Heavy marijuana use increases schizophrenia in men, study finds
bloomberg.com
bloomberg.com
Autistic adults have significantly low blood serum levels of AEA. Autistic people’s neurons prune slower. Schizophrenic people’s neurons prune faster.
It seems the ECS system is the principal driving mechanism behind both conditions. We need a lot more research in this area, but it could be THC has a positive neurological affect on Autistic people whereas finding a blocker for AEA binding on Microglia may result in a positive neurological affect on Schizophrenic people.
The next few years will be especially interesting.
This is a review not a study. It is designed to give you a broad view of current areas of active research. It does not validate any of the research it discusses. It just says “this is what is out there”.
Welcome to the rabbit hole.
On the same (personal observation) basis, I'd say that schizophrenic people are drawn to cannabis. I have no idea why; perhaps because they're often very marginalized and precarious.
Obviously it was ‘pothead science’ without a mechanism etc but it has been a thing anecdotally for at least as long as the medical push has existed.
Therefore marijuana is a cure-all. ;)
Pliny the Elder would be so proud of me.
I think that there are a number of reasons for this. CBD, exploration/play of mental states, and the hundred+ other cannabinoids may all be a factor.
First, cannabis can contain CBD, which has strong, known anti anxiety and anti-psychotic effects. Couldn't a person vulnerable to episodes recognize this effect when enjoying a higher CBD strain, then seek it out again?
It is very unfortunate for these people that prohibition selected for high THC, low CBD strains.
Second, it can be a great benefit to know, from experience, that smoking a herb can bring on near-psychosis. Certainly, some people try to get a handle on their condition by 'playing' with it in this way.
Learning about the physical feelings and clues that go along with the early stages of an episode may help in some way to feel in control, and even learn to recognize and change the course of a budding episode.
Again, it is more than unfortunate that prohibition and propaganda have prevented any real exploration of these possibilities. For thousands of years shamans have played with mental states, and it was seen as not just positive but necessary.
It is too often seen as heresy if you suggest that psychosis doesn't actually need to be treated with hardcore pharmaceuticals, for life. I do believe though that it could - at least sometimes - be better treated as a mental state which can be self-recognized, and integrated.
Third, cannabis contains hundreds of cannabinoids other than THC and CBD. Some of these may have positive effects on all sorts of things related to schizophrenia and psychosis - mood, humour, insight, metabolism, gut health, etc.
Studies which only examine THC and CBD in isolation can only ever understand so much - these interactions may be a lot more complex than we commonly guess.
My argument is wholly secular and realistic. It's summed up as 'exploration/play of mental states', which applies even to your flashing-lights-and-technicolor straw-man.
It doesn't rely on 'hypnotic movements' or 'rhythmic drumming'; or a monomyth, or cultural surroundings, or 'they did it thus it's natural'. Or flashing lights, or wastelands, or ancestral visions, etc.
Perhaps you could read my comment again, with a little more care and a lot less caricature.
This sounds a lot like saying that people with a predisposition to lung cancer are drawn to cigarettes.
There is no universal trend of people consuming cannabis and developing schizophrenia.
We know that cannabis can act as a catalyst for schizophrenia, but we also know that not everyone who is predisposed to schizophrenia develops it 100% of the time after cannabis use. There are degrees of predisposition, and a bunch of other factors that contribute to this.
many of the most common mental health conditions (personality disorders, and schizophrenia) don't appear till the end of adolescence.
If something is flammable, and so predisposed to burning, and you hold a lit match to it, you did cause the fire. You didn't just trigger it.
Similarly someone can be schizophrenic but have an *episode* caused by weed. The weed didn't make them schizophrenic but it did cause an episode to happen.
(Of course, smoking is still bad for you.)
With enough dose anyone can become psychotic on THC.
I don't think it's as absolute as you're saying.
I found this (relatively) recently published article reviewing Bleuler's Dementia Praecox or the Group of Schizophrenias which is the book where he first publishes the terms "Schizophrenia" and "Autism." Though Bleuler was using the words with his colleagues starting a few years earlier. (Cf. Freud-Jung Correspondences, May 1907[0], you can ctrl-f "autism,""schizophrenia," etc.)
[0]https://archive.org/stream/FreudJungLetters/The-Freud-Jung-l...
Other researchers suggest the boundary between autism and schizophrenia is weaker than is commonly supposed. Common diagnostic tests for ASD perform poorly in distinguishing it from schizophrenia; there is heightened prevalence of each condition among those diagnosed with the other; autism started out as a new name for childhood-onset schizophrenia (in fact the word "autistic" was originally coined to describe schizophrenia), and there is still a lot of dispute about what is the difference between autism and childhood-onset schizophrenia (the former is much more common than the later–subclinical hallucinations are common in children, but clinically significant psychotic symptoms are quite rare)
Nobody really knows, not even the experts.
These are all group-level findings, meaning they aren't true for every individual. You can do a study and find that there is a statistically significant difference in mean X between two samples – autistic vs control or schizophrenic vs control. But pretty much always, although there is a statistically significant difference in the mean, the two samples overlap – which is consistent with this being a factor which only explains some of the cases.
> It seems the ECS system is the principal driving mechanism behind both conditions.
Claims like that ("the principal driving mechanism behind psychiatric diagnosis X is biological difference Y") have been made many times before, and few of them have gone anywhere. I'd be surprised if this one turns out differently.
Both autism and schizophrenia are bundles of different conditions which we've grouped together on the basis of nothing more than overlapping systems. Two people can both have "autism", yet at a biological level they've got two completely different things. The same applies for two people with "schizophrenia". This is why a number of researchers have been arguing that diagnosis-centric research is a dead-end.
I wouldn't be surprised if ECS system issues (or any other system in the brain) turn out to be the cause of some cases of autism and some cases of schizophrenia; but there will be other cases of both in which it isn't the "principal driving mechanism" at all.
Now, clearly, mainstream psychology disassociated these terms sometime in the 60s, when the goal with autism diagnoses was moreso to find and identify "abnormal" children (Hans Asperger famously used Autism diagnoses to euthanize children, that's who "Asperger's Syndrome" is named after!), and Schizophrenia gained its own separate classification. But its interesting to note that there was a time when social disaffection in general was considered a single set of disorders.
Asperger was assigned to identify autistic children for exterminatiom, but mafe the case that certain ones were useful to the Reich, which is why “Asperger’s Syndrome” became the name for the manifestation of autism that was seen as a leader impairmemt.
He did successfully argue that some more intelligent children should be spared, on the grounds they had unique skills which could be valuable to the regime. However, less intelligent children, he was happy to refer to be murdered (in most cases without the knowledge or consent of their parents). He wasn't evil in the way in which many devout Nazis were, just in the more banal way of the many who collaborated in the regime's crimes out of personal self-interest, or through coming to believe its propaganda.
For all of Asperger's sins, he was too humble to actually name a disorder after himself – he called his disorder "autistic psychopathy". Lorna Wing renamed it after him, because the word "psychopath" had become very stigmatised, and Asperger was using it in an older and broader sense than current discussions of "psychopathy", which is prone to confuse the uneducated layperson. Wing was actually one of the people trying to defend Asperger–before her death, she wasn't aware of the further historical research published on this topic after she died, and who knows whether she would have revised her position if she'd lived to see that–it is understandable she'd want to defend one of the major decisions of her career–and she was (at best) dimly aware of this aspect of Asperger's history when she made that decision
I will admit to myself sometimes using "Aspergian" in describing some of my own personality traits, not because I necessarily agree with the term, but simply because it is a useful shorthand which my listener is likely to understand, and as much as I'd love to dump all these details and more on them, it risks overwhelming their time, attention and comprehension
On the other hand, Autism Spectrum Disorder basically doesn't exist, it was designed specifically to cover as many possible definitions of Autism such that nearly anyone, under the right circumstances, could be labeled as Autistic and be given expensive treatment, and I think there is something dangerous in people self-identifying with this label as it only feeds into the larger psychiatry-industrial complex. It's similar to depression--some people legit can't get out of bed in the morning, but the drugs we use to treat it are handed out like candy, are not approved to be used for the terms that they are, and don't even perform better than a placebo.
The problem isn't that some people are "neurodivergent" and others aren't, and neurodivergent people shouldn't be ashamed and should embrace their label. The problem is that everyone is neurodivergent--everyone is "perverse," as Freud famously elucidates in his theory--its just that those who are labeled as "other" under the system get exploited, and everyone else, for fear of the same fate, hide all their psychological proclivities from everyone except from their most intimate acquaintances. And there are some who are lucky enough to avoid both fates, but they are rare among the ruling class, and the commonality of ostensible abnormal psychology among the working class is considered a "problem" to be solved by endless mental health facilities, treatment programs, etc. meanwhile the real pains of being a working class American forces many into addiction, and what they are offered can do nothing much to alleviate the underlying problems which led them there (often times problems, as in the case of the opioid crisis, generated by the very corporate structure which also drives people to treatment for their addiction).
I learned about all what you discuss because I wanted to find a genealogy of "Autism" as a why of critiquing it as a medical category. But I don't know, as I said there is definitely some constellation of symptoms and ways of treating them that would fall under an Autism diagnoses, its just that how such a diagnoses came to exist was not through some pure empirical scientific process but a historical, social process that can't be disassociated from the other socio-economic realities.
He criticises the "autism spectrum" saying that it "is a convention that changes over time and belongs more to the history of science than neurobiology" (a rather scathing remark but put it in an understated way)
On the other hand, he insists that "prototypical autism" should be retained as a real target of scientific investigation, and he proposes that our failure to discover its causes (despite immense research funding into the project) is largely due to going astray by broadening its definition (through the "autism spectrum") to the point that it is approaching meaninglessness
For a different viewpoint, see Lynn Waterhouse et al – https://link.springer.com/article/10.1007/s40489-016-0085-x – who argue the whole category of "autism" (whether a broad "autism spectrum" or a narrow "prototypical autism") is a dead-end, and researchers ought to abandon it and look for new concepts to replace it with. In her book, she proposes (as a temporary measure) replacing "autism" with phenotypes of neurodevelopmental social impairment – which unlike "autism"/"ASD", are only defined in terms of deficits in the social communication domain, but allows those deficits to coexist with deficits in other domains (repetitive behaviours, restricted interests, impulsivity, attention deficits, dyspraxia, dyslexia, epilepsy, intellectual disability, etc)
And then there's Sami Timimi et al's book "The Myth of Autism" which, as well as criticising the science of "autism" (as Waterhouse and, to a lesser degree, Mottron do), goes beyond that to criticising it as a cultural construct, arguing that the harm it causes outweighs its benefits
> The problem isn't that some people are "neurodivergent" and others aren't, and neurodivergent people shouldn't be ashamed and should embrace their label. The problem is that everyone is neurodivergent
To quote Timimi, "We are all (humanity) simply neurodiverse" – https://www.madinamerica.com/2018/04/the-scientism-of-autism...
Just sounds like they've been diagnosing by symptom because they didn't know the actual etiology. Once it's known shouldn't they just change the diagnosis to be the new, more specific condition? Seems like diagnosis is still the goal?
Well, we don't know the aetiology (in most cases), so while restructuring diagnosis on the basis of aetiology is defensible as a long-term goal, we are nowhere being able to achieve that yet. The argument is, designing research around the current symptom-focused diagnostic categories is blocking progress in research. Two people with the same diagnostic label may have completely different aetiologies, two people with the same aetiology may have completely different labels, two people with the same aetiology one of them may have a label and the other may have none – the same underlying brain dysfunction may manifest with very different symptoms in different individuals, depending on its interaction with other biological factors, and their social environment. If we want to understand "what's really going on", it can be better to put everyone in the same sample (both diagnosed with various diagnoses and undiagnosed), then look for patterns in that big sample. I think this paper is a great example of doing that, with the help of machine learning – https://www.nature.com/articles/s41398-019-0631-2 – but it needs replication.
Do you know of any literature I can read about the mechanisms behind this?
I have autism. Tho I didn't know it back then. I've had multiple minor psychoses from using marihuana recreationally. I know they're minor (with one on the mediocre side) because I've also had a longer episode likely related to stress. Oh, and marihuana was decriminalized back then. From my perspective, the last thing I need, is THC, and your post hasn't convinced me otherwise.
Also, take note of the headline. It mentions men. So for about 50% of society, its unknown. Actually, the reach is even lower, as they looked into men aged 21-30.
Honestly, if I compare marihuana to psilocybin I'd say the latter is more predictable. But either way, it all has to be standardized. Recreational usage of marihuana is not, and this is problematic, even though it is decriminalized here (and has been for many decades here). The fact people cannot buy psilo's anymore here shivers me in that regard; they either grow their own (not standardized) or have to resort to things like truffles.
Nice guy, probably on the spectrum, started smoking weed to help him chill out in social situations. Turned into a heavy user.
Few years later he ended up hospitalized due to psychosis, ended up on schizophrenia meds. Spend 2 years working a shit job medicated up to his eyeballs, smoking weed regularly.
He met a girl after I wanna say ~2 years and got off the weed... and didn't have a lick of psychosis. Eventually got off the meds, working a job just fine, does a lot of mountain biking. Can't say what he's doing now but when me and the ex split he'd basically turned his life around, and it was mostly due to getting lots of exercise and cutting out the marijuana.
Delusions of persecution are the most common form of schizophrenia. But drug users are indeed persecuted. Perhaps has no effect, but I could imagine it to be relevant if you constantly have to hide your usage. It certainly is not helpful.
Association between cannabis use disorder and schizophrenia stronger in young males than in females (May 4 2023)
https://www.cambridge.org/core/journals/psychological-medici...
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.
That is - not based any particular rate of consumption (which is of course difficult to measure reliably, especially in prohibitionist countries like Denmark). But "continued use despite negative consequences".
And that seems to be the crux of the matter: what the article is saying, basically, is that "people who continue to use despite negative consequences ... continue to suffer negative consequences." Which is rather different from: "Heavy use, by itself, brings these consequences."
This really seems like bad journalism for the sake of clickbait.
It might be an article about a controversial statement someone made, but they'll never quote or link to what was actually said and instead only talk about the drama surrounding it. When the article is about the text of a proposed law, the law is rarely linked to and is often not even named. It feels like I see way more links to random people's tweets from news sources than links to actual sources. I guess commentary gets more clicks than content, but I the content is what actually matters and is usually what I'm interested in.
That's an inaccurate paraphrase. What they're saying is that people who continue to use despite negative consequences are more likely to suffer this particular negative consequence. Not as strong a statement as the headline, perhaps, but also not as weak as your misparaphrase.
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.
This is especially lame when they have access to the Danish population registry with its rich metadata and very large _n_, and could so easily control for a lot of confounds, by doing within-family comparisons. (Spoilers: the correlations would shrink a lot if you compare siblings or better yet, twins. Tip to the authors if you're reading this: 'controlling for parental history of schizophrenia', for something as rare as schizophrenia where so few are diagnosed but will still be carrying heavy liability, doesn't control for genetic factors.) They could have done some actual science, and contributed some knowledge; instead, all they did was waste everyone's time by contributing yet another meaningless highly-confounded piece of research to add to the pile of other equally useless correlates on SCZ/marijuana, a pile which did not need increasing. What a waste.
The authors (whose freshman stats classes were presumably as good as yours) were evidently well aware of this distinction - which is why they took the trouble to say 'association' rather than 'causation' in the title.
So the pedantry here seems rather misplaced.
The authors themselves cover up and ignore the many past results demonstrating confounding, fail to do better when they so easily could have, and then have the sheer unmitigated chutzpah, the incredible gal, to just say "assuming causality" right in the abstract to immediately start advertising huge inflammatory claims like "one-fifth of cases of schizophrenia among young males might be prevented by averting CUD." (again, from the abstract, and repeated throughout). Yes, and 'assuming the moon is made of cheese', we could save a ton on moon base supplies and might avert one-fifth of moon base costs by mining the cheese... But I don't advise going to the media about your exciting new research about how NASA could trim its budgets.
I don't blame the people reporting on this for getting it wrong, when the authors spin it so hard that a CD would explode.
What I'm not so sure about is to what extent we can, starting from that -- make inferences about the authors' broader motives, or to speak of their "gall" and how unmitigated it was. And frankly, I don't particularly care.
Not that you shouldn't care, though. But if you want to criticize them "personally", perhaps a letter to the original journal would do the trick? Or at least get it it of your system? Because I kind of doubt they're taking the trouble to dig into the fine print of this thread, or to otherwise allow their morning coffee ritual to be upended by this withering analysis of yours.
There's evidence that the reason for the split is that psychosis is itself damaging. Once someone has a psychotic episode, they are much likelier to have more. But the earlier a psychotic episode is interrupted, by anti-psychotics or therapy, the better outcomes are. So the implication is that many people have some degree of vulnerability to schizophrenia, and only those who have psychotic breaks develop the full condition.
That's a possible causal explanation for a link between marijuana and schizophrenia. Someone who's got some vulnerability to psychosis, but wouldn't otherwise have developed schizophrenia, might be pushed over the edge by heavy drug use. This jives also with anecdotal reports of people who've had really terrible reactions to other psychedelics.
There's a fascinating account by a psychologist who's also schizophrenic. He didn't have his first psychotic break until he was 33, far later than average. He talks about the personality traits of schizophrenics, how he noticed something was off and got early therapy, and how he credits that with delaying a psychotic break and improving his outcomes.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2632294/
Not a doctor or scientist, just regurgitating research I read for personal interest.
I don't think it was ever considered binary. Rather, previously the variance was explained in terms of discrete subtypes and comorbidities. I guess now the field is moving toward a model that is more fluid and away from a rigid ontology, at least to the extent the ontology deigned to reflect distinct pathogeneses.
I'm tempted to believe that there's an improved appreciation that progression isn't inevitable, and can be halted with management. But whatever assumptions the literature made on that score (and I'm not familiar with the literature), I'd bet most patient clinicians have always appreciated this. Understanding the why's and how's was always and still remains the problem.
It several years to recover from but I think some of the damage is permanent. I feel like I've lost a lot of memory function but I can't remember what things were like before. And it's difficult to separate that out from medication side-effects at this point.
What I do know is caffeine gives me panic attacks now (even decaf coffee is too much) and I can't function well enough to hold a job without medication.
Coffee makes me jittery, but green tea gives me focused attention. I just don't enjoy the taste of green tea that much, so I drink coffee and take L-theanine (extract of green tea) pills to calm me down a bit.
My experiment with it went pretty badly as it took out my mood stabilizer. (Oops.) That took me for a wild ride for the next 3 weeks after I stopped it.
After I mentioned this to my psychiatrist, she was rather insistent about not self-medicating. This included vitamins. A great number of things interact poorly with my medication mix. (e.i. Magnesium can interfere with absorption.)
At this point, I treat anything available over the counter the same way I treat prescription medications. I do research and clear anything potentially psychoactive with my psychiatrist. I do use natural things like melatonin. I just need to make sure are safe to take.
During pregnancy (common), but continuing after birth of our first child (rare?), my wife no longer could handle with coffee with caffeine. She tried, but no it does not work.
I'm skipping on alcohol however, I quit that, it makes me too damn tired. Even one dosage has that effect. I cannot stand it anymore. And its not that I dislike the effect. On the contrary, though I limited usage before. Furthermore, I'm prone to addiction/obsessive behavior, it runs in the family somewhat (as part of hyperfocus of autism, I suspect). Nowadays, I can feel a bonbon with alcohol, or tiramisu with alcohol. I really ought to say no to such, too.
Long story short I cannot summarize all of this but I do have a remaining question: I'm curious how you're dealing with alcohol usage.
A single, tiny sip of scotch hits me fast. I immediately start feeling depressed and irritable. Even a couple sips of 2% beer has a noticeable effect for half an hour. It’s incredibly unpleasant.
It’s no great loss because I didn’t drink much before. I do miss scotch though.
An anecdotal observation of this in media is when comedian Owen Benjamin took a "Stars of Death" edible on the Joey Diaz podcast. It was argued that this was the point his big break with reality occurred (delusions and conspiracy seen everywhere). Another interesting observation is that THC seems to intensify the effect of amphetamines like Adderall. With the increase in ADHD and the presumable fix of amphetamine style drugs like Adderall common marijuana usage could intensify the amphetamine high massively which can exacerbate delusions and psychosis even further. Owen himself was known to use Adderall before shows to maintain focus. Quite an interesting area of research.
Once it wears off though, my sleep's not great. At least it's no worse than it was before starting medication, I've just never been able to sleep well.
You're talking about half the the drug combo in question, I'm not sure that's a useful anecdote. As I said to others, I would not recommend adding weed to your vyvance though, unless you are interested in personally experiencing the topic of this thread.
But you're right that the narcissism of small differences is often made manifest in chemistry.
Just wanted to say though, if someone is getting a "high" from Adderall or Ritalin, they're not taking it medicinally, and that's the problem with these discussions, it's very easy to conflate prescribed use with abuse, which ignores the fact that recreational dosages are far higher than medicinal.
In the context of medication and schizophrenia, the authors take is interesting:
“The message is do not only change what is inside your head but that which your head is inside of…
Recognizing the causes of the crisis as having been multifactorial made me also recognize that all ameliorative efforts had to be multilevel, impinging on everything from brain biochemistry to self-concept and social scenario.”
Spectrum is not the opposite of binary. You probably mean gradient, from your context.
This is more than just a pedantic observation. Autism spectrum disorder is often misconstrued by the general public as a gradient, which is not accurate.
If one accepts the dimensional model of psychiatric diagnosis, then almost all psychiatric disorders are "gradients" – ASD included. If you are calling the dimensional model "not accurate", I disagree
I think the biggest thing where the general public misconstrues things is with "autism"="spectrum". The DSM-5 contains both the autism spectrum and the schizophrenia spectrum, although the former is conceptualised as a single disorder, the latter as a family of related disorders. There is also a brief mention of the concept of the "obsessive-compulsive spectrum", although that concept did not make it into the main body of the text. In the research literature, you'll find heaps more "spectrums" proposed – for example, the "disruptive behaviour disorder spectrum" (composed of ADHD, oppositional-defiant disorder, conduct disorder and antisocial personality disorder) and the "bipolar spectrum" (bipolar I, bipolar II, cyclothymia – some add other conditions such as disruptive mood dysregulation disorder)
The book follows an American family who gave birth to 12 children, 6 of whom were later diagnosed with schizophrenia in their teens.
It’s interesting because the book gives lots of insight into the historical to modern research on the condition. In the past psychologists thought schizophrenia was caused by the environment and/or bad childhood. But most of the research right now is pointing towards a genetic cause.
Were these identicals raised apart, or together? Are there enough of each to see a difference in rates between those raised together and apart?
Whatever the triggers are, I can't help but think that they're subtle and unmemorable.
Strictly logically speaking, this is consistent with it being genetic + random chance (where the odds are determined only by your genes) - meaning no identifiable environmental factors. Not saying it is (nor would I know).
This seems to be pretty compelling observations for various disorders like Alzheimer's, various autoimmune conditions, etc. being caused or exacerbated by previous infections.
It was the case for me. I apparently have the genes for a semi-rare autoimmune condition (Guttate Psoriasis) that was triggered after a bout of some kind of viral illness. Typically, step throat is the trigger for many with the disorder, but that was not the case for me.
With siblings it is likely both generics and environment are similar. In terms of trauma and episode triggering events, imagine the stress of living with a large family where several are schizophrenic.
I hope this isn’t taken the wrong way - id very much like to know if my genetic ancestry made me more or less susceptible to things like schizophrenia.
Wrt SZ, not only is it very badly understood but a lot of the symptoms can be attributed to biochemical disorders and that does not necessarily imply a genetic predisposition at all.
Caffeine can induce psychosis, so can THC. For instance, caffeine is an adenosine antagonist, which itself is a dopamine antagonist.
So from a DSM pov, a lot many people can be diagnosed SZ when in fact, the amplitude of the disorder is caused by repeated psychoactive substance abuse.
Even owning a cat (parasites) is thought to be a possible cause for schizophrenia.
Then again, who knows what lies in people heads too? Perhaps that the thoughts they hear are real and some people just can't process it properly which drive them to do strange things. We discount people's experience but there are so little ways to non-intrusively explore people's internal state. A true scientist wouldn't discount that possibility too.
Psychosis is a positive symptom.
But by changing the neuro-transmitter balance when treating psychosis with anti-psychotic medication, negative symptoms can also appear.
Depending on who establishes the diagnostic, you can be diagnosed as schizophrenic while you are simply in one of the phase (acute or post) of psychosis.
In general, if you repeatedly suffer from bouts of psychosis, you will get a diagnosis even though the real trigger has not been established.
Also, the presence of negative and/or positive symptoms differs from people to people so even that is not clear-cut.
Myopia is almost non-existent in hunter gatherer societies.
One of my best friends was schizophrenic and he described the experience as being in the back of the car with someone else driving. A literal observer to his own life. That kind of scared me because I have strong internal dialogues with myself, especially if I'm in conflict over something. He assured me it's nothing like thinking or hearing your own voice; these voices are in fact someone else and the state of your mind makes the experience feel real.
Related to this, some schizophrenics think that thoughts are being placed in their head by something external or that they perceive thoughts from other people. Telepathy is also a common rationalization.
However when consuming THC these symptoms are heightened to something that feels like 50x and they occur even when awake and moving around.
The symptoms are also heightened a little bit when consuming alcohol and especially when trying to sleep.
If I stay up very late it's also a lot more intense when trying to sleep.
I consume a lot of caffeine in general, but I don't think it heightens my symptoms directly. Maybe indirectly it makes me stay up longer depending on when I consume.
(I've had cats most of my life too!)
How do you grade your visualization? Can you create a scene in your head and control it 100%?
How often do you get a random song stuck in your head?
I think that more people are prone to this than they think but they are simply not aware.
Some people start realizing things when they end up trying some kinds of meditation practice and since they are not in control and somewhat clueless about what's happening internally, for some of them it sends them off the rails (hence the stories we hear about meditation triggering psychosis etc...)
Some people never experience such things as well. For some, it comes later.
Talking to oneself is fine. Feeling external thoughts, emotions and even minor loss of self agency in motor control is something else and I think that some rationalizations could make sense. But the current lack of understanding is leading people to handwave (not every scientist is so handwavy of course).
There is an issue of depersonalization such as seems to be the case with your friend. All these things are really not understood and the nervous system alongside the brain is quite inscrutable for now.
I have issues with attention, such that I easily get distracted when trying to focus on something.
I struggle holding a visual image in my head as it easily deteroitates, it's also very faint. I'm not sure what's normal here but I remember I could do this more easily when using THC, even when the effects start wearing down. It's also easier to do in the morning when I wake up before I start moving.
I feel like I have some song stuck in my head all the time. It's almost always a new song when I wake up from sleep.
I also have somatic tinnitus from what I understand. It's not like the beeping you get in your ear once in a while, it comes more from the center, is very high frequency with many overlapping frequencies and sounds a bit modulated. It also gets louder if I clench my teeth or stretch muscles.
Another interesting thing about schizophrenia is it's much more common in cities, even after controlling for drug use and ethnicity[1]. Which again makes it seem like something that was rare in the past.
[1]: https://www.cambridge.org/core/journals/the-british-journal-...
I think it's widely accepted, albeit in a somewhat loose way, that the reason "schizophrenia" was not previously attested is because society explained the behaviors differently and often in less negative terms such that there was less positive feedback that negatively effected progression and manifestation. An archetypal example would be that someone who experienced hallucinations might be understood to be highly spiritual, a mystic, or just quirky. Moreover, people lived in more tightly knit family and social groups, so someone who had trouble taking care of themselves would be more likely to live with or near compassionate family members. And if someone did become a poorly kempt recluse, that didn't by itself turn them into complete social pariahs, so they could more easily have some minimal normative social relations. OTOH, if someone just completely fell apart and died from exposure, or antagonized the wrong person and was killed, the cause wouldn't have been attributed to a mental disease, per se.
And the effect of culture goes even deeper. Hallucinations among those living in modern, western societies tend to be more paranoid and violent; more likely to involve the threat of "the government" or "they" than, say, a beneficent god or playful tree fairy. Or more specifically, as seen in many recent anti-Asian assaults, acting out racial animus received from the culture. The increased negativity in hallucinations and behaviors feeds back into progression directly (more stress from the hallucinations) and indirectly (people are more afraid and wary of you, so you more quickly become separated from supportive social networks).
They probably had some sort of mental health disorder. Schizophrenia seems to have similar symptoms.
So it's impossible to say if schizophrenia is a modern environmental illness.
FWIW I find it hard to imagine that modern life, even in cities, is more stressful than the life of a peasant in medieval Europe - someone who would be constantly torn between instinct and the threat of eternal agony in hell, and would also be terrorised by the very real threats of war, starvation, plague, and more mundane but still deadly illnesses.
Not that modern homelessness and poverty, workplace aggression and bullying, relationship breakdowns, and the threat of physical violence aren't stressful in their own way.
If there is an environmental component I'd guess it's at least as likely to be chemical as social. But maybe there's some difference in social stress types that everyone has missed.
He told me that he didn't think the drugs caused the mental illness but we're often the trigger. That is these kids already had a mental illness that had not started to present symptoms until it was triggered.
My father was not opposed to drug use. He had a history of recreational drug use and many of his life long friends are heavy marijuana users. So I don't think this observation came from an anti drug bias.
I don't know how cannabis works for people with bipolar. Laing used to interpret all psychotic disorders as the same thing. I'm not sure that's right. It seems to me that the different types of bipolar are suffficiently distinct that it's unsafe to declare them variants of the same condition. And I'm pretty sure they're not on a continuum with schizophrenia.
I don't know; I'm neither a doctor nor a therapist. It's just that a surprising proportion of the people I've known well have turned out to have some kind of psychotic disorder. Perhaps they're attracted to me, or me to them. Either way, perhaps I could be used as a kind of diagnostic sign.
The key take away for me was that he was working with young people. I suspect these people may have ended up in mental health care but much later in life.
If this were true you'd expect less of the later in life diagnoses to be drug related. I have no data on that.
> “The study estimated that 15% of schizophrenia cases in men could be averted if they avoided cannabis use disorder”
If a neurotoxic drug such as cannabis causes psychosis in someone who would otherwise never have become psychotic without the drug, then whether you call it a cause or a trigger is quibbling over semantics.
I'm not qualified to guess but I suspect it would be possible. Then if it's possible the rate that it happens would be important. If it's rare then it might not be important in the discussion of causes of mental health problems.
That's not a settled debate; not remotely.
There are many reasons to believe cannabis is neuroprotective. Especially when using safe, high CBD, high cannabinoid varieties; a rather vital distinction.
And it's not semantics, because you can't make the assumption that people would "never have become psychotic without the drug". On a population scale, such an effect would have stood out by now if it had much strength at all.
In my opinion it is neurotoxic, based on studies I have seen (such as this one that we are commenting on) plus my own direct personal experience. Even without the psychoactive components, the smoke is carcinogenic (like tobacco) and toxic to all cells, including neurons. Go take a massive bong hit, then tell me your mind and lungs feel healthy. Cannabis is blatantly toxic filth.
> because you can't make the assumption that people would "never have become psychotic without the drug"
Somehow you are ignoring the entire point of the article/study that we are commenting on.
No, it isn't. It's medicine, and remarkably harmless recreation. It saves many lives, and enhances quality of life for millions of people. It has a smorgasbord of health benefits.
It does have side effects, and drawbacks. It's not a panacea, and it doesn't suit every one. It's not for kids (except when it's medically worth it).
But calling it "blatantly toxic filth" is wildly inflammatory... Which is funny, because cannabis reduces inflammation. With far less toxic effects than most anti-inflammatories.
> you are ignoring the entire point of the article/study that we are commenting on.
I disagree with the methods and conclusion. As do plenty of people here, who have pointed out the flaws with the article and the study, for example, the very serious correlation/causation issues.
To talk about schizophrenia and cannabis without ever mentioning CBD is remarkably dishonest. THC concentration merits a single sideways mention. This is bad science and worse journalism, and it smells like big pharma.
Which wouldn't surprise me at all. Cannabis hurts their profits. Painkiller use goes way down after legalization and decriminalization - as do prescription painkiller deaths.
Try reading the article before commenting.
I like sugar, salt and caffeine. I consume them to a degree that causes me low lever physical harm. I enjoy them and am happy with the cost. Many cannabis users do the same with cannabis but some seems to think it's a magic cure all. I'm strongly sceptical of such claims.
How do you measure neurotoxicity on yourself?
>Go take a massive bong hit, then tell me your mind and lungs feel healthy.
Smoking is far from the only way to consume cannabis.
>the smoke is carcinogenic (like tobacco)
All smoke is carcinogenic, because it is smoke. This is not a function of cannabis, but a function of organic matter.
If you consume it, and it subjectively and objectively harms your mental health and cognitive abilities, then basic common sense and reasoning tells you it is harmful to the brain (neurotoxic).
This is my opinion based on my experience. If you smoked this shit and it gave you an extra 20 IQ point boost, then congratulations.
> All smoke is carcinogenic, because it is smoke.
That's the point. Neurons don't get healthier from carcinogens.
Objectivity is good. So how often do you measure these things, what tools do you use, and what data do you collect? How do you analyze the data?
>then basic common sense and reasoning tells you it is harmful to the brain (neurotoxic).
"Neurotoxic" does not mean "alters your cognition"
"Alters your cognition" does not mean "harmful to the brain"
"Basic common sense" is not a synonym for "science"
>That's the point. Neurons don't get healthier from carcinogens.
There's no evidence to indicate that cannabis is carcinogenic or neurotoxic. In fact, there is evidence to suggest it has neuroprotective effects [0].
The carcinogens come from burning plant matter (or really, burning almost anything). There are many ways to consume cannabis and its derivative products without burning it or inhaling smoke. By your logic, all plant matter is carcinogenic because it's possible to burn it and inhale the smoke. Time to ban trees and vegetables?
[0] https://www.frontiersin.org/articles/10.3389/fphar.2020.5956...
I explained this was my opinion based on experience multiple times so you're just arguing with a strawman. You are absolutely wasting your time here and completely missed the point.
Try reading the article if you want to see a study showing scientific evidence of the neurotoxicity of weed.
Yes, that's the subjective part, but you also argued that it is objectively neurotoxic. Where is your evidence for that? Where is the objectivity?
Objectively worse performance in life and in mentally taxing work. It really isn't that complicated.
Go smoke a massive bong hit then do a calculus exam and compare your score.
>Objectively worse performance in life and in mentally taxing work.
Very interesting! I'd love to learn more. Please show us the data supporting this assertion.
>Go smoke a massive bong hit then do a calculus exam and compare your score.
I don't smoke, so I took a cannabis edible or vaped some concentrate. My calculus exam score improved. Now what? You still haven't provided any evidence for your claim that cannabis is objectively neurotoxic.
"Objective" is not a synonym for "strongly-held opinion"
You can't demand a study/citation for someones personal experience. That is absurd. You are being an absolutely illogical clown.
I was talking about my opinion and direct personal experience. I explained this multiple times but you are incapable of understanding this basic concept.
"Objective" means observable and measurable. Are you genuinely so clueless that you believe no one can perceive anything objective about their own performance and abilities and actions in the external world?
>You can't demand a study/citation for someones personal experience. That is absurd.
Personal experience is subjective. I am not questioning your subjective experience, because that would indeed be absurd.
What I am questioning is your claim that cannabis is objectively neurotoxic. I am asking you to substantiate your claim about this supposed objective fact.
Where is the evidence? Show us.
>Objective" means observable and measurable.
Correct. Observable AND measurable. Observing is not enough to claim something as an objective fact. Where are your measurements about these observations? Where is the evidence about the "objectively neurotoxic" effects of cannabis?
>Are you genuinely so clueless that you believe no one can perceive anything objective about their own performance and abilities and actions in the external world?
Perception is inherently subjective. Feelings are not facts.
You are welcome to perceive all sorts of things, but that doesn't make these perceptions factual, objective, or even grounded in consensus reality. Some people perceive that the Earth is flat. Does that make Flat Earth an objective fact? Obviously not, because we can disprove these perceptions with concrete replicable measurements using instruments that do not wholly depend on the fallible perceptions of humans.
You keep using the word objective without any evidence, and when questioned about it you deflect by saying it's a subjective observation. Which one is it?
This entire conversation feels crazy-making. What I am trying to explain to you is the scientific method, something most children learn in grade school.
The article doesn't say anything about the neurotoxicity of weed. It doesn't even contain the word "toxic". The study doesn't talk about neurotoxicity or use that word either.
Are you commenting on the right article?
You can find studies showing that even pure THC is neurotoxic. It depends on dosage and frequency.
It turns my neurotic brother into a short-tempered asshole. He uses the stuff several times daily.
Guess people react differently to a whole variety of substances. Who knew?
Example: gaming while stoned. I might get one game of online chess while high that represents my absolute peak level - I've beaten up to 2300+ rated players...the only problem is I'll turn around and loose to someone 400-500 points lower than me in the very next game. While high, my mind wanders like no other.
I already cut my marijuana with 50% CBD, and that's still plenty strong that I only need a single hit to be plenty high.
I can't for the life of me understand why there's a race to the highest imaginable THC percentage, when it so clearly has an adverse effect on the experience.
The "mids" I used to smoke back in my teenage years gave a better (read: more fun and relaxing) high than most of the "dank" weed I've smoked as an adult.
The mental health aspect of this is very serious though. I've seen some real burnout and moreso, social withdrawal. In Canada, we're sounding this all out in real time, and some days the drugs seem like palliative care for an old culture and society whose end is being hastened.
I don't really drink either, so my vices now are limited to vaping and a very occasional small dose of mushrooms.
/shrug, worse problems to have I guess.
Also, it doesn't make much sense to me to draw correlations between "high potency" cannabis and these outcomes. The potency of the cannabis shouldn't matter nearly as much as the amount of total THC consumed within a single session or whatever, right? I would think it's just harder to consume a ton of THC when the potency is lower.
edit: The commenter lisasays has found and linked the actual study the article is based off of. Apparently it just wasn't linked in the article.
I thought his discussion about it was interesting. Clearly there was other stuff going on, but he apparently felt his cannabis use was enough of a contributing factor that he decided to stop. https://www.youtube.com/watch?v=JBvc7Ny4iUk
So if you continue it - REM sleep deprivation has side effects.
and if you stop it - your body will try to make up for lost time (REM) and make you hallucinate a lot.
maybe all of this is related to schizophrenia
The explanation "increased THC content causes more schizophrenia" is clearly more plausible than "more schizophrenia causes increased THC content".
In 2000 Denmark was spending 2496$ yearly per capita on healthcare, in 2012 it was 6004$(taking inflation into account: 2496$ in 2000 was 3,327.91$ in 2012)
Maybe they just got better at detecting it?
Your reasoning is akin to saying that it's likely that vaccines cause autism because of some overlapping charts, correlation is not causation.
My understanding is that the ratio of THC to CBD is significant; CBD seems to protect against some of the more alarming effects of THC.
I'm glad to see research on this, but I hope it doesn't spawn another wave of reflexive & unthinking anti-drug legislation.
If you start believing that this is reality, then it becomes "delusions of reference."
I later learned this can be related to low folate or B12, and suspect that was also a cause.
Interestingly enough, I'm also fairly confident I'm autistic.
I have the homozygous C677T SNP and recently started taking methyl folate and methylated B12 and noticed I get much better sleep and less brain fog.
the consequences should fall on the vendors and growers on a licensing perspective, just like alcohol or food vending
I wish marijuana use wasn’t assumed to be “smoking” by default
most questionnaires and even dating apps are like do you smoke marijuana
When smoking normally, it‘s easier to stop when things become overwhelming.
no matter how familiar they are with smoking
I suspect it's a combination of bad design (a single gummy being >=10mg) and the fact that most people just don't read and comprehend the labels.
The Kiva mints are a good go-to if you’re in CA and looking for lower dose edibles.
You don't have to eat the whole edible. The higher-dose ones are a lot cheaper per mg, and I just split 'em.
[EDIT] Oh but you are correct that ones with more of the other compounds from MJ can have very different effects. I never, ever get giggly on straight THC gummies (mostly just tired) but will on some full-spectrum (that is, that went through a process that focused on extracting more than just THC) gummies or vapes. That's the stuff I stick to if I'm aiming for recreational use—for sleepy time, straight THC is fine, though I have found that full spectrum indica extracts can have a better effect on that front at lower THC doses (but availability's spotty and they're more expensive, so I don't usually bother to track down the Good Stuff)
I don't think the general public knows (or cares) much about potency, actually.
Also, they were plenty aware that legalization wouldn't stop a certain segment of the population from harming themselves through overconsumption, no matter what was done to try to convince them otherwise.
Disagree. I think recreational cannabis users are well aware of potency. Here in Canada, all cannabis products have the THC/CBD content on the label, and our shops offer strengths across the spectrum, according to preferences.
Admittedly, some users will get "the strongest available", but the people I know have specific preferences. Having this information available to consumers is one of the best things about regulating the trade.
The general, non-using public I (and the commenter above) were talking about.
you say "likely lead to a competitive race" as though that hasn't already been going on for the last decade or more. it's happening now, and has been happening for a long time. it makes sense for everyone to produce a higher yielding plant. it's more efficient, less biomass waste, less physical footprint required, etc.
a lot of medical cannabis patients require very high doses of THC. if you are a caregiver who can only grow X crops per year, legally, you want them to produce as much as possible. this sort of regulation is just bonkers. let people live. let the experiment play out. stop regulating out of fear.
There are biological limits to potency - probably about the level of where we are now, in fact.
A better example would be 4loko when it introduced caffeine, which is contrary to the point you were trying to make.
Ordinary marijuana is measured fractions of an ounce or in grams. A half gram in a bowl, which is a lot, contains many doses. I've never heard of this heavy marijuana, but it should be easy enough to identify and avoid.
I blame the highly potent breeds since NLX.
The THC concentration is so high that it's too much. Nowadays weeds are even more potent than NLX. Of course our brains can't handle that.
IMHO those kinds of super weeds are harmful and should be banned.
I'm speaking from my own experience and have seen many friends on stationary observation.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3927252/
First sentence: Cannabis is a known risk factor for schizophrenia. There's more, but read it for yourself.
Huge.
If you are one of the many who comment with confidence on this issue, but are not aware of the distinction, please consider looking into it.
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
Science is done based on the evidence that is found, and this counts as some evidence. Does it answer every question? Of course not. Does it help improve our understanding of the occurrence of it? Yes.
Correlation is not causation, but where there's smoke, there's often a fire—as these findings continue to be validated (and there have been other studies that find similar links), it becomes more and more relevant to understand why there is such a correlation—to find a causal mechanism, if it exists, or to confirm that it's just spurious correlation.
Actually, as the replication crises shows, most smoke from papers either isn't real / doesn't point to a fire. So that maybe is a flawed line of reasoning. Correlation (if the research is done carefully to avoid intentional or unintentional p-hacking, and free of fraud) can point to maybe do a follow-up study (or do lots of different kinds of studies to do a good meta analysis that can try to establish causation) but the replication crisis indicates the good studies are swamped by the meaningless ones.
"Avoid generic tangents."
You could in fact replace "cannabis" and "schizoprehnia" with "foo" and "bar" and you'd have a template for a shallow dismissal of published studies.
> You could in fact replace "cannabis" and "schizoprehnia" with "foo" and "bar" and you'd have a template for a shallow dismissal of published studies.
Indeed, replacing with foo and bar would be valid, and the fact that this is the case, i.e. that correlation is not evidence of causation in general, remains a deep and important statement about reality. It is particularly important to correct this when the headline is direct misinformation about what the study found. Do you think code snippets using foo/bar as placeholders are shallow or uninformative? There is a good reason they are often used in programming discussions: to demonstrate that whatever is being shown applies in general.
I read the article looking for evidence of causation and didn't see it, so it could be either way. Maybe the actual study was more clear on this point.
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.
Holy reefer madness! I'd bet it's probably a lot lower than the correlation between alcohol and drunk fights, murders and spousal abuse. Yet society seems to be perfectly willing to tolerate it.
Uh, is it even reasonable to try and find these correlations? We could probably say that the vast majority of mass shootings were conducted by somebody who had previously used ibuprofen or drank alcohol. Is that meaningful or even useful information?
So it is not a problem unless i already have schizophrenia.
(MJ is an ancient medicine, it can't and won't cause any disease; proper use is a remedy for many)
We're coming out of the era of "marijuana bad. marijuana addictive. gateway drug. gives you cancer. makes you kill your parents." etc etc and moving into actually trying to figure out general guidelines for when it's good/bad. I don't think trying to determine these boundaries is fear or misinformation necessarily. I think it certainly can be weaponized in either direction, but for people looking to determine if it's right for them, this is useful information.
And you're saying overconsumption is bad...can you define this? Just in this thread, there was someone who started their journey with it on a 15mg edible. That's insanely high for a beginner but maybe they read somewhere it was fine, or they had a psychonaut friend misguide them, or they just jumped right in with no frame of reference at all. The point is, if people are doing shit like that, it makes sense for there to be more of a general awareness of "here are the bad things that can happen."
I suppose Cannabinoid Hyperemesis Syndrome does not count? I love the plant probably more than most, but like most things -- it has it's good parts and it's parts.