The importance of homocysteine as a risk factor is becoming much more familiar to us. A constantly increasing number of studies have been published that show homocysteine to be a predictor of potential health problems. It is clear now that raised plasma homocysteine concentrations both predict and precede the development of cardiovascular disease including stroke. A study published this year in the British Medical Journal1 showed clearly that homocysteine levels in blood plasma predicts risk of death from cardiovascular disease in older people even better than any conventional measure of risk including cholesterol, blood pressure or smoking.

Raised levels of homocysteine are also linked to Alzheimer’s, dementia, declining memory, poor concentration and judgment and lowered mood2. It is clear that women with high homocysteine levels find it harder to conceive and are at risk from repeated early miscarriage3. High homocysteine has also been linked to migraines, and those with conditions such as diabetes and osteoporosis are at increased risk of raised homocysteine levels. Homocysteine has therefore been shown to play a crucial role as a key marker for disease development determining longevity and health throughout a person’s life.

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Why is homocysteine harmful?
Homocysteine is a naturally occurring amino acid with the formula HSCH2CH2CH(NH2)CO2H, a derivative of protein that is found in blood plasma when body chemistry is out of balance. It is a homologue of the amino acid cysteine, differing by an additional methylene (-CH2-) group. Homocysteine is not obtained from the diet, instead, it is biosynthesized from methionine via a multi-step process that probably occurs in every cell of the body.

Methionine is an amino acid, ingested as a component of food protein, and is found primarily in meats, eggs, dairy products, fish, chicken, seeds, nuts and some vegetables. Methionine is activated to S-adenosylmethionine (SAM) by the enzyme methionine adenosyltransferase. Circulating levels of homocysteine are usually low due to its rapid metabolism via one of two pathways: a cobalamin (vitamin B12) and folate dependent re-methylation pathway that regenerates methionine, or a pyridoxal 5’ phosphate (PLP, vitamin B6) dependent trans-sulphuration pathway that converts homocysteine into cysteine.