Vitamin D has extensive effects. Widespread assumption that vitamin D is a pure “bone vitamin” is still existent. This is far from true. Vitamin D is transformed into a bioactive form in the skin only after exposure to UV radiation. Bioactive vitamin D, which then again is converted in the body into the active vitamin D hormone, finally docks to the vitamin D receptor (VDR) to unfold its effects.
Patients with a carcinoma of the mammary gland usually do not have enough active vitamin D in the blood. Furthermore, a correlation between the aggressiveness of the tumor and a low vitamin D level could be determined, i.e. the lower the vitamin D level, the more aggressive the tumor. It has also been shown that the prognosis for patients with low vitamin D3 status deteriorates. [1]
Furthermore, the “expression” of the vitamin D receptor on the tumor cells is reduced, i.e. fewer vitamin D receptors are present in the breast tumor cell. The already lacking vitamin D is even less effective.
The vitamin D3 formed in the skin is converted in the liver to the pre-hormone 25 (OH) D calcifediol. Then it is completely converted in the kidney into the calcitriol (1,25- (OH) 2D3), the active hormone.
The lower the calcifediol levels in the blood serum, the higher is the concentration of a tumor progression factor in breast cancer patients (ID1), i.e. a blood serum factor which provides information to the stage of the tumor. [1]
It is important to inform the general public about these facts. A vitamin D intake with already existing illness is in any case sensible, but a lot of suffering could be prevented, if sufficient prophylactic substitution with vitamin D would be carried out.
The common assumption that sufficient vitamin D in a varied diet can be obtained, must unfortunately be rejected as ineffective.
Also, it should be investigate whether substances, which can influence the VDR (vitamin D receptor) positively, are meaningful.
These include substances such as resveratrol and curcumin.
Literature:
[1] Authors: D Feldman: Department of Medicine, Stanford School of Medicine, Stanford University, CA 94305, United States; Stanford Cancer Institute, Stanford University, CA 94305, United States
Medical Journal: The Journal of Steroid Biochemistry and Molecular Biology