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 & biobehavioral reviews, vol. 65, pp. 185-194, doi: 10.1016/j.neubiorev.2016.03.017.

Attached Files
Name Description MIMEType Size Downloads

Title A review of vulnerability and risks for schizophrenia: beyond the two hit hypothesis
Author(s) Davis, Justin
Eyre, Harris
Jacka, Felice N.ORCID iD for Jacka, Felice N. orcid.org/0000-0002-9825-0328
Dodd, SeetalORCID iD for Dodd, Seetal orcid.org/0000-0002-7918-4636
Dean, OliviaORCID iD for Dean, Olivia orcid.org/0000-0002-2776-3935
McEwen, Sarah
Debnath, Monojit
McGrath, John
Maes, Michael
Amminger, Paul
McGorry, Patrick D.
Pantelis, Christos
Berk, MichaelORCID iD for Berk, Michael orcid.org/0000-0002-5554-6946
Journal name Neuroscience & biobehavioral reviews
Volume number 65
Start page 185
End page 194
Total pages 10
Publisher Elsevier
Place of publication Amsterdam, The Netherlands
Publication date 2016-06
ISSN 1873-7528
Summary 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.
Language eng
DOI 10.1016/j.neubiorev.2016.03.017
Field of Research 110999 Neurosciences not elsewhere classified
110319 Psychiatry (incl Psychotherapy)
Socio Economic Objective 920209 Mental Health Services
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2016, Elsevier
Persistent URL http://hdl.handle.net/10536/DRO/DU:30083399

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
Connect to link resolver
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.

Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 149 times in TR Web of Science
Scopus Citation Count Cited 150 times in Scopus
Google Scholar Search Google Scholar
Access Statistics: 946 Abstract Views, 1 File Downloads  -  Detailed Statistics
Created: Wed, 11 May 2016, 14:20:27 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.