EDITORIAL article

Front. Psychiatry

Sec. ADHD

Volume 16 - 2025 | doi: 10.3389/fpsyt.2025.1627536

This article is part of the Research TopicADHD and Anxiety: Causality Sequences Through a Biopsychosocial ModelView all 11 articles

Editorial: ADHD and Anxiety: Causality Sequences Through a Biopsychosocial Model

Provisionally accepted
  • 1George Mason University, Fairfax, United States
  • 2Howard University, Washington DC, United States
  • 3shanxi medical university, Shanxi, China

The final, formatted version of the article will be published soon.

ADHD and anxiety frequently co-occur, yet the directionality and mechanisms of their relationship remain debated. The biopsychosocial model posits that genetic predispositions, neurobiological processes, cognitive traits, and environmental contexts jointly shape psychopathology. Our Topic asked: does ADHD symptomatology drive anxiety (or vice versa), or do shared heritable risks underlie both? We encouraged work using longitudinal data, causal inference (e.g., Mendelian randomization), neuropsychological testing, preclinical models, and epidemiology to dissect these sequences.Working Memory & Inhibitory Control Deficits. Michael J. Kofler and colleagues experimentally compared competing models of working memory and inhibitory control in children with ADHD, finding that deficits in both "hot" and "cool" executive functions contribute to attentional lapses and anxiety symptoms (Working memory and inhibitory control deficits in children with ADHD) Frontiers. Fatty Acids & ADHD Risks. In a Mendelian randomization framework, Kangning Zhou and coauthors identified plasma fatty acid profiles causally linked to ADHD risk, implicating lipidmetabolism pathways that may also influence anxiety via neuroinflammation (Plasma fatty acids and attention deficit hyperactivity disorder: a Mendelian randomization investigation) Frontiers.Genetic & Socioeconomic Interplay. Xiaojuan Deng and team combined genetic instruments (GWAS data) with socioeconomic indicators to show that both inherited variants and environmental deprivation jointly influence risk for ADHD and anxiety, highlighting geneenvironment correlation rather than pure causality (Exploring the genetic and socioeconomic interplay between ADHD and anxiety disorders using Mendelian randomization) Frontiers.between ADHD, anxiety disorders, and head-and-neck cancer, suggesting that pleiotropic genetic loci may underlie neurodevelopmental and somatic risks (Gene-level connections between anxiety disorders, ADHD, and head and neck cancer) Frontiers.Ruixiang Wang and colleagues demonstrated that enriching neonatal rats' environments reversed ethanol-induced attention deficits and anxiety behaviors, providing a translational model of how early interventions may reset ADHD-anxiety trajectories (Environmental enrichment reverses prenatal ethanol exposure-induced attentiondeficits in rats) Frontiers.Conceptual Analysis of Stress & Anxiety. Petr Bob and Michal Privara reviewed neurodevelopmental disorganization processes that create vulnerability to both ADHD and anxiety, arguing for hierarchical brain-organization models to guide future treatment strategies (ADHD, stress, and anxiety) Frontiers.Nationwide Comorbidities in Japan. Takashi Okada et al. used population-based registries to document the high prevalence of anxiety and other psychiatric comorbidities among individuals diagnosed with ADHD, underscoring that shared healthcare pathways may facilitate integrated care (Psychiatric comorbidities of attention deficit/hyperactivity disorder in Japan: a nationwide population-based study) Frontiers.Together, these studies support a multifactorial causality model in which shared genetic risks, early neurodevelopmental disruptions, executive-function deficits, and environmental contexts converge to produce overlapping ADHD and anxiety phenotypes. Mendelian randomization work (Deng et al., Zhou et al.) This Research Topic advances our understanding of ADHD-anxiety comorbidity by integrating genetic, neurobiological, cognitive, and environmental perspectives. By unraveling complex causality sequences, these contributions pave the way for precision interventions that address both disorders simultaneously, ultimately improving outcomes for individuals across the lifespan.

Keywords: ADHD, Anxiety, Comorbidity, biopsychosocial model, Mendelian randomization

Received: 12 May 2025; Accepted: 16 May 2025.

Copyright: © 2025 Cao, Teng and Liu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Hongbao Cao, George Mason University, Fairfax, United States

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