Pediatric chronic pain is pervasive and associated with myriad adverse consequences, yet due consideration has not been given to the mental health disturbances that often present alongside chronic pain and the etiological mechanisms that potentially underlie both. The current study…
Pediatric chronic pain is pervasive and associated with myriad adverse consequences, yet due consideration has not been given to the mental health disturbances that often present alongside chronic pain and the etiological mechanisms that potentially underlie both. The current study examined the etiology underlying chronic pain and internalizing symptomology in middle childhood, considering both independent and co-occurring symptom presentations. Phenotypic parent-offspring associations across chronic pain and internalizing symptomology were also examined. Lastly, nuclear twin family models were tested to determine the extent to which genetic and environmental factors underlie parent-offspring transmission. The sample comprised 795 children (399 families; Mage= 9.7 years; SD = 0.92) and their parents drawn from the Arizona Twin Project. Results indicated that chronic pain was highly heritable (78%), whereas internalizing symptomology was modestly heritable (32%) and further subject to moderate shared environmental influence (50%). Moreover, 9% of the variance in chronic pain was explained by additive genetic factors shared with internalizing symptomology. Maternal chronic pain and internalizing symptomology were positively associated with both child chronic pain and internalizing symptomology. The association between maternal chronic pain and child chronic pain was more pronounced for girls than boys, whereas the association between maternal internalizing symptomology and child internalizing symptomology was more pronounced for boys than girls. Paternal chronic pain was not significantly associated with child chronic pain but was unexpectedly associated with lower child internalizing symptomology. The negative association between paternal chronic pain and child internalizing symptomology was more pronounced for boys than girls. Paternal internalizing symptomology was not significantly associated with child chronic pain but was positively associated with child internalizing symptomology. Lastly, the best fitting reduced nuclear twin family models for both chronic pain and internalizing symptomology retained additive genetic, sibling-specific shared environmental, and nonshared environmental parameters, where parent-offspring transmission was solely explained by shared genetics and sibling-specific shared environmental factors further accounted for co-twin resemblance. Results provide novel insight into common liabilities underlying chronic pain and internalizing symptomology in middle childhood, parent-offspring associations across chronic pain and internalizing symptomology, and the etiological mechanisms that explain symptom aggregation across generations.
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Prior research has established a relation between parenting behaviors and symptoms of child psychopathology, and this association may be influenced by both genetic and environmental factors. Gene-environment correlation, or the influence of a child’s genes on the environment they receive,…
Prior research has established a relation between parenting behaviors and symptoms of child psychopathology, and this association may be influenced by both genetic and environmental factors. Gene-environment correlation, or the influence of a child’s genes on the environment they receive, represents one possible mechanism through which genes and environment combine to influence child outcomes. This study examined evocative gene-environment correlation in the relation between parenting and symptoms of child psychopathology in a sample of 676 twins (51.5% female, 58.5% Caucasian, 23.7% Hispanic/Latinx, primarily middle class, MAge=8.43, SD=.62) recruited from Arizona birth records. Using univariate ACE twin biometric models, genetic influences were found to moderately contribute to internalizing symptoms (A=.47, C=.25, E=.28), while externalizing (A=.86, E=.14) and ADHD (A=.84, E=.16) symptoms were found to be highly heritable. The genetic influences for positive (C=.54, E=.46) and negative (C=.44, E=.56) parenting were smaller and found to be nonsignificant. The correlations between parenting and types of psychopathology were examined and bivariate Cholesky decompositions were conducted for statistically significant correlations. Negative parenting was moderately positively correlated with externalizing and ADHD symptoms; the relation between externalizing symptoms and negative parenting was found to be due to shared genetics, whereas the relation between negative parenting and ADHD symptoms was due to the shared environment. The mixed results regarding the role of gene environment correlation in relations between parenting and child psychopathology indicate that further research on the mechanisms of this relation is needed.
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The tendency for psychopathology to aggregate within families is well-documented, though little is known regarding the level of specificity at which familial transmission of symptomology occurs. The current study first tested competing higher-order structures of psychopathology in adolescence, indexing general…
The tendency for psychopathology to aggregate within families is well-documented, though little is known regarding the level of specificity at which familial transmission of symptomology occurs. The current study first tested competing higher-order structures of psychopathology in adolescence, indexing general and more specific latent factors. Second, parent-offspring transmission was tested for broadband domain specificity versus transmission of a general liability for psychopathology. Lastly, genetic and environmental mechanisms underlying the familial aggregation of psychopathology were examined using nuclear twin-family models. The sample was comprised of five hundred adolescent twin pairs (mean age 13.24 years) and their parents drawn from the Wisconsin Twin Project. Twins and parents completed independent diagnostic interviews. For aim 1, correlated factors, bifactor, and general-factor models were tested using adolescent symptom count data. For aim 2, structural equation modeling was used to determine whether broadband domain-specific transmission effects were necessary to capture parent-offspring resemblance in psychopathology above and beyond a general transmission effect indexed by the latent correlation between a parental internalizing factor and offspring P-factor. For aim 3, general factor models were fitted in both generations, and factor scores were subsequently extracted and used in nuclear twin-family model testing. Results indicated that the bifactor model exhibited the best fit to the adolescent data. Familial aggregation of psychopathology was sufficiently accounted for by the transmission of a general liability. Lastly, the best fitting reduced nuclear twin-family model indicated that additive genetic, sibling-specific shared environmental, and nonshared environmental influences contributed to general psychopathology. Parent-offspring transmission was accounted for by shared genetics only, whereas co-twin aggregation was additionally explained by sibling-specific shared environmental factors. Results provide novel insight into the specificity and etiology of the familial aggregation of psychopathology.
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Sibling interactions are natural contexts for learning about the appropriate expression of emotions. The emotionally charged nature of sibling interactions creates a convenient context to explore emotional reactivity and regulation. The purpose of this study was to examine the relations…
Sibling interactions are natural contexts for learning about the appropriate expression of emotions. The emotionally charged nature of sibling interactions creates a convenient context to explore emotional reactivity and regulation. The purpose of this study was to examine the relations among parent-reported sibling relationship quality, observed sibling prosocial and antisocial behaviors displayed when playing a competitive marble game, and children's emotions coded from videotape. The sample consisted of 58 twin children who are currently participating in the longitudinal Arizona Twin Project. Parents completed the Sibling Relationship Questionnaire online at 5 and 8 years. Additionally, a competitive marble game interaction between the siblings took place in the home at 8 years and was videotaped for objective coding of prosocial, antisocial, and control behavior. Facial expressions were also coded from videotape using Emotient FACET software across the marble game interaction. Three mean composites of emotion were created, including positive and negative emotional facial expressions. Results showed that parent reported warmth did not predict the occurrence of positive emotions during the sibling interaction. However, siblings with high conflict showed less fear during the interaction. Parent reports of warmth predicted the extent to which siblings differed on emotion expression, however conflict did not. Parent ratings of conflict and warmth did not predict the extent to which the sibling dyad was emotionally intense. Findings regarding genetic and environmental effects were in line with previous reports of genetic influence on prosocial behavior and negative emotion, and expressions of joy being influenced by the environment. This study investigated noteworthy aspects of the sibling relationship that appear to promote children's adaptive development.
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