For what it's worth, here's a cut and paste job from
www.medibolics.com
Reversing Plaque in Arteries (July, 2001)
by Michael Mooney
There is an interesting theory on the use of Vitamin C combined with the amino acid lysine (and perhaps proline) for cardiovascular health, and potentially reversing plaque in the arteries.
It makes enough biochemical sense that I am adding 2 grams of lysine to my dietary supplement intake. I am considering proline, too. (I already take 4,000 mg of Vitamin C twice per day.) Lysine and proline are harmless amino acids, so it can't hurt, and may do some good over the long term.
Interesting reading on preventing or reversing cardiovascular disease, based on the work of Drs. Linus Pauling, involves monitoring lipoprotein (a) in blood tests, and reducing it with Vitamin C. Lysine (and proline) supplementation are supposed to augment the effect of Vitamin C. This is not new information, but I had not bothered to read anything about it before now.
I have been taking high dose Vitamin C for 34 years, and have almost no measurable arterial plaque by Ultrafast CT scan (one extremely small spot measuring 34, where 0-100 is low plaque, 100- 400 is medium and above 400 is extensive plaque), but I have not been taking lysine (or proline). This is interesting enough that I have decided to start taking lysine.
To read more, go to:
http://www.medical-library.net/sites/vitamin_c_and_vascular_disease.html
(Below this are abstracts on Lp(a) and HIV and Lp(a) and cardiovascular disease.)
As stated on the above web site:
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The presently accepted levels of lipoprotein(a) are the following.
0 - 20 mg/dl: low risk
20 - 40 mg/dl: moderate risk
Greater than 40 mg/dl: high risk
Interesting Facts About Lipoprotein(a):
1. Lipoprotein(a) levels are largely determined by inheritance.
2. Special diet does not influence lipoprotein(a) levels.
3. None of the available cholesterol lowering drugs lower lipoprotein(a) blood levels.
4. Ascorbate and niacin both lower lipoprotein(a) blood levels.
5. L-lysine and L-proline, two natural amino acids, can prevent the apo(a) adhesive from sticking, serving as a kind of Teflon coating. Of these, L-proline is several times more powerful than L-lysine. These aminos also assist to shrink the plaque which is already present.
6. Lipoprotein(a) blood level is the single greatest risk factor predicting the restenosis of vessels used in bypass surgery.
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SOME STUDIES ON LIPOPROTEIN (a)
Serum lipid levels associated with increased risk for cardiovascular disease is associated with highly active antiretroviral therapy (HAART) in HIV-1 infection.
Int J STD AIDS 2000 Jul;11(7):451-5 (ISSN: 0956-4624)
Koppel K; Bratt G; Eriksson M; Sandstrom E
The long-term effects of fat metabolism, storage and utilization in HIV-1 infected patients on highly active antiretroviral therapy (HAART) including a protease inhibitor are profound and cause increasing concern. The main importance of these lipid/metabolic disorders lies in their assumed contribution to an increased risk of coronary heart disease (CHD). In the general population increased levels of lipoprotein(a) [Lp(a)] constitute an independent risk factor for CHD by itself as well as in combination with increased levels of cholesterol and low density lipoprotein (LDL)-cholesterol, respectively. Two hundred and fifty-six patients with 27 +/- 7 months HAART and 84 treatment-naive HIV-1 positive patients were screened for cardiovascular risk factors. The subjective perception of fat wasting and/or accumulation in different sites of the body, which was possible to evaluate in 235 patients on HAART and 73 treatment-naive patients, the levels of plasma triglycerides (TG), cholesterol, LDL and high-density lipoproteins (HDL)-cholesterol, LDL/HDL ratio and Lp(a) were
measured. Of the patients on HAART, 42% (98/235) reported abnormal fat distribution as compared with 4% (3/73) of the treatment-naive patients (P<0.0001). The levels of TG, cholesterol and LDL-cholesterol, but not HDL-cholesterol or Lp(a) were higher (P<0.0001) in the HAART group as compared with the naive group. Very high Lp(a) levels (> 700 mg/l) were more common among HAART patients as compared with naive, 14% (36/256) vs 2% (2/83); P=0.0022. The Lp(a) levels correlated to the levels of LDL-cholesterol, but not to total cholesterol, HDL-cholesterol or TG, and did not differ between patients with and without subjective perception of abnormal fat distribution. A significant number of the HAART patients had very high levels of Lp(a) and various combinations of increased lipid values associated with considerably increased risk for CHD. The elevation of Lp(a) did not relate to any other clinical or laboratory parameter than to
LDL-cholesterol.
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Association of lipoprotein(a), prostaglandin I(2)--synthesis stimulating plasma factor, biological half-life of prostaglandin I(2)and high-density lipoproteins in HIV-1 infection of different stages.
Prostaglandins Leukot Essent Fatty Acids 2000 Nov;63(5):309-14
Kritz H; Efthimiou Y; Stamatopoulos J; Najemnik C; Sinzinger H
Patients with human immunodeficiency virus show increased atheroembolism and premature arterial events (stroke, myocardial infarction), but no increased venous thromboembolism. This paper describes an association of elevated lipoprotein(a), a decreased prostaglandin I(2)(PGI(2)) synthesis stimulating plasma factor, diminished PGI(2)-stability in plasma and decreased high-density lipoprotein-cholesterol and apolipoprotein A. It is unclear to what extent these biochemical findings represent an acute phase reaction only or a disturbance in the prostaglandin system. Definitely, they are resulting in severe hemostatic imbalance decreasing local PGI(2)-availability with a dramatic reduction in the cytoprotective capacity favouring the onset of premature arterial events seen in some of the patients.
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Lipoprotein(a) as a risk factor for coronary artery disease in hemodialysis patients.
Kidney Int Suppl 1999 Jul;71:S242-4 (ISSN: 0098-6577)
Ohashi H; Oda H; Ohno M; Watanabe S; Sakata S
BACKGROUND: We studied whether lipoprotein(a) [Lp(a)] is an independent risk factor for coronary artery disease (CAD) in hemodialysis (HD) patients. METHODS: A serum concentration of Lp(a) was measured in 212 patients with chronic glomerulonephritis and 56 patients with diabetic nephropathy (a total of 268 patients). The causes of death during five years of follow-up were studied and classified into either cardiovascular or noncardiovascular events. RESULTS: The mortality of these 268 HD patients during the observation period was 26.1%. Seventy-eight percent were due to cardiovascular events. Those who died of cardiovascular events had significantly higher serum Lp(a) levels than those died of noncardiovascular events. The relative risk of death from CAD was 0.71 in HD patients with a Lp(a) concentration above 30 mg/dl. CONCLUSIONS: This study indicates that the serum Lp(a) levels are independent indicators of the future risk of death from CAD in HD patients.
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Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig.
Proc Natl Acad Sci U S A 1990 Dec;87(23):9388-90 (ISSN: 0027-8424)
Rath M; Pauling L [Find other articles with these Authors]
Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306-2025.
Lipoprotein(a) [Lp(a)] is an extremely atherogenic lipoprotein. Lp(a) has been found in the plasma of humans and other primates, but until now only in a few other species. The mechanism by which it exerts its atherogenicity is still poorly understood. We observed that Lp(a) has been found in the plasma of several species unable to synthesize ascorbate and not in other species. We have now detected apoprotein(a) in the plasma of the guinea pig. We induced atherosclerosis in this animal by dietary ascorbate depletion and, using SDS/PAGE and subsequent immunoblotting, we identified Lp(a) as accumulating in the atherosclerotic plaque. Most importantly, adequate amounts of ascorbate (40 mg per kg of body weight per day) prevent the development of atherosclerotic lesions in this animal model and the accumulation of Lp(a) in the arterial wall. We suggest an analogous mechanism in humans because of the similarity between guinea pigs and humans with respect to both the lack of endogenous ascorbate production and the role of Lp(a) in human atherosclerosis.
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Hypothesis: lipoprotein(a) is a surrogate for ascorbate.
Proc Natl Acad Sci U S A 1990 Aug;87(16):6204-7 (ISSN: 0027-8424)
Rath M; Pauling L [Find other articles with these Authors]
Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306.
The concept that lipoprotein(a) [Lp(a)] is a surrogate for ascorbate is suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals. Properties of Lp(a) that are shared with ascorbate, in accordance with this hypothesis, are the acceleration of wound healing and other cell-repair mechanisms, the strengthening of the extracellular matrix (e.g., in blood vessels), and the prevention of lipid peroxidation. High plasma Lp(a) is associated with coronary heart disease and other forms of atherosclerosis in humans, and the incidence of cardiovascular disease is decreased by elevated ascorbate. Similar observations have been made in cancer and diabetes. We have formulated the hypothesis that Lp(a) is a surrogate for ascorbate in humans and other species and have marshaled the evidence bearing on this hypothesis.
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For a more detailed explanation of this theory, click here.
Michael Mooney
www.medibolics.com
