The Etiology of ADHD

A multiple exposure shot of many images of a boy in a blue shirt with his eyes closed

Genetic and environmental factors

Over the past decades, concepts of ADHD have evolved from narrow behavioral symptom clusters to broader notions of deficient self-regulation; and from a focus on lower brain centers to theories that involve frontal and prefrontal regulation (Hinshaw 1994; Hynd, Horn, Voller et al 1991). Conceptions of underlying mechanisms must be able to account for a wide range of problems including those of academic, social and cognitive dimensions. For example, DSM-IV field trials separated dimensions of inattentive/restless from impulsive/hyperactive behaviors. It is possible that varying subgroups of ADHD (and co-morbid conditions) may relate to various vulnerability factors, which may push the child past the threshold of disorder.

Further large-scale genetic studies are needed to determine genetic versus environmental influences on ADHD, oppositional defiant disorder and conduct disorder as well as relationships to language and learning disabilities (Levy, Hay, McLaughlin et al 1996).


Biological brain differences have been reported in children and adults with learning/language, behavior and attention difficulties including ADHD and slow learning disability (SLD). Differences have been described in anatomy, electrical activity, psychological functions, brain metabolism and blood flow and these may show “normalization” with medical treatment (Matochik, Liebenauer, King et al 1994). These findings largely fall within the spectrum of normal.

Genetic factors

There is evidence for genetic factors as shown by higher concordance in monozygotic than dizygotic twins for increased ADHD (Levy, Hay, McStephen et al 1997; Levy, Hay, McLaughlin et al 1996; Gilles, Gilger, Pennington et al 1992; Goodman and Stevenson 1989).

Recent reports indicate possible mutations in dopamine transporter genes (Cook, Stein, Krakowski et al 1995) or receptor genes (D4 receptor gene ÷ Ebstein, Novick, Umansky et al 1996) which may predispose to ADHD.

Congenital factors

Retrospective accounts suggest numerous congenital factors may be related to ADHD. However, there is no compelling evidence for specificity of perinatal (Levy, Hay, McLaughlin et al 1996) or congenital factors (Cantwell and Hanna 1989).

Maternal substance abuse during pregnancy may be associated with ADHD (Steinhausen, Willms and Spohr 1993). Substances such as cocaine and nicotine (Nichols and Chen 1981) may also induce ADHD-related symptoms.

Diet and environmental agents

Available evidence does not strongly support the role of food additives in ADHD (Kavale and Forness 1983; Conners 1980; Levy, Dumbrell, Hobbes et al 1978). Recent evidence from a population study has failed to confirm a relationship between allergy and ADHD (McGee, Stanton and Sears 1993).

There is, however, evidence that exposure to lead, even at sub-clinical toxicity levels, is associated with small but significant decrements in intellectual performance and with distractible impulsive behavior (Fergusson, Horwood, Lynskey 1997 and 1993a; Needleman, Schell, Bellinger et al 1990).

Familial factors

Familial factors are very difficult to separate from genetic factors, but the concept of “goodness of fit” between parent and child temperament may be important (Thomas and Chess 1977). The interaction of family, genetic and psychosocial factors are discussed by Biederman, Faraone, Keenan et al (1990) and by Biederman, Millberger and Faraone et al (1995). The interaction of child and family factors influencing referral of children with hyperactivity is discussed by Woodward, Dowdney and Taylor (1997).


A number of studies have shown co-morbidity of ADHD with oppositional defiant disorder (Hinshaw 1992; Biederman, Newcorn and Sprich 1991; Biederman, Munir and Knee 1987; Werry, Reeves and Elkind 1987) and conduct disorder in both clinic (Biederman, Newcorn and Sprich 1991; Barkley 1990a; Lahey, Schaughnency, Hynd et al 1987; Yule and Rutter 1985; Stewart, Cummings, Seiger et al 1981) and community samples (Szatmari, Boyle and Gifford 1989). Schachar and Tannock (1995) tested patterns of cognitive, developmental risk and psychological factors characterizing the “pure” forms of ADHD and conduct disorder. They found that the ADHD group was significantly impaired on cognitive measures, while the Conduct Disorder group was exposed to significantly greater environmental adversity. Fergusson, Horwood and Lynskey (1993b) reported confirmatory factor analyses reflecting distinctive but highly correlated disruptive childhood behaviours.

Co-morbidity with learning disability

children with ADHD are more likely to be placed in special education classes (or special classes for behavior disorder) than are normal controls (Barkley 1990a). A number of studies have reported co-morbidity with learning disability (Cantwell and Baker 1991; Hynd, Semrud-Clikeman, Lorys et al 1991; Barkley 1990a; McGee, Williams, Moffatt et al 1989) and speech problems (Cantwell and Baker 1992b; Semrud-Clikeman, Biederman, Sprich-Buckminster et al 1992; Berry, Shaywitz and Shaywitz 1985). The reported association between learning disability and ADHD varies from 10 per cent to 90 per cent, depending on dimensional or categorical diagnosis of learning disability, study selection, relationship to overall ability and measurements. Many studies have failed to control for intelligence level. An additional unresolved issue is the relationship of attention deficit disorder without hyperactivity to learning disability (Cantwell and Baker 1992b; Kataria, Hall, Wong et al 1992; McGee and Share 1988). The Dunedin study shows that hyperactivity is more significant in ADHD children with or without reading disability than in children with only a reading disability, or in a comparison group (Pisecco, Baker, Silva et al 1996).

McGee, Williams, Moffitt et al (1989) found up to 80 per cent of 11 year-old boys with ADDH (DSM-III criteria) were at least two years delayed with learning disabilities.

Key points – etiology

The etiology of ADHD is essentially unknown. All of the above factors have been implicated as playing some role. However, to date, their relative importance has not been determined. It is likely that a variety of contributing factors may operate in a vulnerable child to result in the behaviors of ADHD.

Many studies show co-morbidity of ADHD with learning disability, speech problems, oppositional defiant disorder and Conduct Disorder in both clinical and community samples. Depending on the stringency of academic and psychometric tools used for the diagnosis of learning disorders, the association with learning disability varies from 10 per cent to 90 per cent. Further research is needed to clarify this association.

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