Evidence map›Paper›PMID 25522433›Full record

ArticleThe international journal of neuropsychopharmacology2014

Genotypes do not confer risk for delinquency but rather alter susceptibility to positive and negative environmental factors: gene-environmentinteractions of BDNF Val66Met, 5-HTTLPR, and MAOA-uVNTR [corrected].

Kent W Nilsson, Erika Comasco, Sheilagh Hodgins, Lars Oreland, Cecilia Åslund

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The international journal of neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Differential susceptibility effects of theFrontiers in psychiatry · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Personality as an intermediate phenotype for genetic dissection of alcohol use disorder.Journal of neural transmission (Vienna, Austria : 1996) · 2018
    Review
  15. Article
  16. Review
  17. Article
  18. New Clinically Relevant Findings about Violence by People with Schizophrenia.Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2017
    Review
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Kent W NilssonCentre for Clinical Research, Uppsala University, County Hospital, S-721 89 Västerås, Sweden (Drs Nilsson and Åslund); Department of Neuroscience, Uppsala University, BMC, Box 593 S-751 24 Uppsala, Sweden (Drs Comasco and Oreland); Karolinska Institutet, Stockholm Sweden, and Département de Psychiatrie, Université de Montréal, Montréal, Canada (Dr Hodgins). kent.nilsson@ltv.se.
Erika ComascoCentre for Clinical Research, Uppsala University, County Hospital, S-721 89 Västerås, Sweden (Drs Nilsson and Åslund); Department of Neuroscience, Uppsala University, BMC, Box 593 S-751 24 Uppsala, Sweden (Drs Comasco and Oreland); Karolinska Institutet, Stockholm Sweden, and Département de Psychiatrie, Université de Montréal, Montréal, Canada (Dr Hodgins).
Sheilagh HodginsCentre for Clinical Research, Uppsala University, County Hospital, S-721 89 Västerås, Sweden (Drs Nilsson and Åslund); Department of Neuroscience, Uppsala University, BMC, Box 593 S-751 24 Uppsala, Sweden (Drs Comasco and Oreland); Karolinska Institutet, Stockholm Sweden, and Département de Psychiatrie, Université de Montréal, Montréal, Canada (Dr Hodgins).
Lars OrelandCentre for Clinical Research, Uppsala University, County Hospital, S-721 89 Västerås, Sweden (Drs Nilsson and Åslund); Department of Neuroscience, Uppsala University, BMC, Box 593 S-751 24 Uppsala, Sweden (Drs Comasco and Oreland); Karolinska Institutet, Stockholm Sweden, and Département de Psychiatrie, Université de Montréal, Montréal, Canada (Dr Hodgins).
Cecilia ÅslundCentre for Clinical Research, Uppsala University, County Hospital, S-721 89 Västerås, Sweden (Drs Nilsson and Åslund); Department of Neuroscience, Uppsala University, BMC, Box 593 S-751 24 Uppsala, Sweden (Drs Comasco and Oreland); Karolinska Institutet, Stockholm Sweden, and Département de Psychiatrie, Université de Montréal, Montréal, Canada (Dr Hodgins).

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious evidence of gene-by-environment interactions associated with emotional and behavioral disorders is contradictory. Differences in findings may result from variation in valence and dose of the environmental factor, and/or failure to take account of gene-by-gene interactions. The present study investigated interactions between the brain-derived neurotrophic factor gene (BDNF Val66Met), the serotonin transporter gene-linked polymorphic region (5-HTTLPR), the monoamine oxidase A (MAOA-uVNTR) polymorphisms, family conflict, sexual abuse, the quality of the child-parent relationship, and teenage delinquency.

methodsIn 2006, as part of the Survey of Adolescent Life in Västmanland, Sweden, 1 337 high-school students, aged 17-18 years, anonymously completed questionnaires and provided saliva samples for DNA analyses.

resultsTeenage delinquency was associated with two-, three-, and four-way interactions of each of the genotypes and the three environmental factors. Significant four-way interactions were found for BDNF Val66Met × 5-HTTLPR×MAOA-uVNTR × family conflicts and for BDNF Val66Met × 5-HTTLPR×MAOA-uVNTR × sexual abuse. Further, the two genotype combinations that differed the most in expression levels (BDNF Val66Met Val, 5-HTTLPR LL, MAOA-uVNTR LL [girls] and L [boys] vs BDNF Val66Met Val/Met, 5-HTTLPR S/LS, MAOA-uVNTR S/SS/LS) in interaction with family conflict and sexual abuse were associated with the highest delinquency scores. The genetic variants previously shown to confer vulnerability for delinquency (BDNF Val66Met Val/Met × 5-HTTLPR S × MAOA-uVNTR S) were associated with the lowest delinquency scores in interaction with a positive child-parent relationship.

conclusionsFunctional variants of the MAOA-uVNTR, 5-HTTLPR, and BDNF Val66Met, either alone or in interaction with each other, may be best conceptualized as modifying sensitivity to environmental factors that confer either risk or protection for teenage delinquency.

Indexed as

Gene-Environment InteractionGenetic VariationAdolescentBrain-Derived Neurotrophic FactorChild Abuse, SexualEpistasis, GeneticFamily ConflictFemaleGenotypeHumansJuvenile DelinquencyMaleMonoamine OxidaseParent-Child RelationsPolymorphism, Single NucleotideRisk FactorsBDNF protein, humanBrain-Derived Neurotrophic FactorMonoamine Oxidasemonoamine oxidase A, humanSerotonin Plasma Membrane Transport ProteinsSLC6A4 protein, humanbrain-derived neurotrophic factorgene-environment interactionjuvenile delinquencymonoamine oxidaseserotonin plasma membrane transport proteins

Identifiers

PMID25522433
PMCPMC4376552

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Registered trials

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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.