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ADHD / Hyperactivity - Articles Surfing
In past centuries the health of children was mainly threatened by ignorance of basic hygiene, inadequate sanitation, contaminated water, poor nutrition and infectious diseases. Epidemics of cholera and other water borne diseases contributed to the death of thousands of children. Scarlet fever, measles, whooping cough, diphtheria and typhoid did the same. Identification of harmful bacteria and development of methods of immunisation resulted to a large extent in the eradication of infectious diseases. With the advent of modernisation conditions such as hyperactivity, attention deficit disorder and other learning disabilities as well as an increase in chronic illnesses such as asthma, eczema, etc. have been seen. This brochure attempts to summarise observations concerning hyperactivity, and its treatment from a dietetic viewpoint. The information, advice and recommendations are of a general nature and are not specific to the particular circumstances of an individual.
Hyperactivity in history
The hyperactive child and adult have probably been around since the emergence of modern man. Descriptions of clinical patterns as early as 400 BC appear similar to those currently labelled as hyperactive. Heinrich Hoffman, a German physician, first described hyperactivity in 1845. Since then, the hyperkinetic syndrome, commonly labelled as hyperactivity has captured public attention in practically every developed country in the world as increasingly more children have been and are diagnosed as hyperactive. Hyperactive characters abound in literature and cartoons, the main characters in the popular cartoons, Dennis the Menace and Bart Simpson being classic examples.
Hyperactive children usually have Attention Deficit Disorder (ADD), leading experts to classify the malady together as ADHD (Attention Deficit Hyperactive Disorder). In the USA many children are labelled hyperactive or as suffering with ADD when they attend school. There is some concern about "labelling" children when they do not respond in an acceptable way to the school, perhaps reflecting an inadequacy in the teachers rather than the pupils. Medication to suppress hyperactive children is often prescribed with side-effects such as dizziness, headaches, drowsiness, blurred vision, gastrointestinal problems and depression.
Incidence of hyperactivity
The incidence varies from country to country depending on the criteria used for diagnosis. In the USA the rate ranges from 5 to 22%. In Australia the rate of incidence ranges from 8 to 12%.1 In the United Kingdom a small number of children are diagnosed as hyperactive although referrals to child guidance clinics have increased.2 Hyperactivity is believed to affect 10% of the South African population and is found in every ethnic and socio-economic group.13
Characteristics of hyperactive children
Describing the characteristics of hyperactive children is daunting because many of the symptoms are present in all children to some degree at some time. Hyperactivity has been found to be between four and nine times more common in boys.2,3
The hyperactive baby is restless, has feeding problems and colic (intermittent and unexplained crying) and often has sleeping problems. Some fall asleep late and with difficulty while others wake up frequently or early. The baby often cries incessantly and parents find that no amount of comforting, nursing or cuddling pacifies the child.
The hyperactive toddler lives in a constant state of overstimulation, is constantly moving, unable to sit still, always into everything and touching every object in sight. As the child becomes older the description changes. They are always in motion, constantly fidgeting or shuffling their feet, can not stay at an activity long and can not read without quickly losing interest. A large percentage of hyperactive children have an abnormal thirst with a normal urine output. Other symptoms are lack of concentration, temper tantrums, impatience, quick frustration, clumsiness and sleep disturbances. Hyperactive infants and adolescents usually have a depressed immune system. Asthma, hay fever, otitis, eczema and other atopic conditions are common.
Most authorities agree that the major features of hyperactivity can be categorized as academic difficulties and behavioural abnormalities. Impulsiveness, low frustration tolerance, short attention span, aggressiveness and low self-esteem are some of the symptoms exhibited. Almost all hyperactive children have a high IQ, but poor concentration means they perform less well than they should in school and often complain of headaches, asthma, hayfever and other respiratory disorders.
The characteristics of the hyperactive child tend to intensify from birth to about 3 to 4 years of age, but may have subsided by the time the child reaches 10 to 12 years of age. The child becomes more controlled and the hyperactivity could to some extent be outgrown.4
Hyperactivity and allergies
Allergies to cereals and milk, even mother's milk is often commonplace. For many years paediatricians and paediatric allergists have reported that a higher percentage of children with allergies have learning disabilities and/or hyperactivity compared with those children who do not have allergies.9 It has been estimated that up to 10% of primary school children suffer from allergic reactions which exhibit in the classroom as behaviour and concentration problems.14
An allergy is an abnormal body reaction resulting from sensitivity to certain substances. The most common types of allergies are asthma, eczema and hay fever. Often symptoms are not recognised as resulting from an allergy and will be treated over and over with medications which may help superficially. As soon as the medication is stopped, the symptoms flare up again.
Causes of hyperactivity
Data pertaining to the cause of hyperactivity is incomplete, but various factors have been linked to hyperactivity. These include among others genetic factors, smoking during pregnancy, artificial additives in food, refined dietary sugar and environmental pollutants. Inborn temperamental variations with chemical differences in the brain are thought by some physicians to be the cause. The reason for these differences is unknown, but may be due to genetic differences or anomalies in the development of the baby before birth.
1. Prenatal influences
Very little is known about prenatal influences but there is a possibility that small birth size may sometimes lead to hyperactivity. Other variations in the mother's biological processes during pregnancy may contribute to the development of hyperactivity.5 It is well documented that the use of alcohol during pregnancy may result in mental retardation (foetal alcohol syndrome) and hyperactivity. The amount of alcohol, if any, that can be safely taken during pregnancy is unknown.6
2. Inborn temperamental differences
Although uncertain, many child psychiatrists reason that inborn temperamental differences caused by chemical differences in the brain may result in hyperactivity.5
The brain is an extraordinary complex interconnection of nerve cells. It receives information from inside the body via nerve impulses, collates this information and responds by initiating nerve impulses and secreting chemical substances or neurotransmitters (dopamine and noradrenaline). When released, neurotransmitters, transmit signals across synapses to other neurons in the brain. These pass from the brain to other parts of the body to stimulate, regulate and co-ordinate activities in other organs and systems.
When there is a deficiency of a particular neurotransmitter, the nerve cells can not function effectively and the portion of the brain that it "operates" will not function correctly. Successful functioning of the nervous system depends on the release of sufficient quantities of neurotransmitters. Hyperactive children are probably deficient in some neurotransmitters.5 In many hyperactive children the quantity of these transmitters probably increases with age, explaining why hyperactive children improve as they grow older.
3. Heavy metal poisoning
Heavy metals such as lead, copper, cadmium and aluminium are thought to be a cause for hyperactivity, especially where children live in industrialised areas. These metals all affect the nervous system. The lead content of environmental air has risen due to the higher lead content of petrol and increased car ownership. Cadmium from parental cigarette smoke and aluminium from food cooked in aluminium foil containers also affect the nervous system.4,6
4. Food preservatives, additives, flavorants and colorants
An allergist, Dr Benjamin Feingold,7 has proposed that hyperactivity is caused by artificial food preservatives, flavors, colorants and natural salicylates. He reported that 30 to 50% of hyperactive children could improve if these were omitted from the diet. His hypothesis stemmed from his observations that in some people salicylates cause allergic reactions such as asthma and eczema. When treating the asthma by removing salicylates from the diet, he noted a behaviour change as well as the disappearance of the asthma symptoms.
Since many patients who are allergic to salicylates also react to artificial colors and flavors, Dr Feingold further postulated that food colors and flavors may also have a behavioural effect similar to that of salicylates in those people who are sensitive to them.
The food colorant tartrazine increases the urinary excretion of zinc. Food colors and flavors are found in foods such as luncheon meats, sausages, hot dogs, jams, sweets, cake mixes and flavored cold drinks. Dietary sources of salicylates are found in apples, peaches, oranges, tea and worcester sauce.
Most dietary-crossover studies eliminating foods containing salicylates, food colors and flavors by a number of researchers have not been able to substantiate Dr Feingold's theories. Some studies, on the other hand, have provided data in support of the Feingold diet. The final answers are not yet in as there is insufficient evidence on whether the Feingold diet genuinely works.
5. Deficiency of nutrients
5.1. Essential fatty acids
Research4,8 concludes that hyperactive children have a deficiency of essential fatty acids (EFAs) either due to an inability to absorb EFAs adequately from the gastrointestinal tract or because their EFA requirements are higher. A deficiency of EFA in animals causes a constant thirst which is one of the symptoms of numerous hyperactive children.
EFAs are needed to form Prostaglandins (PGE) which are vital regulators in the body. They participate in the regulation of blood pressure, heart rate, blood clotting and the central nervous system. They are essential because the body cannot manufacture them and has to obtain them from dietary sources. There are two EFAs essential to man - linoleic acid and cis alpha linolenic acid.
EFAs are converted by the enzyme delta-6-desaturase to gammalinoleic acid (GLA) which is then converted to another substance called dihomo-gamma-linolenic acid. This in turn is converted to hormone-like substances called eicosanoids of which there are two groups - prostaglandins and leukotrienes. Cis alpha linolenic acid is converted to a substance termed eicosapentaenoic acid (EPA) which is in turn also converted to prostaglandin.
The source of the problem is that the enzyme necessary for the conversion process does not seem to work efficiently in the hyperactive child and adult, with a resultant deficiency of PGE and leukotrienes. The enzyme deficiency or inhibition could be attributed to among others elevated blood glucose levels, a diet consisting of too much saturated fat, refined sugar, the intake of alcohol and deficiencies of zinc, magnesium and vitamin B6.4
Preliminary studies on the effects of supplementation with essential fatty acids in Canada, USA, United Kingdom and South Africa have reported some degree of improvement.2,4
5.2 Other Nutrients
Two-thirds of hyperactive children studied were deficient in zinc.2 A deficiency of zinc, magnesium and vitamin B6 blocks the formation of GLA.
A number of nutrients are essential to the proper functioning of the nervous system and these are discussed under the heading - treatment of hyperactivity.
Clinical observations and parent reports suggest that refined sugars especially cane sugar triggers hyperactive behaviour. Two theories have been proposed for this reaction. One is that a diet consisting of refined carbohydrates influences the level of EFA. Another possibility is that certain sugars (glucose) influence brain neurotransmitter levels and therefore the activity levels in hyperactive children.
Researchers designed a study where children were given one of three different breakfasts; one high in carbohydrates, especially refined sugar; the second high in protein and the third high in fat. After each meal children were challenged with fructose, glucose and placebos. Children reported by their parents as hyperactive after eating sugar did indeed show an increase in activity level when challenged with glucose after eating a high carbohydrate meal.9
Normal children challenged with sucrose had more problems with attention after a high carbohydrate breakfast than after a high protein breakfast. The reverse was true for children with hyperactivity.12
Another study showed that of 261 hyperactive children who had five hour glucose tolerance tests performed on them, 74% had abnormal glucose tolerance curves. The predominant abnormality accounting for 50% of these results was a low, flat curve similar to that seen in hypoglycaemia. Hypoglycaemia is a potent stimulus for the production of epinephrine which could affect behaviour.10
Sugar may on occasion aggravate existing behaviour disorders. Reducing the intake of sugar should be encouraged. Rigid sugar free diets can be burdensome and socially inhibiting for the hyperactive child. The area of sugar intake and behaviour requires much more research before any recommendations can be made.
A study on the use of artificial sweeteners suggests that some hyperactive children become non-compliant and more aggressive when given large doses of aspartame.9
Treatment of hyperactivity
It is important to rectify the essential fatty acid deficiency. The enzyme necessary for the conversion process of essential fatty acids does not seem to work efficiently in the hyperactive child and adult. Essential fatty acids need to be provided in a form which can be readily utilized. Human breast milk contains relatively large amounts of GLA. Another important source of GLA is the oil of the evening primrose flower which contains 9% gammalinoleic acid (GLA) while fish oil contains 20% eicosapentaenoic acid (EPA). These oils which are commercially available should be provided in a ratio of 2 GLA to 1 EPA (e.g. 500 mg Evening Primrose Oil to 250 mg Fish Oil).4
Zinc, vitamins B6, C and E are catalysts necessary to metabolize the essential fatty acids.6 Since most hyperactive children appear to be deficient in these nutrients supplementation with them makes good sense.
The B-group vitamins are particularly vital to the hyperactive child as one of their main functions is to regulate the central nervous system. Vitamin B1, thiamin, is involved in the maintenance of the central nervous system. A deficiency of Vitamin B2, riboflavin, may lead to central nervous system symptoms such as headache, irritability and fatigue. Vitamins B6 and C are involved in neurotransmitter synthesis.
Calcium acts as a co-factor in biochemical reactions in the body and takes part in the generation of nerve impulses throughout the nervous system. Magnesium which is necessary for the growth and repair of body cells also assists the transmission of nerve impulses to the muscles and acts together with calcium. Vitamin D aids the absorption and utilization of calcium and magnesium.
Zinc and chromium play a role in sugar balance by enhancing the action of insulin in promoting uptake of glucose. A glucose tolerance factor has been identified as a natural form of chromium which seems to potentiate the action of insulin. Supplementation with chromium has been shown to reduce glucose levels and to improve glucose tolerance.11 Since abnormal glucose tolerance levels have been seen in some hyperactive children supplementing with chromium and zinc may help.
Although all the amino acids have certain unique functions in the body a few are worth singling out. Four primary amines, serotonin, dopamine, norepinephrine and acetylcholine are synthesised from amino acid precursors and appear to be under dietary control. Dopamine and norepinephrine are synthesised from tyrosine and phenylalanine (phenylalanine is metabolized to tyrosine), serotonin is synthesised from tryptophan and acetylcholine is synthesised from choline. Deficiencies of L-Taurine and glycine which both aid the regulation of the nervous system are possibly liked to hyperactivity, epilepsy and anxiety.
The beneficial effects of large doses of vitamin C to alleviate common symptoms of allergy have been described, but not substantiated in controlled studies. Anecdotal reports suggesting that lysine tablets relieve the symptoms of food allergy in some individuals are also undocumented.11 Methyl Sulphine Methane and calcium assist in allergic sensitivities.
Although Feingold's hypothesis has not been experimentally confirmed, elimination of food additives, colors, flavors and salicylates may be of benefit and is worth a try. Exclusion of sugar and refined carbohydrates is also recommended. If such a diet is to be followed, attention should be paid to its possible nutritional inadequacies and there should be some nutritional counselling and vitamin supplementation. Small, frequent meals consisting of protein and unrefined carbohydrates should be emphasized.
There appears to be a relationship between brain function and nutrition. Studies on the effect of evening primrose oil and fish oil on hyperactivity have shown improvement in behaviour patterns and learning ability. The diet of the hyperactive child should be supplemented with these oils as well as magnesium, zinc, calcium, vitamin C and the B-complex vitamins.
The keys to managing the hyperactive child are dietary control, discipline and lots of tender loving care. All children have strengths and weaknesses. By recognising and accepting the diversity of human personalities and abilities a foundation will be laid for all hyperactive children to achieve their scholastic and developmental potential.
Research activity has increased and it is hoped that future research and clinical findings will lead to better treatment and understanding of hyperactivity.
For access to correct combinations of specialised nutrients, see 'ADHD / Hyperactivity' under 'Children's Needs' on http://wellness.oppiweb.com
1. Serfontein G. Add in adults - help for adults who suffer from attention deficit disorder. Simon and Schuster, Australia. 1994: 9
2. Matthews P. Fast Food. Nursing Times. March 1986.
3. Colten H.R; Food Hypersensitivity, food allergies and hyperkinesis. Suskind R.M; Textbook of Pediatric Nutrition. Raven Press, New York, 1981: 553-562.
4. Van der Merwe C.F. Hyperactivity, Medunsa. August 1992.
5. Wender P.H; Wender E. The Hyperactive Child and the Learning Disabled Child - a Handbook for Parents. Crown Publishers, 1978: 22.
6. Barnes B; Colquhoun I. The Hyperactive Child - what the family can do. Thorsons Publishers, Northamptonshire. 1984: 19, 77.
7. Feingold B. Why your child is hyperactive. New York: Random House, 1985.
8. The Hyperactive Children's Support Group. Information sheet - Health Visitor, 1980, 57;1: 87-93
9. Silver L.B. Attention-Deficit Hyperactivity disorder. Clinical guide to diagnosis and treatment. Washington: American Psychiatric Press Inc, 1992: 129-134.
10. Langseth L; Dowd J. Glucose tolerance and hyperkinesis. Food Cosmet. Toxicol. 16:129. 1978.
11. Krause M.V; Mahan L.K. Food Nutrition and Diet Therapy. A textbook of nutritional care. Philadelphia: W.B. Saunders Company, 1984: 633-668.
12. Kinsbourne M. Sugar and the hyperactive child. New England Journal of Medicine. Feb 3, 1994: 355-356.
13. Edmonds T.L. Hyperactivity, following a special diet could help. Longevity. July 1995: 88-89.
14. Ryan B.J. Cerebral Hazards in relation to food and environmental chemicals. The Hyperactive Children's Support Group of Southern Africa. Newsletter 25, Fourth quarter 1995.
ADD - Attention Deficit Disorder. Developmental dysfunction of the central nervous system.
Allergy - Unusual sensitiveness to the action of particular foods, pollens, dust, etc.
Amino acid - Organic acid containing the group nitrogen, especially as a constituent of protein.
Asthma - Disease especially allergic of respiration.
Diphtheria - Acute infectious bacterial disease with inflammation of mucous membranes, especially throat.
Eczema - Inflammation of skin.
Enzyme - Any of a unique class of proteins which accelerate a broad spectrum of biochemical reactions.
Food Additives - Added to food to color, preserve or flavor.
Hay Fever Summer disorder caused by allergy to pollen or dust often with asthmatic symptoms.
Neurotransmitter - Chemical substances when released, transmit signals across synapses to other neurons in the brain to stimulate, regulate and co-ordinate activities in other organs and systems of the body.
Otitis - Inflammation of the ear.
Salicylate - Salt of salicylic acid. Found in almonds, apples, apple cider, apricots, blackberries, cherries, cloves, cucumbers, currants, gooseberries, grapes, nectarines, oil of wintergreen, oranges, peaches, pickles, plums, prunes, raisins, raspberries, strawberries and tomatoes. Food with added salicylates for flavoring may be ice-cream, bakery goods (except bread), candy, chewing gum, soft drinks, jam, cake mixes.
Typhoid - Infectious bacterial fever with eruption of red spots on chest and abdomen with severe intestinal irritation.
Worcester - Pungent sauce first made in Worcester (United Kingdom).
Copyright © 1995 - Photius Coutsoukis (All Rights Reserved).
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