Parent-child conflict as an etiological moderator of childhood conduct problems: an example of a 'bioecological' gene-environment interaction.
- Authors
- Burt, S A; Klump, K L
- Year
- 2014
- Journal
- Psychological medicine
- PMID
- 23746066
- DOI
- 10.1017/S0033291713001190
- PMCID
- PMC5798251
BACKGROUND: Prior research has suggested that, consistent with the diathesis-stress model of gene-environment interaction (G × E), parent-child conflict activates genetic influences on antisocial/externalizing behaviors during adolescence. It remains unclear, however, whether this model is also important during childhood, or whether the moderation of child conduct problems by negative/conflictive parenting is better characterized as a bioecological interaction, in which environmental influences are enhanced in the presence of environmental risk whereas genetic influences are expressed most strongly in their absence. The current study sought to distinguish between these possibilities, evaluating how the parent-child relationship moderates the etiology of childhood-onset conduct problems. METHOD: We conducted a series of 'latent G by measured E' interaction analyses, in which a measured environmental variable was allowed to moderate both genetic and environmental influences on child conduct problems. Participants included 500 child twin pairs from the Michigan State University Twin Registry (MSUTR). RESULTS: Shared environmental influences on conduct problems were found to be several-fold larger in those with high levels of parent-child conflict as compared with those with low levels. Genetic influences, by contrast, were proportionally more influential at lower levels of conflict than at higher levels. CONCLUSIONS: Our findings suggest that, although the diathesis-stress form of G × E appears to underlie the relationship between parenting and conduct problems during adolescence, this pattern of moderation does not extend to childhood. Instead, results were more consistent with the bioecological form of G × E which postulates that, in some cases, genetic influences may be most fully manifested in the absence of environmental risk.
(a) The extended univariate gene–environment interaction (G × E) model. (b) The bivariate G × E model. A, C and E represent genetic, shared environmental, and non-shared environmental influences, respectively. For ease of presentation, the co-twin variables and paths are omitted here, though they are estimated in the models. In model 1a (van der Sluis et al. 2012), the variance decomposition of Conduct Problems (CP) was modeled as a function of parent–child conflict (the moderator, M). To circumvent possible rGE confounds, the parent–child conflict values of both twins were entered in a means model of CP. Linear moderation was then modeled on the residual CP variance (i.e. that which does not overlap with parent–child conflict), separately for each component of variance (i.e. βxM, βYM and βZM for a, c and e paths, respectively). The non-linear moderators are not shown. In model 1b (Purcell, 2002), the moderator is entered twice: once as a variable that is allowed to correlate with the outcome and once as the moderator. AC and AU, respectively, represent genetic influences on CP held in common with the moderator and those unique to CP. Interactions with the moderator (e.g. βacM and βauM) are added to these common and unique genetic influences. Only the latter are thought to index ‘true’ G × E. The same interpretation holds for C and E effects.
Moderation of Diagnostic and Statistical Manual of Mental Disorders (DSM)-oriented Conduct Problems (CP) by parent–child conflict. (a) Full linear ACE moderation model, as reported in Tables 2 and 3. (b) Best-fitting linear C moderation-only model, as reported in Tables 2 and 3. A, C and E represent unstandardized genetic, shared, and non-shared environmental influences, respectively. These unstandardized estimates index absolute changes in genetic and environmental influences on CP with level of parent–child conflict. Of note, because variance is a second-order statistic, the linearity in the best-fitting linear model is at the level of effect rather than the level of variance component (Purcell, 2002); as a result, the variance components may appear to shift non-linearly even though the model itself is linear.
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| Title | Year | PMID |
|---|---|---|
| Genetic influences on conduct disorder. | 2018 | 27350097 |
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| Genetic influences on conduct disorder. | Salvatore JE et al. | — | 2018 | → |
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| Parental involvement as an etiological moderator of middle childhood oppositional defiant disorder. | Li I et al. | — | 2017 | → |
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| Genetic Influences on Peer and Family Relationships Across Adolescent Development: Introduction to the Special Issue. | Mullineaux PY et al. | — | 2015 | → |
| Parental involvement moderates etiological influences on attention deficit hyperactivity disorder behaviors in child twins. | Nikolas MA et al. | — | 2015 | → |
| The quality of the interparental relationship does not moderate the etiology of child conduct problems. | Burt SA et al. | — | 2015 | → |
| The etiology of the association between child antisocial behavior and maternal negativity varies across aggressive and non-aggressive rule-breaking forms of antisocial behavior. | Klahr AM et al. | — | 2014 | → |