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Although largely ignored by most researchers, the theory of evolution may be relevant to the study of schizophrenia and to other psychiatric conditions. Fields as diverse as psychology, pharmacology, genetics, anthropology, ethnology, and cross-cultural studies enhance our understanding of human behaviours, while simultaneously interfacing with evolutionary theory. A development in any of these fields can potentially reveal the elusive mechanisms of psychiatric disorders. Other medical ailments such as sickle cell anemia and lactose intolerance are already better understood through our recognition of man’s history and evolutionary principles. This paper reviews major attempts to understand schizophrenia through evolutionary perspectives. Evolutionary thinking begins with Charles Darwin’s theory of natural selection, which explains how species change through time (1). Slight variations that exist among members of a species become “selected” and ubiquitously spread through future generations if there is preferential survival of offspring with the particular useful trait. This process, cursorily expressed as “survival of the fittest,” is comprehensively and eloquently explained in Darwin’s book On the Origins of Species, published in 1859. It is a simple, yet powerful, idea that has influenced our understanding of almost every biological mechanism. The theory of evolution has itself evolved over the last one and one-half centuries, with modifications and improvements. The essence of the idea, however, remains unchanged. Evolutionary forces cannot be ignored in conditions that have genetic underpinnings and a long history. Schizophrenia almost certainly possesses a significant genetic component (2,3). It has long been known that schizophrenia commonly aggregates in families (4,5). Environmental influences cannot entirely explain this fact, because adoption studies demonstrate an increased risk of schizophrenia in biological relatives of adoptees with schizophrenia (6–8). In addition, twin studies show substantially higher monozygotic concordance rates (approximately 40%), compared with dizygotic concordance rates (about 15%) (9). Although schizophrenia seems to be an ancient condition, this cannot be determined conclusively (10,11). Jeste’s review of ancient writings dating back to Mesopotamia produced descriptions of aberrant behaviours that closely resembled schizophrenia. Accurately dating schizophrenia is not currently possible, although a minimum estimate may correspond to the last wave of ancient migrations into Australia. Australian Aboriginals became effectively isolated from the rest of humankind about 60 000 years ago (12). Schizophrenia has been observed in Australian Aboriginals and in other remote populations (13,14). Because schizophrenia crosses all cultures in approximately the same frequency, its presence was likely well established before the formation of the oldest genetically isolated racial enclaves (15). Evolutionary perspectives about schizophrenia can be divided into 2 major groups: 1) theories that assume schizophrenia to be a completely disadvantageous byproduct of human brain evolution and 2) theories that propound evolutionary advantages associated with the condition itself. TheoriesSchizophrenia as a Disadvantageous Byproduct of Human Brain Evolution To those who view schizophrenia as an evolutionary, disadvantageous phenotype, the condition is seen in its traditional perspective as a disorder or disease. This formulation makes schizophrenia analogous to an ailment such as vertebral disc herniation. Any advantage of bipedal locomotion is unfortunately mitigated by vulnerability toward herniated discs, just as schizophrenia may be an unfortunate byproduct of human brain evolution. Among the first comprehensive attempts to understand mental illness through evolutionary theory is Farley’s argument that schizophrenia could be an extreme variant of normal social behaviour (16). Noting significant variation in human social behaviours, he conjectured that social skills must be under polygenic control. The extremes of distribution resulted in persons who were maladjusted, chronically overaroused, and vulnerable to psychotic breakdown. Many symptoms of schizophrenia, such as paranoid delusions and disordered thinking, could be viewed as outliers on a normal continuum. Psychosis would be the toll exacted for the benefit of adaptive social skills genes. The author acknowledged the most prominent flaw in his hypothesis: it “fails to explain why psychosis can so readily be divided into at least two major categories.” Randall also supports the assertion that schizophrenia could be an inevitable consequence of normal brain evolution (17,18). Specifically, “abnormalities of functional connection between specialized areas in the human brain may underlie the symptoms which constitute the schizophrenia syndrome.” In this evolutionary model, novel neural pathways are established randomly, resulting in either advantageous “supernormal connections” or nonadaptive “misconnections.” Randall’s conclusion: a “biological trial and error of connection would produce a range of behavioural variants,” including schizophrenia. Although there may be evidence for modified neural pathways in schizophrenia, the suggestion that neural misconnections occur randomly denies the orderly and specific constellation of symptoms typically observed in any given neuropathological condition. Likewise, it does not provide a mechanism for the propagation and maintenance of pathology. Randall explains that girls with schizophrenia would usually be asymptomatic at the initiation of sexual maturity, thereby allowing the propagation of their genes. This argument, however, only diminishes the negative selection pressure on those afflicted without completely eradicating the presumed disadvantages of schizophrenia. Millar used Maclean’s concept of the triune brain to speculate on the etiology of schizophrenia (19). Briefly, the triune concept proposes that the human brain contains the evolutionary remnants of 3 brains: the reptilian (upper brain stem), the paleomammillary (limbic), and the neomammillary (cortical). According to this model, each successive brain that is introduced incorporates and modifies previous functions. Millar suggested that schizophrenia could reflect “some failure of integration between the limbus and the cortex.” Similar concepts outlining the essence of schizophrenia pathology have been formulated, such as the cognitive dysmetria hypothesis of Andreason and others (20). Millar’s concept, however, lacks specificity and therefore could be applied to any disease involving cortical function. Over the last decade, Crow has developed an intricate argument outlining schizophrenia’s possible evolutionary pathway (21–27). In fact, he believes that the evolution of schizophrenia and language are intimately involved. Predisposition toward schizophrenia and other psychotic ailments reflects phenotypic variation associated with the capacity for language. The possible lack of cerebral asymmetry observed in schizophrenia, along with alterations in speech, ties the illness to language. Mating characteristics of early man could have spurred a sexual-selection pressure, resulting in increased intelligence. Amplifying early man’s existing tendency toward cerebral asymmetry may have precipitated unique evolutionary achievements. By the evolutionary mechanism of neoteny, a delay in the maturation of cerebral structures could have occurred, thereby increasing cerebral plasticity. Enhanced cerebral flexibility would boost intelligence and would usher the emergence of language. A disadvantageous byproduct of a cerebral flexibility would be a concomitant variation in psychological functioning, resulting in personality disorders and psychosis. Crow’s intricate argument, though interesting, relies on several contentious suppositions. First, Crow suggests that psychosis is intimately linked to language dysfunction. Schizophrenia can certainly cause disordered language; however, the illness also impacts heavily on social behaviours and executive functions. Further, delusions and hallucinations are commonly observed amidst normal syntax. Second, to bolster the assertion that schizophrenia and language evolved rapidly—perhaps both originating in a single gene—Crow’s concept utilizes the controversial evolutionary theory of punctuated equilibria (28,29). This reasoning appears to ignore observations of symbol use in primates and to disregard other evidence that indicates language likely evolved gradually over several million years (30). Third, Crow’s formulation seems to rely on a continuum model of psychosis, suggesting that schizophrenia and bipolar disorder share a common etiology. Although credible, readers who are unprepared to abandon Kraepelin’s categorical model of psychosis may not accept Crow’s conclusions. Yeo and others have proposed “the developmental instability model of schizophrenia” (31). According to this model, an inability to buffer the deleterious effects of mutations, pathogens, or toxins makes certain individuals prone to developing the illness. This paradigm’s major strength may be that it is compatible with the stress diathesis model of schizophrenia and that 3 possible evolutionary mechanisms are provided: mutation, host–pathogen coevolution, and homozygosity at key alleles. Even so, each suggestion lacks any substantial corroborating evidence and therefore should be considered speculative. Saugstad presents an interesting pathophysiological model that connects certain frontal lobe disorders, such as schizophrenia, dyslexia, and infantile autism, to delayed cerebral maturation (32). The accompanied evolutionary explanation is cursory: schizophrenia is viewed simply as a disadvantageous phenotype within the bounds of “normal variation.” Although normal variation can sometimes be pronounced, nature does not typically produce substantial numbers of distinct phenotypes with reduced fecundity.
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