Omega-3 Fatty Acids and Heart Health

Omega-3 reduces risk of death from cardiovascular causes by between 30 to 50% following a myocardial infarction

 

Lancet. 1999 Aug 7;354(9177):447-55.

From October, 1993, to September, 1995, 11,324 patients surviving recent (< or = 3 months) myocardial infarction were randomly assigned supplements of n-3 PUFA (1 g daily, n=2836), vitamin E (300 mg daily, n=2830), both (n=2830), or none (control, n=2828) for 3.5 years.

The Italian GISSI study says taking just 850 mg of EPA DHA Omega-3 per day showed a dramatic reduction of sudden death.

This risk reduction isn’t from cholesterol reduction.

The risk reduction comes from:

• reduction in triglycerides
• reduction in inflammation
• providing antiarrhythmic properties
• improved endothelial function

Follow up Report

Omega-3 Fatty Acids and Heart Failure
Curr Atheroscler Rep. 2009 Nov;11(6):440-7.

Abstract
During the past three decades, the protective role of omega (n)-3 polyunsaturated fatty acids (PUFA), mainly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in patients with coronary heart disease has been widely reported. The Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-Heart Failure (GISSI-HF) study, a large-scale clinical trial, recently showed that n-3 PUFA (850-882 mg/d) reduced mortality and admission to the hospital for cardiovascular reasons in patients with chronic heart failure (HF) who were already receiving recommended therapies. The favorable effects of n-3 PUFA in GISSI-HF suggest that marine fish oils could confer protection in HF mainly through their antiarrhythmic action and in part by influencing the mechanisms related to HF progression. This article reviews recent clinical and experimental evidence on the effect of n-3 PUFA in coronary heart disease, with particular attention on HF and its pathophysiologic mechanisms.

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Homocysteine Basics

Homocysteine is an amino acid that inflicts damage to the inner arterial lining (endothelium) and other cells of the body. All homocysteine in the body is biosynthesized from methionine, an essential amino acid found abundantly in meats, seafood, dairy products, and eggs. Vegetables, with few exceptions (eg, sesame seeds and Brazil nuts), are low in methionine; even such protein-rich legumes as beans, peas, and lentils contain relatively small amounts of methionine compared to animal-derived foods.

Homocysteine exists in several forms (Jacobsen 1998); the sum of all homocysteine forms is termed ‘total homocysteine.’ Protein-rich diets contain ample amounts of methionine and consequently produce significant levels of homocysteine in the body (Verhoef 2005).

A study published in the journal Medical Hypothesis (1998, 51[3]:179-221) provides evidence that aging may be exclusively a result of cellular "demethylation," or, said differently, the aging process is caused by the depletion of enzymatic "remethylation" activity that is required to maintain and repair cellular DNA. This study suggests that aging may be reversible if aged cells could be programmed to remethylate rather than demethylate.

Homocysteine induces cellular damage by interfering with the methylation process. Methylation will be compromised if homocysteine is elevated, and elevated homocysteine is a warning sign that the methylation cycle is not functioning properly. Homocysteine may also damage cells directly by promoting oxidative stress.

Homocysteine is metabolized through two pathways: remethylation and transsulfuration (See Homocysteine Metabolic Pathways below). Remethylation requires folate and B12 coenzymes; transsulfuration requires B6 coenzyme (Selhub 1999a).

■ Elevated blood levels of homocysteine have been linked with a wide range of health disorders including heart disease, stroke, macular degeneration, hearing loss, migraine, brain atrophy, dementia and cancer.

■ A high-protein diet, especially one that includes red meats and dairy products, is also high in methionine, the parent compound of homocysteine. Following such a diet can increase blood levels of homocysteine.

■ Numerous factors, including prescription drug use, smoking, coffee and alcohol consumption, advancing age, genetics, and obesity contribute to elevated homocysteine levels.

■ Many people carry a genetic variation that is linked with elevated homocysteine levels. People carrying this gene variant suffer from an impaired ability to metabolize folic acid to its active form, but may achieve a significant reduction in plasma homocysteine by taking an active folate (5-MTHF) supplement.

■ Vitamin B2, B6, and B12 supplements as well as those containing choline and TMG work together with folate to maintain homocysteine levels within a healthy range.

■ As humans grow older, homocysteine levels increase substantially. However, although these increased levels are “normal,” they are still associated with higher risk of various health problems.

■ Although some clinical testing laboratories consider homocysteine levels of up to 15.0 µmol/L as normal, I believe this is too high for optimal health and therefore recommends keeping homocysteine levels < 7-8 µmol/L.

■ A program of regular exercise may help people recovering from a heart attack, bypass surgery, or angioplasty to modestly reduce homocysteine levels.

B Vitamins

Cataplex G (Riboflavin) and Homocysteine Reduction.

Vitamin B2 (riboflavin) has long been known to be a determinant of plasma homocysteine levels in healthy individuals with the 5-MTHFR C677T gene variant that causes hyperhomocysteinemia (Hustad 2000). Homocysteine is highly responsive to riboflavin (riboflavin is required as a co-factor by MTHFR), specifically in individuals with the MTHFR 677 TT genotype (McNulty 2006).

A four-week randomized placebo-controlled double-blind trial found that 10 mg/day oral riboflavin supplementation for 28 days lowered plasma homocysteine concentrations in 42 subjects (60 to 94 years) with low riboflavin status (Tavares 2009).

Homocysteine Reduction Treatment Protocol


Individuals who wish to reduce their elevated blood levels of homocysteine may want to adopt the following treatment protocol. Depending upon a number of factors including age, gender, health, diet, drugs, and genetics, this could require taking multiple supplements that work in concert to effectively reduce homocysteine and the risk of vascular disease.

General Guidelines:

■ Reduce methionine-rich foods: Particularly red meats and dairy products. Although methionine is an essential amino acid, it is also suspected to indirectly promote atherosclerotic plaque growth by increasing homocysteine levels.

■ Exercise: In a cardiac rehabilitation program following bypass surgery, angioplasty, or heart attack, 76 participants experienced a modest 12% reduction in homocysteine just by engaging in a program of regular exercise (Ali 1998).

■ Decrease or eliminate: Alcohol, coffee (filtered and unfiltered), and smoking.

■ Weight loss: obesity is associated with higher homocysteine.

The remethylation (or detoxification) of homocysteine requires the following minimum factors: (1) folic acid, (2) vitamin B12, (3) zinc, and (4) TMG.

The following nutrients can provide an effective starting point as a means of reducing homocysteine:

■ Folic Acid B12: 1-2 mg is another option that has been used for years to reduce homocysteine levels.

■ Cataplex B12: (cobalamin): 1 mg daily

■ Cataplex G: (riboflavin): 10 mg daily

■ B6 Niacinaminde: 100 mg daily

■ Zinc Liver Chelate: 30 to 60 mg daily

■ Choline: 250 to 500 mg daily.

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