Forbidden knowledge thread - For things they don't want you to know, but you do know, and now we want to know

Can you expand on this? Do you mean cancer, or severe psychological effects as well?

I think, like cocaine, it is a drug that is favored due to very small physical effects (though smoking will fuck up your lungs no matter what, and cocaine has physical effects that are just... not visible) but yes, the psychological effects are severe. Also, it's not really true that it is not addictive.
 
I think, like cocaine, it is a drug that is favored due to very small physical effects (though smoking will fuck up your lungs no matter what, and cocaine has physical effects that are just... not visible) but yes, the psychological effects are severe. Also, it's not really true that it is not addictive.
QRD on the psychological effects then? Just redpill me if you can. I'm genuinely curious. Everyone says "it makes you lazy" which is a valid observation but it sounds like what you know goes deeper than that.
 
And then Hitler ended up killing himself. I Don't think this was a coincidence, was it shame from years of having to deal with her abuse? Worth speculation. There's nothing else that could have contributed to his untimely demise.

Rumour has it he even had two testicles until she ripped one out.
 
QRD on the psychological effects then? Just redpill me if you can. I'm genuinely curious

Right:


The chemical composition of tobacco smoke has been extensively examined, and the presence of known and suspected carcinogens in such smoke has contributed to the link between tobacco smoking and adverse health effects. The consumption of marijuana through smoking remains a reality and, among youth, seems to be increasing. There have been only limited examinations of marijuana smoke, including for cannabinoid content and for tar generation. There have not been extensive studies of the chemistry of marijuana smoke, especially in direct comparison to tobacco smoke. In this study, a systematic comparison of the smoke composition of both mainstream and sidestream smoke from marijuana and tobacco cigarettes prepared in the same way and consumed under two sets of smoking conditions, was undertaken. This study examined the suite of chemicals routinely analyzed in tobacco smoke. As expected, the results showed qualitative similarities with some quantitative differences. In this study, ammonia was found in mainstream marijuana smoke at levels up to 20-fold greater than that found in tobacco. Hydrogen cyanide, NO, NOx, and some aromatic amines were found in marijuana smoke at concentrations 3–5 times those found in tobacco smoke. Mainstream marijuana smoke contained selected polycyclic aromatic hydrocarbons (PAHs) at concentrations lower than those found in mainstream tobacco smoke, while the reverse was the case for sidestream smoke, with PAHs present at higher concentrations in marijuana smoke. The confirmation of the presence, in both mainstream and sidestream smoke of marijuana cigarettes, of known carcinogens and other chemicals implicated in respiratory diseases is important information for public health and communication of the risk related to exposure to such materials.


The use of cannabis can lead to an acute toxic psychosis, 'flashbacks', depersonalization, derealization and marked cognitive and psychomotor impairment. Further research is needed to establish whether a functional psychosis can be provoked, aggravated or prolonged by cannabis intake. Perhaps of greatest significance among the physical sequelae is the potential to suppress the immune system, impair reproduction, produce respiratory disease and increase the risk of lung cancer.


Recent advances in the understanding of brain cannabinoid receptor function have renewed interest in the association between cannabinoid compounds and psychosis. In a 3-day, double-blind, randomized, and counterbalanced study, the behavioral, cognitive, and endocrine effects of 0, 2.5, and 5 mg intravenous delta-9-tetrahydrocannabinol (Δ-9-THC) were characterized in 22 healthy individuals, who had been exposed to cannabis but had never been diagnosed with a cannabis abuse disorder. Prospective safety data at 1, 3, and 6 months poststudy was also collected. Δ-9-THC (1) produced schizophrenia-like positive and negative symptoms; (2) altered perception; (3) increased anxiety; (4) produced euphoria; (5) disrupted immediate and delayed word recall, sparing recognition recall; (6) impaired performance on tests of distractibility, verbal fluency, and working memory (7) did not impair orientation; (8) increased plasma cortisol. These data indicate that Δ-9-THC produces a broad range of transient symptoms, behaviors, and cognitive deficits in healthy individuals that resemble some aspects of endogenous psychoses. These data warrant further study of whether brain cannabinoid receptor function contributes to the pathophysiology of psychotic disorders.


The main ingredient in cannabis, Δ9-tetrahydrocannabinol (THC), can elicit acute psychotic reactions in healthy individuals and precipitate relapse in schizophrenic patients. However, the neural mechanism of this is unknown. We tested the hypothesis that THC psychopathology is related to changes in electroencephalography (EEG) power or inter-regional coherence. In a within-subjects design, participants (n=16) were given intravenous THC (1.25 mg) or placebo under double-blind conditions, during EEG recordings. Using fast-Fourier transform, EEG data were analyzed for power and coherence in the delta (1–3.5 Hz), theta (3.5–7 Hz), alpha (8–13 Hz), beta (14–25 Hz), low-gamma (30–40 Hz), and high-gamma (60–70 Hz) bands during engagement in the n-back test of working memory (WM). Compared with placebo, THC evoked positive and negative psychotic symptoms, as measured by the positive and negative syndrome scale (p<0.001) and slowed WM performance (p<0.05). Under THC, theta power was specifically reduced, (p<0.001) regardless of WM load; however, the reduction showed no relationship with psychotic symptoms or WM impairment. Coherence between bi-frontal electrodes in the theta band was also reduced by THC (p<0.05) and these reductions correlated with the change-in positive psychotic symptoms (rho=0.79, p<0.001). Bi-frontal specificity was suggested by the absence of a relationship between psychotic symptoms and fronto-parietal coherence. The results reveal that the pro-psychotic effects of THC might be related to impaired network dynamics with impaired communication between the right and left frontal lobes.


TL;DR THC makes you an schitzo

During the processing of oddball stimuli, relative to placebo,Δ9-THC attenuated activation in the right caudate but augmented it in the right prefrontal cortex.Δ9-Tetrahydrocannabinol also reduced the response latency to standard relative to oddball stimuli. The effect ofΔ9-THC in the right caudate was negatively correlated with the severity of the psychotic symptoms it induced and its effect on response latency. The effects of CBD on task-related activation were in the opposite direction of those ofΔ9-THC; relative to placebo, CBD augmented left caudate and hippocampal activation but attenuated right prefrontal activation.


Paranoia is receiving increasing attention in its own right, since it is a central experience of psychotic disorders and a marker of the health of a society. Paranoia is associated with use of the most commonly taken illicit drug, cannabis. The objective was to determine whether the principal psychoactive ingredient of cannabis—∆9-tetrahydrocannabinol (THC)—causes paranoia and to use the drug as a probe to identify key cognitive mechanisms underlying paranoia. A randomized, placebo-controlled, between-groups test of the effects of intravenous THC was conducted. A total of 121 individuals with paranoid ideation were randomized to receive placebo, THC, or THC preceded by a cognitive awareness condition. Paranoia was assessed extensively via a real social situation, an immersive virtual reality experiment, and standard self-report and interviewer measures. Putative causal factors were assessed. Principal components analysis was used to create a composite paranoia score and composite causal variables to be tested in a mediation analysis. THC significantly increased paranoia, negative affect (anxiety, worry, depression, negative thoughts about the self), and a range of anomalous experiences, and reduced working memory capacity. The increase in negative affect and in anomalous experiences fully accounted for the increase in paranoia. Working memory changes did not lead to paranoia. Making participants aware of the effects of THC had little impact. In this largest study of intravenous THC, it was definitively demonstrated that the drug triggers paranoid thoughts in vulnerable individuals. The most likely mechanism of action causing paranoia was the generation of negative affect and anomalous experiences.


Marijuana and Δ9-tetrahydrocannabinol (THC) increase heart rate, slightly increase supine blood pressure, and on occasion produce marked orthostatic hypotension. Cardiovascular effects in animals are different, with bradycardia and hypotension the most typical response. Cardiac output increases, and peripheral vascular resistance and maximum exercise performance decrease. Tolerance to most of the initial cardiovascular effects appears rapidly. With repeated exposure, supine blood pressure decreases slightly, orthostatic hypotension disappears, blood volume increases, heart rate slows, and circulatory responses to exercise and Valsalva maneuver are diminished, consistent with centrally mediated, reduced sympathetic, and enhanced parasympathetic activity. Receptor-mediated and probably nonneuronal sites of action account for cannabinoid effects. The endocannabinoid system appears important in the modulation of many vascular functions. Marijuana's cardiovascular effects are not associated with serious health problems for most young, healthy users, although occasional myocardial infarction, stroke, and other adverse cardiovascular events are reported. Marijuana smoking by people with cardiovascular disease poses health risks because of the consequences of the resulting increased cardiac work, increased catecholamine levels, carboxyhemoglobin, and postural hypotension.


Struve and colleagues9 tentatively suggested that electroencephalographic abnormalities were more pronounced in longer-duration cannabis users, even when adjusting for the greater age of these subjects. Most ominously, Solowij7 found a strong correlation between duration of cannabis use and increased processing negativity to complex irrelevant stimuli in a selective attention task, even in users with a mean of 2 years' abstinence.


Marijuana and its psychoactive constituents induce a multitude of effects on brain function. These include deficits in memory formation, but care needs to be exercised since many human studies are flawed by multiple drug abuse, small sample sizes, sample selection and sensitivity of psychological tests for subtle differences. The most robust finding with respect to memory is a deficit in working and short-term memory. This requires intact hippocampus and prefrontal cortex, two brain regions richly expressing CB1 receptors. Animal studies, which enable a more controlled drug regime and more constant behavioural testing, have confirmed human results and suggest, with respect to hippocampus, that exogenous cannabinoid treatment selectively affects encoding processes. This may be different in other brain areas, for instance the amygdala, where a predominant involvement in memory consolidation and forgetting has been firmly established. While cannabinoid receptor agonists impair memory formation, antagonists reverse these deficits or act as memory enhancers. These results are in good agreement with data obtained from electrophysiological recordings, which reveal reduction in neural plasticity following cannabinoid treatment, and increased plasticity following antagonist exposure. The mixed receptor properties of the pharmacological tool, however, make it difficult to define the exact role of any CB1 receptor population in memory processes with any certainty. This makes it all the more important that behavioural studies use selective administration of drugs to specific brain areas, rather than global administration to whole animals. The emerging role of the endogenous cannabinoid system in the hippocampus may be to facilitate the induction of long-term potentiation/the encoding of information. Administration of exogenous selective CB1 agonists may therefore disrupt hippocampus-dependent learning and memory by ’increasing the noise’, rather than ’decreasing the signal’ at potentiated inputs.


Very heavy use of marijuana is associated with persistent decrements in neurocognitive performance even after 28 days of abstinence. It is unclear if these decrements will resolve with continued abstinence or become progressively worse with continued heavy marijuana use.


The results of this meta-analysis suggest that marijuana use by drivers is associated with a significantly increased risk of being involved in motor vehicle crashes

Also, from WIkipedia

The fungi Aspergillus flavus,[111] Aspergillus fumigatus,[111] Aspergillus niger,[111] Aspergillus parasiticus, Aspergillus tamarii, Aspergillus sulphureus, Aspergillus repens, Mucor hiemalis (not a human pathogen), Penicillium chrysogenum, Penicillium italicum and Rhizopus nigricans have been found in moldy cannabis.[110] Aspergillus mold species can infect the lungs via smoking or handling of infected cannabis and cause opportunistic and sometimes deadly aspergillosis.[112] Some of the microorganisms found create aflatoxins, which are toxic and carcinogenic. Mold is also found in smoke from mold-infected cannabis,[110][111] and the lungs and nasal passages are a major means of contracting fungal infections

 
QRD on the psychological effects then? Just redpill me if you can. I'm genuinely curious. Everyone says "it makes you lazy" which is a valid observation but it sounds like what you know goes deeper than that.

The reason cocaine is traditionally a preferred drug for a lot of people has another reason in that it has a very short half life in the system, and will normally be hard to detect under standard drug tests past a few days of consumption. That's also why the Police take it a lot. Cocaine is also a discreet drug and socially acceptable drug within specific circles of society which makes it far easier to get away with an addiction compared to weed that would normally need to be smoked.

The psychological side effects to THC isn't detrimental to a majority of people, however, if someone is predisposition to schizophrenia then it can trigger it pretty badly.

One of the main issues with weed is that strains have been selectively bred to induce the strongest concentration of THC. Your parents and grandparents would likely be blitz off 1 modern joint.
 
A severed rattlesnake head can still bite and inject venom for a couple of hours after decapitation. I was hiking with some friends out in the Sonoran Desert and our lead guy had a western diamondback strike his boot. Didn't penetrate. He shot it with a .45 ACP snakeshot round basically separating the head from the body.

He touched the side of its jaw with a stick, and sure as shit, it bit the stick hard and you could see the drops of venom on the tips of the fangs. Buried the head and took the rest with us to skin and cook when we got back to camp. Had extra room in my pack so I carried it. I could feel that thing writhing and moving around for a good hour and-a-half after he killed it.
 
A severed rattlesnake head can still bite and inject venom for a couple of hours after decapitation. I was hiking with some friends out in the Sonoran Desert and our lead guy had a western diamondback strike his boot. Didn't penetrate. He shot it with a .45 ACP snakeshot round basically separating the head from the body.

He touched the side of its jaw with a stick, and sure as shit, it bit the stick hard and you could see the drops of venom on the tips of the fangs. Buried the head and took the rest with us to skin and cook when we got back to camp. Had extra room in my pack so I carried it. I could feel that thing writhing and moving around for a good hour and-a-half after he killed it.
Same is true for moccasins and copperheads, presumably just all venomous snakes. I have a bit of a moccasin problem in the woods behind my house and whenever I kill one I make sure to cut the head off, stab it through the top of the skull to prevent it from biting while I dig a hole, and then bury it so that my animals don't step on it or play with it or anything.
 
This is a myth and is absolutely false. You don't have to have a predisposition to get fucked up by THC.

It's not a myth. I know you went through the University of Google searches to derive your opinion, however that does not reflect the current understanding of the drug. I don't know what your definition of "absolutely false" is, however it clearly doesn't come from the majority of studies done on THC's causative nature of mental illness.
 
It's not a myth. I know you went through the University of Google searches to derive your opinion, however that does not reflect the current understanding of the drug. I don't know what your definition of "absolutely false" is, however it clearly doesn't come from the majority of studies done on THC's causative nature of mental illness.

LOL at the 'University of Google'

I just took the sources of the Wikipedia text instead of copying the text itself and just claiming that repeated consumption of cannabis causes cognitive impairment and severely affects things like attention, perception or memory, with the bonus of turning you into an schitzo. I thought they're good as entry level.

I guess, since you cannot ask for sauce to try and refute me like a redditor, now we're going and discrediting the sources provided. I shall imagine, from your comment, using Google Scholar would not be deemed appropriate by you.

If you take a look at those studies, you would have concluded, in between all the dumb science-speak, that cannabis does alter how your brain works. That does mean that it doesn't matter if you are not predisposed to a psychotic breakdown, the drug does alter your brain in such a way that it will create that possibility.

Please, note that all these studies come with the "More research is needed" typical disclaimer.

Now I'm asking you some questions:

Are there studies that claim there are no links between tobacco and cancer, yes or no?

Is there any vested interest on Science (tm) denying a link between cancer and tobacco, yes or no?

Would such a vested interest in driving this outcome be able to disrupt research about it creating confusion, yes or no?

Would such a vested interest obsess over very direct relationships, attacking more complex studies on the relationship between tobacco and cancer, yes or no?

Does such a vested interest have the capacity to affect who gets funds or not in any way, yes or not?

And finally,

Is there a vested interest and concerted effort in normalizing consumption of cannabis, yes or no?

Is there a growing industry around cannabis yes or no?

Are you a consumer of cannabis, yes or no?

I rest my case, your honour.
 
Can you expand on this? Do you mean cancer, or severe psychological effects as well?
Any substance like THC or shrooms that have hallucinogenic-like effects risk permanently altering your brain and thinking patterns. The problem is when people smoke weed, what's actually brain damage isn't noticeable or even perceived or interpreted as brain damage. If you frequently smoked in college or high school, your brain has been permanently chemically altered just in small ways you don't necessarily realize. That's why weed makes people into such useless NEETS over time. They're too zonked out to do anything.

Also, think of how people smoke weed. Do you think those cheap plastic or glass pipes and bowls from the gas station are safe? Or that burning the cheap papers has no negative effects? The reality is the LARP that weed is safe, is fucking not true. No drug is safe. They're lying to you and always have been. That goes double for you faggots who have been microdosing shrooms.
 
Any substance like THC or shrooms that have hallucinogenic-like effects risk permanently altering your brain and thinking patterns. The problem is when people smoke weed, what's actually brain damage isn't noticeable or even perceived or interpreted as brain damage. If you frequently smoked in college or high school, your brain has been permanently chemically altered just in small ways you don't necessarily realize. That's why we'd makes people into such useless NEETS over time. They're too zonked out to do anything.
I know about all of this but I'm looking for more details on the permanent effects that goes beyond "it makes you gay forever". I've heard that smoking weed permanently alters speech patterns and makes your speech more monotone which I've noticed in people before and I'm sure that isn't the only thing.
 
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I know about all of this but I'm looking for more details on the permanent effects that goes beyond "it makes you gay forever". I've heard that smoking weed permanently alters speech patterns and makes your speech more monotone which I've noticed in people before and I'm sure that isn't the only thing.
Anecdotal, but I've seen the same thing and I know of at least one person in my circle who had a psychotic break after smoking weed. They're doing better now, but they did everything "right". No cheap stuff, no weird gas-station paraphernalia, didn't even have any issues for a bit until one day BAM! World's worst panic attack, and it didn't stop.
They had to go to the hospital and everything. Don't know what the hospital told them, I just know they had anxiety issues for years after it happened.
 
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