Evidence map›Paper›PMID 27073049›Full record

ReviewNeuroscience and biobehavioral reviews2016

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

Justin Davis, Harris Eyre, Felice N Jacka, Seetal Dodd, Olivia Dean, Sarah McEwen, Monojit Debnath, John McGrath, Michael Maes, Paul Amminger and 3 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuroscience and biobehavioral reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 8 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

152 citing papers in PubMed, 8 syntheses or guidelines pooled it.

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92 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Justin DavisDeakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia. Electronic address: justinbdavis19@gmail.com.
Harris EyreDeakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia.
Felice N JackaDeakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia; University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia; Centre for Adolescent Health, Murdoch Children's Research Institute, Melbourne, Australia; Black Dog Institute, Sydney, Australia.
Seetal DoddDeakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia; University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia.
Olivia DeanDeakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia; University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia.
Sarah McEwenSemel Institute for Neuroscience and Human Behavior, UCLA, United States.
Monojit DebnathDepartment of Human Genetics, National Institute of Mental Health and Neurosciences, Bangalore, India.
John McGrathQueensland Brain Institute, The University of Queensland, Brisbane, 4072, Queensland, Australia; Queensland Centre for Mental Health Research, The Park Centre for Mental Health, Wacol, Queensland 4076, Australia.
Michael MaesDeakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia.
Paul AmmingerQueensland Brain Institute, The University of Queensland, Brisbane, 4072, Queensland, Australia; Orygen, The National Centre of Excellence in Youth Mental Health and Orygen Youth Health Research Centre, 35 Poplar Rd., Parkville, 3052, Australia.
Patrick D McGorryOrygen, The National Centre of Excellence in Youth Mental Health and Orygen Youth Health Research Centre, 35 Poplar Rd., Parkville, 3052, Australia; Centre of Youth Mental Health, University of Melbourne, 35 Poplar Rd., Parkville, 3052, Australia.
Christos PantelisUniversity of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia; Department of Human Genetics, National Institute of Mental Health and Neurosciences, Bangalore, India; Melbourne Neuropsychiatry Centre, The University of Melbourne & Melbourne Health, Parkville, 3052, Australia; Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, 30 Royal Parade, 3052, Parkville, Australia.
Michael BerkDeakin University, IMPACT Strategic Research Centre, School of Medicine, Barwon Health, P.O. Box 291, Geelong, 3220, Australia; University of Melbourne, Department of Psychiatry, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia; Queensland Centre for Mental Health Research, The Park Centre for Mental Health, Wacol, Queensland 4076, Australia; Orygen, The National Centre of Excellence in Youth Mental Health and Orygen Youth Health Research Centre, 35 Poplar Rd., Parkville, 3052, Australia; Centre of Youth Mental Health, University of Melbourne, 35 Poplar Rd., Parkville, 3052, Australia; Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, 30 Royal Parade, 3052, Parkville, Australia.

Funding

Biological Mechanisms of Enhanced Neuroplasticity in First-Episode SchizophreniaK01MH099431 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MCEWEN, SARAH CHRISTINE · 2012 to 2016
$829k
NIMH NIH HHS K01 MH099431
6 · The paper itself

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.

Indexed as

SchizophreniaEnvironmentGenetic Predisposition to DiseaseHumansPhenotypeRisk Factors

Identifiers

PMID27073049
PMCPMC4876729

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.