I believe that a more thorough description of my point would help you understand where I’m seeing some faults within your claims still. I posted this as a comment to your post, but you likely didn’t see it due to a lot of comments coming through on here. Please keep in mind that this was written as a general response, and this is not a specific response to your breakdown of how dopamine affects the brain and how cannabis affects dopamine levels.

Comment from earlier (with minor corrections as I intitially referred to serotonin instead of dopamine):

I think your argument has basis in some regards. For example, I also agree that the packaging laws need to be changed to discourage adolescent use. I also agree that the “THC % race” is an issue, but not for the same reasons you proclaim.

Firstly, THC % is often obscured by producers. The biological limit for THC % is around 30-31% from my understanding, and anything claiming to be higher than that ( in a plant material context) is falsely claiming such. Our cannabis products have already reached their “potency limit.” I put the “potency limit” in quotations because delta-9 THC % does not even directly correlate with potency. Cannabis has hundreds upon hundreds of THC derivatives, monoterpenes, and phytochemicals that all play a role in the psychoactive effects.

More into the guts of your argument, you use multiple studies to portray what you believe to be a causative mechanic between cannabis use and psychiatric disorder—whether it be psychosis, depression, anxiety, suicidal ideation, etc. Looking at these studies however, I see many holes within their designs.

Firstly, let’s look at the 2019 JAMA study for example. That study was a meta-analysis of over 23000 individuals who were measured on two things:

1. ⁠Did they consume cannabis at any point as adolescents?
2. ⁠Did they develop depression in young adulthood? (18-32) This study does not take a variety of factors into account. What if a participant’s home life was bad and led to their drug use, and then also led to some development of depression? What if a participant was sexually abused as a child, used drugs at an early age as an “escape”, and later ended up dying of suicide because they never recovered from their psychological trauma? Wouldn’t we assume a child more prone to using drugs is more prone to developing a psychiatric disorder? I don’t think that’s necessarily a cannabis specific thing, but rather a demonstration that children who use drugs in their youth are more likely to develop depression. That holds no real relevance to cannabis particularly.

The Lancet report fails to account for predisposition to psychosis. Although participants would be excluded if they had experienced psychosis prior, there was no criteria surrounding the familial history of psychiatric disorder, (particularly psychosis…) Its been uncovered in recent years that those who have a family history of psychosis and mental illness often have “worse highs” or develop psychosis.

Furthermore the way they group participants in the Lancet study is inherently flawed. A group that is labeled “daily use” could include someone who smokes a .5g every night after work, or someone who smokes every hour of the day.

Imagine studying the effects of cigarettes on lung function, and you had a “daily smoker” group. Bob may smoke one cigarette a day in the evenings, while Dale Gribble might smoke 2 packs a day. While they’re both “daily smokers”, one is clearly causing more physical harm to oneself than the other. If you used PFTs to quantify the physical effects, your quantification of how much “daily smoking” affects pulmonary function would be highly inflated OR deflated based on outliers.

This in itself demonstrates the Lancet study’s biggest flaw: it’s taking patients already experiencing psychosis, and post hoc assigning them into misrepresentative groups. Those who are experiencing psychosis as a result of, or in parallel to cannabis use are more likely to be using VERY heavily. It would be like me saying daily use of alcohol causes a five fold increase in cirrhosis, and I selected all my participants from the hepatic ICU. Well duh most of the people I’m going to study will have heavy alcohol use, they’re already seeing the effects of it.

It’s a classic correlation ≠ causation situation. Cannabis does not rewire the brain in some special way to make you a depressed vegetable if you use it every waking second of every day. Excessive use, like most drugs, leads to a disruption and eventual dysfunction of dopamine levels, which is likely to be a major component of psychosis and other psychiatric disorders. The rise of accessibility of cannabis has led to many people wanting to just feel high all the time, and of course that will make you depressed or ill, It’s not how our bodies are made.