People who use cannabis in their 20s and 30s are developing psychosis years earlier than non-users, according to our new study , published today in the journal Biological Psychiatry.
Authors
- Matthew Large
Conjoint Professor, Discipline of Psychiatry and Mental Health, UNSW
- Carly Stevens
Casual Academic, Biomedical Sciences, UNSW
This challenges the idea that delaying cannabis use until your mid-20s - when people believe their brain has finished developing - is a safer option to avoid the risks of psychosis.
Our research found that for people who were susceptible to psychosis, cannabis use in their 30s was associated with an earlier onset of psychosis by 6.3 years.
Cannabis use is becoming increasingly common. More than 2.5 million Australians use prescribed or illicit cannabis each year . It's also increasing in potency.
But for many users, the psychiatric harms of cannabis are likely to outweigh any medical benefit. In fact, there is little evidence it's effective for anxiety, depression or insomnia .
What is psychosis?
Psychosis is a spectrum of disorders, characterised by reality distortion. At the core of psychosis is the more severe and chronic form, schizophrenia.
A person with psychosis may experience confusion, mood swings and hallucinations - seeing or hearing something or someone who isn't there. They may have false beliefs and might not make sense to others while speaking.
Psychosis affects around 0.5% of Australians of Australians. There is a strong genetic component to schizophrenia and psychosis. Environmental factors, including cannabis use, also play a role.
How does cannabis impact psychosis
The most active ingredient of cannabis is delta-9-tetrahydrocannabinol, or THC. Both prescribed and illicit cannabis usually contain THC, often in high doses . However, prescribed cannabis is also available without THC.
THC works by locking onto the cannabis receptors, which are part of the brain's endocannabinoid system.
When naturally functioning, the endocannabinoid system helps maintain physiological balance by regulating processes including appetite, immunity, memory, mood, pain, sleep and stress responses.
The cannabis plant evolved to exploit this system by producing the mind-altering compound THC, which acts as a skeleton key for the cannabinoid receptors.
Past research has found people who frequently use cannabis are more likely to experience psychosis and greater harms from psychosis.
In 2011, our research group showed cannabis use was associated with an earlier age of onset of psychosis .
This was widely assumed to mostly affect younger people because of prevailing beliefs about the vulnerability of the developing adolescent brain to cannabis exposure.
What we found
Our new research casts the link between cannabis and earlier psychosis onset in a different, and ultimately more worrying, light.
We examined 149 studies involving more than 71,000 people over the past 15 years. Most involved people with schizophrenia, from Europe, North America and Australia.
We found cannabis use was associated with an earlier age at psychosis onset by 2.5 years on average.
This finding was more severe in later-onset psychosis: cannabis users who developed psychosis in their late 20s had an onset of 4.4 years earlier on average.
This difference increased to more than 6.3 years in people who developed psychosis aged 30 or over.
Interestingly, we found no evidence of earlier onset of psychosis for people who developed it under 20.
Why does this matter?
Earlier onset of psychosis is associated with worse clinical outcomes, greater functional impairment and struggles with self care.
Losing years of healthy life to psychosis in your 20s or 30s means missing years that could have been spent studying, building a career, travelling, starting a family, and developing strong relationships and support networks.
What might be going on?
Across the lifespan, cannabis use is associated with a dramatic decrease in healthy life years due to psychosis.
While our 2011 research suggested exposure of the adolescent brain interfered with crucial pathways, our new research points to the possibility of an additional factor: a cumulative effect of cannabis as a brain toxin.
It's unclear why we didn't see the same acceleration of psychosis in people under 20. It could be that genetics plays a larger role in the onset of psychosis in this age group, while cannabis may be a more significant contributor in people in their 20s and 30s.
But more research is needed to understand how cannabis interacts with psychosis, including the biological mechanisms to explain the associations.
What were the limitations?
Our study was a meta-analysis, which involves group-level data. It doesn't take into account individual characteristics of participants that could influence the results - for example, exposure to traumatic experiences in childhood.
We also used age groups instead of the specific ages of all participants. This might result in a finding that was stronger or weaker than the one we found.
Finally, we couldn't drill down into the potency of the cannabis products used, or the way cannabis was used (for example, smoking a joint or eating gummies). The potency of products varied between studies.
Users and prescribers need to know the harms
Some 40 years of research has consistently shown an association between cannabis and psychosis .
There is also emerging evidence that cannabis is associated with a range of other psychiatric harms, including anxiety and depression .
But the medicalisation and monetisation of cannabis has hampered knowledge and acceptance about its now well-established harms.
Now Australians can access high-potency cannabis without any appropriate health warning. This might prove to be one of the biggest public health bungles in Australian history.
Our research shows detailed public health warnings are urgently needed to explain the potential psychiatric risks associated with cannabis use across the lifespan.
The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.
