to hypotheses concerning the role of discrimination stress, such as those of Thayer and Friedman (2004).
These various studies offer conceptual lenses for considering evidence of genetic influences on ethnic differences in health and disease. Several recent examples illustrate the pertinent evidence being presented.
Differential responsiveness to therapy has been identified by Exner et al. (2001), who compared black and white patients with left ventricular dysfunction on response to Enalapril therapy. Briefly, black patients displayed no significant reduction of risk for hospitalization for heart failure within 36 months of therapy, while white patients experienced a 44 percent reduction in risk. Other such racial differences have been identified, such as greater resistance among black kidney and liver transplant patients to immunosuppression (Nagashima et al., 2001). The mechanisms underlying these physiological differences may, of course, be environmental, genetic, or some combination of these effects.
Research that more explicitly implicates genetic factors can be illustrated by that of Splawski et al. (2002), who found a particular allele (described as Y1102) of a gene (SCN5A) to be associated with arrhythmia in blacks. This allele is found in about 13 percent of blacks and in about 19 percent of West Africans and Caribbeans, but it has not yet been identified in whites or Asians. Y1102 increases the risk of arrhythmia but is not a sufficient cause—most carriers of the allele never display arrhythmia. The conjecture is that the gene operates in the context of other risk factors, including possibly the use of certain medications.
A further example is provided by Karter et al. (2002), who examined the complications experienced by diabetics who participated in the same medical care program. The results differed by type of complication: blacks, Asians, and Hispanics had a substantially lower incidence of myocardial infarction than did whites; blacks experienced more strokes than whites; Asians had many fewer lower extremity amputations; and whites had lower incidence of end-stage renal disease. Complication susceptibility is clearly not the exclusive attribute of any one group.
Contextual scrutiny of genetic factors thus can lead to discoveries of important gene-gene and gene-environment interactions. For instance, there is evidence that the apoE genotype is less of a risk factor in Hispanic or black populations than in Caucasian populations (Sahota et al., 1997). Whether these differences are due to gene-gene interactions, gene-environment interactions, or both remains to be demonstrated.
Increasingly, reference is made to the prospects of individualized medicine, in which the preventive or intervention strategies will be tailored to