Efa Dietary Supplement With Vitamin E Articles & Resources

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).

The neurobiological etiology of AD/HD has been postulated to be associated with deficiencies in catecholamines, such as norepinephrine and dopamine, (75) with little discussion concerning the physiological origins of the multifaceted mechanisms required to generate such neurotransmitters. Likewise, the therapeutic effect of Ritalin[R] is thought to be linked to its effects on norepinephrine and dopamine. (76) In contrast to this view of neurotransmitters as isolated variables that exist independent of the whole organism, this study protocol attempted to restore and regulate neurotransmitters in test subjects by supplementing the diet with amino acid precursors (., tyrosine) likely to be deficient in the subject as determined by symptoms. For instance, since tyrosine is the precursor for dopamine and norepinephrine, and deficiencies in these excitatory neurotransmitters are likely to be a factor in inattentiveness, subjects who displayed predominantly inattentive symptoms (as opposed to hyperactivity) were provided with extra tyrosine as

part of their supplement regimen. In addition, vitamin and mineral co-factors for neurotransmitter formation were supplemented. Other etiological factors were addressed by nutrients as indicated.

Patients and Methods

Twenty children diagnosed with AD/HD by a clinical child psychologist were divided into two groups by parental choice. Ten subjects were prescribed Ritalin by a family physician. The other 10 were prescribed dietary supplements by a certified nurse clinical specialist. Supplementation consisted of a multiple vitamin, a multiple mineral, phytonutrients, essential fatty acids and phospholipids (soy lecithin), probiotics, and amino acids (Table 1a and 1b). The dietary supplements chosen were those most likely to address the eight etiological factors previously noted and as outlined by Gant. (77) All children in the Ritalin group received prescribed doses of 5-15 mg Ritalin 2-3 times daily, as determined by the prescribing physician.

To be eligible, children had to be 7-12 years old, and were required to be without any other medication or treatment, street drugs, or other nutritional or botanical supplements. The psychologist screened patients to rule out co-morbid disorders. These criteria were selected because previous studies of specific treatment for AD/HD children encouraged diagnostic heterogeneity (not molecular or biological heterogeneity) to reduce factors that may affect treatment response. (78) For example, children found to have coexisting conduct disorder or oppositional defiant disorder were screened out of this study.

Subsequent to diagnostic screening, parents were given literature regarding AD/HD, information about conventional drug treatment (Ritalin), and a booklet describing unconventional (alternative) treatments with dietary supplements. Parents who chose Ritalin were referred back to their family physicians to acquire a prescription, while parents who chose dietary supplement treatment were referred to a psychiatric nurse clinical specialist for counseling regarding types, amounts, and frequency of administration of supplements. Parents were also informed and signed a consent form to allow the data to be included in a doctoral dissertation for a clinical psychology program.

Diagnostic methods included a developmental history, an assessment of DSM-IV diagnostic criteria, (1) the Conner's Parent Rating Scale (1989-1990). (79) and the Intermediate Visual and Auditory/Continuous Performance Test (IVA/ CPT). (80) The Conner's Parent Rating Scale--Revised: Long Form (CPRS-R:L) was developed to assess a wide range of childhood behavioral difficulties, including conduct disorders, problems of cognition, social difficulties, and anxiety. The revised version has achieved excellent reliability and validity.

The IVA/CPT has high reliability and validity in diagnosing and assessing AD/HD treatment efficacy as well as medication titration. The IVA/CPT is a computerized, standardized test developed for the assessment of response inhibition and attention problems. This test is characteristically unique because it tests for auditory as well as visual distractibility. The test analysis yields detailed reports on 22 different scales. The six primary composite quotient scales are: (1) prudence, in which the subject thinks before acting and avoids impulsive errors of commission; (2) consistency, in which most of the subject's response times are clustered within a narrow range; (3) stamina, which is the subject's response times as maintained for the duration of the test; (4) vigilance, in which the subject identifies all targets by avoiding inattentive errors of commission; (5) focus, in which the subject shows no evidence of momentary lapses; and (6) speed, in which the subject response times are rapid, providing evidence that the brain's resources are dedicated to the task at hand. The quotient scores have a mean of 100 and a standard deviation of 15, the same as is utilized for most standardized IQ tests. The printed IVA/ CPT results are presented in the form of graphs that allow comparisons to a normative sample and for test-retest evaluation. It is then possible to quickly compute the change in quotient scores between any two IVA/CPT tests in order to evaluate treatment effects.

Scores for the six primary scales of the IVA/CPT are obtained lot both visual and auditory performance. There are two major quotients derived from these six scales. Prudence, consistency, and stamina comprise a Full Scale Response Control Quotient (FSRCQ), while vigilance, locus, and speed comprise a Full Scale Attention Control Quotient (FSACQ). These global composite quotient scales allow efficient summary and evaluation of the test results.

Statistical Analysis/Results

The primary outcome measure used was the IVA/CPT. (80) Figure 1 illustrates the results of pre- and post-treatment IVA/CPTs for a patient treated with nutritional supplements. Figure 2 "subtracts" the outcomes of the pre-treatment IVA/CPT from the posttreatment results and displays a net gain on both the FSRCQ, which measures impulsivity, and the FSACQ, which measure inattentiveness. Note these two global measurements of impulsivity and inattentiveness are further broken down into visual and auditory responses (., visual inattentiveness versus auditory inattentiveness), and the FSRCQ has a third category of motor restlessness (fidgetiness) as well. Figure 1 further subdivides the IVA/CPT categories into "pru" (prudence), "con" (constancy), "sta" (stamina), "vig" (vigilance), "foe" (focus), and "spd" (speed).

[FIGURES 1-2 OMITTED]

Comparison of the Ritalin treatment group and the group treated with dietary supplements was accomplished using a WINKS two-way analysis of variance with repeated measures as well as Tukey multiple comparisons.

The data was collected from the CPRSR:L and IVA/CPT. The CPRS-R:L and IVA/CPT were both administered pre-treatment. The IVA/ CPT was re-administered after four weeks of treatment for both groups. Retesting of the Ritalin group subjects was conducted two hours after their recommended dose, due to peak effect occurring within 1-3 hours. In contrast, no peak time was advised for the alternative treatment group. Subsequently, t-tests and tests for homogeneity of variance were used to analyze data on all sub-tests of the CPRS-R:L. Results of these analyses were used to evaluate equivalence or differences between groups. Statistical analysis used in assessing differences resulting from treatment within and between the dietary supplement and Ritalin groups was a two-way repeated measures analysis of variance for each of the scales of the IVA/CPT. Subsequent post-hoc comparisons were carried out where significant F ratios were found. The scores were compared by utilizing a WINKS two way analysis of variance with Tukey WSD post-hoc comparison. (81)

The FSRCQ yielded significant pre-test to post-test differences for both the Ritalin and the alternative treatment groups (Figures 3 and 4). Subjects in both groups showed significant (p [less than or equal to] ) gains in the FSRCQ. Increases in FSACQ were also found to be significant (p[less than or equal to] ) for both the Ritalin and the alternative treatment groups (Figures 3 and 4). Comparative analyses indicated there were no significant differences in the level of improvement between the two groups. Thus, the effect of Ritalin versus dietary supplement treatment was found to be essentially the same, and both treatments were found to be effective after four weeks of use.

[FIGURES 3-4 OMITTED]

Increases in the four sub-scales or subquotients that comprise these two major scales were found to be significant as follows:

(1) Auditory Response Control Quotient (ARCQ (p [less than or equal to] ))

(2) Visual Response Control Quotient (VRCQ (p [less than or equal to] ))

(3) Auditory Attention Quotient (AAQ (p [less than or equal to] ))

(4) Visual Attention Quotient (VAQ (p [less than or equal to] ))

Post-hoc tests indicated homogeneity of variance for both groups on all sub-quotients and no significant between-group differences (Figures 3 and 4).

Discussion

This study compared outcomes of two distinct paradigms of AD/HD treatment--the pharmaceutical (Ritalin) and the nutraceutical (dietary supplements). Ritalin's therapeutic effect has been hypothesized to result from presynaptic dopamine transporter inhibition, thus increasing the availability of the neurotransmitter dopamine, (82) especially in the frontal lobes of the cerebral cortex. (83) Dietary supplements used in this study also potentially increase catecholamine(dopamine, norepinephrine, and epinephrine) synthesis by precursor loading (tyrosine is the precursor to dopamine and norepinephrine (84)) and delivering B-vitamin (vitamins B3, B6, and folic acid) and mineral (iron and copper) cofactors. Vitamin C is also a cofactor for the synthesis of the neurotransmitter norepinephrine, imbalances of which are also linked to AD/HD, (82) and may be beneficial in reducing toxicity of some heavy metals, such as lead. Phospholipids and essential fatty acids are necessary for cell membrane repair, especially in the developing central nervous system, and may improve synaptic physiology and neurotransmitter efficiency. (85) These essential lipids have also been utilized for gut enterocyte repair, which, along with reinnoculation of friendly flora and the administration of probiotics, could mitigate food allergy. Formal allergy testing, desensitization procedures, or rotation/elimination of potentially allergenic foods were not done in this study.

Reviews of the physiological and anatomical brain abnormalities in AD/HD suggest AD/HD arises idiopathically or that such brain abnormalities are caused by a genetic predisposition. (83) If such anatomical and physiological abnormalities were to arise spontaneously in genetically susceptible individuals, without known biochemical cause(s), it would follow that optimal treatment of AD/HD should be palliative, symptom management with medications. The 70 studies that support the eight risk factor categories as well as the positive outcomes in this study suggest AD/HD does not arise spontaneously, but in fact is caused by a combination of factors. This evidence suggests the physiological and anatomical brain abnormalities in AD/HD are not pre-programmed and inevitable, but are instead an expression of genetic vulnerabilities to the noted risk factors. Certain individuals may have genetically-imposed, heightened requirements for certain nutrients. If such individuals are not provided with optimum targeted nutrition, they may be significantly more vulnerable to the physiological and anatomical brain abnormalities associated with AD/HD symptoms.

Regardless of the various biological, psychological, or psychosocial factors that are ultimately found to cause AD/HD, this study found that synergistic combinations of dietary supplements directed at the more probable underlying etiologies of AD/HD, as determined by previous studies, (6-74) were equivalent to Ritalin treatment as measured by improvements of attention and self-control using IVA/CPT testing. The means for both treatment groups demonstrating the greatest subject impairment were found in the Full Scale Attention Control Quotient and the Visual Attention Quotient. This is consistent with the validity study for the IVA/CPT, where "comparisons of pre- and post-IVA/CPT scores can reliably be interpreted to reflect possible medication, treatment, or environmental effects." (80)

These findings support the effectiveness of a combined vitamin, mineral, amino acid, probiotic, essential fatty acid, and phospholipid treatment in improving attention and self-control in children with AD/HD. This combined nutritional approach more or less addressed eight likely risk factors. Further studies that target nutritional treatments to the unique, a priori, laboratory-determined risk factors of each test subject would go far beyond such vague empiricism and potentially achieve even better outcomes, based on treatment of the unique biochemical heterogeneity of each individual test subject.

Table 1a. Supplements Used in the Alternative Treatment
Group

Gastrointestinal and Immune Support (Risk Factor #1)

(1) Lactobacillus acidophilus and bifidus

(2) Lactoferrin (5 mg)

(3) Silymarin (5 mg)

Sulfur-Containing Supplements and Glycine (Risk Factor #2)

(1) Taurine (275-425 mg)

(2) Glycine (700-1830 mg)

(3) Methionine (25-75 mg)

(4) N-acetylcysteine (NAC) (0-10 mg)

(5) L-cysteine (0-25 mg)

(6) Glutathione (20 mg)

(7) alpha Lipoic acid (5 mg)

(8) Garlic extract (200 mg)

Amino Acids (Risk Factors #3 and #6)

(1)Tyrosine (900-1800 mg)

(2) Histidine (25-75 mg)

(3) Glutamine (600-1400 mg)

(4) alpha Ketoglutarate (AKG) (25-75 mg)

(5) L-carnitine (30 mg)

Minerals (Risk Factor #4)

(1) Magnesium (as magnesium glycinate) (220-480 mg)

(2) Calcium (as calcium ascorbate) (110-170 mg)

(3) Potassium (as glycerol phosphate)(46-70 mg)

(4) Chromium (as nicotinate) (140-200 mcg)

(5) Selenium (as methionate) (26-32 mcg)

(6) Zinc (as monomethionate) (9-15 mg)

(7) Manganese (as arginate) ( mg)

(8) Boron (as citrate) (1200-800 mcg)

(9) Copper (as tyrosinate) (.4 mg)

(10) Silica (4 mg)

(11) Molybdenum (as chelate) (5-40 mcg)

(12) Vanadium (chelate) (2-20 mcg)

(13) Iron (as glycinate)(1-2 mg)

Table 1b. Supplements Used in the Alternative Treatment Group

Essential Fatty Acids and Phospholipids (Risk Factor #5)

(1) Salmon oil 1000 mg (EPA 180 mg; DHA 120 mg)

(2) Borage oil 200 mg(GLA 45 mg)

(3) Purified Soy Lecithin (Phosphatidyl choline 50-150 mg;
Inositol 20-25 mg)

(4) Choline bitartrate (.5 mg)

Agents to Support Thyroid Functioning (Risk Factor #7)

(1) Iodine (from kelp) (25-150 mcg)

(2) Tyrosine (900-1800 mg)

B Vitamins and Phytonutrients (Risk Factor #8)

(1) Vitamin B1 (as thiamine and thiamine pyrophosphate)
(.5 mg)

(2) Vitamin B2 (as riboflavin and riboflavin phosphate)
(.5 mg)

(3) Vitamin B3 (as niacin and niacinamide) (75-140 mg)

(4) Vitamin B5 (as D-calcium pantothenate and pantethine)
(50-70 mg)

(5) Vitamin B6 (as pyridoxine and pyridoxal-5-phosphate)
(43-86 mg)

(6) Vitamin B12 (cyanocobalamin) (90-175 mcg)

(7) Folic acid (435-760 meg)

(8) Biotin (20-400 mcg)

(9) PABA (.5 mg)

(10) Vitamin E (140-200 IU)

(11) Vitamin C (750-1000 mg)

(12) Vitamin A (as vitamin A and beta carotene) (2000-4500 IU)

(13) Vitamin D3 (40-100 IU)

(14) Vitamin K (20 mcg)

(15) Royal bee jelly (source of biopterin) (75-150 mg)

(16) Dimethyl glycine (10 mg)

(17) Citrus bioflavonoids (10-20 mg)

(18) Proanthocyanidins (grape seed) (5 mg)

(19) Bilberry extract (20 mg)

(20) Soy constituents (saponins, isoflavones, phytosterols) (20 mg)

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Karen Harding, PhD--appointed Harvard Medical School Fellow at McLean Hospital in Belmont, Massachusetts for an internship in child/adolescent psychology and for a post-doctoral program in neuropsychology.

Richard Judah, PhD--practicing psychologist in central Massachusetts; 25 years of experience working with children with learning, attentional, and behavioral problems; faculty of the Department of Graduate Psychology and Counseling at Vermont College of Union Institute and University.

Charles Gant, MD, PhD--has practiced integrative and orthomolecular medicine for 25 years, currently in Washington, DC. He is best known for his work in biomolecular/nutritional medicine as it relates to brain physiology and psychotherapeutics.

Correspondence address: National Integrated Health Associates, 5225 Wisconsin Ave., Suite 401, Washington, DC 20015