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Linus Pauling Heart Protocol -- Pauling Therapy for Heart Disease -Vitamin C Cobb Reversing Heart Disease Linus Pauling Last Interview by Linus Pauling

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TitleLinus Pauling Heart Protocol -- Pauling Therapy for Heart Disease -Vitamin C Cobb Reversing Heart Disease Linus Pauling Last Interview
CreatorLinus Pauling
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LanguageEnglish
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Subjectlinus pauling, vitamin c lysine, lysine, lippoprotein a
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Uploaderarchive0517
Identifierlinus-pauling-heart-protocol-vitamin-c-lysine
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Linus Pauling Heart Protocol -- Pauling Therapy for Heart Disease -Vitamin C Cobb Reversing Heart Disease Linus Pauling Last InterviewThe Cure for Heart Disease:CondensedBy Owen R. Fonorow, Copyright 2004'READER'S DIGEST' VERSIONCardiovascular Diseases Those few species that fail tosynthesize ascorbic acid (vitamin C) are prone to a formof ‘heart disease’ that is not prevalent in other species.The theory that Cardiovascular Disease (CVD) is relatedto a deficiency of vitamin C was first proposed by theCanadian physician G. C. Willis in 1953. He found thatatherosclerotic plaques form over vitamin-C-starvedvascular tissues in both guinea pigs and human beings.In 1989, after the discoveries of the Lp(a) cholesterolmolecule (circa 1964) and its lysine binding sites (circa1987), Linus Pauling and his associate Matthias Rathformulated a unified theory of heart disease andinvented a cure. Vitamin C and lysine (and proline) inlarge amounts become Lp(a) binding inhibitors thatrestore vascular health and are patented to destroyatherosclerotic plaques.Chronic scurvy. Heart disease is a misnomer; theunderlying disease process reduces the supply of bloodto the heart and other organs leading to angina ("heartcramp"), heart attack and stroke. The disease ischaracterized by scab-like build-ups that grow on thewalls of blood vessels. The correct terminology for thisdisease process is chronic scurvy, a slower form of theclassic vitamin C deficiency disease.The hypothesis that CVD is an ascorbic acid (vitamin C)deficiency disease was first conceived and tested inCanada. Willis devised a method of photographingplaques with X-rays and observed that atheroscleroticplaques were not uniformly distributed throughout thevascular system; rather these "blockages" areconcentrated near the heart, where arteries areconstantly bent or squeezed.Another Canadian, Paterson, had found that the tissuesof heart patients were generally depleted of vitamin C,and it was well known that vitamin C is required forstrong and healthy arteries. Willis reasoned that onlythe mechanical stress caused by the pulse could explainthe typical pattern of atherosclerosis. To Willis, the bodywas laying down plaque precisely where it was neededin order to stabilize the vascular system.By the late 1980s, medical researchers had madeseveral intriguing discoveries.First came the discovery that heart disease begins witha lesion, a crack or stress fracture, in the arterial wall.The question became, and remains, as to the cause ofthese lesions in human beings since they do not arise inmost other animals. Then a variant of the so-called"bad" LDL cholesterol called lipoprotein(a), or Lp(a) forshort, was studied and found to be really bad.  Lp(a) issticky because of receptors on the surface of themolecule called lysine binding sites. Work that led tothe 1987 Nobel prize in medicine discovered that lysine(and proline) binding sites cause the formation ofatherosclerotic plaques. Then, Beisiegel et. al. inGermany examined plaques post mortem and foundonly Lp(a), not ordinary LDL cholesterol.Lp(a) was the genetic difference between beings thatsuffer cardiovascular disease and those that do not.Lp(a) had evolved only in species that do not make theirown vitamin C - e.g. humans and guinea pigs.Pauling and Rath repeated the earlier Willisexperiments, but this time they monitored Lp(a). Theydiscovered that it becomes elevated in guinea pigsdeprived of vitamin C, but not in the controls. Theseexperiments connected elevated-Lp(a) with low serumvitamin C. They realized that in most species, sufficientascorbic acid will prevent stress fractures, but in thosespecies that suffer chronic scurvy, Lp(a) had evolved topatch cracked blood vessels.As chronic scurvy progresses, the liver produces moreLp(a) molecules. As the number of Lp(a) moleculesincreases, they tend to deposit on top of existing plaqueformations. When the healing process overshoots, thearteries narrow and the flow of blood is reduced.This problem has a solution. The Lp(a) molecule has afinite number of lysine binding sites - points ofattachment to lysine. Pauling’s invention - the cure forheart disease - is to increase the serum concentration ofthe amino acid lysine enough to make the Lp(a)unattractive. As more lysine enters the blood stream,the probability increases that floating Lp(a) moleculeswill bind with it (rather than with the patches of plaquesgrowing on the arterial walls.)After all the Lp(a) molecule’s binding receptors are filledwith the free lysine floating in the blood, the Lp(a)molecule becomes as harmless as ordinary LDLcholesterol.Pauling and Rath called the substances that treatchronic scurvy and destroy existing plaques Lp(a)binding inhibitors. Vitamin C, to increase collagenproduction and to improve the health and strength ofarteries, and lysine, to prevent and to dissolve Lp(a)plaques, are the primary binding inhibitors. Thesesubstances taken together are clinically effective.Linus Pauling believed that chronic scurvy can beprevented with an orthomolecular daily intake ofbetween 3,000 to 10,000 mg or more vitamin C. Thisamount approximates what the animals synthesize, andmatching animal production is the reason Paulingingested 18,000 mg daily.Pauling and Rath's invention for destroying existingatherosclerotic plaques is the large amount of anotheressential nutrient, the amino acid lysine. Pauling filmeda video lecture in which he recommended that heartpatients take between 2,000 and 6,000 mg of lysinedaily with their vitamin C (more if serum Lp(a) iselevated). Neither vitamin C nor lysine have any knownlethal dose.The Lp(a) binding inhibitors become the PaulingTherapy for heart disease only at high dosages,between vitamin 3 to 18 g ascorbic acid and 3 to 6 glysine. In his video, Pauling recounts the first caseswhere his high vitamin C and lysine therapy quicklyresolved advanced cardiovascular disease in humans.The effect is so pronounced, and the inhibitors are sonontoxic, that Pauling doubted a clinical study was evennecessary. Recently, the amino acid proline was found to be aneven more effective Lp(a) binding inhibitor than lysine invitro. Adding between .5 and 2 g proline may be ofsignificant additional benefit.When serum Lp(a) is elevated, Lp(a) binding inhibitorscan profoundly interfere with the disease process.Binding inhibitor formulas that include proline havebeen documented to lower Lp(a) in six to 14 months. Incases where Lp(a) is not reduced, binding inhibitorsbecome even more important to neutralize Lp(a)regardless of their effect on serum Lp(a).Recently a reevaluation of the Framingham Heart studythat Lp(a) and not ordinary LDL is highly predictive ofCVD and Oxford found that elevated Lp(a) increases therisk of heart attack and stroke by 70%.The on-going lack of scientific curiosity or interest byorganized medicine in the Pauling/Rath theory andPauling's high-dose therapy  may well be recognized asthe greatest lapse of the 20th century.Heart disease orthomolecular protocolNOV 2005: UPDATED PROTOCOL HERETake Vitamin C as ascorbic acid (or sodiumascorbate, but this form may be less effective) up tobowel tolerance (3 to 18 g per day in divideddoses.)The half-life of vitamin C in the bloodstream is 30 minutes. NIH findingsindicate minimum 500 mg every 4 hoursleads to highest sustained blood levels,take more before bed, trips, etc. Troublewith bloating/gas/diarrhea after yourvitamin C? Try Liposomal Vitamin C1.Take Lysine. 2 to 3 g daily for prevention and from3 to 6 g daily for the greatest therapeutic benefit.2.Supplement Coenzyme Q10 (100 - 300 mg) (Note:Vitamin C and several vitamins will help stimulateyour own synthesis of CoQ10. CoQ10 is a vitalsubstance for energy and proper heart function.Popular drugs interfere with your body's ownproduction of CoQ10, and they may lead to heartfailure)3.Take Proline from 250 mg to 2000 mg daily. (Thisadded factor may lower elevated Lp(a) within 6 to14 months.)4.NEW: Eliminate man-made/processed fats,such as trans and hydrogenated fats, andsupplement Omega-3 rich oils. "Research has5. shown that an Omega-3 Index of 8 percent to 10percent reduces a person's relative risk of deathfrom coronary heart disease by 40 percent, andfrom sudden cardiac death by 90 percent." Thisbenefit probably results from restored insulinmediated glucose/vitamin C uptake into cells. [See:Protocol for Reversing Diabetes Type II byEliminating Hydrogenated and Trans Fats andadding Omega-3 oils... ]Note: Following an Atkins-style diet will eliminatemost trans fats because these "poisons" appearmostly in processed carbohydrate foods such ascookies, crackers, snacks, etc. Butter is vastlysupperior to margarine. Natural saturated fats arevastly superior to any fats or oils processed forlonger shelf life.NEW: Eliminate ordinary sugar and refinedcarbohydrates. New research confirms Dr. JohnEly's 30-year theory that sugar (glucose) competeswith ascorbic acid (Vitamin C) for insulin-mediateduptake into cells. Taking sugar can effectivelycrowd out the Ascorbate. The effect of the PaulingTherapy is reportedly much more pronounced andimmediate when sugar is eliminated (and goodOmega-3 fatty acids are added.)6.Follow Paulings general heart and cardiovascularrecommendations provided in his book HOW TOLIVE LONGER AND FEEL BETTER , e.g., Vitamin E -800 to 3200 iu ,Vitamin A - 20,000 to 40,000 iu ,andSuper B-Complex, esp. Vitamins B6 and B37.Supplement the mineral Magnesium (300 to 1500mg) and avoid Manganese (No more than 2 mg.USDA researchers report that elevated manganese,more than 20 mg daily, competes with magnesiumuptake in the heart causing irregular heart beats.)Manganese alters mitochodrial integrity in the hearts of8. swine marginally deficient in magnesium ... These resultssuggest that high Mn, when fed in combination with low Mg,disrupts mitochondrial ultrastructure and is associated withthe sudden deaths previously reported.Eat salt, only unrefined salt, Brownstein discoveredliterature that a low-salt diet can cause the body tochange its hormonal balance as it attempts toretain sodium. This leads to a 400% chance ofheart attack in those with high blood pressure andlow sodium intake [*]. Refined (ordinary table salt)is poisonous, but unrefined salt has over 80minerals and can be considered a necessary"health food."9.Avoid supplemental calcium, and supplementvitamin K for proper calcium metabolism, especiallyif you have taken antibiotics or blood thinners inthe past.10.11.  Add a good mineral/multivitamin   Supplement the amino acids Taurine, Arginine andCarnitine (1 to 3 g).12.Owen Fonorow, NaturopathVitamin C FoundationPO Box 3097, Lisle IL 60532www.VitaminCFoundation.org630-416-1438VitaminCfoundation.orgTheCureForHeartDisease.comPaulingTherapy.comHearttechnology.com