Longitudinal associations between adolescents' individualised risk for depression and inflammation in a UK cohort study

Rachel M. Latham, King's College London, Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, London, UK; ESRC Centre for Society and Mental Health, King's College London, London, UK.
Christian Kieling, Department of Psychiatry, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil; Child and Adolescent Psychiatry Division, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil.
Louise Arseneault, King's College London, Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, London, UK; ESRC Centre for Society and Mental Health, King's College London, London, UK.
Brandon A. Kohrt, Division of Global Mental Health, George Washington University, Washington, DC, USA.
Terrie E. Moffitt, King's College London, Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, London, UK; Department of Psychology and Neuroscience, Duke University, Durham, NC, USA; Psychiatry and Behavioral Sciences, Duke University, Durham, NC, USA; Center for Genomic and Computational Biology, Duke University, Durham, NC, USA; PROMENTA, Department of Psychology, University of Oslo, Norway.
Line J. Rasmussen, Department of Psychology and Neuroscience, Duke University, Durham, NC, USA; Department of Clinical Research, Copenhagen University Hospital Amager and Hvidovre, Hvidovre, Denmark.
Thiago Botter-Maio Rocha, Department of Psychiatry, Universidade Federal Do Rio Grande Do Sul, Porto Alegre, Brazil; Child and Adolescent Psychiatry Division, Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil.
Valeria Mondelli, King's College London, Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; National Institute for Health Research Mental Health Biomedical Research Centre, South London and Maudsley NHS Foundation Trust and King's College London, London, UK.
Helen L. Fisher, King's College London, Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, London, UK; ESRC Centre for Society and Mental Health, King's College London, London, UK. Electronic address: helen.2.fisher@kcl.ac.uk.

Document Type

Journal Article

Publication Date

3-1-2022

Journal

Brain, behavior, and immunity

Volume

101

DOI

10.1016/j.bbi.2021.12.027

Keywords

Adolescence; Adversity; Biomarkers; Major depressive disorder; Mental health; Prevention; Psychopathology; Risk factors; Transition to adulthood

Abstract

Inflammation is associated with poor physical and mental health including major depressive disorder (MDD). Moreover, there is evidence that childhood adversity - a risk factor for MDD - becomes biologically embedded via elevated inflammation. However, the risk of developing MDD arises from multiple sources and yet there has been little investigation of the links between individuals' constellation of MDD risk and subsequent inflammation. We therefore examined associations between individual risk for MDD calculated in early adolescence and levels of inflammation six years later. We use data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative UK birth cohort of 2,232 children followed to age 18 with 93% retention. Participants' individual risk for developing future MDD was calculated at age 12 using a recently developed prediction model comprising multiple psychosocial factors. Plasma levels of three inflammation biomarkers were measured at age 18: C-reactive protein (CRP), interleukin-6 (IL-6), and a newer biomarker, soluble urokinase plasminogen activator receptor (suPAR), which is thought to reflect the level of systemic chronic inflammation. MDD risk scores calculated at age 12 were positively associated with levels of suPAR (but not CRP or IL-6) at age 18 after adjusting for key covariates (b = 1.70, 95% CI = 0.46 - 2.95, p = 0.007). Adolescents at high risk of MDD (risk scores ≥ 90th centile) had significantly higher mean levels of suPAR six years later than adolescents who had been identified as low risk (risk scores ≤ 10th centile) (b = 0.41, 95% CI = 0.18 - 0.64, p < 0.001). Findings support the notion that childhood psychosocial risk for MDD leads to increased levels of low-grade inflammation. If replicated in studies with repeated assessments of inflammation biomarkers throughout childhood and adolescence, these findings would support targeted interventions to reduce inflammation, as measured by suPAR, for adolescents at high risk of MDD to potentially prevent development of depression and physical health problems related to chronic inflammation.

Department

Psychiatry and Behavioral Sciences

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