Homocysteine is an amino acid that inflicts damage to the inner arterial lining (endothelium) and other cells of the body.
In 1968, a Harvard researcher observed that children with a genetic defect that caused them to have sharply elevated homocysteine levels suffered severe atherosclerotic occlusion and vascular disorders similar to what is seen in middle-aged patients with arterial disease. This was the first indication that excess homocysteine might be an independent risk factor for heart disease.
Life Extension has identified elevated homocysteine as one of 17 independent risk factors for cardiovascular disease, anyone of which can initiate and propagate vascular disease. Among such risk factors, homocysteine’s role in cardiovascular and cerebrovascular disease continues to be misunderstood by mainstream medicine.
Much of this confusion stems from highly publicized results of clinical trials that used B vitamins to reduce blood levels of homocysteine yet failed to prevent cardiovascular events in people with advanced atherosclerosis.1,2 Life Extension believes these studies were seriously flawed, most notably because they used doses of B vitamins that were too low to reduce homocysteine to Life Extension’s recommended optimal range of <8 µmol/L. At present, medical testing laboratories consider a homocysteine number between 11‒15 µmol/L as the upper limit of “normal” despite robust clinical data to the contrary.3,4 Consequently, many doctors remain misinformed as to the optimal target range for homocysteine and the doses of homocysteine-lowering nutrients required to achieve this optimal range.