Parent psychological states predict changes in inflammatory markers in children with asthma and healthy children

Abstract

Previous research has shown that parent mental health is associated with asthma morbidity in children. However, the biological pathways explaining these relationships are not known. The present study tested whether parent psychological characteristics could predict longitudinal changes in inflammatory markers in children with asthma and a comparison group of healthy children.

For this, 33 healthy children (17 m/16 f; 13.5 years) and 50 children with asthma (37 m/13 f; 13.3 years) were assessed at two time points on average 208 days apart. Parent depression (CES-D) and perceived stress (PSS) were assessed at baseline, child depression (CDI) and anxiety (RCMAS) at follow-up. Asthma-relevant inflammatory markers eosinophil cationic protein (ECP) and stimulated interleukin-4 (IL-4) production were measured at baseline and at follow-up.

Hierarchical regression analyses controlling for asthma severity and medication use revealed that higher levels of parental perceived stress at baseline were associated with greater increases over time in children’s IL-4 production (β = .29, p = .019) as well as ECP release (β = .27, p = .004). Additionally, higher levels of parental depression at baseline were associated with increases in ECP over time (β = .19, p = .046). There was no evidence that these associations were mediated by child depression or anxiety.

These results demonstrate that parental stress and depression at baseline predict increases in children’s inflammatory profiles over a six month period. This pattern appeared in both children with asthma and healthy children, and was not due to effects on child psychological states. These changes in inflammatory makers may represent one biological mechanism underlying the association between parental distress and child asthma morbidity.

Introduction

Asthma is a chronic condition that affects a large number of children. In the year 2000, more than five percent of all children in the United States below 18 years were reported to have had an asthma attack and, in 1999, asthma was estimated to be “responsible for two million emergency department visits, 478,000 hospitalizations with asthma as a primary diagnosis, and 4426 deaths” in the US (NHLBI, 2002).

Research has documented that psychosocial factors play an important role in childhood asthma. Two of the most prominent psychosocial factors that have been linked to childhood asthma are parental stress and depression. For example, parental life stress has been linked to decreases in functional status and increases in hospitalizations (Weil et al., 1999), as well as increases in health care service utilization and symptoms (Shalowitz et al., 2001) in children with asthma. Furthermore, in a prospective study, stressful life events predicted an increased likelihood of asthma attacks in the weeks following an event (Sandberg et al., 2004, Sandberg et al., 2000). Similar findings have been reported for parental depression. Maternal depression has been linked to health care service utilization and symptoms (Shalowitz et al., 2001), hospitalizations (Brown et al., 2006, Weil et al., 1999), and emergency department visits (Bartlett et al., 2001) in children with asthma. Several studies further suggest that maternal depressive symptoms prospectively predict asthma morbidity (Bartlett et al., 2004, Klinnert et al., 2001).

In summary, these studies consistently demonstrate that parental stress as well as parental depression play an important role in childhood asthma morbidity. Nevertheless, the question that remains is how the psychosocial experiences of one person (parent) get ‘under the skin’ of another person (child) to impact physical health. The present study takes one step toward answering this question by asking whether parent psychological states are linked with asthma-relevant inflammatory processes in children. If so, this would begin to provide researchers with plausible mechanistic models for the clinical research linking parent psychosocial traits to childhood asthma morbidity.

The primary goal of this study was to test the ability of parental depression and stress to predict children’s inflammatory profiles. Both parental depression and stress were included because they are the psychosocial variables most consistently linked to outcome measures in childhood asthma. However, perceived stress and depression are different constructs. Perceived stress relates to the extent a person appraises a situation as stressful, thus involving a cognitive appraisal process, while depression refers to changes in mood, which can be temporary or longer lasting and interfere with daily life (i.e., mood disorder). Therefore we investigated perceived stress and depression separately given the possibility that they might each operate via different pathways. In order for these associations to be meaningful, it is important to document whether parental psychological states can predict change over time in inflammatory markers relevant to asthma; hence, in the present study we measured inflammatory markers in children twice over a 6 month period. We were further interested whether these relationships would be specific to children with asthma, and therefore included a comparison group of healthy children. Lastly, we sought to address the possibility that one reason why parental stress and depression would be associated with child immune markers is because parents’ mood influences children’s mood, which in turn influences child’s immunological processes. We therefore tested whether child depression and anxiety represent one pathway by which parent psychological states get translated into child biological profiles.