~Cardiovascular Disease Comprehensive 12 - Therapeutic M-O

Magnesium-- reduces blood pressure, is a calcium antagonist, tempers the sympathetic nervous system, is beneficial in arrhythmias and mitral valve prolapse, increases the number and sensitivity of insulin receptors, has antidiabetic properties, encourages the methylation process, prevents toxic buildup of homocysteine, reduces calcium levels, is a vasodilator, and opposes platelet aggregation

Magnesium, a potent vasodilator, may prove to be a better hypotensive in some individuals than calcium (50% of magnesium-depleted patients are hypertensive, a condition often remediable with supplementation).

The British Medical Journal reported that magnesium supplementation lowered blood pressure by a mean of 12/8 mmHg (systolic and diastolic pressures) in 19 of 20 subjects (Dyckner et al. 1983). Magnesium reduces blood vessel contractibility by regulating levels of bradykinin, angiotensin II, prostaglandins, serotonin, epinephrine, norepinephrine, and dopamine; as a result, vessels vasodilate and blood pressure decreases.

Besides being a hypotensive mineral, magnesium is absolutely essential to proper cardiac function, allowing relaxation of the heart and supporting normal heart rhythms. In a study of patients admitted to coronary care units experiencing arrhythmias, 100% had complete resolution when administered IV magnesium over a 5-hour period. Dr. Bart Chernow (a surgeon at Sinai Hospital in Baltimore, MD) reports that magnesium injections following bypass surgery reduced heart rhythm irregularities 50%, without side effects (Alternative Medical News staff). After 3 months of oral magnesium supplementation, platelet-dependent thrombosis typically is reduced 35% in 75% of patients.

In a study in the American Journal of Clinical Nutrition, researchers from the U.S. Department of Agriculture reported the effects of a magnesium-deficient diet on 22 healthy postmenopausal women ages 47-78. The women all ate the same meals for 6 months as they lived together under close supervision, taking in about 130 mg of dietary magnesium each day. Half the women also took an additional 280 mg of magnesium in supplemental form for 81 days while the other half received a placebo; during the second half of the study period, the groups crossed over to the other treatment category.

The researchers assessed magnesium levels in urine and blood regularly, as well as heartbeat patterns through electrocardiograms. Not surprisingly, serum and urine concentrations of magnesium were lower on the controlled diet, but heart rhythms were also significantly affected by lesser amounts of magnesium. A lack of magnesium provoked the heart into rhythmic abnormalities, as well as more frequent heartbeats. The researchers concluded that the cardiac muscle is more sensitive to magnesium intake than skeletal muscle and that a deficiency has the potential to cause dangerous cardiac irregularities (Klevay et al. 2002).

Calcium channel blockers are popular as antiarrhythmics and antispasmodics (to read more about calcium channel blockers, consult the sections devoted to Beta-Blockers and Calcium Channel Blockers appearing in this protocol). By relaxing arterial smooth muscles and reducing stress on the myocardium (the thick middle layer of the heart), magnesium delivers many of the effects of a calcium channel blocker (Whitaker 1995b).

Magnesium turns off activity in the sympathetic nervous system. By blocking the release of excitatory hormones (epinephrine and norepinephrine), the "fight or flight" response of the sympathetic nervous system is inhibited (Gonzalez 2000). Although the therapeutic profile of magnesium is similar to a beta-blocker, the drug should not be abruptly stopped and magnesium commenced; without a gradual withdrawal of the drug, a rebound could occur, provoking a heart attack.

In mitral valve prolapse, the valve separating the left atrium from the left ventricle protrudes into the left atrium. Of patients participating in an evaluation, 85% were found to have low magnesium levels, suggesting that a deficiency plays a role in the disturbance (Fernandes et al. 1985; Galland et al. 1986; Murray 1996). Numerous studies indicate that magnesium lessens mitral valve prolapse symptoms, palpitations, fatigue, breathing difficulties, and nonanginal chest pains. Others have observed improvement in exercise tolerance and reduced stress within the heart itself (Shechter et al. 2000). Comment: Low magnesium levels also are associated with angina attacks in men. It appears that as magnesium status drops, the frequency of angina attacks increases (Satake et al. 1996).

Too much calcium in the bloodstream may be a forerunner to aortic stenosis (Bonow et al. 1998). Magnesium hinders the absorption of calcium; therefore supplementing with at least 500 mg a day could inhibit the excesses of calcium hardening the cusps of valves (for a comprehensive look at aortic stenosis, consult the section of this protocol dedicated to Valvular Disease).

Magnesium plays an important role in the prevention and treatment of Syndrome X and diabetes. It benefits these conditions by increasing the number and sensitivity of insulin receptors (Waterfall 2000).

In addition, increased homocysteine concentrations cause abnormal metabolism of magnesium in vascular smooth muscles cells, priming these cells for homocysteine-induced atherogenesis, cerebral vaso-spasm, and stroke. Researchers from State University of New York propose that vitamin B6, vitamin B12, and folic acid, together with physiological levels of magnesium, are needed to prevent magnesium depletion and occlusive cerebral vascular diseases induced by homocysteinemia (Li et al. 1999).

Magnesium status is integral in various drug therapies. Recent controlled studies have shown that treatment with magnesium significantly reduced the frequency and complexity of ventricular arrhythmias in digoxin-treated patients with congestive heart failure. In fact, magnesium improved the efficacy of digoxin (digitalis) in slowing the ventricular response in atrial fibrillation. The complex and potentially life-threatening interactions between magnesium and some cardiovascular drugs suggest that magnesium status should be carefully monitored in patients receiving cardiac pharmaceuticals (Crippa et al. 1999).

Unfortunately, the test used by the majority of physicians to measure magnesium levels is worse than useless, according to Dr. Sherry A. Rogers, an environmental medicine specialist. Dr. Rogers refers to this test as "the most dangerous test in medicine" for if it is used, it too often shows misleading normal levels. The assumption that adequate amounts of magnesium exist when, in fact, deficiency states exist may be a fatal mistake. A study in the Journal of the American Medical Association reported that about 90% of practicing physicians never think to check magnesium levels, even in patients who are severely depleted (Whang et al. 1990). Note: Magnesium deficiency is better detected by measuring mono-nuclear blood cell magnesium, as opposed to serum levels.

A dosage suggestion is 500-1500 mg daily of magnesium bound to succinate, citrate, or aspartate. Magnesium oxide, in larger doses, can cause loose stool.

Reader's guide to magnesium-rich foods, enhancers, and antagonists Magnesium is found in most foods, particularly nuts, whole grains, legumes, brown rice, dark green vegetables, and fish (Balch et al. 1997).

Magnesium enhancers include the B-complex (especially vitamin B6), vitamin C, calcium, essential fatty acids, and essential amino acids. The body's requirement for magnesium increases if using alcohol, taking higher amounts of vitamin D, or if exposed to fluoride, tobacco, or unrelenting stress. Cod liver oil, calcium (excessive intake), and iron decrease magnesium absorption. Diuretics and chronic diarrhea can seriously deplete many minerals, including magnesium.

Niacin (Vitamin B3)-- lowers Lp(a), reduces fibrinogen, normalizes blood lipids, and acts as a vasodilator

Nicotinic acid and nicotinamide are types of the vitamin niacin; although related, they are different in their therapeutic delivery. Nicotinamide, often marketed as a superior lipid-lowering version of niacin, actually has little effect in lowering blood lipids (Segrest 2000). It is nicotinic acid that modulates most all lipid parameters, lowering total cholesterol, LDL, VLDL, Lp(a), and triglyceride levels, while increasing HDL cholesterol. Nicotinic acid has, in fact, won favor with the FDA, adding it to a list of other remedials capable of lowering triglycerides.

Because of niacin's broad-spectrum effectiveness against hyperlipidemia, niacin can act independently or in concert with other drugs. Dr. B. Greg Brown (of the University of Washington, Seattle) reported to the American Heart Association that a combination of a statin drug (which lowers LDL cholesterol) and niacin (which raises HDL cholesterol) brought the progression of atherosclerotic disease to a standstill. According to Brown, a niacin-simvastatin combination resulted in a 70% reduction in heart attacks, strokes, and other disease-related events. According to Brown, "This represents twice the reduction seen with statins alone." Simvastatin (Zocor) plus niacin increased HDL levels 30% over baseline, while Zocor alone increased HDL only 7-10% (Kerr 2000). In addition, nicotinic acid can act independently, accomplishing what no drug can currently do: lower Lp(a); 1500 mg a day of niacin reduced Lp(a) an average of 20%; 3000 mg a day reduced Lp(a) an average of 26% (Berkeley Heart Lab).

Niacin has properties that are the opposite of those of nicotine. Nicotine, a toxic substance in tobacco, is a vasoconstrictor; niacin is a vasodilator. Niacin's vasodilating quality makes it beneficial in the treatment of hypertension and various forms of heart disease.

In 1991 a group of scientists found that small amounts of niacin in combination with chromium, lowered cholesterol levels by an average of 14% and improved the total cholesterol-HDL ratio 7% (Urberg et al. 1987; Cichoke 2001). This finding is valuable since niacin has some significant side effects, making it less justifiable in large doses. Articles appearing in the American Journal of Cardiology and the Journal of Cardiovascular Risk confirmed niacin's hypolipidemic value and also reported that low-dose niacin was effective in reducing plasma fibrinogen levels in subjects with peripheral vascular disease (Philipp et al. 1998; Ma et al. 1999).

If used independently, 1-3 grams of niacin is sometimes required to lower cholesterol levels, a dosage that can cause side effects ranging from nuisance complaints to significant endangerments. Allergic-like reactions, such as itching and flushing, are common, but niacin can also disrupt liver function, causing elevations of liver enzymes.

Other risks associated with niacin:
  • Individuals dosing with niacin may experience a rise in uric acid, an increase that can bring on a gout attack (Goldberg 1998). Recall that individuals with Syndrome X often present with higher levels of uric acid.
  • Niacin may interfere with folate and homocysteine metabolism and actually increase plasma homocysteine levels (Desouza et al. 2002). Dr. David Blankenhorn was the first to discover the niacin-homocysteine connection at USC in the CLAS study. Niaspan, an extended-release niacin, raised homocysteine levels in some, but not all people; the amount is generally between 1-4 micromol/L and appears to be dose-dependent (Berkeley Heart Lab).
  • Niacin may deplete SAMe, a pivotal player in methylation. If niacin does decrease SAMe, a likely consequence would be an elevation of plasma homocysteine (McCarty 2000). Note: Concurrent TMG supplementation may represent a cost-effective way to prevent niacin-mediated depletion of SAMe and thus avoid hepatotoxicity (and possibly other adverse niacin side effects). The lack of sufficient detoxification (due to SAMe depletion) appears to explain many of the adverse effects associated with niacin dosing.
  • Niacin can also increase blood glucose levels. In nondiabetic patients, 1500 mg a day of Niaspan (an extended-release niacin) increased fasting blood glucose levels 2.5-11% following a 2-hour glucose load. Using 3000 mg a day of immediate-release niacin, fasting blood glucose increased 4.1% and 11.6% following a 2-hour glucose load. The niacin effect in Type II diabetic patients is currently under investigation (Berkeley Heart Lab). However, it is speculated that individuals predisposed to Type II diabetes may have a poorer response to niacin (in regard to glucose management) compared to individuals without a diabetic inclination.
Considering these negatives, large-dose niacin may be too great a price to pay for the benefits. If a decision is made to use high-dose niacin, some practitioners report that an aspirin taken 30 minutes before the dose markedly reduces some of the lesser side effects, for example, the allergic-like symptoms.

Reader's guide to vitamin B3 sources, enhancers, and antagonists: Good sources of niacin are lean meats, whole grains, brewer's yeast, peanuts, eggs, poultry, fish, and green, leafy vegetables. Milk; some cheeses, for example, cheddar cheese; bananas; and turkey are good sources of tryptophan (a precursor to niacin) (Braly 1985).

Vitamin B3 enhancers (in regard to absorption) are the B-complex (especially vitamins B1, B2, and B6), vitamin C, magnesium, zinc, protein, and essential fatty acids. Antagonists to niacin absorption are alcohol, coffee, excess sugar, antibiotics, and steroids.

Olive Leaf Extract-- according to botanist James Duke, the cardiac properties found in olive leaf extract include antioxidants, antiaggregates, antiarrhythmics, anti-inflammatories, cyclooxygenase inhibitors, diuretics, hypotensives, vasodilators, antispasmotics, antidiabetics, platelet activating factor inhibitors, weight modulators, antiperiodontics, antihyperlipidemics, and plaque fighters

Olive leaf extract (Olea europaea), although historically regarded as a medicinal for fever and malaria, is also valuable in the treatment of cardiovascular disease. Olive leaf extract has been shown in both laboratory and clinical settings to have antidiabetic, hypotensive, and vasodilating properties (Petkov et al. 1972; Gonzalez et al. 1992; Fehri et al. 1994). Researchers documented that an aqueous extract of olive leaves inhibits ACE, the enzyme that converts angiotensin I to angiotensin II (Duke 1992). The vasoconstricting nature of angiotensin II terminates in an increase in blood pressure, a sequence that olive leaf extract disrupts.

According to Dr. Duke, chemicals contained in O. europaea are regarded as calcium antagonists, diuretics, and anti-inflammatories. In addition, olive leaf protects LDL cholesterol against oxidation and inhibits the production of thromboxane A2 and platelet-activating factor (PAF). These functions discourage vasoconstriction and platelet clumping (Duke 1992; Petroni et al. 1995; Mindell 1998).

Chelation therapy, in conjunction with an aggressive supplemental program that relied heavily upon olive leaf extract, has proved remedial among select senior subjects who have suffered multiple heart attacks and arrhythmias. A suggested dosage is one to two 500-mg olive leaf extract capsules, administered 3 times daily with meals.

Continued . . .

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