~Cardiovascular Disease Comprehensive 14 - Therapeutic T
Taurine-- has hypotensive and diuretic activity, tempers the sympathetic nervous system, is beneficial in CHF and arrhythmias, and has digitalis-like mentality
Taurine is the most important and abundant of the amino acids in the heart, surpassing the combined quantity of all the others. Under high stress conditions--hypertension and many forms of heart disease--the need for taurine increases to compensate for either an accompanying impairment of taurine metabolism or increased requirements. Dr. H. Kohaski and colleagues (Japan) suggest that entry-level taurine may have been low and, as the stress of hypertension progresses, taurine levels drop even lower (Kahashi 1983; Braverman et al.1987).
Taurine has a diuretic action that benefits hypertensive individuals, as well as patients with congestive heart failure. Taurine elicits much of its diuretic action by preserving potassium and magnesium and by promoting sodium excretion (Atkins 1996b).
Taurine also reduces blood pressure by acting as an antagonist to the blood pressure-increasing effect of angiotensin, a circulating protein that is activated by renin, a hormone secreted by the juxtaglomerular cells in the kidneys in response to a drop in blood pressure (Braverman et al. 1987). When both blood and urine taurine levels decrease, renin is activated and angiotensin is formed. As a result blood vessels vasoconstrict, water and salt are retained, and blood pressure increases. Taurine suppresses renin and breaks the renin-angiotensin feedback loop. Dr. Robert Atkins, a complementary physician with a creditable cardiology background, amplifies the positive results of scientific literature, stating that taurine would be his choice were he selecting a single nutrient to treat hypertension.
Dr. Y. Yamori (a Japanese researcher who established an amino acid-stroke association) studied a strain of rats, genetically susceptible to strokes. Yamori found the rats had a much lower incidence of stroke, dropping from 90% to 20%, if their diet was supplemented with methionine, taurine, and lysine (Yamori et al. 1983; Braverman et al. 1987).
Japanese researchers found that 3 grams of taurine, administered daily to patients with congestive heart failure, was more effective than 30 mg of CoQ10 (Azuma et al. 1992). The Japanese, who use taurine widely in the treatment of various forms of heart disease, found that 4 grams of taurine, given for 4 weeks, brought relief to 19 of 24 patients with congestive heart failure. Taurine appears to act much like the drug digitalis, increasing the contractility of cardiac muscle and the force of the pumping action.
Taurine appears to impact cardiac arrhythmias through various pathways. For example, some forms of cardiac irregularities are helped by taurine because it regulates membrane excitability and scavenges free radicals. In addition, taurine protects potassium levels inside heart cells, which, when imbalanced, can cause electrical instability and cardiac arrhythmias (Braverman 1987; Chahine et al. 1998).
Some types of premature ventricular contractions and arrhythmias respond to taurine because the amino acid tends to dampen activity in the sympathetic nervous system (SNS) and the outpouring of epinephrine. As the SNS is quieted, the heart tends to beat less aggressively and the blood pressure is lowered. Lastly, Lebanese researchers showed that the incidence of ventricular fibrillation and ventricular tachycardia were significantly reduced when taurine therapy was utilized (Braverman 1987; Chahine et al. 1998). A suggested dosage is 1500-4000 mg daily.
Testoterone-- modulates cholesterol levels, dilates blood vessels, improves circulation, lessens angina attacks, and reduces blood pressure
Testosterone, a muscle-building hormone, appears to do far more than promote the development of male secondary sexual characteristics. There are, in fact, many testosterone-receptor sites in the heart that play a role in maintaining heart muscle protein synthesis and strength (Bricout et al. 1994).
If testosterone levels are normal, cholesterol is more easily managed, and blood has an easier route as it flows through dilated vessels. One study showed that circulation to the heart improved 68.8% in patients receiving testosterone therapy (Wu et al. 1993). A testosterone delivery patch applied to men with low testosterone levels increased exercise time on a treadmill and (according to trial participants) increased quality of life. Improved emotional health (important to the heart) and a decrease in the incidence of angina attacks reflect some of the benefits of upgrading testosterone levels (English et al. 2000).
Typically, fibrinogen, triglycerides, and insulin levels are higher if testosterone levels are low (Marin 1995; Kryger 2002). In addition, the elasticity of the coronary arteries diminishes, contributing to the development of arteriosclerosis. Blood pressure increases, but the growth hormone decreases, further weakening the heart muscle. Abdominal fat, the most dangerous form of obesity, increases.
Physicians who check for testosterone deficiencies or testosterone-estrogen imbalances have in some cases been able to discontinue cardiac and hypertension medications. Improved EKGs confirm subjective reports of improvement. Since testosterone testing is noninvasive, the risk-benefit ratio swings heavily in favor of testing. For information about safely increasing testosterone levels, refer to the Male Hormone or Female Hormone Modulation protocols.
Thiamine (Vitamin B1)-- is beneficial in some forms of cardiac arrhythmias, palpitations, enlarged heart, elevated venous pressure, and congestive heart disease
Cardiac arrhythmia refers to a deviation from the normal pattern of the heartbeat. Arrhythmias can be caused by a variety of underlying medical conditions that should be addressed by a qualified cardiologist. Arrhythmias are not always clinically significant because rather benign events can spur healthy hearts to enter irregular patterns of beating. Yet, arrhythmias should be taken seriously, and a diagnosis made as to the causative factors provoking the disturbed beat. Stress, electrolyte imbalance, ischemia, hypoxia, ventricular enlargement, occlusions, an insulin rush, or derangement in the autonomic nervous system can drive a heart into irregular rhythms.
Since thiamine has proved correctional for some types of arrhythmias, there appears to be linkage between irregular heartbeats and beriberi, a disease caused by a deficiency of or an inability to assimilate thiamine. Cultures that depended upon rice, a high carbohydrate food, as a dietary mainstay found the milling process, that is, the removal of the brown coat rich in thiamine, to be their undoing. Beriberi swept through the population with epidemic force.
Cardiac arrhythmias may manifest among heavy drinkers as thiamine deficiencies occur, and symptoms of beriberi appear. But, heavy imbibers are not the only individuals susceptible to thiamine deficiency. Infirm individuals, as well as those who are elderly and malnourished, are at particular risk. Long-term diuretic usage can also contribute to a thiamine deficiency through urinary loss. It is not uncommon for heart palpitations, deranged heart rhythms, and elevated venous pressure to occur as patients become thiamine deficient (Whiting 1989). Additional cardiovascular manifestations of wet beriberi are myocardial lesions, sodium and water retention, and biventricular myocardial failure. Typically, clinical improvement occurs quickly following vitamin B1 therapy (Blanc et al. 2000).
In 1995, 30 patients with severe heart failure and taking furosemide (Lasix, a diuretic) were enrolled in a heart study. Although furosemide was unsuccessful in improving their cardiac condition, 200 mg of thiamine (a day) dramatically improved heart function (Shimon et al. 1995). Some patients may experience improvement from 200-250 mg a day; other individuals may require 500-1000 mg daily. (A full spectrum vitamin B supplement should always accompany single B vitamin supplementation.)
Reader's guide to vitamin B1 food sources, enhancers, and antagonists: Lean pork, wheat germ, and whole grains (particularly brown rice) are considered to be excellent sources of thiamine. Meat, poultry, egg yolk, fish, legumes, peas, sunflower seeds, nuts, and brewer's yeast represent other good thiamine choices.
Vitamin B1 enhancers are all others of the B complex, vitamin C, vitamin E, and manganese. Alcohol, coffee, antacids, and excesses of sugar and refined carbohydrates decrease thiamine absorption.
Tocotrienols-- are antioxidants, decrease platelet aggregation, and have statin mentality
Tocotrienols have been until recently the lesser known half of vitamin E. A major functional difference between tocotrienols and tocopherols appears to be the ability of tocotrienols to more aptly decrease cholesterol synthesis in the liver. Both tocotrienols and tocopherols appear to be potent antioxidants, with some research demonstrating greater antioxidant protection and less oxidative damage when supplementing with tocotrienols (Serbinova et al. 1991).
Cholesterol lowering statin drugs -- Lipitor, Lescol, Mevacor, Pravachol, and Zocor -- operate at the level of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase. HMG-CoA reductase is a rate-limiting enzyme that participates in cholesterol synthesis. The cholesterol cascade occurs as follows: (1) acetyl-CoA is converted to HMG-CoA, (2) HMG-CoA is reduced to mevalonic acid by the enzyme HMG-CoA reductase, and (3) several steps convert mevalonic acid to squalene and then to cholesterol.
Tocotrienols, particularly gamma and delta, accelerate the degradation of HMG-CoA reductase, altering the functionality of the enzyme responsible for cholesterol synthesis (Parker et al. 1993). The statin drugs, though acting at the level of HMG-CoA reductase, approach the enzyme differently. Statin drugs do not degrade the enzyme but competitively inhibit its binding. The inhibition of the binding mechanism leads to a higher production of HMG-CoA reductase, which may explain the side effects, such as liver toxicity, associated with statin usage.
Studies indicate that roughly 75% of hypercholesterolemic individuals respond favorably to tocotrienol supplementation. The most impressive cholesterol reductions occur when tocotrienol supplements are combined with dietary changes (a high fiber/low fat diet). In a 12-week double-blind trial, those who responded to tocotrienol therapy saw a reduction of approximately 23% in total cholesterol and a 32% reduction in LDL cholesterol using dietary modification plus tocotrienol supplements. Tocotrienols alone yielded a 16% decrease in total cholesterol and a 21% decrease in LDL cholesterol (Quereshi et al. 1993; ACCM 1998). HDL levels do not appear to respond to tocotrienol supplementation, but apo-B, a protein component found in LDL, VLDL, and IDL cholesterol, is lowered. Thromboxanes are also considered toco-trienol responsive (Qureshi et al. 1997).
The Kenneth Jordan Heart Research Foundation (New Jersey) reported the results of 50 patients with narrowing of the carotid artery who were treated with either a placebo or tocotrienols: 25 patients (some with carotid stenosis greater than 49%) received 650 mg of tocotrienols plus tocopherols; a control group of 25 patients, with comparable closure, received a placebo. Each group was evaluated every 6 months for the first year and every year thereafter with ultrasonography. In the placebo group, 15 patients showed worsening of the stenosis, eight remained stable, and two showed some level of improvement. In the tocotrienol plus tocopherol group, three patients showed minor worsening, 12 remained stable, but 10 patients showed regression of stenosis. Participants experienced a simultaneous drop in triglycerides and LDL cholesterol (Papas undated; Tomeo et al. 1995; Watkins et al.1998).
The late Karl Folkers, a pioneer in CoQ10 research, observed that drugs inhibiting HMG-CoA reductase activity cause a simultaneous decrease in CoQ10 levels (Folkers et al. 1990). The reason for this is that the HMG-CoA enzyme also plays a role in CoQ10 synthesis. Individuals using either statin drugs or tocotrienols may wish to increase their intake of CoQ10; a decrease in CoQ10 could negate any benefit garnered from a hypocholesterolemic drug.
According to Andreas M. Papas, Ph.D., appropriate tocotrienol dosages are as follows: 100 IU of mixed tocopherols and 100 IU of tocotrienols if young and healthy and without a family history of heart disease; 200 IU of mixed tocopherols and 200 IU of toco-trienols for young adults with some cardiac risk factors or healthy people up to 50 years of age without risk factors; 400 IU of mixed tocopherols and 400 IU of tocotrienols for people who have a personal or family history of chronic heart disease. The latter dosage includes senior subjects and those under severe stress and eating a poor diet.
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