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Interaction between environmental and familial affective risk impacts psychosis admixture in states of affective dysregulation.

Authors
  • Radhakrishnan, Rajiv1
  • Guloksuz, Sinan1
  • Ten Have, Margreet2
  • de Graaf, Ron2
  • van Dorsselaer, Saskia2
  • Gunther, Nicole3
  • Rauschenberg, Christian3
  • Reininghaus, Ulrich3
  • Pries, Lotta-Katrin3
  • Bak, Maarten3
  • van Os, Jim3
  • 1 Department of Psychiatry,Yale University School of Medicine,New Haven, CT,USA.
  • 2 Department of Epidemiology,Netherlands Institute of Mental Health and Addiction,Utrecht,The Netherlands. , (Netherlands)
  • 3 Department of Psychiatry and Neuropsychology,School for Mental Health and Neuroscience, Maastricht University Medical Centre,Maastricht,the Netherlands. , (Netherlands)
Type
Published Article
Journal
Psychological Medicine
Publisher
Cambridge University Press
Publication Date
Aug 01, 2019
Volume
49
Issue
11
Pages
1879–1889
Identifiers
DOI: 10.1017/S0033291718002635
PMID: 30284529
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Evidence suggests that cannabis use, childhood adversity, and urbanicity, in interaction with proxy measures of genetic risk, may facilitate onset of psychosis in the sense of early affective dysregulation becoming 'complicated' by, first, attenuated psychosis and, eventually, full-blown psychotic symptoms. Data were derived from three waves of the second Netherlands Mental Health Survey and Incidence Study (NEMESIS-2). The impact of environmental risk factors (cannabis use, childhood adversity, and urbanicity) was analyzed across severity levels of psychopathology defined by the degree to which affective dysregulation was 'complicated' by low-grade psychotic experiences ('attenuated psychosis' - moderately severe) and, overt psychotic symptoms leading to help-seeking ('clinical psychosis' - most severe). Familial and non-familial strata were defined based on family history of (mostly) affective disorder and used as a proxy for genetic risk in models of family history × environmental risk interaction. In proxy gene-environment interaction analysis, childhood adversity and cannabis use, and to a lesser extent urbanicity, displayed greater-than-additive risk if there was also evidence of familial affective liability. In addition, the interaction contrast ratio grew progressively greater across severity levels of psychosis admixture (none, attenuated psychosis, clinical psychosis) complicating affective dysregulation. Known environmental risks interact with familial evidence of affective liability in driving the level of psychosis admixture in states of early affective dysregulation in the general population, constituting an affective pathway to psychosis. There is interest in decomposing family history of affective liability into the environmental and genetic components that underlie the interactions as shown here.

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