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User:Erinororke/sandbox

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Evolution of Schizophrenia

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Hypotheses

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Social brain hypothesis

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A social brain refers to the higher cognitive and affective systems of the brain that evolved as a result of social selection and serves as the basis for social interaction; it is the basis of the complexity of social interactions of which humans are capable[1]. Mechanisms that compromise the social brain include emotional processing, theory of mind, self-referencing, prospection and working memory[1]. As schizophrenia is foremost a disorder of the consciousness, it has been suggested that schizophrenia exists as an unwanted byproduct of the evolution of mainly the prefrontal cortex and medial temporal brain regions constituting the social brain[2][3]. Cortical disinhibition of these regions show the associated positive symptoms of hallucinations and delusions[4]. Other regions, however, such as the anterior cingulate, parietal cortex, thalamus, and cerebellum, show reduced cognitive performance, but there is no clear evidence that these regions are further reduced as schizophrenia progresses [3]. A reduction in mitochondrial viability may account for the cognitive impairment of these regions due to an inability for the brain to properly process information through propagation of signals[5]. Thus, patients with social brain regional impairments show associated negative symptoms of inability to grasp social goals, which serves as an indication of a defect in theory of mind[2]. Under an increasingly selective pressure induced by an increasingly complex social lifestyle, the regions of the brain have grown as a means of accommodation and in turn have given rise to vulnerable neural systems that allow for psychoses such as schizophrenia to appear[2].  

*NOTE: italics indicate parts added and order of already existing sentences have been rearranged as well as the inclusion of new sources  

Language hypothesis

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A plausible evolutionary explanation for the persistence of schizophrenia in the population is the idea that schizophrenia is an anomaly of the mechanism that allowed humans to develop language[6]. Tim Crow suggests the hypothesis that schizophrenia emerged as a trade-off of lateralization and specialization of the two hemispheres of the brain when language evolved[7][8]. Language is thought to have developed due to a critical change on the sex chromosome and can be understood as bi-hemispheric, with one dominant and one non-dominant hemisphere[8][9]. Additionally, language is partially the result of lateralization of the Broca's area and Wernicke's area, both located on the left hemisphere of the brain. Crow hypothesized that symptoms associated with schizophrenia can be explained as a failure to establish dominance for speech in one hemisphere [7][8]. Angrilli et al. 2009 tested Crows hypothesis by measuring brain activity while individuals affected by schizophrenia performed phonological tasks[10]. They found that compared to healthy individuals, patients affected by schizophrenia failed to achieve left hemisphere dominance [10]. This provides strong evidence that the evolution of speech may have subsequently predisposed humans to schizophrenia and could explain the prevalence of the disease.

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Creativity hypothesis

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Some evolutionary psychologists hypothesize that there is a link between psychotic disorders such as schizophrenia and increased levels of creativity. Anecdotal evidence shows that many prominent artists and innovators had, on some level, psychosis (with schizophrenia on the far end of the spectrum). These include mathematician John Nash, painter Vincent Van Gogh, Eduard Einstein (son of Albert Einstein), and French playwright Antoin Artuad, and authors Virginia Woolf and Sylvia Plath. [11][12] However, recent research attempts to quantify this relationship while subsequently revealing its complex nature[13]. Crespi et al. 2007 exemplified this complex relationship when they discovered significant evidence for positive selection on 28 genes related to schizophrenia [14]. The fitness hypothesis proposes that the byproducts of schizophrenia, such as creativity, translate to better courtship abilities and thus reproductive success[15]. A study conducted by Nettle and Clegg 2005, provides evidence for this hypothesis as well [16]. Nettle was able to establish a relationship between the presence of schizotypy traits with creativity and enhanced mate selection, defined by number of mates [16]. Despite the negative consequences of schizophrenia, the disease persists in the population as the extreme end of a creative spectrum that may provide innovative methods in mate selection and reproduction.

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  1. ^ a b Burns, Jonathan (2006-06-01). "The social brain hypothesis of schizophrenia". World psychiatry: official journal of the World Psychiatric Association (WPA). 5 (2): 77–81. ISSN 1723-8617. PMC 1525115. PMID 16946939.
  2. ^ a b c Burns, Jonathan Kenneth (2004-12-01). "An evolutionary theory of schizophrenia: cortical connectivity, metarepresentation, and the social brain". The Behavioral and Brain Sciences. 27 (6): 831–855, discussion 855-885. ISSN 0140-525X. PMID 16035403.
  3. ^ a b Abbott, Christopher; Bustillo, Juan. "What have we learned from proton magnetic resonance spectroscopy about schizophrenia? A critical update". Current Opinion in Psychiatry. 19 (2): 135–139. doi:10.1097/01.yco.0000214337.29378.cd.
  4. ^ Howes, Oliver D; Murray, Robin M. "Schizophrenia: an integrated sociodevelopmental-cognitive model". The Lancet. 383 (9929): 1677–1687. doi:10.1016/s0140-6736(13)62036-x.
  5. ^ Clay, Hayley B.; Sillivan, Stephanie; Konradi, Christine (2011-05-01). "Mitochondrial dysfunction and pathology in bipolar disorder and schizophrenia". International Journal of Developmental Neuroscience. Schizophrenia. 29 (3): 311–324. doi:10.1016/j.ijdevneu.2010.08.007. PMC 3010320. PMID 20833242.
  6. ^ Huxley, Julian; Mayr, Ernst; Osmond, Humphry; Hoffer, Abram (1964-10-17). "Schizophrenia as a Genetic Morphism". Nature. 204 (4955): 220–221. doi:10.1038/204220a0.
  7. ^ a b Crow, T. J (2000-03-01). "Schizophrenia as the price that Homo sapiens pays for language: a resolution of the central paradox in the origin of the species". Brain Research Reviews. 31 (2–3): 118–129. doi:10.1016/S0165-0173(99)00029-6.
  8. ^ a b c Brüne, Martin (2004-03-01). "Schizophrenia—an evolutionary enigma?". Neuroscience & Biobehavioral Reviews. 28 (1): 41–53. doi:10.1016/j.neubiorev.2003.10.002.
  9. ^ Crow, Timothy J. "Is schizophrenia the price that Homo sapiens pays for language?". Schizophrenia Research. 28 (2–3): 127–141. doi:10.1016/s0920-9964(97)00110-2.
  10. ^ a b Angrilli, Alessandro; Spironelli, Chiara; Elbert, Thomas; Crow, Timothy J.; Marano, Gianfranco; Stegagno, Luciano. "Schizophrenia as Failure of Left Hemispheric Dominance for the Phonological Component of Language". PLoS ONE. 4 (2). doi:10.1371/journal.pone.0004507. PMC 2637431. PMID 19223971.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  11. ^ "Famous People With Schizophrenia: List of Schizophrenic Celebrities". mentalhealthdaily.com. Retrieved 2016-03-13.
  12. ^ Claridge, Gordon, Ruth Pryor, and Gwen Watkins. Sounds from the Bell Jar: Ten Psychotic Authors. New York: St. Martin's, 1990. Print.
  13. ^ Burch, Giles St J.; Pavelis, Christos; Hemsley, David R.; Corr, Philip J. (2006-05-01). "Schizotypy and creativity in visual artists". British Journal of Psychology (London, England: 1953). 97 (Pt 2): 177–190. doi:10.1348/000712605X60030. ISSN 0007-1269. PMID 16613648.
  14. ^ Crespi, Bernard; Summers, Kyle; Dorus, Steve (2007-11-22). "Adaptive evolution of genes underlying schizophrenia". Proceedings. Biological Sciences / The Royal Society. 274 (1627): 2801–2810. doi:10.1098/rspb.2007.0876. ISSN 0962-8452. PMC 2288689. PMID 17785269.
  15. ^ Shaner, Andrew; Miller, Geoffrey; Mintz, Jim (2004-09-01). "Schizophrenia as one extreme of a sexually selected fitness indicator". Schizophrenia Research. 70 (1): 101–109. doi:10.1016/j.schres.2003.09.014. ISSN 0920-9964. PMID 15246469.
  16. ^ a b Nettle, Daniel; Clegg, Helen (2006-03-07). "Schizotypy, creativity and mating success in humans". Proceedings. Biological Sciences / The Royal Society. 273 (1586): 611–615. doi:10.1098/rspb.2005.3349. ISSN 0962-8452. PMC 1560060. PMID 16537133.
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