Statins ruin optical signaling in arteries.
Today's quantum factoid: Just as lava tubes are excellent insulators of moving lava, so too has nature built your arteries to be excellent insulators for the light in your red blood cells. Insulators do not allow much loss of heat or light to the surroundings. In atherosclerosis, arteries lose this ability. The first step in crafting a life you want is to get rid of everything you don’t want. Act as if you were on fire from within always because this is how nature built you

Your arteries need sunlight to create NO which dilates blood vessels filled with blood = 93% water.

Ultraviolet light denitrosylates proteins and releases nitric oxide in free form. In a lab dish, two minutes under a UV lamp free nearly all the nitric oxide that has been bound to proteins. Blue and green light have a much weaker effect on NO liberation. Red light works best to release NO when UV light is present.


Sunlight or the photons that make up the light that falls to Earth are timeless because the energy in light has not yet been converted to heat by cells. Light photons never experience time because they have to interact with matter to create heat. The heat creates entropy and this creates the illusion of time because the atoms in our cells account for it like a ledger. That LEDGER is found in our hydrogen bonding cohesiveness in water networks that our mitochondria make. Very soon modern quantum biology will find and report in the literature that the significance of the hydrogen bond for physiology is greater than that of any other single structural feature in human biology.


Artificial intelligence/light is not the same as intelligence gained in Nature. Its noise will affect the periodicity of clocks. A clock is anything that undergoes irreversible that alter the flow of entropy in cells: these changes allow energy to spread out altering the flow of time by allowing more atomic particles into a broader larger area. Anytime size and shape changes occur we know thermodynamics of how entropy flows has been altered. Time is essentially a ledger for the actions of light on the atoms inside your mitochondria. Time is proof that work was done by light on atoms of water in our cells. The timekeeper or clock is our mitochondrial heteroplasmy rate in tissues because it makes the water that contains the ledger of time. A mitochondrion is the Oracle of biology.

RBCs are inside arteries. what is the deal with them: RBCs have no DNA or mitochondria
The transcription of clock genes is sensitive to metabolic and electronic changes in water production and hydrogen bonding in mitochondrial reduction and oxidation (redox) reactions; however, circadian cycles in protein oxidation have been reported in anucleate cells, where no transcription occurs. RBCs are such a cell and act as a light ferry to the mitochondria that are floating in water changed by sunlight in our arteries. The change in hydrogen bonds is the key to the mysteries of life.
https://forum.jackkruse.com/index.php?threads/redox-is-linked-to-rbcs-circadian-clocks.22813/

Statins are mitochondrial toxins because of their effect on CoEnzQ10. There are many ways in which they increase coronary artery calcification. One way is depletion of Vitamin K2 from the gut, another is lack of sun to control calcium flows, and another is direct arterial melanopsin damage liberating Vitamin A to cause intimal damage and a loss of arterial NO.

Sufficient production of vital biochemicals such as Geranylgeraniol (GGPP) is required to maintain endotoxin tolerance in macrophages in our arteries once the damage occurs. Macrophages are the hallmarks of CVD/Atherosclerosis, contributing to plaque development, inflammation, and the promotion of thrombosis. Geranylgeraniol is downstream of Mevalonate in the cholesterol synthesis pathway, and GGPP synthesis is inhibited by Statins, as is CoQ10 and K2. Vitamin K2 is the cofactor for matrix Gla-protein activation, which PROTECTS arteries from calcification.


Statin use is independently associated with increased calcification in patients, & using an animal model of hypercholesterolemia, we present a molecular mechanism whereby statins promote the calcification of atherosclerotic plaque. https://www.ahajournals.org/doi/10.1161/ATVBAHA.119.313832

 

areas of arterial damage have pockets of hypoxia. Thiamine deficiency from the damage can cause pseudohypoxia in mitochondria = lower autophagy and apoptosis efficiency in mitochondria = mitochondrial less thermally efficient = higher heteroplasmy rate = change in water hydrogen bonds = arterial aging = peripheral arterial disease = https://patreon.com/posts/32419906