~Cardiovascular Disease Comprehensive 11 - Therapeutic H

~Cardiovascular Disease Comprehensive 11 - Therapeutic H
Hawthorn Berry (Crataegus oxyacantha)-- normalizes blood pressure; is beneficial to dieters and those with congestive heart failure; prevents premature ventricular contractions and hypoxia; has diuretic and antioxidant potential; lowers cholesterol; acts as a vasodilator; is an ACE inhibitor, beta-blocker, and anti-inflammatory; increases exercise tolerance; and reduces the incidence of tachycardia and palpitations

Dr. James Duke, botanist, says that when hawthorn is evaluated chemically, it appears that the herb covers most of the cardiovascular bases. For example, it contains a calcium-antagonist (magnesium), ACE inhibitors (procyanidins), and beta-blockers (catechin, epicatechin, and procyanidins), plus numerous diuretics, cholesterol-lowering compounds, anti-inflammatories, and antioxidants (Duke 2000b).

The hawthorn berry is considered a smart herb with adaptogenic qualities in regard to normalizing blood pressure. Hawthorn gains much of its hypotensive and weight management properties through its diuretic action. Also, its ACE inhibiting factors interrupt the renin-angiotensin sequence, resulting in lower blood pressure and improved cardiac output (Duke 2000b). Clinicians compare the effectiveness of hawthorn to Captopril, a drug prescribed for congestive heart failure (CHF) and hypertension that also works by inhibiting ACE. (Hawthorn, although helpful in blood pressure management, should not be regarded as the sole therapeutic for hypertension.)

The bioflavonoid content of hawthorn appears to be responsible for much of the herb's cardiac potential, that is, dilating blood vessels, enhancing vitamin C absorption, and protecting against vascular breaks or leaks. Bioflavonoids are powerful antioxidants that not only protect against free-radical damage, but also increase oxygen delivery and blood flow to the heart. This reduces the effort and stress imposed upon the heart to circulate blood, and as an additional bonus, a reduction in blood pressure usually occurs. The risk of stroke was, in fact, 73% lower among individuals who consumed greater amounts of flavonoid-rich foods compared to individuals who consumed less (Keli et al. 1996; Roanoke Times 1996).

During the Middle Ages, hawthorn was used to treat dropsy, a condition now recognized as CHF. Today, European physicians still use hawthorn to treat early signs of CHF, relying upon the herb to strengthen the heart and the power of cardiac contractions. Drugs that have the ability to power up the heart can cause cardiac irregularities; conversely, it appears hawthorn can energize the heart without prompting arrhythmias. Hawthorn, in fact, has a normalizing effect upon the heartbeat, lessening the incidence of tachycardia (a heart rate greater than 100 beats per minute) and palpitations (Santillo 1990).

Studies confirm the multiplicity of hawthorn's actions:
  • Various clinicians report an excellent patient response, treating valvular insufficiency, heart fibrillations, and hypoxia with hawthorn (Santillo 1990; Ritchason 1995; Duke 1997).
  • Hawthorn appears to stabilize heart rhythm and increase exercise tolerance (Duke 1997). Problem-free exercise occurs as the heart becomes stronger and less taxed by exertion.
  • Hawthorn reduces cholesterol levels and the size of existing atherosclerotic plaque (Wegrowski 1984).
Hawthorn is best used long-term because the active constituents do not produce rapid results. It may take 4-8 weeks for improvement in subjective complaints and increased exercise tolerance. Although it is regarded as gentle and safe for chronic usage, a physician should evaluate the patient's drug list before adding hawthorn to the total package. A dosage suggestion is 250-900 mg daily.

Homocysteine-Lowering Nutrients and Elimination Pathways

Homocysteine, a naturally occurring amino acid, is derived from methionine and produced in small amounts by the body. When homocysteine is not detoxified or reduced through metabolic processes (i.e., remethylation or transsulfuration) and begins to accumulate, various biological failures occur. According to some experts, homocysteine is now recognized as the single greatest biochemical risk factor for heart disease (McCully 1996) (for an introduction to homocysteine, consult Newer Risk Factors appearing earlier in this protocol).

The published literature emphasizes that folic acid, vitamin B12, and zinc (nutrient cofactors) and trimethylglycine (a methyl donor) are critical to the remethylation of homocysteine, the most common detoxification pathway. Remethylation occurs as methyl groups are donated to homocysteine to transform it to methionine and S-adenosylmethionine (SAMe) (Porter et al. 1993; Undas et al. 1993; Malinow et al. 1998; Baker-Racine 2002).

SAMe, the chief methyl donor, is crucial to the methylation process. Initially, methionine reacts with ATP to produce SAMe. SAMe is then used for methylation and a byproduct of this reaction, homocysteine, is recycled back to methionine. This cyclic dance continues faultlessly, unless something throws it out of sync.

Too much methionine will disrupt the delicate balance. Flesh foods and dairy products are rich in methionine and require greater amounts of nutrient cofactors to preserve the methylation process. Chronic inflammation, high intensity exercise, and age can also put the brakes on methylation. When this occurs, the cycle is broken, and homocysteine detoxification stagnates. The problem comes full circle, as excessive amounts of homocysteine interfere with the methylation process.

Trimethylglycine (TMG), also called betaine, emerges as one of the most important nutrients to prevent and reverse existing heart disease, in part by supporting remethylation (Baker-Racine 2002). TMG usually causes a substantial lowering of homocysteine, but regular dosing must continue to sustain the improvement. The dosage varies from one to eight 500-mg tablets a day, depending upon the amount needed to maintain healthy levels (below 7 micromol/L of blood).

Choline, another methyl donor, can act independently (not requiring cofactors) to lower homocysteine levels, but it only influences remethylation in the liver and kidneys, leaving the heart and brain less protected. Methylating factors, as vitamin B12 and folic acid, add additional protection.

The second means of homocysteine disposal is via the transsulfuration pathway, a sequence dependent upon vitamin B6. This pathway converts homocysteine to the powerful antioxidants cysteine and glutathione, but a deficiency of the B6-dependent enzyme, cystathione-B-synthase, can hamper this process. An alternative is to take larger doses of vitamin B6, but this course is not without risk. Chronic megadose vitamin B6 supplementation (300-500 mg daily) can result in neurological symptoms that typically fade when the dosage is reduced or discontinued. Careful monitoring to determine the lowest vitamin B6 dose capable of controlling homocysteine levels is essential.

Some individuals lack the enzyme necessary to convert vitamin B6 to its active form (Robinson et al. 1995). In this case, use the biologically active pyridoxal-5-phosphate to control elevations in homocysteine. Note: Vitamin B6 is also a reliable diuretic, making it of particular advantage to patients with high blood pressure and congestive heart failure.

For most individuals, hyperhomocysteinemia is a modifiable cardiovascular risk factor. In fact, about one-half of individuals with hyperhomocysteinemia respond favorably to vitamin B6 supplementation. Researchers selected 421 patients, mildly hyperhomo-cysteinemic, to determine their response to vitamin B6 (250 mg daily). After 6 weeks of vitamin B6 supplementation, 56% of the patients had normal homocysteine levels. Non-normalized homocysteine concentrations were treated with a combination of supplements, vitamin B6 (250 mg daily) and/or folic acid (5 mg daily) and/or TMG (6 grams daily). The more aggressive treatment normalized homocysteine levels in 95% of the remaining cases (Franken et al. 1994).

Another 20% of hyperhomocysteinemic patients have a mutation in the gene, methylenetetrahydrofolate reductase, disrupting the conversion of folic acid to 5-methyltetrahydrofolate, an active contributor in the methyl donation pathway of folate. In this incidence, it is necessary to use 5-methyltetrahydrofolate supplementation to bypass the metabolic block (James et al. 1999; Bland 2000a) (additional information regarding methylenetetrahydrofolate reductase appears in the section devoted to Heredity, one of the traditional risk factors, in this protocol).

A Polish study showed that administering folic acid (5 mg a day), vitamin B6 (300 mg a day), and B12 (1000 microgram a day) over an 8-week period reduced benchmark homocysteine levels by one-half (from 20 micromol/L to 10 micromol/L) and also reduced thrombin, an intermediate in the production of fibrinogen (Undas et al. 1999). Individuals with low folate status, regardless of age or sex, have a 69% greater risk of fatal heart disease compared to individuals with higher levels (greater than 13.6 nanomol/L) (Morrison 1996; Pirisi 2001; Tice et al. 2001). It is theorized that properly administered folate might prevent as many as 13,500-50,000 premature deaths annually (Boushey et al. 1995).

The New England Journal of Medicine reported that a combination of folic acid, vitamin B12, and pyridoxine reduced homocysteine levels and also the necessity for revascularization procedures. (Revascularization refers to restoring adequate blood supply by means of a coronary bypass or angioplasty.) Researchers concluded that this inexpensive nutritional therapy, with minimal side effects, should be considered as adjunctive therapy for all patients undergoing coronary angioplasty (Schnyder et al. 2001).

The American Journal of Clinical Nutrition reported that a chemical component of coffee and black tea (chlorogenic acid) could raise plasma homocysteine levels (Olthof et al. 2001). Another team of researchers targeted unfiltered coffee as being most contributory to hyperhomocysteinemia (Grubben et al. 2000). On the other hand, a diet rich in fruits and vegetables may decrease the risk of heart disease (7-9%) by reducing blood levels of homocysteine. Fresh and unaltered foods have a more reliable nutrient bank and are capable of delivering more homocysteine-lowering vitamins and minerals.

It should be noted that niacin may increase plasma homocysteine levels (from 1-4 micromol/L) in some people (Desouza et al. 2002; Berkeley Heart Lab). Researchers at Pantox Laboratories (California) explain that niacin appears to interfere with homocysteine clearance by depleting SAMe. 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 (McCarty 2000).

Administering homocysteine-lowering nutrients is so individualized that testing is essential to determine adequate dosages. To assume that homocysteine is not a threat (because you have the B vitamins in your supplemental protocol) is not a guarantee that the dosage is appropriate to render protection. The following daily supplements (used alone or in combination) have demonstrated homocysteine-lowering effectiveness: 500-9000 mg of TMG, 800-5000 mcg of folic acid, 1000-3000 mcg of vitamin B12, 250-3000 mg of choline, 250-1000 mg of inositol, 30-90 mg of zinc, 100-500 mg of vitamin B6, and 200-800 mg of SAMe. SAMe is of value in lowering homocysteine levels only if folic acid and vitamins B6 and B12 are also present; without nutrient cofactors, SAMe will eventually break down into homocysteine.

Note: Extremely important data were recently published showing that pretreatment with 800 IU of vitamin E and 1000 mg of C (before an oral methionine load to experimentally produce homocysteine) blocked the damaging effects of hyperhomocysteinemia. Coagulation and circulating adhesion molecule levels significantly increased after methionine ingestion alone but not after methionine ingestion with vitamins (Nappo et al. 1999).

Reader's guide to food sources, enhancers, and antagonists to homocysteine-lowering B vitamins: Medications to treat congestive heart failure commonly result in multiple B vitamin deficiencies, disrupting disposal systems for homocysteine clearance (Sinatra 2001). Also, B vitamins are considered unstable when exposed to the heating process, but the following foods represent the most nutrient-dense choices:

Vitamin B6 appears in most foodstuffs, but the best sources are brewer's yeast, carrots, chicken, eggs, fish, meat, peas, spinach, sunflower seeds, walnuts, and wheat germ.

Complimentary nutrients in regard to vitamin B6 absorption are the full B complex, vitamin C, magnesium, potassium, and zinc. Antidepressants, alcohol, coffee, exercise (to excess), estrogen therapy, and oral contraceptives appear to either increase the need for vitamin B6 or reduce its status. Diuretics and cortisone drugs block its absorption, and theophylline, an oral bronchodilator, antagonizes pyridoxal phosphate synthesis (Ubbink et al. 1996).

Vitamin B12, the most complex of the B vitamins, should be of special interest to vegans who, after chronic abstinence from animal products, can become seriously depleted in this nutrient. However, most vitamin B12 deficiencies occur not because of inadequate dietary consumption, but rather because of poor absorption. The intrinsic factor, a substance secreted by the gastric mucosa, is essential for the absorption of B12, transporting cyanacobalamin (vitamin B12) across the membranes of the ileum (the distal end of the small intestine).

Animal derivatives, eggs, fish and marine life, beef and pork, and milk and dairy products are good sources of vitamin B12. Nutrients considered B12 enhancers are others of the B complex (especially folic acid and vitamin B6), vitamin C, iron, potassium, sodium, and calcium.

Medications to treat gout, anticoagulant drugs, and potassium supplements may block the absorption of vitamin B12 from the digestive tract (Balch et al. 1997). For optimal B12 utilization, avoid coffee, alcohol, smoking, and laxatives.

Folate-rich foods are liver, wheat germ, legumes, green leafy vegetables, beets, citrus fruits, most fish, pork, and whole grains. Fortification of enriched grain products with folic acid is associated with a substantial improvement in folate status in middle aged and older adults (Jacques et al. 1999).

Folic acid is most efficient when combined with vitamin B12, biotin, pantothenic acid, and vitamin C. According to the Committee on Dietary Allowances, heat and oxidation (occurring during cooking and storage) can destroy as much as half of the folate in foods. Sulfa drugs interfere with the bacteria in the intestines that manufacture folic acid, and Streptomycin totally destroys it. Methotrexate depletes folate, causing a transient elevation in homocysteine, and phenytoin (an antiepileptic drug) interferes with folate metabolism. Lastly, oral contraceptives, alcohol, coffee, and smoking are also considered folic acid antagonists.

Continued . . .

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