PREVENTION: If you are otherwise healthy with no known genetic pre-disposed risk of heart disease in your family tree, then you would want to consider:
3000 mg/ (1 gram) of vitamin C per day, along with 1000 to 2000 mg of an essential amino acid (L-Lysine) and possibly 500 mg to 1000 mg of a non-essential amino acid (L-Proline)
MILDLY THERAPEUTIC: If you do have heart disease or stroke in your immediate family and in your gene pool (I.E) Mother, father, sister, brother has had a heart attack or stroke or diagnosed with heart disease)
3000 to preferably 6000 mg of Vitamin C each day and 2000 to 3000 mg of L-Lysine along with 1000 mg of L-Proline
THERAPEUTIC: If you yourself have had a heart attack or stroke and/or signs of heart disease then:
6000 mg of Vitamin C (MINIMUM) and up to 8000 mg or more along with 4000 to 5000 mg of L-Lysine and up to 2000 mg of L-Proline.
In addition depending on what site you visit additional nutrients of benefit include Vitamin E, Vitamin D3, CO-enzyme Q10, magnesium Omega 3 fatty acids, and others.
I am currently on 8000 to 10,000 mg of vitamin C (From a product called C-salts / SEE my other posts of types of vitamin C), I also take 4000 to 5000 mg of L-Lysine either by tablet form along with 1000 mg of L-Proline. (I usually also drink a WHEY protein shake every day which contains all the amino acids and the one I use has apprx 1600 mg of L-Lysine and 1100 mg of L-Proline)
(There are cautions on different sites and in my many blog posts of this subject of NOT jumping into mega doeses of vitamin C if you are on some sort of blood thinner.) Blood thinners would be considered coumadin, plavix, even 81 mg aspirin a day therapy, and could include (BUT NOT LIMITED TO) warfarin, heparin, lovenox, fragmin, eliquis, pradaxa, xarelto.
ANOTHER CAUTION is too much Vitamin K from otherwise healthy GREEN SMOOTHIES , green leafy vegetables etc.
PLEASE consult with your doctor, cardiologist, or naturopath etc. BEFORE TAKING HIGH DOESES OF VITAMIN C IF ON ANY SORT OF BLOOD THINNER REGIMEN.
Following is a LINK with more detailed information on Vitamin C and Dr. Pauling's recommendations:
http://drculik.blogspot.com/2008/07/vitamin-c-for-heart-disease-per-linus.html
EXCERPT:
Vitamin C for Heart Disease per Linus Pauling
THE BASIC ORTHOMOLECULAR RECOMMENDATIONS FOR CONTROLLING HEART DISEASE By Owen R Fonorow, Naturopath
Linus Pauling specifically recommended high oral doses of vitamin C and the amino acid lysine.
Other elements in the following Pauling Therapy protocol, ordered by importance, account for many variables. These recommendations are based on the experience of more than a decade recommending Pauling's protocol, and they feature Pauling's earlier advice published in 1986. This protocol is designed to help overcome a poor diet, advancing age, or the use of prescription drugs commonly given to heart patients.
PROTOCOL
Cardiologist have been kept in the dark about the vitamin C connection. Few cardiovascular drugs benefit heart patients. Several exacerbate heart conditions and should be eliminated in favor of the following othomolecular protocols:
1. Take Vitamin C as ascorbic acid (or sodium ascorbate, but this form may be less effective) up to bowel tolerance (6 to 18 g per day in divided doses.)
The half-life of vitamin C in the blood stream is 30 minutes. NIH findings indicate that a minimum of 500 mg every 4 hours leads to highest sustained blood levels. Take more before bed, trips, etc. Trouble with bloating/gas/diarrhea after your vitamin C? Try Liposomal Vitamin C
2. Take Lysine 3000 to 6000 mg (3 to 6 g) daily for the maximum therapeutic value. Take 2000 to 3000 mg (2 to 3 g) daily for prevention.
3. Supplement Coenzyme Q10 (100 - 300 mg)
Note: Vitamin C and several vitamins will help stimulate your own synthesis of CoQ10. CoQ10 is a vital substance for energy and proper heart function. Popular drugs interfere with your body's own production of CoQ10, and they may lead to heart failure.
4. NEW: Eliminate man-made/processed fats, such as trans fats and hydrogenated oils. Supplement Omega-3 rich oils, e.g. evening primrose, flaxseed, and certain fish oils.
"Research has shown that an Omega-3 Index of 8 percent to 10 percent reduces a person's relative risk of death from coronary heart disease by 40 percent, and from sudden cardiac death by 90 percent." This benefit probably results from restored insulin-mediated glucose/vitamin C uptake into cells. [See: Protocol for Reversing Diabetes Type II by Eliminating Hydrogenated and Trans Fats and adding Omega-3 oils... ]
Note: Following an Atkins-style diet will eliminate most trans fats because these "poisons" appear mostly in processed carbohydrate foods such as cookies, crackers, snacks, etc. Butter is vastly supperior to margarine. Natural saturated fats are superior to any fats or oils processed for longer shelf life.
5. Take the amino acid proline from 250 mg to 2000 mg daily.
This factor, added to Pauling's original protocol, and recommended by Mathias Rath, may lower elevated Lp(a) within 6 to 14 months. It is difficult to suggest an optimum dose for everyone because the healthy body can manufacture its own proline. A few alternative doctors recommend 2 g (2000 mg), but the Tower HeartTechnology formula has produced consistent good results. It can apparently lower Lp(a) with smaller dosages of proline.
6. Follow Linus Pauling's heart and cardiovascular recommendations as provided in his book 1986 HOW TO LIVE LONGER AND FEEL BETTER
Linus Pauling's Basic Vitamin Advice is Centered on Vitamin C, and adds: Natural Vitamin E - 800 iu (to 3200 iu) Gamma Tocopherol
Per Doctor Sinatra's Miracle of CoQ10 book, an epidemiological WHO study found that low vitamin E is highly predictive of heart attack. Their findings were that heart attack is 70% more likely when serum levels of vitamin E are low, than because of either high blood pressure or high cholesterol.
Vitamin A - 20,000 to 40,000 iu
Super B-Complex
Daily Multiple Vitamin/Mineral
Low Sugar
Plenty of Water NEW: Eat salt, but only unrefined salt,
Brownstein discovered literature that a low-salt diet can cause the body to change its hormonal balance as it attempts to retain sodium. This leads to a 400% chance of heart attack in those with high blood pressure and low sodium intake [*]. Refined (ordinary table salt) is poisonous, but unrefined salt has over 80 minerals and can be considered a necessary "health food."
7. Supplement Magnesium (150 to 1500 mg) Certain chelated forms are better absorbed and you need less.
8. Reduce supplemental Manganese (no more than 2 mg).(More than 20 mg daily can lead to irregular heart beats according to the USDA)
Manganese alters mitochondrial integrity in the hearts of swine marginally deficient in magnesium ... These results suggest that high Mn, when fed in combination with low Mg, disrupts mitochondrial ultrastructure and is associated with the sudden deaths previously reported.
9. NEW: Eliminate ordinary sugar and refined carbohydrates.
New research confirms Dr. John Ely's 30-year theory that sugar (glucose) competes with ascorbic acid (Vitamin C) for insulin-mediated uptake into cells. Consuming too much sugar and refined carbs can effectively crowd out Vitamin C.
10. Supplement Vitamin K (1 to 40 mg) to help regulate calcium from soft tissues into bones
Note: Prescription blood "thinning" drugs such as Warfarin and Coumadin interfere with vitamin K. These drugs should never be prescribed for heart patients. They have been proven to cause rapid calcification of soft tissues in animal studies [*] and there is evidence that they cause hard arteries in humans. Unfortunately, these drugs are routinely prescribed. Patients on "rat poison" style blood thinners should avoid vitamin K until they find a nutritionally oriented physician to help wean them. Blood thinner substitutes to the prescription drugs include: 2000 IU Unique-E (from A. C. Grace), arginine (3000 mg), grape seed extract, fish (Omega-3) oils, etc.
11. Avoid supplemental calcium
12. Add a good mineral/multivitamin
13 Supplement the amino acids Taurine, Arginine and Carnitine (1 to 3 g).
The Cure for Heart Disease: Condensed By Owen R. Fonorow
Cardiovascular Diseases Those few species that fail to synthesize ascorbic acid (vitamin C) are prone to a form of ?heart disease? that is not prevalent in other species. The theory that Cardiovascular Disease (CVD) is related to a deficiency of vitamin C was first proposed by the Canadian physician G. C. Willis in 1953. He found that atherosclerotic plaques form over vitamin-C-starved vascular tissues in both guinea pigs and human beings. In 1989, after the discoveries of the Lp(a) cholesterol molecule (circa 1964) and its lysine binding sites (circa 1987), Linus Pauling and his associate Matthias Rath formulated a unified theory of heart disease and invented a cure. Vitamin C and lysine (and proline) in large amounts become Lp(a) binding inhibitors that restore vascular health and are patented to destroy atherosclerotic plaques.
Chronic scurvy. Heart disease is a misnomer; the underlying disease process reduces the supply of blood to the heart and other organs leading to angina ("heart cramp"), heart attack and stroke. The disease is characterized by scab-like build-ups that grow on the walls of blood vessels. The correct terminology for this disease process is chronic scurvy, a slower form of the classic vitamin C deficiency disease.
The hypothesis that CVD is an ascorbic acid (vitamin C) deficiency disease was first conceived and tested in Canada. Willis devised a method of photographing plaques with X-rays and observed that atherosclerotic plaques were not uniformly distributed throughout the vascular system; rather these "blockages" are concentrated near the heart, where arteries are constantly bent or squeezed.
Another Canadian, Paterson, had found that the tissues of heart patients were generally depleted of vitamin C, and it was well known that vitamin C is required for strong and healthy arteries. Willis reasoned that only the mechanical stress caused by the pulse could explain the typical pattern of atherosclerosis. To Willis, the body was laying down plaque precisely where it was needed in order to stabilize the vascular system.
By the late 1980s, medical researchers had made several intriguing discoveries.
First came the discovery that heart disease begins with a lesion, a crack or stress fracture, in the arterial wall. The question became, and remains, as to the cause of these lesions in human beings since they do not arise in most other animals. Then a variant of the so-called "bad" LDL cholesterol called lipoprotein(a), or Lp(a) for short, was studied and found to be really bad. Lp(a) is sticky because of receptors on the surface of the molecule called lysine binding sites. Work that led to the 1987 Nobel prize in medicine discovered that lysine (and proline) binding sites cause the formation of atherosclerotic plaques. Then, Beisiegel et. al. in Germany examined plaques post mortem and found only Lp(a), not ordinary LDL cholesterol.
Lp(a) was the genetic difference between beings that suffer cardiovascular disease and those that do not. Lp(a) had evolved only in species that do not make their own vitamin C - e.g. humans and guinea pigs.
Pauling and Rath repeated the earlier Willis experiments, but this time they monitored Lp(a). They discovered that it becomes elevated in guinea pigs deprived of vitamin C, but not in the controls. These experiments connected elevated-Lp(a) with low serum vitamin C. They realized that in most species, sufficient ascorbic acid will prevent stress fractures, but in those species that suffer chronic scurvy, Lp(a) had evolved to patch cracked blood vessels.
As chronic scurvy progresses, the liver produces more Lp(a) molecules. As the number of Lp(a) molecules increases, they tend to deposit on top of existing plaque formations. When the healing process overshoots, the arteries narrow and the flow of blood is reduced.
This problem has a solution. The Lp(a) molecule has a finite number of lysine binding sites - points of attachment to lysine. Pauling?s invention - the cure for heart disease - is to increase the serum concentration of the amino acid lysine enough to make the Lp(a) unattractive. As more lysine enters the blood stream, the probability increases that floating Lp(a) molecules will bind with it (rather than with the patches of plaques growing on the arterial walls.)
After all the Lp(a) molecule?s binding receptors are filled with the free lysine floating in the blood, the Lp(a) molecule becomes as harmless as ordinary LDL cholesterol.
Pauling and Rath called the substances that treat chronic scurvy and destroy existing plaques Lp(a) binding inhibitors. Vitamin C, to increase collagen production and to improve the health and strength of arteries, and lysine, to prevent and to dissolve Lp(a) plaques, are the primary binding inhibitors. These substances taken together are clinically effective.
Linus Pauling believed that chronic scurvy can be prevented with an orthomolecular daily intake of between 3,000 to 10,000 mg or more vitamin C. This amount approximates what the animals synthesize, and matching animal production is the reason Pauling ingested 18,000 mg daily.
Pauling and Rath's invention for destroying existing atherosclerotic plaques is the large amount of another essential nutrient, the amino acid lysine. Pauling filmed a video lecture in which he recommended that heart patients take between 2,000 and 6,000 mg of lysine daily with their vitamin C (more if serum Lp(a) is elevated). Neither vitamin C nor lysine have any known lethal dose.
The Lp(a) binding inhibitors become the Pauling Therapy for heart disease only at high dosages, between vitamin 3 to 18 g ascorbic acid and 3 to 6 g lysine. In his video, Pauling recounts the first cases where his high vitamin C and lysine therapy quickly resolved advanced cardiovascular disease in humans. The effect is so pronounced, and the inhibitors are so nontoxic, that Pauling doubted a clinical study was even necessary.
Recently, the amino acid proline was found to be an even more effective Lp(a) binding inhibitor than lysine in vitro. Adding between .5 and 2 g proline may be of significant additional benefit.
When serum Lp(a) is elevated, Lp(a) binding inhibitors can profoundly interfere with the disease process. Binding inhibitor formulas that include proline have been documented to lower Lp(a) in six to 14 months. In cases where Lp(a) is not reduced, binding inhibitors become even more important to neutralize Lp(a) regardless of their effect on serum Lp(a).
Recently a reevaluation of the Framingham Heart study that Lp(a) and not ordinary LDL is highly predictive of CVD and Oxford found that elevated Lp(a) increases the risk of heart attack and stroke by 70%.
The on-going lack of scientific curiosity or interest by organized medicine in the Pauling/Rath theory and Pauling's high-dose therapy may well be recognized as the greatest lapse of the 20th century.
Linus Pauling specifically recommended high oral doses of vitamin C and the amino acid lysine.
Other elements in the following Pauling Therapy protocol, ordered by importance, account for many variables. These recommendations are based on the experience of more than a decade recommending Pauling's protocol, and they feature Pauling's earlier advice published in 1986. This protocol is designed to help overcome a poor diet, advancing age, or the use of prescription drugs commonly given to heart patients.
PROTOCOL
Cardiologist have been kept in the dark about the vitamin C connection. Few cardiovascular drugs benefit heart patients. Several exacerbate heart conditions and should be eliminated in favor of the following othomolecular protocols:
1. Take Vitamin C as ascorbic acid (or sodium ascorbate, but this form may be less effective) up to bowel tolerance (6 to 18 g per day in divided doses.)
The half-life of vitamin C in the blood stream is 30 minutes. NIH findings indicate that a minimum of 500 mg every 4 hours leads to highest sustained blood levels. Take more before bed, trips, etc. Trouble with bloating/gas/diarrhea after your vitamin C? Try Liposomal Vitamin C
2. Take Lysine 3000 to 6000 mg (3 to 6 g) daily for the maximum therapeutic value. Take 2000 to 3000 mg (2 to 3 g) daily for prevention.
3. Supplement Coenzyme Q10 (100 - 300 mg)
Note: Vitamin C and several vitamins will help stimulate your own synthesis of CoQ10. CoQ10 is a vital substance for energy and proper heart function. Popular drugs interfere with your body's own production of CoQ10, and they may lead to heart failure.
4. NEW: Eliminate man-made/processed fats, such as trans fats and hydrogenated oils. Supplement Omega-3 rich oils, e.g. evening primrose, flaxseed, and certain fish oils.
"Research has shown that an Omega-3 Index of 8 percent to 10 percent reduces a person's relative risk of death from coronary heart disease by 40 percent, and from sudden cardiac death by 90 percent." This benefit probably results from restored insulin-mediated glucose/vitamin C uptake into cells. [See: Protocol for Reversing Diabetes Type II by Eliminating Hydrogenated and Trans Fats and adding Omega-3 oils... ]
Note: Following an Atkins-style diet will eliminate most trans fats because these "poisons" appear mostly in processed carbohydrate foods such as cookies, crackers, snacks, etc. Butter is vastly supperior to margarine. Natural saturated fats are superior to any fats or oils processed for longer shelf life.
5. Take the amino acid proline from 250 mg to 2000 mg daily.
This factor, added to Pauling's original protocol, and recommended by Mathias Rath, may lower elevated Lp(a) within 6 to 14 months. It is difficult to suggest an optimum dose for everyone because the healthy body can manufacture its own proline. A few alternative doctors recommend 2 g (2000 mg), but the Tower HeartTechnology formula has produced consistent good results. It can apparently lower Lp(a) with smaller dosages of proline.
6. Follow Linus Pauling's heart and cardiovascular recommendations as provided in his book 1986 HOW TO LIVE LONGER AND FEEL BETTER
Linus Pauling's Basic Vitamin Advice is Centered on Vitamin C, and adds: Natural Vitamin E - 800 iu (to 3200 iu) Gamma Tocopherol
Per Doctor Sinatra's Miracle of CoQ10 book, an epidemiological WHO study found that low vitamin E is highly predictive of heart attack. Their findings were that heart attack is 70% more likely when serum levels of vitamin E are low, than because of either high blood pressure or high cholesterol.
Vitamin A - 20,000 to 40,000 iu
Super B-Complex
Daily Multiple Vitamin/Mineral
Low Sugar
Plenty of Water NEW: Eat salt, but only unrefined salt,
Brownstein discovered literature that a low-salt diet can cause the body to change its hormonal balance as it attempts to retain sodium. This leads to a 400% chance of heart attack in those with high blood pressure and low sodium intake [*]. Refined (ordinary table salt) is poisonous, but unrefined salt has over 80 minerals and can be considered a necessary "health food."
7. Supplement Magnesium (150 to 1500 mg) Certain chelated forms are better absorbed and you need less.
8. Reduce supplemental Manganese (no more than 2 mg).(More than 20 mg daily can lead to irregular heart beats according to the USDA)
Manganese alters mitochondrial integrity in the hearts of swine marginally deficient in magnesium ... These results suggest that high Mn, when fed in combination with low Mg, disrupts mitochondrial ultrastructure and is associated with the sudden deaths previously reported.
9. NEW: Eliminate ordinary sugar and refined carbohydrates.
New research confirms Dr. John Ely's 30-year theory that sugar (glucose) competes with ascorbic acid (Vitamin C) for insulin-mediated uptake into cells. Consuming too much sugar and refined carbs can effectively crowd out Vitamin C.
10. Supplement Vitamin K (1 to 40 mg) to help regulate calcium from soft tissues into bones
Note: Prescription blood "thinning" drugs such as Warfarin and Coumadin interfere with vitamin K. These drugs should never be prescribed for heart patients. They have been proven to cause rapid calcification of soft tissues in animal studies [*] and there is evidence that they cause hard arteries in humans. Unfortunately, these drugs are routinely prescribed. Patients on "rat poison" style blood thinners should avoid vitamin K until they find a nutritionally oriented physician to help wean them. Blood thinner substitutes to the prescription drugs include: 2000 IU Unique-E (from A. C. Grace), arginine (3000 mg), grape seed extract, fish (Omega-3) oils, etc.
11. Avoid supplemental calcium
12. Add a good mineral/multivitamin
13 Supplement the amino acids Taurine, Arginine and Carnitine (1 to 3 g).
The Cure for Heart Disease: Condensed By Owen R. Fonorow
Cardiovascular Diseases Those few species that fail to synthesize ascorbic acid (vitamin C) are prone to a form of ?heart disease? that is not prevalent in other species. The theory that Cardiovascular Disease (CVD) is related to a deficiency of vitamin C was first proposed by the Canadian physician G. C. Willis in 1953. He found that atherosclerotic plaques form over vitamin-C-starved vascular tissues in both guinea pigs and human beings. In 1989, after the discoveries of the Lp(a) cholesterol molecule (circa 1964) and its lysine binding sites (circa 1987), Linus Pauling and his associate Matthias Rath formulated a unified theory of heart disease and invented a cure. Vitamin C and lysine (and proline) in large amounts become Lp(a) binding inhibitors that restore vascular health and are patented to destroy atherosclerotic plaques.
Chronic scurvy. Heart disease is a misnomer; the underlying disease process reduces the supply of blood to the heart and other organs leading to angina ("heart cramp"), heart attack and stroke. The disease is characterized by scab-like build-ups that grow on the walls of blood vessels. The correct terminology for this disease process is chronic scurvy, a slower form of the classic vitamin C deficiency disease.
The hypothesis that CVD is an ascorbic acid (vitamin C) deficiency disease was first conceived and tested in Canada. Willis devised a method of photographing plaques with X-rays and observed that atherosclerotic plaques were not uniformly distributed throughout the vascular system; rather these "blockages" are concentrated near the heart, where arteries are constantly bent or squeezed.
Another Canadian, Paterson, had found that the tissues of heart patients were generally depleted of vitamin C, and it was well known that vitamin C is required for strong and healthy arteries. Willis reasoned that only the mechanical stress caused by the pulse could explain the typical pattern of atherosclerosis. To Willis, the body was laying down plaque precisely where it was needed in order to stabilize the vascular system.
By the late 1980s, medical researchers had made several intriguing discoveries.
First came the discovery that heart disease begins with a lesion, a crack or stress fracture, in the arterial wall. The question became, and remains, as to the cause of these lesions in human beings since they do not arise in most other animals. Then a variant of the so-called "bad" LDL cholesterol called lipoprotein(a), or Lp(a) for short, was studied and found to be really bad. Lp(a) is sticky because of receptors on the surface of the molecule called lysine binding sites. Work that led to the 1987 Nobel prize in medicine discovered that lysine (and proline) binding sites cause the formation of atherosclerotic plaques. Then, Beisiegel et. al. in Germany examined plaques post mortem and found only Lp(a), not ordinary LDL cholesterol.
Lp(a) was the genetic difference between beings that suffer cardiovascular disease and those that do not. Lp(a) had evolved only in species that do not make their own vitamin C - e.g. humans and guinea pigs.
Pauling and Rath repeated the earlier Willis experiments, but this time they monitored Lp(a). They discovered that it becomes elevated in guinea pigs deprived of vitamin C, but not in the controls. These experiments connected elevated-Lp(a) with low serum vitamin C. They realized that in most species, sufficient ascorbic acid will prevent stress fractures, but in those species that suffer chronic scurvy, Lp(a) had evolved to patch cracked blood vessels.
As chronic scurvy progresses, the liver produces more Lp(a) molecules. As the number of Lp(a) molecules increases, they tend to deposit on top of existing plaque formations. When the healing process overshoots, the arteries narrow and the flow of blood is reduced.
This problem has a solution. The Lp(a) molecule has a finite number of lysine binding sites - points of attachment to lysine. Pauling?s invention - the cure for heart disease - is to increase the serum concentration of the amino acid lysine enough to make the Lp(a) unattractive. As more lysine enters the blood stream, the probability increases that floating Lp(a) molecules will bind with it (rather than with the patches of plaques growing on the arterial walls.)
After all the Lp(a) molecule?s binding receptors are filled with the free lysine floating in the blood, the Lp(a) molecule becomes as harmless as ordinary LDL cholesterol.
Pauling and Rath called the substances that treat chronic scurvy and destroy existing plaques Lp(a) binding inhibitors. Vitamin C, to increase collagen production and to improve the health and strength of arteries, and lysine, to prevent and to dissolve Lp(a) plaques, are the primary binding inhibitors. These substances taken together are clinically effective.
Linus Pauling believed that chronic scurvy can be prevented with an orthomolecular daily intake of between 3,000 to 10,000 mg or more vitamin C. This amount approximates what the animals synthesize, and matching animal production is the reason Pauling ingested 18,000 mg daily.
Pauling and Rath's invention for destroying existing atherosclerotic plaques is the large amount of another essential nutrient, the amino acid lysine. Pauling filmed a video lecture in which he recommended that heart patients take between 2,000 and 6,000 mg of lysine daily with their vitamin C (more if serum Lp(a) is elevated). Neither vitamin C nor lysine have any known lethal dose.
The Lp(a) binding inhibitors become the Pauling Therapy for heart disease only at high dosages, between vitamin 3 to 18 g ascorbic acid and 3 to 6 g lysine. In his video, Pauling recounts the first cases where his high vitamin C and lysine therapy quickly resolved advanced cardiovascular disease in humans. The effect is so pronounced, and the inhibitors are so nontoxic, that Pauling doubted a clinical study was even necessary.
Recently, the amino acid proline was found to be an even more effective Lp(a) binding inhibitor than lysine in vitro. Adding between .5 and 2 g proline may be of significant additional benefit.
When serum Lp(a) is elevated, Lp(a) binding inhibitors can profoundly interfere with the disease process. Binding inhibitor formulas that include proline have been documented to lower Lp(a) in six to 14 months. In cases where Lp(a) is not reduced, binding inhibitors become even more important to neutralize Lp(a) regardless of their effect on serum Lp(a).
Recently a reevaluation of the Framingham Heart study that Lp(a) and not ordinary LDL is highly predictive of CVD and Oxford found that elevated Lp(a) increases the risk of heart attack and stroke by 70%.
The on-going lack of scientific curiosity or interest by organized medicine in the Pauling/Rath theory and Pauling's high-dose therapy may well be recognized as the greatest lapse of the 20th century.
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