The starting point of this study was the assumption that the behavioural and developmental deficits of hyperactivity might be triggered by too high an intake of phosphate. The study involved twelve boys and three girls, aged between four and sixteen years. In their home environments these children had been given Mrs Hafer's minimal phosphate diet for at least six weeks - in some cases for up to two years - to remove excess phosphate from their system. During this period they all improved markedly. Improvements were noted by the researchers, family members, teachers and the children themselves; they were confirmed by evidence in the form of improved school marks and reports.

The children were then given a series of clinical, blood and psychological tests, to determine whether there were any indications of problems arising from the low phosphate diet. No problems were discovered. Blood and EEG examinations revealed no adverse effects of the phosphate-reduced diet among this group of subjects, even in the case of subjects who had been on the diet for one to two years.

Next, half of them were given a dose of phosphate and the other half were given a placebo. Two observers endeavoured, independently of one another, by observing the behaviour of the children, to judge which subjects had received the phosphate dose and which the placebo. Upon the administration of a controlled dose of phosphate an increase in the specific behavioural symptoms of hyperactivity became very quickly and very obviously apparent. The first symptoms were identifiable within half an hour of the ingestion of the phosphate dose. The researchers were of the opinion that it was highly unlikely that the results they observed were brought about by a placebo or psychotherapeutic effect, since their subjects had been on the same diet in the home situation for as long as two years. In addition, there was considerable supportive evidence of improvement in the form of school reports. The evidence in the form of the reappearance of symptoms of hyperactivity upon the ingestion of phosphate also made this an unlikely factor.

The researchers pointed out that, in contrast to their experience with the minimal phosphate diet, the generally accepted treatment of hyperactivity with stimulants such as methylphenidate (Ritalin) and amphetamines (Dexamphetamine) has the disadvantage of a whole range of side effects and the danger of misuse can further restrict the use of these therapies. No minimum age for the introduction of the diet appears to be indicated, especially as the specific behavioural manifestations of hyperactivity had already become apparent in some cases when infants were taken off baby food and put onto a normal diet. They commented that since the diet would need to be continued for years, at least until the onset of puberty, regular checks of all aspects which it might affect would be advisable. Occasional, clinically controlled ingestion of trial doses of phosphate would afford evidence as to the necessity of continuation of the diet.

Mrs Hafer's own son, Michael, was one of the children involved in this study. He had been doing well on the diet for some considerable time and, like the other fourteen children involved, had been psychologically unobtrusive before the administration of the phosphate dose. She comments: "Our son returned home after the test with an uncontrollable logorrhea (an excessive flow of speech). The next morning he was still so disturbed that within two school lessons he had received three hours of detention and been the subject of several entries in the class discipline book; then, in despair, he ran away from school."

Reference: Unpublished research report (in the original German); copy available on request from PhosADD Australia.