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This story asserts that ADHD is a disease caused by biomedical factors, particularly within the modalities of neurology and genetics. There has been a long history of ADHD being understood through a biomedical lens, although differing explanations have been presented regarding the source of the differences and abnormalities proposed by researchers. In their critical review of the evolution of ADHD since the 1900s, Mayes and Rafalovich (2007)

noted over twenty diagnostic terms for the behaviours we have now come to understand as ADHD. Many of these terms imply a biomedical aetiology and include: encephalitis lethargica, minimal brain damage, mild retardation, minimal brain dysfunction and hypokinetic impulse disorder.

ADHD is considered one of the most heritable psychiatric conditions (Faraone

et al., 2005), with heritability estimates from twin and family studies of around

0.7 (Tarver et al$FFRUGLQJWR%DUNOH\WZLQVWXGLHVIXUQLVKµWKH

most inclusive evidence that genetics can contribute to ADH'¶ S 68). However, although many of the twin studies (e.g. Thapar et al., 1995; Sherman et al., 1997; Heiser et al., 2006) conclude that monozygotic twins are more concordant for ADHD, critics (e.g. Joseph, 2009) have argued that researchers have based their conclusions on a traditional assumption that the environments of monozygotic and dizygotic twins are equal. As highlighted by Cooper (1999), there are difficulties in controlling experiential influences that are commonly shared by members of the same family.

Studies seeking to identify the genetic causes of ADHD have employed two approaches: the genome scan, surveying all genes unselectively; and the candidate genome approach, which has focused specifically on the genes related to the mechanism of action of the medication used to treat ADHD (e.g. dopamine and norepinephrine transporter and receptor genes) (Franke et al., 2009). In particular, UHVHDUFKKDVIRFXVHGRQJHQHVLQYROYHGZLWKWKHEUDLQ¶V dopamine receptors, and it has been suggested that there is a dopamine deficiency in children with ADHD (Spencer et al., 2005). Researchers

supportive of this hypothesis emphasise the therapeutic benefits of methylphenidate, known to be a dopamine agonist: Gizer et al. (2009) conducted a meta-analysis of commonly studied candidate genes and found candidate gene polymorphisms in the dopaminergic and serotonergic systems, which they describe as moderately associated with ADHD. However, these genome-wide scans have not identified any regions that are consistently implicated, and researchers have acknowledged that this is not VXUSULVLQJJLYHQWKDW$'+'LVVRµSKHQRW\SLFDOO\YDULDEOH¶)XUPDQ

In summary, no single genetic risk factor has been identified, making it likely that ADHD develops as the result of the interaction between multiple genetic risk variants, each of small effect (Thapar et al., 2013).

Research has also been directed towards finding a neuroanatomic locus for the disorder, with ADHD being associated with a number of morphological brain abnormalities (Tarver et al., 2014). These proposed abnormalities have been identified through use of neuroimaging techniques such as magnetic resonance imaging (MRI) and computerized transaxial tomography (CTT), comparing the brains of children with ADHD with those of children who do not meet the criteria for a diagnosis. Studies have associated ADHD with reduced global brain volume (Castellanos et al., 2002), reduced grey matter in regions forming part of the fronto-striatal circuits (involving executive functions) (Bush

et al., 2005; Nakao et al., 2011), cortical thinning (Batty et al., 2010) and

delayed cortical development (Shaw et al., 2007). However, critics have argued that these studies have failed to control for potentially critical

confounders known to affect brain imaging results (Furman, 2009), including prior or current medication use, pre- and perinatal complications, effects of co- morbidity and treatment effects in participants with multiple diagnoses, and generally inadequate use of control populations with other pathologies.

Barkley (1990, 1997, 1998), a prominent researcher in the field of ADHD, identifies important relationships between behavioural inhibition, executive mental functions and self-FRQWURO ZKLFK KH KDV OLQNHG WR D µGHYHORSPHQWDO IDLOXUH LQ WKH EUDLQ FLUFXLWU\¶ +LV WKHRU\ VXJJHVWV WKDW WKH RQVHW RI $'+' LV related to deficiencies in key areas of the brain, including working memory, internalised speech and motivational appraisal, leading to difficulties with self- regulation and impulse control. He asserts that deficiencies in these areas lead to poor response inhibition, which QDUURZV FKLOGUHQ¶V UDQJH RI RSWLRQV and choices of actions. Cortese (2012) also suggests that ADHD is likely to be the result of structural abnormalities in a complex network of brain regions and connecting circuitry.

Whilst it is not the intention of this chapter to provide a detailed account of all biomedical theories, it is accepted that within this domain, ADHD has also been linked to biological risk factors, including maternal smoking during pregnancy (Langley et al., 2005), low birthweight (Johnson et al., 2010) and nutritional deficiencies (Stevens, 1995; Arnold, 2005; Cortese et al., 2012).

In summary, neurobiological theories are far from conclusive, particularly as neurological research has been limited to a small percentage of the general

population (Doggett, 2004). Doggett, who conducted a review of research into WKHEUDLQVRILQGLYLGXDOVGLDJQRVHGZLWK$'+'FRQFOXGHGWKDW µZKLOH$'+' brains are different, they also have many of the same developmental and neurological features as other types of EUDLQV«WKHUHIRUH VFLHQWLVWV FDQQRW agree with certainty that ADHD children have a unique and identifiable brain EOXHSULQW¶  S. 74). Given its heterogeneity, it is perhaps unlikely that there is a single identifiable genetic or neurological cause of ADHD; rather, it is more probable that children and adults with similar symptoms have different underlying problems that may not result from a single cause. As Rafalovich has cautioned, µit would be premature to say that neurology has found the answer¶ (2004, p. 414).