A review of vulnerability and risks for schizophrenia: beyond the two hit hypothesis

Davis, Justin, Eyre, Harris, Jacka, Felice N., Dodd, Seetal, Dean, Olivia, McEwen, Sarah, Debnath, Monojit, McGrath, John, Maes, Michael, Amminger, Paul, McGorry, Patrick D., Pantelis, Christos and Berk,Michael (2016) A review of vulnerability and risks for schizophrenia: beyond the two hit hypothesis. Neuroscience and Biobehavioral Reviews, 65 185-194. doi:10.1016/j.neubiorev.2016.03.017

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Author Davis, Justin
Eyre, Harris
Jacka, Felice N.
Dodd, Seetal
Dean, Olivia
McEwen, Sarah
Debnath, Monojit
McGrath, John
Maes, Michael
Amminger, Paul
McGorry, Patrick D.
Pantelis, Christos
Title A review of vulnerability and risks for schizophrenia: beyond the two hit hypothesis
Journal name Neuroscience and Biobehavioral Reviews   Check publisher's open access policy
ISSN 1873-7528
Publication date 2016-06-01
Year available 2016
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1016/j.neubiorev.2016.03.017
Open Access Status File (Author Post-print)
Volume 65
Start page 185
End page 194
Total pages 10
Place of publication Kidlington, Oxford, United Kingdom
Publisher Pergamon Press
Language eng
Subject 3206 Neuropsychology and Physiological Psychology
2805 Cognitive Neuroscience
2802 Behavioral Neuroscience
Abstract Schizophrenia risk has often been conceptualized using a model which requires two hits in order to generate the clinical phenotype—the first as an early priming in a genetically predisposed individual and the second a likely environmental insult. The aim of this paper was to review the literature and reformulate this binary risk-vulnerability model. We sourced the data for this narrative review from the electronic database PUBMED. Our search terms were not limited by language or date of publication. The development of schizophrenia may be driven by genetic vulnerability interacting with multiple vulnerability factors including lowered prenatal vitamin D exposure, viral infections, smoking intelligence quotient, social cognition cannabis use, social defeat, nutrition and childhood trauma. It is likely that these genetic risks, environmental risks and vulnerability factors are cumulative and interactive with each other and with critical periods of neurodevelopmental vulnerability. The development of schizophrenia is likely to be more complex and nuanced than the binary two hit model originally proposed nearly thirty years ago. Risk appears influenced by a more complex process involving genetic risk interfacing with multiple potentially interacting hits and vulnerability factors occurring at key periods of neurodevelopmental activity, which culminate in the expression of disease state. These risks are common across a number of neuropsychiatric and medical disorders, which might inform common preventive and intervention strategies across non-communicable disorders.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: HERDC Pre-Audit
Queensland Brain Institute Publications
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