Cannabis' Effects on the Brain

GoldenBud

Well-Known Member
After hours of reading online, it seems like THC does only 1 thing in our brain: Raising the Dopamine concentration in the Synapses for longer time. it replaces the Anandamide function. "Stronger Anandamide"
 
GoldenBud,

EverythingsHazy

Well-Known Member
After hours of reading online, it seems like THC does only 1 thing in our brain: Raising the Dopamine concentration in the Synapses for longer time. it replaces the Anandamide function. "Stronger Anandamide"
Idk about that. There is a lot of data showing associations with certain brain regions being smaller, with increased risks for schizophrenia in people who are predisposed to getting it, and with worse results in certain cognitive tests. Whether they are all causative or not is a different story, but they are worth looking into, IMO.

Also, Cannabis use has been shown, more and more as time passes, to have negative effects on adolescents.
 
EverythingsHazy,

EverythingsHazy

Well-Known Member
Can I have the source?
There are a few. I haven't fully read all of the papers, and what I have already read doesn't seem to be a particularly strong indicator of causality, however, here is one:

Long-term cannabis users and the five comparison groups.​

Long-term cannabis users showed significantly smaller volumes than cannabis nonusers in the left and right total hippocampus and five of 12 subfields (tail, hippocampal amygdala transition area, CA1, molecular layer, dentate gyrus), and significantly smaller volumes than midlife recreational cannabis users in the left and right hippocampus and three of 12 subfields (tail, CA1, and molecular layer) (Figure 2; see also Table S5 in the online supplement). Long-term cannabis users generally did not show significantly smaller volumes in left and right total hippocampus or hippocampal subfields than long-term tobacco users, long-term alcohol users, or cannabis quitters.

Dose-response associations.​

Participants who used cannabis more persistently had smaller volumes than less persistent users in the left and right hippocampus and numerous hippocampal subfields, after adjusting for sex. Most associations were nonsignificant after additional covariate adjustment (see Table S6 in the online supplement). Adjusting for total brain volume slightly attenuated associations (see Table S7 in the online supplement).

As you can see, there seems to be somewhat of an association, at least at first glance of the study, but it doesn't seem to be particularly strong.

There's also some data on cortical thinning, in regards to adolescent use:

All BCN algorithms strongly suggested a directional relationship from adolescent cannabis use to accelerated cortical thinning. While BCN modeling alone does not prove a causal relationship, these results are consistent with a body of animal and human research suggesting that adolescent cannabis use adversely affects brain development.

I'll be looking into some of these studies in greater depth, but there are a lot of them, and I haven't been able to, yet.
 

XpeeN

Well-Known Member
thanks.

Either use Cannabis and enjoy the high or don't use it and enjoy your life. Not using and constantly desiring it or using and constantly worrying about it is soul destroying and pointless.
It's not about being in a constant worrying, we just want to educate ourself and get to know the facts about a thing that we use quite frequently. You could say this on almost every subject and just cancel science's doing and researching all together. Imagine if people would follow this path of logic about junkfood, or even worse, cigarettes.
 

bhasma

Well-Known Member
It's not about being in a constant worrying, we just want to educate ourself and get to know the facts about a thing that we use quite frequently. You could say this on almost every subject and just cancel science's doing and researching all together. Imagine if people would follow this path of logic about junkfood, or even worse, cigarettes.
Education is important and scientific research is invaluable, but I'm not sure why some Cannabis users are so keen to find research that condemns their usage. My comment could have been posted in "Random Thoughts" and was not meant to discourage critical thinking. This thread began with the idea that Cannabis use shrinks the brain, and I don't think there is any credible evidence that this occurs. It is very obvious that too much junk food is likely to cause obesity, and any long term smoker must admit that smoking diminishes lung function. The tobacco and fast food industries have tried hard to convince people that their products are perfectly safe, but only a fool would believe them. Cannabis has been used by humanity for thousands of years, without any notable harm. I have met lifelong heavy users in their 90s whose mind seemed sharp as a tack, and I have used heavily for over 40 years without any mental problems. I think it is clear that Cannabis can exacerbate pre-existing psychological conditions and can interfere with the development of an adolescent mind, but otherwise I cannot see any problem.
 

EverythingsHazy

Well-Known Member
Education is important and scientific research is invaluable, but I'm not sure why some Cannabis users are so keen to find research that condemns their usage.
If one wants to be aware of the negatives of something, it's best to try one's best to reduce confirmation/desirability bias in one's research. Anyone who wants to know the truth about the potential negatives of Cannabis use would be wise to look for the bad stuff, and then use the information he finds to make an informed decision, instead of staying willfully blind to the reality of the situation.

This thread began with the idea that Cannabis use shrinks the brain, and I don't think there is any credible evidence that this occurs.
In my OP, I presented two arguments, one for each side of the brain volume reduction argument.

It is very obvious that too much junk food is likely to cause obesity, and any long term smoker must admit that smoking diminishes lung function. The tobacco and fast food industries have tried hard to convince people that their products are perfectly safe, but only a fool would believe them. Cannabis has been used by humanity for thousands of years, without any notable harm.
Are the things that are more damaging than Cannabis use? Certainly.
Does that affect the safety profile of Cannabis use? Not at all.

Also, there is no proof that Cannabis use over the last few thousand years has caused no harm. Just because certain harms weren't recorded doesn't mean that they didn't exist. We don't have volumetric brain scans of people from that long ago that can be used to discern any possible negative changes in that domain. We also don't have studies on the mental health of Cannabis users from the ancient past, which could be used to show whether or not there is a connection between Cannabis use and things liek depression, increased anxiety, increased suicide risk, and/or psychosis/schizophrenia.

I have met lifelong heavy users in their 90s whose mind seemed sharp as a tack, and I have used heavily for over 40 years without any mental problems. I think it is clear that Cannabis can exacerbate pre-existing psychological conditions and can interfere with the development of an adolescent mind, but otherwise I cannot see any problem.
I'm sure you know that meeting people who have made it to old age despite having harmful habits isn't proof that their behaviors are safe. I know people who drink way more than what has been shown to be quite damaging to the brain, liver, etc., and yet they are still very successful and seem quite healthy. There are people who chain smoke and drink like fish, and still make it to 95. The stats still show that both of those habits are very bad to have.

Furthermore, even if one makes it to a certain age without having any serious health issues, there is always the possibility that one could've been healthier, smarter, mentally sharper, and/or less at risk of certain issues for the remaining portion of his/her life, etc..
A lot of times, issues go undetected until they do enough damage to cause serious issues. A lot of smokers and drinkers think they are "doing fine", until they get their cancer diagnosis, and it's unlikely that said cancer was caused completely by that person's last drink/cig.

-----------------------------
To summarize... I am not saying that Cannabis should be demonized, or even that I wouldn't use it. I'm not saying that it's terribly harmful, either. What I am saying, is that, for many people, it's worth knowing the facts about it, as much as possible given the current research, and making educated decisions based on those.
 
EverythingsHazy,

bhasma

Well-Known Member
Nothing I have said was intended as scientific proof of anything, simply personal observations. I have spent my life seeking facts, and regarding Cannabis I have seen no strong evidence (apart from possible dependency and consequent withdrawal, and the precipitation or exacerbation of pre-existing psychological frailties) that Cannabis and it's products are harmful to the brain. The sublime poetry of the Rig Veda was composed and remembered by sages and priests who drank soma (which included Cannabis) and many saints and sadhus, philosophers, artists, musicians, writers, scientists, even doctors, have regularly used Cannabis without permanent brain damage. That may not be scientific evidence, but it does show that for most people Cannabis has no practical implications for brain function. And there is a long tradition of using Cannabis as a medicine, with gathering scientific evidence of it's medicinal benefits. Occasional use is surely harmless, and regular use is not for everyone, but the risks are overblown.

And personally, I find the mindset of "if you want to find the bad you must dig for the bad", while ignoring the mountain of good, quite depressing so perhaps I should bow out of this thread.
 
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MinnBobber

Well-Known Member
The real title should be “What are cannabis effects on our Endocannabinoid System (ECS)?

The ECS uses ingested cannabinoids to help it fully function , to maintain homeostasis of our body systems.

Our Cannabinoids are merely a supplement to our body’s own endogenous cannabinoids.

You must have a basic knowledge of the ECS to understand what cannabis really does !

IMO, this thread and some seemed to search hard for the negative studies and seemed to ignore the positives or not look closely at which are good unbiased studies and which are biased and given little weight.

Sifting thru a dozen years of reading cannabis studies , the bottom line for me is:
Cannabis is a substance with miraculous healing powers , a huge huge bank of benefits, and a very small list of negatives for 99.99% of people.

It is a supplement for your ECS , and by far the most valuable supplement there is.
You shouldn’t smoke it but you should have a daily dose….
 
MinnBobber,
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EverythingsHazy

Well-Known Member
That may not be scientific evidence, but it does show that for most people Cannabis has no practical implications for brain function. And there is a long tradition of using Cannabis as a medicine, with gathering scientific evidence of it's medicinal benefits. Occasional use is surely harmless, and regular use is not for everyone, but the risks are overblown.

And personally, I find the mindset of "if you want to find the bad you must dig for the bad", while ignoring the mountain of good, quite depressing so perhaps I should bow out of this thread.
A lot of people drink alcohol without ever noticing it's negative effects on their brains/bodies, but that doesn't mean there aren't any. It just means they are lucky enough for them not to have been bad enough to recognize, and/or that they may have been attributed to something else, if they were noticed.

The thing about the good evidence, is that it doesn't negate the bad. It's worth looking at both sides, but when you want to find the bad about something, looking for the good isn't going to help you much.

The real title should be “What are cannabis effects on our Endocannabinoid System (ECS)?

The ECS uses ingested cannabinoids to help it fully function , to maintain homeostasis of our body systems.

Our Cannabinoids are merely a supplement to our body’s own endogenous cannabinoids.

You must have a basic knowledge of the ECS to understand what cannabis really does !

IMO, this thread and some seemed to search hard for the negative studies and seemed to ignore the positives or not look closely at which are good unbiased studies and which are biased and given little weight.

Sifting thru a dozen years of reading cannabis studies , the bottom line for me is:
Cannabis is a substance with miraculous healing powers , a huge huge bank of benefits, and a very small list of negatives for 99.99% of people.

It is a supplement for your ECS , and by far the most valuable supplement there is.
You shouldn’t smoke it but you should have a daily dose….
I was curious specifically about Cannabis' effects on the brain. It has effects, some good and some bad on various other parts of the body, but those can be discussed in another thread.

Do you have any sources that support the notion that our ECS needs or even benefits (on average) from phytocannabinoids?

The fact that the ECS has the word "cannabinoid" in it is a bit misleading, since it is meant to use our endocannabinoids, rather than being there to benefit from consumption of phytocannabinoids, which while similar, aren't the same chemicals.

If you have any studies that support any of the following, or anything else that's positive about Cannabis use, feel free to drop them here. because I would like to be able to confidently say that it's much better than it is bad:
1. Because of our ECS, Cannabis use is beneficial for homeostasis.
2. Daily Cannabis use is beneficial for most people.
3. Cannabis is a useful supplement for our ECS.
4. The ECS doesn't fully function without Cannabis consumption.
5. Anything else you find interesting.
 
EverythingsHazy,

bhasma

Well-Known Member
And on the association between cannabis use and increased risk for schizophrenia:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181719/
The data presented above indicate that:
(i) future schizophrenia patients have premorbid behavioral abnormalities that might increase their propensity to use cannabis;
(ii) cannabis use and schizophrenia might be the manifestations of a common brain pathology;
(iii) schizophrenia patients have dysfunctions of the endogenous cannabinoid system independent of cannabis use.
The nature of the association between cannabis use and schizophrenia awaits further elucidation from research into the biology of schizophrenia, but, at this point in time, based on the available evidence, it seems premature to claim that cannabis use causes schizophrenia.

Good evidence (whether good or bad) is best.

While there is no evidence that things can fall up, the search for antigravity continues, although I generally expect the opposite.

And the side effects of tea may include: anxiety, sleep disturbance, faster breathing, headache, increased urination, irregular heartbeat, nausea, vomiting, nervousness, restlessness, ringing in the ears, tremors, high blood pressure and anaemia. But I think it's worth the risk.

And there are very many neurodiverse individuals (with disorders such as schizophrenia, autism, ADHD and depression) who suffer with dopamine dysregulation, and cannabinoid supplementation is often their best medicine.
 
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bhasma,
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EverythingsHazy

Well-Known Member
And on the association between cannabis use and increased risk for schizophrenia:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181719/
The data presented above indicate that:
(i) future schizophrenia patients have premorbid behavioral abnormalities that might increase their propensity to use cannabis;
(ii) cannabis use and schizophrenia might be the manifestations of a common brain pathology;
(iii) schizophrenia patients have dysfunctions of the endogenous cannabinoid system independent of cannabis use.
The nature of the association between cannabis use and schizophrenia awaits further elucidation from research into the biology of schizophrenia, but, at this point in time, based on the available evidence, it seems premature to claim that cannabis use causes schizophrenia.
Interesting paper. Read through it, just now.

It's worth noting that it's not an experiment, for anyone who isn't going to read it, themselves, but rather a review of some other data, and that it's from 2005, which is a limitation that definitely shouldn't be discounted, given the fact that Cannabis use patterns and research has come quite a long way in the past 18 years.

The indications that you quoted from the "conclusion" section are part of their proposed alternative to the causality explanation. They aren't definitive, but they are interesting, nonetheless.

Here is the data that they reviewed, as well as some criteria that are commonly used when reviewing epidemiological data:
Review of the Data
The first longitudinal study of the relationship between cannabis use and later schizophrenia utilized data on cannabis use by 50 000 18-year-old recruits Into the Swedish army, and ascertained hospitalization for schizophrenia using a hospitalization registry After a 15-year follow-up, they found that frequent cannabis use (more than 50 times In a lifetime) was associated with a sixfold Increased risk for later hospitalization for schizophrenia. After controlling for possible confounders, the odds ratio (OR) was 2.3.6 This same cohort was later reanalyzed using the same design,7 27 years after cannabis use had been ascertained. They found that use of cannabis at least once by age 18 was associated with Increased risk for later schizophrenia, and, when adjusted for nonpsychotic diagnosis at conscription, low IQ, poor social Integration, cigarette smoking, and behavioral disturbances In childAddress for correspondence: Shlomo Noy MD, PhD, Director, Rehabilitation Hospital, Sheba Medical Center, Tel-Hashomer 52621, Israel (e-mail: snoy@netvision.net.il) hood, the OR was 1.5. Frequent cannabis use (more than 50 times In a lifetime) was associated with a threefold Increased risk for schizophrenia.

The Netherlands Mental Health Survey and Incidence Study (NEMESIS)8 assessed a random sample of 4104 persons aged 18 to 64 and followed them for 3 years. Compared with persons not reporting cannabis use at baseline, persons using cannabis at baseline were 2.8 times more likely to manifest psychotic symptoms at follow-up, after controlling for age, gender, ethnic group, education, unemployment, single marital status, urbanicIty, and discrimination. A dose-response relationship was present, with the highest risk (adjusted OR=6.8) for the highest level of cannabis use.

The Dunedin Multidlscipllnary Health and Development Study9 examined 759 persons from a general population birth cohort of individuals born In Dunedin, New Zealand. They assessed cannabis use at ages 15 and 18, and presence of schizophreniform disorder was ascertalned at age 26. Their results Indicated that use of cannabis at age 15 was associated with higher incidence of schizophreniform disorder (OR=3.1) after controlling for social class and presence of psychotic symptoms at age 11. Finally, In a similar longitudinal, historical- prospective design, 50 413 male adolescents who had been suspected of having behavioral or personality dis-turbances were asked about cannabis use In the Israeli draft board. Self-reported drug use was associated with a twofold Increase in later hospitalization for schizophrenla, after adjustment for intellectual and social functioning, and the presence of a nonpsychotic psychiatric diagnosis at the draft board assessment.
Continued in following post...
 
EverythingsHazy,

EverythingsHazy

Well-Known Member
Inferring causality from epidemiological data Is often problematic, and the classic criteria suggested by Hill are often used when deliberating over these Issues. The Hill criteria Include strength, consistency specificity, biological gradient, temporality, coherence, and plausibility

[Strength]

Regarding the strength of the association, an OR of 2, especially for a relatively rare Illness like schizophrenia, does not represent a particularly strong association, but on the other hand, many other, well-established risk factors for Illness have similar ORs, such as cigarette smoking and later lung cancer, and hypercholesterolemia and later atherosclerotic cardiovascular disease. The data across these different studies are remarkably consistent, using different patient populations and different research methodologies, with very similar results.

[Specificity]
Several of the studies on the topic examined the specificity of the relationship between cannabis use and schizophrenia: Zammlt et al, Van Os et al, and Arseneault et al9 controlled for use of other drugs in their analyses, thus addressing the Issue of specificity of exposure. Van Os et al8 found that cannabis use was not associated with other psychotic disorders, whereas Arseneault et al9 and Weiser et al did not find an association between cannabis use and later depression, Indicating specificity of outcome.

[Biological Gradient]
The presence of a biological gradient Is supported by the presence of a dose-response relationship, with increasing amounts of cannabis used associated with Increasing risk for psychosis8 or schizophrenia.

{Temporality]
As these are all longitudinal studies, which assessed cannabis use at baseline and ascertained later appearance of psychotic Illness, the temporality criterion Is clearly met.

[Coherence]
Coherence refers to how the proposed association relates to the generally known facts regarding the illness. This seems problematic, as the use of cannabis has Increased tremendously over the past four decades: according to the National Survey on Drug Use and Health (NSDUH, previously known as the National Household Survey on Drug Use) , “... the percentage of young adults aged 18 to 25 who had ever used marijuana was 5.1% In 1965, but Increased steadily to 54.4% In 1982. Although the rate for young adults declined somewhat from 1982 to 1993, it did not drop below 43% and actually Increased to 53.8% by 2002. This represents an Increase of approximately 10fold In the use of cannabis In adolescents; If cannabis does, in fact, cause psychotic illness, then one would expect that the prevalence of psychotic illness would Increase In parallel to the greatly Increased use of the “causative” substance In the Western world. This is clearly not the case, as there are reports both of Increases and decreases In the prevalence of schizophrenia in the Western world, with no clear evidence of a significantly Increased prevalence that would be expected If the use of a causative substance Increased 10-fold.

In addressing this Issue, some authors have suggested that cannabis use in early adolescence Is associated with particularly strong association with later psychotic Illness, and that this Is a fairly new phenomenon, In that cannabis use among adolescents under the age of 16 years In the USA has appeared only since the early 1990s. This Indicates that the hypothesized effect of cannabis use on the prevalence of schizophrenia will only be observed in the years to come. However, data from the NSDUH14 Indicate that there has been a significant Increase in cannabis use In this age group as well: the number of 12 to 17 year olds using cannabis for the first time rose from 9.2 per 1000 in 1965, to 58.2 per 1000 In 1980, and to 83.2 per 1000 in 1996. Thus, there has been a very significant Increase In cannabis use In young adolescents as well, which would be expected to lead to an increase of schizophrenia In the population, If cannabis were In fact causative.

[Plausibility]
Regarding biological plausibility, there are some reports on changes In the endogenous cannabinoid system In schizophrenia, which might be related to the effects of cannabis on the brains of patients; this will be discussed in greater detail below. To summarize, based on commonly accepted criteria for causality, there seems to be a reasonable case to be made for cannabis causing schizophrenia; this is clearly delineated In a recent review.

From what I've read, so far, I wouldn't be confident claiming that Cannabis use causes schizophrenia in people who aren't predisposed to get it, but I also wouldn't be comfortable dismissing the correlations, even though I would prefer that they end up not being indicative of a causal relationship. Given the fact that schizophrenia is such a terrible affliction, and one that seems to be lifelong, once it starts, I believe that it's worth giving serious consideration.

I'll see if I have any more recent papers to share, a bit later, because I don't have any on hand.
 
EverythingsHazy,

bhasma

Well-Known Member
Time to read and repeat part of the evidence, but no time to read the counter arguments, leaving the conclusions apparently unsupported? This seems like bias confirmation. The results of previous work are not questioned, only the conclusions. I haven't posted any "experiments" here, only balanced reviews of the evidence. The authors present an explanation of all the findings, based on the work of others and their own work, and based on all the information they came to a considered conclusion.

The strength of the association, especially for a relatively rare illness like schizophrenia, does not represent a particularly strong association ... Several of the studies on the topic examined the specificity of the relationship between cannabis use and schizophrenia: Zammlt et al., Van Os et al. and Arseneault et al. controlled for use of other drugs in their analyses, thus addressing the issue of specificity of exposure. Van Os et al. found that cannabis use was not associated with other psychotic disorders, whereas Arseneault et al. and Weiser et al. did not find an association between cannabis use and later depression ... Coherence refers to how the proposed association relates to the generally known facts regarding the illness. This seems problematic, as the use of cannabis has increased tremendously over the past four decades ... This represents an increase of approximately 10-fold in the use of cannabis in adolescents. If cannabis does, in fact, cause psychotic illness, then one would expect that the prevalence of psychotic illness would increase in parallel to the greatly increased use of the "causative" substance in the Western world. This is clearly not the case, as there are reports both of increases and decreases in the prevalence of schizophrenia in the Western world, with no clear evidence of a significantly increased prevalence that would be expected if the use of a causative substance increased 10-fold ... There has been a very significant increase in cannabis use in young adolescents as well, which would be expected to lead to an increase of schizophrenia in the population, if cannabis were in fact causative.

We present an alternative explanation, based on the work of others and ourselves on premorbid adjustment and schizophrenia ... Several studies suggest that adolescents who manifest abnormal behavior or personality traits may be at high risk of later manifesting schizophrenia as adults ... Persons with obsessive-compulsive disorder, social phobia, and panic attacks were at increased risk for future schizophrenia ... The traits of depression, anxiety, internalized anger, social alienation, and withdrawal are associated with increased risk for future schizophrenia ... 18 year olds with personality disorders or neurosis were at increased risk for future schizophrenia ... Neuroticism at age 16 was associated with increased risk for later schizophrenia ... These nonpsychotic psychiatric disorders are associated with increased rates of cannabis use ... The National Comorbidity Survey found that 90% of respondents with cannabis dependence had a lifetime mental disorder, compared with 55% without cannabis dependence. Antisocial personality disorder and conduct disorder had the strongest associations with cannabis dependence, followed by anxiety and mood disorders ... In adolescents aged 13 to 17, cannabis use was associated with depression and conduct problems ... These data raise the possibility that future schizophrenia patients have increased rates of premorbid behavioral disturbances and psychiatric diagnoses, and these, in turn, are associated with increased rates of cannabis use. One might say that future patients are using cannabis as self-medication of premorbid behavioral disturbances and psychiatric diagnoses ... These epidemiological data are supported by studies indicating that similar neuropathologies might be involved in both cannabis use and schizophrenia, and other reports indicating that patients with schizophrenia have impairments in the endogenous cannabinoid system ... Research on the neurobiology of drug abuse and schizophrenia indicates that the mesolimbic dopamine system is involved in both cannabis abuse and schizophrenia ... Furthermore, dysregulation in cortical, temporal, limbic, and mesoaccumbens circuits is implicated both in schizophrenia and in substance abuse disorders, and behavioral disturbances modulated by the hippocampus and mediated by the nucleus accumbens are associated with schizophrenia and with cannabis abuse ... Developmental neuropathology in hippocampal and prefrontal cortical pathways contributes to vulnerability to both schizophrenia and cannabis use, via dysfunctional interactions with the nucleus accumbens ... The density of cannabinoid receptors has been found to be increased in the anterior cingulate cortex and dorsolateral prefrontal cortex in schizophrenia patients compared with controls. These findings were independent of cannabis use .. Two studies on the genetics of the central cannabinoid receptor have reported an association between polymorphisms of the CNR1 gene and schizophrenia ... Levels of the endogenous cannabinoid anandamide have been found to be elevated in the blood and cerebrospinal fluid of patients with schizophrenia, independent of cannabis use ... All of these findings point to possible structural and functional impairments in the endogenous cannabinoid system in schizophrenia patients ... We suggest that these impairments in the endogenous cannabinoid system might be related to the slightly increased propensity of future schizophrenia patients to smoke cannabis, and are also associated with increased risk for schizophrenia.

And since the conclusions have been muddied I will repeat them:

(i) future schizophrenia patients have premorbid behavioral abnormalities that might increase their propensity to use cannabis;
(ii) cannabis use and schizophrenia might be the manifestations of a common brain pathology;
(iii) schizophrenia patients have dysfunctions of the endogenous cannabinoid system independent of cannabis use.


If more recent research actually disproves these conclusions I am interested, but otherwise I'm tired of repetition.
 
bhasma,

EverythingsHazy

Well-Known Member
Time to read and repeat part of the evidence, but no time to read the counter arguments, leaving the conclusions apparently unsupported? This seems like bias confirmation. The results of previous work are not questioned, only the conclusions. I haven't posted any "experiments" here, only balanced reviews of the evidence. The authors present an explanation of all the findings, based on the work of others and their own work, and based on all the information they came to a considered conclusion.

...

And since the conclusions have been muddied I will repeat them:

(i) future schizophrenia patients have premorbid behavioral abnormalities that might increase their propensity to use cannabis;
(ii) cannabis use and schizophrenia might be the manifestations of a common brain pathology;
(iii) schizophrenia patients have dysfunctions of the endogenous cannabinoid system independent of cannabis use.


If more recent research actually disproves these conclusions I am interested, but otherwise I'm tired of repetition.
I quoted what they found, and didn't cherrypick anything. I even left in the "strength" and "coherence" sections, which support their alternative explanation.

The conclusions were not "muddied", at all, nor do they prove that anything I have said is incorrect. They simply support the presented possible alternative explanation.

I stick by what I said, and I think that it's quite fair, given the info presented in the paper that you shared:
From what I've read, so far, I wouldn't be confident claiming that Cannabis use causes schizophrenia in people who aren't predisposed to get it, but I also wouldn't be comfortable dismissing the correlations, even though I would prefer that they end up not being indicative of a causal relationship. Given the fact that schizophrenia is such a terrible affliction, and one that seems to be lifelong, once it starts, I believe that it's worth giving serious consideration.

I know that a lot of Cannabis users don't like to hear anything negative about it, and you don't have to participate in such discussions if you don't want to, but IMO they are worth having, especially when they're based on actual research, like this, instead of being solely focused on speculation and opinion.
 
EverythingsHazy,
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