To digress, as I mentioned in the first blog post of this series the reason, I have not blogged about vitamin D3 and its direct role in destroying/preventing cancer, is because it was not clear to me how vitamin D3 was involved. It was only recently after more research on my part on recent scientific articles that I stumbled on the connection.
Recent articles leading to a better understanding of the CYP24A1 gene and the vitamin receptor (VDR) receptor. One of the functions of this gene is the destruction of the active form of vitamin D3. Thus, preventing the effects of the active form of vitamin D3 on the immune system and perhaps other intracellular immune functions.
I have yet to come across it but perhaps cancer cells in some way interfere with the intracellular enzyme 1-alpha-hydroxylase the protein that interacts with the blood storage form of vitamin D3 to modify it into the active form. Then intracellular machinery as I previously mentioned further modifies it.
This modified vitamin D3 can by interacting with the VDR initiate the production of genes to then produce enzymes that boost the intracellular immune system and regulate its activity. It effects the intracellular immune system in other ways.
Vitamin D3 is involved in programmed cellular death apoptosis (this may fall under intracellular immune system function) and perhaps in other nonimmune system ways. This occurs in all cells as almost if not every cell has a vitamin D receptor (VDR). Thus, they can activate all the genes that vitamin D3 affects.
Certain cancers can and do possibly affect even those cells those that are involved in in calcium metabolism. That is those cells that are responsible for the endocrine function-calcium metabolism. That is cells for one that are responsible for absorbing calcium from the intestine.
Cells responsible for mobilizing calcium, when stimulated by the active form of vitamin D3 that is in the blood plasma, from skeletal bone and reducing renal excretion. Even in these cells I believe the active form of vitamin D3 in the cell modulates vitamin D receptor and its genes.
As I believe that the active form of vitamin D3 cannot diffuse into or out of cells. Thus, the production of the active form of vitamin D3 outside of the cell does not interfere with the actions of the active form of vitamin in these cells and vis versa.
Well in researching about the CYP24A1 gene defect I stumbled across its effect on promoting the survival of cancer cells. They do this by short circuiting our intracellular immune system. I seem to do that a lot-stumble over “things” and the more I “ambulate” the more likely I am to stumble.
Also, as an aside every time I believe I will have nothing new to blog about vitamin D3 I find something new. This is often from meeting others on our Facebook page Vitamin D Advocacy who post interesting new research on vitamin D3.
Also, the more I research vitamin D3 the more I am amazed how intricately vitamin D3 is involved in so many aspects of our physiology. How genetic defects in the vitamin D receptor and/or the intracellular machinery that interacts with the active form of vitamin D3.
They interact to allow the complex of active form of vitamin D3 and these proteins attach to the vitamin D receptor to turn on gene(s) and produce enzymes. More amazing is how many preventable diseases could be a thing of the past if we raised people’s vitamin D3 levels.
I believe to optimal blood plasma levels. It seems cancer is one of those diseases. In an earlier four part blog posting (The first one here https://judsonsomerville.com/vitamin-d3-cancer-sun-exposure-sunscreen-and-addiction-2-10/) I discussed how the pro-opiomelanocortin (POMC) peptide was involved in addiction, cancer and was affected by vitamin D3. Summarized in a previous blog of this series.
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