Abstract

Depressive symptoms in parents and in youths have been found to relate to disease comorbidity processes in children, including greater disease-related impairment and poorer clinical outcomes. The current study sought to assess whether coming from a family characterized by more depressive symptoms on average would potentiate the effects of changes in youths' own negative mood on the expression of two receptor genes relevant to asthma that are the primary targets of asthma medication, such that the combination of low child negative mood in the context of greater parental depressive symptoms would relate to the lowest levels of gene expression. One-hundred-twenty youths with diagnosed asthma and their parents participated every 6months for 2years. Parents reported on their depressive symptoms, children reported negative mood symptoms, and youths completed blood draws from which expression of Glucocorticoid Receptor (GR) and Beta2 Adrenergic Receptor (β2-AR) genes was extracted. Multilevel linear modeling revealed significant interactions between average levels of parental depressive symptoms and changes in youths' negative mood symptoms predicting gene expression, such that youths expressed significantly less GR and β2-AR during times when they experienced more negative mood symptoms, but this was only true if they came from families with higher levels of average parental depressive symptoms. The current study identifies novel and biologically-proximal molecular signaling patterns that connect depressive symptoms to pediatric asthma while also highlighting the important role of family environment for biological processes that may operate within depression comorbidity.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.