Genetic amplification and the individualization of the parent-child relationship across adolescence

Abstract

Background: Many psychological traits become increasingly influenced by genetic factors throughout development, including several that might intuitively be seen as purely environmental characteristics. One such trait is the parent-child relationship, which is associated with a variety of socially significant outcomes, including mental health and criminal behavior. Genetic factors have been shown to partially underlie some of these associations, but the changing role of genetic influence over time remains poorly understood.

Method: Over 1000 participants in a longitudinal twin study were assessed at three points across adolescence with a self-report measure regarding the levels of warmth and conflict in their relationships with their parents. These reports were analyzed with a biometric growth curve model to identify changes in genetic and environmental influences over time.

Results: Genetic influence on the child-reported relationship with parent increased throughout adolescence, while the relationship's quality deteriorated. The increase in genetic influence resulted primarily from a positive association between genetic factors responsible for the initial relationship and those involved in change in the relationship over time. By contrast, environmental factors relating to change were negatively related to those involved in the initial relationship.

Conclusions: The increasing genetic influence seems to be due to early genetic influences having greater freedom of expression over time whereas environmental circumstances were decreasingly important to variance in the parent-child relationship. We infer that the parent-child relationship may become increasingly influenced by the particular characteristics of the child (many of which are genetically influenced), gradually displacing the effects of parental or societal ideas of child rearing.

Figure 1

Path-diagram of linear ACE growth curve model (for one individual) centered on age at initial assessment. Letters A, C, and E denote additive genetic, common environmental, and unique environmental effect, respectively. I and S denote level at baseline (intercept) and rate of change (slope), respectively, and R denotes the residual effect. Intercept-slope covariance is represented by the path connecting the A, C, and E intercept estimators and the slope.

Figure 2

Unstandardized Variance Components derived from Growth-Curve Model Note. Original unstandardized values of the biometric variance components derive from the parameter estimates from the growth curve model represented in Table 3. A = additive genetic component of variance; C = shared environmental; E = nonshared environmental; P= total phenotypic variance.

Figure 2

Unstandardized Variance Components derived from Growth-Curve Model Note. Original unstandardized values of the biometric variance components derive from the parameter estimates from the growth curve model represented in Table 3. A = additive genetic component of variance; C = shared environmental; E = nonshared environmental; P= total phenotypic variance.