~Atherosclerosis (Coronary Artery Disease), Part 3 - Nutritional Supplementation
THE BENEFITS OF NUTRIENT SUPPLEMENTATION
- Essential Fatty Acids
- Herbal Supplements
- Trace Mineral Supplements
- Supplements for Healthy Coronary Arteries
- B Vitamins
- Vitamin C
- Vitamin E
- Coenzyme Q10
B Vitamins (Homocysteine Lowering Nutrients)
Landmark studies, part of the large Framingham Heart Study started in 1948 demonstrated that high plasma levels of homocysteine and low levels of folic acid and vitamin B6 are associated with increased narrowing of the carotid arteries (Selhub et al. 1995). Numerous studies have reported positive outcomes following the use of B vitamins for reduction of homocysteine. Healthy men with moderate hyperhomocysteinemia had lower concentrations of vitamins B6, B12, and folic acid (25.0%, 56.8%, and 59.1%, respectively). Daily supplementation with these vitamins normalized elevated plasma homocysteine levels within 6 weeks, indicating that moderate vitamin therapy is an efficient and cost-effective method of controlling elevated homocysteine (Ubbink et al. 1993).
Patients and normal volunteers, with or without elevated homocysteine levels (>16 micromoles/L) that received multivitamin supplements showed normalized plasma homocysteine levels, if these levels were initially high, and lower homocysteine levels even if their homocysteine levels were normal. Supplementation with 500 mcg of folic acid led to a substantial reduction of blood homocysteine levels in all populations (den Heijer et al. 1998).
Patients were treated daily with placebo, folic acid (650 mcg), vitamin B12 (400 mcg), vitamin B6 (10 mg), or a combination of the three vitamins for 6 weeks. Folic acid supplementation reduced plasma homocysteine concentrations by 42%; vitamin B12 lowered homocysteine by 15%; but vitamin B6 (in this low dose) caused no significant changes. The combination of all three vitamins reduced homocysteine by 50%. "Folate deficiency might be an important cause of hyperhomocysteinemia in the general population." Supplements containing modest levels of folic acid or combinations of folic acid, B6, and B12 lowered plasma levels of homocysteine (Ubbink et al. 1993).
Heart attack patients were surveyed for dietary intake of vitamins. Higher levels of folic acid were protective and this supports homocysteine as an independent risk factor for cardiovascular disease. Adequate folic acid intake from diet or supplements normalizes levels of plasma homocysteine (Verhoef et al. 1996).
Niacin (nicotinic acid) is a B vitamin that has been used in high doses (1.0–4.5 grams per day) as a treatment for hyperlipidemia, a condition characterized by elevated blood levels of cholesterol and/or fats as triglycerides (TGs). High concentrations of TGs are associated with increased risk of CHD. Niacin reduces cholesterol and TG levels, and increases the concentration of high-density lipoprotein (HDL) associated with reduced risk of CHD (Crouse 1996). Niacin is usually effective at modulating blood lipids, but side effects sometimes dampen enthusiasm for therapy.
Although side effects are dose-related, few studies have determined an optimal dose of nicotinic acid that alters lipid levels with the fewest side effects. Martin-Jadraque et al. (1996) demonstrated that low-dose nicotinic acid treatment significantly lowered TGs, raised HDL concentrations by approximately 22%, and favorably altered the ratio of total cholesterol to HDL in all subjects. Improvement in blood lipid levels was observed in 75% of subjects who tolerated low-dose nicotinic acid therapy. Although the changes induced by lower doses were less than higher doses, the lower dose was better tolerated. Nicotinic acid may also be useful in combination drug therapy for prevention of CHD if higher doses cannot be tolerated. Use of a lower dose should still be beneficial in for producing a moderate rise in HDL levels. Women seem to have a greater LDL response to niacin, but experience more side effects at higher dosages. Lower doses of niacin may be more desirable for women (Goldberg 1998).
Long-term treatment with nicotinic acid (4 g/day for 6 weeks) not only corrects serum lipoprotein abnormalities, but also reduces the fibrinogen concentration in plasma and stimulates fibrinolysis (Johansson et al. 1997).
Epidemiologic evidence (Framingham Heart Study) indicates that a low level of HDL is an independent predictor of CHD. Other findings related to low HDL revealed that (1) it is an independent predictor of the number and severity of atherosclerotic coronary arteries, (2) it predicts total mortality in coronary artery disease patients when total cholesterol is in a desirable range (<200 mg/dL), and (3) it is associated with increased restenosis after angioplasty. Study conclusions were that most medications used to treat dyslipidemias will raise HDL levels modestly; however, niacin appears to have the greatest potential to do so, increasing HDL up to 30% (Kwiterovich 1998).
CAUTION: Side effects associated with niacin consumption include flushing, itching, minor gastrointestinal symptoms, and the possibility of liver damage. A blood test to measure liver enzyme levels is mandatory every 3–6 months because of the potential of niacin to cause liver damage in a minority of people. Niacin cannot be used in individuals with existing liver disease (e.g., hepatitis C, cirrhosis of the liver).
It is possible that niacin raises homocysteine levels because of increased methylation of niacinamide. Niaspan, an extended-release niacin, raised homocysteine levels in a dose-dependent manner in some people, by an amount generally between 1–4 micromoles/L. Niacinamide formed from excess niacin may deplete SAMe, the body's normal agent for methylation. If niacinamide is methylated, it is likely that there would be an elevation of plasma homocysteine.
Individuals may be able to use smaller amounts of niacin if chromium accompanies the dosage. Niacin in combination with chromium lowered cholesterol levels by an average of 14% and improved total cholesterol and HDL/LDL ratio by 7%. This finding is valuable since the side effects of niacin may make it less useful in large doses (Urberg et al. 1987; Cichoke 2004; Berkeley Heart Lab). The typical daily dose of niacin (bound to chromium) is less than 2 mg (not the usual 500-4,500 mg). When niacin-bound chromium is used, mega doses of niacin are no longer needed to lower cholesterol. Niacin-bound chromium can significantly increase levels of protective HDL and decrease the LDL (Cichoke 2004).
A widely publicized study showed that men who took 800 mg daily of vitamin C lived about 6 years longer than those consuming the RDA of 60 mg per day. This study evaluated 11,348 participants over 10 years and demonstrated that high vitamin C intake prolonged average life span and reduced mortality from cardiovascular disease by 42% (Enstrom et al. 1992). A study of 11,178 elderly subjects; aged 67 to 105 years compared vitamin C and vitamin E supplemented subjects to subjects using no vitamin supplements: Use of vitamin E alone reduced death from myocardial infarction (MI) by 63%, cancer mortality by 59%, and overall mortality by 34%. When the vitamin C and E were used together, overall mortality was reduced by 42% (Losonczy et al. 1996).
When vitamin C was co-administered with nitrate drugs (nitroglycerine, NTG), the adverse effects of nitrate tolerance were virtually eliminated. The most significant change was a 310% improvement in the arterial conductivity test (Bassenge et al. 1998). Nitrate drugs sometimes induce dangerous up-regulated activity of platelets that can be reversed with vitamin C supplementation. The findings demonstrated that dietary supplementation with vitamin C can eliminate vascular tolerance and up-regulation of platelet activity during long-term, non-intermittent administration of nitrate drugs (NTG) in humans.
Vitamin supplementation is effective in congestive heart failure (CHF). CHF is associated with a reduced dilation (capacity) of the endothelial lining of the arterial system (flow-dependent dilation). High-resolution ultrasound and Doppler measurements of artery diameter and blood flow following vitamin C (25 mg/min, intra-arterially) determined that vitamin C restored arterial dilatory responses and blood flow in CHF (Hornig et al. 1998). Studies have indicated that antioxidant intake is associated with decreased risk for CHD. Low plasma levels of ascorbic acid predict the presence of an unstable coronary syndrome possibly by influencing the activity surrounding an arterial wall lesion rather than the overall extent of the disease (Vita et al. 1998).
Evidence demonstrates that vitamin E protects against development of atherosclerosis by retarding oxidation of LDL, inhibiting proliferation of smooth muscle cells, reducing platelet adhesion and aggregation, and altering the expression and function of adhesion molecules. Vitamin E attenuates the synthesis of leukotrienes and potentiates release of prostacyclin (which inhibits platelet aggregation and acts as a vasodilator) by up-regulating the expression of cytosolic phospholipase A2. These biological functions of vitamin E may protect against the development of atherosclerosis (Chan 1998).
Studies substantiate the involvement of free radical reactions in the early or developing stages of human disease. Improvement of diet (by increasing antioxidants) lessens degenerative diseases. Degenerative disease is lower following diets with high levels of antioxidants or diets supplemented with vitamin E. By increasing intake of vitamin E-rich foods or vitamin E supplements, it is possible to reduce the risk of many common, disabling human diseases and improve the quality of life, particularly in the elderly (Diplock 1997).
Antioxidant supplements, particularly vitamin E, reduce oxidation of lipoproteins, which promote atherosclerosis. A large study that examined the relationship between the intake of dietary carotene, vitamin C, and vitamin E and subsequent coronary mortality found an inverse association between dietary vitamin E and coronary mortality, supporting the hypothesis that antioxidant vitamins provide protection against CHD (Knekt et al. 1994). Compared to subjects receiving placebo, a significant savings in health-related costs was reported in patients receiving supplemental vitamin E. This was primarily attributed to the fact that the vitamin E-supplemented group had fewer hospital admissions and a 4.4% lower risk of acute MI than the placebo group (Davey et al. 1998).
Large epidemiological studies revealed that higher vitamin E levels in plasma result in a reduced incidence of CHD. Dose-response studies in humans have demonstrated that 400 IU per day of vitamin E increased vitamin E plasma levels twofold and delayed oxidation of LDL (Suzukawa et al. 1998). A study to determine the effects of long-term vitamin E supplementation in 17,894 people (aged 50-98) revealed that the length of time the individual used vitamin E was more important than the amount of the nutrient used. This trend was particularly apparent beyond nine years of usage. Taking 400 IU of vitamin E daily for 10 years or more strikingly reduced the occurrence of heart disease prior to 80 years of age (Passwater 1977).
The type and blend of vitamin E selected for supplementation can affect the end results. Studies show that a-tocopherol may offer better protection against CHD when it is combined with gamma tocopherol. Both a-tocopherol and gamma tocopherol can decrease platelet aggregation, inhibit blood clot formation, protect LDL against oxidation, and increase endogenous superoxide dismutase production (an enzyme with antioxidant activity); however, gamma tocopherol shows greater activity on each function. Unfortunately, gamma tocopherol can be obtained from food, but it is poorly retained because it is excreted in urine following liver metabolism. An a-tocopherol transfer protein, selectively transports a-tocopherol over other forms of vitamin E. Consequently, a-tocopherol is more abundant in body tissues. This does not provide for maximum protection against free radical attack. It is recommended that individuals seeking protective cardiovascular effects from vitamin E include gamma tocopherol, by complexing a-tocopherol (80%) with gamma tocopherol (20%) as an ideal blend.
Coenzyme Q10 (CoQ10; ubiquinone) is a fat-soluble cofactor substance. It is a naturally occurring substance that prevents cell damage due to myocardial ischemia (hypoxia) or subsequent to reestablishment of blood flow to the heart after temporary ischemia.
CoQ10 is involved in several key enzymes in energy production within a cell, and has membrane-stabilizing activity. It functions primarily as an antioxidant. CoQ10 has been used to treat cardiovascular disorders including angina pectoris, hypertension, CHF, and periodontal disease. The inflammatory process within the lining of atherosclerotic blood vessels parallels the chronic inflammation of periodontal disease. People with gum disease carry a greater risk for cardiovascular disease and hypertension. Research suggests that topical application of CoQ10 improves adult periodontitis when used alone, but also in combination with traditional periodontal therapy (Greenberg et al. 1990; Hanioka et al. 1994; Genco 1997).
Numerous studies provide details of the efficacy of CoQ10 in the prevention and treatment of heart disease, as detailed below.
Oral CoQ10 (150 mg daily in 3 doses) was given for 4 weeks to exercising angina patients. Average levels of CoQ10 in plasma increased after CoQ10 treatment and were significantly related to an increase in exercise duration. Side effects were minimal. The study suggested that: "CoQ10 is a safe and promising treatment for angina pectoris" (Kamikawa et al. 1985).
Pretreatment with intravenous CoQ10 minimized myocardial injury caused by cardiac bypass graft (CABG) surgery and improved heart function. Patients undergoing CABG were evaluated for reduced left ventricular capacity following reperfusion. Patients received CoQ10 (5 mg/kg, intravenously) 2 hours before cardiopulmonary bypass. Left ventricular stroke work capacity was significantly elevated at 6 and 10 hours after reperfusion following CAB. The results suggested: "pretreatment with intravenous CoQ10 prevented left ventricular depression in early reperfusion and minimized myocardial cellular injury during CAB followed by reperfusion" (Sunamori et al. 1991).
CHF is characterized by depleted energy status and low CoQ10 levels. Individuals experiencing heart failure (2664 individuals from 173 centers) were administered 50-150 mg of CoQ10 daily. After 90 days of CoQ10 treatment, patient improvement in clinical signs and symptoms was significant: cyanosis, 78.1%; edema, 78.6%; enlarged liver area, 49.3%; dyspnea, 52.7%; palpitations, 75.4%; sweating, 79.8%; subjective arrhythmia, 63.4%; insomnia, 662.8%; vertigo, 73.1%; and nocturia, 53.6%. Improvement of at least three symptoms was observed in 54% of patients, which was interpreted as improved quality of life. The incidence of side effects was low (1.5%) (Baggio et al. 1994).
Effects of oral treatment with CoQ10 (120 mg daily) were compared after 28 days in patients with acute myocardial infarction (AMI). After treatment with CoQ10, angina pectoris, total arrhythmias, poor left ventricular function, and total cardiac events were significantly reduced in the CoQ10 group. The antioxidants (vitamins A, E, C, and beta-carotene), which were initially lower following the AMI, increased more in the coenzyme CoQ10 group. CoQ10 can provide rapid protective effects in patients with AMI if administered within 3 days of the onset of symptoms (Singh et al. 1998).
Many elderly individuals will soon require heart surgery as the general population ages. The outcome of surgery in the elderly, compared to younger individuals, is compromised by age-related reduction of cellular energy production in the myocardium during surgery. Elderly subjects were given CoQ10 prior to heart surgery to improve surgical outcomes and to determine if contractile function of muscle fibers in response to ischemia (and aging) could be reversed. Fibers from subjects over age 70 showed poor recovery of force after simulated ischemia compared to younger patients. This age-associated effect was prevented by pretreatment with CoQ10 (Rosenfeldt et al. 1999). It was hypothesized that CoQ10 pretreatment prior to stress improved recovery of the myocardium after stress (Rosenfeldt et al. 2002). CoQ10 improves heart function in two ways: by fighting free radical attacks during cardiac stress (angioplasty, thrombolysis, and surgery) and improving cellular energy production (Rosenfeldt et al. 1999).
Note: Because of the popular use of "statin" drugs (Zocor®, Lipitor®, Pravachol®, Lescol®, and Mevacor®) it is important to emphasize that statins act by inhibiting HMG-CoA reductase, the rate-limiting enzyme in cholesterol biosynthesis. Drugs inhibiting HMG-CoA reductase activity decrease CoQ10 levels (Folkers et al. 1990) because HMG-CoA reductase is required for CoQ10 synthesis. Individuals using statins ought to increase their intake of CoQ10 to negate the decrease in CoQ10 biosynthesis caused by the statin drugs. Some mainstream physicians are aware of this side effect and administer CoQ10 with statin therapy. CoQ10 is free of toxicity and typically produces no side effects. CoQ10 may change the insulin requirements of people with diabetes so talk to your physician if you have diabetes and plan on taking CoQ10.
Essential Fatty Acids
Omega-3 fatty acids, EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), from fish, flax, or perilla oils, are essential for optimal health. Most Western diets contain predominantly omega-6 fatty acids, in proportions greatly exceeding the omega-3 fatty acids. The so-called "bad" saturated fatty acids and their metabolites (those fats that are solid at room temperature) compete with beneficial EPA and DHA fatty acids. Increasing dietary alpha-linolenic acid and omega-3 fatty acids, while limiting dietary polyunsaturated fat and calorie intake, have important cardiac benefits, including reduction of risk of heart attack and mortality by as much as 70% (Guize et al. 1995).
Scientific studies demonstrate that alpha-linolenic acid (from flax or perilla oil) reduced the incidence of atherosclerosis, stroke, and second heart attacks. When perilla or flax oil is consumed, it requires the enzyme delta-6 desaturase to convert the alpha-linolenic acid into EPA and DHA. Many individuals (particularly those over 50 years of age, who show declining activity of this enzyme) should consider using high-potency fish oil because these products directly provide EPA and DHA. Compared with no fish consumption, a lower risk of death was associated with fish consumption. High proportions of omega-3 fatty acids found in serum lipids were associated with a substantially reduced risk of death (Erkkila et al. 2003).
Thromboxane A2 promotes abnormal blood-clot formation, however, seven days of dietary perilla oil (versus soybean oil) effectively reduced inflammatory cytokine formation and thromboxane A2 production by platelets in rats (Ikeda et al. 1995). Excessive platelet-activating factor (PAF) is a major cause of arterial blood clots that can lead to heart attack and stroke. When compared with high dietary linoleic acid-containing safflower oil (an omega-6 fatty acid), high dietary alpha-linolenic acid-containing perilla oil (an omega-3 fatty acid) decreased PAF production by nearly one half in experimental animals (Oh-hashi et al. 1997). Perilla oil alleviates chronic inflammation, prevents certain types of arrhythmia, maintains cardiac cellular energy output, and preserves cell membrane structure.
Studies reflect the advantages of healthy eating (Renaud 2001). A Mediterranean-type diet has been evaluated after the first heart attack. The diet emphasizes fruits, vegetables, bread, cereals, potatoes, beans, nuts, seeds, and olive oil. Red meat and eggs are restricted. Servings of fish, poultry, and wine are restricted to low to moderate amounts. After four years, there was a 50–70% lower risk of recurrent heart disease (AHA 2004a).
Note: Because EPA/DHA can interfere with blood clotting those who suffer from any type of hemorrhagic disease or who take anticoagulant drugs should inform their doctor they are taking these supplements. Physicians may wish to adjust the dosage of anticoagulant medication based on measures of blood coagulation.
Continued . . .
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