t of these diets on hyperactivity?
- Is there any biological explanation to support an effect of defined diets on hyperactivity?
- If defined diets are effective, how and under what circumstances should they be employed?
- What are the directions for research?
Panel members were drawn from the lay public, biomedical research, pediatrics, nutrition, immunology and allergy, clinical pharmacy, psychiatry and behavioral sciences, genetics, education, epidemiology, biostatistics, environmental health, and law, all relevant to a discussion of diets and childhood hyperactivity.
Childhood hyperactivity, officially termed the "attention deficit disorder with hyperactivity," but variously referred to as "hyperkinetic reaction of childhood," "hyperkinetic syndrome," "hyperactive child syndrome," "minimal brain damage," "minimal brain dysfunction," "minimal cerebral dysfunction," and "minor cerebral dysfunction," is an important health concern affecting afflicted children, their families, and those around them. Traditional therapy for this condition has included behavior modification, educational techniques, psychotherapy, and pharmacotherapy--most prominently amphetamine-like medications.
The 1973 report by Feingold of clinical observations on the benefit of a diet free of salicylates and food additives on hyperactivity focused attention on this new treatment approach. The publication of the Feingold diet in book form came at a time of increasing public concern about environmental pollution and a desire for full knowledge of all additives found in prepared food and the presence of such substances in the diet. These trends, along with a heightened aversion to habitual use of medication, an increase in awareness of the possible causative role of nutritional factors in diseases of many types, a desire for self-involvement in health care, and the frustration encountered in managing childhood hyperactivity, led to the widespread experimentation with the Feingold regimen and other defined diets.
Some controlled, double-blind studies indicate that these diets are only occasionally efficacious. Apparent discrepancies between some clinical impressions of efficacy and much of the available scientific evidence prompted the scheduling of this Consensus Development Conference.
What Constitutes the Hyperactivity Syndrome in Children? Is It a Single Disease or a Cluster of Diseases? Can It Be Graded or Scaled in Quantifiable Variables Such as Attention Span, Learning Ability, and Social Adjustment and By Whom (Teachers, Parents, Medical Personnel)?
Innumerable definitions have been offered for the hyperactivity syndrome in children. The latest of these, in Diagnostic and Statistical Manual III (DSM III) (the American Psychiatric Association), delineates the varied symptomatology in this behavioral syndrome. According to DSM III,"the essential features are signs of developmentally inappropriate inattention, impulsivity, and hyperactivity." Other diagnostic qualifiers include onset prior to the age of 7, a duration of no less than 6 months, and a proven absence of mental illness or mental retardation.
The cluster of symptoms does not represent a single disease, nor is it likely that the etiology is singular; rather, the syndrome may be secondary to (1) organic factors such as trauma, infection, lead intoxication, and significant perinatal hypoxia; (2) predisposing genetic (familial) factors; or (3) psychosocial factors such as anxiety, inadequate parenting, and environmental stresses. In most cases the etiology is unknown and may be the result of synergism of several of the predisposing factors listed above.
The diagnostic process optimally includes the participation of parents, medical personnel, teachers, psychologists, and social workers. Several useful tests and rating scales for quantification of important variables such as attention span, learning ability, and social adjustment are available to those involved in the process; however, a need for more concise assessment tools is apparent. The recent development of electronic devices for measuri