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Attention deficit hyperactivity disorder (ADHD) is one of the most frequently diagnosed childhood psychiatric condition.(1) One in every four children with ADHD has a biologic parent with a current or prior diagnosis of ADHD. In addition, children with fetal alcohol syndrome, lead poisoning, meningitis, or genetic resistance to thyroid hormone have a higher incidence of ADHD symptomatology.(2, 3) Although not a primary cause, a positive association exists between family environment adversity factors (severe marital discord, low social class, large family size, paternal criminality, maternal mental disorder, foster care) and ADHD.(2, 4)
Prior to 1980, a child presenting with short attention span, impulsivity, and hyperactivity was diagnosed with Minimal Brain Dysfunction. However, this diagnosis was controversial because clinicians could not consistently identify specific neurologic deficiencies. In 1980, the American Psychiatric Association made a decision to de-emphasize neurological dysfunction as a basis for diagnosis, and instead, use behavior. The syndrome was called ADD (Attention Deficit Disorder) with or without Hyperactivity. Hyperactivity has now been defined as an essential component and the name has been changed to ADHD.
Although brain studies show no definitive pathophysiologic markers of ADHD, a dysequilibratory disorder of the frontal-neostriatial dopamine systems with widely varying states of arousal has been proposed. Children with ADHD tend to have phasic outbursts of activity and inactivity, resulting in insufficient alertness during dull and repetitive tasks, and overarousal at other times, resulting in ineffective performance. Stimulant drugs may serve as a homeostat to stabilize arousal and thereby temper the spontaneous fluctuations that are characteristic of ADHD.(2, 5) The clinical response with stimulants is not paradoxical and is not diagnostic for ADHD, because asymptomatic children also experience increased attention, decreased motor activity, and improvement on learning tasks when given stimulants.
Onset is typically seen by the age of three, and must be seen by the age of seven. However, the disorder may not require professional attention until the child enters school.
Conventional treatment is often pharmaceutical, but evidence is mounting that many ADHD sufferers can achieve dramatic results with dietary, nutritional, and environmental interventions. Particularly among young children, non-pharmaceutical interventions provide a risk free alternative that can be explored as a first line of treatment. Nutritional interventions include supplementation with magnesium, chromium, and other minerals, elimination of food additives and allergens, and the examining the role of dysbiosis.
Mineral status among those with ADHD has been the subject of several published clinical trials. Deficiencies in magnesium, copper, iron, zinc, and calcium have been identified among children diagnosed with ADHD more often than among "healthy" children. Magnesium deficiency is the most common of the mineral deficiencies associated with ADHD
ADHD may be influenced by dysbiosis. The presence of dysbiotic flora is encouraged by the use of antibiotics, which can destroy "friendly" or probiotic flora normally inhabiting the intestinal mucosa. The average child undergoes multiple courses of antibiotic treatment in the first five years of life, typically without replacement of probiotics. The resulting overgrowth of yeast and other pathogenic flora has been linked to alterations of immune function, food sensitivities, and ADHD. A study reported that high levels of antimetabolites, consistent with fungal or Candida related complex, were identified in the urine of children with ADHD.(6) Supplementing with probiotics is an imp
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