An application of the Biobehavioral Family Model: Examining the impact of maternal depression on child asthma mediated by insecure attachment and child depression.

OBJECTIVE: Child asthma disparities are prevalent in socio-economically stressed single-parent families. Stress impacts childhood asthma mediated by immune and autonomic pathways, but specific family stress pathways are not well established. This study tests the hypothesis, derived from a version of the Biobehavioral Family Model, that single parent maternal depression impacts child asthma mediated by insecure attachment and child depression. METHODS: In a cross-sectional study, children with asthma (age 7-17 years old) from a socio-economically disadvantaged population and their single parent mothers (N = 202) were assessed for depression and attachment security. Child asthma disease activity was assessed by symptom report and lung function tests. Structural equation modeling (SEM) was used to test a model in which caregiver depression impacts child asthma disease activity mediated by insecure attachment and child depression. RESULTS: SEM results indicated that maternal depression statistically predicted child depression (ß = 0.21, p < 0.01) and insecure mother-child attachment (ß = 0.17, p < 0.05). In addition, insecure attachment statistically predicted child depression (ß = 0.50, p < 0.001). Child depression mediated the adverse effects of maternal depression and insecure attachment on child asthma disease activity (ß = 0.43, p < 0.01). There was no direct effect of insecure attachment on child asthma. CONCLUSION: In single-parent families, maternal depression may impact child asthma disease activity, mediated serially by insecure attachment and child depression. Longitudinal and/or intervention studies are needed to establish a causal effect. These findings suggest that caregiver depression and parent-child relationships may be important targets for family intervention. These interventions may help improve child asthma outcomes and reduce health disparities.

Effects of paternal and maternal depressive symptoms on child internalizing symptoms and asthma disease activity: mediation by interparental negativity and parenting.

This study tested a hypothesized model of the relationships among parental depressive symptoms, family process (interparental negativity and negative parenting behavior), child internalizing symptoms, and asthma disease activity. A total of 106 children with asthma, aged 7 to 17, participated with their fathers and mothers. Parental depressive symptoms were assessed by self-report. Interparental and parenting behaviors were observed and rated during family discussion tasks. Child internalizing symptoms were assessed by self-report and by clinician interview and rating. Asthma disease activity was assessed according to National Heart, Lung and Blood Institute guidelines. Results of structural equation modeling generally supported interparental negativity and negative parenting behavior as mediators linking parental depressive symptoms and child emotional and physical dysfunction. However, paternal and maternal depressive symptoms play their role through different pathways of negative family process. (PsycINFO Database Record (c) 2011 APA, all rights reserved).

Depressed children with asthma evidence increased airway resistance: "vagal bias" as a mechanism?

BACKGROUND: Depression is prevalent in pediatric asthma, and implicated in asthma morbidity and mortality. Pathways linking stress, depression, and asthma are unknown. OBJECTIVES: To examine, under controlled laboratory conditions, pathways by which depressive states affect airway function via autonomic dysregulation. METHODS: Participants were 171 children with asthma, age 7 to 17 years, presenting to an emergency department for asthma exacerbation. Forty-five children with asthma and high depressive symptoms (D) were contrasted with 45 with low/no depressive symptoms (ND). Depressive symptoms, asthma disease severity, vagal and sympathetic reactivity to film stressors, airflow (FEV1), and airway resistance were compared between the groups. A subgroup with greater airway reactivity (nonmedicated FEV1<80% predicted) was also studied. Correlations among variables were examined for the entire sample. RESULTS: Groups did not differ in demographics, disease severity, medications, or adherence. The D group with FEV1<80% predicted showed greater airway resistance throughout all conditions (P = .03), and vagal bias in the film stressors. The D group's vagal response was significant for the sad stimuli: family distress/loss (P = .03), dying (P = .003), and death (P = .03). The ND group showed sympathetic activation to sad stimuli: lonely (P = .04) and dying (P = .04). Depressive symptoms were correlated with respiratory resistance (r = .43; P = .001) and vagal bias in scene 3 (r = .24; P = .03), and vagal bias (scene 3) was correlated with postmovie airway resistance (r = 0.39; P = .004). CONCLUSIONS: Children with asthma and depressive symptoms manifest vagal bias when emotionally stressed. Those with depressive symptoms and FEV1<80% manifest greater airway resistance. Depression, vagal bias, and airway resistance were intercorrelated for the full sample.

Testing the Biobehavioral Family Model in pediatric asthma: pathways of effect.

This study uses a laboratory-based multiinformant, multimethod approach to test the hypothesis that a negative family emotional climate (NFEC) contributes to asthma disease severity by way of child depressive symptoms, and that parent-child relational insecurity mediates the effect. Children with asthma (n = 199; aged 7-17; 55% male) reported parental conflict, parent-child relational security, and depressive symptoms. Parent(s) reported demographics, asthma history, and symptoms. Asthma diagnosis was confirmed by clinical evaluation and pulmonary function tests, with disease severity rated by an asthma clinician according to NHLBI guidelines. Family interactions were evoked using the Family Process Assessment Protocol, and rated using the Iowa Family Interaction Rating Scales. Path analysis indicated a good fit of data to the hypothesized model (chi2[1] = .11, p =.74, NFI = .99, RMSEA = .00). Observed NFEC predicted child depression (beta = .19, p < .01), which predicted asthma disease severity beta = .23, p < .01). Relational security inversely predicted depressive symptoms (p = -.40, p < .001), and was not a mediator as predicted, but rather an independent contributor. The findings are consistent with the Biobehavioral Family Model, which suggests a psychobiologic influence of specific family relational processes on asthma disease severity by way of child depressive symptoms.

Maternal depression and parenting in relation to child internalizing symptoms and asthma disease activity.

This study tested a hypothesized model of the relationship between maternal depression and child psychological and physical dysfunction mediated by parenting and medication adherence. A sample of 242 children with asthma, aged 7 to 17, participated with their mothers. Maternal depression was assessed by self-report, and parenting was observed during family interaction tasks. Internalizing symptoms were assessed by self- and clinician reports. Asthma disease activity was assessed according to National Heart Lung and Blood Institute guidelines, and medication adherence was evaluated with a 24-hr recall method. Structural equation modeling indicated that negative parenting partially mediated the relationship between maternal depression and child internalizing symptoms. Child internalizing symptoms, in turn, mediated the associations between both maternal depression and negative parenting and asthma disease activity. Medication adherence did not mediate the link from maternal depression to disease activity. Thus, maternal depression was linked to child psychological dysfunction both directly and indirectly via negative parenting but linked to physical dysfunction only indirectly through psychological dysfunction. These findings suggest that diagnosing and treating depression in mothers of children with asthma would enhance child well-being both psychologically and physically.

Reliability and validity of the Asthma Trigger Inventory applied to a pediatric population.

OBJECTIVE: To test the reliability and validity of the Asthma Trigger Inventory (ATI) applied to a pediatric population. METHOD: Children with asthma (N = 272, 56% male, age 7-17) and their primary caregivers answered together an asthma trigger inventory, ATI (Ritz, Steptoe, Bobb, Harris, & Edwards, 2006) developed for adults. Cronbach's alpha, principal component analysis (PCA), hierarchical regression, and correlations of the ATI subscales with skin prick tests, psychological questionnaires, and disease severity were used to assess the psychometric properties of the ATI. RESULTS: The ATI subscales demonstrated excellent reliability regardless of gender, race, socioeconomic status (SES), or age. PCA confirmed and replicated the theoretical structure of the ATI. Hierarchical multiple regressions illuminated the association of ATI subscales with demographics and asthma history. Evidence in support of construct validity was found in associations between ratings of triggering and disease severity and asthma-related quality of life (PAQLQ). Criterion validity for allergy triggering was partially supported by correlations between ATI animal allergens subscale and the cat dander skin prick test, and construct validity for emotional triggering by associations between the emotional trigger subscale score and the anxiety (STAIC) and depression (CDI, CDI-P, CDRS-R, and CBCL-I) scores. CONCLUSION: The ATI holds promise as a reliable, valid, and useful clinical and research tool to assess the type and degree of asthma triggering in a pediatric population (age 7-17) of varied gender, race, and SES.

Family emotional climate, depression, emotional triggering of asthma, and disease severity in pediatric asthma: examination of pathways of effect.

OBJECTIVES: (a) To assess emotional triggering of pediatric asthma and ascertain its contribution to disease morbidity and functional status; (b) to test whether negative family emotional climate (NFEQ) is associated with depressive and/or anxious symptoms and emotional triggering of asthma attacks in the child. METHOD: Children with asthma (N = 272, 56% male, age 7-17) and their primary caregivers answered together an Asthma Trigger Inventory (Ritz, Steptoe, Bobb, Harris, & Edwards, 2006). Children reported on anxious (STAIC) and depressive (CDI) symptoms and on asthma-related quality of life (PAQLQ). Parent(s) reported on their child's internalizing (CBCL-I) and depressive symptoms (CDI-P). A clinician also rated the child's depression using the structured CDRS-R. Asthma diagnosis was confirmed and disease severity rated according to NHLBI guidelines by an asthma clinician. RESULTS: Path analyses indicated that NFEQ was associated with depressive symptoms, which in turn were associated both directly and indirectly (by way of emotional triggering) with disease severity. Comparison of nested models indicated the possibility of differential roles and pathways for anxious versus depressive symptoms. CONCLUSION: Findings elucidate possible pathways of effect by which family emotional climate and child depressive symptoms may influence pediatric asthma disease severity by way of potentiating emotional triggering of asthma.

Family relational factors in pediatric depression and asthma: pathways of effect.

OBJECTIVE: This study tested a multilevel biobehavioral family model proposing that negative family emotional climate contributes to child depressive symptoms, which in turn contribute to asthma disease severity. Parent-child relational insecurity is proposed as a mediator. METHOD: Children with asthma (N = 112; ages 7-18; 55% male) reported relational security, anxiety, and depressive symptoms. Parent(s) reported demographics, asthma history and symptoms, and family emotional expression. Asthma diagnosis was confirmed by medical history provided by parent and child together, clinical evaluation, pulmonary function tests, and methacholine challenge, with disease severity categorized by National Heart, Lung, and Blood Institute guidelines. Medication adherence was measured prospectively. RESULTS: Path analysis indicated a good fit of data to the hypothesized model (chi2 = 0.072, p =.97, normal fit index = 0.998, root mean square error of approximation = 0.000). Negative family emotional climate predicted child depressive symptoms (beta =.21, p < .04), which predicted asthma disease severity (beta =.35, p < .001), with relational insecurity a partial mediator (beta = -.23, p < .05, beta =.46, p < .001, respectively). Depression was associated with disease severity even after controlling for adherence (r p = 0.38, p < .05). CONCLUSION: Findings are consistent with the proposed family model, suggesting the clinical importance of assessing and intervening in these specific family relational processes when treating children with depression and asthma.