The neurological explanation of ADHD
Since the first descriptions of Attention Deficit Hyperactivity Disorder, more than 10 000 clinical and scientific publications have been published on ADHD and there are clear differences between children (and adults) with and without ADHD.
ADHD is best understood as a bio-psychosocial condition: it’s medical in origin but is affected and influenced by the environment, social and emotional aspects of the person and situation. However, research shows that genetic (hereditary) and neurological factors (such as pregnancy and birth complications, brain damage, toxins and infections) are the main causes of ADHD rather than social factors (such as poor parenting and diet).
ADHD is one of the most genetic conditions – it runs in families, with a heritability chance of almost 60% for a child if a parent has ADHD, and a 70%–80% chance for a twin if the other twin has ADHD.
Family studies confirmed that parents and siblings of probands have a two- to eight-fold increased risk for ADHD. Although some genes contributing to ADHD have been identified, their exact involvement have not been confirmed. These genes are associated with changes in neurotransmitters such as dopamine and serotonin, and also the migration of and communication between neurons (brain cells).
There are differences in the development of self-management systems in the brains of individuals with ADHD (e.g. changes in areas of the brain responsible for concentration, regulation, organisation, planning, time-management, decision-making, etc.).
Research has demonstrated imbalances of neurotransmitters (chemical messengers) such as dopamine and noradrenalin within the brain. In ADHD, the tonic (‘resting state’ or baseline) neural activation is reduced, which allows for a larger-than normal phasic (‘active state’) release of dopamine – causing inattention, hyperactivity, and impulsivity.
Brain imaging studies (scans) of individuals with ADHD have shown structural differences in different areas in the brain involved in decision-making and behaviour, such as the frontostriatal pathways, the cerebellum, temporoparietal lobes, basal ganglia and corpus callosum.
Differences in the amygdala and thalamus (part of the emotional centres or so-called limbic system of the brain) is thought to underlie the emotional and complex sensorial alterations in individuals with ADHD. Functional task-based imaging of the brain has also shown alternations in the brain response to event – some areas are less active than normal (e.g. in the frontal areas where the ‘brakes’ which prevent distractibility, hyperactivity and impulsivity are located), while others are overactive (e.g. the frontoparietal areas involved in mind-wandering).
Electroencephalographic (EEG) studies also showed differences in brainwave activity – consistent with developmentally immature cortical under-arousal, preparatory and inhibitory processes – once again contributing to impulsivity and distractibility.
Animal studies of ADHD have confirmed the involvement of dopaminergic, adrenergic, serotonergic, and cholinergic neurotransmitters in ADHD. Special scans (called Positron Emission Tomography studies) have shown that individuals with ADHD have lower cerebral blood flow and metabolic rates in the frontal region of the brain – where these neurotransmitters play an important role.
Finally, there’s no scientific evidence to prove eating sugar or junk food will cause ADHD. Although some children (both those with and those without ADHD) are particularly sensitive to certain food components (such as artificial colourants, additives, and refined sugar), and others benefit from specific food supplements (such as omegas), dietary intervention alone does not ‘prevent’ or ‘cure’ ADHD.
These studies form the basis for the development of medication intervention: which aims to stimulate the baseline (tonic) activation of dopamine and noradrenaline responsible for guided attention, focus, and organisation of thoughts and actions. However, a healthy balanced diet and regular physical exercise do form part of the ideal integrated treatment approach of children (and adults) with ADHD.