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Comment by ejstronge | Hacker News Reader

Won’t have the space/time to respond fully, but the allusions to bipolar disease and, especially, schizophrenia need to be viewed quite cautiously.

I do not believe these disorders are thought to originate from environmental factors present in late teenage years. Thus, we should expect a large increase in these diagnoses if cannabis is indeed a causative agent that is now more attainable than it used to be.

Also, individuals will instinctively self-medicate (think about a pet favoring a wounded paw). If these disorders reflect structural brain abnormalities - which they do, in large part - we then can’t distinguish whether cannabis use is a compensatory mechanism or a causative mechanism

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There is not one single cause for the onset of psychosis but many factors at play. Cannabis use can be a cause. Early interception of people at risk and treatment, does bring down the number of young people having a first psychosis.

I am not disagreeing that cannabis may be a cause.

This kind of article doesn’t offer any evidence toward the idea outside correlations - and this kind of correlation is very tenuous.

A good example to demonstrate the idea is the outsized use of tobacco products amongst those with ADHD diagnoses. Do we immediately conclude that ADHD rates are influenced by the availability of cigarettes? Or can we instead ask how nicotine may influence neural circuits that are abnormal in ADHD?

The article links to this Lancet study, which does start to go beyond just correlation.

https://www.thelancet.com/article/S2215-0366(19)30048-3/full...

It is a compelling study, but retrospective trials, in general, aren't the correct design to answer this kind of question. I am not saying the results aren't accurate - just that in medicine, there have been instances where a prospective trial offers a different conclusion that that of prior, retrospective trials.

Next, I'm no statistician, but I have never heard of this kind of trial being proof of causality (it can only provide supportive data - but as above, we know that the results may prove incorrect in a stronger study design). There are a lot of confounding factors that make causality a difficult thing to prove in humans.

There is actually a way to prove causality in humans, and I suspect someone will do this for marijuana since it is a hot-button issue: https://archive.cdc.gov/#/details?url=https://www.cdc.gov/ge...

It's really very difficult to untangle, because there's a huge overlap between the known risk factors for schizophrenia and the known risk factors for early and heavy use of cannabis. The best guess based on the available data is that there's a brutal statistical double-whammy - people at risk of psychosis are much more likely to use cannabis heavily [i]and[/i] are more vulnerable to the effects of cannabis.

https://sci-hub.ee/10.1016/j.ajp.2013.03.012

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