~Cardiovascular Disease Comprehensive 8 - Therapeutic C

~Cardiovascular Disease Comprehensive 8 - Therapeutic C
Calcium-- is a hypotensive mineral and an antiarrhythmic, supports healthy bones around gum tissue, and reduces iron overload

Minerals, although usually not considered as focal, are in many ways more important to survival than vitamins. One can live longer with a vitamin deficiency than with a mineral shortage (Whiting 1989). For example, a deficiency of calcium, magnesium, or potassium can force the heart into fatal cardiac arrhythmias. In addition, inadequate mineral intake appears to have a correlation with hypertension. Hypertensive individuals may be unwittingly contributing to the problem by consuming about 18% less dietary calcium than normotensives.

Researchers at the Oregon Health Sciences found that supplemental dietary calcium lowers blood pressure, whereas restricted-calcium diets tend to elevate blood pressure (Geri Clark in Woman's Day). According to research from the Indiana University School of Medicine, a unifying theory showing how calcium reduces blood pressure is not available. A membrane stabilizing effect, natriuresis (the excretion of greater than normal amounts of sodium in the urine), and calcium's ability to control regulatory processes are mechanisms debated (Luft et al. 1990). However, epidemiologic findings suggest that there is a threshold for the protective effect of calcium, below which the risk of hypertension increases at a greater rate. The set point of this threshold may be about 700-800 mg a day, but other variants, such as metabolic type, absorption rates, and genetics may modify this dosage (McCarron et al. 1991).

Calcium is not a universal resolvent for hypertension (Meese et al. 1987). In some cases, clinicians report no significant hypotensive effect in dosages as high as 2.5 grams a day. Patients wishing to try calcium should not withdraw blood pressure medication abruptly but use the drug in combination with calcium over a 3- to 6-month assessment period. During this interval, watchful monitoring may allow a gradual reduction in medication.

According to information published in the journal Stroke, low dietary calcium intake poses a significant risk for women in regard to heart disease and stroke. Researchers analyzed the dietary intake of 85,764 women, compiled from the Nurses' Health Study. After an adjustment for risk factors associated with cardiovascular disease, calcium intake was significantly related to the risk of stroke. Women with the lowest calcium intake (especially from dairy sources) had the greatest risk of heart problems, perhaps because of higher cholesterol levels and a tendency for blood cells to clump. The increase in risk was limited to the lowest quintile of intake; intakes of calcium greater than 600 mg a day did not appear to reduce risk of stroke further (Iso et al. 1999).

Calcium is also of advantage in reducing iron overload. The American Journal of Clinical Nutrition stated that 300 mg of elemental calcium, taken with a meal, reduced the amount of iron absorbed from food by 40% (Hallberg et al. 1998). Amounts larger than 300 mg did not further inhibit iron absorption. Since some individuals become tolerant to calcium-induced iron absorption blockage, it is important to have blood tests periodically to evaluate sustained effectiveness. Calcium is also important in periodontal disease by supporting healthy bone around gums (Balch, et al. 1997).

Calcium citrate is a good choice considering absorption, but calcium citrate malate acid is about 30% better absorbed than calcium citrate. Calcium bis-glycinate was shown to absorb 180% better than calcium citrate and 21% better than calcium citrate malate. A suggested dosage is 1000 mg of elemental calcium a day.

Reader's guide to food sources of calcium: Milk and dairy products are frequently criticized, particularly those that are homogenized. During homogenization, an enzyme appearing in milk (xanthine oxidase) is broken down to a smaller size. The enzyme's altered state allows entry into the bloodstream and a reaction to occur on arterial walls. As a protective gesture, atheromatous materials are laid down at the site of contact. In addition, milk is often challenged as a worthy source of calcium. Its high phosphorous content and magnesium shortfall are thought to impede calcium absorption. Dark green vegetables, salmon (with bones), sardines, most nuts and seeds (especially sesame seeds), blackstrap molasses, root vegetables, and liver are considered to be safer, surer sources of calcium.

The interrelationship of factors acting on absorption

The importance of providing an environment conducive to nutrient utilization cannot be overstated. For example, in an alkaline medium, calcium forms insoluble, nonabsorbable calcium phosphate. Conversely, hydrochloric acid lowers the pH of the digestive tract, providing a favorable milieu for absorption.

Nutrients also play a role, either supporting or opposing absorption. For example, the amino acid lysine (found in milk products, eggs, meat, fish, and fowl) enhances calcium absorption. Other calcium enhancers include vitamin D, vitamin A, vitamin C, and magnesium.

Diets high in sugar alter calcium uptake; coffee, alcoholic beverages, and phosphorous-rich soft drinks also promote increased calcium excretion. Oxalic acid (found in almonds, beet greens, cashews, chard, cocoa, rhubarb, soybeans, and spinach) retards calcium absorption by binding with calcium in the intestines, producing insoluble, nonabsorbable salts. (Oxalic acid is problematic only if the diet is persistently structured around these foodstuffs.) Calcium and tetracycline form an insoluble complex that impairs both mineral and drug absorption.

L-Carnitine-- is an energizer and hypolipidemic, aids weight loss, improves circulation, increases exercise tolerance, and is beneficial treatment in angina, diabetes, congestive heart failure, and cardiac arrhythmias

Robert Crayhon, nutritionist and author, considers carnitine the single most important nutrient in regard to cardiac health. Carnitine, a coenzyme similar to the family of B vitamins, is essential for the burning and transport of long-chain fatty acids, the fuel for cardiac energy. Up to 70% of energy produced by muscles comes from the burning of fats. To expect the normal functioning of heart muscles, the transport of carnitine into tissues is critical (Crayhon 1998).

Lysine and cofactors yield about 25% of the carnitine the body needs for optimal performance. The remaining 75% can come from the diet, if dietary selections are made with a slant toward carnitine-rich protein foods, especially mutton, lamb, and beef. Interestingly, protein foods, those frequently shunned on a heart-healthy diet, raise HDL cholesterol and increase carnitine levels (Crayhon 1998).

Carnitine is often effective in reducing the incidence of cardiac arrhythmias and angina attacks. According to statistics, patients receiving L-carnitine experienced fewer premature ventricular contractions at rest and improved cardiac output (Cacciatore et al. 1991). But if oxygen levels decrease, carnitine also decreases, and the patient may be in jeopardy from two perspectives.

Patients with stable angina, who were evaluated by means of a stress test, were able to exercise longer before abnormalities were detected while on 900 mg of orally administered L-carnitine (Kamikawa et al. 1984). Individuals acting as controls in the study and receiving a placebo experienced distress at 6.4 minutes into the test, while individuals receiving carnitine supplementation extended the period of symptom-free exercise to 8.8 minutes. Researchers also state that carnitine may provide independent benefit in ischemia, when used as monotherapy, or additional benefit when used in combination with conventional beta-blockers or calcium antagonists (Jackson 2001). Although research indicates carnitine may be an effective adjunctive therapy, never discontinue cardiac medications without the consent of your physician.

Carnitine, administered to individuals displaying heart trauma, substantially lessened coronary damage and the risk of occlusion. Arterial plugs were less likely to form as carnitine modulated lipids, with less of the objectionable and more of the beneficial fats produced. After 4 months of carnitine therapy, total cholesterol levels were reduced by about 20%, triglycerides were reduced 28%, and HDL increased 12%. Triglycerides and HDL were more responsive to carnitine supplementation if the diet contained no more than 40% of calories from carbohydrates (Pola et al. 1980, 1983; Murray 1996b).

Carnitine is of value in treating congestive heart failure. A group of 60 men and women (ages 48-73) were selected for a carnitine heart study, having failed conventional treatment. Thirty of the patients were given LPC (L-propionylcarnitine, 500 mg 3 times a day for 180 days), along with their drug regime. At 30 days into the trial, the patients were evaluated for improvement in exercise tolerance and left-ventricular ejection fraction. Compared to controls, both parameters showed significant recovery at the 1-month interval, but improvement was even more pronounced at the 90- and 180-day marks. Exercise tolerance improved 16.4% at 30 days, 22.9% at 90 days, and 25.9% at 180 days; left-ventricular ejection fraction progressively increased 8.4%, 11.6%, and 13.6% throughout the course of the trial (Cacciatore et al. 1991; Mancini et al. 1992; Murray 1996d). Note: L-carnitine has been approved by the FDA, under the name Carnitor, as a therapy for congestive heart failure.

Glycosylated hemoglobin, HbA1c (a hemoglobin molecule chemically linked to glucose), is a test used to evaluate glucose levels over the previous 6-8 weeks. The test measures glycosylation of hemoglobin in the red cells over their lifetime of 90-120 days. HbA1c, for a nondiabetic, is normal at 4-6%; for a diabetic, the goal is to maintain HbA1c less than 7% (7% is an average of 150 mg/dL of glucose). It appears carnitine may have the potential to assist in stabilizing blood glucose levels, so that peaks and valleys are less troublesome to diabetic patients. Carnitine accomplishes this by increasing glucose disposal and improving insulin sensitivity (DeGaetano et al. 1999; Mingrone et al. 1999). A report published in JAMA showed that a significant financial savings ($685-$950 annually) accrued to diabetes within 1 year of improved HbA1c levels (Wagner et al. 2001).

Individuals who are at increased cardiac risk because of obesity may find value in carnitine supplementation. Carnitine, especially when combined with omega-3 fatty acids and a decrease in carbohydrate consumption, promotes weight loss. If used for obesity, begin with 500 mg and gradually increase dosage to 2 grams a day. If an individual is morbidly overweight, larger doses, up to 4 grams a day, may be required (Crayhon 1998). Hypothyroidism, a contributing factor to both obesity and coronary artery disease, frequently parallels carnitine deficiencies.

Some practitioners report better cardiac management when using L-carnitine fumarate, a less hygroscopic and more bioavailable form of the vitamin-like nutrient. Others prefer LPC (L-propionylcarnitine) for the treatment of angina. Acetyl-L-carnitine is touted because of its ability to energize, a result of extremely efficient utilization. Because of the energizing effects of acetyl-L-carnitine, Robert Crayhon, author of The Carnitine Miracle, suggests it be taken no later than 3 p.m. to preserve a restful night's sleep.

As with most supplements, dosage is subjective. Some individuals notice increased energy with 1 gram of L-carnitine or 500 mg of acetyl-L-carnitine a day. Clinical studies frequently use from 1500-3000 mg daily. Because increased energy production begets a greater generation of free radicals, carnitine should always be used with an antioxidant program.

Carnosine-- is an antioxidant, protects against strokes, and reduces AGEs

In January 2001, the Life Extension Foundation hailed carnosine as a substance capable of slowing many of the processes involved in aging, including cardiovascular degeneration. Carnosine, a combination of the amino acids alanine and histidine, accomplishes this in part by playing a dual role in regard to proteins. For example, it yields a protective effect through antioxidant activity and also participates in the repair or removal of damaged proteins. By quenching the destructive potential of the deadly hydroxyl radical and impacting protein degradation that occurs as a result of collagen crosslinking (glycation), carnosine offers significant protection against vascular disease.

Glycation is a reaction that occurs when proteins react with glucose. A series of reactions follow (including the oxidation process), terminating in the formation of an advanced glycosylated end product (AGEs), a protein the body cannot break down. These processes decrease vascular tone and resiliency and are factors that influence the progression of cardiovascular disease and hypertension. Glycated proteins produce 50-fold more free radicals than nonglycated proteins; carnosine may be the most effective antiglycating agent known (Durany et al. 1999).

Russian scientists set out to determine the effect of carnosine upon rats programmed to develop strokes. The first experiment focused upon carnosine as a revitalizer in hypoxic animals (those exposed to low oxygen levels). When oxygen-deprived animals were revitalized with normal levels of oxygen, the carnosine treated rats were able to stand after 4.3 minutes, as compared to 6.3 minutes in the untreated group (Boldyrev 1997).

In the second study, a stroke was simulated in the animals by arterial occlusion. The scientists found that carnosine acts as a neuroprotector in the ischemic brain. Rats treated with carnosine displayed more normal electrocardiograms, less lactate accumulation (a common measure of the severity of injury), and better cerebral blood flow (Stvolinsky et al. 1999).

A suggested dosage is 1000-1500 mg daily. By taking at least 1000 mg a day of supplemental carnosine, the enzyme carnosinase (an enzyme that degrades carnosine) is overwhelmed, thus making the carnosine available in the body. Carnosine should not be used during pregnancy or lactation.

Chondroitin Sulfate-- is an anti-inflammatory and antioxidant and inhibits LDL oxidation

Chondroitin sulfate (CS) is extremely popular in relieving the sore joints of osteoarthritis. In 1968, Dr. Lester Morrison began a 6-year study to determine its value as a cardioprotector. Dr. Morrison divided 120 patients with coronary heart disease into two groups. Lifestyles were not altered during the test period, that is, all participants continued with their prescribed medication and appropriately designed diets. One group also took 1500 mg a day of CS for 4 years, and then 750 mg for another 18 months. After 6 years, four people in the CS group had died, compared to 13 in the nontreated group. Most impressive was the finding that only six people in the CS-treated group had acute cardiac incidents over the 6-year period, while 42 patients in the group that did not receive CS had acute events (Morrison et al. 1969; Morrison et al 1973; Anderson 2002).

Dr. Morrison speculates that the decrease in cardiovascular deaths could be staggering if CS were routinely used by larger numbers of the population. Although further research is needed, it appears CS delivers its cardiovascular protection though anti-inflammatory and antioxidant pathways. A suggested daily dose is one to three 400-mg tablets.

Chromium-- modulates blood glucose levels, lowers cholesterol, and is helpful in weight management

Of the 16 minerals currently deemed essential, none plays a more important role in blood glucose control than chromium. However, the benefits of chromium, a trace mineral, are not limited to modulating errant blood glucose levels. Obesity, coronary heart disease, hypertension, and hyperlipidemia often have a common denominator: insulin insensitivity, a condition worsened by a chromium deficiency. It is estimated that 90% of Americans consume less than the recommended amount of chromium each day, a shortfall that may eventually terminate in some form of ill health. (Note: No recommended dietary allowance (RDA) has been established for chromium, but the ESADDI (estimated safe and adequate daily dietary intake) is 50-200 mcg.)

A group of 180 people with Type II diabetes participated in a study to determine the worth of chromium picolinate (CrP) supplementation in controlling unstable blood glucose levels. The individuals were divided into the following three groups: (1) received only a placebo, (2) received 200 mcg daily of CrP, or (3) received 1000 mcg daily of CrP. Perhaps the finding of greatest interest was the decrease in hemoglobin A1c levels after 4 months (thus signifying increased glycemic control). Hemoglobin A1c dropped from greater than 9% pretreatment to less than 7% in the 1000-mcg-a-day treatment group. Chief Researcher Richard Anderson said: "Nearly all of participants no longer had the classic signs of diabetes. Blood sugar and insulin levels became normal. Most important, the gold standard diagnostic measure of diabetes, blood levels of hemoglobin A1c, sank to normal." This would be considered an optimal response with any diabetes drug regimen (Anderson et al. 1997). Note: The beneficial effects of chromium in individuals with diabetes were observed at levels higher than the upper limit of the ESADDI.

Research is conflicting regarding weight loss with chromium supplementation. While some studies renounce its value, a current study showed that 600 mcg of niacin-bound chromium given to "modestly dieting-exercising African-American women" caused a significant loss of fat and sparing of muscle compared to a placebo group (Crawford et al. 1999). Michael Murray, N.D., reported that individuals using 400 mcg of chromium picolinate for 2 1/2 months lost 4.6 pounds and added 1.1 pounds of muscle, for a total weight loss of 3.5 pounds (Murray 1996).

Typically, chromium decreases total cholesterol and triglycerides 10% and increases HDL 2%. These changes are most observed if initial body chromium levels are very low (Murray 1996). For most individuals, 200-400 mcg of chromium (divided throughout the day) is adequate; higher (supervised) doses may be required if used for Type II diabetes (turn to Niacin in this section to read about the boost chromium gives niacin, requiring lesser amounts of vitamin B3 to manage blood lipids).

Reader's guide to chromium food sources, enhancers, and antagonists: Brewer's yeast, whole grains, mushrooms, corn and corn oil, dairy products, potatoes, and dried beans are examples of chromium food sources; selenium, vitamin E, and essential amino acids enhance its absorption; iron opposes it.

Coenzyme Q10-- lessens the incidence of angina attacks, arrhythmias, cardiomyopathy, congestive heart failure, heart valve irregularities, hypertension, mitral valve prolapse, and periodontal disease; protects LDL cholesterol against oxidation; increases exercise tolerance; burns unwanted fat; supports healthy cholesterol and triglyceride levels; and is beneficial to smokers

Coenzyme Q10 (CoQ10) can be synthesized in the body, but individuals with periodontal disease, hypertension, or cardiovascular diseases are frequently deficient. Heart tissue biopsies in patients with various heart diseases showed a CoQ10 deficiency in 50-75% of cases. A significant finding is that cholesterol-lowering medications (as statin drugs) reduce CoQ10 levels. A CoQ10 deficiency of 25% is associated with illness and a deficit of 75% is associated with death in animals (Bliznakov et al. 1988; Hattersley 1994).

The heart strengthening benefits of CoQ10 make it of significant value in the treatment of congestive heart failure (CHF). Depending upon the degree of cardiac impairment, CoQ10 can be used independently or added to traditional medicine.

Administering CoQ10 (50-150 mg daily) for 90 days to 2664 patients with CHF resulted in the following symptomatic and clinical improvements: cyanosis (bluish skin color), 78.1%; edema, 78.6%; pulmonary crackle, 77.8%; dyspnea, 52.7%; palpitations, 75.4%; sweating, 79.8%; arrhythmia, 63.4%; and vertigo, 73.1%. Fifty-four percent of the patients observed a concurrent improvement in several symptoms, which could be interpreted as an improvement in quality of life (Baggio et al. 1994). A 1-year study involving 640 individuals with CHF showed that patients using CoQ10 were healthier and required less hospitalization (Moriscot et al. 1993).

The ejection fraction (how fully the heart pumps the blood out), end diastolic volume index (the adequacy of the heart to fill with blood), cardiac index (the amount of blood pumped out, considering body size), stroke volume (amount of blood pumped out on each beat of the heart), and cardiac output (the amount of blood pumped out per minute) all improved while using CoQ10 (Judy et al. 1984; Murray 1996). The improvement observed in left ventricular function may prove valuable in preventing left ventricular depression following coronary artery bypass and valvular surgery.

The effects of oral treatment with CoQ10 (120 mg a day) were compared for 28 days in 73 (intervention group A) and 71 (placebo group B) patients with acute myocardial infarction. Following treatment, angina pectoris (9.5% versus 28.1%), total arrhythmias (9.5% versus 25.3%), and poor left ventricular function (8.2% versus 22.5%) were significantly reduced in the CoQ10 group compared to the placebo group. Total cardiac events, including cardiac deaths and nonfatal infarctions, were also significantly reduced in the CoQ10 group compared with the placebo group (15% versus 30.9%) (Singh et al. 1998; Niibori et al. 1999).

Mitral valve prolapse is a common condition associated with a heart murmur. It is often asymptomatic but can produce chest pain, arrhythmia, or leakage of the valve, leading to congestive heart disease. Children with mitral valve prolapse received CoQ10 (2 mg/kg a day) for 8 weeks while eight received a placebo. This dosage proved highly effective in returning heart function to normal in seven of the eight children; none of the placebo-treated patients improved. However, relapse was common among those who stopped taking the medication within 12-17 months but rarely occurred in those who took CoQ10 for 19 months or more. (Oda et al. 1984; Murray 1996b).

The following examples exemplify the breadth of CoQ10's credits:
  • CoQ10 therapy is associated with a mean 25.4% increase in exercise duration and a 14.3% increase in workload (Sacher et al. 1997).
  • The frequency of angina attacks, a squeezing or pressure-like pain in the chest, usually provoked by exercise, decreases by about 53% during CoQ10 supplementation (Murray 1995).
  • CoQ10 has been reported to lower Lp(a), a powerful predictor of cardiac health (Singh et al. 1999; Health Concerns 2002). To read more about Lp(a), consult the section (in this protocol) dedicated to Newer Risk Factors.
  • CoQ10 inhibits oxidation of LDL cholesterol. CoQ10 accomplishes this by attaching to LDL particles circulating in the bloodstream. Were there more riders (CoQ10) than carriers (LDL) the oxidation of LDL cholesterol would be less worrisome (Thomas et al. 1995; LEF 2000).
  • CoQ10's antioxidant activities extend to protect the cells and lungs of smokers. By aiding oxygen delivery, reducing platelet aggregation, and hampering free-radical activity, the brain and heart have significantly greater protection. In addition, current data provide direct evidence for an interactive effect between exogenously administered vitamin E and CoQ10 in terms of uptake and retention, and for a sparing effect of CoQ10 on vitamin E. Vitamin E, in turn, plays a pivotal role in determining tissue retention of exogenous CoQ10 (Ibrahim et al. 2000).
  • Hypertensive patients demonstrated a significant improvement while supplementing with CoQ10. Before treatment with CoQ10, most patients were taking from 1-5 cardiac medications. During the study, overall medication requirements dropped considerably: 43% stopped between 1-3 drugs. Typically, diastolic and systolic blood pressures drop by about 10% with CoQ10 therapy (Langsjoen et al. 1994; Lam 2001).
  • Periodontal disease, a risk factor regarding heart health, responds to CoQ10 supplementation. Gingival pocket depth, swelling, bleeding, redness, pain, exudates, and looseness of teeth were significantly improved using 50 mg of CoQ10 a day (Wilkinson et al. 1977; Murray 1996). The herbs goldenseal and echinacea should accompany CoQ10 supplementation to further reduce oral infection.
  • For the dieter, CoQ10 is good news (Murray 1996). Together with a well-planned diet and exercise program, CoQ10 assists in shedding unwanted pounds.
  • CoQ10's ability to energize the heart is perhaps its chief attribute. The heart is one of the most metabolically active organs in the body, pumping approximately 2000 gallons of blood through 65,000 miles of blood vessels, beating 100,000 times each day (American Heart Association 2002). According to Decker Weiss, N.M.D., the heart requires large amounts of uninterrupted energy to fuel this unbelievable performance. The mitochondria (supplying 95% of the body's total energy requirement) are represented in large numbers (up to 2000 per heart cell).
  • In addition to energy supply, CoQ10 is an important defense system in tissues and muscles, particularly those having large numbers of mitochondria. As the mitochondria produce energy to fuel cellular functions, a plethora of free radicals results (Treatment and Research Newsletter 1998). Heart cells have more CoQ10 than any other cells, a supply critical to ATP production, cardiac function, and free-radical protection (Guyton et al. 1996; Porth et al. 1998).
Despite the large body of clinical evidence demonstrating CoQ10 efficacy, it is tragic that the majority of cardiac physicians still disregard its potential. A suggested dosage is 30-400 mg a day, depending upon the degree of cardiac support required. (Use CoQ10 in divided doses with meals containing fat; use larger doses under physician supervision.)

Reader's guide to CoQ10 food sources: Beef, mackerel, salmon, sardines, peanuts, and spinach.

Conjugated Linoleic Acid (CLA)-- aids in fat loss, reduces cholesterol and triglycerides, and assists in the utilization of beneficial fats Some researchers regard the principal causal factor of obesity to be CLA deficiency. CLA can be obtained from dietary choices such as turkey, lamb, beef, and some fatty dairy products, but the current trend away from meats and fats has caused levels of CLA to drop meaningfully (Ip et al, 1994).

CLA appears reliable in reducing body fat, while preserving lean body tissue. CLA accomplishes this by increasing the basal metabolic rate and impacting the distribution of fat, especially abdominal obesity. (Recall that apple-shaped bodies are considered vulnerable in regard to heart disease.) A Norwegian human study found that CLA-supplemented subjects lost up to 20% of their body fat in 3 months without changing their diet, while the control subjects on an average gained a slight amount of body fat during the same period (Health-N-Energy 2000).

CLA displays hypolipidemic properties as well as the ability to reduce arachidonic acid levels, an initiator of inflammatory leukotrienes (Liu 1998). (Leukotrienes are considered 1000 times more reactive than histamine.)

Researchers set out to determine the effects of CLA on the establishment and progression of experimentally induced atherosclerosis in rabbits. To establish atherosclerosis, New Zealand white rabbits were fed a diet containing 0.1-0.2% of cholesterol for 90 days. Some groups were fed the atherogenic diet and CLA. For effects on progression of atherosclerosis, rabbits with established atherosclerosis were also included in the study. At dietary levels as low as 0.1%, CLA inhibited atherogenesis; at dietary levels of 1%, CLA caused substantial (30%) regression of established atherosclerosis. This is the first example of substantial regression of atherosclerosis being caused by diet alone (Kritchevsky et al. 2000).

Some question whether linoleic acid and CLA accomplish the same tasks. Although the two acids are related, they appear to oppose one another on factors that influence cardiac performance. While the linoleic acid cascade has a greater tendency to stimulate fat formation, CLA inhibits it. Cholesterol is more likely to be oxidized by various factors working off the linoleic cascade, whereas CLA appears to stabilize cholesterol.

Laboratory animals, supplemented with CLA for 36 weeks at a dose 50 times higher than the suggested upper range for human consumption, completed the study without signs of toxicity. A suggested dosage is three to four 1000-mg capsules taken early in the day.

Curcumin-- is anti-inflammatory and hypocholesterolemic, inhibits platelet aggregation, and is protective to smokers

Curcumin, not to be mistaken for the herb cumin, is the yellow pigment of turmeric (Curcuma longa) found in mustard and curry powder. Curcumin has gained popularity because of its antioxidant and antiplatelet aggregating qualities. Curcumin's ability to control platelet aggregation appears directly related to thromboxane inhibition (a promoter of aggregation) and an increase in prostacyclin activity, an inhibitor of aggregation (Srivastava et al. 1985; Toda et al. 1985).

Curcumin is such a powerful antioxidant (comparable to vitamins C and E) that it is considered protective to smokers, lessening free-radical attack and cellular damage. Yet, its cardioprotection extends to reducing blood lipid levels, particularly cholesterol. Rats fed 0.1% curcumin, along with a cholesterol diet, had about one-half of the blood cholesterol as rats fed equal amounts of cholesterol but without curcumin (Rao et al. 1970).

Curcumin also possesses potent anti-inflammatory activity. It is, in fact, comparable to cortisone and phenylbutazone in acute inflammatory conditions and about one-half as effective in chronic models. As curcumin reduces inflammation (a more recently established risk factor for cardiovascular disease), fibrinolysis is promoted and leukotriene formation inhibited (Arora et al. 1971; Chandra et al. 1972; Murray 1994).

Continued . . .

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