72 Chapter 6
IQ, poor memory, poor motor skills, lower heart rate). Not all early
onset cases persist, but a marker for persistence is having a father with a
history of antisocial or criminal behaviour.
Late onset(typically around age 13–15 years) was found in a separate
7% of the population, and while as a group they performed as many
antisocial acts as the early onset group as late teenagers, this level had
halved (but not gone down to normal) by their late twenties. The late
onset group was no more exposed to parenting or neurocognitive risk
factors than the general population.Causes
Genes or environment?
Disruptive behavioural disorders commonly cluster in families, and com-
pared to other child psychiatric disorders, shared environment has a
proportionately greater influence than shared genes. Thus, although twin
studies have shown a high concordance for monozygotic pairs, the con-
cordance for dizygotic pairs is also high. Adoption studies have shown the
influence of the biological parents to be less than that of the adoptive ones.
However, they show a strong interaction effect, whereby the combina-
tion of high congenital risk, as indexed by having criminal or alcoholic
biological parents, plus an unfavourable rearing environment, as indexed
by having alcoholic or criminal adoptive parents, leads to a far higher
rate of antisocial behaviour and criminality than would be expected by
addition (see Box 33.2). This gives grounds for some therapeutic optimism,
since even if a child is born with considerable congenital risk factors, if
the parenting and general rearing environment are favourable, they can
do relatively well. However, genetic influences seem to play a stronger
role in the development of adult antisocial personality and criminality.
Cytogenetic studies have added little so far, and the case studies reporting
that individuals with the XYY karyotype are particularly prone to severe
aggression have not been supported by population-based surveys. Molec-
ular genetic studies are beginning to emerge. For example, the Dunedin
study was the first to show an interesting gene–environment interaction,
whereby children with one particular variant of the monoamine oxidase A
gene are at an increased risk of developing antisocial behaviour, but only
if they receive relatively poor parenting (in the worst third of the popu-
lation); otherwise they are not at increased risk of antisocial behaviour.
Subsequent studies have confirmed this finding, albeit with a relatively
small effect. Within subtypes of antisocial behaviour, those with callous-
unemotional traits have greater heritability – 80% in one study – than
those without, where environmental influences predominate.
Child-based mechanisms
1 Constitutional characteristics proposed include neurotransmitter imbal-
ance, hormonal excess (notably testosterone) and metabolic variations