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      Homocysteine is a naturally occurring amino acid that is required by the human body for the building and maintenance of tissue. It is a normal by-product of protein metabolism, and is derived primarily from meat and dairy products. Homocysteine has come into popular focus over the past several years, as it appears that this amino acid may be a very important marker for cardiovascular disease.

 Relationship to Cardiovascular Disease
      The American Heart Association, and the National Institutes of Health’s (NIH) National Heart, Lung, and Blood Institute (NHLBI), have both recognized that elevated homocysteine levels are a potential risk factor for cardiovascular disease.
      There are a number of theories as to why excess homocysteine apparently has a deleterious effect on blood components and arteries, the results of which lead to either abnormal clotting, impaired blood flow, or both.
      Platelets. It has been suggested that perhaps blood platelets (an essential component in the blood clotting cascade) become abnormally adhesive, thereby causing blood to clot prematurely or excessively. This, in turn, would lead to a much greater risk factor for heart attack and stroke.
      Arterial constriction. Another possibility is that excess homocysteine may restrict arterial dilation (reduce the flexibility of arteries, preventing them from increasing in size to permit larger amounts of blood to flow).
      Plaque formation. A more widely addressed theory is a thickening, and subsequent scarring of tissue on the inside of arterial walls, creating “pockets” allowing the buildup of plaques from excess LDL cholesterol, an atherosclerotic process that in turn leads to restricted blood flow and greater possibility of adverse cardiovascular events.

 The Vitamin B Connection
      The body has a regulatory system, involving the B complex vitamins, that keeps homocysteine at the level required for the amino acid to perform its essential function. Under normal conditions, excess homocysteine is metabolized into another amino acid, methionine, preventing any adverse effects. The question, then, is how does one’s homocysteine become abnormally high? The answer, at least in part, is your diet.
      As mentioned above, homocysteine is abundant in meat and dairy products. It follows that the intake of homocysteine is naturally higher in individuals whose diets lean toward these foods. Numerous studies have shown that homocysteine-methionine metabolism is at least partially regulated by the presence of vitamins B6, B12 and folate, resulting in a higher homocysteine concentration in these same individuals whose diets are also poor in vegetables, whole grains, and other foods naturally high in, or supplemented with these B complex vitamins.
      Vitamin B12 is also an important component in this model, though with special consideration. This vitamin is derived almost entirely from animal products, so normally, the “meat and potatoes” diet also contains sufficient B12 for its contribution to the homocysteine-to-methionine breakdown process. It is known, however, that upwards to a third of all individuals over 50 years of age have vitamin B12 malabsorption, so affected individuals in this age group on similar diets would be at higher risk for elevated homocysteine.
      It is interesting to note that diets high in animal fat and low in fruits and vegetables, traditionally considered a contributing factor to risk of cardiovascular disease, can now be seen to have the homocysteine factor working against them as well. The question that now has the most avid attention of researchers in this area, is which component of this dietary pattern contributes most to the risk of cardiovascular disease, the fat and cholesterol, or the homocysteine?
      Even absent a clear picture of the causative factors, it remains painfully obvious that a moderation of such traditional diets would likely contribute significantly to an overall program of reducing your risk of at least some forms of heart disease and generally improving your overall health.

 The Genetic Factor
      Homocystinuria (elevated homocysteine in the urine) is caused by a relatively uncommon genetic disorder, one that affects sulfur amino acid metabolism resulting from a defect in the enzyme, cystathionine synthetase. This is a far more serious disorder than elevated blood homocysteine resulting from dietary causes, and is characterized by mental retardation, an enlarged liver, and cardiovascular disorders, among others.
      Some relatively new research, however, suggests that genetic mutations may also be contributing to elevated blood homocysteine in some individuals, creating a greater risk of cardiovascular disease than dietary factors alone. It also appears that such mutations may also mimic the folate deficiencies believed to be responsible for neural tube defects (NTDs), resulting in serious birth defects in the newborn, and of course creating a greater risk factor for this disorder as well.

 Can Supplements Help?
      Evaluation of large numbers of individuals at risk for cardiovascular disease has shown a significant correlation between high homocysteine and inadequate B complex vitamin intake, specifically vitamins B6, B12 and folate. It has become all too apparent that B vitamin deficiencies can certainly contribute to the risk associated with cardiovascular disease.
      The importance of folate, in particular, as a nutrient has not been lost on Federal regulators in the U.S. As recently as 1998, food manufacturers have been required to add supplemental folate to processed grains, those typically used in breakfast cereals and similar food products. Ironically, the reason for establishing these new regulations has less to do with the risk of cardiovascular disease than the risk of neural tube defects. However, the change will certainly be a major factor in reduced homocysteine levels in the populations that regularly consume these foodstuffs (at least to the extent that individuals are deficient in folate), thereby reducing their risk of cardiovascular disease in the process.
      Although there is a steady stream of evidence that correlates vitamin B complex deficiency and elevated homocysteine, there is considerably less data to support supplementation of these vitamins as a preventive measure to reduce the risk of cardiovascular disease (relating to elevated homocysteine) in individuals who are not otherwise deficient in these vitamins. This is an area of research that has become the focus of many scientists in the area of nutrition related causes of heart disease.
      An important consideration here is that far more individuals are deficient in the B vitamins than they themselves are aware. Proper supplementation to support poor, or inadequate dietary intake of these vitamins would seem to be very inexpensive insurance to aid in the reduction of homocysteine related risk of cardiovascular disease.

 Other Risk Factors
      Many professionals in the health care community have been quick to point out that lowering homocysteine levels is not the panacea for reducing the risk of cardiovascular disease. Among other factors, there remains the contribution made by diets high in saturated fats and cholesterol toward the risk of heart disease. Although such diets certainly contribute to higher homocysteine levels, fats and cholesterol pose issues of their own to be considered.
      And of course there is the matter of inadequate exercise, poor body weight management, and smoking, all of which contribute to the risk of cardiovascular disease. As with many things in prevention of disease, there is much to consider when addressing matters of your good health.






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