Journal Citation
Joneja, J.M. Diet and behaviour – Myth or science? Journal Of The Canadian Child Psychiatric Bulletin. 1996 5(1):4-15
Article
DIET AND BEHAVIOUR – MYTH OR SCIENCE?
Janice M. Joneja, Ph.D.
INTRODUCTION
Historically, components of the diet have been blamed for almost every disorder that “mankind is heir to”. The food that we actually put into our mouths is arguably the only component of our lives over which we have absolute control. And since we know that the food we eat is the source of most of our body structures, functions and energy, it seems to make sense that the “wrong food” would cause dysfunction in these systems. If we can blame food for bodily dysfunction, be it inability to sleep, intestinal disorder, memory loss, depression, skin rashes, or a runny nose, we are ready to try any diet, however absurd nutritionally, that promises freedom from our misery.
When parents and teachers have to cope every day with an unruly, disruptive, sometimes aggressive child in the home and classroom, and when every attempt at control has met with failure, the idea that the child`s diet is the cause of the problem is often embraced with great enthusiasm, especially if the alternative is behaviour-modifying drugs.
As a result of the many faddish diets that have been promoted as a cure for almost every known disease, medical practitioners have been wary of such claims, and tend to move to the other extreme. The opinion that diet has no role in any disease, except overt nutritional deficiency states such as scurvy, pellagra, rickets, kwashiorkor, etc. is common in conventional western medicine. However, science shows us that neither extreme is true. Components of our food, and the way that our bodies react to them, undeniably can lead to disease and even death. A fatal anaphylactic reaction to food is a dramatic example. The question is: to what extent is food the culprit in the etiology of diseases?
The Role of Diet in Behavioural Disorders
Food as a trigger for behavioural dysfunction may act in a number of ways, for example:
All of these possibilities should be considered when a role for diet in a child`s behaviour is being investigated.
The medical and scientific literature abounds with the results of studies on the role of food components in behavioural dysfunction in children. However, the first criticism that is frequently levelled at these experiments is that the criteria used for selecting the research subjects leaves room for doubt about the diagnosis of the behavioural condition that was being studied (Egger 1987b).
Attention Deficit Hyperactivity Disorder (ADHD)
Attention-deficit hyperactivity disorder (ADHD) is the most recent diagnosis for children with problems in attention, impulse control and overactivity (Barkley 1990) However the diagnosis and etiology of the symptoms that constitute this disorder have been in dispute since the condition was first recognized. More than 90 different terms have been used to describe hyperactive children (Sulzbacher 1976).
Brain Damage as a Cause of Hyperactivity
Early studies on hyperactivity and attention deficit disorders in the 1920`s considered children with behavioural problems as “brain-damaged” usually by infection or trauma (Barkley 1990). In the 1930`s drug treatment for hyperactivity was instituted with amphetamines and other stimulant medications. In the 1950`s “hyperkinetic impulse disorder” was thought to originate from a CNS deficit in the thalamic area (Laufer et al 1957), or in the cortex or subcortical regions of the brain (Knobel, Wolman, and Mason 1959). In the 1950 and early 1960s “minimal brain damage” (MBD) became the designated diagnosis for children with hyperactivity and impulsive behaviour. In the research of the time, there appears a great deal of confusion regarding which aspects of the disorder were neurological in origin, and which were the result of psychological factors stemming from poor parenting and environment (Barkley 1990).
Hyperkinetic Reaction of Childhood
In the 1960`s the Hyperkinetic Reaction of Childhood disorder was recognized (Diagnostic and Statistical Manual of Mental Disorders (DSM-II, American Psychiatric Association, 1968), and the work of Chess (1960) clearly indicated that hyperactivity could be due to neurological dysfunction, but could also occur without any pathology being evident. Since that time an extensive literature on the subject of children`s impulsive, hyperactive, socially disruptive behaviour with attention deficit, and various maladjustment disorders has appeared. A report published in 1977 indicated that less than 5 percent of hyperactive children show any signs of neurological impairment (Rutter 1977)
Current Designations of Behaviour Disorders in Children
The disorder is currently considered to be further subdivisible into several subcategories (ADHD alone; ADHD with oppositional defiant disorder; ADHD with conduct disorder; ADHD with thought/mood disturbance; ADD without hyperactivity; learning disabilities without ADHD (Barkley 1990).
But the debate still continues: to what degree are the symptoms due to a neurological deficit, and how much can be attributed to aberrant environmental factors?
Furthermore, there is no clear consensus that these are scientifically divisible conditions based on physiological differences.
Reaction to Drug Treatment of Childhood Hyperactivity
A great deal of concern arose in the 1970s from the perceived widespread use of stimulant drugs to control children`s hyperactive behaviour (Maynard 1970; Barkley 1990). Some clinicians moved to the opposite extreme and advanced claims that childhood hyperactivity was a perception created by intolerant teachers and parents (Conrad 1975), and was caused by environmental factors rather than any neurological deficit (Barkley 1990).
Hyperactivity and Diet
One of the environmental factors that was considered as a possible cause of the disorder was the child`s diet (Barkley 1990). The idea that dietary components as a cause of aberrant behaviour was not new, and had been considered at various times since it was first suggested in the 1920`s (Cooke 1922, David 1993). Reactions to wheat and corn, as a cause of fatigue, irritability and behaviour problems was suggested again in the 1940`s ( Randolph 1947).
Publications on the relationship between behavioural disorders in childhood and diet can be broadly separated into two major groups: Feingold`s hypothesis and the food allergy hypothesis (Egger 1987b).
The Feingold Hypothesis
In 1975 Dr Benjamin Feingold published an article (Feingold 1975a), and then a book (Feingold 1975b), promoting the theory that a toxic reaction to food additives was responsible for hyperactivity in children. He claimed that up to 70% of his hyperactive patients improved when food dyes, artificial flavours, and natural salicylates were eliminated from their diet. After the publication of Dr.Feingold`s book in 1975 the “Feingold diet” became very popular as a non-drug treatment for childhood hyperactivity. Feingold Associations as sources of information and support for parents were formed in most states within the United States of America (Barkley 1990).
In response to Feingold`s claims, a number of research studies were conducted in an attempt to confirm or refute his theories (Connors 1980; Harley et al 1978). All of these studies can be criticized on the basis of differences in methodology, no clear consensus on diagnostic criteria, inadequate controls and the diversity of the independent variables employed (Egger 1987b). However, the consensus reached was that Feingold`s claims were exaggerated and his findings were anecdotal and lacking in objective evidence. Finally, the idea that diet and food additives were the cause of hyperkinesis was strongly refuted in a statement from the National Advisory Committee on Hyperkinesis and Food Additives (1980). Nevertheless, all the studies had demonstrated that a few hyperactive children did benefit from an additive-free diet (Egger 1987b).
Attention Deficit Hyperactivity Disorder (ADHD) and Allergy
In recent years, the role of food allergy, and intolerance to food additives, in learning and behaviour disorders in children has been the subject of a number of well-conducted studies (Egger, Carter, et al 1985; Egger 1987b; Kaplan, McNicol et al 1989). A comprehensive review of the research in this field appeared in 1992 (Robinson and Ferguson 1992), which discusses current thought on the link between diet and behaviour disorders. An important point made by these reviewers is that: “It must be recognized that adverse effects of foods on behaviour may be either a manifestation of (probably pharmacologically based) food intolerance, or they may be psychologically based (e.g. via suggestion or adverse conditioning).”
Food Allergy and Food Additive Intolerance as a Cause of Behaviour Problems
Convincing evidence for food allergy and intolerance to artificial colours, flavours and preservatives as etiological factors in behavioural disorders in children has been presented by two different research groups: Dr. Josef Egger and his colleagues at the Great Ormond Street Children`s Hospital in London, and Dr Bonnie Kaplan and her colleagues at the Alberta Children`s Hospital in Calgary.
Initially, Egger`s group were investigating the role of foods in childhood migraine. When the migraines were controlled by diet, the children`s behaviour was observed to improve (Egger, Carter, et al 1983). Consequently, the researchers began to study the role of diet in hyperkinesis (Egger, Carter, et al 1985). About 80% of the 76 subjects improved on a very restricted “few foods” diet, and when certain foods and food additives were reintroduced the behaviour deteriorated. Forty-six foods were identified as triggering adverse reactions in different children, including: Milk and dairy products, eggs, wheat and other grains, fruits, nuts, soya bean, meats and fish, as well as artificial food dyes (especially tartrazine), flavourings (glutamates) and some preservatives (benzoates and nitrates) (Egger 1987a; Egger, Carter, et al 1992). Most of the “overactive” children selected for the trials experienced other somatic reactions to foods such as abdominal pains, headaches and seizures, which also responded favourably to the elimination of foods from their diet. On challenge, the time lapse between eating the provoking food and the reaction varied from a few minutes to 7 days, with the average reaction interval being 2-3 days (Egger 1987b). Reactions to the foods and additives were confirmed by double-blind placebo-controlled cross-over trials. Connor`s scores, independent assessment by psychologists and psychiatrists, and parents` observations were used to evaluate the children`s behaviour and symptoms.
The Alberta Children’s Hospital group studied a group of 24 preschool-aged boys for 10 weeks, during which time all food was provided by the research group, thus overcoming the problem of controlling the children`s food intake (Kaplan, McNicol, et al 1987). The possible adverse effect of nutritional deficiency on behaviour was thereby ruled out. The test diet was free from artificial colours, artificial flavours, chocolate, monosodium glutamate, preservatives, caffeine, and any food component that the family had identified as causing an adverse reaction in the child. It was low in simple sugars, and free from dairy products if an adverse reaction to milk had been identified in a specific child (Kaplan, McNicol, et al 1989).
The behaviour of more than half of the children was reported to have improved on the diet, and in addition, other symptoms such as halitosis, night awakening, and inability to fall asleep also improved.
Experimental Design Problems
All of the studies that are designed to demonstrate a role for food components in children`s behaviour are plagued by two major handicaps:
The lack of clear diagnostic criteria for the behavioural conditions that are being studied; and the absence of any definite tests that unequivocally demonstrate allergy to food or intolerance of food additives.
Allergy tests such as skin prick and RAST (radioallergosorbent test) are notoriously unhelpful in the diagnosis of food allergy and intolerance (Egger 1987b; David 1993). The only way to demonstrate an adverse reaction to food components is elimination and challenge: The suspect food or additive is removed from the child`s diet for a specified period of time, and then reintroduced to determine the child`s reactivity to it. Double-blind, placebo-controlled, cross-over food challenge is the standard method used to identify reactive foods to rule out as many confounding variables as possible.
Sugar Regulation in ADHD
Following the decline in the belief that the Feingold diet was an effective management strategy for childhood hyperkinesis, the idea that refined sugar was an important etiological factor in the disorder became very popular (Milich, Wolraich and Lindgren 1986; Wender and Solanto 1991; Wolraich, Lindgren, et al 1994).
“Reactive hypoglycaemia” or “functional hypoglycaemia” (FH) due to sugar in the diet has been blamed for emotional problems, irritability and fatigue (Kanarek and Marks-Kaufman 1991). Claims have been made that reactive hypoglycaemia can give rise to a vast range of aberrant behaviour states, including schizophrenia, neurosis, alcoholism, drug addiction, juvenile delinquency, childhood hyperkinesis, obesity, lethargy, depression, irritability, suspiciousness, bizarre thoughts, hallucinations, mania, anxiety and violent behaviour (Robinson and Ferguson 1992). As a result of these claims, dietary policies have been changed in some correctional institutions in an attempt to control antisocial and violent behaviour (Robinson and Ferguson 1992). However, there have not been any reported studies that conclusively demonstrate low blood sugar levels and impaired insulin response in conditions other than diabetes. The scientific view regarding FH is that the condition is quite rare, but “has become popular because it is a respectable metabolic illness rather than a symptom of psychological distress” (Robinson and Ferguson 1992).
The adverse effect of sugar in sensitive individuals may be mediated by mechanisms other than defective insulin control. A study by Connors on the response to sugar and aspartame in 39 children diagnosed with ADHD indicated that catecholamine control of sugar regulation may be impaired in children with ADHD (Connors, Caldwell, et al 1986). The ADHD children performed significantly worse on behavioural evaluation following a sucrose challenge compared to an aspartame challenge after a breakfast of carbohydrate, but the behaviour improved in these children after a sucrose challenge following a protein breakfast. Normal control children were unaffected by the challenges after either a carbohydrate, protein, or fasting breakfast condition. Blood glucose was reported to be significantly higher at baseline and after the sucrose challenge in the ADHD children than the normal controls. Although insulin levels were not affected, cortisol and growth hormone secretion was suppressed in normals after a carbohydrate meal, but not in the ADHD children; significantly, the hormone response in the two groups was the same after fasting or a protein meal.
Phosphate was also considered as a dietary component that could play a major role in hyperkinesis, based on anecdotal evidence (Hafer 1984). Again, this theory was refuted by controlled studies (Egger 1991). Of interest, however, is the fact that children on either a restricted sugar diet or a restricted phosphate diet would avoid many potentially allergenic foods and a variety of artificial colours and preservatives, that might be the real reason for the apparent improvement in their behaviour (Egger 1991).
Nutritional Deficiencies as a Cause of Unacceptable Behaviour
In 1986 the results of a four-year dietary intervention program in 803 New York City schools affecting 800,000 children was published. All school meals were virtually free from sucrose, all artificial food flavours, artificial food colours and two preservatives (butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT)). Academic achievement rather than behaviour was chosen as a more objective measure of the performance outcome of this intervention. The average percentile rankings of the students in the study on the California Achievement Test (CAT) over the four year test period rose 15.7% from 39.2% to 54.9% with no changes in the school curricula or teaching staff (Schauss 1986b). The hypothesis was made that the improvements in academic achievement were due to diet, especially the reduction in sucrose, which treated marginal malnutrition (Schauss 1986a). Elimination of foods high in sucrose, artificial flavours, artificial colours and preservatives removes many “junk foods” from a child`s diet, giving place to more nutritionally dense foods and a more nutritionally adequate, balanced diet.
Micronutrient Deficiency and Behaviour
Deficiency of micronutrients has been cited as a cause of aberrant behaviour in a number of reports:
The possibility that high levels of one element or nutrient in a child`s diet may directly affect behaviour, for example lead poisoning, has been known for many years. Newer research indicates that an abnormally high level of one nutrient may lead to deficiency in another, the result having an adverse effect on behaviour. Examples of the latter phenomenon are excessive levels of copper impairing zinc absorption (Rapoport,J., 1986; Schauss 1986a)
In another report high carbohydrate consumption was shown to correlate with high cadmium levels in the body, which in turn were claimed to correlate with poorer academic achievement (Lester et al 1982).
The area of micronutrient interactions is a new and presently rather poorly understood field of research. Future studies may reveal significant roles for micronutrient imbalance in disordered behaviour, but for the moment, we can look at this possibility with considerable interest but unfortunately, without any real practical application in clinical practice.
Pharmacologically Active Chemicals in Foods: Caffeine
One of the components of the diet that have been observed to clearly affect behaviour in many people is caffeine (NIN review 1987).
The way that caffeine affects behaviour is not definitely established, although most coffee drinkers are quite clear about their own reactions to the beverage. Reduced aggression (Cherek et al 1983) and reduced academic performance (Gilliland and Andress 1981) have been cited as attributable to caffeine intake, however, other clinicians diasgree with these conclusions (Leviton 1983). It appears that habitual intake is a major factor in the individual differences exhibited in the response to caffeine. Persons who consumed a large quantity of caffeine on a regular basis were more likely to react to caffeine challenge of 300 mg by becoming more alert and experiencing decreased irritability, than persons who did not drink caffeine-containing drinks. The latter group tended to respond to the caffeine challenge with upset stomach and jitteriness (Goldstein et al 1965). Insomnia is a frequent side-effect of high levels of caffeine intake (NIN review 1987).
Caffeine has been found in breast milk and in umbilical cord blood (Bailey et al 1982). Undoubtedly a breast-fed infant will ingest a certain amount of caffeine if the mother drinks caffeine-containing drinks such as coffee or colas. The rate of elimination of caffeine in young infants is much slower than in the adult and presumably the effects will last longer (Aranda et al 1979). The time it takes for the normal adult to eliminate 50% of the caffeine consumed is 3 to 7.5 hours, whereas the new-born infant requires an average of 82 hours (Grant et al 1983).
Methylxanthines such as caffeine appear to act as competitive antagonists for adenosine receptors on cell surfaces and inhibit adenosine effects in a dose-related fashion (von Borstel and Wurtman 1984).
Cola type drinks are good examples of a dietary component that can affect the behaviour of a sensitive child by one or more of the different mechanisms that have been discussed:
Evidence for Other Physiological Mechanisms that may Cause Behavioural Disturbances
The conclusion that behavioural dysfunction can be provoked by foods in a small number of children, based on double-blind, placebo-controlled cross-over procedures, is undeniable (Carter, Urbanowicz et al 1993; Egger 1991). However, many of the mechanisms that are responsible for these reactions are often poorly understood, although a variety of theories have been propounded (Egger 1987b). Recently, a number of studies on the neurological effects of foods in sensitive individuals have begun to shed light on some of the probable physiological responses that may be the cause of some of the behaviour changes. Neurotransmitters and mast cell activation by central nervous system triggers are two of the newest areas being investigated.
Movement Disorders that are Adverse Reactions to Foods
In 1994 Gerrard et al reported three cases of movement disorders that were shown to be triggered by foods. In Case 1 the movement was shaking of the head from side to side, triggered by milk, beef, pork, potatoes, coffee, tea, chocolate, citrus fruits, raspberries and strawberries. In Case 2 the movement was repeated shrugging of the shoulders, triggered by egg and coffee. In Case 3 the movement disorder consisted of rhythmic contraction of the arms and legs, triggered by aspartame. In all cases, skin prick tests to the foods were negative, suggesting that the adverse reaction was not an IgE-mediated event. The reactive foods were all identified by elimination and challenge tests, based on careful food diaries, and confirmed by double-blind placebo-controlled food challenge. In each case, the movement disorder was accompanied by other somatic symptoms which also cleared when the offending foods were eliminated: Case 1 suffered from headaches; Case 2 experienced hoarseness; and Case 3 had chest pains, tachycardia and indigestion. Based on their observations of the response of these patients to drugs, the authors conclude that “in susceptible individuals foods can trigger movement disorders through an action on dopamine and other neurotransmitter pathways in the brain”.
It is conceivable that similar reactions could occur in response to mediators released in an allergic response, or to chemicals in foods.
Interactions of The Immune System and the Nervous System
The immune system and the nervous system form a co-ordinated defence network in the body (Marshall and Waserman 1995). In disease, dysregulation in one system may result in effects in the other. This interaction has been demonstrated in allergic disorders (Ader and Cohen, 1985; Russell, Dark, Cummins, et al 1984).
The mast cells play a key role in allergic diseases (Marshall and Waserman 1995). Preformed inflammatory mediators are stored in the granules within the mast cell and are released in response to signals such as allergen coupled to allergen-specific antibodies (IgE). Histamine, serotonin, proteoglycans and proteinase enzymes are released by the activated mast cell, and secondary mediators such as prostaglandins, leukotrienes and platelet activating factor (PAF) are formed from membrane lipids such as arachidonic acid. Increased vascular permeability, vasodilation, pruritus, and smooth muscle contraction are some of the results.
In addition, recent research has demonstrated that human mast cells can produce a number of cytokines such as tumor necrosis factor a (TNFa), Interleukin 4 (IL-4); IL-5; IL-6; and IL-8 (Marshall and Waserman 1995). There is increasing evidence that both preformed mediators and cytokines can be released from mast cells in response to neuropeptides (Ansel, Brown, Payan et al 1993; Marshall and Wasserman 1995).
In human tissues, mast cells are often found in close anatomical proximity to nerves in the skin, in the airways, and in intestinal tissues such as the duodenal mucosa, colon and appendix. However, although degranulation of mast cells in response to neuropeptides has been seen in rodent models, it has not yet been demonstrated conclusively in humans (Marshall and Wasserman 1995).
Pavlovian Conditioned Release of Inflammatory Mediators
The release of mast cell constituents by stimuli from the central nervous system has been demonstrated in a number of animal experiments. Using rats, MacQueen et al (1989) showed that after activation of sensitized mast cells with egg albumin allergen in conjunction with an audio-visual stimulus, release of mast cell protease II could be achieved by the audio-visual stimulus alone. In a previous study, Russell, Dark, et al (1984) demonstrated sensory conditioned histamine release in guinea pigs. In this case an odour (suphur-smelling or fishy-smelling) was used as the sensory stimulus in animals sensitized to bovine serum albumin. Increased serum histamine was demonstrated in response to the odour alone, but the cellular source of the histamine was not identified.
These preliminary experiments pose the question as to whether such a conditioned release of allergy mediators could also occur in humans. Anecdotal reports certainly indicate that this phenomenon probably does occur in situations where an anaphylactic reaction to a food has been experienced or suggested. In the Allergy Nutrition Clinic at Vancouver Hospital, a number of reported incidents indicate that symptoms of allergy can occur in response to sensory stimuli in the absence of allergen contact.
Case 1 was a 22 year old male, known to be anaphylactic to peanut. He developed urticaria, at first on the face, and later spreading to other upper body surfaces, while standing next to a child spreading peanut butter on a cracker. No peanut butter to his knowledge had come into contact with any part of his body.
Case 2 was a 21 year old male, anaphylactic to peanut, who developed signs of a full-blown anaphylactic reaction (increased heart rate, feeling of doom, sweaty, chilled feeling, chest tightness, breathing difficulty, throat tightening) on several occasions when friends informed him that peanut was an ingredient in a meal he had just consumed. In each case he was taken to the emergency room of the hospital. In fact, no peanut was present in the food.
Case 3 was a kindergarten-aged child who developed signs of an anaphylactic reaction (“felt ill”; breathing difficulty), in response to observing another child eating a peanut butter sandwich on the other side of the classroom.
However, in each of these three cases, there may have been alternative causes for these reactions:
In Case 1, volatilized peanut allergen might have been inhaled.
In Case 2, the so-called anaphylactic reaction might have been a panic attack. On subsequent occasions, the subject`s girl-friend transported him to the emergency room in her car. They then sat outside the hospital until he had calmed down. The symptoms subsided on each occasion, and he did not require any treatment. This raises the question: How often is a panic attack mistaken for an anaphylactic reaction? The symptoms of both can be remarkably similar.
Nurture as the culprit (blame mother!)
Case 3 could also have been due to anxiety, engendered by parents repeatedly reinforcing the message that peanut butter could kill the child after they had been told this by a no-doubt well-intentioned allergist, based on a strong reaction to a skin prick test.
Whatever the cause, the reaction in each case was real. If inflammatory mediators had been released in response to a sensory signal, there are further ramifications of the consequences:
Validity of Double-Blind Food Challenge
Double-blind placebo-controlled food challenge (DBPCFC) for the diagnosis of food allergy using disguised allergen is the “Gold Standard” for food allergy testing (Bock, Sampson, et al 1988) However, this would not be a valid test in cases where a sensory signal is also required for an allergic reaction to be manifest. Even if the DBPCFC demonstrates that the food does not elicit an allergic reaction, in practice, when the food is eaten and the sensory input is present, release of inflammatory mediators might be as life-threatening as if the food were the allergen.
Questions of Management
In the management of sensory-induced adverse reactions to food, is the appropriate approach removal of all the foods suggested to be causing the allergic reaction, or behavioural modification to reduce anxiety and phobia towards the food?
Management of Behaviour Dysfunction that Results from Food Ingestion
When so many different states are considered, which may or may not be attributable to a variety of biochemical or physiological triggers, it is difficult to advocate that diet, either as an etiological factor (for example, a food additive or a natural chemical in the food acting like a “drug”) or as an instrument of deficit (vitamin or mineral deficiencies) could be the major etiological factor in all of these phenomena.
Currently held opinions on the link between food allergy, intolerance and behaviour include:
Reasons for improvement on a modified diet
Several reasons have been proposed for the observation that a surprisingly large number of behaviourally disturbed children improve significantly on a “hypoallergenic diet”. These include:
Undoubtedly most of these factors will have some effect on a child, especially an atopic child.
CONCLUSION
Well-controlled studies have demonstrated that a small number of children diagnosed with ADHD and other behavioural anamolies are sensitive to foods and will respond positively when the appropriate diet is followed. The sensitivity may be due to food allergy, to a pharmacological response to food additives or natural chemicals in foods, to an unusually labile metabolism (especially to sugars and simple carbohydrates), or to a nutritional deficiency, especially in trace elements and vitamins.
Whatever the scientific basis may be, the opportunity to improve the quality of life for the child and family by dietary management is justified, as long as the diet does not pose any psychological, nutritional or economic distress on an already stressed family situation.
The best candidates for dietary intervention are children with poor eating habits and physical as well as behavioral symptoms and a family history of adverse reactions to foods, additives, stimulants and environmental factors (McNicol 1993).
APPENDIX
Management of the behaviourally dysfunctional child with suspected food allergy
The initial elimination diet is formulated to remove any food allergens suspected on the basis of history and appropriate tests, and specific food additives (see below).
A nutritionally adequate diet is prescribed, supplying equivalent nutrients from alternative sources.
This is followed for a period of four weeks.
If significant improvement is achieved, an incremental dose challenge can be implemented to identify specific food allergens and behaviour triggers.
The final diet is designed to restrict the child’s intake of the foods and food additives that provoke symptoms on challenge and to supply a nutritionally adequate, balanced diet from alternative sources.
Long-term compliance of children in follow-up studies on a diet formulated on these principles was reported to be good when improvement in somatic and behaviour symptoms was significant (McNicol and Kaplan, 1992).
Guidelines for diet (Joneja 1995)
These guidelines are initially followed for four weeks
All artificial food colours
Artificial flavours such as monosodium glutamate (MSG) and other glutamates
Preservatives:
Benzoates (especially benzoic acid and benzoyl peroxide)
Butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA)
Nitrates and nitrites
Sulphites
Caffeine
Artificial sweeteners, especially aspartame
THE TEST DIET PLAN
The diet has been planned to remove the foods and food additives which are most likely to be contributing to the problem. This diet is initially followed for four weeks.
If symptoms have not improved in this time, diet is unlikely to be a contributing factor, and there will be no benefit in following the dietary restrictions any longer.
If significant improvement is experienced, foods can be reintroduced individually using sequential incremental dose challenge tests to isolate the dietary offenders.
FOODS AND FOOD ADDITIVES ELIMINATED IN THE TEST DIET
Other Restrictions
Sweeteners, such as sugar, syrups, jam, candy, are used in moderation. Fruit juices should be diluted by one half with water, and low sugar products are recommended. Products and foods with moderate amounts of sugar should be given at the end of the meal and not be used alone for snacks.
Highly scented products such as perfumes, scented cleaners, laundry products should be avoided. Children have been reported to react to scented markers and to whiteout, especially when they are toluene-based.
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