By Carolyn Dean, M.D., N.D.

Attention deficit-hyperactivity disorder (ADHD) is a syndrome characterized by persistent inattentiveness, poor impulse control, and hyperactivity. In 1987 it entered the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders—Third Revision (DSM-IIIR) as a newly defined entity, combining the use in older versions of this publication of the term “hyperactivity” with the condition known as attention deficit disorder (ADD).

How Common is ADHD?

An editorial addressing a 2002 study of the incidence of ADHD commented that although "the published diagnostic criteria lend an aura of objectivity to the diagnosis” of ADHD, “the application of these criteria is based on subjective judgments regarding the accuracy of information given by parents and teachers,” and that this subjectivity would be eliminated “only when and if biological markers can be found to identify the condition.”(1)

The study that the editorial addressed had thoroughly examined the medical and school records of 5,718 children. It had identified children with a clinical diagnosis of ADHD, documented symptoms of ADHD according to the Diagnostic and Statistical Manual of Mental Disorders—Fourth Revision (DSM-IV), and positive results on a questionnaire for ADHD, and had categorized the study subjects into three groups according to these criteria as having definite, probable, or questionable ADHD.

Although the collective incidence of affected children in all three classes was 16%, children with definite ADHD accounted for less than half of this total. The publication Education Week noted that the study helped to clarify some of the confusion about the true incidence of ADHD, which ranges from 1 to 20% (2), but the editorial addressing the study stated that the wide range of incidence numbers reflects the troubling issue of subjective diagnosis of ADHD, in which the common childhood behavior known as “acting out” is confused with true ADHD. Equally noteworthy is that the study reported that 86.5% of children with definite ADHD, 40% of those with probable ADHD, and 6.6% of those with questionable ADHD were all receiving stimulant medication. (3) Concerns about the tendency to medicate ADHD has arisen in many circles along with evidence that the pharmacologic action of Ritalin is much like cocaine. (4-6)

The Behavioral, Social, and Financial Costs of ADHD

An in depth 1999 report on mental health from the U.S. Surgeon General states that although a great many children with ADHD adjust to their condition, some develop problems with conduct and display defiant behavior (7). The report goes on to note that this group is more likely to drop out of school and do poorly in the workforce than children without ADHD. The report furthers points out that as they grow older, some teenagers who have had severe ADHD in childhood experience anxiety or depression (7).

With regard to the economic burden imposed by ADHD, a cost- comparison study found that the overall average yearly cost of medical care for children with the disorder was $1,151, a figure slightly higher than the $1,091 annual cost of care for children with asthma, but significantly above the $712 average yearly cost of care for the general pediatric population (8). However, the study pointed out that because much ADHD-related care occurs within the school and mental health settings, the estimated yearly medical cost for the condition underestimates the total cost of caring for children who have it.

What Causes ADHD?

According to the Surgeon General’s report of 1999, the exact etiology of ADHD remains unknown, but “neurotransmitter (dopamine) deficits, genetics, and perinatal complications have been implicated” in its occurrence (7)

The report notes that chronologically, it was observed shortly after the Second World War that brain-damaged children were often hyperactive, and a label of “minimal brain damage” (MBD) was used to define this condition, but that recent imaging studies have found no evidence of gross brain damage in children with ADHD (7). The subsequent designation of “attention-deficit disorder” (ADD) was adopted by the DSM-III in the late 1970s when it was hypothesized that hyperkinetic children suffered from inattention.

The “dopamine hypothesis” for the cause of ADHD arose in the 1980s when it was found that the symptoms of ADHD responded well to treatment with stimulant drugs such as methylphenidate (Ritalin) that increase the availability of dopamine in the central nervous system. In terms of cerebral function, dopamine is essential for initiating purposive movement, increasing motivation and alertness, reducing appetite, and inducing insomnia--effects often seen when methylphenidate is given to children with a diagnosis of ADHD, and most current research is pursuing the dopamine hypothesis for the disorder.

Additionally, there is a strong focus on finding one or more genes that may underlie ADHD. This is based on the tendency of the disorder to run in families, as evidenced by the fact that from 10% to 35% of children with ADHD have a first-degree relative who had or has the disorder. (9-11)

Nevertheless, the Surgeon General’s report concludes that the overall effects of genetic abnormalities in causing ADHD are probably small, and suggests that nongenetic factors also are important. In this regard, the report notes that some investigators have suggested that exposure to lead or other toxins may be involved, and that episodes of fetal oxygen deprivation, such as occur during some complications of pregnancy, may adversely affect dopamine-rich areas of the brain. The report also point out that hyperactivity and inattention are more common in children whose mothers smoked during pregnancy. (7)

Medical Treatment

The medical treatment of ADHD has focused on pharmacotherapy (12) and on psychosocial, behavioral, and educational strategies that have been recommended for enhancing specific behaviors and potentially improving the educational and social functioning of children with the disorder. (12) The “practice parameters” of the American Academy of Child and Adolescent Psychiatry (AACAP) state that “the cornerstones of treatment” for ADHD are the “support and education of parents, appropriate school placement, and pharmacology” (7), and further, the 1999 report of the Surgeon General states that psychostimulant drugs have been used to treat childhood behavioral disorders since the 1930s and are highly effective for as many as 90% of children with ADHD (7).

The stimulants methylphenidate (Ritalin) and dextroamphetamine (Dexedrine) have been the pharmacologic agents of first choice for the management of ADHD. (12) Ritalin, Dexedrine, and a mixture of amphetamine salts, according to the PDR are rapidly metabolized and exert their peak effects for a period of 1 to 5 hours and therefore may require frequent dosing. (13) They have their greatest effects on symptoms of hyperactivity, impulsivity, and inattention, and the associated features of defiance, aggression, and oppositional behavior, and only small effects on learning, and do not appear to achieve long-term changes in such measures as peer relationships or academic achievement.

Moreover, these medications have frequent side effects that include insomnia, decreased appetite, stomachache, headache, jitteriness, and tics, as well as anecdotally reported rebound symptoms when their use is stopped. More severe side effects have included psychosis and possible retardation of growth, and pemoline has been associated with liver toxicity. (14-16) Because of these drugs’ effects, children who take them should be given regular precautionary monitoring.

For the 10% to 30% of children who do not respond to stimulants or cannot tolerate these drugs, the Surgeon General’s report discusses “other useful medications” such as antidepressants, but also warns of dangerous and potentially lethal effects of tricyclic antidepressants and of controversy surrounding the use of central alpha-adrenergic blocking drugs such as clonidine and guanfacine, to treat ADHD (7). Neuroleptic agents such as chloropromazine, used in schizophrenia, are also on the list of medications for managing ADHD, but pose the risk of tardive dyskinesia, while fenfluramine, benzodiazepines, and serotonin-specific reuptake inhibitors such as fluoxetine have proven ineffective for ADHD. (7)

Nutrition and ADHD

A recent review of the literature found that certain “risk factors” for ADHD clustered around the eight areas of food allergies, thyroid disorders; deficiencies in amino acids, essential fatty acids (EFAs), minerals, and vitamin B deficiencies; heavy metal toxicities; and a diet high in carbohydrate and low in protein. (17)

In 1981, Colquhoun and Bunday noted that hyperactive children exhibited physical disturbances--including excessive thirst, frequent urination, drying and scaling of the skin, and behavioral abnormalities--that had been observed in animals deficient in essential fatty acids (EFAs). (18) They found evidence that EFAs in the diet normally provide a “waterproofing” effect in the skin, but that in children with ADHD this did not seem to occur, resulting in eczema and as well as other abnormalities common in ADHD. Colquhoun and Bunday attributed the problem to a lack of the normal conversion of dietary EFAs into polyunsaturated fatty acids (PUFAs) through metabolism in the liver and gut, and to the crititcal role of PUFAs in perception, cognition, memory, attention, and other cerebral functions. (19)

Corroborating Colquhoun and Bunday’s hypothesis was a report published in the Netherlands in the 1980s and cited by David Horrobin, an investigator of EFAs, in a book devoted to these nutrients. (20) The report from the Netherlands was based on that nation’s highly complete public health records and dated to a period of starvation during the Nazi occupation in the Second World War. The report described highly specific problems, including dyslexia and dyspraxia—later identified as representing ADHD—among children born to women from 4 to 12 months after the period of starvation. (20)

Nutrient Therapy

In the face of the multitude of studies of pharmacotherapy for ADHD, very few studies have been done in the United States on the effect of diet on the disorder, and a recent paper mentioned the neglect of nutrition in ADHD. (21) Several studies reported after Horrobin’s work have found lower levels of EFAs in children with in ADHD, (22-24 ) and at a 1999 conference sponsored by the Georgetown University medical center, Bellanti and colleagues presented evidence that ADHD was worsened by a junk food diet, food dyes, sugar, and yeast overgrowth due to antibiotics and sugar. (25 ) Along similar lines, a study reported in 2002 found that an elimination diet produced behavioral improvement in children with ADHD. (26)

Although sugar has purportedly been discounted as a “trigger” for hyperactive behavior, a study of 203 parents, conducted in 2003, found that two-thirds believed that sugar and diet do affect hyperactivity. (27) Moreover, studies of the relationship of sugar to ADHD have typically used far smaller quantities of sugar than a child ingests in a can of soda or sugared breakfast cereal; (28-32) have observed children for only a few hours after ingesting sugar; have used aspartame, a known neurotoxin as a placebo control for sugar in beverages: (33) and have failed to consider the possible effects of artificial colorings and flavorings in sugared beverages. (34-36) When Schoenthaler and Schauss removed sugar from the diets of thousands of children, they found remarkable improvements in behavior and increases in intelligence quotient. (37-40)

Nutritional supplementation may also have beneficial effects in ADHD. A study reported in 1996 found that children with ADHD had zinc levels that were only two-thirds those of children without the disorder, (41) and a study published in 1997 found that 95% of children with ADHD who were tested for their magnesium level were deficient in this micronutrient. (42) More recently, a small study in which Ritalin and nutritional supplementation with a multivitamin, multiple minerals, phytonutrients, EFAs from fish oil, soy lecithin as a source of phospholipid, acidophilus as a probiotic, amino acids, and supplements for detoxification were compared in children with ADHD found the supplementation regimen as effective as Ritalin, and without the latter’s risk of side effects. (43)

The authors concluded that the study results suggested that the abnormalities in ADHD are not preprogrammed and inevitable, but are instead an expression of genetically determined risk based on individual requirements for specific nutrients, which if not provided in optimum quantities may render affected individuals significantly more vulnerable to ADHD. (43)

Summary

On the basis of the findings described here, it would appear that in the near term, the key to managing ADHD at an intrinsic level, as opposed to “staving off” its effects pharmacologically, is further research in nutrition and its relationship to behavior, focusing particularly on EFAs and the effects of carbohydrates, vitamins, and minerals on cerebral metabolism, and with a genetic answer possibly lying further in the future.

Dr. Carolyn Dean, M.D., N.D.

Proficient in both conventional and alternative medicine Dr. Dean offers private consultations by phone. If you require individualization of the advice offered in this article, you can contact Dr. Dean at www.carolyndean.com or by email at drdean@carolyndean.com. At www.carolyndean.com, under Dean Wellness, you can find a list of food and supplement resources including food-based organic vitamins and angstrom-size minerals that Dr. Dean recommends.

Dr. Dean graduated from medical school in 1978 and holds a medical license in California. She is also a graduate of the Ontario Naturopathic College, now the Canadian College of Naturopathic Medicine, where she sat on the Board of Governors for six years.

Dr. Dean is an expert in difficult to diagnose conditions such as digestive and intestinal disorders (IBS); hormone imbalance and estrogen dominance; and yeast overgrowth as evidenced by three of her books, IBS for DUMMIES, Hormone Balance, and The Yeast Connection and Women’s Health. Another of Dr. Dean’s areas of expertise is magnesium. In her latest book, The Magnesium Miracle she uncovers evidence of magnesium deficiency in 22 health conditions including heart disease, arthritis, PMS, chronic fatigue syndrome, fibromyalgia, and anxiety. Dr. Dean is able to advise what types of magnesium are best suited for these conditions.

Dr. Dean has authored a total of twelve books to share her extensive knowledge in both traditional and alternative medicine. These titles include Natural Prescriptions for Common Ailments, Menopause Naturally, Homeopathic Remedies for Children's Common Ailments, The Miracle of Magnesium, Everything Alzheimer's, Hormone Balance, The Yeast Connection and Women’s Health, IBS for Dummies, Death by Modern Medicine, The Complete Natural Medicine Guide to Women’s Health, Solve it With Supplements, and The Magnesium Miracle.

References

1. Wender EH. Attention-deficit/hyperactivity disorder: is it common? Is it overtreated? Arch Pediatr Adolesc Med 156(3):209-210, 2002.

2. Fine, L. Minimum ADHD Incidence Is 7.5 Percent. Education Week. March 27, 2002.

3. Barbaresi WJ, et al. How common is attention-deficit/hyperactivity disorder? Incidence in a population-based birth cohort in Rochester, Minn. Arch Pediatr Adolesc Med 156(3):217-224, 2002.

4. Rushton JL, Whitmire JT. Pediatric stimulant and selective serotonin reuptake inhibitor prescription trends: 1992 to 1998. Arch Pediatr Adolesc Med 155(5):560-565, 2001.

5. Cox ER, Motheral BR, Henderson RR, Mager D. . Geographic variation in the prevalence of stimulant medication use among children 5 to 14 years old: Results from a commercially insured US sample. Pediatrics 111(2)237-243, 2003.

6. Vastag B. Pay attention: Ritalin acts much like cocaine. JAMA 286(8):905-906, 2001.

7. http://www.surgeongeneral.gov/library/mentalhealth/chapter3/sec4.html

8. Chan E, Zhan C, Homer CJ. Health care use and costs for children with attention-deficit/hyperactivity disorder: national estimates from the medical expenditure panel survey. J Dev Behav Pediatr 23(1 Suppl):S37-S45, 2002.

9. Smalley SL, McGough JJ, Del'Homme M, NewDelman J, Gordon E, Kim T, Liu A, McCracken JT. Familial clustering of symptoms and disruptive behaviors in multiplex families with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2000 Sep;39(9):1135-43.

10. Faraone SV, Biederman J, Mick E, Williamson S, Wilens T, Spencer T, Weber W, Jetton J, Kraus I, Pert J, Zallen B. Family study of girls with attention deficit hyperactivity disorder. Am J Psychiatry. 2000 Jul;157(7):1077-83.

11. Biederman J, Faraone SV, Mick E, Spencer T, Wilens T, Kiely K, Guite J, Ablon JS, Reed E, Warburton R. High risk for attention deficit hyperactivity disorder among children of parents with childhood onset of the disorder: a pilot study. Am J Psychiatry. 1995 Mar;152(3):431-5. )

12. Smucker WD, Hedayat M. Evaluation and treatment of ADHD. Am Fam Physician 64(5):817-829, 2001.

13. Watkins C. Stimulant Medication for AD/HD. Northern County Psychiatric Associates. http://www.baltimorepsych.com/Stimulants.htm

14. Cherland E, Fitzpatrick R. Psychotic Side Effects of Psychostimulants: A 5-Year Review. Can J Psychiatry 1999;44:811–813.

15. Croche AF, Lipman RS, Overall JE, Hung W. The effects of stimulant medication on the growth of hyperkinetic children. Pediatrics. 1979 Jun;63(6):847-50.

16. Marotta PJ, Roberts EA.Pemoline hepatotoxicity in children. J Pediatr 1998;132:894-7.]

17. Gant C, Harding K. Outcome-based comparison of Ritalin® versus food-supplement treated children with AD/HD. Alt Med Rev 8(3):319-330, 2003.

18. Colquhoun I, Bunday S. A lack of essential fatty acids as a possible cause of hyperactivity in children. Med Hypoth 7:673-679. 1981.

19. Ferrie H. EFA and ADHD. Vitality Magazine, April 2000. (see Richardson A. Fatty acids in dyslexia, dyspraxia,, ADHS, and the Autistic Spectrum. Nutrition Practitioner 3(3):18-24, 2001.)

20. Peet M, Glen I, Horrobin DF. Phospholipid Spectrum Disorder in Psychiatry, Marius Press, Carnforth.1999.

21. Schnoll R, Burshteyn D, Cea-Aravena J. Nutrition in the treatment of attention-deficit hyperactivity disorder: a neglected but important aspect. Appl Psychophysiol Biofeedback 28(1):63-75, 2003.

22. Haag M. Essential fatty acids and the brain. Can J Psychiatry 48(3):195-203, 2003.

23. Richardson AJ, Puri BK. A randomized double-blind, placebo-controlled study of the effects of supplementation with highly unsaturated fatty acids on ADHD-related symptoms in children with specific learning difficulties. Prog Neuropsychopharmacol Biol Psychiatry 26(2):233-239, 2002.

24. Richardson AJ, Puri BK. The potential role of fatty acids in attention-deficit/hyperactivity disorder. Prostaglandins Leukot Essent Fatty Acids 63(1-2):79-87, 2000.

25. Bellanti JA, Crook WG, Layton RE (eds,): ADHD: Attention Deficit Hyperactivity Disorder, Causes and Possible Solutions. Sponsored by the Georgetown University Medical Center. November 4-7, 1999, Arlington Virginia. Conference Syllabus.

26. Pelsser LM, Buitelaar JK. Favourable effect of a standard elimination diet on the behavior of young children with attention deficit hyperactivity disorder (ADHD): a pilot study. Ned Tijdschr Geneeskd 146(52):2543-2547, 2002.

27. Dosreis S, Zito JM, Safer DJ, et al. Parental perceptions and satisfaction with stimulant medication for attention-deficit hyperactivity disorder. J Dev Behav Pediatr 24(3):155-162, 2003.

28. Aylsworth J. Sugar and hyperactivity. Priorities: Winter l990, pp. 31-33.

29. Behar D, et al. Diet and hyperactivity. Nutr Behav 1:279-288, 1984.

30. Rapoport JL, et al. Behavioral response to sweeteners in preschool children. Presented at the International Conference on Nutrients and Brain Function, Scottsdale Arizona, February 12, l986.

31. Prinz, R. et al. Associations between nutrition and behavior in 5-year-old children. Nutr Rev .1986

32. Rapoport J. Diet and hyperactivity. Nutr Rev (Suppl):158-161, 1989.

33. Bradstock MK, et al. Evaluation of reactions to food additives: The aspartame experience. Am J Clin Nutr 43:464-469, 1986.

34. Egger J, et al. Controlled trial of oligoantigenic treatment in the hyperkinetic syndrome. Lancet 1:540-545, 1985.

35. Swanson and Kinsbourne. Food dyes impair performance of hyperactive children on a laboratory learning test. Science, March 28, 1980, p. 207.

36. Rowe KS, Rowe KJ. Synthetic food coloring and behavior: A dose- response effect in a double-blind, placebo-controlled, repeated-measures study. Pediatrics 125(5 Pt 1):691-698, 1994.

37. Schoenthaler SJ, et al. The impact of low food additive and sucrose diet on academic performance in 803 New York City public schools. Int J Biosocial Res 8:2, 1986

38. Schoenthaler SJ. The Los Angeles Probation Department Diet-Behavior Program: An empirical analysis of six institutional settings. Int J Biosocial Res 5(2):88-89, 1983.

39. Schoenthaler SJ. Northern California Diet-Behavior Program: An empirical examination of 3,000 incarcerated juveniles in Stanislaus County Juvenile Hall. l983. Int J Biosocial Res 5(2):99-108.

40. Schauss AG. Nutrition and behavior: Complex interdisciplinary research. A review. Nutr Health 3(1-2):9-37, 1984.

41. Toren P, et al. Zinc deficiency in attention-deficit hyperactivity disorder. Biol Psychiatry 40(12):1308-1310, 1996.

42. Starobrat-Hermelin B, Kozielec T. The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactivity disorder (ADHD). Positive response to magnesium oral loading test. Magnesium Res 10(2):149-156, 1997.

43. Gant C, Harding K. Outcome-based comparison of Ritalin® versus food-supplement treated children with AD/HD. Alt Med Rev 8(3):319-330, 2003

---

Article ID: 512