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Homocysteine And Cardiovascular Disease: Evidence On Causality From A Meta-Analysis
David S. Wald, Malcolm Law and Joan K. Morris
BMJ: British Medical Journal
Vol. 325, No. 7374 (Nov. 23, 2002), pp. 1202-1206
Published by: BMJ
Stable URL: http://www.jstor.org/stable/25452960
Page Count: 5
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Objective To assess whether the association of serum homocysteine concentration with ischaemic heart disease, deep vein thrombosis and pulmonary embolism, and stroke is causal and, if so, to quantify the effect of homocysteine reduction in preventing them. Design Meta-analyses of the above three diseases using (a) 72 studies in which the prevalence of a mutation in the MTHFR gene (which increases homocysteine) was determined in cases (n=16 849) and controls, and (b) 20 prospective studies (3820 participants) of serum homocysteine and disease risk. Main outcome measures Odds ratios of the three diseases for a 5 μmol/l increase in serum homocysteine concentration. Results There were significant associations between homocysteine and the three diseases. The odds ratios for a 5 μmol/l increase in serum homocysteine were, for ischaemic heart disease, 1.42 (95% confidence interval 1.11 to 1.84) in the genetic studies and 1.32 (1.19 to 1.45) in the prospective studies; for deep vein thrombosis with or without pulmonary embolism, 1.60 (1.15 to 2.22) in the genetic studies (there were no prospective studies); and, for stroke, 1.65 (0.66 to 4.13) in the genetic studies and 1.59 (1.29 to 1.96) in the prospective studies. Conclusions The genetic studies and the prospective studies do not share the same potential sources of error, but both yield similar highly significant results-strong evidence that the association between homocysteine and cardiovascular disease is causal. On this basis, lowering homocysteine concentrations by 3 μmol/l from current levels (achievable by increasing folic acid intake) would reduce the risk of ischaemic heart disease by 16% (11% to 20%), deep vein thrombosis by 25% (8% to 38%), and stroke by 24% (15% to 33%).
BMJ: British Medical Journal © 2002 BMJ