Schizophrenia Research Trends

118Joseph Polimeni and Jeffrey P. ReissEVOLUTIONARY THEORIES OF SCHIZOPHRENIABASED ON DISEASE MODELSEvolutionary theories related to psychiatry can be broadly divided into those that viewpsychiatric conditions as adaptive and those that consider them disadvantageous byproductsof ordinary brain evolution. To those who frame schizophrenia as a disadvantageousphenotype, the condition is seen in its traditional perspective as a disorder or disease. Thisformulation makes schizophrenia analogous to an ailment such as vertebral disc herniation.Any advantage of bipedal locomotion is unfortunately mitigated by vulnerability towardherniated discs, just as schizophrenia may be an unfortunate byproduct of human brainevolution. In this section, we review the four best-known evolutionary theories ofschizophrenia based on disease models.Among the first comprehensive attempts to understand mental illness throughevolutionary theory was Farley’s hypothesis that schizophrenia could be an extreme variantof normal social behavior [30]. Noting significant variation in human social behavior, heconjectured that social skills must be under polygenic control. The extremes of distributionresulted in persons who were maladjusted, chronically over-aroused and vulnerable topsychotic breakdown. Symptoms such as paranoid delusions and disordered thinking wouldbe considered outliers on a normal continuum. Personality disorder and psychosis would bethe toll exacted for the benefit of adaptive social skill genes. The author acknowledged themost prominent flaw in his hypothesis; it “fails to explain why psychosis can so readily bedivided into at least two major categories.”An assertion that schizophrenia could be an inevitable consequence of normal brainevolution was also put forth by Randall [31-32]. Specifically, “ abnormalities of functionalconnection between specialized areas in the human brain may underlie the symptoms whichconstitute the schizophrenia syndrome”. In this evolutionary model, novel neural pathwaysare established randomly, resulting in either advantageous “supernormal connections” or nonadaptive“misconnections”. Randall’s conclusion; a “biological trial and error of connectionwould produce a range of behavioral variants”, including schizophrenia. Although there maybe evidence for modified neural pathways in schizophrenia, the suggestion that neuralmisconnections occur randomly seems to deny the orderly and specific constellation ofsymptoms typically observed in any given neuropathological condition. Randall’s argumentalso does not provide a mechanism for the propagation and maintenance of pathology.Millar used Maclean’s concept of the triune brain to speculate on the etiology ofschizophrenia [33]. Briefly, the triune concept proposes that the human brain contains theevolutionary remnants of three brains; the reptilian (upper brain stem), paleomammillary(limbic) and neomammillary (cortical). According to this model, each successive brainintroduced, incorporates and modifies previous functions. Millar suggested thatschizophrenia could reflect “some failure of integration between the limbus and the cortex”.Similar concepts outlining the essence of schizophrenia pathology have been formulated suchas the “cognitive dysmetria” hypothesis of Andreason et al. [34]. Millar’s hypothesis,however, lacks specificity and therefore could be applied to any disease involving corticalfunction.