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High Cholesterol Message Board


High Cholesterol Board Index


I can see where Lenin is coming from in his response. I did search and search last night about the Lp(a) correlations and biochemical mechanisms. Appararently, more than just nicotinic acid can lower Lp(a) concentrations. Estrogen treatment and anabolic steroids can do so, too.

The probem is that in studies with Lp(a), different ethnic backgrounds, e.g. African, have higher levels of Lp(a) on average than do Caucasians and Asians. However, many of those studies don't show a correlation between Lp(a) and heart disease, and even the ones they do, the levels change if you examine the ethnic group as a treatement variable. There apparently is a correlation of Lp(a) > 30 mg/dL levels and a higher incidence of CHD in some ethnic groups, but the mechanism is not understood at all.

There have been studies that examine (via radiolabelling) the pathways of LDL formation and Lp(a) formation and these studies indicate that Lp(a) clearance is not the important factor (unlike LDL, where you have the LDL receptors in the liver). The Lp(a) concentration then must be heavily dependent upon the formation rate. I did run across one mention of lysine, but I think that was in reference to binding with Lp(a). Not much else was made to mention in the literature sources, otherwise.

As for formation, I did run across the need for cysteine in the formation process, but I didn't see where the manuscript went so far as to try to link high homocysteine---> high Lp(a). Too much is still left to be understood about the process.

With respect to the Lp(a) deposition and role in formation of plaque ( it can be oxidized...) there still remains the uncertainty about whether it even plays an active role, or if it is some unfortunate victim of incorporation into the foam cells by virtue of its high plasma concentration, and thus gets implicated as a cause for plaque formation...

I don't have an answer as to why the lysine/ascorbic acid treatment has not been examined more extensively in the literature?

I think there is still too much unknown about the Lp(a).

However, like Lenin, I don't take high doses of C and lysine; I am happy with my lipid levels now (as it sounds Hubble is), and the arsenal of supplements I take already, which may (or may not) be helping achieve those values. :D
ARIZONA,

You are avoiding my question. You have said innumerable times that the Pauling-Rath theory of proline-lysine-ascorbate abatement of Lp(a) initiated heart disease seems "VERY PLAUSIBLE" to you. I am asking WHY you feel that way...strong enough to propose it, over and over, as an good, rational, alternative to the current accepted treatment for avoidance and mitigation of heart disease/atherosclerosisis.

Would you like to spell out WHY you consider Pauling/Rath so PLAUSIBLE?

I've given chapter and verse on the IMPLAUSIBITY of each component of the hypothesis/idea. Have you agreed then that it is indeed implausible? Or does it remain "plausible" but in some mystical, indescribable way?

The FACT that something was NEVER tested, though testing could easily be done, is not a reason to asssume it is worthy of consideration, almost certainly the contrary.





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