That high levels of plasma homocysteine could cause an increase in the risk of cardiovascular disease was first hypothesised by Kilmer McKully in the late 1960’s. Since that time, a large body of research has supported the view that homocysteine can cause damage to the endothelial lining of the arteries through oxidative and non-oxidative mechanisms. Plasma homocysteine can be elevated due to a genetic defect of the enzyme cystathionine β-synthase, or through a deficiency of the co-factor vitamins cobalamin, pyridoxal phosphate and folate, required for metabolism of homocysteine. High levels of maternal homocysteine have been hypothesised to be associated with congenital conditions including heart defects and neural tube defects. This might be related to maternal vascular compromise caused by elevated plasma homocysteine levels which have an unknown effect on the developing foetus. Researchers are therefore interesting in determining associations between plasma homocysteine levels in pregnant women and birth defects.
One group of researchers1 investigated the association between the maternal plasma homocysteine levels and the risk of small for gestational-age (SGA) newborns using a meta-analysis of PubMed studies from 1966 to 2010. All studies were included that determined both the maternal plasma homocysteine concentrations and the birth weight, which resulted in 19 studies consisting of 21,326 individuals. Pooling the data resulted in an odds ratio of 1.25 as an estimate of the relative risk of a woman to deliver a SGA offspring when maternal homocysteine levels exceeded the 90th percentile. Linear calculation resulted in an estimate of a 31g decrease in birth weight for a 1 standard deviation increase in maternal homocysteine levels. While these effects are small, they suggest that elevated homocysteine levels in women increase the risk of delivering a SGA offspring, and support the hypothesis that elevated maternal homocysteine may increase the risk of birth defects.
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