Vitamin D3, Cancer, Sun Exposure, Sunscreen and Addiction. 6/10

POMC also is the source of Y-MSH which is involved in regulating the correct balance of sodium in the body. As you can see this rabbit hole is getting deep and fast. Then UV-B light also has antiseptic properties on its own, helping to prevent infections.

But UV-B also is involved in the production of vitamin D3 which causes the release of POMC outside the brain effecting the immune system and protecting us from cancer in multiple ways. As, both sun light in the form of UV-B but also vitamin D3 can and does activate the skin analogue of the hypothalamus pituitary axis (HPA) axis. 1

Well following that train of thought I did some research and sure enough all three forms of vitamin D3 directly activate the analogue of hypothalamus-pituitary-adrenal (HPA) axis in human keratinocytes. Keratinocytes are a type of cell that are most cells in our skin. This is important.

So, in the skin cells-keratinocytes-all three main forms of vitamin D3 activate the HPA axis. 5 To summarize the three main forms of vitamin D3.

1. Cholecalciferol- the form of vitamin D3 produced from UV-B in the skin and taken in oral supplements)
2. Calcifediol (the vitamin D3 form created in the kidneys and the blood storage form and form we measure in blood to determine levels)

3.Calciferol (the active form of vitamin D3 produced in the liver but also, I theorize inside most cells)

As it implies that for one vitamin D3 can cause the release of beta-endorphins.

Which could reduce pain, give us joy and perhaps prevent addiction. Intertwined is how Beta-endorphins base molecule, pro-opiomelanocortin (POMC) can be depending on which tissue and enzyme acts on it so important to our health. One interesting fact is how the body produces POMC.

Those of you who are into cancer genetics are aware of how important mutations in the P53 gene are to developing cancer. For example, mutational inactivation of the p53 gene is noted in nearly half of human tumors. 2 The P53 gene is called the cancer suppressor gene.

P53 is mainly known for repairing DNA of or destroying, damaged cells but it also slows the cell replication cycle. By slowing the cell replication cycle this allows repairs to damaged cell’s DNA to occur. Repair or if necessary, destroy cells infected with viruses, bacteria or so badly damaged they can’t be repaired-cancerous ones. 3,4,5

As UV-B exposure of cells called keratinocytes in the dermis part of the skin results in activation of p53. 6 As a transcription factor, p53 binds directly to the POMC gene promoter which results in the production of POMC. More POMC then potentially more of its products like beta-endorphins and A-MSH production can be released to act on the body.

Thus, through A-MSH producing pigmentation, the sun tan response, to protect from UV-B light. 7 Also protecting from UV-A. Additionally ultraviolet light results in the releasing of beta-endorphins. Creating a positive feedback-reward for sun exposure.

Besides effecting pain, beta endorphins act directly on the immune system by acting on the T-lymphocyte, B-lymphocyte and monocytes. Beta-endorphins also boast natural killer cells for example. These cells are part of the immune system and known to be critical in destroying cancer cells. 8

All are part of our immune system. Also, vitamin D binding protein (DBP) is also involved in the immune system as nothing seems to be wasted and none of the substances related to vitamin D3 seem to have only one use.

As DBP attaches directly to the vitamin D3 when either it is produced in the skin from UV-B exposure or in the liver when absorbed in the gut. This may be how vitamin D3 is DBP also has been shown to be a significantly slow cancer growth. 9

So, so far, we have UV-A, UV-B, beta-endorphins, DBP and the P53 gene all associated with the immune system and/or cancer.

1. Wierzbicka JA, Zmijewski MA, Slominski AT, et al. (5 Dec 2016) Bioactive forms of vitamin D selectively stimulate the skin analogue of the hypothalamus-pituitary-adrenal axis in human epidermal keratinocytes. Mol Cell Endocrinol. 437:312-22.
2. Hamzehloie T, Mojarrad M, Shekouhi S. (Mar 2012). The role of tumor protein 53 mutations in common human cancers and targeting the murine double minute 2-P53 interaction for cancer therapy. Iran J Med Sci. 37(1):3-8.
3. Drayman N, Ben-nun-Shaul O, Oppenheim A, et al. (July 2016). p53 elevation in human cells halt SV40 infection by inhibiting T-ag expression. http://lahav.med.harvard.edu/publications/Drayman2016.pdf/
4. Kastenhuber ER, Lowe SW. (September 17, 2017). Putting p53 in context. Cell. 170: 1062-78.
5. Siegel C, Prusty BK, Rudel T, et al. (November 6, 2014) Tumor suppressor p53 alters host cell metabolism to limit chlamydia trachomatis infection. 9(3):918-29.
6. Oren M, Bartek J. (9 March 2007). The sunny side of p53. Cell. 128(5);826-28.
7. 3. Cui R, Widlund HR, Feige E, et al. (9 March 2007) Central role of p53 in the sun tan response and pathological hyperpigmentation. Cell. 128(5);853-864.
8. Wu J, Lanier LL. (2003). Natural killer cells and cancer. Adv Cancer Res 90:127-56.
9. Kalvin JG, Zhao B, Bielenburg DR, et al. (2010). Vitamin D binding protein-macrophage activating factor directly inhibits proliferation, migration, and uPAR expression of prostate cancer cells. PloS One. 5(10): e13428.

*The information posted above is for educational purposes only. Always check with your doctor before initiating any changes in your medical treatment. If you do not, then The Two-Minute Health Fact, Dr. Judson Somerville, nor The Optimal Dose is responsible!