Elsevier

Journal of Anxiety Disorders

Volume 13, Issue 4, July–August 1999, Pages 371-397
Journal of Anxiety Disorders

Genetic and Environmental Influences on Ratings of Manifest Anxiety by Parents and Children

https://doi.org/10.1016/S0887-6185(99)00011-0Get rights and content

Abstract

Parental reports and children's self-reports of manifest anxiety were obtained from a community-based sample of twin pairs on two occasions approximately 19 months apart, using the Revised Child Manifest Anxiety Scale (Reynolds & Richmond, 1978). In prior cross-sectional studies, a low degree of agreement between parent and child assessments of anxiety was found. Furthermore, parental reports were found to reflect a higher heritability than children's self-reports Eaves et al. 1997, Thapar and McGuffin 1995. The index of temporal stability was moderate for all informants (circa r = .5 to r = .6). To test whether the components contributing to the temporal stability differed between the informants, structural equation models were fitted to the data using the program, Mx: Statistical Modeling (Neale, 1995). The results showed substantial differences in genetic effects according to both gender and informant. For children's self-reports, temporal stability was largely a function of environmental effects, with genetic effects contributing a modest 20%, whereas for parental reports, temporal stability was largely a function of genetic effects. The heritability was higher for parental reports than for boys' self-reports and the genetic covariance between parents and their sons was near zero, indicating that they were reporting on quite different aspects of anxiety. However, for girls, heritability for maternal reports was lower than for self-reports, and the genetic covariance between mother and daughter was about the same as that between mothers and fathers, meaning that they were assessing the same genetically influenced aspect of anxiety. These results highlight the need to focus on gender differences.

Section snippets

Background studies

Evidence of a genetic liability in the development of anxiety disorders has come from studies on both animal and human populations. Indeed, some of the earliest behavioral genetic research with rodents focused on emotional reactivity to stressful situations Broadhurst 1960, DeFries, Hegmann, & Weir 1966. This research led to the development of selected lines of rats (Broadhurst, 1960) and inbred stains of mice that are either reactive or nonreactive in open field stressful situations (DeFries,

Hypotheses and predictions

The accumulated evidence from the cross-sectional studies described above suggest that assessments of vulnerability to anxiety in adolescence reflect genetic variation in liability to a greater extent when parents report on their children than when children report on themselves. In the latter case, environmental circumstances may be more influential; in as much as these are environmental influences shared by siblings, there is some evidence that these are more important for boys than girls. In

Sample

In the 1987/1988 school year, all possible twin pairs known to the public school system of the Commonwealth of Virginia were identified. In the subsequent year, all private schools in Virginia were canvassed. This procedure yielded a target population of 3,264 twin pairs born between 1974 and 1982, who were then solicited via a brief questionnaire to participate in a longitudinal study of adolescent behavior development. Eighty-six percent of the target families responded to this brief request

Results

Descriptive statistics were computed using the SAS Univariate program (SAS Institute Inc., 1990) to determine if the distribution of manifest anxiety scores met the assumption of multivariate normality. The distribution of scores varied somewhat, dependent upon the informant; however, all variables showed evidence of being positively skewed. Scores were therefore subjected to a natural log transformation, which improved their approximation to normality.

The intra-rater Pearson correlations and

Model fitting to estimate genetic and environmental parameters

As a first step, a phenotypic Cholesky decomposition model was fitted to the data to provide a baseline for comparison to a full genetic and environmental (ACE) model. In brief, this provides a means of subdividing the variance according to a set of possible influences (see Neale & Cardon, 1992, for details of the rationale and procedures). For each twin there was up to six observed scores: a child self-report, maternal report, and paternal report on each of two occasions. Thus, for each twin

Discussion

The empirical findings showed differences in the genetic effects according to both gender and informant. The pattern of genetic and environmental variation supported the hypothesis that boys were self-reporting a more environmentally influenced aspect of anxiety. This was reflected in the fact that shared and nonshared environmental influences accounted for 80 to 90% of variation observed in these data for children's self-reports. However, the prediction that this would result in children's

Acknowledgements

This work makes use of the data derived from the Virginia Twin Study of Adolescent Behavioral Development, which is supported by grant no. MH-45268. Lindon J. Eaves, D.Sc. is the principal investigator of this study.

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