ADHD is an extremely complex and multifaceted condition, with diverse aetiological pathways, manifestations, and outcomes. As with so much in the field of ADHD research an exact and universally applicable causal structure has not been identified. This discussion considers the biological basis of the condition, as well as considering gene-environment interactions, and the most comprehensive account of ADHD as a bio-psychosocial condition.


Interestingly enough at its earliest conception in 1798, ADHD was presumed to be neurological in origin. Indeed, even G. Still (1902) account of a moral defect considered the source to be medical.

Biologically ADHD is said to be associated with the neurotransmitter dopamine and norepinephrine (Antshel et al., 2001).These neurotransmitters are associated with regulation of the prefrontal cortex, the neurological basis for the condition. It is not the production or secretion of these chemicals, but the re-uptake of them back into the synapses which has been found to be problematic (Fitzgerald et al., 2007).

Those who advocate the use of psycho-stimulant medication, often cite that methylphenidate (e.g., Ritalin) activate and regulate these neurotransmitters (Barkley, 2006). In addition, the inverse effects of the drug (e.g., it will increase talkativeness and restlessness) in children without the disorder suggests a biological abnormality (Fitzgerald et al., 2007).

The pre-frontal cortex is the brain region believed to be responsible for higher cortical (cognitive) functioning (Fitzerald et al., 2004). Rubia and colleagues (2009) using functioning magnetic resonance imaging (fMRI) provided evidence of ADHD-specific alterations in the frontal lobe, on tests of response-inhibition.

In addition to frontal lobe abnormalities, Barkley (2006) implicates the basal ganglia, which is said to be involved in motor control, automatic learning (habits), cognitive and emotional functioning. The Cerebellum, or little brain, is involved in motor control, cognition, attention, and the reward circuitry. Potentially even the anterior cingulate which functions include connectivity of other brain area, autonomic functioning, rational cognition, and decision-making.

Presently the best evidence suggests that ADHD is indeed attributable to neuronal factors with a significant association to genetic factors. It is often considered to be a highly heritable condition,which tends to cluster in families (Swanson &Castellanos, 2002; Tannock, 1998).

Geneticists suggest a possible association with norepinephrine transporter gene (NET1) and dopamine receptor gene (DRD1) (Fitzgerald et al., 2007; Thome& Reddy, 2009).

Barkley (2006) reviewed several studies suggesting complications during pregnancy, smoking, or exposure to toxins may also represent contributory factors.


There does appear to be ample evidence from both the biological and behavioural sciences to support ADHD legitimacy as a diagnosis. Indeed, the neurobiological basis for ADHD is more accepted (in general) than other less debates conditions. The need for a medical explanation is linked with understanding its origins. Even if it does make certain outcomes and eventualities more likely, biology is not destiny.The simple truth is that ADHD is only observed, and so understood, in terms of how it manifests in context.

As such, there is evidently a clear gene-environment interaction going on. Thus, ADHD and any associated deficits can only be understood in terms of the capacities of the individuals and the demands of the environment.


The view that ADHD arises from a linear gene-environment interaction, is more accurate that either the social or medical reductionist approach, however, it does not explicate the complex pathways and trajectories of the condition.

Each individual interacts with their environment differently, depending on innate factors and previous learning. For example, while siblings may share commonalities they also tend to be affected by different experiences in their shared childhood and develop their own unique personality.

As such, another argument for ADHD as an expressed phenotype (endophenotype) resulting from complex causal sequences, and involves the interaction between multiple genetic and environmental (including social) factors (Nigg, 2004), is probably a more realistic view of the condition, given that biology does not occur within a vacuum. However, adopting such an approach means that clinical diagnosis and the medical model do not fully appreciate the complexities involved in ADHD.

The concept of ADHD represents a complex issue comprising factors such as biology, psychology, cultural and socio-political which cannot be considered in isolation (Thomas, 2004).Thus, the bio-psychosocial model which views ADHD as arising from complex genetic, psychological, socio-cultural, and environmental forces provides us with a more complete picture (Cooper, 2001, 2010).

Authors of the article: Kate Carr-Fanning and Conor Mc Guckin, the School of Education, Trinity College Dublin, 2012


Tannock, R (1998). Attention deficit hyperactivity disorder: Advances in cognitive, neurobiological, and genetic research. Journal of Child Psychology and Psychiatry, 39, 65-99.

Swanson, JM, and Castellanos, FX (2002).Biological Bases of ADHD—Neuroanatomy, Genetics, and Pathophysiology. In P.S. Jensen and J.R. Cooper (eds). Attention deficit hyperactivity disorder: State of the science,best practices, pp. 7-1—7-20. Kingston, New Jersey.

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