Evidence map›Paper›PMID 26666206›Full record

ArticleMolecular psychiatry2016

Genetic and environmental determinants of violence risk in psychotic disorders: a multivariate quantitative genetic study of 1.8 million Swedish twins and siblings.

A Sariaslan, H Larsson, S Fazel

Abstract read
In one paragraph

Article in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Risk factors for interpersonal violence: an umbrella review of meta-analyses.The British journal of psychiatry : the journal of mental science · 2018
    Pooled it
  3. Article
  4. Improving risk assessment in forensic mental health: Temporal validation and clinical refinement of the FoVOx risk tool.European psychiatry : the journal of the Association of European Psychiatrists · 2026
    Article
  5. Aberrant deaths: a conundrum in domestic homicide reviews.Psychiatry, psychology, and law : an interdisciplinary journal of the Australian and New Zealand Association of Psychiatry, Psychology and Law · 2026
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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

3 authors.

A SariaslanDepartment of Psychiatry, Warneford Hospital, University of Oxford, Oxford, UK.ORCID 0000-0002-6151-3278
H LarssonDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
S FazelDepartment of Psychiatry, Warneford Hospital, University of Oxford, Oxford, UK.

Funding

Quasi-experimental studies of early risk factors for severe psychopathologyR01HD061817 · NICHD · TRUSTEES OF INDIANA UNIVERSITY · PI D'ONOFRIO, BRIAN M, LICHTENSTEIN, PAUL · 2010 to 2013
$1.3M
NICHD NIH HHS R01 HD061817Wellcome Trust 095806
6 · The paper itself

Abstract

Patients diagnosed with psychotic disorders (for example, schizophrenia and bipolar disorder) have elevated risks of committing violent acts, particularly if they are comorbid with substance misuse. Despite recent insights from quantitative and molecular genetic studies demonstrating considerable pleiotropy in the genetic architecture of these phenotypes, there is currently a lack of large-scale studies that have specifically examined the aetiological links between psychotic disorders and violence. Using a sample of all Swedish individuals born between 1958 and 1989 (n=3 332 101), we identified a total of 923 259 twin-sibling pairs. Patients were identified using the National Patient Register using validated algorithms based on International Classification of Diseases (ICD) 8-10. Univariate quantitative genetic models revealed that all phenotypes (schizophrenia, bipolar disorder, substance misuse, and violent crime) were highly heritable (h(2)=53-71%). Multivariate models further revealed that schizophrenia was a stronger predictor of violence (r=0.32; 95% confidence interval: 0.30-0.33) than bipolar disorder (r=0.23; 0.21-0.25), and large proportions (51-67%) of these phenotypic correlations were explained by genetic factors shared between each disorder, substance misuse, and violence. Importantly, we found that genetic influences that were unrelated to substance misuse explained approximately a fifth (21%; 20-22%) of the correlation with violent criminality in bipolar disorder but none of the same correlation in schizophrenia (Pbipolar disorder<0.001; Pschizophrenia=0.55). These findings highlight the problems of not disentangling common and unique sources of covariance across genetically similar phenotypes as the latter sources may include aetiologically important clues. Clinically, these findings underline the importance of assessing risk of different phenotypes together and integrating interventions for psychiatric disorders, substance misuse, and violence.

Indexed as

AdultBipolar DisorderComorbidityFemaleGenetic Predisposition to DiseaseHumansMaleMultivariate AnalysisPsychotic DisordersRegistriesRisk FactorsSchizophreniaSiblingsSubstance-Related DisordersSwedenTwins

Identifiers

PMID26666206
PMCPMC4842006

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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.