ADD/ADHD in Children:

Are There Really Alternatives to Ritalin® and Prozac®?

Dana Myatt, N.M.D. and Mark Ziemann, R.N.

Attention Deficit Disorder (ADD), ADD with Hyperactivity (ADHD), and depression represent a continuum of learning and behavioral disabilities that afflict an estimated 5-10% of school-aged children. In the United States, conventional medical treatment of choice is pharmaceutical intervention.

A large body of scientific evidence suggests that these disorders are multi-factorial, representing a special challenge to the holistic physician interested in treating causes as well as symptoms. The concept of “Alternatives to Ritalin and Prozac” is, in the author’s opinion, an allopathic approach to botanical prescribing that is less efficacious than treatments which address specific etiologies. Regardless of the approach, however, botanical medicines have an important role to play in treatment.


Definition (ADD, ADHD) Developmentally inappropriate inattention and impulsivity, with or without hyperactivity (1). The DSM-IV lists 14 signs, 8 of which must be present to make the diagnosis. They are:

  1. Often fidgets with hands or feet and squirms in seat (restlessness),
  2. Has difficulty remaining seated when required to do so,
  3. Is easily distracted by external stimuli,
  4. Has difficulty awaiting turn in games or group situations,
  5. Often blurts out answers before questions are completed,
  6. Has difficulty following through on instructions from others (not due to opposition but to failure of comprehension),
  7. Has difficulty sustaining attention in tasks or play activities,
  8. Shifts from one uncompleted task to another,
  9. Has difficulty playing quietly,
  10. Talks excessively,
  11. Often interrupts or intrudes on others,
  12. Often does not seem to listen to what is being said,
  13. Often loses things necessary for tasks at home or at school,
  14. Often engages in physically dangerous activities without considering consequences.

(Depression) ” . . .  sad and unhappy appearance, apathy and withdrawal, reduced capacity for pleasure, feeling rejected and unloved, difficulty in sleeping, somatic complaints (headache, abdominal pain, insomnia), episodes of clowning or foolish behavior, and persistent self-blame.”(2).


The Current Conventional “Going Line”

According to the U.S. Surgeon General and ICD-10-CM, ADHD is a metabolic form of encephalopathy which impairs the release and homeostasis of neurological  chemicals, and reducing the function of the limbic system. Research indicates that the frontal lobes, their connections to the basal ganglia, and the central aspects of the cerebellum (vermis) are most likely involved in this disorder, as may be a region in the middle or medial aspect of the frontal lobe, known as the anterior cingulate.

There is increasing evidence that variants in the gene for the dopamine transporter are related to the development of ADHD [12]. This evidence is consonant with the theory of inefficacy of dopamine in people with ADD/ADHD; according to other recent studies, some people with ADHD usually have relatively high dopamine transporter levels, which clears dopamine from between neurons before the full effect is gained from dopamine. Stimulant medications used to treat ADHD are all capable of either inhibiting the action of dopamine transporter (as methylphenidate does) or promoting the release of dopamine itself (as the amphetamine-class medications do). Therefore, it is theorized that stimulant medication allows the brain to enhance the effect of dopamine by blocking dopamine transporters or increasing the release of dopamine. Currently this is the most widely accepted model of ADD/ADHD etiology in the scientific and medical community.

New studies consider the possibility that norepinephrine also plays a role. Drugs that manipulate norepinephrine levels in certain brain regions, such as atomoxetine, have shown effectiveness for managing the disorder [13] [14].

It also should be noted that despite the repeated references to the genetics of ADHD being unequivocal, according to Joseph Glenmullen, M.D., clinical instructor in psychiatry at Harvard Medical School “no claim of a gene for a psychiatric condition has stood the test of time, in spite of popular misinformation.”

The Holistic “Going Line”

ADD/ADHD can be caused by a number of factors including Nutritional deficiencies (4,5) inborn errors of metabolism (6), food allergies (7,8,9), heavy metal toxicity (10,11), malabsorption (12), prenatal influences (13,14), genetic influence (15,16), environmental (17) and cultural factors (18), yeast infection (12), food additives (7,19,20), trauma (21), and developmental factors (22).

Scope of the Problem

For ADD, ADHD: An estimated 5-10% of school-aged children are affected. Boys are 10 times more likely than girls to be diagnosed with ADD/ADHD. An estimated 3-5% of ADD/ADHD-diagnosed children will be put on Ritalin (methylphenidate). In 1995, over 6 million prescriptions were written for Americans under age 18(3).

DEPRESSION, once thought to be rare in children, has become an increasingly common diagnosis, though actual numbers are uncertain. There is a higher incidence of depression in families with a history of depressive disorder (2). Depression may occur with or without ADD/ADHD.


The “cure” for ADHD relies on determining the cause. Obviously, if a nutritional deficiency is present and causative, this must be corrected. In another child, heavy metal toxicity may be the cause, in which case the treatment will be different than for those symptoms caused by nutritional imbalance.

Neurotransmitter levels should be evaluated with an NT test (urine is the specimen requirement). Heavy metal toxicity can be easily evaluated with a hair mineral analysis. Food intolerance can be screened for with a saliva test, but elimination/challenge diet is the most accurate method of determination. Yeast overgrowth in the intestinal tract can be screened with a stool test. These tests evaluate for the most common causes of ADD/ADHD. Which of them are necessary can be determined by a careful holistic physician who does an accurate history and physical exam.

Less common causes that may require evaluation include inborn errors of metabolism, trauma (especially birth trauma) and musculoskeletal imbalances.


The “one size fits all” approach of conventional medicine has resulted in millions of US children being put on Ritalin, an amphetamine. New studies show that Ritalin can cause permanent changes in the brain and can also result in hallucinations. Clearly, if there are many different causes of this disorder, there must be a number of different treatments, each distinct and particular to the patient.

A large body of scientific evidence suggests that ADD/ADHD is multi-factorial, meaning that there is usually more than one contributing cause. This presents a special challenge to the diagnosing physician if (s)he is interested in correcting the problem and not just treating symptoms. This may also account for the large number of children placed on drug therapy, which relieves the physician and parents of the responsibility of exploring the numerous causes and contributions to ADD/ADHD. However, due to the far-reaching effects that such attention disorders and behavior problems create, many people have found that it is worthwhile to discover and correct the causes of ADD/ADHD instead of simply “dumbing down” the symptoms with drugs.

Nutritional strategies include:

Diet And Lifestyle:

Diet: Elimination/challenge to discover food allergies, then avoidance of offending foods; avoidance of artificial additives and food colorants (Feingold diet); avoidance of simple carbohydrates (sugars and refined flour products). NO stimulants: colas, chocolate, caffeine- containing foods and beverages unless indicated by an NT evaluation.

Exercise: daily. Exercise helps normalize brain chemistry.


I.) Children’s Multi Vitamin: Optimal dosage according to age and body weight as listed on product label. A deficiency of any vitamin, mineral or trace mineral can lead to impaired mental performance.

II.) Omega-3 Fish Oil: A recent randomized double-blind experiment compared a fatty acid supplement with placebo in children with developmental coordination disorder (which exhibits a high degree of overlap with ADHD diagnoses). Fatty acid supplements improved spelling, reading, and behavior after three months (48). Numerous studies have shown an improvement in cognitive function, in mood, and in vision when omega 3 fatty acid supplements are given. While not directly showing a causal link between ADHD and fatty acids, increased levels of fatty acids have a beneficial effect on related behavior.

Furthermore, creating a deficiency of omega-3 fatty acids in pregnant rats produces pups that are hyperactive and that have altered brain levels of dopamine in the same brain regions as seen in humans and other rat models of hyperactivity. More research, however, is clearly needed before dietary supplements, such as those involving fatty acids can be recommended for clinical use.

III.) L-glutamine: 2,500-3,000mg per day. (This will vary depending on the age and weight of the patient).

IV.) Cal-Mag Amino: (calcium/ magnesium) [Target dose: < 10 years, 1,000mg calcium, > 10 years, 1,200- 1,500 mg calcium with corresponding dose of magnesium].

V.) Grape Seed Extract: 50 mg, 3 times per day with meals.

VI.) L-5-HTP (if indicated by an NT evaluation): dose according to weight in children. In adults, begin with 1 cap, 3 times per day and increase to 2 caps, 3 times per day after two weeks. Use only with medical supervision if antidepressant medications are also being taken.


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2.) Berkow, Robert, MD, editor-in-chief, et al. The Merck Manual of Diagnosis and Treatment, Sixteenth Edition. Merck and Company, N.J., 1992, p. 2269.
3.) John Robbins. Reclaiming our Health: Exploding the Medical Myths and Embracing the Source of True Healing. H.J. Kramer, Inc., 1996.
4.) Prinz RJ, Roberts WR,  Hartman E. Dietary correlates of hyperactive behavior in children. Journal of Consulting and Clinical Psychology, 1980, 48: 760-769.
5.) Thompson HL Malnutrition as a possible factor in Learning Disabilities. Journ Learn Disab 4:27, 1971.
6.) Trattler R. Better Health Through Natural Healing. McGraw-Hill, 1988,p. 360.
7.) Feingold BF. Why Your Child is Hyperactive. New York: Random House, 1975.
8.) Trites RL, Tryphonas H,  Furguson HB. Treatment of hyperactive and learning disordered children. Baltimore, Univ. Park Press, 1980.
9.) Crook WG. Can What a child eats make him dull, stupid, or hyperactive? Journ learn Disab 13:53-58, 1980.
10.) Needleman HL, Gunnoe C, Leviton A, et al. Deficits in psychological and classroom performance of children with elevated dentine lead levels. New Engl Jour of Med, 1979, 300, 13:689-695.
11.) Thatcher RW. Effects of Low Levels of Cadmium and Lead on cognitive functioning in children. Arch Environ Health 37: 159-166, 1982.
12.) Smith, L. Hyper Kids, Shaw/Spelling Assoc., Santa Monica, CA. 1990.
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17.) O’Leary KD, Rosenbaum A, et al.: Flourescent Lighting: A purported source of hyperactive behavior, Jour of Abnorm Child Psych, 6: 1978, p.285-289.
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19.) Rose TL. The functional relationship between artificial food colors and hyperactivity, Jour of Applied Behav Anal, 1978. P.439-446.
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21.) Silver L. Dr. Larry Silver’s Advice to Parents on Attention-Deficit Hyperactivity Disorder, American Psychiatric Press, Washington, D.C. 1993, p.119; p. 175-178.
22.) Dr. Myatt’s personal experience using “Patterning” and “Neurological reprogramming” techniques at the A.R.E. Clinic in Phoenix, AZ.,  based on the work of  Drs. Doman and Delicato of the Institute for the Achievement of Human Potential in Philadelphia, PA.
23.) ChevallierA. The Encyclopedia of Medicinal Plants, D.K. Publishing, New York: 1996.
24.) O’Leary KD. Mommy, I Can’t Sit Still, New Horizon Press, 1984, p.90.
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28.) Weiss RF. Herbal Medicine. AB Arcanum, Gothenburg, Sweden, 1988.
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30.) Ernst E. St. John’s Wort, an anti-depressant? A systematic, criteria-based review. Phytomed, 1995; 2:67-71.
31.) Vorbach EU, et al. Effectiveness and tolerance of the Hypericum extract LI 160 in comparison with imipramine: Randomized double-blind study with 135 outpatients. J Ger Psychiatry Neurol 1994; supplement 1:19-23.
32.) Werbach M, Murray M. Botanical Influences on Illness. Third Line Press, Tarzana, California, 1994, p. 31.
33.) Forester HB, et al. Planta medica, 40:4, p 309, 1980.
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35.) Hendriks H, et al. Planta Medica, 45:150, 1982.
36.) Lindhal G, Lindwall L. Pharmacol Biochem Behav 1989;32:1065-66.
37.) Leathwood P, Chauffard F, et al. Aqueous extract of valerian root (Valerian officinalis) improves sleep quality in man. Pharmacol Biochem Behav 1982; 17:65-71.
38.) Leathwood P, Chauffard F. Aqueous extract of valerian reduces latency to fall asleep in man. Planta Medica 1985; 51:144-148.
39.) Dressing H, Riemann, D, Low M, et al. Are valerian/melissa combinations of equal value to benzodiazepine? Therapiewoche 1992; 42:726-36.
40.) Mennini T, Bernasconi P, In vitro study on the interaction of extracts and pure compounds of valeriana officinalis roots and GABA, benzodiazepine and barbiturate receptos. Fitoterpia 1993; 64:291-300.
41.) Wohlfort R, Hansel R, Schmidt H. Planta Medica 48:120, 1983.
42.) Hoffman D. The Nervous System, Pacific NW Herbal Symposium conference notes, 1996, P. 74-85.
43.) Csupor L. Quantitative determination of kava lactones in Piper methysticum (Forster), Arch Pharm Ber Dtsch Pharm Ges 303 (3): 193-200, March 1970.
44.) Davies LP, Drew CA, Duffield P, et. al.: Kava pyrones and resins: studies on GABAA, GABAB and benzodiazepine binding sites in rodent brain. Pharmacol Toxicol 71 (2): 120-126, Aug 1992.
45.)MunteTF, Heinze HJ, Effects of oxazepam and an extract of kava roots on event-related potential in a word recognition task. Neuropsychobiology 27 (1):46-53, 1993.
46.) Volz HP, Keiser M. Kava-kava extract WS 1490 versus placebo in anxiety disorders— a randomized, placebo controlled 25-week outpatient trial. Pharmacopsychiatry 30 91): 1-S, jan. 1997.
47.) Ruze P.Kava-induced dermopathy: a niacin deficiency? The Lancet 335 (8703):1442-1445, June 1990.
48.) Richardson and Montgomery, Pediatrics, 2005, 115:1360-1366)

Botanical Materia Medica

Group I Medications: Stimulants (Commonly used drugs in this category include methylphenidate [Ritalin], dextroamphetamine [Dexedrine], and pemoline [Cylert]). Mechanism of action: unknown, but proposed to increase the concentration of deficient norepinephrine at the nerve interface (21) or by neurotransmitter modulation at the limbic level (12).

COFFEA arabica, C. canephora – COFFEE
Coffee contains 0.06-0.32% caffeine, theobromine, theophylline and tannins. Caffeine is a strong stimulant, with bronchodilatory and diuretic effects. It’s point of action is the CNS, temporarily improving perception and motor performance (23).  Some physicians have found coffee to be an acceptable alternative to psychostimulant medication, although controlled studies have shown it to be less effective then Ritalin at controlling hyperactivity (24).

COLA acuminata, C. vera, C.nitida- KOLA NUT
Cola nut contains up to 2.5% caffeine (higher than coffee), theobromine, phlobaphene, tannins, anthocyanin, proteins, fats, starch and sugars. The large seeds (nuts) have been used as a digestant and tonic for thousands of years. Kola nut stimulates the CNS (25), increases muscular strength and alertness, and counters lethargy. It has been used historically as an anti-depressant (23).

EPHEDRA sinica, E. vulgaris- EPHEDRA, MA HUANG (Chinese), MORMON TEA
Ephedra contains ephedrine, pseudoephedrine, tannins, saponins, flavones and volatile oils. The main ingredient, ephedrine, mimics adrenaline in the body and acts as a sympathetic nervous system stimulant.  The synthetic alkaloid is a racemic mixture, unlike the whole herb which is levorotatory (28). This may explain why many practitioners find that the whole herb product has significant therapeutic effect at lesser dosages and with fewer side-effects than isolated ephedrine (23).

The seed pulp contains xanthines, a fixed oil, and many unidentified constituents responsible for cocoa’s characteristic flavor. The seeds are also reported to contain an endorphin-like substance that may account for chocolate’s popularity as an antidepressant substance (23).

Damiana contains arbutin, volatile oils, cyanogenic glycosides,resins, gums, and a bitter amorphous principal (damianin). Damiana is best-known as an aphrodisiac and sex stimulant, although there are no reputable studies to support this claim (26). Damiana’s reputation as a CNS tonic and antidepressant is not well-substantiated, but it has been widely esteemed as a stimulant, especially when depression and anxiety occur together (23).

Other stimulant herbs to consider:

PAULLINA cupana, P. sorbilis- GUARANA
Guarana contains the same xanthine derivatives as coffee, with up to 7% caffeine, plus tannins and saponins. Indications are the same as for coffee, but long-term use is not recommended because the high tannin content can impair intestinal absorption (23).

ILEX paraguariensis-MATE
Although Mate contains xanthine derivatives in therapeutically usable amounts (0.2-1.5%), the high tannin content (16%) (23) makes it unsuitable for long-term use, especially in children.

Group II Medications: Antidepressants (Commonly used drugs in this category include tricyclics [Tofranil, Elavil, Norpramin], monoamine oxidase inhibitors (MAOI’s) [Marplan, Nardil], phenothiazines [Mellaril], and serotonin uptake inhibitors [Prozac]). A reported 70-80% of ADD/ADHD children will respond to one of the medications in category I or II or a combination of both (21) and the use of Prozac as a Group II medication is becoming increasingly common in children (27).

Hypericum contains a volatile oil (carophyllene), glycosides ( hypericin and pseudohypericin),  flavonoids, tannins, and resins (23, 25).  It  occupies a special place among antidepressants of all types, being the only proven intermediary between the most powerful psychoactive drugs (Prozac, morphine, opium) and the gentle nervous system effectors such as valerian and hops (28) Various studies have found hypericum as or more effective than certain tricyclics (imipramine, maprotiline) in relieving depression (29,30, 31), with photosensitivity being the only adverse side effect (32).

Group III Medications: “Misc.”:  Antipsychotics and Anti-Seizure Medications (Commonly used drugs in this category include antipsychotics [thioridazine] and anti-seizure medications [Tegretol]). Herbal analogues may have different points of action but serve as antianxiolytics and calmatives. Herbal nervines (tonics) have no equivalent in chemical medicine.

CODONOPSIS pilosula- DANG SHEN (Chinese)
Codonopsis contains triterpenoid saponins, alkaloids (perlolyrin), sterins, glycosides, polysaccharides and Tangshenoside I. Most research on the herb has been conducted in China, where it is regarded as a milder tonic and stimulant than ginseng. Codonopsis has been reported to reduce adrenaline levels (23).

Lemon balm contains flavonoids, triterpenes, polyphenols, tannin and up to .2% volatile oils (citral, carophyllene oxide, linalool, and citronellal). The volatile oils are thought to be the active ingredients (23). German studies have shown that the volatile oils have a CNS calmative effect (33). Balm also has carminative and antispasmodic properties, making it useful in cases where dyspepsia is part of the symptom picture (28). Although relatively safe, it should be used judiciously for long-term management due to its antithyroid effect.

Passion flower contains flavonoids, cyanogenic glycosides, and maltol. Its indole alkaloid content remains in dispute (23).  Passion flower is well researched as a gentle nervous system relaxant and nonaddictive sedative, although it’s mechanism of action is unknown (34).

Skullcap contains flavonoid glycosides (including scutellonin and scutellanein), volatile oil, bitter principals and tannins. The herb enjoys a solid reputation as a nervine, although research is sorely lacking (23,25). The Physiomedicalists (19th-century herbal practitioners) regarded skullcap as a premier herb for hysteria, epilepsy, and rabies – hence the common name “Mad-dogweed.”(23).

Valerian contains valpotriates, glycoside, up to 2% volatile oils (including limonene), alkaloids, choline, tannins and other constituents. Valpotriates are thought to be important in giving valerian its CNS-sedative effect (35). Numerous European studies have confirmed that valerian decreases the sleep latency period and increases quality of sleep without morning “hangover” (36,37,38) and some studies have found it to be superior to the benzodiazepine triazolam (Halcion) (39). Valerian reduces nervous activity by binding to barbiturate (GABA-A) and peripheral benzodiazepine receptors (40).

Hops contains bitter principals (lupulin,lupulon and valerianic acid), up to 1% volatile oils, flavonoids, estrogenic substances and over 100 other compounds (23,25). Hops has a proven sedative action with gastric antispasmodic effects (41).

AVENA sativa- OATS
Oats contain saponins, alkaloids, sterols, flavonoids, starch, proteins (including gluten), fats, minerals (calcium, magnesium, copper, iron, silica and zinc) and B vitamins. Oats have long been used as a nervine; the alkaloid avenine stimulates the CNS in small doses, while larger doses appear to have sedative action (28).

California poppy contains flavone glycosides and alkaloids (protopine,crytopine and chelidonine), which are in the same group of isoquinolines as papverine and narcotine. The effects of poppy are considered to be nervine rather than narcotic, and its antispasmodic and analgesic effects make it useful in children for treating anxiety, nervous tension, and sleep difficulties (42).

PIPER methysticum-KAVA KAVA
Kava kava contains resins (kava lactones) and piperdine alkaloids (43). It is considered a moderately potent anxiolytic, producing stimulation followed by CNS sedation. Large doses may induce sleep. The anti-anxiety effects are similar to oxazepam (44,45), making  it useful in non-psychotic anxiety with or without depression (46). Long-term use may produce “kava dermopathy,” a skin lesion of pigmented scales that occurs predominantly on the soles, palms, forehead, back and shins. The dermopathy retreats with discontinuance of the herb, and there is evidence that this reaction is due to a niacin deficiency (47).

Author’s Note:

Recommended for physicians, parents, and teachers: “Hyper Kids” by Lendon Smith, Shaw/Spelling Assoc., 1990. This workbook provides questionnaires to help physicians and parents sort out causes of ADD/ADHD – from nutrient deficiencies and allergies to malabsorbtion and yeast overgrowth. A very useful resource in differential diagnosis.