Family, twin, adoption, and molecular studies offer strong evidence of a genetic component to AD-HKD. Studies of community (88> and clinic samples*89,9 and 91.) show that relatives of AD-HKD probands have an increased risk for AD-HKD. Moreover, they are also at increased risk for antisocial personality disorder, conduct disorder, and other conditions such as anxiety, mood, and reading disabilities. (52> Twin studies find a markedly higher concordance of AD-HKD for monozygotic (79 per cent) than dizygotic (32 per cent) twins that is consistent with a genetic origin of AD-HKD. (85) Adoption studies(92> provide further evidence of a genetic component to AD-HKD; biological parents of AD-HKD probands are more likely to exhibit AD-HKD or related disorders than adoptive parents. Siblings of children with AD-HKD have two to three times the risk of having AD-HKD than siblings of normal controls. (93> Furthermore, the basic characteristics that comprise the syndrome of AD-HKD are highly heritable (e.g. hyperactivity (9°)).
Inattentive, hyperactive-impulsive, and combined subtypes of AD-HKD have unique but associated genetic influences; there may be different genetic effects for AD-HKD subtypes based on their severity.(5 94,>
The often dramatic effect of stimulant medication on children with AD-HKD, and the concentration of neurones rich in dopamine and norepinephrine in the neural areas involved in executive function, suggest a role for the genes involved in the noradrenergic and dopaminergic systems. (95,96> Molecular genetic research associates AD-HKD with specific candidate genes in the dopaminergic system. AD-HKD is associated with an allele of the dopamine transporter(979 and 99 and the D4 receptor gene (DRD4).(45 There is no evidence of genetic effects in the noradrenergic system such as in the monoamine oxidase system. (10°)
The specific mechanism by which genetic and neurobiological factors influence the development of AD-HKD is unknown. Segregation analysis is consistent with a major locus gene effect that has low penetrance and polygenic transmission, and a genetic risk, which is reflected in a spectrum of psychiatric phenotypes. (93) However, it is likely that multiple genes confer susceptibility to the development of AD-HKD in particular persons. The effects of these susceptibility genes may be potentiated by the environmental neurobiological factors already described.
AD-HKD may be best viewed as the extreme of a behaviour that varies genetically throughout the entire population, rather than as a disorder with discrete determinants^101) The high prevalence of AD-HKD in the general population suggests that it may have had an adaptive function in early human history. As a result, the genes for AD-HKD may have been selected for survival in environments typical of those of early humans. (1°2)
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