Heavy marijuana use increases schizophrenia in men, study finds

I'm guessing that this statistic wouldn't be very helpful or interesting. Even if the number is 100%, they all drink water and eat food too.

A more interesting statistic would be rate of 1st-3rd degree murders committed on different drugs, and/or what percentage of cannabis users commit violent crimes in general.

If anyone wants a technical reason, (as best as I understand), this could very well be a very straightforward consequence of THC sensitizing the D2 receptor, which so far at least has been shown to happen in some parts of the brain (https://www.nature.com/articles/npp201291), as best as I understand.

D2 is the primary receptor that many antipsychotics (especially the newer ones) target -- the first generation by completely blocking it, the third by partially agonizing it -- I.E., partially causing it to activate. However, third generation anitpsychotics activate it at a much lower value than dopamine itself would, so you potentially get fewer of the catastrophic side effects than you would from something like haloperidol or risperidone. However all three generations end up balancing out in the end to where they're actually not too terribly far apart in terms of side effects for the benefit provided, if I understand correctly, third generation antipsychotics like Abilify (aripiprazole) do hold an edge here.

D2 is one of the the receptors used for psychotomimetic models of the brain -- stimulating it tends to bring forward both the positive and negative effects of schizophrenia if I remember correctly. Another psychotomimetic pathway is NMDA antagonism, which makes sense as glutamate is implicated in schizophrenia.

What is interesting is that D2 agonists can help trigger latent schizophrenia, which exists genetically and often becomes obvious in the forefront by the late teens and early twenties. Marijuana use before the brain fully develops also has permanent effects on this brain in the same time range (not saying they're necessarily related). Schizophrenia does have some very clear structural causes -- for example, pyramidal neurons in some parts of the brain, if I remember correctly, are inverted to route information to lower layers in certain parts than higher ones. These are the neurons that collate and process many-to-one inputs->outputs.

One of the interesting things about schizophrenia is that it results (if I recall correctly) in _lower_ brain entropy on the whole, which is not what one might expect with an information routing issue. This means that one might not reap the benefits of having excess information flow, since not only is there noise being added to the system, the confidence of the outputs of the system are increased.

Many people who are schizophrenic tend to have a flat affect and are asocial, and will often have a tendency to safely pull away from society and keep to themselves, for example. They also have a lower tendency to become violent. This partially means, for example, that counterintuitively, that people who are schizophrenic, at least (and I would assume this applies as well to those who have schizophrenic tendencies) tend to have a lower violent crime rate as well. There are outliers, for example in homeless camps intercity, that can make schizophrenics seem more violent, though I would blame this on the human tendency of us valuing long tail events over uneventful ones for determining important information (something absolutely necessary for raw survival in a generally oftentimes cruel and unforgiving world -- society or no. It is unfortunately a useful bias to have).

All in all, this is a very interesting (if very tough, hard, and sad at times, to be quite frank!) topic, and does bear much of our interest and empathy. Please be sure to ground yourself in the science of it all, and I encourage you to keep pursuing knowledge about this subject matter. There is not necessarily much new under the sun, and a lot of these studies are not anything surprising, shocking, or novel, but instead confirmation of certain hypotheses or theories that have been running in the community for quite a while. Of course, we don't know for sure if this what this is -- this is one person who is not in the medical community's take on it (albeit with a fair bit of personal interest and investment in the topic), and someone who is a skilled researcher particular to the subject matter area might give you a different and/or better view on it.

Source for interest in this case is that I am very much interested in psychopharmacology, and it's been an, er, rather involved hobby of mine for a while in terms of the amount of papers and such that I've read on the matter (I also took a graduate class in it for funsies online through the Harvard extension school. I can recommend that experience -- it's not that hard to get into, and you get some _quality_ course material, guest speakers from around the field (!!!!), and lectures).

Feel free to let me know if you have any questions! Much love!!!! <3 :)))) :'D <3

It could, though there is some work I believe on certain receptors which THC also happens to increase the activation of activating latent schizophrenia.

> Interestingly, the journal article doesn't bother to mention how cannabis use disorder (CUD) is defined; however, Bloomberg's description "frequent use despite negative consequences" is essentially that of the DSM, and so is presumably what they're using.

Yes, it does: "CUD was identified in the same registers and supplemented with the somatic part of the National Patient Register, defined as ICD-8 code 304.5 and ICD-10 code F12.X." 304.5 is the diagnostic code for CUD. We can infer that a person with CUD themselves have considered their cannabis use to be problematic. Otherwise they wouldn't have been diagnosed.

FTA: "For example, in Denmark, the incidence of schizophrenia steadily increased from 2000 to 2012 (Kühl, Laursen, Thorup, & Nordentoft, Reference Kühl, Laursen, Thorup and Nordentoft2016), and the schizophrenia population attributable risk fraction (PARF) for CUD increased three- to fourfold over the past two decades, parallel to increases in THC concentration (Hjorthøj, Posselt, & Nordentoft, Reference Hjorthøj, Posselt and Nordentoft2021). The increased THC content may thus, along a potential increase in the prevalence of CUD, be a main driver of the population-level increase in PARF between CUD and schizophrenia."

The explanation "increased THC content causes more schizophrenia" is clearly more plausible than "more schizophrenia causes increased THC content".