Homocysteine: a Risk Factor worth Treating a Concise Update of Important Issues concerning Natural Health Ingredients

lesions in these individuals and he further postulated that moderately elevated homocysteine due to heterozygous mutations in homocysteine related genes or poor vitamin status would also lead to increased risk of cardiovascular disease (4). By the early 1990’s, elevated homocysteine was being considered an independent risk factor for cardiovascular disease (along with cholesterol and other lipid markers, age, gender, smoking status, obesity, hypertension and diabetes). A prospective study of male physicians in 1992 found that acute myocardial infarction (MI) or death due to coronary disease was statistically related to increased homocysteine levels, after adjusting for other risk factors (5). In 1995, a key meta-analysis was published by JAMA in which 27 studies involving over 4,000 subjects concluded that homocysteine was an independent risk factor for cardiovascular disease (CVD) and estimated that 10% of the population’s CVD risk is attributable to elevated homocysteine (6). In total there are nearly 100 retrospective and prospective clinical studies linking homocysteine levels and increase risk of cardiovascular outcomes and numerous reviews of the literature available (7-11). According to a recent meta-analysis of the data, a causal relationship between homocysteine and cardiovascular disease is highly likely (12). The authors conclude that lowering homocysteine 3 μmol/L would reduce the risk of ischemic heart disease by 16%, deep vein thrombosis by 25% and stroke by 24%. Homocysteine is a sulfur amino acid and a normal intermediate in methionine metabolism. When excess homocysteine is made and not readily converted into methionine or cysteine, it is excreted out of the tightly regulated cell environment into the blood. It is the role of the liver and kidney to remove excess homocysteine from the blood. In many individuals with in-born errors of homocysteine metabolism, kidney or liver disease, nutrient deficiencies or concomitant ingestion of certain pharmaceuticals, homocysteine levels can rise beyond normal levels and lead to adverse health outcomes. The role of elevated blood homocysteine levels in clinical practice is still being debated. The central question is whether it is clinically beneficial to measure for and treat elevated levels of homocysteine (1-2). While some consider homocysteine as simply a marker but not a treatable causative agent, or ignore homocysteine as an innocuous metabolite that is coincidental to other treatable risk factors; the weight of the scientific evidence suggests otherwise.