I agree whole-heartedly! Lysine can be very useful! In fact, I am taking 3 grams of it a day as I type this mainly because of Linius Pauling's recommendation of it being beneficial in heart disease. The theory is:
Quote:
The Pauling/Rath hypothesis rests on the pioneering work of two Canadian medical doctors J. C. Paterson, MD and G. C. Willis, MD conducted in the late 1930s through the 1950s. These two medical doctors suspected that the heart disease process is related to the stability of arteries. They noticed that atherosclerotic plaques are not randomly distributed. Plaques usually develop at the same locations in places where blood vessels are stretched or squeezed, i.e., where mechanical forces and stresses are great, e.g., in the coronary arteries.
In 1937, on a hunch, Dr. Paterson measured tissue levels of vitamin C in hospital patients. He showed that heart patients have 80% lower tissue levels of vitamin C in their blood vessels compared to other patients in the hospital. In the 1950s, Willis showed that vitamin C intake correlates to atherosclerosis in both humans and guinea pigs. Willis discovered that 500 mg of vitamin C added to the diet could reverse plaque build-up in about half the human patients. Plaque was not reduced in the controls. Daily vitamin C was 100% effective preventing atherosclerosis in guinea pigs.
Pauling's crucial insight is that our diets lead to heart disease, but not in the way most people think. Our diets have sufficient vitamin C to prevent scurvy, but less than what we need to function optimally and keep our blood vessels flexible and strong. The result is a sub-clinical form of scurvy, i.e., chronic scurvy.
"Knowing that lysyl residues are what causes lipoprotein-(a) to get stuck to the wall of the artery and form plaques, any physical chemist would say at once that the thing to do is prevent that by putting the amino acid lysine in the blood to a greater extent than it is normally." [Linus Pauling, JON, Aug. '94]
Pauling’s invention is to increase the lysine concentration in the blood serum causing Lp(a) to bind with lysine molecules in the blood rendering the Lp(a) inactive.