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Awareness of adult separation anxiety (ASA) is growing, but there is a dearth of knowledge about how separation anxiety aggregates in families. We examined the intergenerational associations of separation anxiety and other forms of internalizing problems in an American community sample of 515 predominantly white children and their parents.
Children's separation anxiety (CSA), depression, and other anxiety disorders were modeled as latent factors using diagnoses from interviews and symptom scores from questionnaires completed by mothers, fathers, and children when children were 9 years old and again 3 years later. Parents' separation anxiety was assessed via a questionnaire and parents' other anxiety, depressive, and substance use disorders were assessed with a diagnostic interview when children were nine. Relationships between parents' and children's psychopathology were modeled using s.e.m.
Mothers' and fathers' ASA were related to all three psychopathology factors in offspring, over and above other parental disorders, in concurrent and prospective analyses. CSA was also related to maternal depression concurrently and prospectively and to maternal anxiety prospectively. Of all paternal psychopathology variables, only ASA was significantly related to children's psychopathology in either model.
Results indicate that parental separation anxiety is an important, but non-specific, risk factor for children's psychopathology. The pathway by which this risk is transmitted may be genetic or environmental, and the observed statistical associations likely also encompass child-to-parent effects.
In this article, we consider an often overlooked model that combines mediation and moderation to explain how a third variable can relate to a risk factor–psychopathology relationship. We refer to it as moderation and mediation in a three-variable system. We describe how this model is relevant to studying vulnerability factors and how it may advance developmental psychopathology research. To illustrate the value of this approach, we provide several examples where this model may be applicable, such as the relationships among parental externalizing pathology, harsh parenting, and offspring psychopathology as well as between neuroticism, stressful life events, and depression. We discuss possible reasons why this model has not gained traction and attempt to clarify and dispel those concerns. We provide guidance and recommendations for when to consider this model for a given data set and point toward existing resources for testing this model that have been developed by statisticians and other methodologists. Lastly, we describe important caveats, limitations, and considerations for making this approach most useful for developmental research. Overall, our goal in presenting this information to developmental psychopathology researchers is to encourage testing moderation and mediation in a three-variable system with the aim of advancing analytic strategies for studying vulnerability factors.
Social anhedonia is well established as a transdiagnostic factor, but little is known about its development. This study examined whether temperament and parenting in early childhood predict social anhedonia in early adolescence. We also explored whether the relationships between early predictors and social anhedonia are moderated by a child's sex. A community sample of children participated in laboratory observations of temperament and parenting practices at age 3 (n = 275). The participants returned at age 12 and completed the Anticipatory and Consummatory Interpersonal Pleasure Scale–Child Version (ACIPS-C). Our results indicated that, at age 3, lower observed sociability predicted higher levels of social anhedonia at age 12. These associations were moderated by child sex, such that males with diminished sociability reported greater social anhedonia. These findings indicate that predictors of early adolescent social anhedonia are evident as early as 3 years of age. However, these effects were evident only for males, suggesting that the pathways to social anhedonia in early adolescence differ as a function of sex.
There is an emerging consensus in developmental psychopathology that irritable youth are at risk for developing internalizing problems later in life. The current study explored if irritability in youth is multifactorial and the impact of irritability dimensions on psychopathology outcomes in adulthood.
We conducted exploratory factor analysis on irritability symptom items from a semi-structured diagnostic interview administered to a community sample of adolescents (ages 14–19; 42.7% male; 89.1% white). The analysis identified two factors corresponding to items from the mood disorders v. the oppositional defiant disorder (ODD) (Leibenluft and Stoddard) sections of the interview. These factors were then entered together into regression models predicting psychopathology assessed at age 24 (N = 941) and again at age 30 (N = 816). All models controlled for concurrent psychopathology in youth.
The two irritability dimensions demonstrated different patterns of prospective relationships, with items from the ODD section primarily predicting externalizing psychopathology, items from the mood disorder sections predicting depression at age 24 but not 30, and both dimensions predicting borderline personality disorder symptoms.
These results suggest that the current standard of extracting and compositing irritability symptom items from diagnostic interviews masks distinct dimensions of irritability with different psychopathological outcomes. Additionally, these findings add nuance to the prevailing notion that irritability in youth is specifically linked to later internalizing problems. Further investigation using more sensitive and multifaceted measures of irritability are needed to parse the meaning and clinical implications of these dimensions.
Reward processing deficits have been implicated in the etiology of depression. A blunted reward positivity (RewP), an event-related potential elicited by feedback to monetary gain relative to loss, predicts new onsets and increases in depression symptoms. Etiological models of depression also highlight stressful life events. However, no studies have examined whether stressful life events moderate the effect of the RewP on subsequent depression symptoms. We examined this question during the key developmental transition from childhood to adolescence.
A community sample of 369 children (mean age of 9) completed a self-report measure of depression symptoms. The RewP to winning v. losing was elicited using a monetary reward task. Three years later, we assessed stressful life events occurring in the year prior to the follow-up. Youth depressive symptoms were rated by the children and their parents at baseline and follow-up.
Stressful life events moderated the effect of the RewP on depression symptoms at follow-up such that a blunted RewP predicted higher depression symptoms in individuals with higher levels of stressful life events. This effect was also evident when events that were independent of the youth's behavior were examined separately.
These results suggest that the RewP reflects a vulnerability for depression that is activated by stress.
Many preschool-age children meet criteria for psychiatric disorders, and rates approach those observed in later childhood and adolescence. However, there is a paucity of longitudinal research examining the outcomes of preschool diagnoses.
Families with a 3-year-old child (N = 559) were recruited from the community. Primary caregivers were interviewed using the Preschool Age Psychiatric Assessment when children were 3 years old (n = 541), and, along with children, using the Schedule for Affective Disorders and Schizophrenia for School-Age Children Present and Lifetime Version when children were 9 and 12 years old.
Rates of disruptive behavior disorders (DBD) decreased from preschool to middle childhood and early adolescence, whereas rates of attention-deficit/hyperactivity disorder (ADHD) increased. Rates of any psychiatric disorder and depression increased from preschool to early adolescence only. Preschoolers with a diagnosis were over twice as likely to have a diagnosis during later periods. Homotypic continuity was present for anxiety disorders from preschool to middle childhood, for ADHD from preschool to early adolescence, and for DBD through both later time points. There was heterotypic continuity between preschool anxiety and early adolescent depression, and between preschool ADHD and early adolescent DBD. Dimensional symptom scores showed homotypic continuity for all diagnostic categories and showed a number of heterotypic associations as well.
Results provide moderate support for the predictive validity of psychiatric disorders in preschoolers. Psychopathology in preschool is a significant risk factor for future psychiatric disorders during middle childhood and early adolescence.
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