~Cardiovascular Disease Comprehensive 13 - Therapeutic P-S

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 AGENTDOSAGELIPOPROTEIN EVALUATEDAMOUNT REDUCED
Lovastatin (Mevacor)20 mgLDL Cholesterol22%
Simvastatin (Zocor)10 mgLDL Cholesterol15%
Policosanol10 mgLDL Cholesterol24%


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).

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.

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.

Continued . . .


Free Shipping in the Continental U.S. on Orders over $50
The statements made here have not been evaluated by the FDA. The foregoing statements are based upon sound and reliable studies, and are meant for informational purposes. Consult with your medical practitioner to determine the underlying cause of your symptoms. Please always check your purchase for possible allergins and correct dosage on the bottle before use.

While we work to ensure that product information is correct, on occasion manufacturers may alter their ingredient lists. Actual product packaging and materials may contain more and/or different information than that shown on our Web site. We recommend that you do not solely rely on the information presented and that you always read labels, warnings, and directions before using or consuming a product. For additional information about a product, please contact the manufacturer. Content on this site is for reference purposes and is not intended to substitute for advice given by a physician, pharmacist, or other licensed health-care professional. You should not use this information as self-diagnosis or for treating a health problem or disease. Contact your health-care provider immediately if you suspect that you have a medical problem. Information and statements regarding dietary supplements have not been evaluated by the Food and Drug Administration and are not intended to diagnose, treat, cure, or prevent any disease or health condition. Life Ex Online assumes no liability for inaccuracies or misstatements about products.