The Native American and Disease Ecology

The long-term result of the development of North American peoples in the absence of contact with others was a healthy population adjusted to its environmental niches. Humankind had multiplied from the founding stock and by the late fifteenth century numbered somewhere between 4.4 million (Ubelaker 1976) and 9.8 million (Dobyns 1966). Within this total, a degree of variety had arisen in the human populations of Nearctica in the course of some 600 generations, reflecting the historical and environmental conditions (Brues 1954; Szathmary 1984).

The genetic characteristics of American Indian populations are sufficiently similar to one another and different from those of other continental groups to permit (as a first approximation) of their description as a "distinct" subgroup of the human species. ... Closer analysis of genetic affinities reveals that over larger areas the genetic continuity takes the modified form of gradients or clines. Thus the frequency of the gene for blood group A decreases from north to south, that for the allele for the Diego factor and the M gene increases from north to south. (Weiner 1971; see also Suarez, Crouse, and O'Rourke 1985)

Throughout the region the B gene is singularly lacking, with almost all Amerindian groups belonging to the O blood group. This situation may explain a particular susceptibility to smallpox on its introduction (Mourant, Kopec, and Domaniewska-Sobczak 1958). Not all scholars agree even on this point, however:

The role of the blood groups in the resistance of certain infections or parasites has been controversial. If it was demonstrated, its importance would be significant in accounting for the repetition of certain factors . . . [I]n the region of pestilential or variolic endemic diseases, the plague would be worse and more frequent among people with type O, and smallpox, among those with type A. (Bernard and Ruffle 1966, trans. Graham)

This interpretation is based on the discovery that Pasteurella pestis possesses an antigen similar to the H antigen, whereas the variola virus has an antigen similar to the A antigen. As people with blood group O are not able to produce any anti-H antibody (which corresponds to the H antigen of P. pestis), they have a very poor prognosis when infected (Vo-gel, Pettenkofer, and Helmbold 1960; Matsunage 1962, 1982). Although anthropologists and others have used these studies to support theories of genetic distance and purity of Amerindian stock (Post,

Neel, and Schull 1968; Roberts 1976; Szathmary 1984), the consensus on the theory of genetic susceptibility to disease is that the case is unproven in the context of the exposure of these peoples to the imported Old World infections (Newman 1976; Ward 1980; Joralemon 1982).

There is, however, increasing evidence in genetic epidemiology that certain conditions are related to genotype—environment interactions. In the case of contemporary North American native peoples, these conditions include inflammation of the inner ear (Gregg, Steele, and Holzheuter 1965), gallbladder disease (Burch, Comess, and Bennett 1968), diabetes (Miller, Bennett, and Burch 1968), and alcoholism (Broudy and May 1983; Social Biology 1985). Indeed, it has been claimed that at the present time

Many Amerindian peoples are experiencing a major epidemic of a series of diseases which include a tendency to become obese at an early adult age, adult onset of diabetes mellitus, the formation of cholesterol gallstones. [T]his epidemic . . . seems to be due to an interaction between susceptible Amerindian genotype(s) and some recently changed aspect of the environment, probably involving dietary components. (Weiss, Ferrell, and Hania 1984)

It would seem, then, that there is evidence of an ecology of disease specifically associated with the continent's native peoples, one of the three major human stocks presently inhabiting the region.

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