Improving the medical assessment of young people with ADHD: Genetic, psychosocial or metabolic issues? (II)
Main Article Content
Abstract
A good understanding of the origin of symptoms is essential to ensure the optimization of therapeutic treatments. This article proposes a critical re-evaluation of both confounding and risk factors associated with attention deficit hyperactivity disorder to avoid over-diagnosis and over-medication as currently observed in Quebec. We provide an in-depth analysis of the nutritional, metabolic, digestive, respiratory and behavioral factors that may contribute to the onset and persistence of symptomatology resembling attention deficit hyperactivity disorder (ADHD), traditionally classified as a neurodevelopmental disorder of genetic origin. Emerging evidence suggests that the symptomatology may result from a multifactorial dysregulation affecting dopaminergic and noradrenergic pathways. It is essential to consider the critical role of nutrition in neurotransmitter synthesis, as deficiencies in amino acids, vitamins, minerals, and essential fatty acids may significantly compromise executive and attentional functions. Among the vulnerability factors, particular attention should be given to the long-term impact of childhood malnutrition on cognitive performance. Optimal therapeutic management of attention deficit hyperactivity disorder (ADHD) also requires evaluating its symptomatology within the broader continuum of metabolic dysfunction, including insulin resistance, glycemic variability, sedentarity and pediatric obesity. These imbalances affect neuroinflammation, neuronal energy production, and neurotransmitter synthesis. In this context, it is relevant to explore the role of the gut microbiota and intestinal permeability in the emergence of symptoms associated with attention-deficit/hyperactivity disorder (ADHD). This includes examining the potential benefits of elimination diets and the behavioral effects of food dyes and additives, thereby highlighting the importance of a personalized, patient-centered approach. Finally, sleep-disordered breathing in children, which has multiple causes, is also common among children with attention deficit hyperactivity disorder and can exacerbate neurocognitive symptoms. To ensure optimal therapeutic direction, it is therefore recommended to evaluate nutritional, metabolic, digestive, respiratory and behavioural factors before making a diagnosis of attention deficit hyperactivity disorder and initiate a treatment. All in all, mental health should not be considered as an isolated entity, but as the expression of a neuro-metabolic imbalance modulated by lifestyle habits on which it is possible to act effectively.
Keywords:
children, adolescents, ADHD, psychostimulants, metabolic assessment, clinical ethics
Article Details
How to Cite
DIONNE, Anne-Isabelle; MONZÉE, Joël.
Improving the medical assessment of young people with ADHD: Genetic, psychosocial or metabolic issues? (II).
Medical Research Archives, [S.l.], v. 13, n. 6, june 2025.
ISSN 2375-1924.
Available at: <https://esmed.org/MRA/mra/article/view/6535>. Date accessed: 17 july 2025.
doi: https://doi.org/10.18103/mra.v13i6.6535.
Section
Review Articles
The Medical Research Archives grants authors the right to publish and reproduce the unrevised contribution in whole or in part at any time and in any form for any scholarly non-commercial purpose with the condition that all publications of the contribution include a full citation to the journal as published by the Medical Research Archives.
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2. Monzée J. Evolution of psychotropic medication prescription in young people: reflection from the Quebec experience. Psychotherapy and Psychosomatics. 2025;94(1):8–14.
3. MSSS-MEES, Protocole: trouble de déficit de l’attention avec ou sans hyperactivité, 2019.
4. Deng MG, Zhou X, Li X, Liu J. Identification of Risk Genes for Attention-Deficit/Hyperactivity Disorder During Early Human Brain Development. J Am Acad Child Adolesc Psychiatry. 2024;S0890-8567(24)01976–2.
5. Li D, Sham PC, Owen MJ, He L. Meta-analysis shows significant association between dopamine system genes and attention deficit hyperactivity disorder (ADHD). Hum Mol Genet. 2006;15(14):2276–84.
6. A. Kirley. Scanning the genome for attention deficit hyperactivity disorder. In D. Gozal D.(ed.). Attention deficit hyperactivity disorder: from gene to patients. Humana Press Inc., 2005.
7. Chen MH, Pan TL, Huang KL et al. Coaggregation of Major Psychiatric Disorders in First-Degree Relatives of Individuals With Attention-Deficit/Hyperactivity Disorder: A Nationwide Population-Based Study. J Clin Psychiatry. 2019;80(3):1812371.
8. Solberg BS, Hegvik TA, Halmøy A et al. Sex differences in parent-offspring recurrence of attention-deficit/hyperactivity disorder. J Child Psychol Psychiatry. 2021;62(8):1010–1018.
9. Monzée J. Neuropsychologie et généticisation: limites scientifiques et éthiques. In Hervé Ch et al.(dir.). Généticisation et responsabilités. Dalloz. 2008:53–78.
10. Peedicayil J. The Role of Epigenetics in the Pathogenesis and Potential Treatment of Attention Deficit Hyperactivity Disorder. Curr Neuropharmacol. 2022;20(9):1642–1650.
11. Storebø OJ, Pedersen N, Ramstad E et al. Methylphenidate for attention deficit hyperactivity disorder (ADHD) in children and adolescents - Assessment of adverse events in non-randomised studies. Cochrane Database Syst Rev. 2018; 5(5):CD012069.
12. Zhang L, Li L, Andell P et al. Attention-Deficit/Hyperactivity Disorder Medications and Long-Term Risk of Cardiovascular Diseases. JAMA Psychiatry. 2024;81(2):178–187.
13. Charney DS, Nestler EJ. Neurobiology of mental illness, Oxford PU, 2004.
14. Yu Y, Herman P, Rothman DL et al. Evaluating the gray and white matter energy budgets of human brain function. J Cereb Blood Flow Metab. 2018;38(8):1339–1353.
15. Galler JR, Bryce C, Waber DP et al. Socioeconomic outcomes in adults malnourished in the first year of life: a 40-year study. Pediatrics. 2012;130(1):e1–7.
16. Roger K, Vannasing P, Tremblay J et al. Early childhood malnutrition impairs adult resting brain function using near-infrared spectroscopy. Front Hum Neurosci. 2024;17:12874–88.
17. Fernstrom JD, Fernstrom MH. Tyrosine, phenylalanine, and catecholamine synthesis and function in the brain. J Nutr. 2007;137(6-Suppl 1):1539S–1547S.
18. Roth W, Zadeh K, Vekariya R, Ge Y, Mohamadzadeh M. Tryptophan Metabolism and Gut-Brain Homeostasis. Int J Mol Sci. 2021;22(6):2973.
19. Bornstein RA, Baker GB, Carroll A et al. Plasma amino acids in attention deficit disorder. Psychiatry Res. 1990;33(3):301–6.
20. Wang LJ, Yu YH, Fu ML et al. Dietary Profiles, Nutritional Biochemistry Status, and Attention-Deficit/Hyperactivity Disorder: Path Analysis for a Case-Control Study. J Clin Med. 2019;8(5):709.
21. Martini D, Godos J, Bonaccio M et al. Ultra-Processed Foods and Nutritional Dietary Profile: A Meta-Analysis of Nationally Representative Samples. Nutrients. 2021;13(10):3390.
22. Moubarac JC, Batal M, Louzada ML et al. Consumption of ultra-processed foods predicts diet quality in Canada. Appetite. 2017;108:512–520.
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