Abstract

The current state of scientific and philosophicalorientation for most biomedical theory and practice isnot adequate to even ask, much less answer, deepquestions of phylogenetic etiology (Wilson, 1993).Much biomedical science lacks a coherence to beadduced from its mongering of study design, outcomecurves and other enthusiasms of the currently reign-ing, largely inductive science. While it is perhapsbetter to make a minor inductive advance than risk acrashing deductive error, theoretical inference, whenrobust, can reframe quantitative data or, at least,identify crisp qualitative incongruencies (Herrick,1915, 1936) with insights, both counterintuitive andnon-obvious, that would never be appreciated by mereexperiment, no matter how clever.These problems are only magnified in psychiatricresearch by its lack of both a foundational theory andcogently integrated intellectual aims. In certainrespects,psychiatryhasbecomeapasticheofaridfacts,abstruse ideological claims and grand speculationsamid a surfeit of plausible but contradictory explana-tions that lack an encompassing framework. It isparticularly difficult to sort out historical questions(such as the past function of phenotypes and theselection of their genes in the environment of theirevolution) since experimental observation is con-strained, largely,tomodern environmentalcircumstan-ces. Of course, empirico-experimental research iswelcome, but quite daunting given the scale of issuesand ethics involved. Meanwhile, psychopathologistshavelonghadavailableonesuchframeworkbeginningwith Darwin’s elegantly reasoned theory of evolution.However, no application has yielded a clear, nec-essary and complete Darwinian explanation for thefact that genes linked to psychopathology, includingthe schizophrenia-spectrum phenotypies, appear be-yond what probable mutation rates and neutral selec-tion might maintain. It is therefore not merelyspeculative to consider schizophrenia may be associ-ated with evolutionarily adaptive features—past orpresent—but an actual imperative from the point ofview of population genetics. Among the many salientapplications of evolutionary science, it is essential to afull understanding of epigenetic conditions, especiallythose with broad and/or high genomic frequency. Thatnotably includes schizophrenia for which classical(pre-genomic/recombinant) epidemiology long agoestablished it as clearly epigenetic (McGuffin et al.,1995; Kendler and Diehl, 1993; Kety et al., 1994;Tienari et al., 1994), familial (Gottesman, 1972;Kendler and Diehl, 1993), and rather highly heritable(Matthysse and Kidd, 1981; McKusick, 1990; Tsuanget al., 1999).Thus, Shaner et al. (in press) present extant data ina newly synthesized manner with some plausibility asto evolutionary heuristics of schizophrenia. As such,this is a laudable effort that should be of interest toreaders of Schizophrenia Research and, indeed,broader audience insofar as it formulates a useful—

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