The brain of a lifelong bully looks different than the general population's
People with lifelong antisocial behavior may share neurological commonalities, a new brain-scan study shows.
One in four people will show patterns of antisocial behavior at least once during their childhood and adolescence. From stealing to bullying, lying, or even committing violence, most people grow out of these behaviors.
But for about 10 percent of the population, antisocial behavior never goes away, persisting into adulthood. In a new study, scientists scanned the brains of 672 people to discover that people who have antisocial conduct throughout their lives have smaller brains than those who do not.
Individuals who showed antisocial behavior consistently up to age 45 had a thinner cortex and smaller surface area in brain regions associated with executive function, motivation, and affect, when compared to people who were not antisocial.
By contrast, the research team didn’t see any widespread structural brain abnormalities in people who exhibited antisocial behavior only during adolescence.
The study’s findings, published Monday in the Lancet Psychiatry journal, suggest these differences in brain structure may make it harder for people to develop the social skills they need to stop them from engaging in the antisocial behavior in the first place, Christina Carlisi, a co-author on the study and researcher at University College London said.
That has implications for diagnosis — and for treatment. If these changes appear in early life, or from birth, then it may be possible to intervene early enough to make a difference in people's lifelong habits and conduct.
“These people could benefit from more support throughout their lives," Carlisi said.
Mapping the brain
The study is not the first to link atypical brain development to antisocial behavior or conduct disorder. But it is the first to map out which areas of the brain may be distinct in people who only show antisocial behavior during early life as compared to people who exhibit this behavior across their lifespan.
To figure out which brain regions — if any — looked and operated differently in lifelong-antisocial behavior, the research team analyzed brain scans from 672 45-year-old participants who are a part of the Dunedin Study. The Study has followed the same group since age three, offering researchers unprecedented information on how people's behaviors change and develop across the lifespan.
Of the 672 participants, 66 percent (441 people) had no history of persistent antisocial behavior, while 23 percent (151 people) had exhibited antisocial behavior during their younger years, and 12 percent (80 people) had “life-course-persistent antisocial behavior.” Members of the latter group showed conduct problems across their life such as physical fighting, bullying, destroying property, lying, truancy (or chronic work absenteeism), and stealing, up to age 45.
Researchers analyzed participants' brain thickness, surface area, size, and other structural details using magnetic resonance imaging (MRI) scans.
Across the entire brain, individuals who showed antisocial behavior through life had (on average) reduced surface area in 282 of 360 brain regions. They also had thinner cortex in 11 of 360 regions, including in areas linked to goal-directed behavior, regulation of emotions, and motivation, all of which can factor into antisocial behavior.
By contrast, the people who had exhibited antisocial behavior only in adolescence did not have widespread differences in brain structure.
“Most people who exhibit antisocial behavior primarily do so only in adolescence, likely as a result of navigating socially difficult years, and these individuals do not display structural brain differences,” Carlisi said.
“It is also these individuals who are generally capable of reform and go on to become valuable members of society."
Nature versus nurture
The findings do not show that lifelong antisocial behavior is rooted in the brain, or destined from birth. It is unclear whether people who do show these behaviors throughout their lives are born with brain differences or if these differences develop over time as a result of the behaviors themselves. They may also stem, in part, from environmental factors like drug use, smoking, or diet.
"It is unclear whether these brain differences are inherited and precede antisocial behavior, 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," Essi Viding, a study co-author and researcher at University College London, said in a statement.
The results jibe with a 2018 study that showed children with antisocial behavior, or who are diagnosed with conduct disorder, are at an increased risk for incarceration and poor physical and mental health later in life. More research is needed to determine how antisocial behavior plays out over a lifetime as well as in the brain.
But the findings have important implications now for the treatment of juvenile offenders, the researchers say.
"Political approaches to juvenile offending often swing back and forth between punitive measures and approaches that give young offenders room to reform," Terrie Moffitt, a study co-author and researcher at Duke University said in a statement.
"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," she said.
"Instead, we need to recognize 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."
Abstract: Background: Studies with behavioural and neuropsychological tests have supported the developmental taxonomy theory of antisocial behaviour, which specifies abnormal brain development as a fundamental aspect of life-course- persistent antisocial behaviour, but no study has characterised features of brain structure associated with life- course-persistent versus adolescence-limited trajectories, as defined by prospective data. We aimed to determine whether life-course-persistent antisocial behaviour is associated with neurocognitive abnormalities by testing the hypothesis that it is also associated with brain structure abnormalities.
Methods: We used structural MRI data collected at 45 years of age from participants in the Dunedin Study, a population- representative longitudinal birth cohort of 1037 individuals born between April 1, 1972, and March 31, 1973, in Dunedin, New Zealand, who were resident in the province and who participated in the first assessment at 3 years of age. Participants underwent MRI, and mean global cortical surface area and cortical thickness were extracted for each participant. Participants had been previously subtyped as exhibiting life-course-persistent, adolescence-limited, or no history of persistent antisocial behaviour (ie, a low trajectory group) based on informant-reported and self-reported conduct problems from the ages of 7 years to 26 years. Study personnel who processed the MRI images were masked to antisocial group membership. We used linear estimated ordinary least squares regressions to compare each antisocial trajectory group (life-course persistent and adolescence limited) with the low trajectory group to examine whether antisocial behaviour was related to abnormalities in mean global surface area and mean cortical thickness. Next, we used parcel-wise linear regressions to identify antisocial trajectory group differences in surface area and cortical thickness. All results were controlled for sex and false discovery rate corrected.
Findings: Data from 672 participants were analysed, and 80 (12%) were classified as having life-course-persistent antisocial behaviour, 151 (23%) as having adolescence-limited antisocial behaviour, and 441 (66%) as having low antisocial behaviour. Individuals on the life-course-persistent trajectory had a smaller mean surface area (standardised β=–0·18 [95% CI –0·24 to –0·11]; p<0·0001) and lower mean cortical thickness (standardised β=–0·10 [95% CI –0·19 to –0·02]; p=0·020) than did those in the low group. Compared with the low group, the life-course-persistent group had reduced surface area in 282 of 360 anatomically defined parcels and thinner cortex in 11 of 360 parcels encompassing circumscribed frontal and temporal regions associated with executive function, affect regulation, and motivation. Widespread differences in brain surface morphometry were not observed for the adolescence-limited group compared with either non-antisocial behaviour or life-course-persistent groups.
Interpretation: These analyses provide initial evidence that differences in brain surface morphometry are associated with life-course-persistent, but not adolescence-limited, antisocial behaviour. As such, the analyses are consistent with the developmental taxonomy theory of antisocial behaviour and highlight the importance of using prospective longitudinal data to define different patterns of antisocial behaviour development.