
in the currently recommended intake of vitamin D is warranted. An
intake for all adults of >/=1000 IU (40 mug) vitamin D
(cholecalciferol)/d is needed to bring vitamin D concentrations in no
less than 50% of the population up to 75 nmol/L. The implications of
higher doses for the entire adult population should be addressed in
future studies.

PMID: 16825677 [PubMed - in process]"


"Med Hypotheses. 2006 Dec 2

Vitamin D toxicity redefined: Vitamin K and the molecular mechanism.

Masterjohn C.
Weston A. Price Foundation, 4200 Wisconsin Ave., NW, Washington DC 20016, United States.

The dose of vitamin D that some researchers recommend as optimally therapeutic exceeds that officially recognized as safe by a factor of two; it is therefore important to determine the precise mechanism by which excessive doses of vitamin D exert toxicity so that physicians and other health care practitioners may understand how to use optimally therapeutic doses of this vitamin without the risk of adverse effects. Although the toxicity of vitamin D has conventionally been attributed to its induction of hypercalcemia, animal studies show that the toxic endpoints observed in response to hypervitaminosis D such as anorexia, lethargy, growth retardation, bone resorption, soft tissue calcification, and death can be dissociated from the hypercalcemia that usually accompanies them, demanding that an alternative explanation for the mechanism of vitamin D toxicity be developed. The hypothesis presented in this paper proposes the novel understanding that vitamin D exerts toxicity by inducing a deficiency of vitamin K. According to this model, vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D. This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined. The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect. If animal experiments can confirm this hypothesis, the models by which the maximum safe dose is determined would need to be revised. Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K.

PMID: 17145139 [PubMed - as supplied by publisher]"