ABSTRACT
Despite these reservations, it is evident that there is a clear genetic component to cardiovascular disease. This is clearly seen in largescale studies in human populations, particularly those that have used a twin paradigm to dissect out environmental and genetic factors. The majority of twin studies in a range of countries have indicated that monozygotic twins (genetically identical) share much closer resemblance of cardiovascular risk including hypertension, than do dizygotic twins who share only 50% of their genome.7
There is equally strong evidence from the Montreal adoption study.8 In this experiment, blood pressure similarities were compared in natural and adopted offspring and between natural and adopted siblings. In general, the correlation of blood pressure measurement was higher between mothers of natural children and fathers of natural children than between parents and adopted offspring. This relationship, which was seen for both mothers and fathers, tends to support the idea that maternal uterine environment cannot be the only explanation for subsequent adult cardiovascular risk. In addition, natural siblings showed a highly correlated level of blood pressure in comparison to adopted siblings. Thus, there is clear evidence that hypertension (and other cardiovascular disorders) do have a genetic component. Estimates suggest that this may contribute up to 30% of the variance in blood pressure within the population. The remainder of this review will concentrate on high blood pressure as a prime example of cardiovascular disease, in which substantial information about genetic factors is now avail-
