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. 2022 Aug 6;26(6):581–606. doi: 10.1007/s40291-022-00609-y

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

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Fig. 1 — ADHD as a complex, multifactorial entity involving interactions across environmental, biological, and behavioral domains. According to current theoretical models of ADHD, such as the ‘mechanistic-cybernetic model’ [2], multiple extrinsic (e.g., environmental factors, blue), intrinsic (genetic, pink; biological and psychological processes, white) and behavioral (green) domains are thought to interact together to shape risk and resilience in ADHD development. Key findings to date from research on both genetic (left-hand side) and environmental (right-hand side) influences on ADHD are highlighted. While this Current Opinion focuses specifically on the potential relevance of epigenetics in ADHD research and clinical practice, it is important to note that epigenetic processes are likely only one of several interconnected domains implicated in the pathophysiology of ADHD. Note: double-headed blue arrows = bidirectional influence; single-headed blue arrow = directional influence; grey dotted arrow = correlated but not causal association. ADHD attention-deficit/hyperactivity disorder, SNP single nucleotide polymorphism, GWAS genome-wide association study, DNAm DNA methylation, BMI body mass index, PGS polygenic score