Cardiovascular Disease Protocol

Note: Extremely important data were recently published showing that pretreatment with 800 IU of vitamin E and 1000 mg of C (before an oral methionine load to experimentally produce homocysteine) blocked the damaging effects of hyperhomocysteinemia. Coagulation and circulating adhesion molecule levels significantly increased after methionine ingestion alone but not after methionine ingestion with vitamins (Nappo et al. 1999).

Reader's guide to food sources, enhancers, and antagonists to homocysteine-lowering B vitamins
Medications to treat congestive heart failure commonly result in multiple B vitamin deficiencies, disrupting disposal systems for homocysteine clearance (Sinatra 2001). Also, B vitamins are considered unstable when exposed to the heating process, but the following foods represent the most nutrient-dense choices:

Vitamin B6 appears in most foodstuffs, but the best sources are brewer's yeast, carrots, chicken, eggs, fish, meat, peas, spinach, sunflower seeds, walnuts, and wheat germ.

Complimentary nutrients in regard to vitamin B6 absorption are the full B complex, vitamin C, magnesium, potassium, and zinc. Antidepressants, alcohol, coffee, exercise (to excess), estrogen therapy, and oral contraceptives appear to either increase the need for vitamin B6 or reduce its status. Diuretics and cortisone drugs block its absorption, and theophylline, an oral bronchodilator, antagonizes pyridoxal phosphate synthesis (Ubbink et al. 1996).

Vitamin B12, the most complex of the B vitamins, should be of special interest to vegans who, after chronic abstinence from animal products, can become seriously depleted in this nutrient. However, most vitamin B12 deficiencies occur not because of inadequate dietary consumption, but rather because of poor absorption. The intrinsic factor, a substance secreted by the gastric mucosa, is essential for the absorption of B12, transporting cyanacobalamin (vitamin B12) across the membranes of the ileum (the distal end of the small intestine).

Animal derivatives, eggs, fish and marine life, beef and pork, and milk and dairy products are good sources of vitamin B12. Nutrients considered B12 enhancers are others of the B complex (especially folic acid and vitamin B6), vitamin C, iron, potassium, sodium, and calcium.

Medications to treat gout, anticoagulant drugs, and potassium supplements may block the absorption of vitamin B12 from the digestive tract (Balch et al. 1997). For optimal B12 utilization, avoid coffee, alcohol, smoking, and laxatives.

Folate-rich foods are liver, wheat germ, legumes, green leafy vegetables, beets, citrus fruits, most fish, pork, and whole grains. Fortification of enriched grain products with folic acid is associated with a substantial improvement in folate status in middle aged and older adults (Jacques et al. 1999).

Folic acid is most efficient when combined with vitamin B12, biotin, pantothenic acid, and vitamin C. According to the Committee on Dietary Allowances, heat and oxidation (occurring during cooking and storage) can destroy as much as half of the folate in foods. Sulfa drugs interfere with the bacteria in the intestines that manufacture folic acid, and Streptomycin totally destroys it. Methotrexate depletes folate, causing a transient elevation in homocysteine, and phenytoin (an antiepileptic drug) interferes with folate metabolism. Lastly, oral contraceptives, alcohol, coffee, and smoking are also considered folic acid antagonists.

M

Magnesium--reduces blood pressure, is a calcium antagonist, tempers the sympathetic nervous system, is beneficial in arrhythmias and mitral valve prolapse, increases the number and sensitivity of insulin receptors, has antidiabetic properties, encourages the methylation process, prevents toxic buildup of homocysteine, reduces calcium levels, is a vasodilator, and opposes platelet aggregation
Magnesium, a potent vasodilator, may prove to be a better hypotensive in some individuals than calcium (50% of magnesium-depleted patients are hypertensive, a condition often remediable with supplementation).

The British Medical Journal reported that magnesium supplementation lowered blood pressure by a mean of 12/8 mmHg (systolic and diastolic pressures) in 19 of 20 subjects (Dyckner et al. 1983). Magnesium reduces blood vessel contractibility by regulating levels of bradykinin, angiotensin II, prostaglandins, serotonin, epinephrine, norepinephrine, and dopamine; as a result, vessels vasodilate and blood pressure decreases.

Besides being a hypotensive mineral, magnesium is absolutely essential to proper cardiac function, allowing relaxation of the heart and supporting normal heart rhythms. In a study of patients admitted to coronary care units experiencing arrhythmias, 100% had complete resolution when administered IV magnesium over a 5-hour period. Dr. Bart Chernow (a surgeon at Sinai Hospital in Baltimore, MD) reports that magnesium injections following bypass surgery reduced heart rhythm irregularities 50%, without side effects (Alternative Medical News staff). After 3 months of oral magnesium supplementation, platelet-dependent thrombosis typically is reduced 35% in 75% of patients.

In a study in the American Journal of Clinical Nutrition, researchers from the U.S. Department of Agriculture reported the effects of a magnesium-deficient diet on 22 healthy postmenopausal women ages 47-78. The women all ate the same meals for 6 months as they lived together under close supervision, taking in about 130 mg of dietary magnesium each day. Half the women also took an additional 280 mg of magnesium in supplemental form for 81 days while the other half received a placebo; during the second half of the study period, the groups crossed over to the other treatment category.

The researchers assessed magnesium levels in urine and blood regularly, as well as heartbeat patterns through electrocardiograms. Not surprisingly, serum and urine concentrations of magnesium were lower on the controlled diet, but heart rhythms were also significantly affected by lesser amounts of magnesium. A lack of magnesium provoked the heart into rhythmic abnormalities, as well as more frequent heartbeats. The researchers concluded that the cardiac muscle is more sensitive to magnesium intake than skeletal muscle and that a deficiency has the potential to cause dangerous cardiac irregularities (Klevay et al. 2002).

Calcium channel blockers are popular as antiarrhythmics and antispasmodics (to read more about calcium channel blockers, consult the sections devoted to Beta-Blockers and Calcium Channel Blockers appearing in this protocol). By relaxing arterial smooth muscles and reducing stress on the myocardium (the thick middle layer of the heart), magnesium delivers many of the effects of a calcium channel blocker (Whitaker 1995b).

Magnesium turns off activity in the sympathetic nervous system. By blocking the release of excitatory hormones (epinephrine and norepinephrine), the "fight or flight" response of the sympathetic nervous system is inhibited (Gonzalez 2000). Although the therapeutic profile of magnesium is similar to a beta-blocker, the drug should not be abruptly stopped and magnesium commenced; without a gradual withdrawal of the drug, a rebound could occur, provoking a heart attack.

In mitral valve prolapse, the valve separating the left atrium from the left ventricle protrudes into the left atrium. Of patients participating in an evaluation, 85% were found to have low magnesium levels, suggesting that a deficiency plays a role in the disturbance (Fernandes et al. 1985; Galland et al. 1986; Murray 1996). Numerous studies indicate that magnesium lessens mitral valve prolapse symptoms, palpitations, fatigue, breathing difficulties, and nonanginal chest pains. Others have observed improvement in exercise tolerance and reduced stress within the heart itself (Shechter et al. 2000). Comment: Low magnesium levels also are associated with angina attacks in men. It appears that as magnesium status drops, the frequency of angina attacks increases (Satake et al. 1996).

Too much calcium in the bloodstream may be a forerunner to aortic stenosis (Bonow et al. 1998). Magnesium hinders the absorption of calcium; therefore supplementing with at least 500 mg a day could inhibit the excesses of calcium hardening the cusps of valves (for a comprehensive look at aortic stenosis, consult the section of this protocol dedicated to Valvular Disease).

Magnesium plays an important role in the prevention and treatment of Syndrome X and diabetes. It benefits these conditions by increasing the number and sensitivity of insulin receptors (Waterfall 2000).

In addition, increased homocysteine concentrations cause abnormal metabolism of magnesium in vascular smooth muscles cells, priming these cells for homocysteine-induced atherogenesis, cerebral vaso-spasm, and stroke. Researchers from State University of New York propose that vitamin B6, vitamin B12, and folic acid, together with physiological levels of magnesium, are needed to prevent magnesium depletion and occlusive cerebral vascular diseases induced by homocysteinemia (Li et al. 1999).

Magnesium status is integral in various drug therapies. Recent controlled studies have shown that treatment with magnesium significantly reduced the frequency and complexity of ventricular arrhythmias in digoxin-treated patients with congestive heart failure. In fact, magnesium improved the efficacy of digoxin (digitalis) in slowing the ventricular response in atrial fibrillation. The complex and potentially life-threatening interactions between magnesium and some cardiovascular drugs suggest that magnesium status should be carefully monitored in patients receiving cardiac pharmaceuticals (Crippa et al. 1999).

Unfortunately, the test used by the majority of physicians to measure magnesium levels is worse than useless, according to Dr. Sherry A. Rogers, an environmental medicine specialist. Dr. Rogers refers to this test as "the most dangerous test in medicine" for if it is used, it too often shows misleading normal levels. The assumption that adequate amounts of magnesium exist when, in fact, deficiency states exist may be a fatal mistake. A study in the Journal of the American Medical Association reported that about 90% of practicing physicians never think to check magnesium levels, even in patients who are severely depleted (Whang et al. 1990). Note: Magnesium deficiency is better detected by measuring mono-nuclear blood cell magnesium, as opposed to serum levels.

A dosage suggestion is 500-1500 mg daily of magnesium bound to succinate, citrate, or aspartate. Magnesium oxide, in larger doses, can cause loose stool.

Reader's guide to magnesium-rich foods, enhancers, and antagonists
Magnesium is found in most foods, particularly nuts, whole grains, legumes, brown rice, dark green vegetables, and fish (Balch et al. 1997).

Magnesium enhancers include the B-complex (especially vitamin B6), vitamin C, calcium, essential fatty acids, and essential amino acids. The body's requirement for magnesium increases if using alcohol, taking higher amounts of vitamin D, or if exposed to fluoride, tobacco, or unrelenting stress. Cod liver oil, calcium (excessive intake), and iron decrease magnesium absorption. Diuretics and chronic diarrhea can seriously deplete many minerals, including magnesium.

N

Niacin (Vitamin B3)--lowers Lp(a), reduces fibrinogen, normalizes blood lipids, and acts as a vasodilator
Nicotinic acid and nicotinamide are types of the vitamin niacin; although related, they are different in their therapeutic delivery. Nicotinamide, often marketed as a superior lipid-lowering version of niacin, actually has little effect in lowering blood lipids (Segrest 2000). It is nicotinic acid that modulates most all lipid parameters, lowering total cholesterol, LDL, VLDL, Lp(a), and triglyceride levels, while increasing HDL cholesterol. Nicotinic acid has, in fact, won favor with the FDA, adding it to a list of other remedials capable of lowering triglycerides.

Because of niacin's broad-spectrum effectiveness against hyperlipidemia, niacin can act independently or in concert with other drugs. Dr. B. Greg Brown (of the University of Washington, Seattle) reported to the American Heart Association that a combination of a statin drug (which lowers LDL cholesterol) and niacin (which raises HDL cholesterol) brought the progression of atherosclerotic disease to a standstill. According to Brown, a niacin-simvastatin combination resulted in a 70% reduction in heart attacks, strokes, and other disease-related events. According to Brown, "This represents twice the reduction seen with statins alone." Simvastatin (Zocor) plus niacin increased HDL levels 30% over baseline, while Zocor alone increased HDL only 7-10% (Kerr 2000). In addition, nicotinic acid can act independently, accomplishing what no drug can currently do: lower Lp(a); 1500 mg a day of niacin reduced Lp(a) an average of 20%; 3000 mg a day reduced Lp(a) an average of 26% (Berkeley Heart Lab).

Niacin has properties that are the opposite of those of nicotine. Nicotine, a toxic substance in tobacco, is a vasoconstrictor; niacin is a vasodilator. Niacin's vasodilating quality makes it beneficial in the treatment of hypertension and various forms of heart disease.

In 1991 a group of scientists found that small amounts of niacin in combination with chromium, lowered cholesterol levels by an average of 14% and improved the total cholesterol-HDL ratio 7% (Urberg et al. 1987; Cichoke 2001). This finding is valuable since niacin has some significant side effects, making it less justifiable in large doses. Articles appearing in the American Journal of Cardiology and the Journal of Cardiovascular Risk confirmed niacin's hypolipidemic value and also reported that low-dose niacin was effective in reducing plasma fibrinogen levels in subjects with peripheral vascular disease (Philipp et al. 1998; Ma et al. 1999).

If used independently, 1-3 grams of niacin is sometimes required to lower cholesterol levels, a dosage that can cause side effects ranging from nuisance complaints to significant endangerments. Allergic-like reactions, such as itching and flushing, are common, but niacin can also disrupt liver function, causing elevations of liver enzymes.

Other risks associated with niacin:

Individuals dosing with niacin may experience a rise in uric acid, an increase that can bring on a gout attack (Goldberg 1998). Recall that individuals with Syndrome X often present with higher levels of uric acid.
Niacin may interfere with folate and homocysteine metabolism and actually increase plasma homocysteine levels (Desouza et al. 2002). Dr. David Blankenhorn was the first to discover the niacin-homocysteine connection at USC in the CLAS study. Niaspan, an extended-release niacin, raised homocysteine levels in some, but not all people; the amount is generally between 1-4 micromol/L and appears to be dose-dependent (Berkeley Heart Lab).
Niacin may deplete SAM-e, a pivotal player in methylation. If niacin does decrease SAM-e, a likely consequence would be an elevation of plasma homocysteine (McCarty 2000). Note: Concurrent TMG supplementation may represent a cost-effective way to prevent niacin-mediated depletion of SAMe and thus avoid hepatotoxicity (and possibly other adverse niacin side effects). The lack of sufficient detoxification (due to SAM-e depletion) appears to explain many of the adverse effects associated with niacin dosing.
Niacin can also increase blood glucose levels. In nondiabetic patients, 1500 mg a day of Niaspan (an extended-release niacin) increased fasting blood glucose levels 2.5-11% following a 2-hour glucose load. Using 3000 mg a day of immediate-release niacin, fasting blood glucose increased 4.1% and 11.6% following a 2-hour glucose load. The niacin effect in Type II diabetic patients is currently under investigation (Berkeley Heart Lab). However, it is speculated that individuals predisposed to Type II diabetes may have a poorer response to niacin (in regard to glucose management) compared to individuals without a diabetic inclination.
Considering these negatives, large-dose niacin may be too great a price to pay for the benefits. If a decision is made to use high-dose niacin, some practitioners report that an aspirin taken 30 minutes before the dose markedly reduces some of the lesser side effects, for example, the allergic-like symptoms.

Reader's guide to vitamin B3 sources, enhancers, and antagonists.
Good sources of niacin are lean meats, whole grains, brewer's yeast, peanuts, eggs, poultry, fish, and green, leafy vegetables. Milk; some cheeses, for example, cheddar cheese; bananas; and turkey are good sources of tryptophan (a precursor to niacin) (Braly 1985).

Vitamin B3 enhancers (in regard to absorption) are the B-complex (especially vitamins B1, B2, and B6), vitamin C, magnesium, zinc, protein, and essential fatty acids. Antagonists to niacin absorption are alcohol, coffee, excess sugar, antibiotics, and steroids.

O

Olive Leaf Extract--according to botanist James Duke, the cardiac properties found in olive leaf extract include antioxidants, antiaggregates, antiarrhythmics, anti-inflammatories, cyclooxygenase inhibitors, diuretics, hypotensives, vasodilators, antispasmotics, antidiabetics, platelet activating factor inhibitors, weight modulators, antiperiodontics, antihyperlipidemics, and plaque fighters
Olive leaf extract (Olea europaea), although historically regarded as a medicinal for fever and malaria, is also valuable in the treatment of cardiovascular disease. Olive leaf extract has been shown in both laboratory and clinical settings to have antidiabetic, hypotensive, and vasodilating properties (Petkov et al. 1972; Gonzalez et al. 1992; Fehri et al. 1994). Researchers documented that an aqueous extract of olive leaves inhibits ACE, the enzyme that converts angiotensin I to angiotensin II (Duke 1992). The vasoconstricting nature of angiotensin II terminates in an increase in blood pressure, a sequence that olive leaf extract disrupts.

According to Dr. Duke, chemicals contained in O. europaea are regarded as calcium antagonists, diuretics, and anti-inflammatories. In addition, olive leaf protects LDL cholesterol against oxidation and inhibits the production of thromboxane A2 and platelet-activating factor (PAF). These functions discourage vasoconstriction and platelet clumping (Duke 1992; Petroni et al. 1995; Mindell 1998).

Chelation therapy, in conjunction with an aggressive supplemental program that relied heavily upon olive leaf extract, has proved remedial among select senior subjects who have suffered multiple heart attacks and arrhythmias. A suggested dosage is one to two 500-mg olive leaf extract capsules, administered 3 times daily with meals.

P

Pantethine--reduces cholesterol, discourages platelet clumping, and has antioxidant activity
Pantethine, a biologically active, intermediate form of pantothenic acid (vitamin B5) and a precursor to coenzyme A, is a powerful natural pharmaceutical that reduces cholesterol, increases heart muscle contractility, slows the heart rate, and has antioxidant activity.

Pantethine (300 mg 3 times daily) reduced serum triglycerides 32%, total cholesterol 19%, and LDL cholesterol 21%; HDL cholesterol levels increased 23% (Arsenio et al. 1986, Murray 1996b). Pantethine further reduces cardiovascular risk by inhibiting platelet clumping and the production of the inflammation-producing chemical, thromboxane A2 (CVR). A dosage suggestion is 300 mg 3 times a day.

Policosanol--is a hypocholesterolemic, protects LDL cholesterol against oxidation, inhibits thromboxane and the proliferation of vascular cells, discourages blood clot formation, inhibits platelet aggregation, and increases exercise tolerance
Policosanol, derived from sugar cane, is a new face on the cholesterol scene in the United States but is a popular hypocholesterolemic in other countries (Mas et al. 1999). The main ingredient in sugar cane is octacosnol, a long-chain fatty alcohol found in the waxy film that covers the leaves and fruit of plants.

Policosanol represents an effective alternative to lowering cholesterol for many people. For example, 10 mg a day of policosanol (over a 6- to 12-week period) lowered LDL cholesterol 20%, reduced total cholesterol 15%, and raised the beneficial HDL cholesterol 7-28%. Doubling the dose (20 mg a day) resulted in the following lipid improvements: LDL cholesterol reduced about 28%, total cholesterol about 20%, and HDL increased by 7-10%. Triglycerides were unaffected. During the course of the trial, participants continued on a low cholesterol diet.

The hypolipidemic effects of policosanol are comparable to many cholesterol-lowering drugs (Prat et al. 1999). The results of a head-to-head study classing popular hypocholesteremic drugs against policosanol.

Comparison of Policosanol to Classic Drug Therapy
CHOLESTEROL-LOWERING AGENT DOSAGE LIPOPROTEIN EVALUATED AMOUNT REDUCED
Lovastatin (Mevacor) .........................................20 mg ......................LDL Cholesterol ......22%
Simvastatin (Zocor) .............................................10 mg .........................LDL Cholesterol ..15%
Policosanol ..................................................10 mg ..................................LDL Cholesterol 24%

Policosanol also outclassed the drugs in regard to increasing levels of the beneficial HDL cholesterol. Yet, a combination of policosanol and gemfibrozil (Lopid) was more hypocholesterolemic than either used singularly. In fact, policosanol even upgraded the efficiency of bezafibrate, a once touted fibrinogen-lowering drug that yielded disappointing results in the Bezafibrate Infarction Prevention Study (Castano et al. 1998; Behar 1999). Bezafibrate in union with policosanol dramatically reduced LDL and total cholesterol. In addition, policosanol appears to replicate another of the objectives of statin drugs, reducing the proliferation of cells. A telltale sign of a diseased vessel is that the smooth lining of the vessel becomes thickened and overgrown with cells.

When comparing the value of a drug to a natural alternative, the safety factors must be considered. Usually, the ramifications of a nutrient, in contrast to a drug, are not side effects but side benefits. For example, the oxidation of LDL cholesterol (a particularly destructive form of cholesterol that creates chronic inflammation) is inhibited by policosanol. As less inflammation and blood vessel destruction occur, fewer foam cells appear (Noa et al. 1996). Conversely, if the oxidation of LDL is not inhibited, metalloproteinase enzymes are aroused, further damaging the vasculature by interfering with the protective nature of HDL cholesterol.

Policosanol combines well with aspirin to inhibit the formation of clots, with each influencing the activity of different platelets (Arruzazabala et al. 1997; Carbajal et al. 1998). The synergistic approach provides more comprehensive protection against platelet aggregation. Another factor in blood clot formation, thromboxane, is repressed after a couple of weeks of policosanol therapy.

Policosanol users can expect an improvement in exercise tolerance. When patients with heart disease were given 10 mg a day of policosanol, exercise capacity and oxygen uptake increased, but ischemia decreased. The improvement in treadmill-ECG tests confirmed that policosanol benefits heart patients, but healthy, physically active individuals also reported increases in exercise tolerance and strength (Stusser et al. 1998). Policosanol not only improved cardiovascular capacity, but also protected against atherosclerotic lesions (thickened fatty streaks in the vasculature).

Policosanol does not appear to interfere with other heart medications. However, it may potentiate the effects of propranolol, a beta-blocker used to treat hypertension. The 10-mg dose has had more than 2 years of clinical testing with no significant ill effects noted, except some patients reported an unexpected weight loss. Blood tests (after about 2 months of policosanol therapy) will allow the individual to adjust the dose commensurate with need. Some individuals will need only 5-10 mg of policosanol to maintain healthy cholesterol levels; others will require 20 mg a day. Note: Policosanol has undergone as many clinical trials as most drugs.

Polyenylphosphatidylcholine (PPC)--is a hypolipidemic, improves exercise tolerance and apoB/apoA-1 ratio, lessens angina attacks, and increases levels of HDL2b
Phosphatidylcholine, the main component of lecithin (a soy product), has a long history as a preventive in arteriosclerosis, cardiovascular disease, and brain derangements. PPC, a newer, polyunsaturated soy derivative, has shown extraordinary promise in managing hypercholesterolemia. It appears that PPC delivers its value by traversing into cholesterol, where direct modulation of the substance occurs. In a study involving 100 participants, PPC lowered total LDL cholesterol by about 15%, reduced triglycerides 32%, and raised HDL levels by about 10% (Klimov et al. 1995; Jordon 2000).

PPC significantly increased apolipoprotein A-1 and only slightly increased apolipoprotein B, while decreasing postprandial triglycerides, VLDL, and IDL (Klimov et al. 1995; Zeman et al. 1995). apoB is a cholesterol particle that is believed to promote heart disease by affecting how cholesterol is transported in arteries and other tissues. It is found not only in LDL cholesterol, but also in VLDL and IDL, other potentially bad cholesterols. On the other hand, apoA-1 is a protective, antiatherogenic particle found in the highly beneficial HDL cholesterol. Researchers concluded that PPC appeared to be an appropriate supplement for patients with decreased concentrations of HDL cholesterol and plasma apoA-1.

The Lancet recently reported the results of a 5 1/2-year trial (the AMORIS, Apoliprotein-Related Mortality Risk Study) evaluating the cardiovascular health of 175,553 men and women. Although all conventional markers were assessed (triglycerides, total cholesterol, and LDL-HDL cholesterol ratio), persons with the greatest absolute risk of dying from a heart attack tended to have the highest ratios of apoB to apoA-1 (Srinivasan et al. 2001; Walldius et al. 2001; GSDL 2001).

Over the course of the study, 864 men and 359 women died from acute myocardial infarctions. When researchers compared their blood results, the apoB-apoA-1 ratio was the strongest predictor of fatal heart attacks. Men with the highest apoB and lowest apoA-1 levels were nearly 4 times as likely to experience a deadly heart attack compared to those with a favorable apo ratio. (In women the relative risk was threefold greater.) apoB proved to be a stronger predictor of risk than LDL cholesterol in both sexes.

The study also showed that the apo ratio remained a strong marker in all age groups, including those patients over age 70, a group in which total cholesterol levels are not considered to be accurate risk indicators for heart attack. Assessing apoB-apoA-1 ratio appears to identify high-risk individuals who have normal-to-low LDL cholesterol, as well as those with diabetes and insulin resistance. Recall that PPC's credits include increasing the desirable apoA-1.

PPC has a positive effect upon HDL levels, particularly the most protective of the HDL family, HDL2b. Individuals attaining longevity often display HDL differentials favoring HDL2b, suggesting that this subfraction renders, among other health benefits, greater cardioprotection. Another of the restorative capacities of PPC is its ability to increase exercise tolerance (Klimov et al. 1995).

Alcohol in moderation appears to prevent atherosclerosis. Heavy drinking has the opposite effect, in part by promoting oxidation of LDL cholesterol. Administering PPC at 2.8 grams/1000 kcal to baboons made alcoholic for experimentation lessened the expected ethanol-induced increase in LDL oxidation (Navder et al. 1999).

Russian researchers compare PPC to niacin in the treatment of angina and hyperlipidemia. While nicotinic acid is a reliable hypocholesterolemic, the clusters of annoying symptoms (flushing and itching) and less benign side effects (liver disruption and GI disturbance) discredit megadose usage in some individuals. Conversely, PPC therapy has no contraindications, side effects, or drug interactions. A suggested dosage is two 900-mg capsules daily.

Potassium--reduces blood pressure, maintains fluid balance, encourages parasympathetic nervous system, and increases insulin sensitivity
Potassium, considered by some to be the major electrolyte, is found almost exclusively in the intracellular fluids of the cell. Sodium is found in the extracellular fluid, but it is equilibrium between potassium and sodium that determines fluid balance and blood pressure regulation. A high potassium-low sodium intake reduces the blood vessel constricting effects of adrenaline, a hormone associated with sympathetic nervous system arousal; the result is lower blood pressure.

Adults (37 in number) with diastolic blood pressure less than 110 mmHg participated in a crossover trial of 32 weeks' duration to determine the hypotensive nature of minerals. Sixty mmol/day of potassium (about 2.5 grams) reduced systolic pressure by an average of 12 mmHg and decreased diastolic pressure 16 mmHg (Patki et al. 1990; Murray 1996). Comment: Results of the DASH study illustrate the necessity for providing adequate amounts of potassium, magnesium, and calcium to control blood pressure. To read more about the study, please turn to the subsection entitled, Does Sodium Restriction Lower Blood Pressure? in this protocol (Bland 2000b).

Hypertensive individuals over 65 years of age may find particular value in potassium, since medications are not always as effective among senior subjects. Administering 2.5 grams a day of potassium for 4 weeks to 18 untreated elderly hypertensive patients resulted in a systolic drop of 12 mmHg and a diastolic reduction of 7 mmHG. All entered the study with systolic blood pressure greater than 160 mmHg and diastolic pressure greater than 95 mmHg (Fotherby 1992; Murray 1996). The results were impressive considering the brevity of the study and the fact that potassium's value is cumulative, meaning a greater response is generally seen with longer supplementation.

Researchers at the Johns Hopkins University School of Medicine advocate increasing potassium to treat and prevent hypertension. A group of seven medical researchers reviewed 33 randomized, controlled trials involving over 2600 participants. The researchers concluded that increased potassium intake is effective in lowering both systolic and diastolic blood pressure (systolic blood pressure dropped an average of 3.11 mmHg and diastolic was reduced 1.97 mmHg) (Whelton et al. 1997).

The hypotensive nature of potassium benefited a group of rats made stroke-prone for experimentation. The rats were divided into two groups. Only 2% of the potassium-supplemented group experienced a fatal stroke, compared to 83% of the untreated group (Alternative Medical News Staff). Cardiologists report using 400 mg of magnesium, 500-1000 mg of calcium, and 500-1000 mg of potassium to treat patients with arrhythmias (Sinatra 1997).

Several factors influence potassium levels. For example, insulin therapy appears to cause a potassium deficiency. Conversely, a diabetic supplementing with potassium may observe increased insulin secretions and responsiveness, reducing insulin requirements. Physical exertion (producing heavy perspiration) or diarrhea and vomiting (resulting in loss of body fluids) can cause a mineral depletion. Always replace minerals, for if not replaced, heart function can quickly depreciate. Symptoms of potassium deficiency are weakness, fatigue, mental confusion, and heart disturbances (Murray 1996).

While the results of potassium studies are impressive, it must be noted that though self-poisoning is uncommon, the consequences are often fatal (Colledge 1988). Potassium supplementation in the form of oral potassium tablets is generally not needed if you are on a good anti-aging diet that includes several servings of fruits and vegetables per day (The estimated safe and adequate daily dietary intake of potassium, as set by the Committee on Recommended Daily Allowances, is 1.9 grams to 5.6 grams per day.)

Most individuals can tolerate excesses of potassium, but individuals taking digitalis, potassium-sparing diuretics, and ACE inhibitors, or individuals with diagnosed kidney disease, should never supplement unless physician prescribed. This cautionary is valid for anyone considering therapeutic dosages of potassium. Due to the potential side effects of potassium on cardiac function, the FDA limits the amount of potassium permitted in nutritional supplements to 99 mg per serving.

Recall that many foods offer reliable potassium stores; subsequently, eating from foods delineated in the potassium food source section should be especially important to individuals with hypertension and cardiac irregularities. It becomes increasingly difficult, however, to provide adequate levels of potassium if taking a diuretic. Patients are commonly told to replace potassium by consuming potassium-rich foodstuffs. Yet, if every milligram of potassium in a banana were retained, it would require eating an entire stock of bananas every day to offset the potassium lost during diuretic therapy (Cuneo et al. 1985; Alternative Medical News Staff).

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