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Antisocial behaviour: just a phase? Brain structure holds clues

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Some people get into trouble in their youth, but only a few go on to engage in life-long antisocial behaviour – for example, stealing, aggression and violence, bullying, and lying. New research from the long-running Dunedin Study reports that people engaging in this persistent anti-social behaviour have structural differences in their brains that are not seen people who were only troublesome in their youth but grew out of it. The authors say their findings cannot prove causation, but provide the first robust evidence to suggest that underlying neuropsychological differences exist in people with life-course-persistent antisocial behaviour and have implications for the way we treat juvenile offenders.

Journal/conference: Lancet Psychiatry

Link to research (DOI): 10.1016/ S2215-0366(20)30002-X

Organisation/s: University of Otago, Rangahau Roro Aotearoa Centre of Research Excellence

Funder: This study was funded by US National Institute on Aging, Health Research Council of New Zealand, New Zealand Ministry of Business, Innovation and Employment, UK Medical Research Council, Avielle Foundation, and Wellcome Trust. It was conducted by researchers from University College London, London, UK, Duke University, USA, King’s College London, London, UK, University of Otago, Dunedin, New Zealand, Rangahau Roro Aotearoa Centre of Research Excellence, Dunedin, New Zealand.

Media Release

From: The Lancet

Peer-reviewed / Observational study / People

Life-course-persistent antisocial behaviour may be associated with differences in brain structure

MRI brain scans suggest there are characteristic differences in brain structure of individuals who exhibit life-course-persistent antisocial behaviour.

Individuals who exhibit life-course-persistent antisocial behaviour – for example, stealing, aggression and violence, bullying, lying, or repeated failure to take care of work or school responsibilities – may have thinner cortex and smaller surface area in regions of the brain previously implicated in studies of antisocial behaviour more broadly, compared to individuals without antisocial behaviour, according to an observational study of 672 participants published in The Lancet Psychiatry journal.

However, there were no widespread structural brain abnormalities observed in a larger group of individuals who exhibited antisocial behaviour only during adolescence.

Previous epidemiological studies have demonstrated marked individual differences in the age of onset and duration of antisocial behaviour. Some individuals display life-course-persistent antisocial behaviour that begins in childhood and lasts into adulthood, whereas for others antisocial behaviour arises in adolescence but desists as they mature into adulthood.

The study is the first to compare structural brain differences using neuroimaging in individuals with either life-course-persistent or adolescent-only antisocial behaviour and those without antisocial behaviour, providing the first robust evidence to suggest that underlying neuropsychological differences are primarily associated with life-course-persistent persistent antisocial behaviour.

Lead author Dr Christina Carlisi, UCL, UK, says: “Our findings support the idea that, for the small proportion of individuals with life-course-persistent antisocial behaviour, there may be differences in their brain structure that make it difficult for them to develop social skills that prevent them from engaging in antisocial behaviour. These people could benefit from more support throughout their lives.” [1]

Continuing, she cautions: “Most people who exhibit antisocial behaviour primarily do so only in adolescence, likely as a result of navigating socially difficult years, and these individuals do not display structural brain differences. It is also these individuals who are generally capable of reform and go on to become valuable members of society.” [1]

The study used MRI brain scans from 672 participants aged 45 years. Based on reports from parents, carers and teachers, as well as self-reports of conduct problems between ages seven and 26 years old, the 672 participants were previously categorised in terms of the patterns of behaviour they exhibited - 12% (80 people) had life-course-persistent antisocial behaviour, 23% (151) had adolescent-only antisocial behaviour, and 66% (441) had no history of persistent antisocial behaviour.

Analysing the brain scans, the authors measured and compared the average cortical thickness and cortical surface area (indices of grey matter – a type of brain tissue – size), between these three groups. They also analysed differences in the surface area and cortical thickness of 360 different regions of the cortex.

On average, across the entire brain, individuals with life-course-persistent antisocial behaviour had a smaller mean surface area and lower mean cortical thickness than people who showed no persistent antisocial behaviour. In addition, people who showed life-course-persistent antisocial behaviour had reduced surface area in 282 of 360 brain regions, and had thinner cortex in 11 of 360 regions, most of which have been previously linked to antisocial behaviour through their involvement in goal-directed behaviour, regulation of emotions, and motivation.

However, widespread differences in brain structure were not found for the adolescence-limited group compared with either non-antisocial or life-course-persistent antisocial groups.

The authors say their findings provide the first robust evidence to suggest that underlying neuropsychological differences exist in people with life-course-persistent antisocial behaviour and have implications for the way we treat juvenile offenders.

Adolescents exhibiting life-course-persistent antisocial behaviour which began in childhood are often diagnosed with conduct disorder, and these children are at an increased risk for incarceration and poor physical and mental health later in life. [2]

Co-author Terrie Moffitt, Duke University, USA, says: “Political approaches to juvenile offending often swing back and forth between punitive measures and approaches that give young offenders room to reform. Our findings support the need for different approaches for different offenders – however, we caution against brain imaging being used for screening, as the understanding of brain structure differences are not robust enough to be applied on an individual level. Instead, we need to recognise that individual development can be one driver of serious repeat offending, but to also appreciate that this is not the case for all juvenile offenders.” [1]

Acknowledging the limitations of their study, co-author Professor Essi Viding, UCL, UK, cautions: “It is unclear whether these brain differences are inherited and precede antisocial behaviour, or whether they are the result of a lifetime of confounding risk factors (eg, substance abuse, low IQ, and mental health problems) and are therefore a consequence of a persistently antisocial lifestyle.”

The authors call for more long-term studies of antisocial behaviour which include multiple measurements of behaviour, brain, genes, and environment to understand how life-course-persistent antisocial behaviour unfolds.

[1] Quote direct from author and cannot be found in the text of the Article.
[2] https://moffittcaspi.trinity.duke.edu/sites/moffittcaspi.trinity.duke.edu/files/rivenbark_jcpp2018_0.pdf

Expert Reaction

These comments have been collated by the Science Media Centre to provide a variety of expert perspectives on this issue. Feel free to use these quotes in your stories. Views expressed are the personal opinions of the experts named. They do not represent the views of the SMC or any other organisation unless specifically stated.

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

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.

Last updated: 18 Feb 2020 12:02pm

Declared conflicts of interest:

None declared.

Dr Gina Forster, Department of Anatomy, University of Otago

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.

Last updated: 18 Feb 2020 12:00pm

Declared conflicts of interest:

None declared.

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