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Hyperactivity - an increasingly common problem
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Professor David Benton
9.1 - March 2008
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When a child displays problem behaviour it is natural for parents to wonder if they are responsible; or, if they are not responsible, whether there is something they can do to help. The number of children with Attention Deficit / Hyperactivity Disorder (ADHD) has progressively increased, with estimates of its prevalence varying between three and nine percent. Frequently, parents blame themselves for the diet they offer and see changes in the food provided as an answer to the problem. However, rather than seeing ADHD as a product of poor parenting, increasingly it is being viewed as a biological phenomenon.
Symptoms
There are three groups of problems associated with ADHD that may occur to different degrees and in different combinations. Inattentiveness, where the child is easily distracted, forgetful and dislikes tasks that require sustained mental effort or attention to detail. Hyperactivity, where there is fidgeting, excessive talking and they have trouble playing quietly as they are always “on the go”. Thirdly impulsivity, where there is difficultly waiting for a turn; the child interrupts and there is a lack of control over what he or she says or does. To attract the diagnosis, symptoms usually start around four years of age and must be present before seven years; they must have continued for more than six months and be displayed in two or more settings such as both school and home.
Parents should not look at the above list and conclude that there is a problem if their child occasionally acts in one of the ways listed, as many normal children occasionally display such behaviour. To attract a diagnosis of ADHD, the relatively intense behaviour will occur frequently and over a long period.
Heredity
As ADHD runs in families, the possibility arises of a genetic mechanism, although shared experiences or exposure to environmental toxins might also play a role. About half the children of parents who in the past have been given the diagnosis of ADHD will themselves develop the disorder. In particular, the study of twins suggests a role for genetics. If one identical twin has ADHD it is more likely that the other twin will also be diagnosed than when non-identical twins are compared. This increased incidence even occurs when the twins have been raised separately. Thus a role for genetics is suggested as identical twins share 100% of their genes, whereas non-identical twins have only 50% in common. When Elia et al.(1) reviewed the topic they concluded that ADHD has a heritability of 0.75 to 0.91, where 1.0 would reflect a 100% genetic contribution and 0 a 100% environmental causation. Clearly there is an important genetically determined predisposition to develop ADHD.
The response of ADHD symptoms to stimulant drugs has led to the examination of genes involved in dopamine systems in the brain. Stimulant drugs are thought to act via dopamine, a brain chemical that sends signals between brain cells. The presence of various genes that regulate dopamine activity has been associated with an increased risk of ADHD. The National Institute of Health in the USA has started the International Multi-centre ADHD Gene project (IMAGE) that samples the DNA of those with ADHD and their relatives. The aim is to identify the relevant genes and study their influence on brain development and response to the environment. It is believed no single gene will be sufficient on its own to cause ADHD. Instead it is expected that the cumulative effect of several genes, and their interaction with the environment, will result in ADHD.
The functioning brain
An early hypothesis was that problems of attention were caused by minor head injuries and therefore for many years ADHD was called “minimal brain damage”. Although some children who have suffered brain injury show signs of behaviour similar to ADHD, the majority of those with ADHD have no history of head injury. More recently, with the development of brain imaging techniques, the structure and functioning of the brains of those with ADHD have been examined. Brain imaging has found that children with ADHD have, on average, four percent smaller brains. Arnsten(2) concluded that those with ADHD tended to have a smaller prefrontal cortex. This part of the brain is particularly associated with human evolution and is often described as the executive centre of the brain: it plays a major role in planning behaviour, problem solving and sustaining attention. It is interesting that the prefrontal cortex is important in impulse control and involves brain circuits that are regulated by dopamine(3). The basal ganglia, areas important for the control of movement, also differ in those with ADHD.
Environmental and dietary influences
Although heredity is important it can never be the only factor. Genes are only influential after interacting with the environment. Various environmental toxins have been discussed including exposure to alcohol in the womb, lead, polychlorinated biphenyls (PCBs) and parental smoking(4). In addition there are problems of attention and an increased incidence of behavioural disorders in those born prematurely(5).
However, in the general population, diet is the most common environmental factor believed to influence ADHD. In particular the Feingold diet is often mentioned, which decreases the intake of synthetic additives and salicylates, (chemicals in food with a similar structure to aspirin). The Feingold theory stimulated a great deal of research, but the ideas have received no support from well-conducted studies(6). There is similarly a widespread belief that sugar is responsible for hyperactivity, although the origin of this idea may be little more than a simplistic assumption that as sugar is a source of physical energy, it is assumed to cause hyperactivity. There can be few other aspects of diet that have been subject to more double-blind trials than sugar. However, a recent review concluded that there was no evidence that sugar adversely influenced the behaviour of children(7). In these studies, the behaviour of children was monitored when they consumed a drink that either contained sucrose or was artificially sweetened. Interestingly, although a child’s behaviour is not influenced by consuming sucrose, it can change the behaviour of the mother. Hoover and Milich(8) studied boys who were reported by their mothers to be “sugar sensitive”. Their mothers were told that their child received a drink containing a large dose of sugar or an artificial sweetener, although all children actually received the placebo. When mothers falsely thought that sugar had been consumed by their son he was rated as more hyperactive. They exercised more control by maintaining physical closeness and were more likely to criticise, look at, and talk to their sons. Clearly the expectation of the mother, rather than the sucrose itself, adversely influenced how the behaviour was perceived.
Although there are reasons to suspect that those with ADHD may differ in their fatty acid status, and there are isolated reports that supplementation may help behaviour, Benton(6) was unable to find a single study in which children with a clinical diagnosis of ADHD benefited from fatty acid supplementation.
In contrast to these negative findings in well-controlled studies some, but not all children with ADHD, have been found to be food intolerant(6); that is they are unable to metabolise food in a normal manner. There are dozens of foods to which an adverse reaction has been demonstrated; wheat, dairy products and chocolate are common problems. However, as the children were studied because their parents suspected that they reacted to food, it is unclear how typical they are of the population. It is probable that those with ADHD have a higher incidence of adverse food-reactions, but they are likely to be a minority of those with the diagnosis. However, it has been recently reported that a cocktail of high doses of food additives caused behavioural problems, such as temper tantrums and poor concentration(9): the novel aspect of the study was that a response was found in a sample of the normal population, irrespective of whether they previously were described as hyperactive. It may be that at least some additives have a more general influence.
Although currently the major emphasis is on biological determinants, it should not be assumed that psychological and social factors cannot play a role. Rutter et al.(10) examined the incidence of mental disorders in children and six risk factors were distinguished: (a) severe marital discord; (b) low social class; (c) large family size; (d) paternal criminality; (e) maternal mental disorders; (f) foster placement. The suggestion was that it was a combination of these risk factors, rather than the presence of a single problem, that impaired development.
Treatment
Many treatments have been used for those with ADHD including drug therapy, psychosocial approaches and the management of the diet. In 1937 a paediatrician in Rhode Island gave stimulants to hyperactive children with the unexpected consequence that they calmed them down. Today drugs related to amphetamine, such as Ritalin, are widely used. Nair et al.(11) concluded that psychostimulants “have been shown to be highly efficacious for treating ADHD” although psychosocial treatments have also been shown to be beneficial. Others have been concerned that the use of stimulants may have no long-term benefit. As most studies have been short-term there is a need to consider the influence of stimulants and other treatments over a period of several years. In the US the National Institute of Mental Health funded the Multimodal Treatment Study of Children with Attention Deficit Hyperactivity Disorder(12) that found medication alone, or in combination with behaviour therapy, resulted in a better outcome than behaviour therapy alone or treatment in the community.
Summary
For a long time it was questioned whether ADHD was a valid diagnosis. However, evidence from many scientific disciplines including psychology, neuroscience and genetics have demonstrated that it is a valid disorder. It is widely believed that ADHD is largely biological in nature, with many proposing that there is a chemical imbalance and structural change of the brain. Environmental toxins and diet may play a role, but the many factors involved means that only rarely will the influence of one predominate.
Professor David Benton D.Sc.
Department of Psychology
University of Swansea
References
- Elia J, Ambrosini PJ, Rapoport JL (1999) Treatment of attention-deficit-hyperactivity disorder. N Engl J Med; 340: 780-788
- Arnsten AF (2006) Fundamentals of attention-deficit/hyperactivity disorder: circuits and pathways. J Clin Psychiatry; 67 (Suppl 8): 7-12
- Winstanley CA (2007) The Orbitofrontal Cortex, Impulsivity, and Addiction: Probing Orbitofrontal Dysfunction at the Neural, Neurochemical, and Molecular Level.
Ann N.Y. Acad Sci; 1121: 639–655 - Banerjee TD, Middleton F, Faraone SV (2007) Environmental risk factors for attention-deficit hyperactivity disorder. Acta Paediatr; 96: 1269-1274
- Aylward GP (2002) Cognitive and neuropsychological outcomes: more than IQ scores. Ment Retard Dev Disabil Res Rev; 8: 234-240
- Benton D (2007) The impact of diet on anti-social, violent and criminal behaviour. Neurosci Biobehav Rev; 31: 752-774
- Benton, D (2008) Sucrose and behavioural problems. Crit Rev Food Sci Nutr (in press)
- Hoover DW, Milich R (1994) Effects of sugar ingestion expectancies on mother-child interactions. J Abnorm Child Psychol; 22: 501-515
- 9. McCann D, Barrett A, Cooper A, Crumpler D, Dalen L, Grimshaw K, Kitchin E, Lok K, Porteous L, Prince E, Sonuga-Barke E, Warner JO, Stevenson J (2007) Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial. Lancet; 370 (9598): 1560-1567
- Rutter M, Cox A, Tupling C, Berger M, Yule W (1975) Attainment and adjustment in two geographical areas. I--The prevalence of psychiatric disorder. Br J Psychiatry; 126: 493-509
- Nair J, Ehimare U, Beitman BD, Nair SS, Lavin A (2006) Clinical review: evidence-based diagnosis and treatment of ADHD in children. Mo Med; 103: 617-621
- The MTA Cooperative Group (1999) A 14-month randomized clinical trial of treatment strategies for attention-deficit/hyperactivity disorder. The MTA Cooperative Group. Multimodal Treatment Study of Children with ADHD. Arch Gen Psychiatry; 56: 1073-1086s
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