The Crowning Achievement of Alternative Medicine A Cure for Heart Disease is a Reality. Copyright 1997 (c) by Owen R. Fonorow Edited by Billie Valentine Revision 2 - 10-07-97 (Final) Vice President Gore deserves to be commended for helping the public gain free access to the MEDLINE database on the National Institute of Health's world-wide-web site. This move is about to send shock waves through the mainstream medical community. Pursuing an interest in the combined work of Linus Pauling and Matthias Rath, MD regarding cardiovascular disease, I began to explore MEDLINE looking for the reason the two men make different recommendations. Dr. Rath recommends both the amino acids proline and lysine for their ostensibly therapeutic value. Dr. Pauling, on the other hand, carefully avoided any reference to proline, and focused his recommendation on much larger (gram) amounts of l-lysine. According to Pauling: "You need lysine to be alive. It is essential, but you can take lysine, pure lysine, a perfectly non toxic substance in food [as supplements] , and that puts extra lysine molecules in the blood. They enter into competition with lysyl residues on the walls of arteries and accordingly count to prevent Lp(a) from being deposited or even will work to pull it loose and destroy atherosclerotic plaques." [Linus Pauling 1994] My curiosity regarding this difference in therapeutic agents and dosage recommendations began a fruitful relationship with the "free" MEDLINE internet search engine Grateful Med. Prior to 1992, there were only a handful of MEDLINE cataloged studies that mention lipoprotein(a) or Lp(a) in the subject or title. However, after Pauling began his lecture series, i.e., from 1992 on, there were, and are more than 1100 studies, papers and letters regarding the importance of Lp(a) as a risk factor in premature coronary vascular disease (CVD). The magnitude of this research is amazing. (The abstracts alone would require about a thousand pages). The pioneering work of Matthias Rath and Linus Pauling, although apparently unknown to most authors, is now supported by a substantial and compelling body of research in the mainstream scientific community. Following are a examples of the conclusions drawn from a sample of these papers, published in mainstream medical journals: Lipoprotein Lp(a) excess has been identified as a powerful predictor of premature atherosclerotic vascular disease in several large, prospective studies1. We measured serum Lp(a) and other lipid parameters... Although triglyceride and LDL, HDL and total cholesterol levels were similar in the restenosis and no-restenosis group before PTCA, Lp(a) was significantly higher in the restenosis group2. This study provides the first evidence in man of a significant role for lipoprotein Lp(a) in unstable angina3. Lipoprotein(a): a potential biological marker for unruptured intracranial aneurysms. The prevalence of elevated Lp(a) levels in ... and the high degree of association of raised Lp(a) with the presence of IAs..4 While the two drugs (pravastatin and simvastatin) caused the expected reduction of plasma total and LDL cholesterol levels, no significant changes in Lp(a) were noted.5 These, along with the other one thousand ninety six MEDLINE abstracts can be obtained from the NIH by simply by searching for "lipoprotein(a)" in the subject or title beginning with year 1992. (A hypertext link to the NIH search engine can be found on the following web page: http://www.internetwks.com/pauling) Although among these hundreds of studies, several did not find Lp(a) to correlate to coronary arteriosclerosis, the vast majority have correlated Lp(a) and found it to be a highly athogenic risk factor. A feat science was never able to accomplish with LDL alone. There has been much research that indicates it is Lp(a), not LDL, which exhibits the Lysine Binding Site (LBS). Thus it is Lp(a) that adheres or binds to lysine residues in damaged arteries. This is now well understood. The lipoprotein(a) found in Rhesus Monkeys, however, does not bind to lysine and has thus been designated as LBS-. The Rhesus monkey Lp(a) does have a "proline binding domain" and thus this peculiar form of Lp(a) LBS- binds to fibrinogen. Furthermore, researchers have been able to show that proline in the test tube may interfere with the so-called "assembly" or creation of lipoprotein(a). Researchers at the University of Chicago were the first to demonstrate this "proline binding region" and thus they have shown that proline and a lysine analog can inhibit the binding of lipoprotein(a) in vitro, i.e., in the test tube. Ms. Olga Klezovitch, Ph.D. wrote to me: "Dear Owen Fonorow: Our study published in Journal of Clinical Investigation demonstrated for the first time that L-proline can inhibit the binding of Lp(a) and apo(a) to fibrinogen in vitro conditions. However, we have no data about the physiological relevance of this finding. It is well established that the binding of Lp(a) to fibrinogen also involves the lysine binding sites of apo(a) (component of Lp(a)), therefore, the presence of lysine and lysine analog dramatically reduces this binding. Once again, the in vivo relevance of this inhibition is unknown." Sincerely, Olga Klezovitch, Ph.D. University of Chicago Department of Medicine For the record, the following MEDLINE abstract prompted me to contact Dr. Klezovitch: "It is now established that the lysine binding site (LBS) of apo(a) kringle IV-10, and particularly Trp72, plays a dominant role in the binding of lipoprotein(a) [Lp(a)] to lysine. To determine the role of the LBS in the binding of Lp(a) to fibrinogen, we examined the binding to plasmin-modified (PM) fibrinogen of human and rhesus monkey Lp(a) species classified as either Lys+ or Lys- based on their capacity to bind lysine Sepharose and to have Trp or Arg, respectively, in position 72 of the LBS of kringle IV-10. We also examined the free apo(a)s obtained by subjecting their corresponding parent Lp(a)s to a mild reductive procedure developed in our laboratory. Our results how that both Lys+ and Lys- Lp(a)s and their derived apo(a)s, bound to PM-fibrinogen with similar affinities (Kds: 33-100 nM), whereas the B(max) values were threefold higher for apo(a)s. Both the lysine analog epsilon-aminocaproic acid and L-proline inhibited the binding of Lp(a) and apo(a) to PM fibrinogen. We conclude that the LBS of kringle IV-10 is not involved in this process and that apo(a) binds to PM-fibrinogen via a lysine-proline-sensitive domain located outside the LBS and largely masked by the interaction of apo(a) with apoB100. The significant difference in the PM fibrinogen binding capacity also suggests that apo(a) may have a comparatively higher athero-thrombogenic potential than parent Lp(a)" Department of Medicine, University of Chicago, Illinois 60637, USA. oklezovi@medicine.bsd.uchicago.edu6 It is important to note, that even with all this research in the form of 1100 studies, I could find no study that investigated the specific claim of Linus Pauling that multi-gram amounts of vitamin C and l-lysine can "completely control, even cure" cardiovascular disease in humans in vivo?! One study, not yet available via MEDLINE at the time of this writing, comes close. This clinical study by researcher Dr. Matthias Rath, soon to be published in the Journal of Applied Nutrition, is valuable. Rath apparently was forced to study his own product himself because it is difficult to get mainstream researchers interested in the benefits of vitamin C. (Vitamin C oriented research can, reportedly, harm ones ability to secure grant money, as many of the readers of this publication know.) Rath was able to demonstrate that deposits can be prevented, and even eliminated over the course of one year. This improvement was statistically significant, compared to the controls whose atherosclerosis increased dramatically. However, it must be said that the amounts of lysine that were investigated are about 10-20% of what an individual normally obtains in their diet -- hardly therapeutic. It is important to differentiate these rather low doses recommended by Dr. Rath with the large dosages recommended by Dr. Pauling. Pauling's recommended 5-6 grams are about 30-40 times Rath's recommended dosage. Empirical Observations I have observed the results of the Pauling vitamin C/lysine therapy, outlined in Pauling's video. What makes the Pauling recommendations so important is the dramatic improvement that usually occurs within two weeks at these high therapeutic levels. Again, in the words of Linus Pauling: "I've got to the point where I think we can get almost complete control of cardiovascular disease, heart attacks and strokes by the proper use of vitamin C and lysine. It can prevent cardiovascular disease and even cure it. If you are at risk of heart disease, or if there is a history of heart disease in your family, if your father or other members of the family died of a heart attack or stroke or whatever, or if you have a mild heart attack yourself then you had better be taking vitamin C and lysine."[Linus Pauling 1994] Linus Pauling did not speak this words lightly. I have seen the result Pauling's recommended therapy had on patients who were considered by their doctors, to be hopeless cases. I have had conversations with people who were, literally, sent home to die, and who then, without exception, had gotten well. They had been told that one or more of their coronary or carotid arteries were 90% or more blocked, and that for one reason or another, surgery was no longer an option. They had suffered heart attacks, coronary by-pass operations, angioplasties, and they almost always complained of severe angina pain. As difficult as it may be for most readers to believe, these are the people that report substantial relief from pain after the Pauling therapy. On more than one occasion this writer has heard: "My angina pain went away after 10 days." I am unaware of any person who, if he/she tried the therapy and if he/she had been in a terminal condition, did not respond. To my knowledge, every person who has adopted the specific Pauling therapy is alive -- beginning with the three cases cited by Pauling in his video lecture. Because of the outstanding success we have formed The Vitamin C Foundation to help spread the word about vitamin C to the medical profession. Although not a doctor (of medicine) I understand, to a degree, the struggle of alternative medicine. What I cannot understand is the passive attitude of many people in the alternative medical movement, nor the attitude of the national media who with either inadvertent disregard or calculated omission overlook this matter. People are suffering, and this suffering can be alleviated or eliminated. What is being ignored is this: The titular head of the Alternative Medicine movement, an American scientist, has discovered a cure for heart disease, a fact that is virtually unknown. Add to this outrage the recent "junk scientist" label Pauling was given on national television. Now that this cure is backed by a large body of mainstream science, why hasn't the alternative movement latched on to this fact? This achievement should be held up to the world as proof of what Alternative Medicine is all about. What can be accomplished. It should show the world that you are the real science in medicine today. Think about the blow to allopathic medicine? They had six years of intense study of Lp(a), yet they are on a snail's pace after the trail blazed by the pioneers of alternative medicine. Not one of these mainstream scientists has offered a similar remedy. But years prior, an American pioneer in alternative medicine who invented the term "orthomolecular medicine" and his associate came up with a cure for heart disease that works, empirically , in every case. Yet very few people know about it, and no one in the mainstream scientific community has studied it. This does show that truth is stranger than fiction. The fact is that vitamin C and lysine are perfectly harmless and non-toxic. Even in the unlikelihood that Pauling and Rath are proven wrong, there would have been no harm done to anyone by ingesting these substances -- substances which are essential for life. Every person in America. Every person in the world should be made aware of this discovery. I can't imagine a valid reason for another coronary by-pass graph operation or an angioplasty. There is one caveat. It will be tempting for mainstream scientists to accept one half of the Pauling/Rath theory. They will accept the Lp(a) aspect, and thus recognize that lysine can prevent and even eliminate plaque. However, reversing the plaque without correcting the underlying lesion will result in fatalities. The Pauling recommendation to vastly increase ascorbic acid (vitamin C) along with lysine is absolutely warranted and must be followed. Vitamin C apparently heals the arteries, stops further atherosclerosis and enhances the anti-plaque properties of lysine. Again, MEDLINE abstracts provide support for this notion. In another remarkable MEDLINE, the University of Chicago authors propose their hypotheses that Lp(a) is a surrogate for vitamin C in "latent scurvy." Apparently, they are unaware of the prior work of Linus Pauling and Matthias Rath: "Latent scurvy is characterized by a reversible atherosclerosis that closely resembles the clinical form of this disease. Acute scurvy is characterized by microvascular complications such as widespread capillary hemorrhaging. Vitamin C (ascorbate) is required for the synthesis of collagen, the protein most critical in the maintenance of vascular integrity. We suggest that in latent scurvy, large blood vessels use modified LDL--in particular lipoprotein(a)--in addition to collagen to maintain macrovascular integrity. By this mechanism, collagen is spared for the maintenance of capillaries, the sites of gas and nutrient exchange. The foam-cell phenotype of atherosclerosis is identified as a mesenchymal genetic program, regulated by the availability of ascorbate. When vitamin C is limited, foam cells develop and induce oxidative modification of LDL, thereby stabilizing large blood vessels via the deposition of LDL. The structural similarity between vitamin C and glucose suggests that hyperglycemia will inhibit cellular uptake of ascorbate, inducing local vitamin C deficiency.7" People familiar with the Pauling/Rath Unified Theory of Heart Disease will recognize its similarity to the above hypothesis. The Future Based on the empirical results, I'm not optimistic that a true, double blind, randomized prospective study can ethically be conducted. It is simply inhumane to deprive any human being of the benefit of this therapy. (Not to mention that when this becomes common knowledge among terminally ill heart patients, they will all be taking vitamin C/lysine on their own.) There is a preliminary study that can, and should be conducted to verify these claims. It is a sad fact that there exists today a pool of heart patients who have been declared "terminal" by their doctors. These are the patients who should be studied first. A group of these patients suffering heart disease only, (i.e. no cancer) should be selected, and *all* should be given Linus Pauling's recommended 3-6 gm vitamin C and 4-6 gm lysine. Their conditions should be verified. Their blood serum, blood pressure and other objective measurements taken, and then they should report their condition to the researchers over the course of one month. If, as I predict, all patients recover to the point that the pain ceases, their blood pressure drops, and all indications of serious illness go into remission, the medical research community can decide then how to proceed with further investigation. Again, whether a private foundation funds such a study, or the Office of Alternative Medicine, National Institute of Health, it is imperative that the Pauling recommended dosages of both Vitamin C and Lysine be used. Reversing the plaque, without healing the underlying lesion, will result in fatalities. If you have personal experience of the Pauling vitamin C/lysine cure, either as a patient or medical practitioner, and are willing to tell your story on video, please do so and send videos to: Owen Richard Fonorow PO Box 3097 Lisle, IL 60532 Fax: 1-630-416-1309 fonorow@internetwks.com http://www.internetwks.com/pauling References 1. Stein JH; Rosenson RS, "Lipoprotein Lp(a) excess and coronary heart disease", Arch of Intern Med 1997, Jun MEDLINE Cit ID: 97326406 2. Horie H, et. al., "Association of acute reduction in Lp(a) with coronary artery restenosis after percutaneous transluminal angioplasty," Circulation, 1997 Jul 1;96(1):166-73, MEDLINE Cit ID: 97379632 3. Stubs P, et. al., "A prospective study of the role of Lp(a) in the pathogenesis of unstable angina", Eur Heart J 1997, Apr 18(4):603-7, Cit ID: 97276136 4. Phillips J, et. al., "Lp(a): a potential biological marker for unruptured intracranial aneurysms", Neurosurgery 1997 May;40(5):1112-5; MEDLINE CIT ID: 97293308 5. Pazzucconi F, "Cholesterol synthesis inhibitors do not reduce Lp(a) levels in normocholesterolemic patients," Pharmacol Res 1996 Set-Oct;34(3-4);131-3 MEDLINE Cit ID: 972041326. 6. Klezovitch O; Scanu AM; Edelstein C, "Evidence that the fibrinogen binding domain of Apo(a) is outside the lysine binding site of kringle IV-10: a study involving naturally occurring lysine binding defective lipoprotein(a) phenotypes," J Clin Invest 1996 Jul 1;98(1):185-917. 7. Price KD; Reynolds RD; Price CS, "Hyperglycemia-induced latent scurvy and atherosclerosis: the scorbutic-metaplasia hypothesis," : Med Hypotheses 1996 Feb;46(2):119-29 1Stein JH; Rosenson RS, "Lipoprotein Lp(a) excess and coronary heart disease", Arch of Intern Med 1997, Jun MEDLINE Cit ID: 97326406 2Horie H, et. al., "Association of acute reduction in Lp(a) with coronary artery restenosis after percutaneous transluminal angioplasty," Circulation, 1997 Jul 1;96(1):166-73, MEDLINE Cit ID: 97379632 3Stubs P, et. al., "A prospective study of the role of Lp(a) in the pathogenesis of unstable angina", Eur Heart J 1997, Apr 18(4):603-7, Cit ID: 97276136 4Phillips J, et. al., "Lp(a): a potential biological marker for unruptured intracranial aneurysms", Neurosurgery 1997 May;40(5):1112-5; MEDLINE CIT ID: 97293308 5Pazzucconi F, "Cholesterol synthesis inhibitors do not reduce Lp(a) levels in normocholesterolemic patients," Pharmacol Res 1996 Set-Oct;34(3-4);131-3 MEDLINE Cit ID: 97204132 6 Klezovitch O; Scanu AM; Edelstein C, "Evidence that the fibrinogen binding domain of Apo(a) is outside the lysine binding site of kringle IV-10: a study involving naturally occurring lysine binding defective lipoprotein(a) phenotypes," J Clin Invest 1996 Jul 1;98(1):185-91 7 Price KD; Reynolds RD; Price CS, "Hyperglycemia-induced latent scurvy and atherosclerosis: the scorbutic-metaplasia hypothesis," : Med Hypotheses 1996 Feb;46(2):119-29 Crowning Achievement Owen R. 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