Archief Roodbont

Folic acid should be used to reduce heart disease and stroke

24 November 2006

There is enough evidence to support using folic acid for heart disease and stroke prevention, experts argue in this week's issue of the British Medical Journal.

They say that, overall, data support a causal link between homocysteine and cardiovascular disease (CVD), and they therefore propose that increased folic acid consumption would reduce the risk of CVD events according to the degree of homocysteine reduction that is achieved.

"Debate remains over whether raised serum homocysteine concentrations cause ischemic heart disease and stroke, and whether folic acid, which lowers homocysteine, will help reduce the risk of these disorders," David Wald (Queen Mary's School of Medicine and Dentistry, London, UK) and colleagues note.

In an attempt to clarify the issue, Wald and team conducted separate meta-analyses of cohort studies, genetic studies, and randomized controlled trials in this field.

The large cohort studies looked at homocysteine levels and the occurrence of ischemic heart disease events (fatal and nonfatal myocardial infarction and sudden cardiac death) and stroke, while genetic studies focused on the link between polymorphisms in the methylenetetrahydrofolate reductase gene (MTHFR) that cause increases in homocysteine and ischemic heart disease, and randomized controlled trials tested the effects on CVD events of lowering homocysteine.

The cohort and genetic studies yielded similar results, indicating a protective effect from lower homocysteine levels, despite not sharing the same sources of possible error.

Meanwhile, although the trials were too small to be conclusive, data were consistent with the expected protective effects of folic acid.

The researchers say that a causal link between homocysteine increases and CVD explains the observations, even if results from any one type of study alone are insufficient to reach that conclusion.

"No single alternative explanation can account for all the observations," they write.

"We therefore take the view that the evidence is now sufficient to justify action on lowering homocysteine concentrations, although the position should be reviewed as evidence from ongoing clinical trials emerges," the authors conclude.

Br Med J 2006; 333: 1114-1117