Nutrition, immunological mechanisms and dietary immunomodulation in ADHD

Abstract

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.

Effect of Pycnogenol® on attention-deficit hyperactivity disorder (ADHD): study protocol for a randomised controlled trial

“…Plasma cytokines for monocytes (interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12, tumour necrosis factor (TNF)-α) and T-cells (IL-4, IL-5, IL-6, IL-10, interferon (IFN)-γ) as well as antibody levels (IgA 1–2 , IgG 1–4 , IgE) by flow cytometry and ELISA, as markers of immune activation state and skewing [21, 46, 47]Identification of peripheral blood mononuclear cells (PBMCs) like neutrophils, CD4, CD8 and B-cells and measurement of their functional responses (e.g. cytokine release) after stimulation, as a marker of immune activation state, skewing and responsivity [21, 46, 47]…”

“…cytokine release) after stimulation, as a marker of immune activation state, skewing and responsivity [21, 46, 47]Intestinal microbial composition, assessed using extreme throughput multiplexed sequencing of 16S ribosomal ribonucleic acid (RNA) gene pools polymerase chain reaction (PCR)-amplified from intestinal content samples [48, 49] …”

“…Plasma cytokines for monocytes (interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12, tumour necrosis factor (TNF)-α) and T-cells (IL-4, IL-5, IL-6, IL-10, interferon (IFN)-γ) as well as antibody levels (IgA 1–2 , IgG 1–4 , IgE) by flow cytometry and ELISA, as markers of immune activation state and skewing [21, 46, 47]…”

“…In addition, immune and oxidative effects of both standard therapy and nutritional supplementation in ADHD are neglected topics in research. Yet, immune and oxidative imbalances linked with ADHD offer potential for appropriate supplementation in ADHD therapy [21]. …”

Temporal Association of Certain Neuropsychiatric Disorders Following Vaccination of Children and Adolescents: A Pilot Case–Control Study

“…These include obsessive–compulsive disorder (OCD) (2, 3), anorexia nervosa (AN) (4), tic disorders (5), attention deficit hyperactivity disorder (ADHD) (6), major depressive disorder (7), and bipolar disorder (8). The precise role immune mechanisms play in these disorders remains to be determined.…”