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Brain abnormalities pre-date pot smoking in heavy users

Long term cannabis use has been known to harm the brain but new research shows some of this damage was there to begin with. Wiros

Cannabis remains the most commonly consumed illicit drug in the world, with more than a third of Australians reporting that they have used it at some point in their lives.

This is despite growing evidence that smoking pot during adolescence is associated with a number of significant harms, including educational underachievement and the later development of mental health disorders.

While few studies have examined whether long-term cannabis use also has detrimental effects on the brain, we have previously found that regular, heavy cannabis use is associated with significant reductions in the hippocampus and amygdala, two key brain regions that are involved in learning and emotion.

We also observed a relationship between brain volume and cannabis use, with greater levels of cannabis exposure associated with smaller hippocampi.

M. Martin Vicente

Although these changes are often attributed to the neurotoxic effects of long-term cannabis use on key brain regions, some abnormalities may predate use and represent markers of vulnerability. Until now, no studies have examined whether structural brain abnormalities are present in adolescents before they begin experimenting with cannabis.

This month, we published new research in the journal Biological Psychiatry that assessed whether adolescents who began smoking cannabis before age 17 demonstrated pre-existing differences in key brain regions. Participants were recruited from primary schools in Melbourne, as part of a larger study examining emotional development.

The participants underwent structural magnetic resonance imaging (MRI) at age 12 and were assessed for cannabis use four years later, at the age of 16. At the follow-up assessment, 28 participants (16 of whom were female) had commenced using cannabis and 93 (43 females) had not.

We found that only regions of the frontal part of the brain – the orbitofrontal cortex (OFC) – predicted cannabis use by age 16, even after controlling for alcohol and tobacco use. Volumes of other brain regions, including the hippocampus and amygdala, did not predict later cannabis use.

Green: the orbitofrontal cortex. Paul Wicks

The OFC plays a primary role in inhibitory control and reward-based decision making. And previous studies of adolescent cannabis users have demonstrated subtle deficits in problem solving, attention, memory and executive functions, as well as abnormalities in this brain region.

In adult cannabis users, decreased activation of the OFC has been associated with faulty decision-making, suggesting that a reduced ability to weigh up the pros and cons of one’s actions might render certain individuals more prone to drug use.

But while our findings suggest that brain regions that underlie inhibitory and decision-making processes influence risk for early cannabis use, it’s unlikely that OFC volume reductions exclusively lead to cannabis use.

Multiple studies suggest that OFC abnormalities occur in other addictive disorders and are not substance-specific. In fact, smaller OFC volumes are likely to be related to other substance use problems later in life, of which adolescent cannabis use might be considered an early marker.


Indeed, our findings are consistent with other research which demonstrates that the most robust predictors of early substance use are those that relate to poor behavioural and emotional control.

Our results also suggest that previously observed structural changes in the amygdala and hippocampus in long-term heavy users are a consequence of chronic cannabis exposure rather than a pre-existing vulnerability. This reinforces the notion that prolonged use of cannabis is neurotoxic to specific brain regions.

In terms of next steps, further prospective studies are required to determine the degree and mechanisms of long-term cannabis-related harm, as well as the time course and extent of brain recovery following abstinence.

In the meantime, we need greater investment in prevention programs that target childhood risk factors, such as social disadvantage, family breakdown and early school failure, which contribute to the development of harmful substance use during adolescence.

And we need to work to strengthen factors that protect young people from developing substance-related harm such as enhancing family attachment, and social and emotional competence.

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