Heritability of children's prosocial behavior and differential susceptibility to parenting by variation in the dopamine receptor D4 gene
Abstract
Theoretical considerations and new empirical evidence suggest that children's development cannot simply be explained by either genes or environment but that their interaction is important to understanding child behavior. In particular, a genetic polymorphism, the exon III repeat region of the dopamine receptor D4, has been the focus of interest regarding differential susceptibility to parental influence. To study environmental and genetic influences on children's prosocial behavior, 168 twin pairs (mean age = 44 months) participated in an experiment that assessed prosocial behavior via three measures: compliant prosocial behavior elicited in response to social requests, self-initiated prosocial behavior enacted voluntarily, and mothers' rating of children's behavior. Genetic effects accounted for 34% to 53% of the variance in prosocial behavior. The rest of the variance was accounted for by nonshared environment and error. Parenting measures of maternal positivity, negativity, and unexplained punishment did not correlate significantly with children's prosocial behavior. However, when parenting was stratified by presence or absence of the child's dopamine receptor D4 7-repeat allele in an overlapping sample of 167 children to model differential susceptibility to parental influence, a richer picture emerged. Positive parenting related meaningfully to mother-rated prosocial behavior, and unexplained punishment related positively to self-initiated prosocial behavior, but only among children carrying the 7-repeat allele. The findings demonstrate that a molecular genetic strategy, based on genotyping of common polymorphisms and combined with a classic twin approach, provides a richer description of how genes and environment interact to shape children's behavior, and allows for the identification of differential sensitivity to parental influence.
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Parenting influences have been demonstrated to be moderated by individual differences in biological sensitivity, such as genetic phenotype and stress reactivity.
“Indeed, parenting influences have been demonstrated to be moderated by individual differences in biological sensitivity, such as genetic phenotype (Bakermans-Kranenburg and van Ijzendoorn, 2011, Knafo et al., 2011) and stress reactivity (Hastings et al., 2014).”
From Adolescent neurobiological susceptibility to social context (2016) · cites this paper as Knafo et al., 2011
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- Authors
- Knafo, A., Israel, S., & Ebstein, R. P.
- Affiliations
- National University of Singapore (SG)
- Venue
- Development and Psychopathology
- Publisher
- Cambridge University Press (CUP)
- Published
- 2011-01-24
- Volume
- 23
- Issue
- 1
- Pages
- 53-67
- ISSN
- 0954-5794 (ISSN-L)
- 1469-2198
- OpenAlex
- W2170207406
- Cited by
- 156
- References
- 105
- Citations by year
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- FWCI
- 19.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Development and Psychopathology (publishedVersion)
- PubMed (publishedVersion)
- National University of Singapore (submittedVersion)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Child and Adolescent Psychosocial and Emotional Development
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Developmental and Educational Psychology › Child and Animal Learning Development
- Keywords
- prosocial behavior, heritability, differential susceptibility, dopamine D4 receptor, 7-repeat allele, gene-environment interaction, parenting, positive parenting, nonshared environment, child behavior, twin pairs
- MeSH terms
- Alleles, Child Behavior, Child Development, Child, Preschool, Female, Heterozygote, Homozygote, Humans, Male, Polymorphism, Genetic, Punishment, Social Behavior, Parenting, Receptors, Dopamine D4
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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