A Model of Perinatal Stress and Childhood Wheezing: ELSPAC-CZ Cohort

Abstract

Background Prenatal origins of wheezing are not fully understood. This study develops a model of mechanisms linking perinatal stress exposure to wheeze phenotypes in children. Methods Data were obtained from 1,849 mother-child dyads participating in ELSPAC-CZ birth cohort. Wheeze phenotypes assessed between birth and age seven years included "never wheeze", "earlyonset transient (EOT) wheeze," "early-onset persistent (EOP) wheeze," and "late-onset (LO) wheeze." Prenatal and postnatal maternal stress exposures were assessed in mid-pregnancy and six months post-delivery, respectively, using an inventory of 42 life events. Results In adjusted models, children in the highest tercile (high) vs. lowest tercile (low) of prenatal life events had a 44% higher risk of EOT wheeze (relative risk ratio [RRR]=1.44, 95% confidence interval [CI]=1.06-1.95, p=0.02) and 69% higher risk of LO wheeze (RRR=1.69, 95% CI=1.13-2.52, p=0.01). High vs. low exposure to postnatal life events predicted a 74% increase in the risk of EOT wheeze (RRR=1.74, 95% CI=1.27-2.38, p<0.001) and 101% increase for EOP wheeze (RRR=2.01, 95% CI=1.23-3.26, p=0.005). Postnatal life events partially mediated between prenatal life events and any wheeze (high vs. low life events: indirect effect OR=1.13, 95% CI=1.06-1.21, p<0.001). Lower respiratory tract infections and secondary smoke partially mediated between postnatal life events and any wheeze (indirect effects OR=1.06, 95% CI=1.02-1.09, p=0.002 and OR=1.02, 95% CI 1.001-1.05, p=0.035, respectively). Conclusions Exposures to prenatal and postnatal life events are risk factors for development of wheezing. Prenatal stress contributes to wheeze directly and also through postnatal life events and respiratory infections.

A review of common influencing factors and possible mechanisms associated with allergic diseases complicating tic disorders in children

“…Another study found that GABA is involved in the pathophysiology of TD, and increased GABA levels may contribute to enhanced control over motor excitability in TS (63). In addition, 5-HT and 5-hydroxyindoleacetic acid levels may play a role in the genesis of TD, but these findings have no significant correlations with the severity of TD (64). In summary, neurotransmitter imbalance has been implicated in the development of TD, but the exact mechanisms involved are still not fully understood.…”