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[[Genomic imprinting]] is an [[epigenetic]] process by which certain [[gene]]s are expressed in a parent-of-origin-specific manner. The imprinted brain theory is a variant of the [[the kinship theory of genomic imprinting|conflict theory of imprinting]] which argues that in [[diploid]] organisms, such as humans, the maternal and paternal set of genes may have antagonistic reproductive interests since the mother and father may have antagonistic interests regarding the development of the child. The conflict theory of imprinting is, according to [[Bernard Crespi]] in a 2008 paper, the only comprehensive theory explaining observed patterns of imprinting in humans and other organisms.<ref name="Crespi2008"/><ref>{{cite web|url=https://www.edge.org/conversation/christopher_badcock-the-imprinted-brain-theory |title= The Imprinted Brain Theory |website=www.edge.org|access-date=2019-08-26}}</ref><ref>{{cite journal | vauthors = Skaar DA, Li Y, Bernal AJ, Hoyo C, Murphy SK, Jirtle RL | title = The human imprintome: regulatory mechanisms, methods of ascertainment, and roles in disease susceptibility | journal = ILAR Journal | volume = 53 | issue = 3–4 | pages = 341–58 | date = 2012 | pmid = 23744971 | pmc = 3683658 | doi = 10.1093/ilar.53.3-4.341 }}</ref><ref>{{cite journal | vauthors = Mokkonen M, Crespi BJ | title = Genomic conflicts and sexual antagonism in human health: insights from oxytocin and testosterone | journal = Evolutionary Applications | volume = 8 | issue = 4 | pages = 307–25 | date = April 2015 | pmid = 25926877 | pmc = 4408143 | doi = 10.1111/eva.12244 }}</ref>
[[Genomic imprinting]] is an [[epigenetic]] process by which certain [[gene]]s are expressed in a parent-of-origin-specific manner. The imprinted brain theory is a variant of the [[the kinship theory of genomic imprinting|conflict theory of imprinting]] which argues that in [[diploid]] organisms, such as humans, the maternal and paternal set of genes may have antagonistic reproductive interests since the mother and father may have antagonistic interests regarding the development of the child. The conflict theory of imprinting is, according to [[Bernard Crespi]] in a 2008 paper, the only comprehensive theory explaining observed patterns of imprinting in humans and other organisms.<ref name="Crespi2008"/><ref>{{cite web|url=https://www.edge.org/conversation/christopher_badcock-the-imprinted-brain-theory |title= The Imprinted Brain Theory |website=www.edge.org|access-date=2019-08-26}}</ref><ref>{{cite journal | vauthors = Skaar DA, Li Y, Bernal AJ, Hoyo C, Murphy SK, Jirtle RL | title = The human imprintome: regulatory mechanisms, methods of ascertainment, and roles in disease susceptibility | journal = ILAR Journal | volume = 53 | issue = 3–4 | pages = 341–58 | date = 2012 | pmid = 23744971 | pmc = 3683658 | doi = 10.1093/ilar.53.3-4.341 }}</ref><ref>{{cite journal | vauthors = Mokkonen M, Crespi BJ | title = Genomic conflicts and sexual antagonism in human health: insights from oxytocin and testosterone | journal = Evolutionary Applications | volume = 8 | issue = 4 | pages = 307–25 | date = April 2015 | pmid = 25926877 | pmc = 4408143 | doi = 10.1111/eva.12244 }}</ref>


== The theory ==
== The hypothesis ==
The imprinted brain theory argues that since it is uncertain if a woman's other and future children have and will have the same father, as well as the father generally having lower [[parental investment]], it may be in the father's reproductive interest for his child to maximize usage of the mother's resources while it may be in the mother's interest to limit this in order to have resources for her other and future children.<ref name="Nature">{{cite journal | vauthors = Badcock C, Crespi B | title = Battle of the sexes may set the brain | journal = Nature | volume = 454 | issue = 7208 | pages = 1054–5 | date = August 2008 | pmid = 18756240 | doi = 10.1038/4541054a | bibcode = 2008Natur.454.1054B }}</ref><ref name="NYT">{{cite web | first = Benedict | last = Carey | name-list-style = vanc | year = 2008 | url = https://www.nytimes.com/2008/11/11/health/research/11brain.html | title = In a Novel Theory of Mental Disorders, Parents' Genes Are in Competition | work = The New York Times }}</ref>{{ums|date=November 2017}}
The imprinted brain hypothesis argues that since it is uncertain if a woman's other and future children have and will have the same father, as well as the father generally having lower [[parental investment]], it may be in the father's reproductive interest for his child to maximize usage of the mother's resources while it may be in the mother's interest to limit this in order to have resources for her other and future children.<ref name="Nature">{{cite journal | vauthors = Badcock C, Crespi B | title = Battle of the sexes may set the brain | journal = Nature | volume = 454 | issue = 7208 | pages = 1054–5 | date = August 2008 | pmid = 18756240 | doi = 10.1038/4541054a | bibcode = 2008Natur.454.1054B }}</ref><ref name="NYT">{{cite web | first = Benedict | last = Carey | name-list-style = vanc | year = 2008 | url = https://www.nytimes.com/2008/11/11/health/research/11brain.html | title = In a Novel Theory of Mental Disorders, Parents' Genes Are in Competition | work = The New York Times }}</ref>{{ums|date=November 2017}} Thus, a genomic imprinting with slight maternal bias would supposedly be associated with factors such as decreased growth, more tractable behavior, and an empathizing and less self-centered personality causing less demands on the mother. The opposite would occur for a slight paternal bias.<ref name="Nature"/><ref name="NYT"/>


⚫
However, an extreme genomic imprinting in favor of maternal genes is argued to cause [[psychosis]] such as in [[schizophrenia spectrum]] disorders while an extreme genomic imprinting in favor of paternal genes is argued to cause [[autism spectrum]] disorders. This claims the symptoms of [[schizophrenia]] are claimed by overempathizing, resulting in [[delusions]] and [[paranoia]], while people with autism seem to be blind to the intentions of others. Certain neuroimaging findings lend support to the hypothesis,<ref>{{cite journal | vauthors = Ciaramidaro A, Bölte S, Schlitt S, Hainz D, Poustka F, Weber B, Bara BG, Freitag C, Walter H | display-authors = 6 | title = Schizophrenia and autism as contrasting minds: neural evidence for the hypo-hyper-intentionality hypothesis | journal = Schizophrenia Bulletin | volume = 41 | issue = 1 | pages = 171–9 | date = January 2015 | pmid = 25210055 | pmc = 4266299 | doi = 10.1093/schbul/sbu124 | quote = Consistent with these studies, it has been hypothesized that ASD and SCZ thus may be located at the extreme ends of a cognitive architecture ranging from a mechanistic hypo-intentional (to treat person as objects) to a mentalistic hyper-intentional (to treat objects as persons) mode of cognition, respectively. }}</ref>{{primary source inline|date=November 2017}} although neuroimaging in schizophrenia is controversial due to the neurological impact of [[neuroleptic]] medication.<ref>{{cite journal|vauthors=Torres, Ulysses S; Portela-Oliveira, Eduardo; Borgwardt, Stefan; Busatto, Geraldo F|title=Structural brain changes associated with antipsychotic treatment in schizophrenia as revealed by voxel-based morphometric MRI: an activation likelihood estimation meta-analysis|work=BMC Psychiatry|date=December 2013|doi=10.1186/1471-244X-13-342|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3878502/}}</ref><ref>{{cite journal|title=Brain Structural Effects of Antipsychotic Treatment in Schizophrenia: A Systematic Review|vauthors=Roiz-Santiañez, Roberto; Suarez-Pinella, Paula; Crespo-Facorro, Benedicto|date=July 2015|journal=Current Neuropharmacology|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4790397/|doi= 10.2174/1570159X13666150429002536}}</ref>
Thus, a genomic imprinting with slight maternal bias would be associated with factors such as decreased growth, more tractable behavior, and an empathizing and less self-centered personality causing less demands on the mother. The opposite would occur for a slight paternal bias.<ref name="Nature"/><ref name="NYT"/>


Traits such as ambivalence seen in [[negative symptoms]] versus the single-minded focus of autistic special interests are also posited to be distinctions,<ref name="Nature" /> although the pronounced similarity and overlap between negative symptomatology seen in the two disorders weakens this claim substantially.<ref>{{cite journal|title=High-functioning autism and schizophrenia: A comparison of an early and late onset neurodevelopmental disorder|vauthors=Goldstein, Gerald; Minshew, Nancy J; Allen, Daniel N; Seaton, Brent E|work=Archive of Clinical Neuropsychology|date=June 2002|url=https://www.sciencedirect.com/science/article/pii/S0887617701001299|doi=10.1016/S0887-6177(01)00129-9}}</ref><ref>{{cite journal|title=Autism Spectrum Disorder and Schizophrenia Are Better Differentiated by Positive Symptoms Than Negative Symptoms|work=Frontiers in Psychiatry|vauthors=Trevisan, Dominic A., Foss-Feig, Jennifer H., Naples, Adam J., Srihari, Vinod, Anticevic, Alan, McPartland, James C.|date=June 2020|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7301837/|doi=10.3389/fpsyt.2020.00548}}</ref>
⚫
However, an extreme genomic imprinting in favor of maternal genes is argued to cause [[psychosis]] such as in [[schizophrenia spectrum]] disorders while an extreme genomic imprinting in favor of paternal genes is argued to cause [[autism spectrum]] disorders. Thus, people with [[schizophrenia]] empathize and read too much into situations and see hidden intentions everywhere, causing [[delusion]]s and [[paranoia]], while people with autism seem to be blind to the intentions of others. This could be confirmed by a recent [[neuroimaging]] study.<ref>{{cite journal | vauthors = Ciaramidaro A, Bölte S, Schlitt S, Hainz D, Poustka F, Weber B, Bara BG, Freitag C, Walter H | display-authors = 6 | title = Schizophrenia and autism as contrasting minds: neural evidence for the hypo-hyper-intentionality hypothesis | journal = Schizophrenia Bulletin | volume = 41 | issue = 1 | pages = 171–9 | date = January 2015 | pmid = 25210055 | pmc = 4266299 | doi = 10.1093/schbul/sbu124 | quote = Consistent with these studies, it has been hypothesized that ASD and SCZ thus may be located at the extreme ends of a cognitive architecture ranging from a mechanistic hypo-intentional (to treat person as objects) to a mentalistic hyper-intentional (to treat objects as persons) mode of cognition, respectively. }}</ref>{{primary source inline|date=November 2017}}


⚫
[[Schizotypal personality disorder]] is argued to be analogous to [[Asperger syndrome]], with both being less severe forms.<ref name="CrespiBadcock2008"/>
There are other contrasts such as [[ambivalence]] vs. single-mindedness.<ref name="Nature" />


Adherents of the hypothesis say it remains compatible with genetic and environmental factors that increase the risk for both schizophrenia and autism, as these are considered to be affected by genomic imprinting differently.<ref name="Crespi2008"/>
⚫
[[Schizotypal personality disorder]] is argued to be analogous to [[Asperger syndrome]] with both being less severe forms.<ref name="CrespiBadcock2008"/>

The theory is compatible with various genetic or environmental factors increasing the risk for schizophrenia and autism since many factors, genetic or environmental, are known to affect genomic imprinting. In the view many different factors may change overall imprinting balance and cause similar disorders.<ref name="Crespi2008"/>


== Supporting evidence ==
== Supporting evidence ==

Revision as of 09:46, 21 January 2021

The imprinted brain hypothesis is an evolutionary psychology hypothesis regarding the causes of autism spectrum disorders and schizophrenia spectrum disorders. It claims that certain autistic and schizotypal traits are opposites, such as autism being associated with literal-mindedness while schizotypal is associated with imagination. Bernard Crespi, one of the primary proponents of the hypothesis, claims that these tendencies show that autism is linked to epigenetic imprinting of the X chromosome, specifically that autistic disorders involve paternal imprinting while schizotypal disorders involve maternal imprinting.

The conflict theory of imprinting

See also: Sexual conflict

Genomic imprinting is an epigenetic process by which certain genes are expressed in a parent-of-origin-specific manner. The imprinted brain theory is a variant of the conflict theory of imprinting which argues that in diploid organisms, such as humans, the maternal and paternal set of genes may have antagonistic reproductive interests since the mother and father may have antagonistic interests regarding the development of the child. The conflict theory of imprinting is, according to Bernard Crespi in a 2008 paper, the only comprehensive theory explaining observed patterns of imprinting in humans and other organisms.[1][2][3][4]

The hypothesis

The imprinted brain hypothesis argues that since it is uncertain if a woman's other and future children have and will have the same father, as well as the father generally having lower parental investment, it may be in the father's reproductive interest for his child to maximize usage of the mother's resources while it may be in the mother's interest to limit this in order to have resources for her other and future children.[5][6][unreliable medical source?] Thus, a genomic imprinting with slight maternal bias would supposedly be associated with factors such as decreased growth, more tractable behavior, and an empathizing and less self-centered personality causing less demands on the mother. The opposite would occur for a slight paternal bias.[5][6]

However, an extreme genomic imprinting in favor of maternal genes is argued to cause psychosis such as in schizophrenia spectrum disorders while an extreme genomic imprinting in favor of paternal genes is argued to cause autism spectrum disorders. This claims the symptoms of schizophrenia are claimed by overempathizing, resulting in delusions and paranoia, while people with autism seem to be blind to the intentions of others. Certain neuroimaging findings lend support to the hypothesis,[7][non-primary source needed] although neuroimaging in schizophrenia is controversial due to the neurological impact of neuroleptic medication.[8][9]

Traits such as ambivalence seen in negative symptoms versus the single-minded focus of autistic special interests are also posited to be distinctions,[5] although the pronounced similarity and overlap between negative symptomatology seen in the two disorders weakens this claim substantially.[10][11]

Schizotypal personality disorder is argued to be analogous to Asperger syndrome, with both being less severe forms.[12]

Adherents of the hypothesis say it remains compatible with genetic and environmental factors that increase the risk for both schizophrenia and autism, as these are considered to be affected by genomic imprinting differently.[1]

Supporting evidence

For empirical evidence regarding growth rates, personality and other characteristics that are argued to support the theory, see below. A direct comparison of autism and schizophrenia risks in relation to birth weight within the same population also supports these claims.[13][non-primary source needed]

Factors such as nutrition during pregnancy can affect imprinting. Schizophrenia is associated with maternal starvation during pregnancy while autism has become increasingly common in affluent societies.[14]

The imprinted brain theory regarding autism spectrum disorders is somewhat similar although not identical with the extreme male brain theory of autism. According to the imprinted brain theory there could be a mismatch and more severe problems when extreme genomic imprinting occurs in the opposite sex, which would explain why female autism (and male psychosis) is often particularly severe, which is a problem for the "extreme male brain" theory which predicts the opposite.[5]

Comparison of Features[1][12]
Area
Autism Schizophrenia
Growth rates
  • is linked to overgrowth of the head and body
  • associated with high or normal birth weight, faster body growth,
  • increased brain size, increased cortical thickness
  • high levels of growth factors
  • is linked to slow development and undergrowth
  • associated with low birth weight, slow maturation
  • smaller brain size, decreased cortical thickness
  • low levels of growth factors.
Cancer risk
  • associated with an increased risk of cancer (different growth rates and growth factors levels may affect cancer risk)[15]
  • associated with a decreased risk of cancer (different growth rates and growth factors levels may affect cancer risk)
Sensory processing
  • typically reduced imagination, literalness and inability at deception[12]
  • enhanced sensory filtering, narrow focus, and repetitive behaviors
  • pain and smell perception seem increased in autistic children
  • reduced or lacking inner speech
  • autism is associated with increased local processing of stimuli relative to global. hyperlexia is almost always associated with autism.[12]
  • typically enhanced imagination, delusions and self-deception[12]
  • reduced sensory filtering, loose associations, and creativity
  • is associated with reduced pain and smell perception
  • is associated with auditory hallucinations and thought insertions
  • global or top-down processing of stimuli seems less affected than local or bottom-up processing. This is also typical for dyslexia which is associated with schizophrenia.
Gaze
  • characterized by avoidance of gaze
  • characterized by increased responsiveness to gaze
Smoking
  • Smoking rate seems to be low in autism.[12]
Body features
Gender identity

Empathy

In both mild and severe autism and severe schizophrenia the theory of mind is impaired. This may occur by different mechanisms, such as by the presence of delusions in schizophrenia. However, there is evidence that people with schizotypal personality have an enhanced theory of mind and increased emphatic ability.[12] Lateralization of brain function is decreased in schizophrenia, possibly due to slower brain development. Autism is associated with reversed lateralization compared to normal, possibly due to brain development in infancy and childhood being faster in the right hemisphere and autism being associated with increased brain growth during this period. The mirror neuron system, involved in the theory of mind and empathy, is developed but dysregulated in schizophrenia while it is underdeveloped in autism. Functional imaging shows overactivation of certain brain regions involved in social functioning in schizophrenia while the same regions are underactivated in autism.[12]

Genetics

Increased paternal age is a strong risk factor for schizophrenia but the rate of ordinary nucleotide mutations appears to be too slow to explain this. However, imprinting is affected by a higher rate of mutation and may thus explain the age effect.[1][better source needed]

Many imprinted genes are expressed mainly or entirely in the brain suggesting that differences in imprinting have important effects on the brain.[1][better source needed]

Prader–Willi syndrome is a genetic disorder caused by loss of a set of normally expressed paternal genes, which are imprinted in the mother. It is associated with a high frequency of psychosis. The sister syndrome Angelman syndrome is caused by a loss of normally expressed maternal genes, which are imprinted in the father, in the same region and is associated with a high frequency of autism.[1][better source needed]

XXX syndrome and XXY syndrome, having an extra X chromosome, are associated with a high frequencies of psychosis. Turner syndrome, females having only one X chromosome, is associated with a high frequency of autism.[1][better source needed]

Some mutations in the MECP2 gene can cause Rett syndrome with autistic symptoms. A different mutation can lead to PPM-X syndrome which includes psychosis. The MECP2 gene is involved in controlling imprinted genes.[1][better source needed]

The Beckwith-Wiedemann syndrome is caused by increased effects of paternally imprinted genes and have increased incidence of autism.[1][18][13]

Fragile X syndrome involves reduced expression of the FMR1 gene which is X-linked which may favor parental genes.[1][19]

Areas off the human genome linked with imprinted genes, psychosis, and parent-of-origin effects each occupy only a very small part of the human genome and overlap of these areas would not be expected if they were unrelated. However, many of the areas overlap.[1]

Data from copy number variation and single gene association studies support shared genetic mechanisms causing schizophrenia and autism.[20][21]

Reception

In a book review in The British Journal of Psychiatry of a 2009 book about the theory, Carl Fredrik Johansson wrote:[22]

"In terms of the plausibility of the theory, it is appealing in its symmetry, offering some compelling examples of how the disorders complement each other in their symptomatology. Testable hypotheses are offered but most remain untested. More significantly, far too little is known about the relationship between genes and the aetiology of these disorders, and the understanding of the struggle for expression between parental genes is at a very early stage."

Stearns et al. commented on new genetic evidence supporting the theory in 2010 in an article in the Proceedings of the National Academy of Sciences of the United States of America:[21]

"Here Crespi, Stead, and Elliot extend such analysis of autism and schizophrenia to the impacts of copy number variants (deletions and duplications), further single-gene associations, growth signaling pathways, and brain growth (16). They make a plausible case that the risk of autism is increased by disruption of maternal interests and the uninhibited expression of paternal interests, and that the risk of schizophrenia is increased by the disruption of paternal interests and the uninhibited expression of maternal interests. This is an unconventional but creative approach to serious mental diseases. If it is correct, it will be one of the least expected and most surprising connections in the history of human evolutionary biology."

A 2011 literature review by Schlomer, Del Giudice, and Ellis in Psychological Review stated regarding the theory:[23]

"Recently, Crespi and Badcock (2008a; Badcock, 2009) argued that genomic imprinting can help explain the evolution of the human brain and the origin of some important psychological disorders. They reviewed a large body of evidence linking imprinted genes to the etiology of autism and psychosis, and proposed that autistic-spectrum conditions are associated with a "paternally biased" pattern of brain development (i.e., over-expression of paternal genes and/or under-expression of maternal genes), while psychotic-spectrum syndromes would be associated to a "maternally biased" development. Although Crespi and Badcock’s model is still speculative in several respects, and has been met with criticism by some researchers (e.g., Dickins, Dickins, & Dickins, 2008; Keller, 2008; Thakkar, Matthews, & Park, 2008; but see also Crespi & Badcock, 2008b; Crespi, Stead, & Elliot, 2009), it does hold considerable promise for an integrated evolutionary theory of psychopathology, and may be useful to understand normal variation in personality as well (see Del Giudice, Angeleri, Brizio & Elena, 2010). A better understanding of the genetic and epigenetic basis of autism and psychosis may also permit the development of improved methods for the early diagnosis and treatment of these conditions."

References

  1. ^ a b c d e f g h i j k Crespi B (November 2008). "Genomic imprinting in the development and evolution of psychotic spectrum conditions". Biological Reviews of the Cambridge Philosophical Society. 83 (4): 441–93. doi:10.1111/j.1469-185X.2008.00050.x. PMID 18783362.
  2. ^ "The Imprinted Brain Theory". www.edge.org. Retrieved 2019-08-26.
  3. ^ Skaar DA, Li Y, Bernal AJ, Hoyo C, Murphy SK, Jirtle RL (2012). "The human imprintome: regulatory mechanisms, methods of ascertainment, and roles in disease susceptibility". ILAR Journal. 53 (3–4): 341–58. doi:10.1093/ilar.53.3-4.341. PMC 3683658. PMID 23744971.
  4. ^ Mokkonen M, Crespi BJ (April 2015). "Genomic conflicts and sexual antagonism in human health: insights from oxytocin and testosterone". Evolutionary Applications. 8 (4): 307–25. doi:10.1111/eva.12244. PMC 4408143. PMID 25926877.
  5. ^ a b c d Badcock C, Crespi B (August 2008). "Battle of the sexes may set the brain". Nature. 454 (7208): 1054–5. Bibcode:2008Natur.454.1054B. doi:10.1038/4541054a. PMID 18756240.
  6. ^ a b Carey B (2008). "In a Novel Theory of Mental Disorders, Parents' Genes Are in Competition". The New York Times.
  7. ^ Ciaramidaro A, Bölte S, Schlitt S, Hainz D, Poustka F, Weber B, et al. (January 2015). "Schizophrenia and autism as contrasting minds: neural evidence for the hypo-hyper-intentionality hypothesis". Schizophrenia Bulletin. 41 (1): 171–9. doi:10.1093/schbul/sbu124. PMC 4266299. PMID 25210055. Consistent with these studies, it has been hypothesized that ASD and SCZ thus may be located at the extreme ends of a cognitive architecture ranging from a mechanistic hypo-intentional (to treat person as objects) to a mentalistic hyper-intentional (to treat objects as persons) mode of cognition, respectively.
  8. ^ Torres, Ulysses S; Portela-Oliveira, Eduardo; Borgwardt, Stefan; Busatto, Geraldo FB (December 2013). "Structural brain changes associated with antipsychotic treatment in schizophrenia as revealed by voxel-based morphometric MRI: an activation likelihood estimation meta-analysis". BMC Psychiatry. doi:10.1186/1471-244X-13-342. {{cite journal}}: Vancouver style error: punctuation in name 2 (help)CS1 maint: unflagged free DOI (link)
  9. ^ Roiz-Santiañez, Roberto; Suarez-Pinella, Paula; Crespo-Facorro, Benedicto (July 2015). "Brain Structural Effects of Antipsychotic Treatment in Schizophrenia: A Systematic Review". Current Neuropharmacology. doi:10.2174/1570159X13666150429002536. {{cite journal}}: Vancouver style error: punctuation in name 2 (help)
  10. ^ Goldstein, Gerald; Minshew, Nancy J; Allen, Daniel N; Seaton, Brent E (June 2002). "High-functioning autism and schizophrenia: A comparison of an early and late onset neurodevelopmental disorder". Archive of Clinical Neuropsychology. doi:10.1016/S0887-6177(01)00129-9. {{cite journal}}: Vancouver style error: punctuation in name 2 (help)
  11. ^ Trevisan, Dominic A., Foss-Feig, Jennifer H., Naples, Adam J., Srihari, Vinod, Anticevic, Alan, McPartland, James C. (June 2020). "Autism Spectrum Disorder and Schizophrenia Are Better Differentiated by Positive Symptoms Than Negative Symptoms". Frontiers in Psychiatry. doi:10.3389/fpsyt.2020.00548. {{cite journal}}: Vancouver style error: punctuation in name 2 (help)CS1 maint: unflagged free DOI (link)
  12. ^ a b c d e f g h Crespi B, Badcock C (June 2008). "Psychosis and autism as diametrical disorders of the social brain" (PDF). The Behavioral and Brain Sciences. 31 (3): 241–61, discussion 261–320. doi:10.1017/S0140525X08004214. PMID 18578904.
  13. ^ a b Byars SG, Stearns SC, Boomsma JJ (November 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. Biological Sciences. 281 (1794): 20140604. doi:10.1098/rspb.2014.0604. PMC 4211440. PMID 25232142.
  14. ^ Badcock C (June 2011). "The imprinted brain: how genes set the balance between autism and psychosis" (PDF). Epigenomics. 3 (3): 345–59. doi:10.2217/epi.11.19. PMID 22122342.
  15. ^ Crespi B (August 2011). "Autism and cancer risk". Autism Research. 4 (4): 302–10. doi:10.1002/aur.208. PMID 21823244.
  16. ^ Jones RM, Wheelwright S, Farrell K, Martin E, Green R, Di Ceglie D, Baron-Cohen S (February 2012). "Brief report: female-to-male transsexual people and autistic traits". Journal of Autism and Developmental Disorders. 42 (2): 301–6. doi:10.1007/s10803-011-1227-8. PMID 21448752.
  17. ^ Rajkumar RP (2014). "Gender identity disorder and schizophrenia: neurodevelopmental disorders with common causal mechanisms?". Schizophrenia Research and Treatment. 2014: 463757. doi:10.1155/2014/463757. PMC 4274821. PMID 25548672.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  18. ^ Shuman C, Beckwith JB, Weksberg R (11 August 2016). "Beckwith-Wiedemann Syndrome". In Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJ, Stephens K, Amemiya A (eds.). GeneReviews. University of Washington, Seattle. PMID 20301568. Retrieved 2019-08-26.
  19. ^ Brouwer JR, Willemsen R, Oostra BA (September 2009). "The FMR1 gene and fragile X-associated tremor/ataxia syndrome". American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. 150B (6): 782–98. doi:10.1002/ajmg.b.30910. PMC 4320942. PMID 19105204.
  20. ^ Crespi B, Stead P, Elliot M (January 2010). "Evolution in health and medicine Sackler colloquium: Comparative genomics of autism and schizophrenia". Proceedings of the National Academy of Sciences of the United States of America. 107 Suppl 1: 1736–41. Bibcode:2010PNAS..107.1736C. doi:10.1073/pnas.0906080106. PMC 2868282. PMID 19955444.
  21. ^ a b Stearns SC, Nesse RM, Govindaraju DR, Ellison PT (January 2010). "Evolution in health and medicine Sackler colloquium: Evolutionary perspectives on health and medicine". Proceedings of the National Academy of Sciences of the United States of America. 107 Suppl 1 (Suppl 1): 1691–5. Bibcode:2010PNAS..107.1691S. doi:10.1073/pnas.0914475107. PMC 2868294. PMID 20133821.
  22. ^ Johansson CF (2010). "The Imprinted Brain: How Genes Set the Balance between Autism and Psychosis". The British Journal of Psychiatry. 196 (4): 334–335. doi:10.1192/bjp.bp.109.071084.
  23. ^ Schlomer GL, Del Giudice M, Ellis BJ (July 2011). "Parent-offspring conflict theory: an evolutionary framework for understanding conflict within human families". Psychological Review. 118 (3): 496–521. doi:10.1037/a0024043. PMID 21604906.
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