Issues with the VDR and the intracellular machinery and to overcome these defects is discussed here: : https://judsonsomerville.com/vitamin-d3-vitamin-d-receptors-and-why-you-may-not-see-results-from-taking-optimal-doses-of-vitamin-d3-1-2/ That by overcoming these defects allows activation of vitamin D3 and initiation of its gene expression.
The blog posting is two parts and discussed these “cofactors” for lack of a better term. These cofactors help boost the function of the vitamin D receptor (VDR). The most interesting of these cofactors is strenuous exercise. In my opinion and experience perhaps the most effective of the cofactors and perhaps a major reason exercise is so healthy for us as it significantly Improves the function of what vitamin D3 we do have.
It is also best to include/use these “cofactors” if one has these genetic defects. Even if you are not sure if you have these genetic defects it is wise to use them to assure your bodies best result. Especially if you have one of the cancers discussed in this blog series, a few of which are extremely aggressive and deadly.
Returning to the CYP24A1 gene and cancer cells ability to upgrade its production of 24-hydroxylase enzymes function to neutralize vitamin D3’s ability to kill and/or repair cancer cells. So how can vitamin D3 at optimal blood levels circumvent this defense mechanism of cancer? It may be one or a combination of the following reasons.
It may be that the intracellular concentration of 1,25-hydroxy vitamin D3-the active form becomes so high that it is able to overwhelm the action of the increased production of the 24-hydroxylase enzyme by cancer cells.
Or 25-hydroxy vitamin D3 the blood storage form concentration becomes so high, this form can directly interact with the VDR though much less biologically active than the 1.25 dihydroxy vitamin D3 form, that it becomes high enough that it can sufficiently activate the intracellular immune response at the VDR to repair or kill the cancer cells.
Or a combination of both the concentration of the blood storage form becomes so high as does the active form to overcome the cancerous cells defenses the increased production of the 24-hydroxylase enzyme. 1 Thus the cells can either repair or kill the cancerous cells.
Again, I digress which though allows me to tie together a few points. It is interesting that the blood storage form of vitamin D3 at higher blood levels would be both involved in why people develop hypercalcemia despite the body shutting down the endocrine production of the active form of vitamin D3.
So essentially the cause of the problem. Now in killing cancer sells this same mild but just the same effect which in one case is toxic and in the case of cancer may be the savior. Again, I find the more I research vitamin D3 the more connections I find.
To summarize, vitamin D3 is intricately involved in many cancers. It works through the immune system to kill cancer cells and prevent chronic inflammation that can lead to it. However some cancers have developed means to subvert this.
Chronic infections can lead to the development of cancer. Low vitamin D3 blood plasma levels, genetic defects in the VDR and those of the intracellular machinery that modifies the active form of vitamin D3 all make the development and progression of cancer more likely.
Those with the genetic defect of the CYP24A1 gene may have a lower incidence of the above cancers. Optimal dosing to achieve optimal blood levels or even higher blood levels show great promise and in many anecdotal cases have cured some of these types of cancer.
Certain cofactors may boost the function of defective VDR and perhaps even those that are not to improve one’s ability to fight off these cancers. Bear in mind those cancers that manipulate vitamin D are only the ones I could find. There may be more or perhaps all are affected.
- Lou W, Hershberger A, Johnson C, et al. 4-Hydroxylase in Cancer: Impact on Vitamin D-based Anticancer Therapeutics. J Steroid Biochem Mol bIol. 2013 jul; 136: 252-257.
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