© 2008 American Thoracic Society doi: 10.1164/rccm.200710-1526ED
Exploring Biopsychosocial Influences on Asthma Expression in Both the Family and Community Context
Channing Laboratory Two articles, one in this issue of the Journal (pp. 142–147) and the other published in the October 1, 2007 issue, expand the empirical literature linking psychosocial factors to asthma expression, with each focused on a different developmental stage of the disease. Kozyrskyj and colleagues examined the relationship between maternal distress marked by psychological comorbidities (short-term and persistent) early in a child's life and risk of asthma at age 7 years (1), thus focusing on the onset of asthma. Chen and coauthors (2) examined the relationship between social environmental factors in the family as well as the neighborhood context with asthma-related morbidity among adolescents (aged 9–18 yr), thus focusing on the link between psychosocial factors and disease course once already established. Each of these studies adds significantly to the field.
Kozyrskyj and colleagues (1) examined a large representative cohort (n = The parallel that Kozyrskyj and coauthors draw to work by Essex and colleagues (5) is worth underscoring. Essex and colleagues examined the association of maternal stress beginning in infancy and concurrent stress on hypothalamic–pituitary–adrenal axis activity (i.e., cortisol expression) and later mental health outcomes in preschoolers (aged 4.5 yr). A cross-sectional analysis found that preschoolers exposed to high levels of concurrent maternal stress had elevated cortisol levels. Longitudinal analysis further revealed that stressed children with elevated cortisol also had a history of high maternal stress exposure in infancy. Importantly, children exposed only to high levels of concurrent or early stress had cortisol levels that did not significantly differ from those never exposed to stress. Further analysis of the specific components of maternal stress indicated that maternal depression beginning in infancy was the most potent predictor of children's cortisol expression later on. The influence of maternal depression on childhood asthma outcomes, including being a risk factor for the onset of disease, needs to be studied further in prospective studies with repeated measurements over time. Investigation needs to start even earlier given the burgeoning evidence that the asthma phenotype may be programmed even before birth (6). Future studies that incorporate these stands of overlapping research and strategies for prospectively studying maternal and child psychological functioning and stress reactivity during pregnancy, infancy, and early childhood are needed to continue to elucidate the mechanisms underlying the links between psychological factors (e.g., stress, affective states and traits, frank psychopathology) and asthma development. Specifically, these studies need to address how fetal exposure to stress may influence human immune and neuroendocrine development, whether such effects are independent of postnatal exposures, and how these pathways may, in turn, influence asthma development (6). The role of exposure timing and critical windows of development will need to be considered within a life-course framework (7). By so doing, we will be better able to translate this research into more effective intervention strategies and treatments. Two limitations in the work by Kozyrskyj and coworkers are worth further note. The issue of reverse causality is a significant one in studies designed to examine the effect of stress or other psychosocial factors and asthma onset. Stress and consequent negative emotion or affect (e.g., depression) may be caused by or persist given the added burden on the caregiver of having a child with asthma (8, 9). The authors address this in part by running a sensitivity analysis that omitted children who had been diagnosed with asthma in the first year of life. However, asthma often is manifested between the ages of 3 to 5 years and certainly could have contributed to the more persistent psychopathologies being examined in the current study. In addition, there is concern for residual confounding by access to health care related to socioeconomic status that may explain why they find these effects in higher income homes. This finding is notable because the psychosocial stress model (i.e., differential experiencing of stress and consequent adverse psychological functioning in lower socioeconomic status groups) remains one of the leading theoretical models explaining health disparities, which is counter to Kozyrskyj and colleagues' findings (10, 11). As such, this finding should be interpreted with caution. The contribution by Chen and colleagues (2) considers the cross-sectional influence of social factors at the family, peer, and community levels on asthma morbidity and pulmonary function in adolescents with asthma. This expands the literature in an important way because, traditionally, asthma epidemiology has focused on individual and family factors only. Recently observed epidemiologic trends suggest that asthma may provide an excellent paradigm for understanding the role of broader social contexts (e.g., community-level factors) (12). A particular strength of these analyses is the ability to examine possible pathways, both behavioral and more direct physiologic mechanisms. Interestingly, these authors show that context does matter, such that the underlying mechanism operating between measured social factors and asthma morbidity differed between family and neighborhood indicators. Although family factors seemed to be influencing markers of underlying inflammation, neighborhood problems had a stronger influence through adverse health behaviors (i.e., smoking) in these youth. Such findings buttress those of others who have found that smoking behaviors in youth are socially patterned and related to contextual-level factors, including neighborhood problems and deprivation (13–15). A multilevel approach that explicitly recognizes the embedding of asthma in a broader social context is likely to provide a better understanding of asthma morbidity at different stages of the life course and better inform interventions that work. FOOTNOTES Conflict of Interest Statement: R.J.W. has no financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
Related articles in AJRCCM:
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
14,000) of children enrolled in the Manitoba Health Services insurance plan who were not at high risk for asthma based on maternal history. Data were derived from archived electronic records. The outcome of interest was current asthma at age 7 years defined by automated medical record using methodology validated previously by the investigators. Maternal distress was based on a broad spectrum of psychological comorbidities (e.g., episodic mood disorders, anxiety, dissociative and somataform disorders, adjustment and depressive disorders) as well as pharmacy records documenting prescriptions for antidepressants, anxiolytics, and hypnotics). Although this method has its limitations (