Information provided on this website is intended for your general knowledge and is not meant to be a substitute for professional medical advice and treatment. You should never disregard professional medical advice or delay in seeking an assessment or medical treatment because of something you may have read on this site. You should also not use the information on this web site or the information on links from this site to diagnose or treat ADHD and/or co-morbidities, in yourself or others, without consulting a qualified adult ADHD specialist.
What is Attention Deficit Hyperactivity Disorder (ADHD)?
While everybody to some extent, and at certain times, occasionally has trouble sitting still, paying attention, or controlling impulsive behaviour. many others experience impulsivity, hyperactivity, and inattention at such mal-adaptively high levels that their daily lives at home, at school, at work, and in social settings are disrupted to a considerable and sometimes disabling extent. These people may have a common neurobiological disorder called Attention Deficit Hyperactivity Disorder (ADHD). There is also a less common and more severe form of ADHD called Hyperkinetic Disorder.
Although ADHD is a neurobiological disorder, it is defined at a behavioural level. That means that the symptoms are based upon observations about how people behave: ‘impulsivity’ signifies premature and thoughtless actions; ‘hyperactivity’ a restless and shifting excess of movement; and ‘inattention’ is a disorganised style preventing sustained effort. These symptoms are shown by individuals to different extents, and are influenced by context as well as by the constitution of the individual. People with ADHD may also be clumsy, unable to sleep, have temper tantrums and mood swings and find it hard to socialise and make friends.
Until recently, it was believed that children outgrew ADHD in adolescence, because sometimes hyperactivity seems to lessen in teen years. It is now known, however, that many symptoms continue into adulthood and hyperactivity may instead be experienced as internal restlessness. Undiagnosed ADHD in adults may have severe consequences including academic failure, substance abuse, criminal activity, failed relationships, troubled work relationships, and emotional difficulties such as anxiety and depression.
UK Prevalence & Gender Distribution
ADHD is a common disorder. In the UK, surveys of children between the ages of 5 and 15 years found that 3.62% of boys and 0.85% of girls had ADHD. Hyperkinetic Disorder is less common and prevalence estimates are around 1.5% for boys in the primary school years.
Also, a recent review of longitudinal follow-up studies of individuals diagnosed with ADHD as children found that by age 25 only 15% retained the full ADHD diagnosis. However, a much larger proportion (65%) fulfilled criteria for either ADHD or ADHD in partial remission, indicating the persistence of some symptoms associated with clinical impairments in the majority of cases. It is likely, therefore, that about 0.6–1.2% of adults retain the full diagnosis by age 25 years and a larger percentage (2–4%) have ADHD in partial remission. This is consistent with population surveys in adult populations that estimate prevalence of ADHD in adults to be between 3 and 4%. (CG72 Full Version page 26-27 )
When researchers are conducting studies, they typically use the same definitions of ADHD for both boys and girls, and usually find more boys than girls with ADHD (a ratio of about 3 to 1). The gender ratio for children attending ADHD clinics, however, is usually higher than in the research surveys, which raises the possibility that females with ADHD receive less recognition. Similarly, in adult life, the male-female ratio for ADHD appears to be approximately equal, which again suggests the possibility that the high gender ratios in childhood may be partly a result of under-identifying the problem in girls, or of a different presentation of symptoms in girls. (CG72 Full Version pages 127-128 )
Theories about the causes of ADHD
Research has demonstrated that AD/HD has a very strong neurobiological basis. Although precise causes have not yet been identified, there is little question that heredity makes the largest contribution to the expression of the disorder in the population.
Studies indicate that multiple genes contribute to a susceptibility to ADHD. Pharmacologic, neuroimaging, and animal-model findings suggested
imbalances in monoaminergic (dopaminergic, serotonergic, and noradrenergic) neurotransmission in ADHD. Several studies examined monoaminergic candidate genes for possible genetic association with ADHD in the Irish population, focusing particularly on genes of the dopaminergic and serotonergic systems. Several of the genes were associated with ADHD, including DAT1, DBH, DRD4, DRD5, and 5HT1B (Online Mendelian Inheritance in Man). Also twin studies suggest that around 75% of the variation in ADHD symptoms in the population are because of variable genetic factors. (CG72 Full Version pages 28-29 )
A range of factors may adversely affect brain development during perinatal life and early childhood. These include difficulties during pregnancy; fetal oxygen deprivation; maternal smoking, alcohol consumption, and heroin use during pregnancy; premature delivery; very low birth weight, exposure to high lead levels; a deficiency of zinc; and postnatal injury to the prefrontal regions of the brain. These may all lead to an increase in the risk of having ADHD. These risk factors, however, do not act alone, but may interact with the hereditary factors. For example, the risk of ADHD associated with maternal alcohol consumption in pregnancy may be stronger in those children with a dopamine transporter (DAT) susceptibility gene. Furthermore, there is increased risk of ADHD symptoms in epilepsy and of ADHD in genetic conditions such as neurofibromatosis type 1, and syndromes such as Angelman, Prader-Willi, Smith Magenis, velocardiofacial and fragile X. Secondary ADHD may follow traumatic brain injury. (CG72 Full Version pages 28-29 )
ADHD has been associated with severe early psychosocial adversity, for instance, in children who have survived depriving institutional care. The mechanisms are not known but may include a failure to acquire cognitive and emotional control. Disrupted and discordant relationships are more common in the families of young people with ADHD. Discordant family relationships, however, may be as much a consequence of living with a child with ADHD as a risk for the disorder itself. In established ADHD, discordant relationships with a harsh parenting style are a risk factor for developing oppositional and conduct problems. Parents themselves may also have unrecognised and untreated ADHD, which may adversely affect their ability to manage a child with the disorder. (CG72 Full Version pages 28-29 ).
Excessive television viewing, poor child management by parents, or social and environmental factors such as poverty or family chaos have also been suggested by some as possible causes of ADHD, but while these may aggravate symptoms, the evidence for such circumstances is not strong enough to conclude that they are primary causes of ADHD. (CG72 Full Version pages 28-29 )
The influence of dietary factors in ADHD has attracted much public attention: food additives, excessive intake of sugar, colourings and ‘E’ numbers are often regarded as causes of ADHD, and elimination and supplementation diets are widely used, often without professional advice. But the evidence is not strong enough to indicate that these cause ADHD. Nevertheless, epidemiological research indicates a link between additives and preservatives in the diet and levels of hyperactivity amongst a small proportion of children with ADHD.
Reviews have also been conducted on the evidence on associations between ADHD and longchain polyunsaturated fatty acids (PUFA) and these have remarked upon the brain’s need throughout life for adequate supplies, on a relative lack of omega-3 PUFA, and a possibility that males may be more vulnerable because testosterone may impair PUFA synthesis. Scientific uncertainties remain, however, concerning the physiological significance of different measures of PUFA metabolism and they are not used in practice. (CG72 Full Version pages 28-29 )
National Institute for Health and Clinical Excellence (2008) Attention deficit hyperactivity disorder: Diagnosis and management of ADHD in children, young people and adults. CG72. London: National Institute for Health and Clinical Excellence.
The advice in this guideline covers:
- the care, treatment and support that children, young people and adults with ADHD should be offered
- how families and carers can support people with ADHD.
It does not specifically look at:
- the treatment of children younger than 3 years
- the treatment of conditions other than ADHD.
A free electronic copy of the guideline can be accessed from our library here