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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"/>
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"/>


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 delusions and [[paranoia]], while people with autism seem to be blind to the intentions of others. There are other contrasts such as ambivalence vs. single-mindedness.<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. 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. There are other contrasts such as ambivalence vs. single-mindedness.<ref name="Nature"/><ref name="NYT"/>


[[Schizotypal personality disorder]] is argued to be analogous to [[Aspberger syndrome]] with both being less severe forms.<ref name="CrespiBadcock2008"/>
[[Schizotypal personality disorder]] is argued to be analogous to [[Aspberger syndrome]] with both being less severe forms.<ref name="CrespiBadcock2008"/>

Revision as of 21:20, 13 November 2011

The imprinted brain theory is an evolutionary psychology theory regarding the causes of autism spectrum disorders and psychosis.

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 supported by an extensive amount of empirical evidence and is, according to Crespi in a 2008 review, the only comprehensive theory explaining observed patterns of imprinting in humans and other organisms.[1]

The theory

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.[2][3]

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.[2][3]

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 delusions and paranoia, while people with autism seem to be blind to the intentions of others. There are other contrasts such as ambivalence vs. single-mindedness.[2][3]

Schizotypal personality disorder is argued to be analogous to Aspberger syndrome with both being less severe forms.[4]

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.[1]

Supporting evidence

Empirical evidence regarding growth rates and personality are argued to support the theory. Autism is associated with overgrowth of the head and body while schizophrenia is associated with slow development and undergrowth.[1] Schizophrenia has been associated with low birth weight, slow maturation, smaller brain size, decreased cortical thickness, and low levels of growth factors. Autism has been associated with high or normal birth weight, faster body growth, increased brain size, increased cortical thickness, and high levels of growth factors.[4]

Different growth rates and growth factors levels may affect cancer risk. Schizophrenia is associated with a decreased risk of cancer while the opposite occurs for autism.[5]

Factors such nutrition during pregnancy can affect imprinting. Schizophrenia is associated with maternal starvation during pregnancy while autism have become increasingly common in affluent societies.[6]

Reduced imagination, literalness, and inability at deception characterize autism while enhanced imagination, delusions, and self-deception characterizes schizophrenia. Other characteristics of autism are sensory filtering, narrow focus, and repetitive behaviors while schizophrenia is characterized by reduced sensory filtering, loose associations, and creativity. Pain and smell perception seem increased in autistic children while schizophrenia is associated with reduced pain and smell perception.[4]

Autism is associated with reduced or lacking inner speech while schizophrenia is associated with auditory hallucinations and thought insertions.[4]

In schizophrenia global or top-down processing of stimuli seems less affected than local or bottom-up processing. This is also a typical pattern seen in in the processes involved in dyslexia which is associated with schizophrenia. In contrast, autism is associated with increased local relative to global processing and hyperlexia is almost always associated with autism.[4]

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.[4]

Autism is characterized by avoidance of gaze while schizophrenia is characterized by increased responsiveness to gaze. In schizophrenia there is a high rate of smoking, possibly a form of self-medication. Smoking rate seems to be low in autism.[4]

The size of the corpus callosum is increased in schizophrenia while it is decreased in autism. Lateralization of brain function is decreased in schizophrenia, possibly due to slower brain development, while autism is associated with reversed lateralization compared to normal, possibly due to brain development in infancy and childhood being faster in 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 autsim. Functional imaging shows overactivation of certain brain regions involved in social functioning while the same regions are underactivated in autism.[4]

Schizophrenia is associated with a female pattern digit ratio while autism is associated with a male pattern digit ratio.[4]

Increased paternal age is 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]

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

Prader–Willi syndrome is a genetic disorder caused by loss of a set of normally expressed paternally imprinted genes. It is associated with a high frequency of psychosis. The sister syndrome Angelman syndrome is caused of loss by a set of normally expressed maternally imprinted genes in the same region and is associated with a high frequency of autism.[1]

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]

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]

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

Areas off the human genome linked with 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.[7][8]

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.[2]

Reception

In a book review in The British Journal of Psychiatry of a 2009 book about the theory, Carl Fredrik Johansson wrote:[9]

"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:[8]

"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:[10]

"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 Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1111/j.1469-185X.2008.00050.x, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1111/j.1469-185X.2008.00050.x instead.
  2. ^ a b c d Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1038/4541054a, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1038/4541054a instead.
  3. ^ a b c Benedict Carey, In a Novel Theory of Mental Disorders, Parents’ Genes Are in Competition, The New York Times, November 11, 2008, http://www.nytimes.com/2008/11/11/health/research/11brain.html
  4. ^ a b c d e f g h i Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1017/S0140525X08004214, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1017/S0140525X08004214 instead.
  5. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1002/aur.208, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1002/aur.208 instead.
  6. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.2217/epi.11.19, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.2217/epi.11.19 instead.
  7. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1073/pnas.0906080106, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1073/pnas.0906080106 instead.
  8. ^ a b Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1073/pnas.0914475107, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1073/pnas.0914475107 instead.
  9. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1192/bjp.bp.109.071084, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1192/bjp.bp.109.071084 instead.
  10. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1037/a0024043, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1037/a0024043 instead.
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