Prospective association between psychopathological symptoms in childhood and asthma in adolescence: Results from the GINIplus and LISA birth cohort studies

TL;DR

This study finds that childhood psychopathological symptoms are linked to asthma in adolescence, particularly non-atopic asthma, and suggests early intervention may help prevent asthma development.

Contribution

The study is novel in examining the longitudinal association between childhood psychopathology and asthma endotypes in adolescence.

Findings

Psychopathological symptoms at age 10 are associated with asthma at age 15, particularly non-atopic asthma.

Peer problems in childhood are linked to atopic asthma in adolescence.

Puberty onset interacts with psychopathological symptoms to influence atopic asthma risk.

Abstract

Although there is a high co‐occurrence of psychopathological symptoms and asthma, longitudinal studies considering asthma endotypes in childhood and adolescence are scarce. Therefore, this study examined the prospective association between psychopathology in childhood and current atopic and non‐atopic asthma in adolescents, considering sex and puberty‐related characteristics.

The study includes 3584 participants (1790 females, 1794 males) from two German birth cohort studies, GINIplus and LISA. Psychopathological symptoms at age 10 (M = 10.06, SD = .22) were assessed by parent‐reported Strengths and Difficulties Questionnaire (SDQ) and current asthma at age 15 (M = 15.07, SD = .30) was defined as a positive parent‐reported medical diagnosis, wheezing, and/or medical treatment against asthma (at least two criteria). Atopic asthma was characterized as current asthma and a positive specific immunoglobulin E (IgE) test (≥0.35 kU/L), non‐atopic asthma as current asthma without sensitization. Data were analyzed by logistic regression and multinomial regression models, controlling for potential covariates and confounders.

Psychopathological symptoms at age 10 were associated with asthma at age 15 (odds ratio (OR) = 1.69, 95% confidence interval (CI) = 1.04–2.92, p = .035). When examining the endotypes, this effect was replicated only for non‐atopic asthma at age 15 (relative risk ratio (RRR) = 2.92, 95% CI = 1.13–7.60, p = .028), but not for atopic asthma (p = .381). Regarding the SDQ subscales, an association between peer problems at age 10 and atopic asthma at age 15 was revealed (RRR = 2.00, 95% CI 1.01–3.97, p = .048). Furthermore, significant interaction effects of puberty onset with psychopathological symptoms (p = .020), and particularly with peer problems (p = .029), were found on atopic asthma.

The findings highlight the importance of early recognition and treatment of psychopathological symptoms to prevent and reduce development, persistence and exacerbation of asthma endotypes, and point to the necessity for further research into hormonal mechanisms linking psychopathology with atopy.

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