The imprinted brain hypothesis is a hypothesis in evolutionary psychology regarding the causes of autism spectrum and schizophrenia spectrum disorders, first presented by Bernard Crespi and Christopher Badcock in 2008. It hypothesizes that genomic imprinting effects contribute, to some degree, to the diametric (opposite) nature of autism and psychosis (the diametric disorders hypothesis, which is much more general than the imprinted brain idea). The imprinted brain hypothesis is based around genomic imprinting, an epigenetic process through which genes are expressed differently depending upon which parent they are inherited from. Specifically, the imprinted brain hypothesis proposes that autism spectrum disorders are caused to some degree by biases towards paternal gene expression, while psychosis spectrum disorders are caused in some cases by biases towards maternal gene expression. The imprinted brain hypothesis is supported by high rates of autism in Angelman syndrome (which is due to paternal imprinted gene biases) and high rates of psychosis in Prader-Willi-syndrome (which is due to maternal imprinted gene biases). The diametric disorders hypothesis and the imprinted brain hypothesis have been subject to considerable research and testing, with considerable support and some non-supportive evidence, e.g., .
Genomic imprinting
Genomic imprinting is an epigenetic process by which certain genes are expressed in a parent-of-origin-specific manner. The imprinted brain theory represents an application of the kinship theory of genomic imprinting, also known as the conflict theory of genomic imprinting. The kinship theory 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 kinship theory is one of multiple competing major hypotheses regarding genomic imprinting and is supported by proponents of the imprinted brain hypothesis. The precise matter of how genomic imprinting works has not yet been resolved.
Hypothesis and background Proponents of the kinship theory of imprinting argue 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 use more of the mother's resources than other children, while it may be in the mother's interest for a child to take fewer resources and free up more for herself and future children. Thus, genomic imprinting a 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. 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 associated with overempathizing, resulting in delusions and paranoia, while those of autism are caused by underempathizing. Specifically, autism is considered to be a tendency to under-mentalize and under-empathize in a way that treats people as objects, while schizotypy is considered to be the inverse tendency to over-mentalize and over-empathize until objects are treated as people. Certain neuroimaging findings lend support to the hypothesis, although neuroimaging in schizophrenia is controversial due to the neurological impact of neuroleptic medication, and other neuroimaging findings have results inconsistent with the hypothesis. Traits such as the ambivalence seen in negative symptoms versus the single-minded focus of autistic special interests are also posited to be distinctions, although the pronounced similarity and overlap between negative symptomatology seen in the two disorders weakens this claim substantially. The imprinted brain hypothesis was first proposed in 2008 by biologist Bernard Crespi and sociologist Christopher Badcock, neither of whom had previous experience with cognitive science or behavioural genetics. Publishing their first presentation of their claims in the influential cognitive science journal Behavioral and Brain Sciences, the hypothesis attracted significant attention, both interested and critical.
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