David L. Hoffmann B.Sc. (Hons), M.N.I.M.H.
(A generic term for a number of diseases in which the arterial wall becomes thickened and loses elasticity).
The term arteriosclerosis refers to several diseases that involve both arteries of different sizes and different layers of the walls of the arteries. From Greek words that mean “hardening of the arteries, ” the term originally signified the tendency of arteries to become hard and brittle through the depositing of calcium in their walls. This is not, however, an important characteristic of the most familiar form of arteriosclerosis, called atherosclerosis.
Although herbs exist that may be anti-arteriosclerotic, the phytotherapist aims at preventing the disease by treating the causative factors, which include not only hypertension but also diabetes mellitus, smoking, and obesity.
Atherosclerosis is a disease of the arteries characterized by fatty deposits on the intimal, or inner, lining. The presence of fatty deposits, called plaques, leads to an important loss of arterial elasticity with narrowing of the artery. This constriction to smooth blood-flow ultimately deprives vital organs of their blood supply. Clots may lodge in arteries supplying the heart, causing myocardial infarction (heart attack), or the brain, causing stroke. Atherosclerosis may be manifested fairly rapidly in diseases in which the concentration of blood fats (lipids) is raised, as in diabetes.
Half the annual mortality in Western society results from heart and blood-vessel diseases of which atherosclerosis, the most common lethal disease, is the chief cause. This is because of the resultant impact upon the brain, heart, kidneys and other organs of the body. A number of biochemical, physiological and environmental risk factors have been identified that increase the chances of an individual to developing arteriosclerosis.
**hypertension. High blood pressure is critical in the atherosclerotic process, which does not normally occur in the low-pressure pulmonary arteries and veins, despite their being bathed by the same blood concentration of lipids.
**elevated serum lipid levels. The atherogenicity of cholesterol is influenced by the type of lipoproteins, of which there are four that transport it in the blood. The low-density lipoproteins are clearly atherogenic, but the high-density lipoproteins appear to prevent accumulation of cholesterol in the tissues
**obesity promotes all the risk factors,
**cigarette smoking increases the chances of developing this disease as well as many others.
*****diets rich in polyunsaturated oils, hydrogenated or partially hydrogenated oils, and calories appear to be chiefly responsible for high blood cholesterol, and such diets are therefore believed to promote atherosclerosis. THIS IS BECAUSE CHOLESTEROL IS A WARNING SIGN. Cholesterol itself is NOT the problem. The PROBLEMS are the aforementioned risk factors that cause stress to various areas of the body, and in response to those stresses our bodies produce CHOLESTEROL to help repair the stress areas. Therefore, as you can see, CHOLESTEROL is our friend and not to be feared.
a family history of premature atherosclerotic disease appears to indicate either a propensity to higher levels of the risk factors for atherosclerosis or an increased susceptibility to them. Inborn errors in lipid metabolisms also increase susceptibility.
diabetes mellitus is one disease that may lead to arteriosclerosis.
sex. Between the ages of 35 to 44 the death rate from coronary heart disease among white men is 6.1 times that amongst white women. This is thought to be due to hormonal influences. Overt manifestations are rare in either sex before the age of 40 because more than a 75 percent narrowing of the arteries must occur before blood flow is seriously impeded.
aging brings about degenerative arterial changes such as dilatation, tortuosity, thickening and loss of elasticity.
physical inactivity increases the chances of complications developing, but the disease effects both the active and sedentary.
personality type, especially type A (discussed elsewhere) appear to predispose individuals to a range of C-V problems.
lifestyle considerations can contribute depending upon diet, stress levels etc.
There is no doubt that, in most cases, atherosclerosis is a disease directly related to diet and lifestyle. Treatment and prevention include reducing all known risk factors. For many patients, this goal requires a major change in diet and lifestyle. Since so many factors are known to be involved in atherosclerosis, any treatment plan must be individualized to assure optimal results.
According to the American Heart Association:
Nearly 59 million Americans have a form of Cardiovascular disease
Over 100 million Americans are at risk
Every 34 seconds an American dies of Cardiovascular disease
a. Genetic pre-disposition.
b. Diets high in refined carbohydrates (starches, grains an alist sugars), excessive alcohol and caffeine.
c. Endocrine dysfunction (thyroid hypo-function most common).
d. Diabetes or carbohydrate sensitivity resulting in dysinsulinism.
e. High serum Homocystine levels (need for vitamin B6, B12, betaine, and/or folic acid).
f. Serum Lipoprotein(a) levels greater than 10 mg/dl. 11-24 mg/dl are borderline high; >25 mg/dl are very high. If your Lp (a) levels are over 10, you need to take action at once.
a. Eliminate all refined carbohydrates, dairy products (except butter), gluten containing grains, caffeine containing foods such as coffee, (except tea), chocolate and colas and alcohol.
b. Eliminate all hydrogenated fats and oils. use only extra virgin olive oil, fish oils and coconut oil as your only sources of oils.
c. Increase quality protein via sea vegetables and fresh fruits and fish.
d. Sip 1 mouthful of distilled or filtered water every 30 minutes while awake.
e. Eliminate canned food, frozen food and all processed food.
f. Reduce the overall amount of food usually eaten by 40%. Make sure you pick up the difference with a lot of organically frown fresh fruits and vegetables.
1. BIO-MULTI PLUS Iron Free – 1 tablet, 3 times daily after meals.
2. BIO-C PLUS 1000 – 1 tablet, 4 times daily after meals and at bedtime.
3. M S M POWDER – 1/2 teaspoonful 2 to 4 times daily depending on the severity of symptoms. NOTE: Try to take MSM with your Vitamin C.
4. BIOMEGA-3 – 5 capsules, twice daily after meals.
5. E-MULSION 200 – 2 capsules, once daily after a meal.
6. COQ-ZYME FORTE – 2 tablets, once daily after a meal.
Specific Nutrients: When symptoms or condition begins to subside, gradually, as needed, wean yourself from the Specific Nutrients & stay on the Primary Nutrients. If any symptoms re-occur resume taking Specific Nutrients.
7. L-CARNITINE – 2 capsules, 3 times daily after meals.
8. PURIFIED CHONDROITIN SULFATE – 4 tablets, once daily after a meal.
9. LIPOIC ACID – 2 capsules, twice daily after meals to stabilize blood sugar
If serum Homocystine levels are elevated, then take:
10. B12 LOZENGES – One tablet, once daily after a meal.
11. B6 PHOSPHATE – 2 tablets, twice daily after meals.
If Atherosclerosis is severe but your arteries still have sufficient blood flow, then use Linus Pauling’s protocto tC/A> for the Heart:
12. BIO-C PLUS 1000 – 1 tablet, 4 times daily after meals and at bedtime with L-Lysine.
13. L-LYSINE – 2 capsules, 4 times daily after meals and at bedtime with Bio-C Plus 1000.
Pauling’s and Rath’s protocol is used for 6 months and then your condition should be reevaluated. It usually takes, according to their research, about 6 months to stabilize the artery wall and another 6 months to reverse the atherosclerotic plaque process.
Thus, with this program, those patients with early coronary heart disease, healing of the artery wall can lead to complete removal of atherosclerotic deposits. In patients with advanced coronary artery disease, this program can stabilize the artery walls, halt further growth of coronary deposits, and reverse them, at least in part; thus contributing to the prevention of heart attacks.
The latest information on:
SPECIFIC ANTI-ATHEROSCLEROSIS NUTRIENTS — A Summary
1. MAGNESIUM – 300mg, twice daily after meals. Low tissue magnesium causes atherosclerosis.
2. VITAMIN C, L-LYSINE, PROLINE – 1 gram of each 3 times daily after meals for Lp(a) over 10.
3. ZINC – 50 mg daily after a meal. Along with Vitamin C stabilizes the fibrous cap on soft plaque to prevent plaque from loosening.
4. QUERCETIN – 500mg twice daily after meals as an anti-inflammatory.
5. PURIFIED CHONDROITIN SULFATE – 1 gram, 3 times daily after meals to repair the artery walls.
6. FISH OILS (Omega-3 Oils) – 6 grams, twice daily after meals improves all lipid profiles & reverses plaque.
7. VITAMIN B12 – 2000mcg; FOLIC ACID – 800 mcg;
VITAMIN B6 – 25 mg — daily for Homocysteine over 8.
8. AGED GARLIC EXTRACT – 600mg, twice daily to actually reverse atherosclerosis; thins the blood; antiviral & antibacterial.
9. POLICOSANOL – 20 mg daily to raise HDL & lower triglycerides & LDL; reduces inflammation of blood vessels.
10. L-ARGININE – 3000 mg twice daily on empty stomach. Reduces plaque; improves blood flow (nitric oxide precursor); forms new blood vessels (angiogenesis).
11. VITAMIN K DROPS – 10 drops, 3 times daily as a nutrient to repair the arteries.
12. NIACIN – 500 mg, twice daily after meals; reduces LDL; strong vasodilator. Begin with small doses the increase to 500mg twice daily. You may have some flushing at first.
13. WHITE TEA – 1 cupful, twice daily to reduce blood vessel inflammation & stabilize the fibrous cap on the plaque.
14. CA EDTA CHELATION – 300mg IV once weekly for 12 weeks, rest 1 month, then repeat twice more.
ALSO, Raspberries, Walnuts, Pomegranates — these foods are full of Ellagic Acid, a flavonoid which reduces atherosclerosis.
The ideal Cholesterol/HDL ratio should be lower than 4.0 and generally speaking the lower the better.
remain on the Specific Nutrients program for 2 to 3 months and have your condition reevaluated by your physician. If need be then continue for another 2 months before your next evaluation. As your condition improves you can begin eliminating the Specific Nutrients until you remain on only the Primary Nutrients.
ALSO SEE: CHOLESTEROL
Preempting Another Heart Attack
When Henry was referred to us by his physician for thermographic imaging, he had already undergone two coronary bypass surgeries to relieve his angina, or heart pain. The first bypass lasted six years, the second wore out after barely two years. Tests showed that Henry’s coronary arteries were blheald again, despite the successive bypasses. This did not surprise us at all.
Bypass surgery for heart disease accelerates the heart disease process. The cause of ATHEROSCLEROSIS is NOT high cholesterol. It is usually a response to an injury, such as oxidative stress from free radicals. This means toxins in the blood (free radicals), derived both from inappropriate food choices and the normal results of metabolism, cause injury and functional havoc (oxidative stress) in the body’s cells and tissues.
The process of ATHEROSCLEROSIS has two parts. First there is the actual scarring of the artery (from oxidative stress and free radical damage) as it thickens with fibrous and fatty tissue lesions. Second, a matrix of calcium and oxidized cholesterol, known as plaque, forms over this lesion.
Slicing into an artery with a scalpel to graft on a new piece causes great irritation and damage to the artery; the bypass surgery itself creates the site for the next accelerated emergence of ATHEROSCLEROSIS. Angioplasty, which involves the inflation of a miniscule balloon within an artery to mechanically widen it, also imparts stress, damage, and local irritation to the linings of the arteries and can similarly start an atherosclerotic process.
As an artery’s ability to handle blood flow volume diminishes, more scarring and damage to its membranes result, and the risk of an acute blood clotting episode increases. It is the clotting of platelets (red blood cells) that causes a stroke or heart attack.
This is why conventional medicine prescribes aspirin or Coumadin: both thin the blood and inhibit clotting. Aspirin, for example, takes a heart disease patient away from the knife-edge of attack or stroke but should be used only as a short-term palliative. Henry took aspirin for a while to give the chelation therapy (see below) more of an opportunity to work; then he discontinued it except for relief from the occasional headache.
Bear in mind, the entire body is highly traumatized by open-heart surgery; you are put under deep anesthesia and practically split open like a melon. This procedure?it’s considerably stressful, painful, debilitating, and exceptionally expensive?requires a long recovery and generally cannot be repeated more than twice without enormous risk and because you have likely run out of suitable blood vessels to graft.
Bypass surgery does absolutely nothing to change the course of the disease. This type of highly invasive surgery provides only a temporary mechanical improvement in blood flow. Unless the patient radically changes his lifestyle and diet and undertakes targeted nutritional supplementation and chelation detoxification, the arteries will quickly clog up again, as did Henry’s.
BYPASS SURGERY AND ANGIOPLASTY DON?T EXTEND LIFE
His heart pain had returned and he was ready for an alternative approach. Henry had a moderate degree of thickening in the left carotid artery, the major blood supplier to the head. Thermographic imaging showed us that blood circulation into Henry’s head was already diminished; we also discovered he had extensive ATHEROSCLEROSIS in both legs.
Based on our analysis and the clinical information, Henry’s physician recommended that he undergo chelation therapy to detoxify his system and improve his blood circulation. Henry had 45 chelation infusions at the rate of two per week. He also made some changes in his diet and lifestyle: he exercised more, ate more fresh organically raised vegetables and fruits, reduced his meat and salt consumption, and stopped smoking. Generally, a low-fat, high? complex carbohydrate diet with limited amounts of chicken and fish is advisable here. I also suggested that Henry take high doses of vitamin C (5 grams daily in divided doses). Folic acid and vitamin B12 are also helpers in rebuilding arteries.
The treatment goal was twofold: first, quit damaging the arteries and allow them to heal naturally; and second, provide the arteries with proper nutrition to rebuild themselves. With this approach, we have been able to help people defy the usual model of heart attack/die or stroke/become a vegetable by doing nothing more than what should be the state of the art for cardiovascular treatment.
When we examined Henry after the treatment, he reported that his angina had disappeared; in fact, he said it had abated after only ten chelations. Thermographic imaging documented that there was a marked improvement in blood circulation through the left carotid artery; this result also confirmed the success of the chelation therapy. His arterial restriction was reduced from 80% to less than 20%.
Anything less than 20% restriction is considered minimal and therefore non-problematic. Technically, you can find traces of ATHEROSCLEROSIS in nearly anybody. The rate and extent to which it df thops (if at all) and the arterial systems it affects is highly variable among individuals. What’s dangerous about ATHEROSCLEROSIS is that it rarely gives a warning. You may not know you are at risk for a mild heart attack or mini-stroke until it happens. Many people don’t get even this warning. They go from feeling fine to suddenly sustaining a major stroke or heart attack.
Thermography can prevent this atherosclerotic ambush. It helps us identify those people at risk for heart attack or stroke early enough so that effective, noninvasive corrective actions can be taken. Thermography enabled us to monitor Henry’s progress during chelation therapy. First it showed us that Henry was at high risk of having a heart attack or stroke, then later it showed us that his risk was significantly reduced.
Henry’s case highlights the advantages of thermography as a diagnostic tool for heart disease. It is objective, quantitative, completely safe, and highly reliable. In fact, even if you are not at risk for a stroke or heart attack, thermography can detect the earliest signs of ATHEROSCLEROSIS, long before it becomes a problem; this advance warning can enable you to prevent serious heart disease from ever developing.
Blood: is classified into 4 blood types or groups according to the presence of type A and type B antigens on the surface of red blood cells. These antigens are also called agglutinogens and pertain to the blood cells’ ability to agglutinate, or clump together. Type O blood (containing neither type) is found in 47% of the Caucasian population; type A, 41%; type B, 9%; type AB, 3%. Another form of blood grouping is according to Rh-positive and Rh-negative types, based on the distribution of 6 different Rh antigens.
Free radical: is an unstable molecule with an unpaired electron that steals an electron from another molecule and produces harmful effects. Free radicals are formed when molecules within cells react with oxygen (oxidize) as part of normal metabolic processes. Free radicals then begin to break down cells, especially if there are not enough free-radical quenching nutrients, such as vitamins C and E, in the cell. While free radicals are normal products of metabolism, uncontrolled free-radical production plays a major role in the development of degenerative disease, including cancer and heart disease. Free radicals harmfully alter important molecules, such as proteins, enzymes, fats, even DNA. Other sources of free radicals include pesticides, industrial pollutants, smoking, alcohol, viruses, most infections, allergies, stress, even certain foods and excessive exercise.
Chelation therapy: refers to a method of binding up (“chelating”) toxins (e.g. heavy metals) and metabolic wastes and removing them from the body while at the same time increasing blood flowA
removing arterial plaque. One type of chelation therapy involves the chelating agent disodium EDTA given as an intravenous infusion over a 31/2 hour period. Usually 20 to 30 treatments are administered at the rate of 1 to 3 sessions per week. Chelation therapy is especially beneficial for all forms of atherosclerotic cardiovascular disease including angina pectoris and coronary artery disease.
A Unified Theory of Human Cardiovascular Disease Leading the Way to the Abolition of This Disease as a Cause for Human Mortality
Matthias Rath M.D. and Linus Pauling Ph.D
“An important scientific innovation rarely, makes its way by gradually winning over and converting its opponents. What does happen is that its opponents gradually die out and that the growing generation is familiar with the idea from the beginning.”
Until now therapeutic concepts for human cardiovascular disease (CVD) were targeting individual patho-mechanisms or specific risk factor, on the basis of genetic, metabolic, evolutionary, and clinical evidence we present here a unified pathogenetic and therapeutic approach.
Ascorbate deficiency is the precondition and common denominator of human CVD. Ascorbate deficiency is the result of the inability of man to synthesize ascorbate endogenously in combination with insufficient dietary intake. The invariable morphological consequences of chronic ascorbate deficiency in the perivascular wall are the loosening of the connective tissue and the loss of the endothelial barrier function.
Thus human CVD is a form of pre-scurvy. The multitude of patho-mechanisms that lead to the clinical manifestation of CVD are primarily defense mechanisms aiming at the stabilization of the vascular wall. After the loss of endogenous ascorbate production during the evolution of man these defense mechanisms became life-saving.
They counteracted the fatal consequences of scurvy and particularly of blood loss through the scorbutic vascular wall. These countermeasures constitute a genetic and a metabolic level. The genetic level is characterized by the evolutionary advantage of inherited features that lead to a thickening of the vascular wall, including a multitude of inherited diseases.
The metabolic level is characterized by the close connection of ascorbate with metabolic regulatory systems that determine the risk profile for CVD in clinical cardiology today. The most frequent mechanism is the deposition of lipoproteins, particularly lipoprotein (a) [Lp(a)], in the vascular wall.
With sustained ascorbate deficiency, the result of insufficient ascorbate uptake, these defense mechanisms overshoot and lead to the development of CVD. Premature CVD is essentially unknown in all animal species that produce high amounts of ascorbate endogenously. In humans, unable to produce endogenous ascorbate, CVD became one of the most frequent diseases.
The genetic mutation that rendered all human beings today dependent on dietary ascorbate is the universal underlying cause of CVD– Optimum dietary ascorbate intake will correct this common genetic defect and prevent its deleterious consequences.
Clinical confirmation of this theory should largely abolish CVD as a cause for mortality in this generation and future generations of mankind.
We have recently presented ascorbate deficiency as the primary cause of human CVD. We proposed that the most frequent patho-mechanism leading to the development of atherosclerotic plaques is the deposition of LP(a) and fibrinogen/fibrin in the ascorbate-deficient vascular wall.
In the course of this work we discovered that virtually every patho-mechanism for human CVD known today can be induced by ascorbate deficiency. Beside the deposition of LP(a) this includes such seemingly unrelated processes as foam cell formation and decreased reverse-cholesterol transfer, and also peripheral angiopathies in diabetic or homocystinuric patients.
We did not accept this observation as a coincidence. Consequently we proposed that ascorbate deficiency is the precondition as well as a common denominator of human CVD. This far-reaching conclusion deserves an explanation; it is presented in this paper.
We suggest that the direct connection of ascorbate deficiency with the development of CVD is the result of extraordinary pressure during the evolution of man.
After the loss of the endogenous ascorbate production in our ancestors, severe blood loss through the scorbutic vascular wall became a life-threatening condition. The resulting evolutionary pressure favored genetic and metabolic mechanisms predisposing to CVD.
The Loss of Endogenous Ascorbate Production in the Ancestor of Man
With few exceptions all animals synthesize their own ascorbate by conversion from glucose. In this way they manufacture a daily amount of ascorbate that varies between about 1 gram and 20 grams, when compared to the human body weight.
Apparently man and a couple of other mammals never had or lost the ability for endogenous ascorbate production. This may bave been the result of a mutation of the gene encoding for the enzyme L-gulono-g-lactone oxidase (GLO), a key enzyme in the conversion of glucose to ascorbate. As a result, all descendants became dependent on dietary ascorbate intake.
The precondition for the mutation of the GLO gene was a sufficient supply of dietary ascorbate. Our ancestors at that time lived in tropical regions. Their diet consisted primarily of fruits and other forms of plant nutrition that provided a daily dietary ascorbate supply in the range of several hundred milligrams to several grams per day. When our ancestors left this habitat to settle in other regions of the world the availability of dietary ascorbate dropped considerably and they became prone to scurvy.
Fatal Blood Loss Through the Scorbutic Vascular Wall – An Extraordinary Challenge to the Evolutionary Survival of Man
Scurvy is a fatal disease. It is characterized by structural and metabolic impairment of the human body, particularly by the destabilization of the connective tissue. Ascorbate is essential for an optimum production and hydroxylation of collagen and elastin, key constituents of the extracellular matrix. Ascorbate depletion thus leads to a destabilization of the connective tissue throughout the body.
One of the first clinical signs of scurvy is perivascular bunching.
The explanation is obvious: Nowhere in the body does there exist a higher pressure difference than in the circulatory system, particularly across the vascular wall. The vascular system is the first site where the underlying destabilization of the connective tissue induced by ascorbate deficiency is unmasked, leading to the penetration of blood through the permeable vascular wall.
The most vulnerable sites are the proximal arteries, where the systolic blood pressure is particularly high. The increasing permeability of the vascular wall in scurvy leads to petechiae and ultimately hemorrhagic blood loss.
Scurvy and scorbutic blood loss decimated the ship crews in earlier centuries within months. It is thus conceivable that during the evolution of man periods of prolonged ascorbate deficiency led to a great death toll. The mortality from scurvy must have been particularly high during the thousands of years the ice ages lasted and in other extreme conditions, when the dietary ascorbate supply approximated zero.
We therefore propose that after the loss of endogenous ascorbate production in our ancestors, scurvy became one of the greatest threats to the evolutionary survival of man.
By hemorrhagic blood loss through the scorbutic vascular wall our ancestors in many regions may have virtually been brought close to extinction.
The morphologic changes in the vascular wall induced by ascorbate deficiency are well characterized: the loosening of the connective tissue and the loss of the endothelial barrier function. The extraordinary pressure by fatal blood loss through the scorbutic vascular wall favored genetic and metabolic countermeasures attenuating increased vascular permeability.
Ascorbate Deficiency and Genetic Countermeasures
The genetic countermeasures are characterized by an evolutionary advantage of genetic features and include inherited disorders that are associated with atherosclerosis and CVD. With sufficient ascorbate supply these disorders stay latent. In ascorbate deficiency, however, they become unmasked, leading to an increased deposition of plasma constituents in the vascular wall and other mechanisms that thicken the vascular wall.
This thickening of the vascular wall is a defense measure compensating for the impaired vascular wall that had become destabilized by ascorbate deficiency. With prolonged insufficient ascorbate intake in the diet these defense mechanisms overshoot and CVD develops.
The most frequent mechanism to counteract the increased permeability of the ascorbate-deficient vascular wall became the deposition of lipoproteins and lipids in the vessel wall. Another group of proteins that generally accumulate at sites of tissue transformation and repair are adhesive proteins such as fibronectin, fibrinogen, and particularly apo(a). It is therefore no surprise that LP(a), a combination of the adhesive protein APO(a) with a low density lipoprotein (LDL) particle, became the most frequent genetic feature counteracting ascorbate deficiency.’
Beside lipoproteins, certain metany ic disorders, such as diabetes and homocystinuria, are also associated with the development of CVD. Despite differences in the underlying pern -mechanism, all these mechanisms share a common feature: they lead to a thickening of the vascular wall and thereby can counteract the increased permeability in ascorbate deficiency. In addition to these genetic disorders, the evolutionary pressure from scurvy also favored certain metabolic countermeasures.
Ascorbate Deficiency and Metabolic Countermeasures
The metabolic countermeasures are characterized by the regulatory role of ascorbate for metabolic systems determining the clinical risk profile for CVD. The common aim of these metabolic regulations is to decrease the vascular permeability in ascorbate deficiency. Low ascorbate concentrations induce vasoconstriction and hemostasis and affect vascular wall metabolism in favor of atherosclerogenesis.
Towards this end ascorbate interacts with lipoproteins, coagulation factors, prostaglandins, nitric oxide, and second messenger systems such as cyclic monophosphates. It should be noted that ascorbate can affect these regulatory levels — In lipoprotein metabolism low density lipoproteins (LDL), LP(a), and very low density lipoproteins (VLDL) are inversely correlated with ascorbate concentrations, whereas ascorbate and HDL levels are positively correlated.
Similarly, in prostaglandin metabolism ascorbate increases prostacyclin and prostaglandin E levels and decreases the thromboxane level. In general, ascorbate deficiency induces vascular constriction and hemostatis, as well as cellular and extracellular defense mechanism in the vascular wall.
In the following sections we shall discuss the role of ascorbate for frequent and well established patho-mechanisms of human CVD. In general, the inherited disorders described below are polygenic. Their separate description, however, will allow the characterization of the role of ascorbate on the different genetic and metabolic levels.
APO(a) and LP(a), the Most Effective and Most Frequent Countermeasure
After the loss of endogenous ascorbate production, APO(a) and LP(a) were greatly favored by evolution. The frequency of occurrence of elevated LP(a) plasma levels in species that had lost the ability to synthesize ascorbate is so great that we formulated the theory that APO(a) functions as a surrogate for ascorbate.
The culprit: A “sticky” relative of LDL called lipoprotein(a) or Lp(a).
In most population studies the genetic pattern of high APO(a) isoform/low LP(a) plasma level was found to be the most advantageous and therefore most frequent pattern. In ascorbate deficiency LP(a) is selectively retained in the vascular wall. APO(a) counteracts increased permeability by compensating for collagen, by its binding to fibrin, as a proteinthiol antioxidant, and as an inhibitor of plasmin-induced proteolysis. Moreover, as an adhesive protein APO(a) is effective in tissue repair processes.
Chronic ascorbate deficiency leads to a sustained accumulation of LP(a) in the vascular wall. This leads to the development of atherosclerotic plaques and premature CVD, particularly in individuals with genetically determined high plasma LP(a) levels. Because of its association with APO(a), Lp(a) is the most specific repair particle among all lipoproteins. LP(a) is predominantly deposited at predisposition sites and it is therefore found to be significantly correlated with coronary+potrvical, and ceaw10al atherosclerosis but not with peripheral vascular disease.
The mechanism by which ascorbate re-supplementation prevents cardiovascular disease is by maintaining the intergral structure of the vascular wall.
In addition, ascorbate exerts in the individual a multitude of metabolic effects that prevents the development of CVD. If the predisposition is a genetic elevation of LP(a) plasma levels the specific regulatory role of ascorbate is the decrease of APO(a) synthesis in the liver and thereby the decrease of LP(a) plasma levels.
Moreover, ascorbate decreases the retention of LP(a) in the vascular wall by lowering fibrinogen synthesis and by increasing the hydroxylation of lysine residues in vascular wall constituents, thereby reducing the affinity for LP(a) binding.
In about half of the CVD patients the mechanism of LP(a) deposition contributes significantly to the development of atherosclerotic plaques. Other lipoprotein disorders are also frequently part of the polygenic pattern predisposing the individual patient to CVD in the individual.
Other Lipoprotein Disorders Associated with CVD
In a large population study Goldstein et al. discussed three frequent lipid disorders, familial hypercholesterolemia, familial hypertriglyceridemia, and familial combined hyperlipidemia. Ascorbate deficiency unmasks these underlying genetic defects and leads to an increased plasma concentration of lipids (e.g. cholesterol, triglycerides) and lipoproteins (e.g. LDL, VLDL) as well as to their deposition in the impaired vascular wall.
As with LP(a), this deposition is a defense measure counteracting the increased permeability. It should, however, be noted that the deposition of lipoproteins other than LP(a) is a less specific defense mechanism and frequently follows LP(a) deposition. Again, these mechanisms function as a defense o0066for a limited time. With sustained ascorbate deficiency the continued deposition of lipids and lipoproteins leads to atherosclerotic plaque development and CVD. Some mechanisms will now be described in more detail.
Hypercholesterolemia, LDL-receptor Defect
A multitude of genetic defects lead to an increased synthesis and/or a decreased catabolism of cholesterol or LDL. A well characterized although rare defect is the LDL receptor defect. Ascorbate deficiency unmasks these inherited metabolic defects and leads to an increased plasma concentration of cholesterol-rich lipoproteins, e.g. LDL, and their deposition in the vascular wall. Hypercholesterolemia increases the risk for premature CVD primarily when combined with elevated plasma levels of LP(a) or triglycerides.
The mechanisms by which ascorbate supplementation prevents the exacerbation of hypercholesterolemia and related CVD include an increased catabolism of cholesterol. In particular, ascorbate is known to stimulate 7-a-hydroxylase, a key enzyme in the conversion of cholesterol to bile acids and to increase the expression of LDL receptors on the cell surface. Moreover, ascorbate is known to inhibit endogenous cholesterol synthesis as well as oxidative modification of LDL.
Hypertriglyceridemia, Type III Hyperlipidemia
A variety of genetic disorders lead to the accumulation of triglycerides in the form of chylomicron remnants, VLDL, and intermediate density lipoproteins (IDL) in plasma.
Ascorbate deficiency unmasks these underlying genetic defects and the continued deposition of triglyceride-rich lipoproteins in the vascular wall leads to CVD development. These triglyceride-rich lipoproteins are particularly subject to oxidative modification, cellular lipoprotein uptake, and foam cell formation. In hypertriglyceridemia nonspecific foam-cell formation has been observed in a variety of organs.”
Ascorbate-deficient foam cell foesseion, although a less specific repair mechanism than the extracellular deposition of LP(a), may have also conferred stability . Ascorbate supplementation prevents the exacerbation of CVD associated with hypertriglyceridemia, Type III hyperlipidemia, and related disorders by stimulating lipoprotein lipases and thereby enabling a normal catabolism of triglyceride-rich lipoproteins.
Ascorbate prevents the oxidative modification of these lipoproteins, their uptake by scavenger cells and foam cell formation.
Moreover, we propose here that, analogous to the LDL receptor, ascorbate also increases the expression of the receptors involved in the metabolic clearance of triglyceride-rich lipoproteins, such as the chylomicron remnant receptor.
The degree of build-up of atherosclerotic plaques in patients with lipoprotein disorders is determined by the rate of deposition of lipoproteins and by the rate of the removal of deposited lipids from the vascular wall. It is therefore not surprising that ascorbate is also closely connected with this reverse pathway.
Hypoalphalipoproteinemia is a frequent lipoprotein disorder characterized by a decreased synthesis of HDL particles. HDL is part of the ‘reverse-cholesterol-transport’ pathway and is critical for the transport of cholesterol and also other lipids from the body periphery to the liver.
In ascorbate deficiency this genetic defect is unmasked, resulting in decreased HDL levels and a decreased reverse transport of lipids from the vascular wall to the liver. This mechanism is highly effective and the genetic disorder hypoalphalipoproteinemia was greatly favored during evolution.
With ascorbate supplementation HDL production increases, leading to an increased uptake of lipids deposited in the vascular wall and to a decrease of the atherosclerotic lesion.
During spring and summer seasons the ascorbate content in the diet increased significantly and mechanisms were favored that decreased the vascular deposits under the protection of increased ascorbate concentration in the vascular tissue.
It is not unreasonable for us to propose that ascorbate can reduce fatty deposits in the vascular wall within a relatively short time.
In an earlier clinical study it was shown that 500 mg of dietary ascorbate can lead to a reduction of atherosclerotic deposits within 2 to 6 months.”
This concept, of course, also explains why heart attack and stroke occur today with a much higher frequency in winter than during spring and summer, the seasons with increased ascorbate intake.
The patho-mechanism in this case involves the structural similarity between glucose and ascorbate and the competition of these two molecules for specific cell surface receptors.”
Elevated glucose levels prevent many cellular systems in the human body, including endothelial cells, from optimum ascorbate uptake. Ascorbate deficiency unmasks the underlying genetic disease, aggravates the imbalance between glucose and ascorbate, decreases vascular ascorbate concentration, and thereby triggers diabetic angiopathy.
Ascorbate supplementation prevents diabetic angiopathy by optimizing the ascorbate concentration in the vascular wall and also by lowering insulin requirement-”
Homocystinuria is characterized by the accumulation of homocyst(e)ine and a variety of its metabolic derivatives in the plasma, the tissues and the urine as the result of decreased homocysteine catabolism.”
Elevated plasma concentrations of homocyst(e)ine and its derivatives damage the endothelial cells throughout the arterials of venous system. Thus homocystinuria is characterized by peripheral vascular disease and thromboembolism. These clinical manifestations have been estimated to occur in 30 per cent of the patients before the age of 20 and in 60 per cent of the patients before the age of 40.
Ascorbate supplementation prevents homocystinuric angiopathy and other clinical complications of this disease by increasing the rate of homocysteine catabolism.
Thus, ascorbate deficiency unmasks a variety of individual genetic predispositions that lead to CVD in different ways. These genetic disorders were conserved during evolution largely because of their association with mechanisms that lead to the thickening of the vascular wall. Moreover, since ascorbate defiency is the universal cause of these diseases, ascorbate supplementation is the universal therapy.
The Determining Principles of This Theory
The determining principles of this comprehensive theory are schematically summarized:
1. CVD is the direct consequence of the inability for endogenous ascorbate production in man in combination with low dietary ascorbate intake.
2. Ascorbate deficiency leads to increased permeability of the artery wall by the loss of the endothelial barrier function and the loosening of the vascular connective tissue.
3. After the loss of endogenous ascorbate production scurvy and fatal blood loss through the scorbutic vascular wall rendered our ancestors in danger of extinction. Under this evolutionary pressure over millions of years genetic and metabolic countermeasures were favored that counteract the increased permeability of the vascular wall.
4. The genetic level is characterized by the fact that inherited disorders associated with CVD became the most frequent among all genetic predispositions. Among those predispositions lipid and lipoprotein disorders occur particularly often.
5. The metabolic level is characterized by the direct relation between ascorbate and virtually all risk factors of clinical cardiology today. Ascorbate deficiency leads to vasoconstriction and hemostasis and affects the vascular wall metabolism in favor of atherosclerogenesis.
6. The more effective and specific a certain genetic feature counteracted the increasing vascular permeability in scurvy, the more advantageous it became during evolution and, generally, the more frequently this genetic feature occurs today
7. The deposition of LP(a) is the most effective, most specific, and therefore most frequent of these mechanisms. LP(a) is preferentially deposited at predisposition sites. In chronic ascorbate deficiency the accumulation of LP(a) leads to the localized development of atherosclerotic plaques and to myocardial infarction and stroke.
8. Another frequent inherited lipoprotein disorder is hypoalphalipoproteinemia. The frequency of this disorder again reflects its usefulness during evolution. The metabolic upregulation of HDL synthesis by ascorbate became an important mechanism to reverse and decrease existing lipid deposits in the vascular wall.
9. The vascular defense mechanisms associated with most genetic disorders are nonspecific. These mechanisms can aggravate the development of atherosclerotic plaques at predisposition sites.
Other nonspecific mechanisms can lead to peripheral forms of atherosclerosis by causing a thickening of the vascular wall throughout the arterial system. This peripheral form of vascular disease is characteristic for angiopathics associated with Type III hyperlipidemia, diabetes, and many other inherited metabolic diseases.
10. Of particular advantage during evolution and therefore particularly frequent today are those genetic features that protect the ascorbate-deficient vascular wall until the end of the reproduction age. By favoring these disorders nature decided for the lesser of two evils: the death from CVD after the reproduction age rather than death from scurvy at a much earlier age. This also explains the rapid increase of the CVD mortality today from the 4th decade onwards.
11. After the loss of endogenous ascorbate production the genetic mutation rate in our ancestors increased significantly. This was an additional precondition favoring the advantage not only of APO(a) and LP(a) but also of many other genetic countermeasures associated with CVD.
12. Genetic predispositions are characterized by the rate of ascorbate depiction in a multitude of metabolic reactions specific for the genetic disorder.” The overall rate of ascorbate depletion in an individual is largely determined by the polygenic pattern of disorders. The earlier the ascorbate reserves in the body are depleted without being re-supplemented, the earlier CVD develops.
13. The genetic predispositions with the highest probability for early clinical manifestation require the highest amount of ascorbate supplementation in the diet to prevent CVD development. The amount of ascorbate for patients at high risk should be comparable to the amount of ascorbate our ancestors synthesized in their body before they lost this ability: between 1000mg and 20,000 milligrams per day.
14. Optimum ascorbate supplementation prevents the development of CVD independently of the individual predisposition or patho-mechanism. Ascorbate reduces existing atherosclerotic deposits and thereby decreases the risk for myocardial infarction and stroke. Moreover, ascorbate can prevent blindness and organ failure in diabetic patients, thromboembolism in homocystinuric patients, and many other manifestations of CVD.
In this paper we present a unified theory of human CVD. This disease is the direct consequence of the inability of man to synthesize ascorbate in combination with insufficient intake of ascorbate in the modem diet. Since ascorbate deficiency is the common cause of human CVD, ascorbate supplementation is the universal treatment for this disease.
The available epidemiological and clinical evidence is reasonably convincing.
passher clinical co4.4.mation of this theory should lead to the abolition of CVD as a cause of human mortality for the present generation and future generations of mankind.
How To Reduce Your Lp(a) and Decrease Your Risk of Heart Disease
This regimen is recommended ONLY for people with established cardiovascular disease or those who have an elevated LP(a) level. BUT, the researchers do recommend people should take 3000mg of Vitamin C daily on average.
This vitamin regimen is not for general protection from cardiovascular disease.
For most of us, simply following the diet will virtually eliminate the risk of heart disease.
However, if your LP(a) is elevated you will need more aggressive measures.
The most important part of the program will be to follow the diet, which will reduce your insulin levels and improve your HDL/cholesterol ratio. The diet will not alter the LP(a) levels, but it will minimize other risk factors for heart disease.
The mega vitamin therapy increases blood concentrations of important substances and will:
* Strengthen and heal blood vessels,
* Lower LP(a) blood levels and
* Keep LP(a) levels low
* Inhibit the binding of LP(a) molecules to the walls of blood vessels
Unlike ordinary drugs, there are no health risks. We call high intakes of these substances, esp. vitamin C and lysine, The Pauling Therapy. The Pauling Therapy helps treat the root cause and our experience shows it can rapidly reverse advanced heart disease.
How Much Vitamin C And Lysine Should I Take?
The amount will vary between individuals. Seriously ill heart patients require 5-6 grams of vitamin C and 5-6 grams of lysine daily. That is, 5,000 to 6,000 mg of each.
Th prow protocol would also be to include L-carnitine, a natural compound stimulating fatty acid oxidation in the mitochondria. The dose would be 2 grams per day or 500 mg four times a day.
This recommendation comes from a study that was published in October of 2000 from Italian researchers at the University of Milan. (Dirtori Cr, et al: L-Carnitine Reduces Plasma Lipoprotein(a) levels in patients with hyper LP(a). Nutr Metab Cardiovas Dis 2000 Oct 10 (5):247-51.)
Ideally this should be split into four evenly divided doses.
The lysine works by binding to the LP(a) and if you only take it once a day, there will be a large part of the day where you will not be getting protection as the lysine will be eliminated from the blood within a few hours.
The Pauling “mega” dose ranges are based on the degree of illness. In general, Lp(a) binding inhibitors are food substances that are non-toxic and studies have shown they improve health as intake increases. Lesser amounts will have lesser effects. According to his daughter Linda, Linus Pauling’s lysine dosage recommendations were carefully considered. Pauling based his recommendations on knowledge of lysine blood serum levels after intake.
It is not practical to obtain these amounts in food alone. Supplements are required.
It may not be a coincidence that vitamin C, and the amino acids lysine and proline are the fundamental building blocks of collagen. The Pauling Therapy provides these building blocks in ample amounts. Over time, collagen must be replenished for blood vessels to remain healthy and plaque free.
Report after report provides more evidence that the Pauling Therapy, at high doses, works in many people within 14 to 60 days (depending on the daily dosage). A few have reported that the therapy didn’t change their condition, or else required much longer, sometimes over 10 months.
But so far most people (>90%) report relief in weeks rather than months. Lp(a) levels in the blood provide objective evidence. People share their lab reports with us. These reports document drops in serum Lp(a) up to 88%. With longer term use the values continue to decline and usually drop to less than 14. So far, the higher the starting value, the larger the point drop. It is not surprising that most doctors won’t take our word for it and require solid scientific evidence. The question is:
Why haven’t serious clinical studies been run years ago?
Re-growth of plaque is common. Patients risk strokes and other side effects; pieces of plaque may break free during the surgical procedure causing a blockage. According to a recent Discovery-Health channel report, roughly 40% of patients who are put on a heart-lung machine suffer brain damage. On the other hand, to our limited knowledge, there has yet to be single death of a “terminal” patient who adopted and continued the Pauling Therapy.
It would be wise to include a good form of vitamin E, preferrably emulsified. There are many good ones on the market, but make certain that yours is not synthetic and has a mixed form of tocopherols present. Additionally, tocotrienols will also be useful.
Having a hair analysis done from Trace Elements will also help optimize your requirements for specific adjunctive minerals. If you take a mineral that your body does not need, it can actually worsen your condition.
Recent Literature Support For Lp(a) Importance and Reduction
Angles-Cano ; Structural basis for the pathophysiology of lipoprotein(a) in the athero-thrombotic process. Braz J Med Biol Res 1997 Nov;30(11):1271-80.
Lipoprotein Lp(a) is a major and independent genetic risk factor for atherosclerosis and cardiovascular disease. The essen3Edifference between Lp(a2c nd low density lipoproteins (LDL) is apolipoprotein apo(a), a glycoprotein structurally similar to plasminogen, the precursor of plasmin, the fibrinolytic enzyme.
Lp(a) has the capacity tbind to fibrin and to membrane proteins of endothelial cells and monocytes, and thereby to inhibit plasminogen binding and plasmin generation. The inhibition of plasmin generation and the accumulation of Lp(a) on the surface of fibrin and cell membranes favor fibrin and cholesterol deposition at sites of vascular injury.
Moreover, insufficient activation of TGF-beta due to low plasmin activity may result in migration and proliferation of smooth muscle cells into the vascular intima. These mechanisms may constitute the basis of the athero-thrombogenic mode of action of Lp(a).
Price KD; Price CS; Reynolds RD; Hyperglycemia-induced latent scurvy and atherosclerosis: the scorbutic-metaplasia hypothesis. Med Hypotheses 1996 Feb;46(2):119-29.
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.
de la Pena-Diaz A; Izaguirre-Avila R; Angles-Cano E; Lipoprotein Lp(a) and atherothrombotic disease. Arch Med Res 2000 Jul-Aug;31(4):353-9.
High plasma concentrations of lipoprotein (a) [Lp(a)] are now considered a major risk factor for atherosclerosis and cardiovascular disease. This effect of Lp(a) may be related to its composite structure, a plasminogen-like inactive serine-proteinase, apoprotein (a) [apo(a)].
This structure endows Lp(a) with the capacity to bind to fibrin and to membrane proteins of endothelial cells and monocytes, and thereby inhibits binding of plasminogen and plasmin formation. This mechanism favors fibrin and cholesterol deposition at sites of vascular injury and impairs activation of transforming growth factor-beta (TGF-beta) that may result in migration and proliferation of smooth muscle cells into the vascular intima.
Misra A; Risk factors for atherosclerosis in young individuals. J Cardiovasc Risk 2000 Jun;7(3):215-29.
Atherosclerosis starts in childhood, and is accelerated in some individuals. A cluster of clinical and biochemical factors constitute the risk profile for many of them, perhaps most important being metabolic insulin resistance syndrome.
Insulin resistance and its components for children and adolescents, especially obesity and dyslipidemia, are generators of hypertension, glucose intolerance and complications of atherosclerosis in adulthood. Some individuals are genetically predisposed, particularly those with the family history of such disorders.
For many subjects, there is ‘tracking’ of metabolic and lifestyle factors from early age to adulthood. Several new risk factors of atherosclerosis (e.g. level of lipoprotein (a), hyperhomocysteinemia, low birth weight and adverse in-utero environment, and possibly inflammatory markers) are current and potentially future areas of research concerning children and young individuals.
Chong PH; Bachenheimer BS Current, new and future treatments in dyslipidaemia and atherosclerosis. Drugs 2000 Jul;60(1):55-93.
Nicotinic acid has been made tolerable with sustained-release formulations, and is still considered an excellent choice in elevating HDL cholesterol and is potentially effective in reducing lipoprotein(a) [Lp(a)] levels, an emerging risk factor for coronary heart disease (CHD).
Although LDL cholesterol is still the major target for therapy, it is likely that over the next several years other lipid/lipoprotein and non-lipid parameters will become more generally accepted targets for specific therapeutic interventions. Some important emerging lipid/lipoprotein parameters that have been associated with CHD include elevated triglyceride, oxidized LDL cholesterol and Lp(a) levels, and low HDL levels.
Conventional medicine is largely confined to treating the symptoms of this disease. Calcium antagonists, beta-blockers, nitrates, and other drugs are prescribed to alleviate angina pain. Surgical procedures such as angioplasty and coronary bypass surgery applied to improve blood flow mechanically. Hardly any conventional medicine targets the underlying problem: the instability of the vascular wall, which triggers the development of atherosclerotic deposits.
The Unified Theory of Dr. Rath and Dr. Pauling provides a breakthrough in our understanding of these causes and leads to effective prevention and treatment of coronary heart disease. The primary cause of coronary heart disease and other forms of atherosclerotic disease is a chronic deficiency in vitamins and other essential nutrients in millions of vascular wall cells. This leads to instability of the vascular walls, to lesions and cracks, to atherosclerotic deposits, and eventually to heart attacks or strokes. Since the primary cause of cardiovascular disease is a deficiency of essential nutrients in the vascular wall, a daily optimum intake of these essential nutrients is the primary measure to prevent atherosclerosis and to help repair wall damage.
Scientific research and clinical studies have already documented the particular value of vitamin C, vitamin E, beta-carotene, lysine, proline, and other ingredients of Dr. Rath’s and Dr. Pauling’s program in the prevention of cardiovascular disease and in improving the health of patients with existing cardiovascular disease.
A comprehensive Nutritional Supplement Program comprising selected essential nutrients to help prevent cardiovascular disease naturally and to help repair existing damage. SEE: ATHEROSCLEROSIS PROGRAM. The following documents health improvements from patients with coronary heart disease and other forms of cardiovascular disease, who have benefited from this program.
Recommendations for patients with cardiovascular disease is to start immediately with this natural cardiovascular program and inform your doctor about it. Follow the suggested comprehensive Nutritional Supplement Program in addition to your medication. Vitamin C and E are natural ?blood thinners.? If you are on blood thinning medication you should talk to your doctor about the vitamins you take so that additional blood tests can be performed and your prescription medication may be decreased. Do not change any medication without consulting your doctor. The key is to eventually wean yourself off of all medications.
Prevention is better than treatment. The success of this essential nutrient program in patients with existing atherosclerosis and cardiovascular disease is based on the fact that the millions of cardiovascular cells are replenished with cell fuel for optimum cell function. A natural cardiovascular program able to correct an existing health condition is, of course, your best choice to prevent this condition in the first place.
A Comprehensive Nutritional Supplement Program Can Help Reverse Coronary Heart Disease
Millions of people die every year from heart attacks because no effective treatment to halt or reverse coronary artery disease has been available. Therefore, other researchers (Dr. Rath, Dr. Pauling) decided to test the efficacy of a Comprehensive Nutritional Supplement Program for the Number One health problem of our time: Coronary Atherosclerosis. If this nutritional supplement program is able to stop further growth of coronary atherosclerosis, the fight against coronary artery disease can be won and the goal of eradicating heart disease becomes reality.
To measure the success of the Nutritional Supplement Program the researchers did not primarily look at risk factors circulating in the blood stream. They focused directly on the key problem, thginaherosclerotic deposits inside the walls of the coronary arteries. A fascinating new diagnostic technique had just become available that allowed them to measure the size of the coronary deposits non-invasively: UltraFast Computed Tomography.
The Ultrafast CT measures areas and density of the calcium deposits without any needles or radioactive dye involved; then the computer automatically calculates their size by determining the Coronary Artery Scan (CAS) score. The higher the CAS score, the more calcium has accumulated, indicating more advanced coronary artery disease. Compared to angiography and treadmill tests, UltraFast CT is the most precise diagnostic technique available today to detect coronary artery disease already in its early stage. This diagnostic test allows detection of deposits in coronary arteries long before a patient notices any angina pectoris or other symptoms. Moreover, since it measures directly the deposits in the artery walls, it is a much better indicator for a person’s cardiovascular risk than any measurements of cholesterol or other risk factors in the bloodstream.
They studied 55 patients with various degrees of coronary artery disease. Changes in the size of the coronary artery calcifications in each patient were measured over an average period of one year without a Nutritional Supplement Program followed by a period of one year with the Nutritional Supplement Program. In this way, heart scans of the same person could be compared without and with the Nutritional Supplement Program. This study design had the advantage that the patients served as their own controls. The dosages of essential nutrients given were about the same amounts listed in the Nutritional Program listed in this Web Site at ATHEROSCLEROSIS.
The results of this landmark study were published in the Journal of Applied Nutrition in 1996. This study measured for the first time how aggressive coronary artery disease grows until eventually a heart attack or heart disease occurs. Without the comprehensive supplement program, the coronary calcifications increased at an exponential rate, with an average growth of 44% every year. Thus, without vitamin-mineral protection, coronary deposits add about half their size every year.
When patients started a comprehensive vitamin-mineral program this trend was reversed and the average growth rate of coronary calcifications actually slowed down. Most significantly, in patients with early stages of coronary heart disease, this essential nutrient program stopped further growth of coronary heart disease within one year. Thus, this study also gives us valuable information about the time it takes until this program shows its natural healing effect on the artery wall. While for the first six months the deposits in these patients continued to grow, although at a decreased pace, the growth essentially stops during the second six months on this program. Of course, any therapy that stops coronary artery disease in its early stages will prevent many heart attacks later on.
It is not surprising that there is a delay of several months until the healing effect of the Nutritional Supplement Program on the artery wall becomes noticeable. Atherosclerotic deposits develop over many years or decades, and it takes several months to control this aggressive disease and start the healing process. More advanced stages of coronary heart disease may take still longer before the vascular healing process is measurable. To answer these questions, research is continuing this line of study.
Can already existing coronary deposits be reversed in a natural way? The answer is yes. In individual patients theses researchers documented natural reversal and complete disappearance of early coronary artery deposits within about one year. The ongoing study will tell us how long the natural reversal takes in patients with advanced coronary artery disease.
In patients with early coronary heart disease, this healing of the artery wall can lead to the complete natural removal of atherosclerotic deposits (see above).
In patients with advanced coronary artery disease, this program can stabilize the artery walls, halt further growth of the coronary deposits, and reverse them, at least in part; thus contributing to the prevention of heart attacks.
Clinical Studies Document Prevention of Cardiovascular Disease with Nutritional Supplements
Dr. James Enstrom and his colleagues from the University of California at Los Angeles investigated vitamin intake of more than 11,000 Americans over ten years. This government-supported study showed that people who took at least 300 mg per day of vitamin C in their diet or in form of a multivitamin-mineral supplement, compared to 50 mg contained in an average American diet, could reduce their heart disease rate up to 50% in men and up to 40% in women. The same study showed that an increased intake of vitamin C was associated with an increased life expectancy of up to six years.
The Canadian physician, Dr. G. C. Willis, showed that dietary vitamin C could reverse atherosclerosis. At the beginning of his study, he documented the atherosclerotic deposits in his patients by angiography (injection of a radioactive substance followed by X-ray pictures). After this documentation, half of the study patients received 1.5 grams of vitamin C per day. The other half of the patients received no additional vitamin C. The control analysis, on average, after 10 to 12 months, showed that in those patients who had received additional vitamin C, the atherosclerotic deposits had decreased in 30% of the cases. In contrast, no decrease in atherosclerotic deposits could be seen in those patients without vitamin C supplementation. The arterial deposits in these patients either remainons.he same or had further incres1294Amazingly, this important clinical study was conducted more than 40 years ago and was never followed up.
Europe: More Vitamins, Less Heart Disease
One of the largest studies about the importance of vitamins in the prevention of cardiovascular disease was conducted in Europe. It is a well-known fact that cardiovascular diseases are more frequent in Scandinavia and northern European countries as compared with Mediterranean countries. Professor Gey, from the University of Basel in Switzerland, compared the rate of cardiovascular disease in these countries to the blood levels of vitamin C and beta-carotene, as well as cholesterol. His findings were remarkable:
People in northern European countries have the highest rate of cardiovascular disease and, on average, the lowest blood levels of vitamins.
Southern European populations have the lowest cardiovascular risk and the highest vitamin blood levels.
An optimum intake of vitamin C, E and A had a much greater impact on decreasing the risk for cardiovascular disease than lowering of cholesterol levels.
This study finally provides the scientific answer to the ?French Phenomenon? and to the low rate of heart attacks in France, Greece, and other Mediterranean countries. The decisive factor for the low cardiovascular risk in these countries is an optimum intake of vitamins in the regular diets of these regions. Certain dietary preferences, such as the consumption of wine and olive oil, rich in bioflavonoids and vitamin E, seem to be of particular importance.
Vitamin E and Beta-Carotene Also Decrease Your Cardiovascular Risk
Optimum dietary intake of vitamin E and beta-carotene also significantly reduce the cardiovascular risk. In several large-scale clinical studies, the importance of these vitamins for optimum cardiovascular health has been ump mented:
The Nurses? Health Study included more than 87,000 American nurses, ages 34 to 59. None of the study participants had any signs of cardiovascular disease at the beginning of the study. In 1993, a first result was published in the New England Journal of Medicine. It was shown that study participants taking more than 200 units of vitamin E per day could reduce their risk for heart attacks by 34%, compared to those receiving only 3 units, corresponding to the average daily intake of vitamin E in America.
The Health Professional Study included over 39,000 health professionals, ages 40 to 75. At the beginning of the study, none of the participants had any signs of cardiovascular disease or diabetes, or elevated blood cholesterol levels. The study showed that people taking 400 units of vitamin E per day could reduce their risk for heart attack by 40%, compared to those taking only 6 units of vitamin E per day. In the same study, an increased intake of beta-carotene was also shown to significantly decrease the cardiovascular risk.
The Physicians Health Study included over 22,000 physicians, ages 40 to 84. From this study in patients with existing cardiovascular disease, published by Dr. Hennekens in 1992, it was shown that in those patients, 50 mg of beta-carotene per day could cut the risk for suffering a heart attack or stroke in half.
The following table summarizes the results of these last clinical studies:
Vitamin C intake lowers cardiovascular risk by 50%, documented in 11,000 study participants over 10 years.
Vitamin E supplementation lowers cardiovascular risk by one-third, documented in 87,000 study participants over 6 years.
Beta-carotene supplementation lowers cardiovascular risk 30%, documented in more than 87,000 study participants over 6 years.
No prescription drug has ever been shown to be as effective as these vitamins in preventing heart disease.
Vitamin C, vitamin E and beta-carotene are all essential components of a comprehensive Nutritional Supplement Program. Moreover, this program comprises the natural amino acids, lysine and proline, as well as the other natural substances that have been shown in numerous scientific studies to optimize cardiovascular health.
The main cause of atherosclerotic deposits is the biological weakness of the artery walls caused by chronic vitamin and nutritional deficiencies. The atherosclerotic deposits are the consequence of this chronic weakness; they develop as a compensatory stabilizing cast of nature to strengthen these weakened blood vessel walls.
Why Animals Don’t Get Heart Attacks
According to the statistics of the World Health Organization, each year more than 12,000,000 people die from the consequences of heart attacks and strokes. Amazingly, while cardiovascular disease has become one of the largest epidemics ever to haunt mankind, these very same heart attacks are essentially unknown in the animal world. The following paragraph from the renowned textbook of veterinary medicine by Professor H. A. Smith and T. C. Jones documents these facts:
?The fact remains, however, that in none of the domestic species, with the rarest of exceptions, do animals develop atherosclerotic disease of clinical significance. It appears that most of the pertinent pathological mechanisms operate in animals and that atherosclerotic disease in them is not impossible; it just does not occur. If the reason for this could be found it might cast some very useful light on the human disease.?
These important observations were published in 1958. Now, almost four decades later, the puzzle of human cardiovascular disease has apparently been solved. The solution to the puzzle of human cardiovascular disease is one of the great advances in medicine.
Here is the main reason why animals don’t get heart attacks: With few exceptions, animals produce their own vitamin C in their bodies. The daily amounts of vitamin C produced vary between 1000 mg and 20,000 mg, when compared to the human body weight. Vitamin C is the cement of the artery wall, and optimum amounts of vitamin C stabilize the arteries. In contrast, we human beings cannot produce a single molecule of vitamin C ourselves. Our ancestors lost this ability generations ago when an enzyme that was needed to convert sugar molecules (glucose) into vitamin C became defunct. This change in the molecules of inheritance (genes) of our ancestors had no immediate disadvantage since, for thousands of generations, they relied primarily on plant nutrition such as cereal, fruits and others, which provided the daily minimum of vitamins for them. Nutritional habits and dietary intake of vitamins changed considerably in this century. Today, most people do not receive sufficient amounts of vitamins in their diet. Still worse, food processing, long-term storage and overcooking destroy most vitamins in the food. The consequences are summarized in the picture above.
The single most important difference between the metabolism of human beings and most other living species is the dramatic difference in the body pool of vitamin C. The body reservoir of vitamin C in people is on average ten to 100 times lower than the vitamin C levels in animals
How Does Vitamin C Prevent Atherosclerosis?
Vitamin C contributes in many different ways to the prevention of cardiovascular disease. It is an important antioxidant and it serves as a cofactor for many biochemical reactions in the body cells. The most important function of vitamin C in preventing heart attacks and strokes is its ability to increase the production of collagen, elastin, and other reinforcement molecules in the body. These biological reinforcement rods constitute the connective tissue, about 50% of all proteins in our body. Collagen has the same structural stability function for our body as iron reinforcement rods have for a skyscraper building. Increased production of collagen means improved stability for the 60,000-mile-long walls of our arteries, veins, and capillaries.
The Scientific World Knows the Facts
The close connection between vitamin C deficiency and the instability of body tissue was established long ago. Professor Lubert Stryer of Stanford University takes the following from the world-famous textbook on biochemistry. While the vitamin C-collagen-connection is firmly established, the paramount importance of this connection for heart disease has apparently been overlooked or neglected.
Defective Hydroxylation is one of the Biochemical Lesions in Scurvy
The importance of the hydroxylation of collagen becomes evident in scurvy. A vivid description of this disease was given by Jacques Cartier in 1536, when it afflicted his men as they were exploring the Saint Lawrence River: ?Some did lose all their strength and could not stand on their feet…others also had all their skins spotted with spots of blood of a purple color: then did it ascend up to their ankles, knees, thighs, shoulders, arms and necks. Their mouths became stinking, their gums so rotten, that all the flesh did fall off, even to the roots of the teeth which did also almost all fall out.?
The means of preventing scurvy was succinctly stated by James Lind, a Scottish physician, in 1753: ?Experience indeed sufficiently shows that as greens or fresh vegetables with ripe fruits, are the best remedies for it, so they prove the most effectual preservatives against it.? Lind urged the inclusion of lemon juice in the diet of sailors. The British navy reasted his advice some 40 years later.
Scurvy is caused by a dietary deficiency of ascorbic acid (vitamin C). Primates and guinea pigs have of t the ability to synthesize ascorbic acid and so they must acquire it from their diets. Ascorbic acid, an effective reducing agent, maintains prolyl hydroxylase in an active form, probably by keeping its iron atom in the reduced ferrous state. Collagen synthesized in the absence of ascorbic acid is insufficiently hydroxylated and, hence, has a lower melting temperature. This abnormal collagen cannot properly form fibers and thus causes the skin lesions and blood vessel fragility that are so prominent in scurvy.
Atherosclerosis Is an Early Form of Scurvy
While these facts were known 250 years ago, they are still not applied in medicine today. The fact is, the main cause of heart attacks and strokes is a scurvy-like condition of the artery wall.
1. Optimum intake of vitamin C leads to an optimum production and function of collagen molecules. A stable blood vessel wall does not allow atherosclerotic deposits to develop. Optimum availability of vitamin C in their bodies is the main reason why animals don’t get heart attacks.
2. Total depletion of the vitamin C body reserves, as they occurred in sailors of earlier centuries, leads to a gradual breakdown of the body’s connective tissue, including the vessel walls. Thousands of sailors died from hemorrhagic blood loss through leaky blood vessel walls within a few months.
3. Atherosclerosis and cardiovascular disease are exactly between these two conditions. Our average diet contains enough vitamin C to prevent open scurvy, but not enough to guarantee stable reinforced artery walls. As a consequence, millions of tiny cracks and lesions develop along the artery walls. Subsequently, cholesterol, lipoproteins, and other blood risk factors enter the damaged artery walls in ordany o repair these lesions. With chronically low vitamin intake, however, this repair process continues over decades. Over many years this repair m,ess continues and can overcaw10nsate or overshoot and atherosclerotic deposits develop more thickly. Deposits in the arteries of the heart eventually lead to heart attack; deposits in the arteries of the brain lead to stroke
Vitamin C Deficiency Causes Atherosclerosis – The Proof
It is possible to prove that too low a dietary intake of vitamin C alone, without any other factors involved, directly causes atherosclerosis and cardiovascular disease. To prove this, researchers had to conduct an animal experiment with guinea pigs, exceptions in the animal world because they share with humans the inability to produce their own vitamin C. Two groups of guinea pigs received exactly the same daily amounts of cholesterol, fats, proteins, sugar, salt, and all other ingredients in their diet, with one exception – vitamin C. Group B received 60 mg of vitamin C per day in their diet, compared to the human body weight. This amount was chosen to meet the official recommended daily allowance for humans in the U.S. In contrast, group A received 5,000 mg of vitamin C per day compared to human body weight.
The vitamin C deficient animals of Group B developed atherosclerotic deposits, particularly in the areas close to the heart. The aortas of the animals in Group A remained healthy and did not show any deposits. The artery sections from animals with high vitamin C intake showed an intact cell barrier between the bloodstream and the artery wall. The almost parallel alignment of the collagen molecules in the artery wall makes stability visible. In contrast, the arteries of the vitamin C deficient animals have lost the protection (defective barrier cell lining) and stability (fragmented collagen structure) of their arteries.
The previous experiment underlines our modern definition of cardiovascular disease as a vitamin deficiency condition. This new understanding is summarized on the facing page:
1. Lesions. The main cause of coronary artery disease is the instability and dysfunction of the blood vessel wall caused by chronic vitamin deficiency. This leads to millions of small lesions and cracks in the artery wall, particularly in the coronary arteries. The coronary arteries are mechanically the most stressed arteries because they are squeezed flat from the pumping action of the heart more than 100,000 times per day, similar to a garden hose which is stepped upon.
2. Beginning Repair. Repair of the artery walls then becomes necessary. Cholesterol and other repair factors are produced at an increased rate in the liver and are transported in the bloodstream to the artery walls, which they enter in order to mend and repair the damage. Because the coronary arteries sustain the most damage, they require the most intensive repair. NOTE:(You should now be asking yourself: ?Why take cholesterol-lowering drugs if the artery wall is compromised??).
3. Ongoing Repair. With continued vitamin deficiency over many years, the repair process in the artery walls continues with respect to how much damage there is to the artery wall. Atherosclerotic plaques form predominantly at those locations in the cardiovascular system with the most intensive repair: the coronary arteries. This is why infarctions occur primarily at this very same location and why the most frequent cardiovascular events are infarctions of the heart, not infarctions of the nose or ears.
The Natural Reversal of Cardiovascular Disease
The basis for the reversal of atherosclerosis is the initiation of a healing process in the artery wall that has been weakened by chronic vitamin deficiency. Besides vitamin C, which stimulates production of collagen molecules, other constituents of a comprehensive Nutritional Supplement Vitamin Program are essential for this healing process.
In a microscopic cross-section of an atherosclerotic plaque deposit in a human coronary artery, lipoproteins (fat molecules) are in the center of the deposits. Two of these lipoprotein(a) molecules (one lipoprotein (a) and one LDL molecule) are among thousands of lipoprotein molecules in this plaque.
Around the core of the plaque a local ‘tumor? forms from muscle cells typical for the artery wall. This ?muscle cell tumor? is another way by which the body stabilizes the vitamin-deprived artery wall. The deposition of lipoproteins from the bloodstream and the muscle cell tumor in the artery wall are the most important factors that determine the size of the plaque and, thereby, the growth of coronary heart disease. Any therapy that is able to reverse these two mechanisms of atherosclerosis must also reverse coronary heart disease itself. The ingredients of a comprehensive Nutritional Supplement Program synergistically affect both mechanisms in the following ways:
1. Stability of the artery wall through optimum collagen production. The collagen molecules in our body are proteins composed of amino acids. Collagen molecules differ from all other proteins in the body by the fact that they make particular use of the amino acids lysine and proline. We already know that vitamin C stimulates the production of collagen in the cells of the artery wall. An optimum supply of lysine, proline, and vitamin C is a decisive factor for the optimum regeneration of the connective tissue in the artery walls and, therefore, for a natural healing of cardiovascular disease.
2. Decrease of the ?muscle cell tumor? in the artery wall. With an optimum supply of essential nutrients, the muscle cells of the artery walls produce sufficient amounts of functional collagen, thereby guaranteeing optimum stability of the wall. In contrast, vitamin deficiency leads to the production of faulty and dysfunctional collagen molecules by the arterial muscle cells. Moreover, these muscle cells multiply themselves, forming the atherosclerotic ‘tumor.? Dr. Aleksandra Niedzwiecki and her colleagues investigated this mechanism in detail. They found that vitamin C, in particular, could inhibit the growth of the atherosclerotic ‘tumor.? In the meantime, other studies have shown that vitamin E also has this effect. AND, do not forget MSM, as sulfur is also very important to the formation of good quality collagen.
3. ?Teflon? protection of the artery wall and reversal of fatty deposits in the artery walls. Lipoproteins are the transport molecules by which cholesterol and other fat molecules circulate in the blood and are deposited in the artery walls. For many years, it has been thought that the primary transport molecule responsible for the deposition of fat in the artery walls is LDL (low-density lipoprotein, or ?bad cholesterol?). Today, we know that the most dangerous fat transport molecules are not LDL molecules, but a variant, called lipoprotein(a). The letter (a) can stand for ?adhesive? and characterizes an additional sticky protein, which surrounds the LDL molecules. By means of this sticky protein the lipoprotein(a) molecules accumulate inside the artery walls. Thus, it is not the cholesterol or LDL-cholesterol level that determines the risk for cardiovascular disease; it is the amount of lipoprotein(a) molecules.
The primary therapeutic aim to prevent fatty deposits in the artery wall is therefore to neutralize the stickiness of the lipoprotein molecules and to prevent their attachment to the inside of the artery walls. This can be achieved by means of ?Teflon? substances for the artery walls. The first generation of these ?Teflon? agents has been identified. They are the natural amino acids LYSINE and PROLINE. They form a protective layer around the lipoprotein(a) molecules, which has a twofold effect: preventing the deposition of more fat molecules in the artery wall and releasing lipoprotein molecules that had already been deposited inside the artery walls. Releasing fat molecules from the atherosclerotic deposits leads to a natural reversal of cardiovascular disease. Molecule by molecule is released from the atherosclerotic plaques into the bloodstream and transported to the liver, where these molecules are burned. It is important to understand that this is a natural process, and complications that frequently accompany angioplasty and other mechanical procedures do not occur.
4. Antioxidant protection in the bloodstream and artery walls. An additional mechanism accelerating the development of atherosclerosis, heart attacks and strokes, is biological oxidation. Free radicals, aggressive molecules occurring in cigarette smoke, car exhaust, and smog, damage the lipoproteins in the bloodstream and also the tissue of the artery walls. By doing so, they further extend the size of atherosclerotic plaques. Vitamin C, vitamin E, beta-carotene, and other components of a comprehensive Nutritional Supplement Program contain some of the strongest natural antioxidants, protecting the cardiovascular system from oxidative damage.
The reversal of fatty deposits in the artery wall is a process common in Nature. Bears and other hibernators, for example, use it regularly. During several months of winter sleep (hibernation) these animals do not eat, and therefore get no vitamins in their diet. Moreover, during hibernation the vitamin C production in their bodies decreases to a minimum. As a consequence, fat molecules and other factors from their blood are deposited in the artery walls and lead to a thic theng of these walls. In spring, after these animals arise from hibernation, their vitamin supply increases dramatically from their diet and from their body’s vitamin production. With this increased vitamin supply, the fatty deposits in the artery walls of these animals gradually reverse, and the artery walls retain their natural stability and function.
CONCLUSION: THE LIPID HYPOTHESIS OF ATHEROSCLEROSIS
The lipid hypothesis currently dominates the field of atherogenesis. Dissidents have been classified as biased or extremists not cognizant of the strong epidemiological evidence” for links between dietary fat and coronary heart disease (CHD).’ The truth of this statement, based on the philosophical approach of those who favor a middle of the road course, is not inviolate and depends on logic and the weight of evidence for and against the dietary lipid hypothesis. The voices of dissidents are drowned by the majority and their research grants and publications run the gauntlet of appraisal by lipid protagonists. There is increasing public awareness of the scientific confusion that prevails and genuine worldwide concern the public is being subjected to changes in lifestyle, the chronic effects of which, as yet unknown, are potentially hazardous.
Epidemiology, of particular value in acute infectious and occupational diseases, has less applicability to ubiquitous chronic degenerative diseases such as atherosclerosis. The first step in the investigation of atherogenesis should be to become acquainted with the pathology and to appreciate that atherosclerosis is ubiquitous and not species-specific. Unfortunately most investigators are not well acquainted with the modern pathology of the disease. Rather than appraising the basic scientific evidence many have assumed the lipid hypothesis is valid because of the weight of opinion. Pathologists too have had preconceived ideas which led to misappraisal and misrepresentation of the pathology of the cholesterol-fed animal and familial hypercholesterolemla (FH) on which all the prolipid epidemiological studies rely in vain for biological plausibility. Warnings that the pathology of these conditions differs substantially from spontaneous atherosclerosis were either not heeded or simply ignored.
With the best of intentions many clinical attempts have been made over the years to search for epidemiological factors which might be used to interrupt the chain of events from the initiation of atherosclerosis to the development of clinical and possibly fatal complications of the end-stage disease. Unfortunately no such factor has yet been identified in atherosclerosis analogous to the role of swamps or mosquitoes in malaria or the contamination of the water supply in typhoid epidemics. Some lipid protagonists have mistakenly believed that cholesterol and latterly low density lipoproteins (LDL) fulfill such a role but that is not the case. The empirical approach was unlikely to be successful since atherosclerosis is ubiquitous with a prolonged developmental phase prior to the onset of complications and because correlations of indirect observations were sought with an unsatisfactory surrogate. It is also unlikely that a universal disease in man which is also widespread in lower animals would be due to an essential circulating metabolite or to environmental factors as postulated by the growing school of CHD epidemiology. The difficulties do not excuse the basic errors in methodology that pervade CHD epidemiology.
The basis and evidence for the lipid hypothesis has been reviewed from a broad perspective revealing the poor pathology that so obviously misled early investigators. However misplaced faith in the validity of the pathological and experimental evidence cannot excuse the unscientific methodology on which the epidemiological case has been based. The methodological flaws are mostly indicated as basic errors listed in text books of epidemiology. Errors due to incompetence, lack of logic or ignorance, even though unintentional, are nevertheless scientific misrepresentation. It should be of concern to all that so many have willingly and unquestioningly accepted the fallacious epidemiological methodology and data for so many years and still do so. In the face of the current evidence, lipid protagonists continue to allege success for the cholesterol lowering program and are unwilling to face reality and the possibility that they are wrong.