Brain structure and antisocial behaviour – Expert Reaction

Lifelong antisocial behaviour may be associated with differences in brain structure, reports a new study.

An observational study published today in The Lancet Psychiatry examined MRI brain scans of more than 600 participants from the Dunedin Study. The scans suggest there are characteristic differences in brain structures between people who are anti-social adolescents, and those who continue to have troubles into adulthood.

The SMC asked experts to comment on the research.

Dr. Gina Forster, Department of Anatomy, University of Otago, comments:

“The key importance of this new study is the ability to distinguish between antisocial behaviour in adolescence vs. that which persists into adulthood. By doing so, it is clearer that only individuals who continue to exhibit antisocial behaviour into mid-life have a smaller brain surface area and thinner cortex in brain area associated with emotional and cognitive control.

“Studies in the past have often been limited to cross-section analysis at one time-point in an individual’s life. Here the examination of the Dunedin Study cohort has allowed a person’s behaviour to be observed over their life span. This longitudinal view is critical. Antisocial behaviour in adolescence, for example, can be transient and in response to rapidly changing physical, emotional and social demands. By recognising this, the new study provides a more detailed picture of how brain structure is associated with persistent antisocial behaviour, and has important therapeutic implications for supporting these individuals as adults.

“As with all studies of brain structure and behaviour, there are caveats. It is not clear what causes changes to brain structure and whether these in turn, directly result in antisocial behaviour. Furthermore, structural brain alterations are calculated as an average over many (in this case 600+) individuals, and it may be difficult to apply this to a single individual case for assessment or therapeutic purposes. However, technologies are improving to such allow individual-level based brain analysis so that the information gained by the current study could be readily applied in the future.”

No conflict of interest.

Devon Polaschek, Professor of Psychology and Director of the NZ Institute for Security and Crime Science Te Puna Haumara, University of Waikato, comments:

“This is an interesting study in that it represents another piece of information about how people on lifecourse persistent (LCP) vs. adolescence limited offending trajectories differ. At the same time we need to be mindful of not overinterpreting these findings; the authors are careful not to go beyond what can be concluded from this design.

“I am not all that surprised to find that people who were allocated at age 26 years to the life-course persistent trajectory in the Dunedin study have some differences detectable on MRI scans at the age 45. First, LCP men in particular were noted in quite early childhood to have differences in neuropsychological functioning, along with numerous differences in behaviour. It seems plausible, though not inevitable, that decades of having a brain that works differently might lead to observable differences in the surface of that brain.

“In fact, research on these same people at age 26 showed them to have poorer functioning across multiple life domains, including physical and mental health, as well as more persistent antisociality. Two decades on, assuming that the gap has continued to widen on all of these indices between them and the less dysfunctional members of the cohort, it would be surprising if nothing was “showing” inside their skulls. I am sure some members of the cohort look much older on the outside than others by now too. Some combination of inheritance and a lifetime of accumulating lifestyle factors that go with that inheritance has perhaps left its mark.

“But is brain structure the ‘why’ of lifecourse antisocial behaviour? The findings of this study cannot answer this question, as the researchers also note. Had these differences been present and detected early in life, it would be more believable that they may have ’caused’ lifecourse persistent offending, since causes need to precede in time the effects they are seeking to explain. But even then, wouldn’t we still be asking what caused their brains to have less surface area and thinner cortical layers?

“Perhaps the more surprising finding is that people with adolescence-limited antisocial behaviour also showed some cortical thinning compared to non-antisocial controls. People who limited their antisocial behaviour to adolescence were originally described by Terrie Moffitt in her groundbreaking 1993 developmental taxonomy work as ‘normal’ while those who did no antisocial behaviour at all were thought to be at risk of other types of maladjustment. Of course time has shown that this concern was not well founded, but it is interesting to find that their brains are now being used as the benchmark against which other brains are compared.”

No conflict of interest.