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.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"
Can I have the source?There is a lot of data showing associations with certain brain regions being smaller
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:Can I have the source?
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).
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.
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.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.
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.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.
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.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.
In my OP, I presented two arguments, one for each side of the brain volume reduction argument.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.
Are the things that are more damaging than Cannabis use? Certainly.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'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.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.
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.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.
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.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….
Interesting paper. Read through it, just now.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.
Continued in following post...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.
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.
I quoted what they found, and didn't cherrypick anything. I even left in the "strength" and "coherence" sections, which support their alternative explanation.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.
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.