Homocysteine and Cardiovascular Disease Post 1

Cardiovascular disease remains by far the leading cause of premature death for men and women in the U.S., the disease itself the consequence of a variety of factors, both hereditary and environmental.

Of the major risk factors, namely, high low-density lipoprotein (LDL), cholesterol and/or low high-density lipoprotein (HDL) cholesterol, old age, male gender, premature menopause in women, hypertension, smoking, diabetes mellitus and a family history of heart attack, three are related to diet: HDL and LDL cholesterol levels, hypertension and diabetes. Much research time has been spent exploring potential dietary intervention strategies and preventative measures.

For several decades, the debate on diet and cardiovascular disease has been dominated by the classic diet-heart hypothesis that proposes an adverse effect of dietary saturated fat and cholesterol and a beneficial effect of polyunsaturated fatty acid (PUFA) intake. However, recent research suggests that the diet-heart relationship is much more complex than previously recognized. No doubt, dietary lipids play a significant role in the development and prevention of this chronic disease, however, it is becoming clear that myriad of other dietary factors work synergistically and may prove to be just as, if not more, important in maintaining the health of the heart.

Antioxidants are emerging as protective factors, as well as numerous other phytochemicals often overlooked in fruits and vegetables. Moreover, deficiencies and/or excesses in certain vitamins, minerals and trace elements appear to effect the health status of the heart. There is also increasing evidence that high levels of homocysteine, an amino acid partially regulated by folic acid and vitamin B12, may contribute to the development of cardiovascular disease.

Coronary Heart Disease (CHD) is the most common form of cardiovascular disease and involves both atherosclerosis and hypertension. A heart attack (myocardial infarction) is usually the consequence of three events: 1) the narrowing of coronary arteries by atherosclerosis, 2) the rupture of an atheromatous plaque and 3) the formation of a blood clot (thrombus) in a narrowed artery. Atherosclerosis is the accumulation of cholesterol-rich deposits along the inner walls of the arteries.

It first appears in arteries as fatty streaks, slightly raised yellow areas which contain foam cells. Over time, these fatty streaks collect minerals and they enlarge to form fibrous plaques which stiffen the arteries and tighten their passage. Arteries narrowed by plaques are unable to expand normally with each heartbeat, thereby causing blood pressure to rise with each pulse and the artery walls to undergo further damage.

When the body’s tissues are injured, platelets and several clotting factors known as eicosanoids are released into the blood to stimulate coagulation. Consequently, soluble fibrinogen is converted into insoluble fibrin which, along with the platelets and red blood cells, aggregates at a damaged point in the artery wall to form a thrombus. The blood clot gradually expands until it reaches a narrow artery where it is blocked from passage. Consequently, the heart is robbed of oxygen and nutrients resulting in myocardial infarction.

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