Gene-environment interaction in the determination of levels of haemostatic variables involved in thrombosis and fibrinolysis.

Although a specific genotype may be associated in healthy subjects with modest differences in levels of a risk factor for thrombosis, this effect may be larger or smaller in subgroups of subjects. Documenting such gene-environment interactions is important if genotype information is ever to be used in a clinical or diagnostic setting, and understanding the molecular mechanisms of such interactions is vital to be able to use the information to develop novel therapeutic approaches for reducing the risk of myocardial infarction. This review focuses on gene-environment interactions detected to date for the G-455A beta fibrinogen gene promoter polymorphism. Carriers of the A allele, representing roughly 20% of the population, consistently have on average 7-10% higher fibrinogen levels than those with the genotype GG. Data will be presented to demonstrate interaction between gender, smoking habit, age, presence of ischaemic disease and level of physical exercise, in the determination of the magnitude of this A-raising effect and thus on an individual's plasma fibrinogen levels.