populations usually exceeds by far that between groups. For instance, Hartl and Clark (1997) present an analysis of data from Nei (1975) with respect to a group of enzyme variants, showing that only about 7 percent of the total genetic variation of Caucasoid, Negroid, and Mongoloid racial groups could be assigned to differences among the groups; 93 percent of the variation was within groups. The important consequence is that membership in a particular socially defined race is not a reliable or unambiguous marker for possession of any particular allele (except, perhaps, for such characteristics as skin color).
The literature also presents a picture of great complexity in the relationships of genes to racial and ethnic health differences. First, it is essential to understand that genetic influence is mediated through a causal nexus comprising the anatomy, biochemistry, physiology, immunology, endocrinology—all of the complex of structures and functions—of the human organism. This is, of course, the same causal nexus through which environmental influences are mediated.
Such complex causal networks are usually characterized by converging and diverging processes derived from multiple inputs from both genetic sources and environmental sources. Multiple redundant pathways with feedback loops may provide for compensatory mechanisms, in which one pathway adjusts for inadequacies in another pathway. Consequences of differences or changes in one of the input elements can be enormously influenced by both genetic and environmental context. The dynamics of these complex causal nexuses underlying health and disease phenotypes is frequently manifest as interactions of genes with genes, genes with environments, or environments with environments.
The resulting causal field is not homogeneous, of course. Some of the inputs and some of the mediating pathways may have a greater impact than others. Some genetic and some environmental variables are sufficiently potent that their influence is apparent in all or most system contexts. In systems terms, there may be nodes within the network that are describable as having a broad “span of control” (Simon, 1973) or as being “soft spots” (Waddington, 1977). In genetic parlance, a gene providing input to a node of this kind may be referred to as a major gene, or a Mendelian gene, or, recklessly, as “the gene” for this or that phenotype. Even the effects of such a major gene, however, may be subject to fine tuning by its companion genes or by the environmental milieu in which all of them operate. Some long-recognized genetic phenomena represent such effects: variable expressivity, in which individuals with the same genotype at a particular