Psychosis, Hype And Baloney

A tenfold increase in cannabis use was not accompanied by any significant increase in psychosis. That should tell anyone with a little bit of common sense that if the link exists, it is a very minor one in terms of its overall impact on our society. Lets assume the link exists and that cannabis increases your risk or psychosis by 30%. What is the prevelance of psychosis to begin with in our society? About 0.8%. So that would mean if you smoked weed the odds would go up from 0.8% to 1.04%. If 10000 people were to smoke weed, there would be 24 additional cases. So thats a 24/10000 or about a 0.24% chance that weed would give you a psychosis you wouldn't have already gotten. And this is all assumming the symptomology really indicates psychosis and that there is causation, not just correlation.

I never said "why didn't they use DSM as opposed to the scale they did use". Regardless of the scale they used, the "psychotic symptoms" used in these scales are not symptoms of psychosis in wide variety of real life contexts. And there is way too much opportunity for bias in choosing 10 out of 90 symptoms. Why are you ignoring the opportunities for bias in this sort of research. What they are focusing on are some of the accute effects of weed, which are harldy anything like full blown psychosis. Statistics are only as good as the underlying data. This data is very questionable.

Your peicemeal numbers aren't showing me anything about the increase in psychotic symptoms not being related to paranoid type answers. In fact, you are saying they all increased, so you contradict your self. And you are only address 3 of the ten symptoms that they used. The 7 other symptoms prove weed causes psychosis? The problem with all of these diagnostic criterea for mental illnesses is that they are not derived empirically, and are instead derived by committee and are full of cultural bias.

This bullshit is nothing but a sophisticated form of reefer madness. The intent of the these studies is to produce prohibitionist fears. This is science with a political agenda. Scientists today still aren't sure what causes schizophrenia and many other mental illness, but they damned sure weed does.
 
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"These models are designed to adjust for possible variables that might confound the results and to assess whether the marijuana use caused the symptoms or vice versa."

This is the part of the article that I don't get. How can any mathematical model distinguish between causality and reverse-causality?

..Because I'm not at all surpised that regular marijuana users are mentally different from straight-edge people. You spend any time with stoners, and you'll know that regular marijuana users tend to be far from conventional: many have ideas, beleifs and habits that are far from the social norm. But how can any mathematical model prove that they weren't already different in many respects even before they started smoking?

After all, there must be REASONS why some people grow up to be potheads and others never smoke. Its obviously not just by chance; in order to take that first toke you must already have BROKEN THE LAW, not to mention have (at least indirect) contact with a drug dealer, and have friends who are smokers. Is it any suprise that such people will be (statistically) different from those people who live their lives without ever taking a toke?

I'm sure if you did a study on people engaging in any unconventional activity (say, S&M or motorbike racing) you'd find differences between them and the general population.
 
gloggawogga said:
A tenfold increase in cannabis use was not accompanied by any significant increase in psychosis. That should tell anyone with a little bit of common sense that if the link exists, it is a very minor one in terms of its overall impact on our society. Lets assume the link exists and that cannabis increases your risk or psychosis by 30%. What is the prevelance of psychosis to begin with in our society? About 0.8%. So that would mean if you smoked weed the odds would go up from 0.8% to 1.04%. If 10000 people were to smoke weed, there would be 24 additional cases. So thats a 24/10000 or about a 0.24% chance that weed would give you a psychosis you wouldn't have already gotten. And this is all assumming the symptomology really indicates psychosis and that there is causation, not just correlation...
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That's the beauity of having an effective public health model to work with. If any of these figures were true we would immediately see them reflected in the general substance using population.

Just as you've pointed out, the reality simply doesn't correspond with the study's findings. :)
 
No, you're both assuming the correlation between psychotic symptomatology and an increase in inpatient numbers, which isn't legitamate.

Then you attack the diagnostic questions. Which I think is generally fair enough. But studies using the full DSMIV diagnostic test find an increase too. Now while you might find fault in the fine points of DSM, there is no way that someone who is found to be psychotic under the DSMIV techneque doesn't have something seriously seriously wrong with them.

Your peicemeal numbers aren't showing me anything about the increase in psychotic symptoms not being related to paranoid type answers. In fact, you are saying they all increased, so you contradict your self. And you are only address 3 of the ten symptoms that they used. The 7 other symptoms prove weed causes psychosis?
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I don't quite understand what you mean there. I said that the people who smoked cannabis at a younger age had more psychotic symptomes, then the older group. If this was soley due to cannabis-induced paranoia, then you would see simpley a decrease in paranoid symptomes.. but you didn't see that. 2 out of 3 went the other way, while 1 decreased slightly.
 
No, you're both assuming the correlation between psychotic symptomatology and an increase in inpatient numbers, which isn't legitamate.
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No. We are observing that the lack of increase in inpatient numbers means a lack of overal social impact of the alledged link, assuming it exists at all.

Now while you might find fault in the fine points of DSM, there is no way that someone who is found to be psychotic under the DSMIV techneque doesn't have something seriously seriously wrong with them.
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Really?? Thats your prejudicial judgement value. Are you aware that DSMIV also includes a category for "spiritual problems", including "spiritual emergence", "mystical experience", "shamanic crisis". etc. and the symptomology for many of these overlaps the symptomology for psychosis? How do you know pot isn't giving some of these people some sort of spiritual emergence? Or how do you know the symptomology isn't the result of simple cultural/social differences not taken into account at all in DSM? Have you ever been arrested? Have you ever had to stand before a judge and admit that you are 'bad' because you smoke weed? Have you ever had to pee in a cup to avoid prison? Have you had your career destoyed by a drug charge? Have you been to prison? DSM in its history and still today has pathologized minorities, woman, children, the elderly, the poor, prisoners, drug users, gays, and pretty much everything else that isn't upper class white male.

Moreover, how is there "something seriously seriously wrong with them" when pot smokers can function satisfactorily as members of society, and are not increasing inpatient numbers? Maybe there is "something seriously seriously wrong" with DSM, as in like being based completely on subjective value judgements and a complete lack of scientific method.

I said that the people who smoked cannabis at a younger age had more psychotic symptomes, then the older group. If this was soley due to cannabis-induced paranoia, then you would see simpley a decrease in paranoid symptomes.... but you didn't see that. 2 out of 3 went the other way, while 1 decreased slightly.
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?????

The numbers you posted shows all 3 of them increasing. But I don't see why paranioa should necessarily increase or decrease between younger and older smokers. I can see reasons why it might go in either direction. You will have to spell this out more clearly, including your assumptions about the dynamics of paranoia in pot culture.
 
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wow do you guys remember that JAMA study where they IV'ed a few monkeys with like 3x a normal dose of MDMA once every three hours over a 9 hour period?

and then of course the entire prohibitionist community jumped on it like it were valid scientific proof that MDMA is neurotoxic (and a few of the monkeys not only suffered permanent brain trauma, but some were murdered via overdose).

i mean no shit.

if i went around IV'ing caffiene all day and never took in any food or water, I might experience some nasty physical side effects too. Caffiene is deadly and a threat to our teens! It must be banned! Those korean bastards are manufacturing it like flinstones vitamins and giving it out to our children in shopping malls and dance parties!! ><

yeah this article reminds me a lot of those days.

of course when JAMA refuted its own study, it was a 3 sentence blurb that got no attention (except within the anti-prohibition community) and more (political?) non-scientific oriented media went on claiming there was scientific proof that mdma is a killa drug.

no shit if you are schizo marijuana is gonna make that worse. ive smoked pot fairly regularly for about 7-8 years, and naturally I know hundreds (possibly thousands) of people who are the same, who never experienced any sort of "psychosis" nor know anyone who has.

total

load

of

bullshit

kthxbye
 
No. We are observing that the lack of increase in inpatient numbers means a lack of overal social impact of the alledged link, assuming it exists at all.
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moreover, how is there "something seriously seriously wrong with them" when pot smokers can function satisfactorily as members of society, and are not increasing inpatient numbers?
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What proof do you have for this statement? I've allready argued that you wouldn't notice an increase of 10% of total psychotic patients spread out over many years... or at least I don't think you would... and no one has supplied any actual statistics.

While the arguement that potentially people can still function fine is potentially true, it still doesn't negate anything in the original article, they never said they couldn't, you're just aruging about views on psychotic behaviours, which although very pertinent in some cases, isn't here.

The numbers you posted shows all 3 of them increasing. But I don't see why paranioa should necessarily increase or decrease between younger and older smokers. I can see reasons why it might go in either direction. You will have to spell this out more clearly, including your assumptions about the dynamics of paranoia in pot culture.
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Hehe.. yeah, getting a little mixed up there between arguements in different places. Yeah, I showed ALL of that paranoid type symptomes increased when the cohort was sampled at 21 vs 18. BUT the total psychotic symptomes "caused" by cannabis was higher at 18. So this doesn't fit with the idea that the correlation between psychotism and cannabis is soley due to an increase in paranoid type symptomes caused by acute cannabis.

I.e. Dependent cannabis users have higher rates of "psychotic symptomes", when they are young, but lower rates of paranoid symtomes.

Anyway, I still think we are argueing at cross purposes on most points. I agree that the choice of questions was poor. I also agree that this paper doesn't necesarily that cannabis cause "functional" (i.e. semiperminent) psychotic behaviour (though we don't know whether or not the excluded acute effects).
 
Once again you go after the weakest statement and ignore the stronger overriding facts, as well as the social context of the statement.

Regardless of my statement, there no scientific validity to the study at all, period. The "psychotic symptoms" were chosen arbitrarily and no scientific method whatsoever has ever been used in determining any of these symptoms. These symptoms are determined by committee and are full of cultural bias. Put simply, there is no scientific proof that observation of "psychotic symptoms" can't be symptoms of many other things, including even healthy things, and it is entirely a subjective matter that they are called "psychotic symptoms" to begin with. Yet, it is taken completely for granted that these symptoms are "psychotic symptoms" and not anything else. This isn't science, this is a game of cultural semantics.

As far as the 18 or 21 year olds, there could be many reasons for those result. 18 and 21 year olds are at very different stages of development and in very different social conditions. Pot culture, like any other culture, is full of complex dynamics. Picking on a little point like that isn't going to give the study an validity as its fundamental assumptions are flawed.
 
I don't really follow... but it doesn't matter... you might be interested to read a reply from the articles PI. (I see something that hadn't clicked with me before: They did full factor-anaylsis, which showed that the increase in "psychotic symptomes" didn't just reflect the increase in a few questions, and that the increase in responses was spread out equally over the questions (or more, they were significantly stacked onto a few of the questions).

1. Were the 10 questions used from the SCL-90 independently validated as a reliable measure of psychotic symptoms.
2. Was Social Anxiety disorder adequately controlled for- it seems to say in the paper that it was.
3. Is it possible that subjects were intoxicated with cannabis at the time of interview?
4. Do you have any further breakdown of the questions ( of the 10) that were checked. "Seeing things that other people can't see" may be a more convincing measure than "not trusting people"


1. The measurement of psychotic symptoms: The measure of psychotic symptoms was based on a factor analysis of the SCL 90 symptoms which we reported in an earlier paper on this topic.I enclose a copy of the paper.The results suggest that the scale is factorially valid and of
adequate reliability.

2. Control for social anxiety: There is some confusion in the discussion about this matter with some writers claiming that we were measuring social anxiety rather than psychotic symptoms. The factor analysis in the previous paper demonstrates that this was not so since the SCL 90 symptoms formed a coherent dimension which spanned the full item set. Had the results been contaminated by social anxiety there would have been evidence of two dimensions one reflecting social anxiety and the other the remaining symptoms. This did not occur.

3. Is it possible that some subjects were intoxicated with cannabis at the time of interview:It is possible but very unlikely since our interviewers are asked to complete an assessment of the respondent's demeanour during the interview.This is necessary for ethical purposes to
assess adverse reactions to the interview. None of these assessments reported that the respondent was cannabis intoxicated at the time of interview but one needs to bear in mind that, by definition, daily users would have used cannabis less than 24 hours prior to the interview.

4. Further breakdown of questions:You suggest that we could break down the questions further to examine individual items.We have looked at the individual items and none of them in isolation is significantly related to psychotic symptoms but most are somewhat more frequent amongst cannabis users.This is what one would expect if cannabis use had a small diffuse effect on levels of psychotic symptoms.It is also important to place this research in context.Our study was one of a growing number of studies that has examined the cannabis/psychosis link.These studies have used a range of measures ranging from diagnoses of psychosis in the large Swedish studies to measures of symptoms in smaller samples.In all cases, studies have found increased rates of psychosis/psychotic symptoms amongst cannabis users and in all cases these associations have persisted after control for confounding factors.Given this evidence, it becomes increasing difficult to argue that the linkages between cannabis and psychosis/psychotic symptoms are merely due to measurement shortcomings.
 
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