The role of psychosocial adversity in the aetiology and course of attention deficit hyperactivity disorder

Rev Colomb Psiquiatr (Engl Ed). 2023 Jan-Mar;52(1):65-72. doi: 10.1016/j.rcpeng.2021.02.007.
[Article in English, Spanish]

Abstract

Introduction: Attention deficit/hyperactivity disorder (ADHD) has genetic and environmental aetiological factors. There are few publications on the environmental factors. The objective of this review is to present the role of psychosocial adversity in the aetiology and course of ADHD.

Methods: A search was carried out in the following databases: PubMed, ScienceDirect, SciELO, ClinicalKey, EMBASE, Lilacs, OVID, APA and PsycNET. English and Spanish were selected without being limited by type of study or year of publication. Finally, a qualitative synthesis was conducted.

Results: ADHD development could be related to exposure to adverse factors in the family, school or social environment. It has been proposed as an explanatory mechanism that adversity interacts with genetic variants and leads to neurobiological changes. There may also be a gene-environment correlation whereby individual hereditary characteristics increase the risk of exposure to adversity, and indirectly increase the probability of developing ADHD. Research on psychosocial adversity represents a big challenge, not only due to the complexity of its construct, but also to the effect of subjective perception of a given event.

Conclusions: ADHD aetiology is complex and involves the interaction of both genetic and environmental factors, in which these factors correlate and cause the disorder. The study of the role of psychosocial adversity in ADHD is fundamental, but it remains a task that entails great difficulties.

Keywords: Aetiology; Attention deficit/hyperactivity disorder; Etiología; Impacto psicosocial; Problemas sociales; Psychosocial impact; Social problems; Trastorno por déficit de atención con hiperactividad.

Publication types

  • Review

MeSH terms

  • Attention Deficit Disorder with Hyperactivity* / etiology
  • Humans
  • Social Environment