Vitamin D can force cancer cells to differentiate back into normal

Danny and I already discussed this topic on a recent podcast, but I decided to post the studies anyways, considering how important the topic is. While progesterone and testosterone are the most well-known differentiating factors in humans, the role of vitamin D has gone largely unnoticed. The studies below demonstrate that vitamin D is a powerful differentiating agent, and can cause the regression of even advanced tumors when used in doses proven to be safe for most people (5,000 IU – 10,000 IU daily). The studies cover both in-vitro and in-vivo models and the third link is a human case report. Importantly, at least two of the studies (second and third to last) demonstrate that the “inactive” cholecalciferol (25-OH-D3, commonly used as a supplement) is just as active in terms of differentiating effects as the “active” form known as 1,25-OH-D3 (calcitriol). Moreover, cholecalciferol has a much lower risk of causing hypercalcemia compared to calcitriol, and in fact may lower elevated levels of calcitriol that are seen in many chronic inflammatory conditions.

“…Several investigators reported that 1,25-dihydroxyvitamin D3 (vD3) and its active metabolite cholecalciferol (calcitriol, DHCC) causes monocytic differentiation of leukemia cells. This appears to be due in part to down-regulation of expression of cell cycle related proto-oncogenes (e.g., c-myc). Differentiation inducing effect was also seen against certain solid tumors including prostatic cancer and squamous cell carcinoma.”

“…In a number of studies, vD3 was evaluated as a growth inhibitor. In tissue culture studies it was found effective in osteosarcoma, squamous cell carcinoma, breast cancerprostate cancer, and leukemias.”

“…The antiproliferative effect of 1,25(OH)2D 3 has been confirmed in vivo. In high doses the sterol inhibits growth of human malignant melanoma and colonic cancer xenografts in immune suppressed mice [23] and of nitrosomethylurea-induced mammary tumours in rats [24], while administration of I~(OH)D 3 reduced the number of lung metastases after implantation of Lewis lung carcinoma cells into mice [25]. The fact that 1,25(OH)2D 3 stimulates fibronectin synthesis in several human cancer cell lines may be related to the possible antimetastatic effect of the hormone [26].”

“…From the data currently available it seems clear that 1,25(OH)2D3 has a regulatory effect on cell growth and proliferation. However, high doses of the sterol are needed. Therefore, it remains to be established whether 1,25(OH)2D3 can produce long-term antitumour effects without unacceptable toxicity, like the development of hypercalcemia. In this light, the recent development of new vitamin D analogues which have potent effects on cell proliferation and differentiation in vitro without inducing severe hypercalcemia is of interest [27-29].”