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The imprinted brain theory is an evolutionary psychology theory regarding the causes of autism spectrum disorders and psychosis.
The conflict theory of imprinting
[edit]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
[edit]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 schizoaffective disorder 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, 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
[edit]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 factors may affect cancer risk. Schizophrenia is associated with a decreased risk of cancer while the opposite occurs for schizophrenia.[5]
Autism is characterized by avoidance of gaze while schizophrenia is characterized by increased responsiveness to gaze.[4]
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.[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]
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.[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 to 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.[6][7]
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]
External links
[edit]- In a Novel Theory of Mental Disorders, Parents’ Genes Are in Competition - NYT article
- The Imprinted Brain - Blog about the theory by one of the creators
References
[edit]- ^ a b c d e f g h i j Crespi, B. (2008). "Genomic imprinting in the development and evolution of psychotic spectrum conditions". Biological Reviews. doi:10.1111/j.1469-185X.2008.00050.x.
- ^ a b c d Badcock, C.; Crespi, B. (2008). "Battle of the sexes may set the brain". Nature. 454 (7208): 1054–1055. doi:10.1038/4541054a. PMID 18756240.
- ^ 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
- ^ a b c d e f g Crespi, B.; Badcock, C. (2008). "Psychosis and autism as diametrical disorders of the social brain". Behavioral and Brain Sciences. 31 (3): 241–261, discussion 261–320. doi:10.1017/S0140525X08004214. PMID 18578904.
- ^ Crespi, B. (2011). "Autism and cancer risk". Autism Research. 4 (4): 302–310. doi:10.1002/aur.208. PMID 21823244.
- ^ Crespi, B.; Stead, P.; Elliot, M. (2009). "Colloquium Paper: Comparative genomics of autism and schizophrenia". Proceedings of the National Academy of Sciences. 107: 1736–41. doi:10.1073/pnas.0906080106. PMC 2868282. PMID 19955444.
- ^ Stearns, S. C.; Nesse, R. M.; Govindaraju, D. R.; Ellison, P. T. (2010). "Colloquium Paper: Evolutionary perspectives on health and medicine". Proceedings of the National Academy of Sciences. 107: 1691. doi:10.1073/pnas.0914475107.