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Guillermou's avatar

Yes Randall, one of the functions that vitamin C plays in the body is to help maintain the collagen network. The mechanisms that allow this regulation and that justify its use as an antiaging treatment are listed below:

1) Prevents the autoinactivation of the enzymes lysyl and prolyl hydroxylase, key enzymes in the collagen synthesis process, and its physiological cross-linking at the cellular and tissue level.-----

2) It directly activates the transcription of factors involved in collagen synthesis and stabilizes messenger RNA (mRNA), which regulates the synthesis of type I and III collagens.----

3) Increases the activity of the collagen expression gene by increasing the synthesis of the tissue inhibitor of MMP-1 and, consequently, decreases collagen degradation.----.

Reactive oxygen species (ROS) are being generated continuously in our body, to avoid their negative effects we need them to be neutralized, and this work is carried out by two different families of scavengers:

Enzymatic scavengers such as glutathione peroxidase, superoxide dismutase and catalases.

Non-enzymatic scavengers such as β-carotene, vitamin C and vitamin E; both groups of scavengers depend on selenium.

Vitamin E is a fat-soluble antioxidant composed of 4 tocopherols and 4 trienols, with alpha-tocopherol being the most abundant form. Its function is to protect cell membranes from oxidative stress. The transport of vitamin E to the deeper layers of the stratum corneum is carried out by the secretion of the sebaceous glands.

Excessive sun exposure can deplete the skin's vitamin E levels. Topical use of vitamin E reduces lipid peroxidation, photoaging, immunosuppression, and photocarcinogenesis.

Vitamin C and vitamin E have an antioxidant effect on the skin and reduce oxidative stress, interacting with each other, in such a way that vitamin C regenerates oxidized vitamin E, favoring the maintenance of the skin's antioxidant reservoir.

https://www.intechopen.com/online-first/85565 (2023)

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Guillermou's avatar

Thanks Randall. While plaque is made up of a variety of substances: fibrinogen / fibrin; lipoproteins; cholesterol and other fatty particles, as mentioned, the main glue-like substance that initially binds to the arterial walls is lipoprotein (a), abbreviated Lp (a). Heart disease begins with an injury, crack, or stress fracture, in the arterial wall. Work that led to the 1987 Nobel Prize in Medicine discovered that lysine (and proline) binding sites cause the formation of atherosclerotic plaques. Lp (a) was the genetic difference between beings that suffer from cardiovascular diseases and those that do not. Lp (a) had evolved only in species that do not make their own vitamin C such as humans and guinea pigs.

Pauling and Rath realized that the species suffering from chronic scurvy, Lp (a) had evolved to patch cracked blood vessels. As chronic scurvy progresses, the liver produces more Lp (a) molecules. As the number of Lp (a) molecules increases, formations tend to settle on the existing plate. When the healing process is overrun, the arteries narrow and blood flow is reduced.

This problem has a solution. The Lp (a) molecule has a finite number of lysine binding sites - lysine attachment sites. The cure for heart disease is to increase the serum concentration of the amino acid lysine enough to bind Lp (a)

Lp (a) binding inhibitors are converted to Pauling Therapy for heart disease only in high doses, between vitamin 3 to 18 g of ascorbic acid and 3 to 6 g of lysine. In his video, Pauling recounts the first cases where his high vitamin C and lysine therapy quickly resolved advanced cardiovascular disease in humans.

THE CURE FOR HEART DISEASE: CONDENSED

https://cardiacos.net/wp-content/uploads/ArticulosMedicos/20170813/2004---Heart-cure.pdf

LINUS PAULING PROTOCOL

https://asociacionaibb.com/linus-pauling-protocol/

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