Reader's guide to potassium food sources, enhancers, and antagonists: Potassium is abundant in most food selections, e.g., 1 banana has 440 mg, 1 medium orange (263 mg), 1 medium peach (308 mg), cup of apricots (318 mg), avocado (680 mg), cantaloupe (341 mg), cup cooked lima beans (581 mg), 1 medium potato (782 mg), 1 medium raw tomato (444 mg), 1 stalk of celery (130 mg), 3 ounces of light chicken (350 mg), 3 ounces of cod (345 mg), 3 ounces of flounder (498 mg), and 3 ounces of salmon (378 mg). Asparagus, carrots, spinach, apples, plums, strawberries, watermelon, roast beef, pork, haddock, and tuna are other reliable sources.

Potassium enhancers (regarding absorption) are vitamin B6, calcium, magnesium, and essential fatty acids. Antagonists to potassium include excesses of sodium, sugar, stress, alcohol, and coffee, plus steroids, diuretics, and laxatives.

Proanthocyanidins--are antioxidants, ACE inhibitors, and beneficial to smokers; reduce platelet aggregation, protect endothelium against white blood cell adherence, increase exercise tolerance
Many names aptly describe the flavonoids found in pine bark, grape seed, citrus peel, lemon tree bark, peanuts, and cranberries. The scientific community once referred to this entire family as pycnogenols, a term now considered outdated. Today pycnogenols are recognized by terms such as proanthocyanidins, oligomeric proanthocyanidin complexes (OPCs), or procyanidolic oligomers (PCOs). In the United States, Pycnogenol is a registered trademark for Horphag Ltd. of Switzerland, identifying a PCO derived from French maritime pine trees.

Much discussion as to whether pine bark or grape seed extract delivers the most medicinal advantage still leaves the question unresolved. Dr. Michael Murray states that while both are excellent sources of proanthocyanidins, grape seed extracts are available that contain from 92-95% PCO content; pine bark extracts vary from 80-85%. An overwhelming majority of the published clinical and experimental trials over the past 20 years have been performed using the grape seed extract, not the extract of pine bark (Murray 1995b).

Peter Rohdewald, Ph.D., reported that nitric oxide (NO) became the molecule of the year in 1993 when, among other functions, it was determined that NO was a powerful vasodilator (Rohdewald 1999). NO is produced in the endothelial cells from arginine, a process controlled by the enzyme, endothelial nitric oxide synthase. Scientists became additionally excited when it was determined that PCOs stimulate endo-thelial nitric oxide synthase, producing more NO. This action counteracts the vasoconstricting effects of the stress hormone adrenaline and also diminishes the threat of platelets clumping.

Studies indicate that PCOs may be an alternative to aspirin. Among 180 poststroke patients receiving 500 mg a day of aspirin for 2 years, 21% were forced to stop medication because of side effects; more than 41% experienced an increase in bleeding time. John D. Folts (University of Wisconsin) reported that flavonoids benefited laboratory monkeys, reducing the incidence of platelet aggregation and blocked arteries with efficiency equal to or greater than aspirin. Adrenaline can completely wipe out the positive effects of aspirin, but it has no degrading effect on flavonoids. PCOs offer neither GI toxicity nor an effect on coagulation, suggesting a better risk-benefit ratio compared to aspirin (Folts 1997; Watson 1999; Duke 2000b).

Research cited in The Lancet showed an inverse relationship between flavonoid intake and the risk of heart attack, that is, the more flavonoids ingested, the less the incidence of heart disease (Hering et al. 1993). PCOs provide some of the most beneficial classes of plant flavonoids available.

Consider the multiple pathways PCOs employ to protect against heart disease:

Inhibits ACE (the angiotensin-converting enzyme) (Duke 2000b). This means that the production of angiotensin II (a vasoconstricting compound) is blocked and sodium and water retention decreases. These actions decrease blood pressure and improve cardiac output; a decrease in heart size usually follows.

Protects the endothelium from leukocyte adherence, a process that lessens the threat of occlusion (Cooke et al. 1997; Rohdewald 1999).

Increases intracellular vitamin C levels, a function that strengthens capillary and blood vessel walls (Schwitters et al. 1993; Murray 1995b).

Appears to offer about 50 times more antioxidant protection than vitamin C or vitamin E, an action that assists in shielding LDL cholesterol from the cardiac damaging oxidation process (Murray 1995b).

Lowers blood cholesterol levels, even shrinking the size of cholesterol deposits appearing in the arteries of laboratory animals (Wegrowski et al. 1984).

Increases treadmill endurance (improvement confirmed by electrocardiograms and stress tests) and reduces myocardial ischemia and cardiovascular deterioration (Petry et al. 2001).

Regarded as beta-adrenergic receptor blockers, reducing sympathetic nervous system activity and the "fight or flight syndrome" (Duke Database 1992).

Reports from the Institute of Pharmaceutical Chemistry (Germany) indicate that PCOs lower platelet aggregation in heavy smokers without increasing the risk of bleeding (Rohdewald 1999). Tests confirm that the platelet aggregation index was reduced to levels closely challenging those found in nonsmokers, in part by inhibiting the synthesis of thromboxane, a compound derived from inflammatory prostaglandins, that increases platelet aggregation (Putter et al. 1999).

For most individuals, 100 mg daily of PCO (grape seed-skin extract) appears adequate. Therapeutic doses are 150-300 mg a day.

Note: While proanthocyanidins do not prolong bleeding time when used independently, if used with anticoagulant drugs, caution is advised.

S

Selenium--prevents ventricular tachycardia, is a hypolipidemic, and improves diabetic symptoms, congestive heart failure, and cardiomyopathy
Cardiomyopathy is defined as any disease that affects the structure and function of the heart. For example, the heart may become disabled as fibrous tissue partially replaces the heart muscle; the fibrous tissue degrades the heart's performance, and the blood no longer moves efficiently. The World Health Organization recognizes cardiomyopathy as a selenium deficiency. In addition, French researchers showed that chronic heart failure (associated with oxidative stress) appears to be relieved by selenium supplementation. Selenium may play a role in the clinical severity of the disease, rather than in the degree of left ventricular dysfunction (de Lorgeril 2001).

Selenium limited the incidence of ventricular tachycardia--that is, at least three consecutive ventricle complexes with the heart rate more than 100 beats a minute--from 91% in the control group to 36% in the selenium-treated group; irreversible ventricular fibrillation was reduced from 45% in the control group to 0% in the selenium group (Tanguy et al. 1998). Luoma et al. (1984) noted that 97 mcg of selenium a day increased the ratio of HDL-LDL cholesterol, while inhibiting platelet aggregation. It is reported that a 1% increase in HDL reduces the risk of a heart attack or stroke 4%.

Korpela et al. (1989), in a 6-month double-blind trial involving 81 heart attack patients, found that 100 mcg of selenium reduced the number of cardiovascular events to one nonfatal heart attack, while the group not receiving the selenium suffered four fatal heart attacks and two nonfatal heart attacks. Among men free of stroke at the outset, low serum selenium was associated significantly with stroke mortality, an adjusted relative risk of 3.7 (Virtamo et al. 1985).

Selenium brought blood glucose levels, malondialdhyde (a breakdown product of peroxidized polyunsaturated lipids), and glutathione concentrations to near control levels in almost all diabetic patients. A suggested dosage is 200-300 mcg daily.

Reader's guide to selenium food sources, enhancers, and antagonists
Quantities found in foods are dependent upon the selenium content of the soil, but typically whole grains, wheat germ, broccoli, onions, tomatoes, Brazil nuts, brewer's yeast, garlic, eggs, and seafood are classed as selenium sources.

Selenium enhancers include most antioxidants and essential fatty acids. Antagonists to selenium absorption are heavy metals (mercury and cadmium), excesses of iron, saturated and trans fats, unresolved stress, and indulgences in alcohol and tobacco.

Taurine--has hypotensive and diuretic activity, tempers the sympathetic nervous system, is beneficial in CHF and arrhythmias, and has digitalis-like mentality
Taurine is the most important and abundant of the amino acids in the heart, surpassing the combined quantity of all the others. Under high stress conditions--hypertension and many forms of heart disease--the need for taurine increases to compensate for either an accompanying impairment of taurine metabolism or increased requirements. Dr. H. Kohaski and colleagues (Japan) suggest that entry-level taurine may have been low and, as the stress of hypertension progresses, taurine levels drop even lower (Kahashi 1983; Braverman et al.1987).

Taurine has a diuretic action that benefits hypertensive individuals, as well as patients with congestive heart failure. Taurine elicits much of its diuretic action by preserving potassium and magnesium and by promoting sodium excretion (Atkins 1996b).

Taurine also reduces blood pressure by acting as an antagonist to the blood pressure-increasing effect of angiotensin, a circulating protein that is activated by renin, a hormone secreted by the juxtaglomerular cells in the kidneys in response to a drop in blood pressure (Braverman et al. 1987). When both blood and urine taurine levels decrease, renin is activated and angiotensin is formed. As a result blood vessels vasoconstrict, water and salt are retained, and blood pressure increases. Taurine suppresses renin and breaks the renin-angiotensin feedback loop. Dr. Robert Atkins, a complementary physician with a creditable cardiology background, amplifies the positive results of scientific literature, stating that taurine would be his choice were he selecting a single nutrient to treat hypertension.

Dr. Y. Yamori (a Japanese researcher who established an amino acid-stroke association) studied a strain of rats, genetically susceptible to strokes. Yamori found the rats had a much lower incidence of stroke, dropping from 90% to 20%, if their diet was supplemented with methionine, taurine, and lysine (Yamori et al. 1983; Braverman et al. 1987).

Japanese researchers found that 3 grams of taurine, administered daily to patients with congestive heart failure, was more effective than 30 mg of CoQ10 (Azuma et al. 1992). The Japanese, who use taurine widely in the treatment of various forms of heart disease, found that 4 grams of taurine, given for 4 weeks, brought relief to 19 of 24 patients with congestive heart failure. Taurine appears to act much like the drug digitalis, increasing the contractility of cardiac muscle and the force of the pumping action.

Taurine appears to impact cardiac arrhythmias through various pathways. For example, some forms of cardiac irregularities are helped by taurine because it regulates membrane excitability and scavenges free radicals. In addition, taurine protects potassium levels inside heart cells, which, when imbalanced, can cause electrical instability and cardiac arrhythmias (Braverman 1987; Chahine et al. 1998).

Some types of premature ventricular contractions and arrhythmias respond to taurine because the amino acid tends to dampen activity in the sympathetic nervous system (SNS) and the outpouring of epinephrine. As the SNS is quieted, the heart tends to beat less aggressively and the blood pressure is lowered. Lastly, Lebanese researchers showed that the incidence of ventricular fibrillation and ventricular tachycardia were significantly reduced when taurine therapy was utilized (Braverman 1987; Chahine et al. 1998). A suggested dosage is 1500-4000 mg daily.

Testoterone--modulates cholesterol levels, dilates blood vessels, improves circulation, lessens angina attacks, and reduces blood pressure
Testosterone, a muscle-building hormone, appears to do far more than promote the development of male secondary sexual characteristics. There are, in fact, many testosterone-receptor sites in the heart that play a role in maintaining heart muscle protein synthesis and strength (Bricout et al. 1994).

If testosterone levels are normal, cholesterol is more easily managed, and blood has an easier route as it flows through dilated vessels. One study showed that circulation to the heart improved 68.8% in patients receiving testosterone therapy (Wu et al. 1993). A testosterone delivery patch applied to men with low testosterone levels increased exercise time on a treadmill and (according to trial participants) increased quality of life. Improved emotional health (important to the heart) and a decrease in the incidence of angina attacks reflect some of the benefits of upgrading testosterone levels (English et al. 2000).

Typically, fibrinogen, triglycerides, and insulin levels are higher if testosterone levels are low (Marin 1995; Kryger 2002). In addition, the elasticity of the coronary arteries diminishes, contributing to the development of arteriosclerosis. Blood pressure increases, but the growth hormone decreases, further weakening the heart muscle. Abdominal fat, the most dangerous form of obesity, increases.

Physicians who check for testosterone deficiencies or testosterone-estrogen imbalances have in some cases been able to discontinue cardiac and hypertension medications. Improved EKGs confirm subjective reports of improvement. Since testosterone testing is noninvasive, the risk-benefit ratio swings heavily in favor of testing. For information about safely increasing testosterone levels, refer to the Male Hormone or Female Hormone Modulation protocols.

Thiamine (Vitamin B1)-- is beneficial in some forms of cardiac arrhythmias, palpitations, enlarged heart, elevated venous pressure, and congestive heart disease
Cardiac arrhythmia refers to a deviation from the normal pattern of the heartbeat. Arrhythmias can be caused by a variety of underlying medical conditions that should be addressed by a qualified cardiologist. Arrhythmias are not always clinically significant because rather benign events can spur healthy hearts to enter irregular patterns of beating. Yet, arrhythmias should be taken seriously, and a diagnosis made as to the causative factors provoking the disturbed beat. Stress, electrolyte imbalance, ischemia, hypoxia, ventricular enlargement, occlusions, an insulin rush, or derangement in the autonomic nervous system can drive a heart into irregular rhythms.

Since thiamine has proved correctional for some types of arrhythmias, there appears to be linkage between irregular heartbeats and beriberi, a disease caused by a deficiency of or an inability to assimilate thiamine. Cultures that depended upon rice, a high carbohydrate food, as a dietary mainstay found the milling process, that is, the removal of the brown coat rich in thiamine, to be their undoing. Beriberi swept through the population with epidemic force.

Cardiac arrhythmias may manifest among heavy drinkers as thiamine deficiencies occur, and symptoms of beriberi appear. But, heavy imbibers are not the only individuals susceptible to thiamine deficiency. Infirm individuals, as well as those who are elderly and malnourished, are at particular risk. Long-term diuretic usage can also contribute to a thiamine deficiency through urinary loss. It is not uncommon for heart palpitations, deranged heart rhythms, and elevated venous pressure to occur as patients become thiamine deficient (Whiting 1989). Additional cardiovascular manifestations of wet beriberi are myocardial lesions, sodium and water retention, and biventricular myocardial failure. Typically, clinical improvement occurs quickly following vitamin B1 therapy (Blanc et al. 2000).

In 1995, 30 patients with severe heart failure and taking furosemide (Lasix, a diuretic) were enrolled in a heart study. Although furosemide was unsuccessful in improving their cardiac condition, 200 mg of thiamine (a day) dramatically improved heart function (Shimon et al. 1995). Some patients may experience improvement from 200-250 mg a day; other individuals may require 500-1000 mg daily. (A full spectrum vitamin B supplement should always accompany single B vitamin supplementation.)

Reader's guide to vitamin B1 food sources, enhancers, and antagonists.
Lean pork, wheat germ, and whole grains (particularly brown rice) are considered to be excellent sources of thiamine. Meat, poultry, egg yolk, fish, legumes, peas, sunflower seeds, nuts, and brewer's yeast represent other good thiamine choices.

Vitamin B1 enhancers are all others of the B complex, vitamin C, vitamin E, and manganese. Alcohol, coffee, antacids, and excesses of sugar and refined carbohydrates decrease thiamine absorption.

Tocotrienols--are antioxidants, decrease platelet aggregation, and have statin mentality
Tocotrienols have been until recently the lesser known half of vitamin E. A major functional difference between tocotrienols and tocopherols appears to be the ability of tocotrienols to more aptly decrease cholesterol synthesis in the liver. Both tocotrienols and tocopherols appear to be potent antioxidants, with some research demonstrating greater antioxidant protection and less oxidative damage when supplementing with tocotrienols (Serbinova et al. 1991).

Cholesterol lowering statin drugs--Lipitor, Lescol, Mevacor, Pravachol, and Zocor--operate at the level of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase. HMG-CoA reductase is a rate-limiting enzyme that participates in cholesterol synthesis. The cholesterol cascade occurs as follows: (1) acetyl-CoA is converted to HMG-CoA, (2) HMG-CoA is reduced to mevalonic acid by the enzyme HMG-CoA reductase, and (3) several steps convert mevalonic acid to squalene and then to cholesterol.

Tocotrienols, particularly gamma and delta, accelerate the degradation of HMG-CoA reductase, altering the functionality of the enzyme responsible for cholesterol synthesis (Parker et al. 1993). The statin drugs, though acting at the level of HMG-CoA reductase, approach the enzyme differently. Statin drugs do not degrade the enzyme but competitively inhibit its binding. The inhibition of the binding mechanism leads to a higher production of HMG-CoA reductase, which may explain the side effects, such as liver toxicity, associated with statin usage.

Studies indicate that roughly 75% of hypercholesterolemic individuals respond favorably to tocotrienol supplementation. The most impressive cholesterol reductions occur when tocotrienol supplements are combined with dietary changes (a high fiber/low fat diet). In a 12-week double-blind trial, those who responded to tocotrienol therapy saw a reduction of approximately 23% in total cholesterol and a 32% reduction in LDL cholesterol using dietary modification plus tocotrienol supplements. Tocotrienols alone yielded a 16% decrease in total cholesterol and a 21% decrease in LDL cholesterol (Quereshi et al. 1993; ACCM 1998). HDL levels do not appear to respond to tocotrienol supplementation, but apo-B, a protein component found in LDL, VLDL, and IDL cholesterol, is lowered. Thromboxanes are also considered toco-trienol responsive (Qureshi et al. 1997).

The Kenneth Jordan Heart Research Foundation (New Jersey) reported the results of 50 patients with narrowing of the carotid artery who were treated with either a placebo or tocotrienols: 25 patients (some with carotid stenosis greater than 49%) received 650 mg of tocotrienols plus tocopherols; a control group of 25 patients, with comparable closure, received a placebo. Each group was evaluated every 6 months for the first year and every year thereafter with ultrasonography. In the placebo group, 15 patients showed worsening of the stenosis, eight remained stable, and two showed some level of improvement. In the tocotrienol plus tocopherol group, three patients showed minor worsening, 12 remained stable, but 10 patients showed regression of stenosis. Participants experienced a simultaneous drop in triglycerides and LDL cholesterol (Papas undated; Tomeo et al. 1995; Watkins et al.1998).

The late Karl Folkers, a pioneer in CoQ10 research, observed that drugs inhibiting HMG-CoA reductase activity cause a simultaneous decrease in CoQ10 levels (Folkers et al. 1990). The reason for this is that the HMG-CoA enzyme also plays a role in CoQ10 synthesis. Individuals using either statin drugs or tocotrienols may wish to increase their intake of CoQ10; a decrease in CoQ10 could negate any benefit garnered from a hypocholesterolemic drug.

According to Andreas M. Papas, Ph.D., appropriate tocotrienol dosages are as follows: 100 IU of mixed tocopherols and 100 IU of tocotrienols if young and healthy and without a family history of heart disease; 200 IU of mixed tocopherols and 200 IU of toco-trienols for young adults with some cardiac risk factors or healthy people up to 50 years of age without risk factors; 400 IU of mixed tocopherols and 400 IU of tocotrienols for people who have a personal or family history of chronic heart disease. The latter dosage includes senior subjects and those under severe stress and eating a poor diet.

Vitamin A and Beta-Carotene--lower fibrinogen levels and heart disease risks and increase insulin sensitivity
Dexter Morris, M.D. (University of North Carolina), says that phytochemicals keep your heart healthy. "The 60-80 age group has a much greater risk of heart disease than younger people do. If your diet is rich in fruits and vegetables, you can reduce risk," according to Morris. In a study begun in 1973, researchers kept track of 1883 men ages 35-59 who had high cholesterol levels. Over the next 20 years, the men who had the highest levels of carotenoids in their blood had 60% fewer heart attacks and deaths (Morris 2001).

Dr. J.E. Manson of the Women's Hospital in Boston reported that those taking 25,000 IU of beta-carotene daily had 22% fewer heart problems and strokes than those taking less than 10,000 IU daily (Friend 1991; Passwater undated). Dr. Monika Eichholzer (scientist at the University of Bern, Switzerland) reported similar findings after tracking 2974 people for 12 years. The relative risk of ischemic heart disease was increased (1.53%) among those lowest in plasma carotene concentrations (Eichholzer et al. 1992).

High vitamin A and beta-carotene serum levels have been reported to reduce fibrinogen levels in humans and animals (Green 1997). Animals fed a vitamin A-deficient diet have an impaired ability to break down fibrinogen, but when injected with vitamin A, they produce tissue plasminogen activators that break down fibrinogen, reducing the risk of clot formation.

Vitamin A is beneficial to individuals with Syndrome X and diabetes. A study involving 52 patients indicated that vitamin A enhanced insulin-mediated glucose disposal (Facchini et al. 1996a). Since beta-carotene must be converted in the body to vitamin A, an adaptation some individuals lack, diabetics may do better using vitamin A rather than beta-carotene.

It should be noted that the protection of beta-carotene is not absolute. In fact, if the individual is consuming greater amounts of alcohol, beta-carotene may actually increase the risk of intracerebral hemorrhage (Leppala et al. 2000). A blend of phytoextracts (alpha-carotene, beta-carotene, lutein, and lycopene) appears to offer more comprehensive cardiac protection than using beta-carotene alone.

For example, individuals participating in the Toulouse study who had higher blood levels of lutein also had a lower incidence of coronary artery disease (Howard et al. 1996). The Los Angeles Atherosclerosis study uncovered a relationship between thickenings in the carotid arteries (an indicator of systemic atherosclerosis) and blood levels of lutein (Dwyer et al. 2001). Participants with the highest blood levels of lutein showed virtually no artery wall thickening, while those with the lowest lutein levels showed increased arterial thickness. In addition, lutein reduces the oxidation of LDL cholesterol, a declaration the Life Extension Foundation first made to members in 1985.

A current Finnish study evaluated 725 middle-aged men free of coronary heart disease and stroke at the study baseline. Men in the lowest quartile of serum levels of lycopene had a 3.3-fold risk of an acute coronary event or stroke compared with other trial participants with higher lycopene levels. In a second study, the same researchers assessed the association between plasma concentrations of lycopene and intima-media thickness (IMT) of the common carotid artery wall in 520 asymptomatic men and women. After adjusting for common cardiovascular risk factors, low plasma levels of lycopene were associated with an 18% increase in IMT in men as compared with men in whom plasma levels were higher than median. In women, the difference did not remain significant after the adjustments (Rissenen et al. 2002).

German researchers reported that plasma levels of alpha-carotene may represent a marker of atherosclerosis in humans. Measuring alpha-carotene levels (among other antioxidants) may be of clinical importance as a practical approach to assess atherogenesis and/or its risk (Kontush et al. 1996).

Some individuals are susceptible to vitamin A toxicity even when the dosage is low. This occurs because of a challenged liver and fewer detoxification mechanisms. Beta-carotene, on the other hand, is generally regarded as nontoxic (more about vitamin A toxicity). Appropriate dosages for most individuals are 5000 IU of beta-carotene and/or 10,000 IU of vitamin A daily. Several supplements are available that provide the carotenoids alpha-carotene, beta-carotene, lutein, and lycopene.

Reader's guide to vitamin A food sources, enhancers, and agonists.
The richest sources of vitamin A are foods of animal origin, i.e., liver, fish liver oil, milk and milk products, butter, and eggs. Yellow fruits and green and yellow vegetables will also help meet vitamin A requirements.

Enhancers to vitamin A absorption are vitamin C, calcium, magnesium, vitamin E, B complex, choline, and essential fatty acids. Vitamin A antagonists are laxatives and some cholesterol-lowering drugs (Questran). Coffee, alcohol, excess iron supplementation, sugar, tobacco, and mineral oil can also interfere with vitamin A absorption. Food sources of lutein are kale, Brussels sprouts, corn, collards, spinach, and egg yolks. Egg yolks have tiny amounts of lutein--about 0.2 mg a yolk--because chickens eat corn (Carper 2002). Lycopene is present in tomatoes and several other red fruits.

Vitamin C--lessens risk of stroke and heart attack; strengthens blood vessels; reduces blood pressure, fibrinogen levels, Lp(a), inflammation, and C-reactive protein (CRP); promotes gingival healing; is a reliable antioxidant and diuretic; and is highly beneficial to smokers and those exposed to secondhand smoke

Linus Pauling, a Nobel Prize winner, showed that the body often forms atherosclerotic plaque to repair a wound inflicted upon an artery. When adequate amounts of vitamin C are available, an injured artery is repaired without involving atheromatous materials. In the absence of adequate levels of vitamin C, Lp(a), acting as a surrogate for vitamin C, must participate in the repair. Lp(a) does what it must, but the health of the artery is compromised as plaque is added to the vessel. If ascorbate levels had been adequate, Lp(a) would not have been necessary; without adequate vitamin C, the need for Lp(a) is enormous.

Vitamin C Lowers Lp(a)
Kathie M. Dalessandri, M.S., M.D., was inspired by a report appearing in the Archives of Internal Medicine relating to the ability of vitamin C to lower Lp(a). Dr. Dalessandri, a general surgeon in Point Reyes Station, CA, was displeased with her own Lp(a) levels. She was well aware of the dangers associated with Lp(a), particularly when linked with other risk factors as a family history of heart disease. Dr. Dalessandri (53 years old at the time) was taking hormone replacement therapy and niacin, but the niacin became problematic and had to be discontinued. After reviewing the literature, she decided upon 3 grams a day of both ascorbic acid and L-lysine monohydrochloride as a natural regime against the elevated Lp(a). Dr. Dalessandri reports that her Lp(a) dropped 14 mg/dL, a reduction of 48% after 6 months. She was also pleased that she was able to take vitamin C and lysine without side effects (Dalessandri 2001).

Matthias Rath, M.D., in Eradicating Heart Disease, says that animals do not have heart attacks and strokes because their bodies manufacture vitamin C, a genetic adaptation humans lack. Most mammals produce impressive amounts of vitamin C, the human equivalency of 2000-13,000 mg daily. Under periods of stress the same animal's needs for vitamin C may skyrocket, but the body complies by producing prodigious amounts. Man cannot adapt to stress with the same efficiency as lower animals because of a lack of L-gulonolactone oxidase, an enzyme needed to produce vitamin C from glucose. Dr. Rath states that because of this genetic flaw and inadequate dietary vitamin C, cardiovascular disease can emerge as a form of early scurvy (Rath 1993).

An ascorbic acid deficit contributes to the development of vascular lesions (wounds or injuries) by altering collagen metabolism (Rath 1993). Vitamin C produces many collagen molecules, supporting a strong and elastic blood vessel wall. Over time, arterial collagen must be replenished. If vitamin C is not present in large enough quantities, collagen is not produced, and blood vessels become thin and weak.

Vitamin C levels are lower in patients who have had heart attacks, both fatal and nonfatal events. Randomly selected Finnish men (1605 individuals who were 42-60 years old) entered a study evidencing no signs of preexisting heart disease. Among men with a vitamin C deficiency, 13.2% had a heart attack compared to 3.8% who were not vitamin C deficient. After adjusting for other confounding factors, men who were deficient in vitamin C had 3.5 times more heart attacks than men who were not vitamin C deficient (Nyyssonen et al. 1997).

The most significant report emanated from UCLA, where it was announced that men who took 300-400 mg of vitamin C a day lived 6 years longer than those who received less than 50 mg daily. The study (which evaluated 11,348 participants over a 10-year period) showed that long-term, high vitamin C intake extended average lifespan and reduced mortality from cardiovascular disease 45% (Enstrom et al. 1992; Hansen 2000).

Researchers from the Boston University School of Medicine reported that vitamin C appears effective in lowering mild cases of hypertension. The patients lowered systolic and diastolic blood pressure by about 9% with a daily dose of 500 mg of ascorbic acid (Stauth 2001). The value of vitamin C as a hypotensive nutrient may come by way of its antioxidant activity, possibly by protecting the body's supply of NO, a vasodilator. (Free radicals appear to lower NO levels.) Depriving test animals of antioxidants, such as vitamin C, glutathione, and vitamin E, resulted in oxidative stress and higher blood pressure.

The heart is one of the most vulnerable of all organs to free-radical oxidative stress. Vitamin C can respond to this risk by exerting its antioxidant properties, acting independently, or by prompting the production of other antioxidants. For example, 3 grams of vitamin C increased white blood cell glutathione levels fourfold and plasma glutathione levels eightfold (Jain et al. 1994; Murray 1996b).

Vitamin C is beneficial in reducing fibrinogen levels. In a report published in the journal Atherosclerosis, heart disease patients were given either 1000 or 2000 mg a day of vitamin C to assess its effect on the breakdown of fibrinogen. At 1000 mg a day, there was no significant change in fibrinolytic activity. At 2000 mg of vitamin C a day, fibrinolytic activity increased 62.5% (Bordia 1980).

Inflammation, a newer risk factor for heart disease, is reduced by vitamin C. Each winter (in most countries) there is a 15-30% increase in deaths from cardiovascular and respiratory disease. Researchers in the United Kingdom followed 96 men and women for 1 year to assess the impact of winter stress upon the heart and circulatory system. It appears some of the increase in winter cardiovascular mortality may be related not only to a rise in fibrinogen, but also to an increase in other inflammatory markers, such as C-reactive protein. This cycle may be spurred as winter infections increase and vitamin C intake (because of less availability of fruits and vegetables) decreases. The conclusion of the study was that vitamin C might be able to influence cardiovascular risk and the resulting thrombotic tendency by modulating the inflammatory response to infection (Woodhouse et al. 1997).

Cardiovascular Disease Protocol Pg (1) (2) (3) (4) (5) (6) (7) (8) (9) (10) (11) (12) (13) (14)

These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease