Outcome-based comparison of Ritalin® versus food-supplement treated children with AD/HD - Original Research

Alternative Medicine Review, August, 2003 by Karen L. Harding, Richard D. Judah, Charles E. Gant

Abstract

Twenty children with attention deficit/ hyperactivity disorder (AD/HD) were treated with either Ritalin[TM] (10 children) or dietary supplements (10 children), and outcomes were compared using the Intermediate Visual and Auditory/Continuous Performance Test (IVA/ CPT) and the WINKS two-way analysis of variance with repeated measures and with Tukey multiple comparisons. Subjects in both groups showed significant gains (p[less than or equal to] 0.01) on the IVA/CPT's Full Scale Response Control Quotient and Full Scale Attention Control Quotient (p[less than or equal to] 0.001). Improvements in the four sub-quotients of the IVA/CPT were also found to be significant and essentially identical in both groups: Auditory Response Control Quotient (p [less than or equal to] 0.001), Visual Response Control Quotient (p[less than or equal to] 0.05), Auditory Attention Quotient (p[less than or equal to] 0.001), and Visual Attention Quotient (p[less than or equal to] 0.001). Numerous studies suggest that biochemical heterogeneous etiologies for AD/ HD cluster around at least eight risk factors: food and additive allergies, heavy metal toxicity and other environmental toxins, low-protein/ high-carbohydrate diets, mineral imbalances, essential fatty acid and phospholipid deficiencies, amino acid deficiencies, thyroid disorders, and B-vitamin deficiencies. The dietary supplements used were a mix of vitamins, minerals, phytonutrients, amino acids, essential fatty acids, phospholipids, and probiotics that attempted to address the AD/ HD biochemical risk factors. These findings support the effectiveness of food supplement treatment in improving attention and self-control in children with AD/HD and suggest food supplement treatment of AD/HD may be of equal efficacy to Ritalin treatment.

Introduction

Attention deficit/hyperactivity disorder (AD/HD) is classified by the Diagnostic and Statistical Manual of Mental Disorders--Fourth Edition (DSM-IV) as a mental disorder primarily characterized by a "persistent pattern of inattention and/or hyperactivity-impulsivity that is more frequent and severe than is typically observed in individuals at a comparable level of development." The DSM IV explicitly defines the meaning of the term "disorder." (1)

"In DSM-IV, each of the mental disorders is conceptualized as a clinically significant behavioral or psychological syndrome or pattern that occurs in an individual and that is associated with present distress (e.g., a painful symptom) or disability (i.e., impairment in one or more important areas of functioning).... Whatever its original cause, it must currently be considered a manifestation of a behavioral, psychological, or biological dysfunction in the individual.... In DSM-IV, there is no assumption that each category of mental disorder is a completely discrete entity with absolute boundaries dividing it from other mental disorders or from no mental disorder. There is also no assumption that all individuals described as having the same mental disorder are alike in all important ways. The clinician using the DSM-IV should therefore consider that ... individuals sharing a diagnosis are likely to be heterogeneous even in regard to the defining features of the diagnosis and that boundary cases will be difficult to diagnose in any hut a probabilistic fashion."

Although individuals diagnosed with AD/ HD share a similar range of outward behavioral symptoms, the underlying causalities are "likely to be heterogeneous," (2) a term defined as "of unlike natures, composed of unlike substances" and "consisting of dissimilar or diverse ingredients or constituents." (3) Such heterogeneity could be within biological, psychological, and/or social levels of organization (The Biopsychosocial Model) (4) or could vary widely within each level of organization for each individual with AD/HD. At least at the biological level of the biopsychosocial model, an extensive literature review by Kidd strongly supports a heterogeneous molecular etiology for AD/HD, with each individual likely to have a unique array of abnormalities expressed symptomatically as AD/HD. (5)

There is a complex body of information suggesting multiple, heterogeneous, biochemical etiologies for AD/HD. For purposes of discussion and clinical utility, the information can be assembled into eight general etiological categories: (1) food and additive allergies; (6-25) (2) heavy metal toxicity and other environmental toxins; (26-36) (3) low-protein, high-carbohydrate diets; (37-39) (4) mineral imbalances; (40-52) (5) essential fatty acid (EFA) and phospholipid deficiencies; (53-57) (6) amino acid deficiencies; (58-63) (7) thyroid disorders; (64-67) and (8) B-vitamin and phytonutrient deficiencies. (68-74)

Each of the publications noted above examines only the relationship of AD/HD to a single or a few risk factors. Furthermore, within each etiological category, the studies primarily examine only the relationship of AD/HD to a single or a few variables within each category. Exemplary variables included, but were not limited to, various food and additive allergies, two toxic metals (aluminum and lead), several B-vitamin (B1, B3, and B6) deficiencies, several amino acid (tryptophan, tyrosine, and D- and L-phenylalanine) deficiencies, thyroid abnormalities, a high-carbohydrate and low-protein diet, endogenous protein and carbohydrate metabolic abnormalities, EFA deficiencies of the omega-3 series, and abnormalities in several essential minerals (iron, selenium, zinc, copper, phosphorus, calcium, and magnesium).