Adulthood asthma as a consequence of childhood adversity: a systematic review of epigenetically affected genes

Abstract

There is an accumulating data that shows relation between childhood adversity and vulnerability to chronic diseases as well as epigenetic influences that in turn give rise to these diseases. Asthma is one of the chronic diseases that is influenced from genetic regulation of the inflammatory biomolecules and therefore the hypothesis in this research was childhood adversity might have caused epigenetic differentiation in the asthma-related genes in the population who had childhood trauma. To test this hypothesis, the literature was systematically reviewed to extract epigenetically modified gene data of the adults who had childhood adversity, and affected genes were further evaluated for their association with asthma. PRISMA guidelines were adopted and PubMed and Google Scholar were included in the searched databases, to evaluate epigenetic modifications in asthma-related genes of physically, emotionally or sexually abused children. After retrieving a total of 5245 articles, 36 of them were included in the study. Several genes and pathways that may contribute to pathogenesis of asthma development, increased inflammation, or response to asthma treatment were found epigenetically affected by childhood traumas. Childhood adversity, causing epigenetic changes in DNA, may lead to asthma development or influence the course of the disease and therefore should be taken into account for the prolonged health consequences.

Emerging trends in epigenetic and childhood trauma: Bibliometrics and visual analysis

“…Houtepen identified a locus in the Kit ligand gene (KITLG; cG27512205) which associated with cortisol stress response using genome-wide analysis, and shedding light on the neurobiological pathways behind individual’s vulnerability to stress ( 31 ). Saygideger conducted a meta-analysis and revealed that childhood trauma induces asthma or other chronic inflammatory diseases by influencing genes such as NR3C1 and FKBP5, which mediate immune inflammation ( 43 ). The above studies suggest that FKBP5 methylation, NR3C1 methylation, KITLG methylation, and inflammatory phenotypes have been the focus of epigenetic studies in the field of childhood trauma in recent years.…”