Homocysteine is an amino acid derived from the consumption of meat (including red meat, chicken, and fish). Hyperhomocysteinemia is an increase in the level of homocysteine in the blood. There is a strong relationship between hyperhomocysteinuria, carotid artery stenosis and stroke. Of all the risk factors responsible for stroke, hyperhomocysteinemia is the one most directly influenced by diet. Folate, vitamin B12, and vitamin B6 are required for the metabolism of homocysteine. Deficiencies in folate, vitamin B6, and vitamin B12 can lead to increased plasma homocysteine concentrations. Deficiencies in these nutrients are risk factors for ischemic stroke. Remarkably, supplementation of these nutrients (folate, vitamins B6 and B12) can lead to a decrease and even the normalization of elevated homocysteine levels. One study concluded that this could be effectively accomplished after fifteen weeks of vitamin therapy. The efficacy of these vitamins in lowering homocysteine levels has been verified by other studies.
Elevated homocysteine levels can further the progression of pre-existing atherosclerosis. A more problematic reality is that homocysteine can cause vascular narrowing and occlusion without the presence of associated atherosclerosis. In other words, it can cause a stroke by itself! Strokes associated with hyperhomocysteinuria have specific characteristics that can aid in their diagnosis. The effect of elevated homocysteine is multifactorial, involving both the vascular wall structure and the coagulation system. Researchers Stuart A. Lipton (Children’s Hospital in Boston) and Jonathan S. Stambler (Duke University) reported in the Proceedings of the National Academy of Sciences that even mild elevations of homocysteine in the blood can be lethal to nerve cells. Mild hyperhomocysteinemia was found to be lethal to those brain cells that contain N-methyl-D-aspartate (NMDA) glutamate receptors.
Studies now demonstrate increased levels of homocysteine may cause brain atrophy and vascular disease, and therefore may be related to the development of dementia and possibly Alzheimer’s disease. Studies have demonstrated that elderly people who had greater brain atrophy were twice as likely to have high homocysteine levels. It is believed that elevated homocysteine in Alzheimer’s disease is not the direct cause or result of Alzheimer’s disease but rather is related to the well-documented association with vascular disease. The most effective means for lowering plasma homocysteine is vitamin B supplementation.
In summary, elevated homocysteine levels can lead to vascular pathology through a variety of mechanisms. Homocysteine can cause atherosclerosis, thrombosis, and hypercoagulable states. Even a moderate elevation of homocysteine is an independent risk factor for the development of stroke. It is also neurotoxic to brain cells having NMDA glutamate receptors. Deficiencies in folate, vitamin B6, and vitamin B12 can lead to increased plasma homocysteine concentrations. Supplementing the diet with these nutrients can decrease and even normalize elevated homocysteine levels.