Title: Attention Deficit Hyperactivity Disorder

Key words: cognitive disorders, inattention, impulsivity, nor-adrenergic dysregulation, cognitive function, caudate nucleus, glucose utilisation, frontal lobes, basal ganglia, serotonin (5HT), chocolate, methylxanthine, food allergy, food intolerance, hyposensitisation, Feingold diet, zinc, omega-3 fatty acids, dietary modification

Date: Aug 2000

Category: 13. Specific Conditions

Type: Article

Author: Dr van Rhijn

 

 

Attention Deficit Hyperactivity Disorder

 

What Diet Can Do?

 

Introduction

Attention Deficit Hyperactivity Disorder (ADHD), a childhood psychiatric disorder affects 1%1 (0.02 – 20%) of the childhood population. The gender ratio boys:girls is 9:1 but girls equal boys in ADD cognitive disorders. Primary characteristic symptoms include inattention, distractibility, impulsivity, social disinhibition, hyper-excitability, hyperactivity, excessive restlessness, low frustration tolerance, aggressive behaviour and sleep disturbances, impairing the child's ability to function2 socially, interpersonally and academically. The assessment for and diagnosis of ADHD is complicated by the lack of a specific test or marker for the disorder3.

 

Neurobiological Basis

Neurobiological and pharmacological data provide support for a nor-adrenergic (NA) network dysregulation hypothesis that may underlie the ADHD pathophysiology. The NA system has associations with modulating higher cortical functions (attention, alertness, vigilance, execution). Pharmacological NA activation is known to affect cognitive function (attention, arousal) profoundly and is also known to be deficient in ADHD4. Brain imaging (MNR) studies found ADHD significantly associated with a decrease in the rostral body area, suggesting neurobiological involvement of frontal-subcortical circuits5 with underlying NA function dysregulation. Normal asymmetry reversal of the caudate nucleus head, especially in ADHD male children, was due to a smaller left caudate nucleus6.

 

ADHD behavioural symptoms might reflect disinhibition from normal dominant hemispheric control, possibly correlated with deviations in asymmetric caudate-striatal morphology and deficiencies in associated neurotransmitter systems. Topographic EEG mapping confirmed that certain provoking foods influence clinical symptoms and was associated with increased β-1 electrical activity in the fronto-temporal brain areas7. SPECT studies suggested perfusion disorders with reduced glucose utilisation, involving the frontal lobes and basal ganglia (dopamine), resulting in disinhibition, awkwardness and clumsiness in executing complex tasks. Therapeutic stimulants do not target specific neurobiological deficits but exert compensatory effects involving pre-synaptic inhibitory autoreceptor stimulation, reduced dopaminergic and nor-adrenergic pathway8 activity.

 

The role of central serotonergic function has also been suggested in the neurobiological mechanisms in ADHD9. Excessive carbohydrate intake increases the ratio of tryptophan:large neutral amino acids10, thereby enhancing serotonin11 production and subsequent mood modulation. Chocolate provides numerous amino acids, tyrosine, tryptophan, anandomides (cannabinoid), phenylalanine, phenylethylamine and theobromine (a methylxanthine like caffeine) that may act as neurotransmitter precursors. Systemic absorption of toxic metabolites from chronic dysbacteriosis such as tartaric acid & arabinose (candidiasis) and DHPPA  (clostridium) are associated with hyperactive behaviour (alteration in the HVA/VMA ratio). Enzyme deficiencies (phenolsulphotransferase) result in metabolic failure of phenolic amine compounds that may act as neurotransmitters12,13.

 

The role of Nutrition and Dietary Intervention

Numerous studies confirmed food allergies and intolerance as important contributors of the hyperkinetic syndrome (HD14,15 and ADHD16,17) and disruptive behaviour secondary mediated by neurotransmitters. Main culprits18 appear to be sugar, chocolate, milk, wheat, oranges, eggs, nuts, preservatives, colourings, flavourings and additives. The majority of hyperkinetic behaviour, as well as physical symptoms, improved on an oligoantigenic diet19 but this can be nutritionally inadequate. Hyposensitisation with enzyme-potentiated desensitisation (EPD) may enable children with food induced ADHD to tolerate provoking foods20. The improvements claimed by using the Feingold diet (eliminating artificial colourings, flavourings, salicylates) were not confirmed by some researchers21.

 

Low zinc (co-factor of delta-6-desaturase required for EFA conversion) levels were found in hyperactive children given tartrazine (E102), suggesting higher zinc excretion rates were associated with behaviour and emotional status22. ADHD subjects have significantly lower plasma and red cell EFAs23,24,25 and boys with omega-3 fatty acid deficiencies displayed more behaviour problems, temper tantrums, impulsivity and sleep disturbances26,27. Omega-6 supplementation either showed no28 or mild29 behavioural improvements and ADHD symptoms may be reduced by dietary addition of saccharides required for glycoconjugate synthesis30.

 

Dietary modification (elimination of ‘soft drinks’& junk foods) with nutrient supplementation (Fe, Zn, Se, EFAs) and healthy diets, showed considerable behavioural improvement for HA, dyslexia and allergic children (all had low zinc levels)31, and a 45% reduction of rule violations culminating in disciplinary action32.

 

Conclusion

The cause of the complex ADHD is multi-factorial, involving both environmental and biological determinants. Although not fully understood, it is clear that dietary factors, intolerance, EFA33 and amines play a major part, and may be utilised as an alternative therapy (60%) ADH34.

 

 

References

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