Psychotic Potheads

[Techne]

Research seems to suggest you are either psychotic or likely going to be if you area pothead/weed smoker etc .

Researchers warn of reefer madness

Teenagers and young adults who use cannabis face increased risk of psychosis, research published in the British Medical Journal shows.

Experts from Germany, the Netherlands and London’s Institute of Psychiatry studied 1,900 people aged between 14 and 24 over a period of eight years.

The study found that those who started using cannabis only after the experiment had begun and those who used it before and after both had a higher risk of psychotic symptoms than those who had never used it.

“Cannabis use is a risk factor for the development of incident psychotic symptoms,”[/B] the report concluded.

“Continued cannabis use might increase the risk for psychotic disorder by impacting on the persistence of symptoms.”Robin Murray, professor of psychiatric research at the Institute of Psychiatry, said the latest results backed up claims that the drug caused long-term psychological effects.

“This study adds incremental information to the already fairly solid evidence that continued use of cannabis increases risk of psychotic symptoms and psychotic illness,” he said.

“In short, this study adds a further brick to the wall of evidence showing that use of traditional cannabis is a contributory cause of psychoses like schizophrenia,” he added.

Cannabis Use Precedes the Onset of Psychotic Symptoms in Young People, Study Finds

Long-Time Cannabis Use Associated With Psychosis

To make things worse:
Queen's University researcher connects cannabis use and sexual dysfunction

 

[OverKill69]

Those must be the only university graduates to never have lit up!

WAHAHAHAHA!

 

[Pavan]

cannabis helped me through my engineering degree.. no lies

 

[Bizkit87]

i also believe that pot can make you pshy;ackljva;lv a;lvjas vja;sdklvja ..... ERM ALL IS OK ON THIS SIDE, WEED IS FRIENDLY AND GOOD, RECOMMEND TO YOUR FRIENDS....

 

[San-DraX]

Hmmmmmmm....something to ponder about

 

[stricken]

i been bongin it up for 10 years now... still waiting for psychosis... perhaps some unwanted obsessive compulsiveness here and there... but still nothing major. ;D

 

[Sherbang]

Research seems to suggest you are either psychotic or likely going to be if you area pothead/weed smoker etc .

I see no evidence here that cannabis causes psychosis.

What they conclude in this study is that cannabis, when used by adolescents, is a risk factor for the development of incident psychotic symptoms. They were measuring the incidence and persistence of subclinical expression of psychosis in the general population (that is, expression of psychosis below the level required for a clinical diagnosis). "For most individuals, subclinical expression of psychotic phenomena is transitory and never progresses to psychotic illness."
See the full report here: http://www.bmj.com/content/342/bmj.d738.full

 

[Kornhub]

It has also caused schizophrenia-saw on carte blanche. Hell all drugs come with risks...some like this are rare though.

 

[Valis]

Oh bollocks! These people use flawed methodologies to get the answers they want. This is not science.

Let me ask them just one question; It is true that rates of cannabis use has increased, yet rates of psychosis and schizophrenia has stayed exactly the same. Also rates do not vary with usage of cannabis. Countries that have low rates of cannabis use have exactly the same incidence of psychosis and schizophrenia as countries that have high rates of cannabis use!

The only link that exists between cannabis use and psychosis is the one in their imaginations.

 

[Sherbang]

Oh bollocks! These people use flawed methodologies to get the answers they want. This is not science.
.

Actually this is science - the research is sound - what flaws in the methodology are you referring to?
What's flawed is the sensationalist media reporting of the study.

 

[Techne]

From the abstracts:
Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study

Objective To determine whether use of cannabis in adolescence increases the risk for psychotic outcomes by affecting the incidence and persistence of subclinical expression of psychosis in the general population (that is, expression of psychosis below the level required for a clinical diagnosis).

Design Analysis of data from a prospective population based cohort study in Germany (early developmental stages of psychopathology study).

Setting Population based cohort study in Germany.

Participants 1923 individuals from the general population, aged 14-24 at baseline.

Main outcome measure Incidence and persistence of subthreshold psychotic symptoms after use of cannabis in adolescence. Cannabis use and psychotic symptoms were assessed at three time points (baseline, T2 (3.5 years), T3 (8.4 years)) over a 10 year follow-up period with the Munich version of the composite international diagnostic interview (M-CIDI).

Results In individuals who had no reported lifetime psychotic symptoms and no reported lifetime cannabis use at baseline, incident cannabis use over the period from baseline to T2 increased the risk of later incident psychotic symptoms over the period from T2 to T3 (adjusted odds ratio 1.9, 95% confidence interval 1.1 to 3.1; P=0.021). Furthermore, continued use of cannabis increased the risk of persistent psychotic symptoms over the period from T2 to T3 (2.2, 1.2 to 4.2; P=0.016). The incidence rate of psychotic symptoms over the period from baseline to T2 was 31% (152) in exposed individuals versus 20% (284) in non-exposed individuals; over the period from T2 to T3 these rates were 14% (108) and 8% (49), respectively.

Conclusion Cannabis use is a risk factor for the development of incident psychotic symptoms. Continued cannabis use might increase the risk for psychotic disorder by impacting on the persistence of symptoms.

Association Between Cannabis Use and Psychosis-Related Outcomes Using Sibling Pair Analysis in a Cohort of Young Adults

Context Prospective cohort studies have identified an association between cannabis use and later psychosis-related outcomes, but concerns remain about unmeasured confounding variables. The use of sibling pair analysis reduces the influence of unmeasured residual confounding.

Objective To explore the association between cannabis use and psychosis-related outcomes.

Design A sibling pair analysis nested within a prospective birth cohort.

Setting Births at a Brisbane, Australia, hospital.

Participants Three thousand eight hundred one young adults born between 1981 and 1984 as part of the Mater-University Study of Pregnancy.

Main Outcome Measures Cannabis use and 3 psychosis-related outcomes (nonaffective psychosis, hallucinations, and Peters et al Delusions Inventory score) were assessed at the 21-year follow-up. Associations between duration since first cannabis use and psychosis-related outcomes were examined using logistic regression adjusted for sex, age, parental mental illness, and hallucinations at the 14-year follow-up. Within 228 sibling pairs, the association between within-pair differences in duration since first cannabis use and Peters et al Delusions Inventory score was examined with general linear modeling. The potential impact of attrition was examined.

Results Duration since first cannabis use was associated with all 3 psychosis-related outcomes. For those with duration since first cannabis use of 6 or more years, there was a significantly increased risk of (1) nonaffective psychosis (adjusted odds ratio, 2.2; 95% confidence interval, 1.1-4.5), (2) being in the highest quartile of Peters et al Delusions Inventory score (adjusted odds ratio, 4.2; 95% confidence interval, 4.2-5.8), and (3) hallucinations (adjusted odds ratio, 2.8; 95% confidence interval, 1.9-4.1). Within sibling pairs, duration since first cannabis use and higher scores on the Peters et al Delusions Inventory remained significantly associated.

Conclusions Early cannabis use is associated with psychosis-related outcomes in young adults. The use of sibling pairs reduces the likelihood that unmeasured confounding explains these findings. This study provides further support for the hypothesis that early cannabis use is a risk-modifying factor for psychosis-related outcomes in young adults.

And from the editorial:
Cannabis and the increased incidence and persistence of psychosis

...A causal association is also biologically plausible; a double blind provocation study found that intravenous tetrahydrocannabinol provokes positive and negative psychotic symptoms in a dose dependent way in healthy volunteers and people with schizophrenia...

...The evidence on cannabis and psychosis has influenced the decision in the UK to retain criminal penalties for cannabis use, despite evidence that removing such penalties has little or no detectable effect on rates of use.12 An informed cannabis policy should be based not only on the harms caused by cannabis use, but also on the harms caused by social policies that attempt to discourage its use, such as criminal penalties for possession and use.9 12

 

[Pavan]

Yeah I agree, this is 100% science and its been a test conducted over several years with a relatively substantial sample space. I agree with Korn, all drugs come with their risks - and sometimes only certain people are effected (adversely) by using them. It's almost the same concept as people who experience different feelings when smoking - i have never once experienced paranoia but a few of my mates get uber-paranoid... it effects everyone differently, and thats where the risk truly lies.

 

[EchoZA]

perhaps some unwanted obsessive compulsiveness here and there... but still nothing major. ;D

Nothing wrong with obsessing about munchies

 

[Sherbang]

From the abstracts:
Conclusion Cannabis use is a risk factor for the development of incident psychotic symptoms. Continued cannabis use might increase the risk for psychotic disorder by impacting on the persistence of symptoms.

Conclusions Early cannabis use is associated with psychosis-related outcomes in young adults. The use of sibling pairs reduces the likelihood that unmeasured confounding explains these findings. This study provides further support for the hypothesis that early cannabis use is a risk-modifying factor for psychosis-related outcomes in young adults.

...A causal association is also biologically plausible;

Risk factors are correlational and not causal (correlation does not imply causation). For example, being young cannot be said to cause measles, but young people are more at risk. In the same way, adolescents who smoke cannabis may be more at risk of developing psychosis-related outcomes but it cannot be said, based on this study, that cannabis causes psychosis-related outcomes.

It should be noted that self-reported psychotic symptoms were assessed rather than clinically-diagnosed psychotic problems.

The study had several limitations, some of which the authors have noted:

- It relied on self-reported information about both psychotic symptoms and cannabis use. This could potentially introduce error, although the authors say this possibility was minimised through their interviews being conducted by trained clinical psychologists.
- The study did not adjust for family history of psychosis, a possible confounding factor. The authors say they may have indirectly adjusted for this to some degree, though.
- The authors say they used a “broad outcome measure” to represent psychotic experiences, rather than clinically relevant psychotic disorder. However, they say that psychotic experiences show “continuity” with psychotic disorders.
- The study may have had its results influenced by “selective recall” about cannabis use and psychotic symptoms, i.e. the participants may have intentionally or unintentionally modified their answers to support their personal views on the matter. The long-term nature of this study may increase the risk of this occurring as the participants would have known the purpose and methods of the study and could have modified their answers at later interviews.

In conclusion, this study’s findings are a valuable addition to the research on the possible association between cannabis use and psychotic symptoms, particularly because it was able to show that use of cannabis preceded psychotic symptoms. However, further research is required into any association between use of cannabis and more long lasting, clinically diagnosed psychotic disorders.

http://todaysvitalhealth.com/more-evidence-on-cannabis-psychosis/

 

[Techne]

Risk factors are correlational and not causal (correlation does not imply causation).

Yes, I know, that is why the editorial states that "A causal association is also biologically plausible; a double blind provocation study found that intravenous tetrahydrocannabinol provokes positive and negative psychotic symptoms in a dose dependent way in healthy volunteers and people with schizophrenia... "

 

[murraybiscuit]

it's a lot of reading.
so let's say there's causal proof. but exactly what is that factor in quantifiable terms?

1. how much do you have to smoke and for how long in order to be at risk?
2. if everybody stopped smoking weed tomorrow, what real numbers would we be talking, expressed as a total of all schizophrenia sufferers, and as a percentage of the population?
3. can we link cannabis-induced schizophrenia with bob marley, marcus garvey and the rastafarian preoccupation with heile selassi as the true messiah? /joke

it would be helpful to put this further into context: we could compare weed with, say, tobacco, alcohol and fast-food consumption to see its general risk to society in terms of health, economics and behaviour.

 

[Sherbang]

Yes, I know, that is why the editorial states that "A causal association is also biologically plausible; a double blind provocation study found that intravenous tetrahydrocannabinol provokes positive and negative psychotic symptoms in a dose dependent way in healthy volunteers and people with schizophrenia... "

Well, a causal association may be biologically plausible, but that is not what this study shows. The fact that something is only plausible means nothing in science.
I agree injecting THC might create psychotic symptoms, of course, but I've never met anyone who does that.

 

[Sherbang]

it's a lot of reading.
so let's say there's causal proof. but exactly what is that factor in quantifiable terms?

Let's not say that, because there isn't.

 

[Techne]

Well, a causal association may be biologically plausible, but that is not what this study shows. The fact that something is only plausible means nothing in science.
I agree injecting THC might create psychotic symptoms, of course, but I've never met anyone who does that.

Well, this was an epidemiological study so they never intended to study the causal mechanisms associated with the correlation. Other studies are needed to fully understand the causal mechanisms (if any). I think cannabinoid receptors and their activation or deactivation are likely candidates.

 

[bk.ru]

Techne getting pwned by joelus again.