Heart disease reversal: AA, CoQ10, vitamins, L-Lysine & L-Proline     (From 1991)

Pauling and Rath contribute, with several published papers, to the understanding of the molecular interactions resulting in the formation of atherosclerotic plaques.  Then they put the pieces together to save the life of a critically ill colleague.  This paper is a marvelous tour-de-force in biochemical analysis. L-Lysine is the critical element. L-Proline is now added to improve current (2011) arteriosclerosis treatments.  The original Pauling paper is preserved by John Ely of the University of Washington.  It contains the essence of the solution to how to keep these plaques from forming, to reverse their formation, and to produce an inexpensive dietary cure for a large number of persons. Side note: Co-author, Matthias Rath, (Germany) uses AA+L-Lysine+L-Proline+EGCG to control the spread of cancer. 


Lysine and Proline are found in abundance, inexpensively, in gelatin and homemade soup made from boiling bones. Search for Nutrients. See Results for Lysine and Proline.


[Descriptors: Arteriosclerosis, atherosclerosis, stroke prevention, heart disease, peripheral artery disease, brain hypo-oxygen, plaque formation, plaque removal, angina]


[A]melioration of effort angina by the use of high-dose L-lysine and ascorbate in a man with severe coronary artery disease (CAD).

[Journal Orthomolecular Medicine, 1991]

L. Pauling:  Lysine/Ascorbate-Related Amelioration of Angina (Arterial Sclerosis)


Edited extract from the website to increase readability:


This regimen was based on the hypothesis that, in thrombotic atherosclerosis, lipoprotein(a) [Lp(a)]‹ size-heterogeneous, LDL- like particles displaying independent risk activity for CAD ‹initiates plaque formation by binding to fibrin in the damaged arterial wall. This postulated mechanism correlates with the findings that apoliprotein(a) [apo(a)] has a striking homology to plasminogen and the Lp(a) accumulates in atherosclerotic lesions in the arteries of man (Rath et al., 1989)and the hypoascorbic guinea pig (Rath and Pauling, 1990a, 1990b) and in occluded bypass venous grafts (Cushing et al., 1989).


[I]t was known that Lp(a) binds to lysine-Sepharose, immobilized fibrin and fibrinogen (Harpel et al., 1989); and the epithelial-cell receptor for plasminogen ( Gonzalez-Gronow et al., 1989). This binding specificity correlates with the genetic linkage on chromosome six and striking homology of apo(a) and plasminogen ‹highly conserved multiple kringle-four domains, a kringle-five domain, and a protease domain (McLean et al., 1987).


Moreover, using the molecular evolutionary clock, the loss in primates of the ability to synthesize ascorbate (Zuckerkandl and Pauling, 1962; Rath and Pauling, 1990a) and acquisition of Lp(a) (Maeda et al., 1983) both appear to have occurred about 40 million years ago.


These observations and the presence of Lp(a) in sclerotic arteries (Rath et al., 1989; Rath and Pauling, 1990b) and in venous grafts (Cushing et al., 1989) indicate that atherosclerosis may be initiated by excess binding of Lp(a) to fibrin in vascular wall clots, thus interfering with normal fibrinolysis by plasmin. This thrombogenic activity, which is postulated to reside in plasmin-homologous domains of Lp(a), may help to stabilize the damaged vascular wall, especially in ascorbate deficiency (Scanu, Lawn, and Berg, 1991; Rath and Pauling, 1990a). Once bound to fibrin, the LDL-like domain of Lp(a) could promote atheromas (Scanu, Lawn, and Berg, 1991).


In this scenario, high-dosage lysine could inhibit or reverse plaque accretion by binding to Lp(a).


Independently, lysine benefits the heart as a precursor with methionine in the synthesis of L-carnitine, the molecule that carries fat into mitochondria for the synthesis of adenosine triphosphate (ATP) bond energy needed for muscular and other cellular activities (Cederblad and Linstedt, 1976). While his intake of 60 mg of CoQ-10, also required for ATP synthesis, prior to the addition of lysine improved his sense of well being, it did not suppress his angina.


Ascorbate without lysine also did not ameliorate angina, but it is needed as an antioxidant to protect the vascular wall against peroxidative damage and in hydroxylation reactions both in the synthesis of carnitine and in the conversion of procollagen to collagen (hydroxylation of prolyl and Iysyl residues) (Myllyla et al., 1984) to strengthen the extracellular matrix of the wall.


Dosage:  6 g of ascorbate (acid form), 60 mg CoQ-10; a multivitamin tablet with minerals; additional vitamins A, E and a B-complex; lecithin; and niacin, on advice of his cardiologist to try to raise his HDL level.


Nevertheless, he still had to take nitroglycerin sublingually to suppress angina during a daily two mile walk and when working in his yard. This effort angina continued to worsen, imparting a feeling of impending doom that was reinforced by his cardiologist's admonition during a check-up in March 1991 that a fifth angiographic test and a fourth bypass operation were no longer options. Also, the saphenous veins from his groin regions and legs had all been used for previous grafts.


In this predicament and with his history of restenosis, I suggested that he continue ascorbate and add 5 g of L-lysine daily (ca., six times the lysine derived from dietary protein) to try to mitigate the atherosclerotic activity of Lp(a). After reading the 1990 Rath and Pauling reports and their manuscript titled "Solution to the puzzle of human cardiovascular disease", he began taking 1 g of lysine in early May 1991 and reached 5 g (in divided doses eight hours apart) by mid-June. In mid-July, his HDL was, as usual, a low 28 mg/dl. A low-normal 0.9 mg/dl blood creatinine indicated that lysine could be increased, if needed.


He could now walk the same two miles and do yard work without angina pain and wrote, "the effect of the lysine borders on the miraculous". By late August, he cut up a tree with a chain saw, and in early September started painting his house.


By late September, possibly from over-exertion, he again began to have angina symptoms during his walks, but after stopping strenuous work and increasing lysine to 6 g [calculated to provide a peak 280,000 molar excess in the blood over his then 6 mg/dl of Lp(a) to help compensate for the relatively high dissociation constant of lysine-Lp(a)] these symptoms stopped entirely by mid-October.


His blood creatinine was still a normal 1.2 mg/dl. He attributes his newfound well being to the addition of lysine to his other medications and vitamins. His wife and friends comment on his renewed vigor.


Whatever the patho-mechanisms of atherosclerosis, the addition of lysine to medications and vitamins, including ascorbate, markedly suppressed angina pectoris in this intractable case of CAD. [coronary artery disease]


End of edited extract.

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