Elevated homocysteine levels have been observed more frequently among women with certain pregnancy complications, including preeclampsia (elevated blood pressure that can lead to dangerous consequences), placental abruption (where the placenta detaches from the uterus), recurrent pregnancy loss, and giving birth to a small, low-birth-weight baby (called intrauterine growth restriction).
This week's PLoS Medicine reports on a comprehensive study that reveals that levels of the amino acid, homocysteine, have no significant effect on the risk of developing coronary heart disease. This concludes the ongoing argument of the previously suggested benefits of lowering homocysteine with folate acid.
But research failed to bear out the theory: in a seven-year study of 12,064 heart-attack survivors, published in 2010, participants who took daily supplements of folic acid and vitamin B12 had 28% lower levels of homocysteine in the blood, but no reduction in heart events or stroke, compared with people taking placebo.
In the genetic condition called homocystinuria, there is a deficiency or lack of an important mediator molecule (enzymes) in the complicated homocysteine breakdown pathway. This leads to severely elevated levels of homocysteine.
Elevated plasma homocysteine levels are associated with carotid atherosclerosis and an increased risk of stroke.8,10 Atherosclerosis and stroke, in turn, increase the risk of clinical Alzheimer's disease.2,4 Hyperhomocysteinemia has been related to cerebral microangiopathy,44 endothelial dysfunction,45 impaired nitric oxide activity,46 and increased oxidative stress47 — all factors associated with the aging of the brain.
Clinical testing laboratories consider a homocysteine value between 5 to 15 µmol/L as healthy. The Life Extension Foundation believes that an upper limit of 15 µmol/L is too high for optimal health. Studies indicate that adults with homocysteine values ≥6.3 µmol/L are at increased risk of atherosclerosis (Homocysteine Studies Collaboration), heart attack and stroke (Broxmeyer 2004).
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.
So far, no controlled treatment study has shown that folic acid supplements reduce the risk of atherosclerosis or that taking these vitamins affects the development or recurrence of cardiovascular disease. Researchers are trying to find out how much folic acid, B-6 and/or B-12 are needed to lower homocysteine levels.
High-risk patients with high homocysteine levels should increase their intake of B-vitamins in their diet. These vitamins can be found in a wide variety of fruits, green, leafy vegetables, and grain products fortified with folic acid.
Homocysteine is a common amino acid (one of the building blocks that make up proteins) found in the blood and is acquired mostly from eating meat. High levels of homocysteine are related to the early development of heart and blood vessel disease.