As I was discussing at the end of the last blog post defects in the vitamin D receptor (VDR), machinery that modifies the active form of vitamin D3 so it can activate the VDR and vitamin D3 deficiency can result in one being more susceptible to cancer progressing. 

Not sure if these factors make one more prone to contracting cancer as probably need exposure to a carcinogenic agent. Exposure that is to initiate the cancer. Like I discussed with chronic infections where the P53 gene is shut of or have chemical agents damage the P53 gene to reduce or stop it function.

Though in some with certain genetic make ups they may be more prone to developing cancer and doing so spontaneously. The key is in my opinion in preventing  those cancers listed above and future ones that operate the same way from developing is optimal dosing to achieve optimal blood levels of vitamin D3

That is those cancers listed above that proliferate by inactivating the active forms of vitamin D3. Optimal blood level’s may in most cases cure these cancers. Except possibly in those cases where the patient has such severe defects in the VDR or intracellular machinery that modifies the active form of vitamin D3. Thus not able to produce enough of the active for of vitamin D3 to overcome these defects.

Those people with genetic defects with the CYP24A1 gene that is responsible for producing the 24-hydroxylase enzyme present an interesting situation. The 24-hydroxylase is the enzyme that breaks down the active form of vitamin D3. 

As depending on the severity of the CYP24A1 gene defect they cannot produce the 24-hydroxylase enzyme or do so in reduced amounts. Thus the concentration of the active form of vitamin D3 is not reduced or only slightly so. 

Thus there is enough of it available to kill the cancer cells or severely limit its growth. Possible with severe defects these cancers cannot form.  So what happens concerning these cancers in the other cases where there is some CYP24A1 gene function. Probably a spectrum. This is probably what happens in those with milder and easier to treat cases. 

I am curious to know and to know how much of a reduction in the person’s ability to produce this enzyme is needed to result in a mild case or these cancers not forming at all. I also wonder if those with this genetic issue are less likely to contract these cancers. 

Again probably a spectrum depending on the extent of the genetic defect and resulting decreased or minimal ability to produce this enzyme. Certainly, an interesting area for research and hopefully one that is pursued. Back to the issues that make one more prone to contracting these cancers.

So even in those with one, a combination or all the four factors I discussed above that make one more prone to having a worse response to cancer there is hope. As certain “cofactors” that I discussed in my blog posts about helping to overcome VDR and vitamin D3 intracellular machinery that allows it to activate this receptor: 


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