The clinical definition of “ADHD” dates to the mid-20th century, when physicians developed a diagnosis for a set of conditions variously referred to as “minimal brain damage”, “minimal brain dysfunction”, “learning/behavioral disabilities” and “hyperactivity”. Researchers speculate that earlier references to the condition, as mentioned in the examples below, have been made throughout history.
In 493 BCE, physician-scientist Hippocrates described a condition that seems to be compatible with what we now know as ADHD. He described patients who had “quickened responses to sensory experience, but also less tenaciousness because the soul moves on quickly to the next impression.” Hippocrates attributed this condition to an “overbalance of fire over water.” His remedy for this “overbalance” was “barley rather than wheat bread, fish rather than meat, water drinks, and many natural and diverse physical activities.” Shakespeare made reference to a “malady of attention” in King Henry VIII, which at least “proves” that people don’t pay attention when other things are on their mind.
In 1845, Dr. Heinrich Hoffmann (a German physician and poet who wrote books on medicine and psychiatry) became interested in writing for children when he couldn’t find suitable materials to read to his 3-year-old son. The result was a book of poems, complete with illustrations, about children and their undesirable behaviors. One, “The Story of Fidgety Philip,” was a description of a little boy who could be interpreted as having ADHD. On the other hand, it could also be interpreted as merely a moral fable exaggerating children’s normal “improper” behavior to amuse young children and encourage them to behave properly.
In 1902, the English pediatrician George Still gave a series of lectures to the Royal College of Physicians in England, describing a condition which some have claimed is analogous to ADHD. Dr. Still described a group of children with significant behavioral problems caused, he believed, by hereditary.
In 1918–19, the world-wide influenza pandemic left many survivors with encephalitis, affecting their neurological functions. Some of these exhibited immediate behavioral problems similar to what we now call ADHD. This caused researchers and doctors to believe that the condition was the result of injury rather than heredity. Not until 1960 was the concept of hyperactivity again described as being caused by heredity (Hyperactive Child Syndrome”) and not brain damage.)
Until the early 1990s, Europeans saw hyperkinesis as unusual and associated with retardation, brain damage, and conduct disorders; in the U.S., however, following observations in 1966 that the condition existed without any objectively observed pathological disorder or injury, researchers changed the terminology from Minimal Brain Damage to Minimal Brain Dysfunction. It may be noteworthy to mention that food additives such as flavoring and coloring were introduced into the food supply earlier in the U.S. than in Europe.
In 1968, displaying the psychoanalytical influences of that time, psychiatry officially codified a condition called “hyperkinetic reaction of childhood.” The name Attention Deficit Disorder (ADD) was first introduced in the 1980 DSM-III. Further revisions to the DSM were made in 1987 and 1994, and today’s DSM-IV describes three groupings within ADHD, which can be simplified as: mainly inattentive; mainly hyperactive-impulsive; and both in combination.
In January of 1982, the National Institute of Health held a Consensus Development Conference on Defined Diets and Childhood Hyperactivity. Their conclusions were published in an NIH Consensus Statement 1982 Jan 13-15;4(3):1-11 The 1982 NIH panel’s findings relating to diet therapy, was:
- The Feingold diet is a valid option for the treatment of childhood hyperactivity.
- While some children were clearly helped, the scientific studies did not support the clinical reports of 60 to 70% success.
- But the studies were seriously flawed, and dealt almost exclusively with dyes, and thus were not a valid test of the Feingold diet.
Their report states:
“Controlled challenge studies have primarily involved the administration of food dyes to children, but have not included other food flavors or preservatives that are allegedly implicated in the causation of hyperactivity. Therefore, these controlled challenge studies do not appear to have addressed adequately the role of diet in hyperactivity.”
Although not even named as a distinct condition until 1968, by 1996 ADHD accounted for at least 40% of child psychiatry references.
In 1998, another Consensus Development Conference on stimulant drug and other treatments for ADHD was held by the NIH. They failed to reach a consensus on how to define ADHD, although calling it the “most commonly diagnosed behavioral disorder of childhood.” It was reported that the disorder is more prevalent in the United States than elsewhere.
The 23 nonstimulant treatments for ADHD which were reviewed by L. Eugene Arnold were totally ignored, with diet therapy alone mentioned only in passing, with the statement that “some of the dietary elimination strategies showed intriguing results suggesting future research.”
In their section on effective treatments, the panel concluded that:
- It cannot be determined if the combination of stimulants and psychosocial treatments can improve functioning with reduced dose of stimulants;
- there are no data on the treatment of ADHD, Inattentive type;
- There are no conclusive data on treatment in adolescents and adults with ADHD;
- There is no information on long-term treatment;
- There is a need for development of methods targeted to cognitive problems such as deficiencies in working memory and language deficits.
This was the meeting at which one doctor (mentioned above under “What Causes ADHD?”) complained in exasperation to the reporters that “diagnosis is a mess!!”
Dr. Arnold later published his review of the non-stimulant treatments which the panel had almost totally ignored. It can be seen here.
As the 1998 conference was being organized, and responding to the ongoing complaint that there was no long term research on the safety or efficacy of stimulant medication, a 14-month study known as the Multimodal Treatment Study of ADHD (MTA Study), had already been initiated. It involved more than 570 children with ADHD at 6 sites in the United States and Canada. Results generally showed that medication alone was more effective than psychosocial treatments alone, but that their combination was beneficial for some children. More than 40 studies have subsequently been published from this same data. [Note: Diet was not included in this study, and although this is often billed as the “largest study on ADHD ever done,” the Schoenthaler study on over a million children whose diet had been changed was much larger.]
In 2004, Bateman et al did a study in England on toddlers from the general population. The children were given a modest amount of coloring (only 20 mg) plus some sodium benzoate preservative. Their reaction was sufficient for Bateman to conclude that “this suggests that benefit would accrue for all children if artificial food colours and benzoate preservatives were removed from their diet.“
In 2007, a followup study (McCann 2007) was also published in England, showing that in the general population (children not diagnosed with anything), a modest amount of mixed coloring and a preservative elicited increased hyperactive symptoms and decreased attention span in both toddlers and older children. This study led to a radical change in the food supply of England and Europe, as supermarkets and international suppliers scrambled to replace the synthetic colorings and preservatives with safer, natural colorings and natural preservatives.
To date, the United States has not responded in any way to this development.