Nutrition, immunological mechanisms and dietary immunomodulation in ADHD
Open accessAbstract
Attention-deficit hyperactivity disorder (ADHD) etiology is not completely understood, but common comorbid dysfunction of the gastrointestinal and immune system suggests that these systems may be affected by a common genetic background and molecular mechanisms. For example, increased levels of specific cytokines were observed in ADHD. Moreover, ADHD has a high comorbidity with both Th1- and Th2-mediated disorders like ear infections, eczema and asthma. A common pathophysiological mechanism was suggested to underlie both asthma and ADHD, while several genes that are linked to ADHD have immune functions. Furthermore, immunological recognition of food provoking ADHD-like behavior was suggested. An immune imbalance, probably requiring a predisposing genetic background, is therefore suggested to contribute to ADHD etiology, with immune dysregulation being more likely than a single subcellular defect. However, next to allergic mechanisms, also pharmacological mechanisms (especially in case of food additives) might be involved. In addition, though cellular (cytokine-related) rather than antibody-mediated immune mechanisms seem involved, specific immune-inflammatory markers other than antibodies have not been systematically studied in ADHD. Substantial alterations implicated in ADHD apparently occur in the immune system and epigenetic regulation of gene expression. As a result, chronic inflammation and oxidative stress could develop, which can lead to ADHD symptoms, for example by chronic T-cell-mediated neuroinflammation. If immune pathways contribute to ADHD, both its diagnosis and treatment should be reconsidered. Modulation of immune system activity might have potential in ADHD treatment, for example by nutritional approaches providing safe and low-cost ADHD therapy, but further research in these fields is implicated.
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Neuroinflammation is hypothesized to affect brain growth and thereby raises the risk of neurodevelopmental disorders through pathways such as glial activation, increased oxidative stress, problems related to neuronal growth and impaired NT activity.
“Neuroinflammation is hypothesized to affect brain growth and thereby raises the risk of neurodevelopmental disorders through pathways such as glial activation, increased oxidative stress, problems related to neuronal growth and impaired NT activity [60].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [60]
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Experimental — accuracy not yet measuredPro-inflammatory cytokines such as TNFβ, IFNα, IL-1, IL-5, and IL-16 are found upregulated, whereas the anti-inflammatory cytokines IL-4 and IL-13 are downregulated, resulting in an inflammatory process that causes neuronal damage and contributes to ADHD symptomatology.
“Pro-inflammatory cytokines such as tumour necrosis factor beta (TNFβ), interferon alpha (IFNα), interleukin-1 (IL-1), IL-5, and IL-16 are found upregulated, whereas the anti-inflammatory cytokines IL-4 and IL-13 are downregulated, resulting in an inflammatory process that causes neuronal damage and contributes to ADHD symptomatology [60].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [60]
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Experimental — accuracy not yet measuredSeveral risk genes have been found in the human genome, but only a limited number of small impact size ADHD genes have been identified.
“Several risk genes have been found in the human genome [59], but only a limited number of small impact size ADHD genes have been identified [60].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [60]
Citation [60] is attached to the claim that only a limited number of small-effect ADHD genes have been identified. The retrieved passages from our indexed copy contain bibliographic information and ADHD-related keywords, but none addresses the number or effect size of identified genes (searched for genetic factors, ADHD risk genes, and small effect size). (LLM, conf=0.70)
Experimental — accuracy not yet measuredLow cortisol promotes an imbalance in pro-inflammatory Th1/anti-inflammatory Th2 cytokine profile making a more pro-inflammatory environment in ADHD, which can be related to a defective Treg regulation.
“This promotes an imbalance in pro-inflammatory T helper 1 cell (Th1)/anti-inflammatory T helper 2 cell (Th2) cytokine profile making a more pro-inflammatory environment in ADHD [60, 102], which can be related to a defective regulatory T cell (Treg) regulation.”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [60]
No passage from our indexed copy addresses the proposed link between low cortisol, a Th1/Th2 cytokine imbalance, and defective Treg regulation in ADHD. Searches for cortisol, Th1, Treg, and pro-inflammatory cytokines returned no substantive passage; the only returned text was bibliographic information with no section or page. (LLM, conf=0.70)
Experimental — accuracy not yet measuredNeuroinflammation is hypothesized to increase the risk of neurodevelopmental disorders and impaired NT activity.
“Neuroinflammation is hypothesized to increase the risk of neurodevelopmental disorders and impaired NT activity [60].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [60]
No eligible full-text passage in our copy addresses whether neuroinflammation increases the risk of neurodevelopmental disorders or impairs neurotransmitter activity. Searches for neuroinflammation, neurodevelopmental disorders, and neurotransmitters returned no matching full-text passage; the only substantive match was labeled Abstract, which cannot decide this verdict. (LLM, conf=0.68)
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References 103 · Cited by 114
- Authors
- Verlaet, A. A. J., Noriega, D. B., Hermans, N., & Savelkoul, H. F. J.
- Affiliations
- University of Antwerp (BE)
- Wageningen University & Research (NL)
- Corresponding author
- Verlaet, Annelies A. J.
- Venue
- European Child & Adolescent Psychiatry
- Published
- 2014-02-04
- Volume
- 23
- Issue
- 7
- Pages
- 519-529
- ISSN
- 1018-8827 (ISSN-L)
- 1435-165X
- OpenAlex
- W2051024010
- Cited by
- 114
- References
- 103
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 6 · 2023: 8 · 2022: 15 · 2021: 13 · 2020: 17 · 2019: 9 · 2018: 10 · 2017: 8 · 2016: 7 · 2015: 3 · 2014: 1
- FWCI
- 0.87
- Type
- journal article
- Language
- en
- Open access
- green
- research.wur.nl
- Licence
- www.springer.com/tdm (tdm)
- Locations
- European Child & Adolescent Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Socio-Environmental Systems Modeling (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- attention deficit hyperactivity disorder, dietary immunomodulation, immune dysregulation, cytokines, Th1/Th2 imbalance, food allergy, food additives, epigenetic regulation, chronic inflammation, oxidative stress, neuroinflammation, gastrointestinal dysfunction, asthma comorbidity, ADHD etiology
- MeSH terms
- Attention Deficit Disorder with Hyperactivity, Child, Humans, Nutritional Status, Immunomodulation
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