Evolution of schizophrenia

The evolution of schizophrenia refers to the theory of natural selection working in favor of selecting traits that are characteristic of the disorder. Positive symptoms are features that are not present in healthy individuals but appear as a result of the disease process. These include visual and/or auditory hallucinations, delusions, paranoia, and major thought disorders. Negative symptoms refer to features that are normally present but are reduced or absent as a result of the disease process, including social withdrawal, apathy, anhedonia, alogia, and behavioral perseveration. Cognitive symptoms of schizophrenia involve disturbances in executive functions, working memory impairment, and inability to sustain attention.[1]

Given the high numbers of individuals diagnosed with schizophrenia (nearly 1% of modern-day populations), it is unlikely that the disorder has arisen solely from random mutations.[2] Instead it is believed that, despite its maladaptive nature, schizophrenia has been either selected for throughout the years or exists as a selective by-product.

Hypotheses

Social brain hypothesis

A social brain refers to the higher cognitive and affective systems of the brain, evolving as a result of social selection and serving as the basis for social interaction; it is the basis of the complexity of social interactions of which humans are capable.[3] Mechanisms comprising the social brain include emotional processing, theory of mind, self-referencing, prospection and working memory.[3] Patients display defects in various regions of the social brain, such as an inability to grasp social goals, which serves as an indication of a defect in theory of mind.[4]

As schizophrenia is foremost a disorder of the consciousness, it has been suggested that schizophrenia exists as an unwanted byproduct of the evolution of the prefrontal cortex and other brain regions constituting the social brain.[4] Under increasingly selective pressure induced by increasingly complex social living, the regions of the brain have grown as a means of accommodation and in turn have given rise to vulnerable neural systems, allowing for psychoses such as schizophrenia to appear.[4]

Social advantage hypothesis

This hypothesis refers to the worship of psychics and seers in the times of early civilization; the hallucinatory behavior and delusions brought by schizophrenia may have been highly regaled and allowed the individual to be conferred the title of saint or prophet, raising him on the social spectrum and allowing for social selection to act on the behalf of the disorder.[2] This hypothesis lacks evidence and has not aided in explaining the continued persistence of schizophrenia in modern-day society where people showing symptoms of schizophrenia are typically not identified as saints or prophets.[2]

Physiological advantage hypothesis

This hypothesis maintains that schizophrenics possess a physiological advantage in the form of disease or infection resistance, a theory that has found basis in diseases such as sickle-cell anemia.[2] In one particular study, NAD, an energy carrier found in animals and yeast, is found to be capable of diminishing infectivity of tuberculosis when present in large quantities; this is done by repressing gene expression.[5] However, M. tuberculosis bacterium has been shown to be capable of acting as a drain on NAD supply.[5]

Studies in kynurenine pathway activation reveal that M. tuberculosis infection of the pathway causes niacin receptors in the pathway to indicate high levels of niacin, a precursor to NAD that makes de novo synthesis of NAD from tryptophan unnecessary. This change creates the illusion that NAD levels are adequate and that tryptophan conversion is unnecessary.[5] Coevolution with M. tuberculosis has resulted in an attempt to overcome this illusion in a variety of manners, including the up-regulation of niacin receptors and up-regulation of de novo synthesis of NAD from tryptophan via the kynurenine pathway.[5]

An enzyme implicated in the initiation of the kynurenine pathway, tryptophan 2,3-dioxygenase (TDO2) is found to activate during niacin-deficient conditions and is also found to be in increased levels in schizophrenic brains.[5] In the postmortem brain tissue of schizophrenics, the protein for the high affinity niacin receptor was significantly decreased and, as a result, would allow for the up-regulation of mRNA transcript for the niacin receptor.[5]

Shamanistic hypothesis

This hypothesis purports that schizophrenia is a vestigial behaviour that was once adaptive to hunting and gathering tribes. Psychosis prompts shamans to communicate with the spirit world, which results in the formation of religious myths. The shamanistic theory posits that the universal presence of shamanism in all hunting and gathering societies is likely due to heritable factors – the same heritable factors that support the worldwide distribution of schizophrenia. One modern version of the theory has invoked the evolutionary mechanism of group selection in order to explain the apparent genetic-based task specialization of shamanism.[6]

Immune system Hypothesis

Perinatal exposure
It has been suggested that acute neuroinflammation during early fetal development may contribute to schizophrenia pathogenesis. The risk of schizophrenia is higher among those who experienced prenatal maternal viral infections like influenza, rubella, measles, and polio as well as bacterial or reproductive infections.The brain is highly sensitive to environmental insults during early development. Factors common to the immune response to a variety of pathogens are mediators in linking the commonalities between prenatal/perinatal infection and neurodevelopmental disorders. One hypothesis suggests that enhanced expression of proinflammatory cytokines and other mediators of inflammation in the maternal, fetal, and neonatal compartments may interfere with brain development, thereby increasing the risk for long-term brain dysfunction later in life.[1]

Increased Pro-inflammatory Cytokines
Another hypothesis seeking to explain why schizophrenia occurs aim at understanding the activation of the immune system. The activation of the inflammatory response system mediated by cytokines may play a key role in the pathogenesis of schizophrenia.[7] Evidence suggests that serum levels of IL-2, IL-6, IL-8, and TNF-α are significantly elevated in patients with chronic treatment-resistant schizophrenia.[8][9][10] Nuclear factor-kappa B regulates the expression of cytokines and an increase in NF-κB levels leads to an increase in proinflammatory cytokine levels [7]

Brain-derived Neurotrophic Factor
Individuals with schizophrenia have lower levels of brain-derived neurotrophic factor or BDNF. BDNF is responsible for promoting the proliferation, regeneration, and survival of neurons. It is also important for the regulation of cognitive function, something individuals with schizophrenia have trouble doing. Lower BDNF expression is associated with increased IL-6 expression, and increased cortisol levels. The more pro-inflammatory cytokines in circulation, the more the BDNF production decreases. This implies that an excess amount of pro-inflammatory cytokines negatively affects BDNF production. This, in turn, affects the presence and severity of psychosis in individuals with schizophrenia.[11]

Self-domestication hypothesis

The theory of self-domestication asserts that during the late Pleistocene period, archaic humans split from their hominid ancestors and underwent behavioral changes that led to a reduction of aggression and an increase in “tameness”.[12] As a result of this transformation, changes to humans’ biological, morphological, physiological, and genetic development occurred; leading to anatomical changes in size, craniofacial structure, and brain structural differences, as well as changes in behavior related reduced levels of stress hormones and delayed maturation of the adrenal glands.[13] The self-domestication hypothesis for evolution of schizophrenia observes the importance our self-domesticated evolution, with emphasis on its contribution to the altered genetic development of the neural crest and our relaxed our social cultural niche. Adaptations related these domesticated changes favored the emergence of complex cognitive abilities, including advanced linguistic cognition.[13]

The self-domestication hypothesis suggests that schizophrenia results from hypofunction of the neural crest development, triggered by the selection for domesticated “tameness”, and emphasize the domestic characteristics that make up the clinical phenotype of schizophrenia. Deficits related to language production and processing are prevalent in both positive and negative symptoms of schizophrenia.[13] In addition, schizophrenic patients often demonstrate more marked domesticated traits at the morphological, physiological, and behavioral levels; including craniofacial abnormalities, desensitized cortical response to stress, and disorganized speech.[13]

A study published in 2017 targeted various candidate genes (FOXD3, RET, SOX9, SOX10, GDNF) with overlapping function in relation to schizophrenia, domestication, and neural crest development, and found the largest number of brain area expressions include to be in the frontal cortex, associate striatum nucleus, and hippocampus.[13] Although the results do not reflect the molecular events that occurred during early neural development or evolution, they provide insight into the molecular network that underlies the impaired cognitive and social scenarios that act in the schizophrenic brain, and further suggest that self-domestication, language processing, and schizophrenia have an intimately intertwined relationship.[13]

Extended maturation time hypothesis

This hypothesis synthesizes two previous hypotheses for the evolution of schizophrenia involving humans’ development of functional brain asymmetry in the neocortex (Crow’s theory) and improvement of fatty acid metabolism (myelin production), while adding a third dynamic of mechanistic cortical growth over an extended period of time, referred to as the balloon model theory, in order to describe the variations in human cognition that when abnormally defected, can lead to psychiatric conditions like schizophrenia. The balloon model theory describes cortical growth as a mechanism similar to an expanding balloon, where stretching of the myelin to the surface disentangles neighboring neuronal columns and enables the affected cortex to better differentiate signals.[14]

Cortical growth is affected by genetics, environment, nutrition, and time.[14] Human life history is unique because it delays the end of brain growth until the third decade of life, which allows environmental factors to exert influence, via balloon-like cortical growth and stretching, to impose much greater variability and plasticity in the final outcome of brain maturation.[14] However, the increase of variability in brain maturation outcomes also has increased humans’ susceptibility for disorders like schizophrenia. The onset of schizophrenia usually occurs between the ages of 16-30, and regions of the brain that mature last, including the frontal and temporal lobes, show more variable in maturation outcome and are also highly associated with symptoms of schizophrenia, as opposed to brain regions that develop earlier, such as the motor and somatosensory cortices.[14] Thus, humans’ collaborative evolution of functional asymmetry in the neocortex, improvement of fatty acid metabolism, and unique cortical growth maturation has been a driving force for the development of our variable complex cognition, but has left us susceptible for developing extreme variants in the form of mental disorders.

Sexual selection hypothesis

This hypothesis builds upon Crespi and Badcock’s imprinted brain theory of autism and psychosis by suggesting that the behavioral traits associated with autism and schizophrenia have been beneficial for individual reproductive, mating, and parental strategies; and therefore, have been maintained throughout the human population via sexual selection.[15] Under this hypothesis, autistic- and schizotypy-like traits exist as diametric opposites joined on the same spectrum of normal cognition, and most people display moderate degrees of one or both types of traits.[16]

When the spectrum of traits intertwine with the dynamics of genomic imprinting and principles of sexual selection within the context of bipaternal investment patterns, traits act as ornaments of mating behavior.[15] Whereas autistic-like traits are selected for based on their display of mechanistic and practical intelligence for obtaining resources that indicate support for a long-term relationship, schizotypy-traits demonstrate verbal and artistic creativity that indicate strong genetic fitness for a short-term mating strategy.[15]

Therefore, variation in different cognitive traits remain adaptive life-history, reproductive, and paternal strategies according to the local ecological conditions and personal characteristics. Although the hypothesis proposes that the cognitive traits do not originate by means of sexual selection and likely evolved for reasons unrelated to mating, the behavioral effects dictated by the genetic autistic- and schizotypy-traits remain varied in the environment and remain under selection; only extreme variants of either of the traits result in their respective clinical condition.

Evolutionary Advantage

Creativity is an essential tool for human development and survival. Schizophrenia is more than a tragic risk for creative people: Its persistence in the gene pool is essential. It is there “because of shared genetic linkages to creativity. ”Schizotypal thinking is often viewed as sharing features with creative thought, such as cognitive flexibility and divergent thinking via unusual but meaningful associations. These commonalities, coupled with the observed heritability of both constructs, suggest that there may be genetic factors common to both creativity and schizophrenia.”.[17] There are many creative and famous people with schizophrenia.

See also

References

  1. 1 2 Meyer U, Feldon J, Dammann O (2011). "Schizophrenia and autism: Both shared and disorder-specific pathogenesis via perinatal inflammation?". Pediatric Research. 69 (5): 26R. doi:10.1203/PDR.0b013e318212c196. PMC 3086802.
  2. 1 2 3 4 Erlenmeyer-Kimling, L.; Paradowski, William (Nov–Dec 1966). "Selection and Schizophrenia". The American Naturalist. 100 (916): 651–665. doi:10.1086/282458.
  3. 1 2 Burns, Jonathan (5 June 2006). "The Social Brain Hypothesis of Schizophrenia". World Psychiatry. 2. 5 (2): 77–81. PMC 1525115. PMID 16946939.
  4. 1 2 3 Burns, Jonathan (2004). "An Evolutionary Theory of Schizophrenia: Cortical Connectivity, Metarepresentation and the Social Brain". Behavioral and Brain Sciences. 27 (6): 831–855. doi:10.1017/s0140525x04000196.
  5. 1 2 3 4 5 6 Miller, Christine L. (2009). "The Evolution of Schizophrenia: A Model of Selection by Infection, with a Focus on NAD". Current Pharmaceutical Design. 15: 100–109. doi:10.2174/138161209787185805.
  6. ↑ Polimeni, J. Shamans Among Us: Schizophrenia, Shamanism and the Evolutionary Origins of Religion. EvoEbooks 2012
  7. 1 2 Song XQ, Lu LX, Li WQ, Hao YH, Zhao JP (2009). "The interaction of nuclear factor-kappa B and cytokines is associated with schizophrenia". Biol Psychiatry. 65 (6): 8. doi:10.1016/j.biopsych.2008.10.018.
  8. ↑ Zhang XY, Cao LY, Song C, Wu GY, Chen da C, Qi LY, Kosten TR (2008). "Lower serum cytokine levels in smokers than nonsmokers with chronic schizophrenia on long-term treatment with antipsychotics". Psychopharmacology. 201 (3): 383–389. doi:10.1007/s00213-008-1295-4.
  9. ↑ Zhang XY, Zhou DF, Zhang PY, Wu GY, Cao LY, Shen YC (2002). "Elevated interleukin-2, interleukin-6 and interleukin-8 serum levels in neuroleptic-free schizophrenia: Association with psychopathology". Schizophrenia Research. 57 (2–3): 247–258. doi:10.1016/S0920-9964(01)00296-1.
  10. ↑ Yang Zhang X, Feng Zhou D, Yuan Cao L, Yan Zhang P, Ying Wu G (2002). "Decreased production of interleukin-2 (IL-2), IL-2 secreting cells and CD4+ cells in medication-free patients with schizophrenia". Journal of Psychiatric Research. 36 (5): 331–336. doi:10.1016/S0022-3956(02)00023-7.
  11. ↑ Mondelli V, Cattaneo A, Murri MB, Forti MD, Handley R, Hepgul N, Pariante CM (2011). "Stress and inflammation reduce brain-derived neurotrophic factor expression in first-episode psychosis: A pathway to smaller hippocampal volume". Journal of Clinical Psychiatry. 72 (12): 1677–1684. doi:10.4088/JCP.10m06745. PMC 4082665.
  12. ↑ Brüne, M. (2007). "On human self-domestication, psychiatry, and eugenics". Philosophy, Ethics, and Humanities in Medicine. 2 (1): 21. doi:10.1186/1747-5341-2-21.
  13. 1 2 3 4 5 6 Benítez-Burraco, A., Di Pietro, L., Barba, M., Lattanzi, W. (2017). "Schizophrenia and Human Self-Domestication: An Evolutionary Linguistics Approach". Brain, Behavior, and Evolution. 89 (3): 162–184. doi:10.1159/000468506.
  14. 1 2 3 4 Seldon, H. L. (2007). "Extended neocortical maturation time encompasses speciation, fatty acid and lateralization theories of the evolution of schizophrenia and creativity". Medical Hypotheses. 69 (5): 1085–1089. doi:10.1016/j.mehy.2007.03.001.
  15. 1 2 3 Del Giudice, M., Angeleri, R., Brizio, A., & Elena, M. R. (2010). "The evolution of autistic-like and schizotypal traits: A sexual selection hypothesis". Frontiers in Psychology. 1. doi:10.3389/fpsyg.2010.00041.
  16. ↑ Byars, S. G., Stearns, S. C., & Boomsma, J. J. (2014). "Opposite risk patterns for autism and schizophrenia are associated with normal variation in birth size: phenotypic support for hypothesized diametric gene-dosage effects". Proceedings of the Royal Society B: Biological Sciences. 281 (1794): 20140604–20140604. doi:10.1098/rspb.2014.0604. PMC 4211440.
  17. ↑ Powers, Ron (2017). No One Cares About Crazy People: The Chaos and Heartbreak of Mental Health in America (Kindle ed.). Hachette Books.
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