Work by scientists such as Dr Neil Ward, of the Chemistry Department, University of Surrey and advisor to HACSG, has emphasised the importance of zinc status, ingestion of additives and heavy metal burden (such as lead, cadmium and mercury) in children with ADHD symptoms.

Early work found that zinc deficiency caused hyperactivity (HA) syndrome in rats (Pediatr Res, 1975; 9: 94-7) and that additives such as tartrazine (E102), one of 15 azo dyes permitted in food, can trigger hyperactive behaviour in some children (Arch Gen Psychiatry, 1981; 38: 714-8; J Pediatr, 1994; 125: 691-8). One double blind, placebo controlled study of HA children by Ward and co workers showed that tartrazine reduced blood and saliva zinc levels while increasing urinary zinc output (J Nutr Med, 1990; 10: 415-31). These changes were related to deterioration in both behaviour and emotional expression.In a further study of HA children, Ward confirmed that they had significantly lower zinc and iron levels compared with controls in blood, urine and washed scalp hair (J Nutr Environ Med, 1997; 7: 333-42). HA children known to react to synthetic colouring showed a significant reduction in their blood zinc levels and an increase in urinary zinc output in response to ingesting either tartrazine or sunset yellow (E119). Many HA children also showed significantly high levels of aluminium, cadmium and/or lead in their urine or hair. Raised aluminium levels are associated with antisocial behaviour in children (Biol Trace Elem Res, 1986; 11: 5), while cadmium has an adverse effect on brain metabolism, in particular, a depressive effect on levels of norepinephrine, serotonin and acetylcholine (Ward, 1990, op cit).

Moderate zinc deprivation in prepubertal monkeys was found to adversely affect visual attention and short term memory with no effects on growth rate and no signs of zinc deficiency (Am J Clin Nutr, 1994; 60: 238-43). Zinc deficiency can cause a hyperadrenal condition (Physiol Behav, 1979; 22: 211-5), and adrenergic and dopaminergic dysfunction has been implicated in ADHD (Synopsis of Psychiatry, 7th edn, Baltimore: Williams & Wilkins, 1994: 1063-8). It may also be associated with a reduction in melatonin secretion (Int J Neurosci, 1990; 52: 239-41) which, in turn, leads to reduced serotonin secretion, linked to aggressive behaviour.

Most recently, Ward summarised the evidence for dietary and trace element benefit in a study of supplementation in ADHD children (Nutr Pract, 2000; 2: 43-5). Of those given either trace elements, such as zinc, iron and selenium, or EFAs, or a combination of the two, the “most dramatic improvement” in blood and hair levels, and in reduction of behavioural problems over a 10 week period, was seen with the combined dietary modification.

In his latest, as yet unpublished, analysis, Ward has also found a progressive decline in blood zinc levels in four children using Ritalin over 12 months.

Given that zinc is an essential cofactor in over 100 enzymes and in the conversion of EFAs to LC-PUFAs, zinc status and appropriate supplementation, plus assessment of synthetic food additives and heavy metals, appears to be of primary importance in treating ADHD children.

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