Vitamin C Affects ADHD Medications

Nutrient therapy for AD (H) S

 

Prevalence

ADHD is the most common child psychiatric disease. The figures vary between 2% for severe and 19% for lighter, subclinical forms [2]. However, as previously assumed, it is not just a childhood disease. In around 70% of those affected, ADHD persists even in adulthood, which, however, is often associated with a shift in symptoms [3].

The symptoms

Three core symptoms characterize ADHD:

  • the attention deficit, the inability to deliberately direct the attention in a targeted manner, to concentrate,
  • hyperactivity, excessive physical restlessness,
  • a pronounced impulsiveness, sudden, rash action.

According to the valid diagnostic criteria (ICD 10, DSM IV) [4], the core symptoms must persist in pronounced form for at least six months, the intensity of which varies considerably from patient to patient.

A distinction is made between three basic types of ADHD (Fig. 1), whereby the transitions are fluid:

  • the mixed type with problems in the area of ​​attention and hyperactivity in roughly the same form,
  • the predominantly inattentive type (daydreamer) and
  • the predominantly hyperactive-impulsive type in which hyperactivity is the dominant symptom.

ADHD is usually already impressive due to the peculiarities of pregnancy and infancy (baby babies). Those affected often learn to walk early on and are constantly on the move from then on. While hyperactivity dominates in childhood, this symptom diminishes in adults, with attention deficit becoming more prominent.

Frequent comorbidities

The most common comorbidities are reading and spelling weakness (dyslexia) or its counterpart, arithmetic weakness (dyscalculia; in every 3rd case), anxiety, depression, disorders of social behavior and tic disorders (uncontrolled muscle twitching mainly in the facial area and / or uncontrolled Vocalizations).

Diagnosing ADHD

In the absence of clear and easily measurable biological markers, the diagnosis is based on the behavior and medical history of the patient. In addition to standardized parent and teacher questionnaires, partial performance tests (e.g. the Hamburg-Wechsler intelligence test for children, HAWIK-R) or more modern computer-aided diagnostic systems are used to measure attention (Qb test). Video diagnostics, in which certain exercises can be recorded and behavioral patterns evaluated, is still rarely used, but very informative.

Neurotransmitter imbalance

ADHD is hereditary, as shown by twin, adoption and family studies [6]. References to ADHD can therefore often be found in the certificates of parents and grandparents [7]. If there is no genetic disposition, the clinical picture cannot be triggered by social or educational errors, but these can have a favorable or unfavorable influence on an existing ADHD clinical picture.

ADHD is related to at least 15 genetic defects that cause a disturbance in the balance of the neurotransmitters dopamine (drive), norepinephrine (attention) and serotonin (impulsiveness, mood) (Fig. 2). In addition to receptor defects, enzyme defects play a role.

Drug therapies aim to compensate for the imbalance of the neurotransmitters. Stimulants (methylphenidate: Ritalin®, Medikinet®, Equasym®, Concerta®) largely influence the dopamine metabolism and improve the symptoms associated with it. Atomoxetine (Strattera®), recently approved for ADHD therapy in Germany, is a norepinephrine reuptake inhibitor. Occasional liver damage (1: 50,000) after administration of atomoxetine in England prompted the British Pharmaceutical Authority (MHRA) to warn the prescribers.

Specific nutritional deficiencies in AD (H) D patients

ADHD patients are relatively often deficient in the ω-3 fatty acid docosahexaenoic acid (DHA), the ω-6 fatty acids arachidonic acid (AA) and γ-linolenic acid (GLA) as well as the minerals magnesium and zinc, which are among others. play a role as co-factors in the metabolism of fatty acids. The deficits can also be determined and quantified with a blood test. There is a particular connection between the DHA plasma level and the concentrations of the serotonin, noradrenaline and dopamine metabolites in the cerebrospinal fluid. Correlations between the extent of nutrient deficiency and ADHD symptoms have also been described [9, 10, 11, 12].

The connection between the nutrient deficiency in the blood plasma and the disturbances in the neurotransmitter metabolism is probably due to the prostaglandins formed from the fatty acids [13]. In addition, a deficiency in DHA and AA changes the structure of the nerve cell membrane, which contains these fatty acids in equal parts, and therefore possibly impairs signal transmission.

Improvement of the nutrient supply

In various clinical studies with ADHD patients, balanced diets with a daily dose of approx. 500 mg DHA, approx. 100 mg GLA, approx. 40 mg AA as well as 200 mg magnesium and 10 mg zinc have proven to be effective [14, 15, 16]. Suitable preparations are, for. B. Addy plus, Omefa or Focus IQ.

In principle, it is possible, but not very practical, to supply the relevant nutrients in sufficient quantities by choosing certain foods (Tab. 1 and 2).

Side effects of methylphenidate

Children affected by ADHD often show an extremely one-sided food choice because of the inwardly directed attention deficit, and it is difficult to make the diet even remotely balanced. If treatment with methylphenidate is carried out, this problem usually worsens further [17]: The substance was used as an appetite suppressant for weight loss long before it was approved for the therapy of ADHD, and this undesirable effect now occurs frequently and intensely in the children treated. The growth retardation sometimes observed under methylphenidate therapy may be related to this. Conversely, the ADHD symptoms improve after supplementation of the fatty acids and minerals mentioned.

Interestingly, a derivative of the ω-3 fatty acid eicosapentaenoic acid (EPA) achieved positive results in a phase II study in the treatment of patients with severe depression [18]. Further interesting connections with the neuronal fatty acid metabolism exist in the clinical pictures epilepsy and schizophrenia [19].

Balanced diets as a supplement to medicinal therapy

Supplementing methylphenidate therapy with balanced diets is possible and makes sense. There are numerous, partly double-blind, randomized studies on this, but the number of patients has always been small. The first positive effects were usually already apparent after two to three weeks. The result was better tolerability of the drug (fewer psychosomatic complaints such as headaches, abdominal pain, anxiety, difficulty falling asleep, loss of appetite, restricted choice of food). The best effects were achieved in the areas of mood, aggression, oppositional behavior. The hyperactivity decreased, whereas the attention span and the ability to concentrate did not increase significantly.

Supplements in Practice

For milder cases of ADHD, supplementation of the nutrients mentioned together with adequate behavioral therapy is often sufficient. In the case of patients undergoing medical treatment, the supplementation should be discussed with the doctor. If the therapy works well in drug-treated patients, the doctor can reduce the dosage of the drug if necessary.

Address for the authors:
Dr. Georg Keller
North Rhine Chamber of Pharmacists
Poststrasse 4, 40213 Düsseldorf

literature
[1] Fegert, Glaeske, Janhsen, Ludolph, Ronge: Investigation of drug supply for children with hyperkinetic disorders based on performance data from the statutory health insurance. Project report, University of Bremen and University Medical Center Ulm, December 2002.

[2] Döpfner, M: Hyperkinetic disorders. In F. Petermann (Ed.): Textbook of clinical child psychology, 4th edition, pp. 153-189. Göttingen, 2000.

[3] Wenwei, Y .: An Investigation of the Adult Outcome of Hyperactive Children in Shanghai. Chin. Med. J. 109, 877 – 880 (1996).

[4] ICD 10 = International Statistical Classification of Diseases and Related Health Problems, 10th Revision, WHO; DSM IV = Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, American Psychiatric Association.

[5] Skrodzki, K .: The hyperkinetic syndrome, quoted in Schulz, J .: ADHD, the “fidgety philipp syndrome” - causes and therapeutic options. Naturopathic Practice 55, 1572 (2002).

[6] Bennett, H .: Gene targets related to phospholipid and fatty acid metabolism in schizophrenia and other psychiatric disorders: an update. Prostaglandin Leukot. Essent. Fatty Acids 63, 47– 59 (2000).

[7] Krause, J., Krause, K.-H .: ADHD in adulthood. The attention deficit / hyperactivity disorder in adults. Stuttgart 2003.

[8] Holsboer-Trachsler, Vanoni: Depression and sleep disorders in practice. Binningen, 1998.

[9] Hibbeln, J.R., et al .: Essential Fatty Acids Predict Metabolites of Serotonin and Dopamine in Cerebrospinal Fluid among Healthy Control Subjects, and Early- and Late-Onset Alcoholics. Biol. Psychiatry 44, 235–  242 (1998).

[10] Burgess, Stevens, Zhang, Peck: Long-chain polyunsaturated fatty acids in children with attention deficits hyperactivity disorder. At the. J. Clin. Nutr. 71, 327– 330 (2000).

[11] Arnold, Pinkham, Votolato: Does zinc moderate essential fat- ty acid and amphetamine treatment of attention-deficit / hyperactivity disorder? J. Child Adolesc. Psychopharmacol. 10, 111 – 117 (2000).

[12] Burgess: Attention deficit hyperactivity disorder: observational and interventional studies. NIH workshop on omega-3 essential fatty acids and psychiatric disorders. National Institutes of Health, Bethesda, 1998, Sep. 2 - 3.

[13] Horrobin, C. Interactions between zinc, essential fatty acids and prostaglandines. Med. Hypoth. 6, 277 –296 (1980).

[14] Starobrat-Hermelin, K .: 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, 149 –  156 (1997).

[15] Akhondzadeh, et al .: Zinc sulfate as an adjunct to methylphenidate for the treatment of attention deficit hyperactivity disorder in children. A double blind and randomized trial. BMC Psychiatry 4, 9 (2004).

[16] Richardson, A.J., Puri, B.K .: 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. Neuropsy- chopharmacol. Biol. Psychiatry 26, 233 – 239 (2002).

[17] Schmidt, et al .: Effect of dextroamphetamine and methylphenidate on calcium and magnesium concentration in hyperactive boys. Psychiatric Res. 54, 199 – 210 (1994).

[18] (was): Hope for patients with severe depression? German Apoth. Ztg. 145, 821– 822 (2005).

[19] Baumeister, F.A.M., et al .: The Ketogenic Diet, Renaissance of a Forgotten Therapy. Children adolescent med. 3, 76 - 81 and 120 - 126 (2003).