High homocysteine is consistently associated with an increased risk of atherosclerosis, coronary artery disease and thrombosis. Whether lowering it through supplements also reduces the risk of heart attacks or death has, however, not been demonstrated.
Homocysteine is an amino acid that occurs naturally in your blood as a by-product of metabolism. An elevated level, also known as hyperhomocysteinaemia, is consistently associated in studies with a higher risk of hardening of the arteries (atherosclerosis), coronary artery disease and venous thrombosis (blood clots in the veins). To give an impression of the magnitude: every increase of 5 micromoles per litre of homocysteine raises the risk of coronary artery disease by approximately as much as a cholesterol rise of 20 mg/dl. That is not insignificant. Nevertheless, it is important to know that this is an association, not a proven causal relationship: it is not certain that homocysteine itself is the cause, or that it runs parallel with other factors that damage the heart.
Beyond atherosclerosis and thrombosis, homocysteine is also linked in recent literature to atrial fibrillation, a common heart rhythm disorder. The evidence for this is more limited and, here too, it concerns an association, not a proven cause-and-effect relationship.
Some people naturally have higher homocysteine due to a genetic variant in the so-called MTHFR gene (variant C677T). This gene controls an enzyme that breaks down homocysteine. When that enzyme functions less effectively, homocysteine accumulates. The association of this variant with cardiovascular disease is, however, mixed: multiple studies find no predictive value, which means this is not a straightforward story.
Folic acid (vitamin B11) lowers homocysteine in the blood by approximately 25%. Vitamin B6 and B12 also play a role in this. Folic acid supplementation is cheap and safe. The major caveat is: no hard outcome data are available demonstrating that lowering homocysteine through supplements actually reduces the number of heart attacks or deaths from heart disease. Preliminary studies suggested a slowing of atherosclerosis, but evidence of mortality reduction is absent from the available sources.
Elevated homocysteine also interacts with classical risk factors such as smoking and can further amplify overall cardiovascular risk. For women there is an additional nuance: after the menopause, homocysteine rises, presumably due to the decline in oestrogen. Hormone therapy can lower homocysteine by 10-15%, but is not recommended as cardiac protection for other reasons. In children and adolescents, high homocysteine is weakly associated with overweight, but more studies are needed to establish its cardiovascular significance in that age group.
The claims are based on multiple PMIDs (12652107, 15023293, 17917419, 39716283, 34960114, 15511133, 33351941). The research is predominantly observational and associational in nature. No randomised outcome studies are available in the supplied sources that demonstrate mortality reduction through homocysteine lowering.