So, infections and resulting inflammation are bad. As it appears to take what I consider normal, but others consider high blood levels of vitamin D3 to be effective for one against infections. Take tuberculosis which is a notoriously difficult infection to treat.

In one study it took a level of the active form of vitamin D3 in the cell that was approximately 28-40 times the level of again what I consider normal levels of the blood form. 1 Compared to the blood levels currently recommended as normal it is about 333 times as much.

However, the macrophages-the cells that act in our immune system to destroy tuberculous-can absorb the blood form of vitamin D3 and convert it to the active form. 1 Reaching these higher levels in these cells. It is like more likely to happen at those levels I consider normal then the current levels recommended by the government.

The important thing was vitamin D3 was effective. Effective against a notoriously difficult and getting more difficult all the time infection, tuberculosis. As I wrote before the Madison-HannaH effects, like for fighting infections, occurs inside the cells, where the, blood form is converted into the active form of vitamin D3.

Again, see previous blog posting (https://judsonsomerville.com/madison-hannah-effects/). This is, for which I apologize, a complex process but hopefully it is making sense for you. Before you become too comfortable let me confuse you more!

See, macrophages release macrophage migration inhibitory factor (MIF) to help fight infections. Well MIF shuts off P53. 2 Thus, chronic infections can both damage our p53 gene and shut it off. In the short term we can tolerate this but long term it appears to increase our risk of cancer.

Ok so our ability to fight infections if it goes on too long can cause damage that can cause cancers. Sunscreens which I have gone on way longer then I initially planned are not only poisoning both us as well as our environment but potentially affect the p53 gene one of our main ways to treat cancer.

Less sun by whatever means, results in less proopiomelanocortin (POMC) and thus less melanotropin stimulating hormone (MSH). In the skin cells, keratinocytes ultraviolet light is required for p53 to potentially stimulate the production of POMC. 3

Thus, reduced or no ultraviolet light due to sun screen no or less POMC. So, less or no MSH. MSH besides protecting us from ultraviolet light both UV-A and UV-B when produced also forms both the neuropeptide B-MSH and A-MSH.

B-MSH plays a role in weight regulation, and A-MSH which helps maintain the correct energy balance (it does this in the ventromedial nucleus part of the brain where regulation of appetite occurs-this occurs by POMC neuron stimulation that results in satiety.4).

Cancer cells need to be fed and what we eat may affect how well cancer cells grow in our body. Labrador Retrievers, like my dog Ralph who I posted about in an earlier blog, is an example of how a mutation in the POMC gene can result in overeating. 5

Not sure how, if his POMC gene was damaged, by giving him vitamin D3 I was able to overcome this. Possibly more on this in a future blog posting as this is a deep rabbit hole in its self. B-MSH also causes the increased production of melanin that protects the cell’s nucleus from deleterious effects of ultraviolet light.

The melanin accumulates in the cells between where the UV-B enters the cell and the cell’s nucleus to protect its DNA. That is, it acts to absorb the UV-B but also the UV-A before it contacts the cell nucleus. This prevent damage to the cell’s DNA.

Damaged DNA can lead to cancer. That UV-B causes the release of POMC which is broken down to form besides B-MSH also A-MSH. So POMC by forming A-MSH which effects satiety. It reduces hunger which is important as over eating results in obesity.

Obesity causes a state of chronic inflammation. 6 Chronic inflammation increases risk of cancer. It all loops back to itself.

  1. Crowle AJ, Ross EJ, May MH. (Dec 1987). Inhibition by 1,25(oh)2-vitamin D3 of the multiplication of virulent tubercle bacilli in cultured human macrophages. Infect Immun. 55(12):2945-2950.
  2. Hudson JD, Shoaibi MA, Beach DH, et al. (1999). A proinflammatory cytokine inhibits p53 tumor suppressor activity. J Exp Med. 190:1375-1382.
  3. Cui R, Widlund HR, Fisher DE, et al.  (March 9, 2007). Central role of p53 in the suntan response and pathological hyperpigmentation. Cell. 128(5): 853-64.
  4. Varela L, Horvath TL. (December 2012). Leptin and insulin pathways in POMC and AgRP neurons that modulate energy balance and glucose homeostasis. EMBO Reports. 13(12); 1079-86.
  5. Raffan E, Dennis RJ, O’Donovan CJ, et al. (May 2016). “A Deletion in the Canine POMC Gene Is Associated with Weight and Appetite in Obesity-Prone Labrador Retriever Dogs”. Cell Metabolism. 23 (5): 893–900.
  6. Ferrante AW. (2007). Obesity-induced inflammation: a metabolic dialogue in the language of inflammation. Journal of Internal Medicine. 262(4):408-14.

*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!


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