NEW YORK (Reuters Health) - Findings from a genotype-phenotype analysis suggest that high homocysteine levels may play a causal role in stroke. However, a related editorial suggests that confounding factors may still explain the association.
“Our study...provides evidence for a role of homocysteine in the development of stroke, though it must be emphasized that a systemic review of published studies such as this might be affected to some degree by reporting bias,” senior author Dr. Aroon D. Hingorani, from University College London, said in a statement.
In their review, published in the January 15th issue of The Lancet, the researchers looked first for studies linking a C677T polymorphism in the MTHFR gene with homocysteine levels. Then they searched for studies linking this polymorphism to stroke. A total of 111 studies were identified.
Subjects homozygous for the T allele of the polymorphism had homocysteine levels that were, on average, 1.93 micromol/L higher than those of CC homozygotes. Based on observation studies, this degree of elevation should raise the stroke risk by 20%.
Comparing the stroke risks of TT and CC homozygotes, the researchers found that the former group was 26% more likely to sustain a stroke than the latter, a risk that is comparable to the 20% predicted. Moreover, this consistency remained when the subjects were analyzed by age-group, ethnicity and geographic location.
Still, not everyone is convinced by the findings. In a related editorial, Dr. Graeme J. Hankey and Dr. John W. Eikelboom, from Royal Perth Hospital in Western Australia, comment that “these results do not provide conclusive evidence of a causal association between total homocysteine and stroke.”
The editorialists note that the MTHFR polymorphism may raise the stroke risk, not by increasing homocysteine levels, but by predisposing the patient to “unhealthy behaviors, low socioeconomic status, or abnormal physiologic risk factors.”
Source: Lancet 2005;365:194-195,224-232. [ Google search on this article ]
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