The researchers from Wageningen have demonstrated that people with a genetically determined, specific form of reduced homocysteine breakdown have a 16 percent higher risk of developing coronary heart disease. People with the aforementioned reduced breakdown have on average a 25 percent higher homocysteine concentration in their blood from birth onwards, compared to other people.
Homocysteine has been associated with cardiovascular disease for a long time. However, until recently it was not clear whether an increased concentration of this amino acid in the blood was the cause or consequence of cardiovascular disease. This research into people with a genetic predisposition for a high homocysteine concentration in the blood supports the argument that this high concentration is a cause of cardiovascular disease.
Homocysteine is an amino acid (protein building block) which is formed in the body during the breakdown of another amino acid (methionine) obtained from food. The body regulates the homocysteine concentration in the blood with the aid of several B vitamins, including folic acid. Apart from a genetic predisposition, a shortage of these vitamins can also lead to an increased concentration of homocysteine in the blood. Folic acid supplementation is therefore an effective strategy to reduce the quantity of homocysteine in the blood.
The research has also revealed that people with genetically determined, reduced homocysteine breakdown only had an increased risk of heart disease when the folic acid concentration in the blood was low. This result suggests that reducing the homocysteine concentration in the blood by means of folic acid supplementation will reduce the incidence of cardiovascular disease.
The researchers also investigated whether a reduction in the homocysteine concentration in the blood as a result of vitamin B supplementation had a favourable effect on blood clotting in healthy volunteers. The assumption was that homocysteine increases the risk of cardiovascular disease by overstimulating blood clotting (which could eventually result in thrombosis). Despite a considerable reduction in the homocysteine concentration in the blood of people who had received extra vitamin B, no clear effect on blood clotting could be demonstrated.
For further information please contact Dr Mariska Klerk (Division of Human Nutrition and Epidemiology, Wageningen University), tel. 31-317 485-444, fax 31-317-483-342, e-mail: mariska.klerk@wur.nl. Mariska Klerk recently gained her doctorate. Her supervisors were Prof. Frans J. Kok and Prof. Evert Schouten and her assistant supervisor was Dr P. Verhoef.
The research was funded by the Netherlands Organisation for Scientific Research (NWO).