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Cardiovascular Disease Protocol
Artichoke
reduces cholesterol by decreasing the synthesis of cholesterol in the
liver and increasing the conversion of cholesterol to bile acids. (Cholesterol
is a building block for bile acids.) According to Michael Murray, N.D.,
cholesterol levels are sometimes high because of the impaired conversion
of cholesterol to bile acids. Thus, low bile acid levels send a powerful
signal to the liver to provide more cholesterol. Artichoke extract intercepts
this signal, and the liver complies with less cholesterol production
(Murray 1998b).
The flavonoid luteolin appears to be pivotal in the hypocholesterolemic effects of artichoke. Statin drugs reduce cholesterol by competitively inhibiting the binding of HMG-CoA reductase. Tocotrienols also degrade this enzyme. Artichoke research has found no direct inhibition of HMG-CoA reductase. Other enzymatic steps occurring later in the biosynthesis of cholesterol appear unaffected. It seems luteolin inhibits cholesterol below the level of HMG-CoA reductase and therefore spares coenzyme Q10 synthesis. Recall that the cholesterol cascade begins with acetyl-CoA being converted to HMG-CoA. HMG-CoA reductase reduces HMG-CoA to mevalonic acid. Mevalonic acid participates in several steps that reduce it to squalene. Squalene is then converted to cholesterol (Murray 1998b; Sardesai 1998). A suggested dosage is 1 capsule 3 times a day, containing 300 mg of artichoke standardized to contain 13-18% caffeoylquinic acid. Note: The American Journal of Clinical Nutrition recently reported that chlorogenic acid, a component of black tea and coffee, could increase homocysteine levels (Olthof et al. 2001). Chlorogenic acid also appears in artichoke and would therefore be contraindicated in refractory hyperhomocysteinemia. Lastly, individuals with gallstones or biliary tract obstruction should not use artichoke.
Three studies looked at the incidence of stroke subtypes among aspirin users. A 1.69-fold increase in the risk of hemorrhagic stroke occurred among aspirin users, but no increase in ischemic strokes was noted. Secondary prevention trials, evaluated by Drs. Patricia R. Hebert (Yale University) and Charles Hennekens (University of Miami) indicated that aspirin therapy administered to 10,000 persons would prevent about 67 myocardial infarctions and cause approximately 11 hemorrhagic strokes. In November 2001, the New England Journal of Medicine published that over a 2-year period, no difference was found between aspirin and warfarin in the prevention of recurrent ischemic stroke or death or in the rate of major hemorrhage (Hebert et al. 2000; Mohr et al. 2001). The drug disposition of aspirin is persuasive when applied to a cardiovascular model. For example, low-dose aspirin (81 mg) appears to provide partial protection against abnormal blood clot formation, having a 2-day lasting effect on blood platelets. Platelets become less sticky and the risk of a heart attack and transient ischemic attacks (TIAs) is subsequently reduced. Aspirin exerts some of its cardioprotection by inhibiting the enzyme cyclooxygenase, a trigger in the inflammatory process (Newmark et al. 2000). One molecule of aspirin will destroy the cyclooxygenase enzyme for 4-6 hours (read the sections devoted to C-Reactive Protein and The Link Between Infections and Inflammation in Heart Disease to learn how the inflammatory process advances cardiac disease). Aspirin appears to lower C-reactive protein (CRP). In the Physician's Health Study, participants were randomly assigned at baseline to receive 323 mg of aspirin on alternate days and were then followed through first myocardial infarction. The study showed that low dose aspirin reduced heart attack risk by about 44% compared to the control group; the risk was 55% lower than that of placebo-treated men with high CRP levels. The results of this study suggest that in addition to aspirin's antagonism toward platelet clumping, it may also attenuate thrombosis through anti-inflammatory mechanisms (Physicians Weekly 1998a). Aspirin significantly cut the death rate from cardiac disease among 2368 noninsulin-dependent diabetic patients with coronary artery disease. (The aspirin benefit was greater among diabetic patients than nondiabetics.) Diabetic patients using aspirin had a 10.9% mortality risk from cardiac diseases, while diabetics not using aspirin had a 15.9% risk (Harpaz et al. 1998). The aspirin advantage extended to include carotid endarterectomy patients. Individuals using low-dose aspirin (81-325 mg a day) reduced the risk of myocardial infarction, stroke, and death for a 30-day to 3-month interval following surgery. Individuals taking 650-1300 mg were not similarly protected, illustrating that the dose can alter the end response (Taylor et al. 1999). Current information indicates that aspirin can also reduce the level of heart damage during a heart attack. When taking aspirin because one believes they are experiencing an acute heart attack, the aspirin should be chewed rather than swallowed and is best taken within 30 minutes of the onset of symptoms. In conclusion, the Antithrombotic Trialists' Collaboration (representing a review of 287 studies involving 135,000 patients) announced that over 40,000 lives are lost worldwide every year because aspirin is underused. According to the report, aspirin (or other antiplatelet drugs) is protective in most patients at increased risk of occlusive vascular events, including those with acute myocardial infarction or ischemic stroke, unstable or stable angina, previous myocardial infarction, cerebral ischemia, peripheral arterial disease, or atrial fibrillation (Antithrombotic Trialists' Collaboration 2002). Aspirin (75-150 mg a day) appears to be an effective antiplatelet regimen for long-term usage, but in acute settings, an initial loading dose of at least 150 mg may be required. Adding a second antiplatelet drug to aspirin may produce additional benefits in some clinical circumstances (Antithrombotic Trialists' Collaboration 2002). Note: The New England Journal of Medicine recently published that warfarin, in combination with aspirin or given alone, was superior to aspirin alone in reducing the incidence of composite events following an acute myocardial infarction. Warfarin was, however, associated with a higher risk of bleeding (Hurlen et al. 2002). The American College of Chest Physicians suggests that all people over 50 years of age, with one cardiac risk factor and no condition that would negate treatment, consider aspirin therapy. The cautionary includes those individuals who have increased prothrombin time, disturbed gastric mucosa, or hypertension. As acclaimed as low-dose aspirin is, studies have shown that aspirin does not appear comprehensive enough to prevent a heart attack if fibrinogen levels are excessively high. It should also be noted that a concomitant administration of Borage Seed Oil (but not rofecoxib, acetaminophen, or diclofenac) antagonizes the platelet inhibition activity induced by aspirin. Thus, treatment with Borage Seed Oil in patients with increased cardiovascular risk may limit the cardioprotective effects of aspirin (Catella-Lawson et al. 2001).
Bromelain--is
an anti-inflammatory, reduces fibrinogen, lessens risk of blood clots,
is beneficial in atrial fibrillation, is hypotensive, relieves angina,
and is basic to smokers Bromelain lowers blood pressure, breaks down fibrinogen, and relieves angina. It opposes platelet aggregation and is helpful in thrombophlebitis. Many of bromelain's qualities make it particularly valuable to smokers and patients with atrial fibrillation (Murray 1995c; Duke 1997). A suggested bromelain dosage is 1/8-1/4 teaspoon taken between meals to relieve inflammation. The strength of enzymes is often expressed as milk-clotting units (MCU) and gelatin-digestive units (GDU) per gram. One level teaspoon of Life Extension Bromelain Powder (2.9 grams) has enzymatic strength of 3500 MCU or 2000 GDU. Bromelain tablets (500 mg) are also available. Typically, bromelain is used 3 times a day.
Bugleweed is beneficial in the treatment of hypertension and congestive heart failure, ridding water from edematous tissues and organs. It has been called a natural digitalis, milder but with some of the same characteristics as the drug. Bugleweed does not accumulate and is therefore considered nontoxic (Santillo 1990; Ritchason 1995). A suggested dosage is 30-40 drops in a little water 2-4 times a day. (For an explanation regarding milligrams per drop, turn to Angelica, appearing alphabetically in this section.) C Calcium--is
a hypotensive mineral and an antiarrhythmic, supports healthy bones
around gum tissue, and reduces iron overload 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. The interrelationship
of factors acting on 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 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.
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.
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.
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
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).
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These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease
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