Evidence map›Paper›PMID 28696435›Full record

ArticleMolecular psychiatry2018

A direct test of the diathesis-stress model for depression.

L Colodro-Conde, B Couvy-Duchesne, G Zhu, W L Coventry, E M Byrne, S Gordon, M J Wright, G W Montgomery, P A F Madden, Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 7 pooled it
18.4field-weighted citation impact, top 1% of its field
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

138 citing papers in PubMed, 7 syntheses or guidelines pooled it, 286 citations in OpenAlex.

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78 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

16 authors at 6 institutions in 3 countries.

L Colodro-CondeDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia. Lucia.ColodroConde@qimrberghofer.edu.au.
B Couvy-DuchesneDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
G ZhuDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
W L CoventrySchool of Behavioural and Social Sciences, University of New England, Armidale, NSW, Australia.
E M ByrneInstitute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.
S GordonDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
M J WrightQueensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia.
G W MontgomeryInstitute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.
P A F MaddenDepartment of Psychiatry, Washington University School of Medicine, St Louis, MO, USA.
Major Depressive Disorder Working Group of the Psychiatric Genomics Consortium
S RipkeAnalytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA.
L J EavesVirginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA, USA.
A C HeathDepartment of Psychiatry, Washington University School of Medicine, St Louis, MO, USA.
N R WrayQueensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia.
S E MedlandDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
N G MartinDepartment of Genetics and Computational Biology, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
QIMR Berghofer Medical Research Institute · AUUniversity of Queensland · AUWashington University in St. Louis · USMassachusetts General Hospital · USUniversity of New England · AUVirginia Commonwealth University · US

Funding

Molecular Epidemiology of Alcoholism 3 - EDAC FamiliesR01AA013321 · NIAAA · WASHINGTON UNIVERSITY · PI HEATH, ANDREW C. · 2001 to 2005
$4.3M
Genetic Epideniologic Models of Alcohol AbuseR37AA007728 · NIAAA · WASHINGTON UNIVERSITY · PI HEATH, ANDREW C. · 1998 to 2007
$2.2M
Molecular Epidemiology of Alcoholism 1: Candidate GeneR01AA013326 · NIAAA · QUEENSLAND INSTITUTE OF MEDICAL RESEARCH · PI MARTIN, NICHOLAS G · 2001 to 2005
$2.1M
PERSISTENCE &CHANGE IN DRINKING HABITS: TWIN STUDYR01AA007535 · NIAAA · WASHINGTON UNIVERSITY · PI HEATH, ANDREW C. · 1989 to 1996
–
PERSISTENCE AND CHANGE IN DRINKING HABITS--PROJECT TWOR01AA010249 · NIAAA · WASHINGTON UNIVERSITY · PI HEATH, ANDREW C. · 1995 to 1998
–
NIAAA NIH HHS R01 AA007535NIAAA NIH HHS R01 AA010249NIAAA NIH HHS R01 AA013321NIAAA NIH HHS R01 AA013326NIAAA NIH HHS R37 AA007728
6 · The paper itself

Abstract

The diathesis-stress theory for depression states that the effects of stress on the depression risk are dependent on the diathesis or vulnerability, implying multiplicative interactive effects on the liability scale. We used polygenic risk scores for major depressive disorder (MDD) calculated from the results of the most recent analysis from the Psychiatric Genomics Consortium as a direct measure of the vulnerability for depression in a sample of 5221 individuals from 3083 families. In the same we also had measures of stressful life events and social support and a depression symptom score, as well as DSM-IV MDD diagnoses for most individuals. In order to estimate the variance in depression explained by the genetic vulnerability, the stressors and their interactions, we fitted linear mixed models controlling for relatedness for the whole sample as well as stratified by sex. We show a significant interaction of the polygenic risk scores with personal life events (0.12% of variance explained, P-value=0.0076) contributing positively to the risk of depression. Additionally, our results suggest possible differences in the aetiology of depression between women and men. In conclusion, our findings point to an extra risk for individuals with combined vulnerability and high number of reported personal life events beyond what would be expected from the additive contributions of these factors to the liability for depression, supporting the multiplicative diathesis-stress model for this disease.

Indexed as

AdultDepressionDisease SusceptibilityFemaleGene-Environment InteractionGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLife Change EventsMajor Depressive DisorderMaleMiddle AgedMultifactorial InheritanceRisk Factors

Identifiers

PMID28696435
PMCPMC5764823
OpenAlexW2735059498

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.