Genetic epidemiology and schizophrenia: a study of reproductive fitness

Avila, Matthew T.; Thaker, Gunvant K.; Adami, Helene

doi:10.1016/s0920-9964(00)00062-1

Cited by 76 publications

(43 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Nettle and Clegg (2006) have suggested that such an advantage exists, and that it relates to high mating success associated specifically with the artistic creativity that is associated with some components of schizotypy. Avila, Thaker, and Adami (2001) showed increased numbers of offspring in first-degree relatives of people with schizophrenia. However, other studies have shown that there is no reproductive advantage to schizotypal traits (Haukka, Suvisaari, and Lonnqvist 2003;Kendler, Karkowski, and Walsh 1998).…”

Section: The Hypothesismentioning

confidence: 99%

A Reformulation of the Social Brain Theory for Schizophrenia: The Case for Out-Group Intolerance

Abed¹,

Abbas²

2011

pbm

View full text Add to dashboard Cite

This article proposes a reformulation of the social brain theory of schizophrenia. Contrary to those who consider schizophrenia to be an inherently human condition, we suggest that it is a relatively recent phenomenon, and that the vulnerability to it remained hidden among our hunter-gatherer ancestors. Hence, we contend that schizophrenia is the result of a mismatch between the post-Neolithic human social environment and the design of the social brain. We review the evidence from human evolutionary history of the importance of the distinction between ingroup and out-group membership that lies at the heart of intergroup conflict, violence, and xenophobia. We then review the evidence for the disparities in schizophrenia incidence around the world and for the higher risk of this condition among immigrants and city dwellers. Our hypothesis explains a range of epidemiological findings on schizophrenia related to the risk of migration and urbanization, the improved prognosis in underdeveloped countries, and variations in the prevalence of the disorder. However, although this hypothesis may identify the ultimate causation of schizophrenia, it does not specify the proximate mechanisms that lead to it. We conclude with a number of testable and refutable predictions for future research.

show abstract

Section: The Hypothesismentioning

confidence: 99%

A Reformulation of the Social Brain Theory for Schizophrenia: The Case for Out-Group Intolerance

Abed¹,

Abbas²

2011

pbm

View full text Add to dashboard Cite

show abstract

“…(12) The maintenance of schizophrenia in the population despite the reduced fertility of the patients [109] is a partially unsolved puzzle [110] which might be explained by the postulated growth deficiency. Growth-dependent birth weight is the classical example for stabilizing selection in humans [111], a selection against both extremes.…”

Section: Testing the Hypothesismentioning

confidence: 99%

The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia

2002

View full text Add to dashboard Cite

Abstract

Background

A systems approach to understanding the etiology of schizophrenia requires a theory which is able to integrate genetic as well as neurodevelopmental factors.

Presentation of the hypothesis

Based on a co-localization of loci approach and a large amount of circumstantial evidence, we here propose that a functional deficiency of glial growth factors and of growth factors produced by glial cells are among the distal causes in the genotype-to-phenotype chain leading to the development of schizophrenia. These factors include neuregulin, insulin-like growth factor I, insulin, epidermal growth factor, neurotrophic growth factors, erbB receptors, phosphatidylinositol-3 kinase, growth arrest specific genes, neuritin, tumor necrosis factor alpha, glutamate, NMDA and cholinergic receptors. A genetically and epigenetically determined low baseline of glial growth factor signaling and synaptic strength is expected to increase the vulnerability for additional reductions (e.g., by viruses such as HHV-6 and JC virus infecting glial cells). This should lead to a weakening of the positive feedback loop between the presynaptic neuron and its targets, and below a certain threshold to synaptic destabilization and schizophrenia.

Testing the hypothesis

Supported by informed conjectures and empirical facts, the hypothesis makes an attractive case for a large number of further investigations.

Implications of the hypothesis

The hypothesis suggests glial cells as the locus of the genes-environment interactions in schizophrenia, with glial asthenia as an important factor for the genetic liability to the disorder, and an increase of prolactin and/or insulin as possible working mechanisms of traditional and atypical neuroleptic treatments.

show abstract

“…For example, although the prevalence of schizophrenia is typically estimated to be approximately 1% of the population (Avila, Thaker, & Adami, 2001;McGrath, Saha, Chant, & Welham, 2008), Shaw, Hunt, Flynn, Meehan, Robinson, Bickly et al (2006), in a study of 1594 homicide offenders, reported that 5% were diagnosed with schizophrenia. Wallace et al (1998), in a study linking court and psychiatric records, reported similar findings, but noted that substance abuse contributed to violence in most crimes for which people with schizophrenia were convicted.…”

Section: Introductionmentioning

confidence: 99%

Schizophrenia and violence: realities and recommendations

Silverstein

Pozzo

Roché

et al. 2015

Crime Psychology Review

View full text Add to dashboard Cite

Published findings on the relationship between schizophrenia and violence have been mixed, due to differences in study design and quality. In this review, we address the issue with an emphasis on characterizing who is most likely to be violent and when. We conclude that: (1) individuals with schizophrenia are at an increased risk for violence due to specific psychotic symptoms; (2) this risk is increased by brain abnormalities, psychiatric comorbidities, and demographic factors that are not specific to schizophrenia; (3) the majority of violent offenses committed by people with schizophrenia are indistinguishable from offenses committed by others; and (4) despite our knowledge of factors related to increased violence risk and the existence of effective treatments to mitigate this risk, valid risk assessment instruments for this population are lacking, and treatment strategies are rarely employed at any level of psychiatric care. In short, while most people with schizophrenia are not violent and violence committed by people with this condition accounts for only a small percentage of overall violent crime, there is nevertheless a significantly increased risk for violence among subgroups in this population. This has implications for people living with people with schizophrenia, mental health professionals, administrators of psychiatric care facilities, law enforcement personnel, the court system, and policymakers.

show abstract

Genetic epidemiology and schizophrenia: a study of reproductive fitness

Cited by 76 publications

References 24 publications

A Reformulation of the Social Brain Theory for Schizophrenia: The Case for Out-Group Intolerance

A Reformulation of the Social Brain Theory for Schizophrenia: The Case for Out-Group Intolerance

The glial growth factors deficiency and synaptic destabilization hypothesis of schizophrenia

Schizophrenia and violence: realities and recommendations

Contact Info

Product

Resources

About