I've received a ton of DMs and emails about my discussion with Dr. Alexis Cowan on our second podcast on T cells and autoimmunity, so I decided to answer them here.
How do I know that the external process on the integument controls the biochemistry process on the interior? Do you know that supplementation of Vitamin D does not work the same in those with heavily melanated exteriors compared to those with Fitzpatrick one and two skin?
Do you understand the implications?
According to the article above, "Doctors frequently prescribe supplemental vitamin D," Freedman said. "However, we do not know all its effects and how they may differ between the races. The bottom line is that racial differences in calcium handling are seen, and black and white patients have differing risks for bone and heart disease. We should more clearly determine the effects of supplementing vitamin D in black patients with low levels based on existing criteria. We should not assume that the effects of supplementation will be the same between the races." Again, this is not a racial story; it is a story of the biophysics of melanin and how POMC is only translated by UV light frequencies.
ARE THERE ANY OTHER LINES OF EVOLUTIONARY EVIDENCE THAT THESE THINGS ARE LINKED TO OUR INTEGUMENT?
YES THERE IS IN DAIRY TOLERANCE. This is food loaded with calcium. HYPERLINK
This explains this fact: 80 percent of all African Americans and Native Americans are lactose intolerant. They have more melanin in their integument. Over 90 percent of Asian Americans are lactose intolerant, and it is least common among Americans with a Northern European heritage who have Fitzpatrick one or two skin.
This important distinction must be made in El Salvador, where 95% of the population has melanated skin. This implies that supplemental Vitamin D is not a wise choice for them.
Brown & Black races generally have lower vitamin D levels than whites, partly because their darker skin pigmentation limits the amount of the vitamin produced by sunlight. This is protective in environments where melanated skin is optimized.
IMPLICATIONS OF THE SURFACE BIOPHYSICS?
Despite these lower vitamin D levels and dietary calcium ingestion, browns & blacks naturally experience lower rates of osteoporosis and have far less calcium in their arteries based on published studies. Studies further reveal that brown/black patients with diabetes have half the rate of heart attack as whites. This shows us that melanated skin may be a protective effect from blue light and nnEMF exposure. This also shows us that lower levels of calcified atherosclerotic plaque in brown & blacks are associated with a lower risk of heart disease. The irony is in the stroke and heart attack belt in the US, browns & blacks in the general community have higher rates of heart attack than whites. This implies that their circadian mismatch to a higher latitude likely explains their decreased longevity. This is why my pinned tweet exists. Vitamin D is not the best end-all story in longevity. It can be used as a good proxy for whites, but we should not assume the same for browns & blacks. Browns & blacks clearly get disease faster and more severe than whites at the same latitude. This again points to a lack of proper sunlight being the main culprit in disease creation.

Humans have CYP11A1-derived secosteroids in their epidermis and serum. What does it do?
CYP11A1 drives a novel magnetochemical pathway in the vitamin D3 (D3) and 7-dehydrocholesterol (7DHC) metabolic pathways in humans. CYP11A1 initiates it. The CYP11A1 SNP has been previously characterized in vitro papers. It has also been proven to occur in vivo in humans. The researchers in those papers analyzed samples of human serum, epidermis, and pig adrenals for the presence of intermediates and products of these pathways. What did they find, and why did it sway me that the electric state of our membranes is giving direct feedback control to metabolism below inside of cells?
In the paper linked below, the epidermal, serum and adrenal samples showed the presence of D3 hydroxy-derivatives corresponding to 20(OH)D3, 22(OH)D3, 25(OH)D3, 1,25(OH)2D3, 20,22(OH)2D3, 20,23(OH)2D3, 20,24(OH)2D3, 20,25(OH)2D3, 20,26(OH)2D3, 1,20,23(OH)3D3 and 17,20,23(OH)3D3, plus 1,20(OH)2D3 which was detectable only in the epidermis.
Serum concentrations of 20(OH)D3 and 22(OH)D3 were only 30- and 15-fold lower than 25(OH)D3, respectively, and at levels above those required for biological activity as measured in vitro.
They also detected 1,20,24(OH)3D3, 1,20,25(OH)3D3 and 1,20,26(OH)3D3 in the adrenals. Products of CYP11A1 action on 7DHC, namely 22(OH)7DHC, 20,22(OH)27DHC, and 7-dehydropregnenolone, were also detected in serum, epidermis, and the adrenal gland. Thus, research has shown that humans have novel CYP11A1-derived secosteroids in the skin, serum, and adrenal gland. This SNP likely has much to do with why we deleted the Vitamin C gene in the human genome. Moreover, as I told Dr. Cowan, based on the concentrations found in the papers, their biological activity suggests that they act as hormones in vivo.

T cells undergo positive and negative selection in the thymus through T cell receptor (TCR) recognition of peptides presented on major histocompatibility (MHC) proteins. Although the genes encoding MHC proteins are among the most polymorphic, most vertebrates express relatively few MHC alleles individually. Genes only act to alter metabolic flux, as the picture above shows. How the number of MHC alleles expressed affects thymic selection and the TCR repertoire on an individual level remains unclear to centralized science. Decentralized science has a different viewpoint. I think sunlight on the skin changes our microbiome and sculpts it to create free radicals and light changes from the microbiomes, creating a variability response in our CD4 and CD 8 cells.

SUMMARY
This is my current hypothesis. I believe sunlight creates T-cell variability in our skin and gut surfaces, as I mentioned below with Dr. Cowan. I think sunlight stimulates MHC heterozygosity, which improves immunity by reducing receptor variability in T cells. MHC heterozygosity limits T cell receptor variability in CD4 T cells. T cells are essential for recognizing infectious agents through their receptors (TCRs), which engage peptides derived from invaders or auto-antigens bound to major histocompatibility complex proteins (MHC). While much research has focused on MHC peptide specificity, the impact of MHC on the expressed TCR repertoire, especially in MHC heterozygotes, has not been well studied in centralized science. Understanding this decentralized link in medicine should guide personalized autoimmune monitoring and better predictive responses to various new treatments. Sunlight exposure to 380nm and 1280 nm light is mandatory in any autoimmune reversal. It should be from sunlight and not any manmade light.

The blog's parting thought is about pharmaceuticals for autoimmune conditions: The human condition does not require that you take drugs that pharmaceutical companies sell. You do not have a pharmaceutical deficiency or a "chemical imbalance." BigHarma sells these ideas to keep you believing their BS. Pharmaceutical companies demand that you consume what they sell. You can live strong and healthy without them. Learn how and do it. Decentralized medicine and healthcare teach these techniques.
Time is your most valuable asset in life and links to your choices in health span and how you use your monetary energy. Why doesn't the "food guru" get this concept? They spend too much time under ALAN while in a gym reading flawed nutrition data and not enough time reading about the physics of organisms. The erasure of information drives entropy in cells, and this process increases over time. This is a consequence of having a ratio in our universe of 1 billion light photons to every atom. This is why LIGHT> food. All molecular clocks that control circadian biology are flow meters for this entropy measurement. This should tell the ripe mind that circadian biology's light and dark cycles are the key to the biological ENIGMA CODE of all modern diseases, especially autoimmune conditions.
Dr. Jack Kruse
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