• Medientyp: E-Artikel
  • Titel: The Mediating Role of Cardiometabolic Dysregulation on the Relation Between Adverse Childhood Experiences and Adult Cognition
  • Beteiligte: Moliner, Sheyla; Quinn, Jamie M.; Sheffler, Julia
  • Erschienen: Ovid Technologies (Wolters Kluwer Health), 2022
  • Erschienen in: Psychosomatic Medicine
  • Sprache: Englisch
  • DOI: 10.1097/psy.0000000000001093
  • ISSN: 1534-7796; 0033-3174
  • Schlagwörter: Psychiatry and Mental health ; Applied Psychology
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  • Beschreibung: <jats:title>ABSTRACT</jats:title> <jats:sec> <jats:title>Objective</jats:title> <jats:p>Adverse childhood experiences (ACEs) are uncontrollable stressful events during early life that predispose adults to adverse health outcomes, such as impaired cognitive functioning. However, little is known about the factors indirectly impacting this relation. Biological dysregulation may be one pathway that can help explain the relations between ACEs and later cognition. The current study examined the mediating role of cardiometabolic dysregulation on the relation between ACEs and cognition.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p>Our study gathered data from 1053 participants using three waves of the Midlife in the United States longitudinal study. Linear regression analyses and bootstrapped mediation analyses were performed to analyze the direct and indirect associations of cardiometabolic dysregulation on ACEs and cognition.</jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p>Our results showed a significant linear relationship between ACEs and cardiometabolic dysregulation (<jats:italic toggle="yes">b</jats:italic> = 0.152, standard error [SE] = 0.056, <jats:italic toggle="yes">p</jats:italic> = .007), and a significant indirect association, such that cardiometabolic dysregulation mediated the relation between ACEs and cognitive status at wave II (<jats:italic toggle="yes">b</jats:italic> = −0.007, SE = 0.004, <jats:italic toggle="yes">p</jats:italic> = .044) and cognitive status at wave III (<jats:italic toggle="yes">b</jats:italic> = −0.006, SE = 0.003, <jats:italic toggle="yes">p</jats:italic> .042). There was no significant direct or indirect relation when cognitive change was the outcome variable.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusions</jats:title> <jats:p>The present study identifies a combined biological pathway that connects ACEs to cognition in late life. These findings supports the need to empirically determine biological mechanism that can be used to develop targeted clinical interventions to prevent the progression of chronic cognitive impairment.</jats:p> </jats:sec>