DECENTRALIZED MEDICINE #8: PERIPHERAL ARTERY DISEASE ETIOLOGY

The take home: The periodicity of our clocks determines the shape of our lives. Time sculpts us. What happens in your colony of mitochondria every AM writes a story in the arteries of your flesh.

Question:  My hubby tested very high and when I looked into it discovered it is an enzyme released by the white blood cells in response to inflammation and damage to the arteries. does anyone know how much research they is behind this marker and have any info I can take away?

ANSWER

Myeloperoxidase (MPO) is an enzyme stored in azurophilic granules of polymorphonuclear neutrophils and macrophages and released into extracellular fluid in the setting of inflammatory process and is associated with increased ROS/RNS creation due to altered mitochondrial metabolism and altered biophoton release.  This is due to environmental changes that are not light/dark controlled. 

The excess release of endogenous light is not creating enough UV light endogenously and this is not causing translation of POMC to create alpha beta or gamma MSH = less melanin inside and melanin inside deals with excess ROS/RNS production.  As a result of this cascade, myeloperoxidase  rises and it has been correlated with CVD disease because excess MPO has been linked as marker of plaque instability in PAD disease and coronary heart disease. 

The cascade has many other parts associated with it discussed on the forum.

THERE IS A DEEP LESSON HERE------> https://www.instagram.com/p/C-EgRioOefF/

Without full spectrum sunlight, and total darkness at night PATIENTS should expect to have endothelial dysfunction and peripheral arterial damage should be EXPECTED by the decentralized clinician. It is not expected by each because neither are being taught properly about light. Light has no relative power without understanding darkness when it comes to ROS/RNS magnetochemistry. No one involved in any side of science in medical curriculums looks at the data in BigHarma literature to see this data much less understand the clinical significance. 

A lack of NO production at our integument and eye surfaces ALWAYS link PAD by way of intimal thickening = directly to cardiovascular dysfunction. This is why MPO is an arterial disease marker.  The local effect become generalized in the entire organ as the lack of NO production gets worse under ALAN or nnEMF influence. This is why PAD is always linked to cardiovascular disease. The link is the aberrant use of the electromagnetic spectrum to communicate to create NO. Modern light and RF and cell radiation impairs production of NO from arginine by eNOS. When melanin is missing in tissues arterial disease in that tissue is likely and MPO should be expected to rise. 

This, in turn, induces high blood pressure by causing endothelial dysfunction. Mitochondria are intimately involved in importing nitorgen into tissues to create the substrates that eventually become NO when sunlight is present. 

Nitrogen substrates are not created from the direct synthesis by eNOS. Nature provided the clue to me why humans got rid of Vitamin C for glutathione in this AMO physics dance. When Vitamin C is missing in subcutaneous tissues, glutathione become more reactive with locally produced NO. This mimics a radical pair or triad effect we see in avian compass navigation. 

Here is more evidence of magnetochemistry in humans being used. When glutathione and nitric oxide are powered by terrestrial sunlight this allowed humans to produce S-nitrosoglutathione (GSNO). I think this is why human primates lost the majority of their integumentary hair and absorbed more melanin from the hair follicle to the interior. 

SUMMARY

When we lost our dense mammal hair filled with melanin and it went to our interiors, this allowed the skin to become a better charge capacitor for the brain and heart by allowing the skin to become a photoelectric depot station to store massive amounts of nitric oxide. This is why human immune T cells are so common in the skin and why leptin was placed in subcutaneous fat.

Other primates do not have these phenotypes even thought their genomes are close to identical. This tells me magnetochemistry timing induced this evolutionary change. We never need genes to change this. We used timing to change the metabolic pathways in the skin using hair loss and removal of Vitamin C from the radical triad mechanism to do it. As a consequence of this dance using more light on the skin, keratinocytes were able to sense more visible light combinations with purple, blue, and green light to easily photocatalyze the release of NO from glutathione. The picture below explains why it happens. See how it affects eNOS production? Your centralized clinicians are abhorrently ignorant on how light and the non visual photoreceptor system operates.

Not only does NO liberation cause a relaxation of the blood vessels, but it also frees up glutathione to react with hydrogen sulfide gas to produce sulfate to make every other chemical in the skin water soluble to get access to body parts to have global effects in other tissues.

This is how light develops its abscopal effects. No one has figured out how this all works in humans but this is how I have seen it for 20 plus years.

To date no one has published a thing using my ideas. But I can explain why subtraction of Vitamin C in humans links to hair loss. Note below all the pathways that link POMC to Vitamin C, yet no one sees the connections. This also explains most of the integumentary and ocular diseases we see today because all have arterial disease as a preexisting condition.  

This is why childhood obesity has changes in choroid always present if one looks for it.  No pediatrician does.  Most are not skilled enough to examine the retina directly in their offices

These change cascades due to light and dark alterations explains obesity, too. It explained to me why humans get aneurysms and AVMs in the brain as well. When you know better, you do better.  

 CITES

https://forum.jackkruse.com/threads/decentralized-research.29101/page-2