Talk:Tetrahydrocannabinol/Archive 1

Archive 1

Removal of unfounded speculation

Removed the following, "There is no evidence to suggest that THC is physically addictive." Not only was no citation given, making it completely inappropriate, but it is also likely false according to Pharmacotherapeutics: Clinical Reasoning in Primary Care, 2nd Ed. by Kathleen Gutierrez, page 901. Billyrubin2008 (talk) 03:37, 30 March 2011 (UTC)

THC produces ADRENALINE RUSHES

As an experienced smoker and keen scientist, I am quite positive that the increased heart rate and butterfles produced by cannabis equates to a large release of adrenaline, for example after a pipe of Skunk...

It seems CRAZY to me to have a long passage about pharmacology here without any actual metabolic explanation of the cannabis intoxiction:

1/Adrenaline produces a fight or flight response, which in negative circumstances explains very closely the emotional aspect of cannabis paranoid phsychosis.

2/Adrenaline also produces strong mental activity in comparison to boredom for example

3/The fast heart rate and excitement lasts for the first phase of the cannabis intoxication from in between 3 and 45 minutes into the rush.

4/Adrenaline surges causes the days after to seem empty, causing a part of the strong emotional addiction that people get to cannabis, it is a way to administer very large adrenaline doses, particularly with concentrated THC sources.

YOU HEARD IT FROM ME - ADRENALINE - FULL STOP>>> even the society of enocrinology has only very patchy studies on the obvious butterlfy effects of cannabis!!!!! —Preceding unsigned comment added by 90.29.32.173 (talk) 13:51, 1 December 2009 (UTC)

According to the scientific literature it is quite the opposite. Activation of central or peripheral cannabinoid receptors inhibits adrenaline release. The described effects are more likely subjective or caused by the coadministration of nicotine. Panoramix303 (talk) 18:38, 1 December 2009 (UTC)

Pharmacology clarification

I'm not a THC expert, just a persnickety editorial type with an interest in the subject. I couldn't figure out the meaning of some of the sentences in this section, so I cleaned up as best I could. These sentences below I still find incredibly confusing.

THC has analgesic effects that, even at low doses, cause a high, thus leading to the fact that medical cannabis can be used to treat pain.

In the sentence above, I don't understand how analgesic effects cause a high and "lead to the fact that medical cannabis can be used to treat pain." I would think the painkilling effects themselves would be responsible, not their ability to cause a high at low doses. Plus, is the high caused by analgesic effects, as implied here? I kindly request that someone who understands this sentence please reword it to make it clearer.

It's just needlessly verbose. Analgesic covers the fact that it treats pain, & the high is an effect of the analgesia (among other things) and not a cause. -LlywelynII (talk) 16:32, 11 October 2008 (UTC)

CB1 activity in the hunger centers in the hypothalamus increases the palatability of food when levels of a hunger hormone, ghrelin, increase as food enters the stomach.

This is the sentence as I have cleaned it up, since it was a fragment before, with some verb agreement confusion and bad syntax. As far as I can tell from the ghrelin entry, I've got the action of ghrelin now described correctly, but what is the relation to cannabinoid activity? It is still unclear. Does cannabinoid activity trigger a release of ghrelin? Does it accompany the increase of ghrelin through some parallel process? Does it merely make food seem more appealing, with no relation to the hunger hormone itself? I kindly request a clarification here as well, or at least a note that the process is unknown if that's the case. Brooklyntbone (talk) 17:02, 22 December 2007 (UTC)

Purpose of THC?

The article states that thc is a defence mechanism in plants. this seems unlikely as the seeds will not sprout unless the outer layer is removed via digestion in animals.

Removed via digestion by animals??? I don't know where you are getting your info from, but I do know for a fact that people who grow marijuana don't have to eat the seeds and then shit them out to get them to grow.--Metalhead94 (talk) 22:38, 12 August 2008 (UTC)

Its just to dissuade big animals and insects and mice from eating all the seeds from the whole plantation. birds arent silly enough to munch on seeds that they dont digest. they peck them. furthemore i dont think they can survive most larger animals digestive tracks. you can make big studies of how it dissuades different animals and the seed propagation, big topic. —Preceding unsigned comment added by 90.29.17.33 (talk) 16:02, 1 December 2009 (UTC)

Insects lost their cannabinoid receptors during evolution, so unless there is a novel unknown high affinity receptor it is unlikely that THC protects the plant against insects. Panoramix303 (talk) 18:45, 1 December 2009 (UTC)

I think he means the seeds will not be distributed by animals if they can't eat the plants, then walk around pooping the seeds out. But I'm not sure that's the case. Does the THC defence mechanism work by making the animals sick or high, so they learn to avoid the plants? How exactly does this work? 76.115.59.36 (talk) 05:26, 29 January 2009 (UTC)

I have no citation for this, and perhaps someone can help with that, but the production of THC is a reproductive mechanism for the plant. It forms on the trichomes of the buds during the flowering stage to better aid the plant's ability to collect pollen. This is evidenced by the plant producing markedly more THC in a dry, arid environment than it does in a humid one where pollen collection is made much easier by the moisture in the air. In extremely humid environments Cannabis produces very minor amounts of THC. Sh4d0w4x3 (talk) 11:03, 9 June 2009 (UTC)sh4d0w4x3

It would be quite useless for the plant to have the pollen sticking to the trichomes (that are not even sticky if undamaged) instead of the pistil :-S Cacycle (talk) 15:55, 9 June 2009 (UTC)

Doesn't it seem unlikely that the purpose of THC is to defend against herbivores given that one of its effects (at least in humans) is to increase appetite? —Preceding unsigned comment added by 76.169.173.29 (talk) 16:50, 18 March 2010 (UTC)

Insects don't have any known cannabinoid receptors, it is therefore unlikely that they will be affected in the same way like mammals. Panoramix303 (talk) 19:58, 18 March 2010 (UTC)

I said herbivores as in mammals like deer, horses etc. —Preceding unsigned comment added by 76.169.173.29 (talk) 23:06, 18 March 2010 (UTC)

Carboxylation process?

Any chemist would care to explain the transition from thc acid to psychoactive thc? Ksenon 19:56, 12 November 2005 (UTC)

See decarboxylation. Cacycle 17:12, 25 March 2006 (UTC)

Psychoactive components

I think it is not one of the psychoactive componets rather than the only one...

Yup, there are numerous others. Remember me 14:38, 15 Jun 2005 (UTC)

Actually THC seems to be the only psychoactive compound in hemp (with the only exception being the heptyl analog that is present only in very low concentrations). The propyl analog tetrahydrocannabivarin (THCV) is devoid of psychotropic effects up to 100 mg. CBD seems to increase the action of THC but is itself devoid of psychoactive effects, as is CBN. Cacycle 17:25, 15 Jun 2005 (UTC)

While tests have shown that cannibinol and cannabidiol (CBN and CBD respectively) do not show significant psychological effects even at high doses when administered by themselves, their impact on the psychological effects of THC are significant. The presence of CBD has been shown to delay the onset of the effects of THC, while simultaneously lengthening the effects, and altering the subjective feeling experienced by the medical patient. If you have ever talked to a medical patient living in California who has access to both marinol (a pill containing synthetic THC in a sesame oil base) and the plant cannabis, then you are familiar with the profound differences in subjective experience that exist between marinol and cannabis. The varying ratios of CBN/CBD/THC exert a significant impact on the subjective experience of the medicinal user, and many patients have reported an astounding range of effects created by different types of cannabis they purchased from their local Cannabis Club (review the current medicinal use of cannabis in the State of California for more information).

In addition to the psychoactive differences between created by the presence of cannabinoids like CBN and CBD (and many others), there are isomers of THC which exhibit different pharmacological/psychoactive effects. delta-3-THC (also known as delta-8-THC in the older nomenclative system) has anywhere between 1/3 and 1/6 of the psychoactivity of delta-1-THC (http://www.springerlink.com/content/h685591860942585/). Also, according to the book entitled "Marijuana Chemistry" (published by Ronin Publishing), analogs of THC which differ from those found in most cannabis have been found in cannabis local to certain regions of India. I, myself, have not seen spectroscopic analyses to either confirm or disprove the book's suggestion.

Cannabinoids in the human body

Since cannabinoids are not naturally produced in the human body, the search began for the endogenous substance that normally binds to this receptors

In one of the recent American Scientific magazines, there is an extensive article showing that there are cannabinoids that are naturally produced in the human brain. I wish to God I had this article with me so I could rightfully change that line, and add the appropriate information.

Could someone who knows more about this find out which cannabinoids are produced in the brain? There are about three or four of them, I believe. I'll start searching, but I doubt I will find anything...

--Ddhix 2002 20:00, 28 Apr 2005 (UTC)

link to scientific american article unfortunately you need a digital subscription to read it, anyone have one? --Heah 20:11, 28 Apr 2005 (UTC)

Thank you, Heah, for correcting my mistake. Scientific American, lol. Did a Google search, and turned up the full article; The Brain's Own Marijuana. --Ddhix 2002 04:03, 29 Apr 2005 (UTC)

Forgot to mention. In the original article (that is in the magazine), they had chemical structures of these occouring cannabinoids. This would probably be very helpful to the expansion of data for cannabinoids on Wikipedia. --Ddhix 2002 04:05, 29 Apr 2005 (UTC)

One thing not mentioned in the article is what mechanism in the body triggers the release of endocannabinoids. If there were a vitamin, when taken in large doses, that could trigger this, then we would have new "natural" way to "get high", and the government couldn't make it illegal. —Preceding unsigned comment added by 76.175.235.41 (talk) 03:13, 9 November 2007 (UTC)

Interesting thought about the pro-endocannabinoid vitamin hypothesis, but actually introducing THC into the body to create psychoactive effects would be just as "natural" as introducing a vitamin into the body to do the same thing (they are both chemicals). Anyway, I doubt such a "vitamin" exists, but it may be worth some research.--Metalhead94 (talk) 23:11, 12 August 2008 (UTC)

the main endocannabinoid in humans is Anandamine —Preceding unsigned comment added by 71.202.233.31 (talk) 01:41, 6 November 2008 (UTC) Hey Hey Hey smoke weed every day!!! —Preceding unsigned comment added by 97.102.21.55 (talk) 03:13, 25 March 2009 (UTC)

Overlap with Marinol

There seems to be considerable overlap between the two articles in reference to legality in the United States. 24.54.208.177 23:53, 22 May 2005 (UTC)

This is true. Ratification 00:41, 23 May 2005 (UTC)

American centredness

This article was too US centred, and I have removed te reference that implied this drug was just controversial in the US, as well as NPOVing the alleged negative long temr efects, SqueakBox 17:27, May 31, 2005 (UTC)

Hyperbole

I removed the highly from in front of disputed and politicized, the hyperbole makes it harder to read and makes an otherwise good article sound less than encyclopedic (it is a little amusing, but not entirely appropriate). While I was there I was bold and put some section headings in that seem to make the article flow a little better. -- pcr^talk 07:37, 10 Jun 2005 (UTC)

THC under the Convention on Psychotropic Substances

I'm confused about THC's current international legal status. I thought it was transferred to less-restrictive Schedule awhile ago, but this says it's in Schedule I of the Convention on Psychotropic Substances: http://www.incb.org/pdf/e/list/green.pdf . Remember me 12:32, 15 Jun 2005 (UTC)

I see now. Dronabinol (specifically, delta-9-tetrahydrocannabinol and its stereochemical variants) is listed there as a Schedule II drug, while THC is listed in Schedule I. I wonder what the difference is. Remember me 12:38, 15 Jun 2005 (UTC)

I notice the footnote says something about trans-delta-9-tetrahydrocannabinol. Remember me 12:41, 15 Jun 2005 (UTC)

The only difference between THC and dronabinol is that THC is synthesized naturally in the cannabis plant whilst dronabinol is synthesized synthetically in a laboratory. They are the exact same thing, though, reguardless of the source. How the DEA justifies this scheduling difference between the two is beyond me. They can't justify it, and they won't, because they have no basis for the scheduling difference to begin with.--Metalhead94 (talk) 13:23, 20 September 2008 (UTC)

Isomerisation

Should it be "is a product of isomerisation of cbd (cannabidiol)" or "is an isomer of cbd"?

Both is true, but that compounds are isomeric does usually not mean that you can isomerize one into the other. So the first statement would be better. Cacycle 10:40, 25 March 2006 (UTC)

cannabis can't be patented; synthetic thc-analogues can be patented

how convenient that where cannabis (which is illegal) cannot be patented and exploited for financial gain by pharmas, thc-analogues can be patented by the researchers (and some of these are legal)

That's often heard but it is a misconception (or maybe a conspiracy theory?). I something is not patented is does not mean it can't be financially exploited. Moreover, new production processes, dosage forms, and related inventions can be patented. There are several companies that produce dronabinol for medical purposes and every physician can prescribe it to you. Beside that, it is usually better to use pure or standardized compounds or analogs for medical purposes in order to minimize unwanted side effects. Cacycle 11:13, 25 March 2006 (UTC)

Please see Sativex for an example of non-patented medicine can be profitable. Anarchist42 18:56, 13 April 2006 (UTC)

Or just look at tobacco or alcohol. No patents on them but they sell like hotcakes. It's government that decides legality, not drug companies; government stands to make loads if they decided to tax pot. But they're afraid too. 76.115.59.36 (talk) 05:34, 29 January 2009 (UTC)

Overdose and death

didn't mean to revert, i wanted to leave an edit summary . . . anyways the toxicity of marijuana is in absolutely no way a contentious issue. If you can document a death go for it, but i can garuntee you won't find one. check out cannabis (drug)#Lethal dose. --He:ah? 05:06, 25 March 2006 (UTC)

There may have been no recorded deaths from cannabis use, but certainly there have been hospitalizations. In my experience as a pharmacologist i have come across several case reports of young children being hospitalized with sedation and respiratory depression following ingestion of either capsules of cannabis oil, or cake prepared with large amounts of cannabis oil. In addition i have come across a case of an epileptic individual suffering an extended seizure subsequent to the consumption of cannabis, and another case of an individual suffering an acute psychotic episode after smoking cannabis and then running out onto a busy road where they were hit by traffic and seriously injured. Any of these cases could potentially have resulted in death. Furthermore this article cites instances of fatality following intravenous injection of cannabis oil;

Kochanowski M, Kala M. Tetrahydrocannabinols in clinical and forensic toxicology. Przeglad Lekarski. 2005;62(6):576-80.

Presumably these deaths occured as a result of cardiac embolism following the injection of such a thick, non-water soluble substance as cannabis oil, but while these may not be THC overdoses per se, they are still acute deaths from misadventure associated with the consumption of cannabis. Also i would note that rats and mice are generally far more resistant to drug overdoses than humans on a weight for weight basis, so citing the high LD50 values found for rodents does not necessarily constitute proof that THC overdose in humans is not possible. Certainly the fact that there is an LD50 value shows that mammals can be made to overdose on this compound, and with CB1 full agonists such as HU-210 lethal overdose is quite possible. I would conceed that it would take a huge amount of highly pure cannabis oil ingested orally to overdose an adult human, but a very small child would require only 1/20th the dose of an adult. Any substance which has the potential to cause both sedation and vomiting, has the potential to cause death through aspiration of vomit if the person goes to sleep on their back and vomits while unconscious. Drug-associated deaths do not only occur because of overdose. Finally i would note that the LD50 values cited are for oral THC, where not all of it will be absorbed. LD50 values for intravenously injected THC are much lower, e.g. 27.5mg/kg (mice); J Med. Chem. 1978 Oct;21(10):1079-81. This value would corrolate to a lethal dose of only 2100mg for a 75kg animal, a challenging amount to inject but by no means impossible.

Meodipt 06:43, 30 January 2007 (UTC)

Is there any data showing what the toxicity is using the FDP? Also, would it be more helpful to list the LD in monkeys? The LD in monkeys for oral administration is >3150mg/kg and the LD₅₀ for intravenous administration is 125mg/kg. See: http://chem.sis.nlm.nih.gov/chemidplus/jsp/common/ChemFull.jsp?MW=314.466 Earthsound 19:46, 30 January 2007 (UTC)

Comparison of acute oral toxicity of cannabinoids in rats, dogs and monkeys; George R. Thompson, Harris Rosenkrantz, Ulrich H. Schaeppi and Monique C. Braude; Mason Research, Institute, Worcester, Massachusetts 01608, USA

Abstract: For preclinical toxicologic evaluation, Δ9-tetrahydrocannabinol (Δ9-THC), Δ8-THC, and Cannabis extract were administered po to rats, dogs and monkeys as solutions in either absolute ethanol, sesame oil, or sesame oil with 2.5–9.0% ethanol. All three compounds were significantly more potent in female than in male Wistar-Lewis and Fischer rats. However, within the dosage range of 225–3600 mg/kg, Δ9-THC and Δ8-THC produced the same lethality, while both isomers were approximately twice as potent as the Cannabis extract. Death due to all three compounds consistently occurred between 36 and 72 hr after treatment regardless of the dose level or sex of the rats. Mortality in rats apparently resulted from severe hypothermia and other central effects. Toxicity was characterized by severe hypothermia, bradypnea, rapid weight loss, inactivity, wide stance, ataxia, muscle tremors, and prostration. Rats treated with equimolar amounts of tetrahydrocannabinol from the three compounds exhibited equivalent diversities and severities of clinical signs. In dogs and monkeys, single oral doses of Δ9-THC and Δ8-THC between 3000 and 9000/mg/kg were nonlethal. Predominant toxic signs in dogs included drowsiness, ataxia, prostration, anesthesia, tremors, mild hypothermia, salivation, emesis, and anorexia. Toxic signs in monkeys included hyperreactivity to stimuli, lethargy, drowsiness, characteristic huddled posture, slow movements, abnormal eating procedures and sedation. Histopathologic alterations did not occur in either dogs or monkeys.

121.200.212.105 (talk · contribs) 06:28, 26 October 2008

And what effects would one experience while undergoing a lethal dose of THC? I've often wondered what one would experience under a lethal dose of LSD, although, it has been generally accepted that there is no such lethal dose of LSD, per se.

First cannabis-based prescription drug?

The last paragraph states that Sativex (approved in 2005) was "the first cannabis-based prescription drug in the world." Wouldn't that honor belong to Marinol (dronabinol), which has been available by prescription in the U.S. for decades? ZZYZX 13:26, 3 September 2006 (UTC)

Marinol is a synthetic molecule similiar to THC, whereas Sativex is a mixture of real THC and CBD molecules collected from natural sources. Anarchist42 19:14, 3 September 2006 (UTC)

Not true. Dronabinol is synthetic Δ⁹-THC, one of the primary cannabinoids found in natural cannabis (but not the only psychoactive one). Sativex, being an extract of botanical cannabis, is a mixture of various cannabinoids (including delta-9-THC). Some believe this to be therapeutically superior to dronabinol. --Bk0 (Talk) 19:31, 3 September 2006 (UTC)

Spectrographic analysis of cannabinoids in human fingerprints

Does anybody know if there has been much research into the detection of cannabinoids likely to be present in the fats or lipids deposited in the fingerprints of marijuana smokers?

Since the dermal ridges in fingerprints are kept constantly wet and oily from certain eccrine glands present on the skin of the fingers and palms, and since the fats and lipids found in fingerprints tend to reflect the unique dietary intakes of particular human individuals, it makes sense to inquire into the saturation point, after which cannabinoids can be successfully detected using spectral analysis of the lipid deposits found on or in a fingerprint.

How much THC would an individual have to be fed (or have to eat) before its presence could be found in a fingerprint? If THC is taken in by smoking, is there such a kind of affinity between the lipids of the fingerprints, and the smoke molecules of marijuana smoke, that the molecules would preferentially bind to the exterior of the fat molecules, but would otherwise be found to be left wanting, that much deeper in?

Spectrographic analysis of lipids is a kind of analysis using low wattage laser light, such that surface and subsurface components can be examined, in turn, according to the frequencies of light transmitted, and the frequencies of light reflected.

Biosynthesis of THC

beginning to add the enzymatic pathway to the frontpage, wanted to get some feedback first....

How to grow THC enzymatically seems a bit long winded. It need to be more succinct and also evaluated more thoroughly.

From olivetol to cannabigerol to tetrahydrocannabinol I think everyone can more or less agree on (there is some room for debate from olivetol to cannabigerol though?) and so it should really be investigated. There are a lot of sources in there too.

That Can't be Correct

I assume when this article states in the toxicity section the LD50 for rats is 1270 mg/kg of body weight eaten for males and 730 mg/kg for females it means in pure THC. But in the marijuana article it makes the same statement, I assume meaning in mg's of cannabis (not pure THC). Does the dissolving of THC in sesame oil dilute it and make up for the lack of plant matter? I think this needs some more explaining, but I'm not in the position to make changes. BeefJeaunt 20:44, 19 December 2006 (UTC)

The marijuana article now says it's the LD50 of THC. Since the composition of THC in marijuana varies, you obviously can't have a LD50 for marijuana, you can simply estimate how much marijuana you have to take to get the LD50 of THC which the article appears to do, at least for smoking Nil Einne 15:03, 21 December 2006 (UTC)

Solubility in water

Please recheck this infor: Solubility (water) 2.8 mg/L (23 °C). Thats not true. Some stoners after read this started to drink water from bongs:DDD Feeeeeeeee217.17.86.86 20:43, 10 January 2007 (UTC)

2.8 mg/L is actually quite insoluble. --Bk0 (Talk) 02:04, 11 January 2007 (UTC)

I saw a discussion where someone misread it as 2.8 g/L...Twin Bird 18:23, 29 March 2007 (UTC)

Neutrality

I think one of those neutrality banners should be on here. because it only seems to say the good things and benefits about thc and none of the risks. sure there are benefits but it must be illegal for some reason. —The preceding unsigned comment was added by 86.129.226.151 (talk) 17:28, 22 January 2007 (UTC).

An unsubstantiated feeling is not enough to place a dispute banner on an article, therefore I will remove it. You might want to check out the petitio principii article... Cacycle 00:05, 1 February 2007 (UTC)

Yeah I agree we need more negative things about THC in this article. For example, yesterday I was stoned and ate all the cereal. Now I have nothing for breakfast. Why didn't I listen to the government! 71.68.17.141 17:09, 2 February 2007 (UTC)

But dont blame THC for your personal problems (greed in eating all the cereal mixed with laziness or poverty in not going out to buy some more), SqueakBox 17:15, 2 February 2007 (UTC)

You know he was joking, right? But in all seriousness, the legal status of Cannabis/THC has no bearing on its health effects. A substance is not required to be dangerous to be illegal. 76.242.40.144 23:45, 24 September 2007 (UTC)BlackHoleSon

just to add to the statment that it has to be illegal for some reason. The history channel ran a program on how it became illegal about a week ago. since i dont remember the exact name of the show (caught it as i was channel surfing), i have looked up an article on the marijuana tax act. This states in it how the actual illegalization was tied into fears of mexican imagration at the beginning of the Great depression. It is alot of information and i will not try to explain it. So here is the site for those interested http://www.druglibrary.org/schaffer/hemp/history/mustomj1.html 69.250.191.120 18:51, 31 July 2007 (UTC)

Yea I think it is really sad that we have these biased clowns called the DEA in the way who continue to ridiculously claim that cannabis has no medical purposes. It's schedule 1, which means supposedly it is not even safe to use cannabis under medical supervision. Anyone who believes that is either insane or VERY gullible IMO. It's a joke, you can't even OD on it and yet there's a lack of safety even for use under medical supervision??? Yeah right, the DEA should be laughed at. Aside from that, the article THC seems perfectly neutral and balanced.

There are numerous articles on marijuana's legal status & its highly dubious history; they're linked from the marijuana page. THC should address the chemical and its research. What doesn't make sense is that THC (100% active compound in marijuana) is schedule III while marijuana (~3% THC) is schedule I, a disparity which possibly should be addressed in this article, but would introduce bias. Better to cover all that hoopla on the mj pages. -LlywelynII (talk) 16:50, 11 October 2008 (UTC)

Poor citation

The information content of this page is great, as is the tone, however, citation needs to be much tighter, especially considering the potentially contentious subject matter. I didn't want to flag the page but could someone tie particular statements to particular sources, and also list those sources at the end of the page. --82.47.208.137 19:54, 5 April 2007 (UTC)

I agree with this, in particular I would like to see a citation for the claim that THC has analgesic effects. Perhaps I could find it easily online but the cite should certainly be in the article and someone more qualified than I should add it. I personally do not find that THC has analgesic effects, I find that it just makes pain easier to ignore. Many other drugs with that property are not considered analgesics. 128.232.246.186 12:50, 10 April 2007 (UTC)

Check out the prescription medication Sativex, which has been through several successfull trials showing analgesic effects. Anarchist42 17:05, 10 April 2007 (UTC)

Let's see, there is this: [1] "The purpose of this study is to find out if cannabis-based medicine compared to a dummy medicine (placebo that contains no active ingredient) can help the central neuropathic pain patients experience as a result of multiple sclerosis." The discription on that page uses the word "analgesi{a,c}" multiple times, but since it is specific to MS, it seems odd to call the effect one of analgesia. The fact that it is only a specific type of pain which is being relieved suggests that it is not the pain itself which is being stopped, but rather some other process is being stopped which was causing the pain. If this is true, which seems logical given other things that we know about THC and the diseases it cures, then to call THC a neurpathic pain analgesic would be like saying that my allergy medication is a sinus pain analgesic. It's simply not that straightforward. Allergy medication causes a different immune response, THC relieves muscle spasms; I doubt that either one acts on pain receptors. According to my own perception, people seem to enjoy thinking that THC is an analgesic because it goes along with their beliefs about the supposed abuse potential of illegal drugs; or perhaps because the pain which is being relieved is internal in origin, they fail to realise that the cause of the pain could be different from the pain itself... I think it would be good if we could decide to change the wording on Wikipedia so as to avoid perpetuating this misconception. I would like to solicit more serious justifications for use of the word "analgesic", and if none are forthcoming then I would like to propose to change the text of the article. A5 23:48, 16 April 2007 (UTC)

THC Presence in Plants other than Cannabis varieties

The article currently states that: "...found in a variety of plants; most abundantly so in the Cannabis plant." implying that it is also present in other plants. In the past I read information contrary to that: that THC is only known to be present in Cannabis. Is there a source with information about other plants containing THC, or is the article to more correctly state something like: "...found in varieties of Cannabis/Hemp plants; most abundantly so in drug varieties (differentiated from varieties better suited for hemp fiber, or seed oil production.) -az —The preceding unsigned comment was added by 69.248.86.178 (talk) 07:02, 1 May 2007 (UTC).

"Cannabinoids are a group of molecules found only in the cannabis plant." However, there are a number of cannabinoids that occur naturally in animals, called endocannabinoids. I believe (and the Cannabinoids article agrees) they meant to convey that the 66+ different cannabinoids are found in no other plant. 64.126.64.197 15:22, 1 September 2007 (UTC)

Is THC an alcohol

it has an OH group linked to a chain of hydrocarbon, but does the extra oxygen stop it from being an alcohol?

The hydroxyl group linked to the phenyl ring makes it a phenol. The heterocyclic oxygen, in the "B" ring, also makes it a pyran.

Vaporization Temperature of THC

The table at the top of this article has a vaporization (Boiling) point of "155-157 °C (vacuum, 0.07 mbar)".

The article, http://www.maps.org/news-letters/v06n3/06359mj1.html#note , has this at the end:

---

Contrary to the initial version of this article, which erroneously stated that THC vaporizes at 155º C, the Merck Manual lists the vaporization point of THC as 200º in vacuum. The vaporization point at normal atmospheric pressure appears to be unknown, but is thought to be in the range 250-400º.

---

Anyone know where the "155-157C" figure comes from? It seems to be on the low side. I found a copy of a THC Material Data Safety Sheet (here: http://www.erowid.org/plants/cannabis/thc_data_sheet.shtml ). It also lists the 200C number but at ".02 mbar" (vs. 155C @ .07mbar this article). I don't know if the .05 mbar is important. I would think it odd that they would list a boiling point of anything at .02 or .07mbar (vacuum conditions). Is the ".02/.07 mbar" relative to standard pressure (1 atmosphere = 1013.25 mb)?

Either way, I can't see it being at 155-157C @ .07 mbar and 200C at .02 mbar. I didn't want to make any changes, as I don't know for sure which is right, but I've seen the 200C use elsewhere. I can't verify 155-157C being used other than here. Athena 06:11, 29 June 2007 (UTC)

The reason that the boiling is done in a vacuum, is that the material will burn before boiling when done at atmospheric pressure. Boiling point will vary with impurities, but the Merck Index is a reliable source.

Extrapolating from 200C at .02mmHg, the boiling point is 390.4 °C at 760 mmHg. Most vaporizers don't go anywhere near that temperature, so there is obviously something wrong here. I believe THC actually starts releasing vapor at its theoretical flash point, 149.3 °C. —Preceding unsigned comment added by 71.201.149.40 (talk) 18:52, 20 December 2008 (UTC)

Boiling in a vacuum is a BOGUS way to state natural properties, as water is commonly held to boil at 100C, not 0C (as it would in a vacuum)!

Article's current temp of 157C is correct -- i.e. from table below: all temps are at 760mgHg pressure (1 std atmosphere):

• THC (Δ-8 tetrahydrocannabinol) 157C
• CBD (Cannabidiol) 160-180C
• CBN (Cannabinol) 185C
• CBC (Cannabichromene) 220C
• CBG (Cannabigerol) MP=22C (no BP given)
• Δ-8 THC (Δ-8 tetrahydrocannabinol) 175-178C
• THCV (Tetrahydrocannabivarin) <220C

Athena (talk) 03:48, 22 July 2011 (UTC)

References

Hi,

I don't have time for it right now, but if someone could go and fix all those PMID refs using, for example, the wikipedia template filling tool, that would be cool, and shouldn't be too hard. --Slashme 09:49, 27 August 2007 (UTC)

Use with AD(H)D

---

Recently, cannabis has even been prescribed to adults and teens who are diagnosed with ADD & ADHD due to the drug's relaxing and calming effects.

---

Are there any resources to this from the research group(s) who studied this? Who is/are the research group(s) and do they have any published pages supporting this?
Then again, I suppose the drugs "relaxing and calming effects" are a fact anyway, but it would definitely improve the quality of the article to cite who has prescribed THC/Cannabis for AD(H)D.
Isangaft220 16:13, 25 September 2007 (UTC)

a few ideas

has anyone ever made an anolouge where one or both of the oxygen atoms are replaced with sulfur? or a alkyl ester? —Preceding unsigned comment added by 202.161.0.236 (talk) 09:10, 27 September 2007 (UTC)

Yes, as far as I remember, check the Beilstein database in your next chemistry library, there is a huge amount of work on THC analogs. Thiols are very different from hydroxy functional groups, e.g. they do not form hydrogen bonds. The SAR of THC shows that the OH group is essential for activity. Cacycle 13:33, 27 September 2007 (UTC)

Who ruined the nice table of physical data for THC? I need it now, and it is gone. Can someone please replace it as it was originally? 116.68.66.211 (talk · contribs) 11:26, 16 October 2007

toxicity

What in the world does all that mean? Layman's terms, please?--Ioscius ^(talk) 03:42, 23 October 2007 (UTC)

Simply put, it means THC cannot kill you. THC is nontoxic.--Metalhead94 (talk) 11:21, 13 September 2008 (UTC)

wording

Changed "Episodes" to "Symptoms" to match cited article 11. Flying Hamster 07:27, 31 October 2007 (UTC)

Hatched wedge vs hatched line

Hi Cacycle,

I see you replaced the png because you preferred the hatched wedge for stereochemistry. IUPAC disagrees, so I replaced the svg diagram. --Slashme 14:46, 5 November 2007 (UTC)

As was pointed out on the structure drawing workgroup page, the new IUPAC recommendations favour wedges for hatched bonds, so I fixed up the svg and re-uploaded it. If it still looks wrong for a bit, that's just because the thumbnail still needs to be updated. --Slashme 06:38, 9 November 2007 (UTC)

Cats

There is a myth that cats cannot metabolize it. Can anyone refute that? Barcovelero (talk) 14:57, 23 December 2007 (UTC)

I have never heard anything like that. Sounds like psuedo-science junk to me. Cats do have some compromised liver function compared with many other mammals, as small amounts of paracetamol (acetaminophen) can be fatal even in small doses due to the fact that cats lack an enzyme to metabolize it. There are a few other drugs that may cause this toxic reation in felines, however, to the best of my knowledge, THC is not among these.--Metalhead94 (talk) 01:25, 5 September 2008 (UTC)

Nomenclature: Change to dronabinol?

Should we change the article name to dronabinol? That is the International Nonproprietary Name. Tetrahydrocannabinol gets 849 unique hits, vs. 657 for dronabinol. See:

• here and
• here

-Ron Duvall (talk) 04:52, 16 February 2008 (UTC)

Tetrahydrocannabinol is usually abbreviated as THC and this gives orders of magnitude higher Google hits than dronabinol. Throughout the scientific literature it is called tetrahydrocannabinol - only in the context of prescription medicine it is called dronabinol. So we should keep it under the current article name. Сасусlе 15:02, 9 March 2008 (UTC)

Second the no. -LlywelynII (talk) 16:45, 11 October 2008 (UTC)

Unclear wording

I'm having trouble interpreting this sentence:

New scientific evidence is showing that THC can prevent Alzheimer's Disease by counteracting the activation of microglia and thus inducing the inflammation of microglia binding to amyloid protein.

Microglia induces inflammation (this is desired), but if THC "counteracts the activation" of microglia, that would seem to mean that the microglia can't do its job of inducing inflammation, wouldn't it? -Pete Davis (19:47, 8 March 2008 (UTC))

You are right, I changed the sentence. Hope it is now clearer to people who are less familiar with the topic. - Panoramix303 (talk) 21:18, 8 March 2008 (UTC)

Half life

This is the old value for the half life time. 4.3-12.6 days Please read the articles before posting such things because it is totally misleading. The value was the terminal half-life time and not the half-life time of THC itself. This makes a huge difference. -- Panoramix303 (talk) 09:17, 13 March 2008 (UTC)

The first paragraph of the "Pharmacology" section

From the first sentence onwards it is mainly just pharmacological history related to, but not about, THC. Not really fitting for a first paragraph and maybe irrelevant as a whole. —Preceding unsigned comment added by 80.222.240.155 (talk) 09:05, 29 June 2008 (UTC)

Merge proposal

Propose that Dronabinol be merged to Tetrahydrocannabinol as they are the same chemical with different names. NJGW (talk) 17:51, 8 July 2008 (UTC)

Full support. Cacycle (talk) 03:59, 9 July 2008 (UTC)

From me too. Icek (talk) 03:35, 11 July 2008 (UTC)

Done. NJGW (talk) 18:44, 31 July 2008 (UTC)

NOOOO bad idea, Marinol is it's own medication, it needs it's own page just like Cesamet, Sativex, etc. —Preceding unsigned comment added by 69.125.245.92 (talk) 02:18, 25 October 2008 (UTC)

Similarity to opioids

I know this may be a little off-subject, but has anyone else noticed that THC has a similar structure to morphine and other opioids. The only difference is the carbon chain on THC and that it lacks a nitrogen atom.--Metalhead94 (talk) 23:42, 26 August 2008 (UTC)

Sorry, but there is not much resemblance, neither in 2D nor, much more significant, in 3D (beside the basic fact that both contain a phenol substructure). Cacycle (talk) 02:30, 27 August 2008 (UTC)

I see the similarity this guy is talking about. You know, since THC has been shown to activate certain opioid receptors, maybe this resemblance has something to do with that, and there is more resemblance than the simplistic phenol substructure. Look at THC, cover the carbon chain with your hand, and it looks like you have a nitrogenless morphine molecule.--206.28.43.251 (talk) 09:42, 30 August 2008 (UTC)

THC does not "activate certain opioid receptors" and there is no similarity if you take into account the three-dimensional structure. Cacycle (talk) 16:50, 30 August 2008 (UTC)

THC dosen't activate certain opioid receptors? Are you sure? I remember reading one article that says THC activates Delta opioid receptors, and I, too, see the similarity it has to opioids, which is interesting.--68.217.167.115 (talk) 15:57, 31 August 2008 (UTC)

Aha, you are mistaken cacycle. Right in the pharmacology section of this article it says cannabinoids activate opioid pathways via the delta-1 opioid receptor, and I still see the similarity with opioids.--68.217.167.115 (talk) 16:19, 31 August 2008 (UTC)

Not to mention the fact that opioid antagonists can block the effects of THC.--Metalhead94 (talk) 16:22, 31 August 2008 (UTC)

This data proves that THC shares similarities with opioids, not only in the structure, but in its pharmacology as well. There is a glaring similarity to opioids, it is founded by scientific evidence. This debate is hereby officially closed.--68.217.167.78 (talk) 01:16, 5 September 2008 (UTC)

THC does not activate opioid receptor directly at the receptor level but indirectly through neuronal pathways that involve opioid signaling. And I guess if you have no experience with chemical formulas they all look the same. Feel free to believe what you want - but either come up with some rational, educated, and referenced arguments or questions or stop messing up talk pages with half-baked original thoughts. Cacycle (talk) 12:36, 5 September 2008 (UTC)

I think the hard working gents in this debate have already given you a rational, educated argument. They have brought up a peculiar chemical similarity, pharmalogical similarity (rather THC stimulates opioid receptors directly or indirectly is irrelevant, it shows a similarity nonetheless). These thoughts should be reguarded as truly interesting rather than "half baked". Yes, I'm singling you out, Cacycle. Can't we get any other person to comment besides you?--206.28.43.138 (talk) 07:36, 7 September 2008 (UTC)

The structural formula of THC and opiates does not share any commonality, except for lines which can be found in any other organic molecule, too. A similar pharmacological profile of THC and opioids is nonsense, too. THC has to many properties, taking a single property and claiming similarity does not work. The same kind of "similiarity" is true for THC and cocaine (increase in dopamine levels), THC and ethanol (anticonvulsive properties), THC and benzodiazepines (antiepileptic properties) and ..... --Panoramix303 (talk) 21:38, 7 September 2008 (UTC)

Hey, Panoramix303, your rebuttal is very flawed. First of all, nothing has been said to imply that THC's actions are restricted to opioid activity. That is obvious. But the fact that it does stir changes in opioid signaling is evidence of some sort of chemical or pharmalogical likeness, rather distant or not. You said "The same is also true for THC and ethanol (anticonvulsive properties)". That is a weak comeback because THC and ethanol have no pharmalogical likeness, not even distant resemblance in the mechanism of action. THC acts primarily on cannabinoid receptors, and ethanol acts as a GABA agonist. Now, here's where the similarty should be obvious. THC activates the delta opioiod receptor through changes in opioid signaling. That is a pharmalogical similarity, not mere likeness of effect. The same applies for benzodiapines, too. I don't know where you got cocaine from, though...--68.217.167.78 (talk) 23:15, 11 September 2008 (UTC)

Does the article have a bias?

It looks to me like this article has a pro-marijuana bias. The article reads as if it were written for a stoner convention, to refute the claims of the "establishment". Seriously, does anyone else think that the article may have derailed after the first section? 74.183.138.133 (talk) 01:31, 22 September 2008 (UTC)

I don't see any bias. There are very straight forward facts about published studies as far as I can tell, much like you would expect to see at the entry for any pharmacological chemical. I do think some review studies should probably be cited for context on some of the studies, like the 2008 Melbourne one with only 15 test cases... and really, how do you find matched controls for the type of person that smokes 5 joints a day for 20 years?! NJGW (talk) 01:51, 22 September 2008 (UTC)

Yes, no bias here. This article presents only referenced scientific findings.--Metalhead94 (talk) 21:23, 25 September 2008 (UTC)

Biased. The LD50 section is way too detailed, any other pharmacological entry would just get a number. The whole article is a collection of bits and pieces and very hard to read, even for people familiar with the subject. Giving a proper reference does not mean something can't be biased, you just have to select the references carefully. -- Panoramix303 (talk) 22:02, 11 October 2008 (UTC)

I'm confused... are you saying the article is biased towards detail? towards poor writing? Please be more specific so we can fix what you see as problems. NJGW (talk) 02:42, 12 October 2008 (UTC)

Sorry for the confusion. In my opinion there are two seperate problems, first the article is biased towards pro-THC and second, the article is a collection of details lacking a general story. I would suggest that the whole article should be rewritten in order to make it more readable. The bias is subject to discussion. -- Panoramix303 (talk) 11:00, 12 October 2008 (UTC)

I agree that the structure and flow could be improved, but a rewrite seems to suggest the article be stubbed... I'm not sure I agree with that as I don't see any fundamental issues that a good editor couldn't fix (I'll get on by the end of the week when I have more time if no one else does). As for the bias, others have said so but been unable to say why they felt that way. Maybe you can explain where you see the bias. NJGW (talk) 15:29, 12 October 2008 (UTC)

Reasons why I believe the article is biased.
1) "THC is also a neuroprotective antioxidant", this a minor property of THC and mentioned in the first, i.e. main, paragraph.
2) the whole LD50 section has only one function, to prove that THC is not toxic
3) the "negative side effects" paragraph states negative effects but at the same time says they need further evaluation and are subject to dispute, e.g. "Conceivable long-term ill effects of THC on humans are disputed. Its status as an illegal drug makes research difficult." The Apolipoprotein C section has also a weasel sentence "currently believed" which reads like "currently believed but not proven and soon disproven".
4) The Dronabinol section is also very POV, e.g. "which has raised much controversy as to why natural THC is still a schedule I drug.", no reference given, e.g. heroine is used as a drug in acute myocardial infarction but still illegal as a recreational drug, different use, different classification.
5) comparison to medical marihuana, the section about CBD contains several mistakes. CBD is anticonvulsive but surely not the major anticonvulsive part of marihuana. The statements might be true but still they are not really related to the article which should be about THC. Again no reference given. "It takes over an hour", i.e. THC is worse than medical marihuana. "Many have said", how many? who? how reliable? "Isolated THC is expensive", 24$ per dose is not expensive. Also it contradicts the statement before that dronabinol is synthetic THC, while here it is isolated THC. "Taking a Marinol pill to manage nausea can be ineffective because nausea can cause the pill to be ejected before it is absorbed by the body." also POV, the same is true for any other antiemetic drug, this is the reason why they are combined with other drugs.
6) some more points: "Recent research has shown that many adverse side-effects, generally known as the "stoner" stereotype, fail to hold up to the scientific method.", no reference given. "Recent studies with synthetic cannabinoids show that activation of CB1 receptors can facilitate neurogenesis,[23] as well as neuroprotection[24], and can even help prevent natural neural degradation from neurodegenerative diseases such as MS, Parkinson's, and Alzheimer's." so what? this article is about THC and not about synthetic CB1 agonists. -- Panoramix303 (talk) 16:49, 12 October 2008 (UTC)

(undent) I made some changes, see what you think. Addressing your points one-by-one:

1) "Minor" is your opinion. I'll let others chime in to reach a consensus.

2) That's what LD50 is about... what changes would you suggest?

3) Just the facts man. No study has been conclusive... please give citation if you think otherwise.

4) Now cited.

5) Now cited. (a couple of citations still missing but marked CN, might have to make minor wording changes)

6) Changed wording and cited.

Honestly those were pretty minor points and all seemed easily addressed (besides the two CN's I placed in the article, I don't want to spend all day hunting down cites for minor points). I thought you meant the article needed a total rewrite. Still, the structure could use a going-over, and I do think some extra material could be removed. NJGW (talk) 17:47, 12 October 2008 (UTC)

Good work! Looks much better now. I agree that the points were minor, but it sums up and quantity transforms into quality. For the LD50 it would suggest a simple statement like "the oral LD50 is X in rats and Y in mice. LD50 by inhalation in rats is Z which would amount to Z2 in a 80 kg male human, roughly equal to Z3 of high potency marihuana". That's it, no reason to elaborate the differences between mice and man or explain the receptor distribution in the brain (e.g. CB1 is the most abundant GPCR in the human brain therefore its overactivation has to certainly lead to death, also a valid statement but simply not true), the saturation of serum lipids is true but not relevant and also unreferenced.

I would suggest to create another article, something like "THC in research" to put in all the in-vivo and in-vitro experiments. Perhaps another article about the regulatory history of THC, it suddenly starts in the 1980s without any history before. Furthermore the first paragraph in the pharmacology section has to be cleaned up. -- Panoramix303 (talk) 18:00, 12 October 2008 (UTC)

Unless there's a pressing need to greatly expand the sections you mention, I don't think we need to spin off any daughter articles. The article is only 40kb long, and we're talking about editing some out... better to keep the information together until it gets unwieldy. NJGW (talk) 18:16, 12 October 2008 (UTC)

Proposed move: Dronabinol

I propose that this page be moved to dronabinol. That is the international term, and therefore we should use it, especially seeing as this is an article from a global point of view (as opposed to, e.g., regulation of tetrahydrocannabinol in the United States.) Simultaneous movement (talk) 19:04, 20 October 2008 (UTC)

I agree in principle terms but in this case it is like Aspirin vs. acetyl salicylic acid. The "trade name" is more common than the INN. Also while dronabinol refers only to THC as a drug, THC is used in the chemical literature and as a research chemical. In this case it would be confusing for the average reader to move the whole article. -- Panoramix303 (talk) 09:47, 21 October 2008 (UTC)

Nah, the guideline says that we link to the name which is commonly used as the name, not necesserily to the official name. Most common used is 'THC' (which as an abbreviation is a difficult case, as it is an abbreviation, which may be used for other things as well), and then tetrahydrocannabinol. --Dirk Beetstra ^{T C} 09:58, 21 October 2008 (UTC)

Isn't it also comparable to the paracetamol/acetaminophen nomenclature debate, though? The latter seems more common (compare the google hits), but we use the former. I think there is also a bit of a bias toward shorter names (all other things being equal) which could account for the outcome of the aspirin/acetylsalicylic acid debate. "Dronabinol" is shorter than "tetrahydrocannabinol."

I think also that using the term "dronabinol" helps avoid the bias introduced by prohibitionists in calling Marinol's active ingredient "dronabinol" while calling cannabis' ingredient "tetrahydrocannabinol," as if they're two different drugs. It's like how they called cannabis "marijuana" (see marijuana (etymology)) because "hemp" and "cannabis" had too many positive connotations in the industrial and medical fields. It seems better to shun arbitrary/nonexistent distinctions that, from the beginning, were designed to confuse people as to the facts at hand.

In any event, redirects and lead paragraphs are the standard ways of clearing up reader confusion about names. For instance, I looked up the SA-7 missile awhile ago, having no clue that it was also called the Strela-2, and understood the nomenclature situation pretty quickly after clicking on it. Simultaneous movement (talk) 15:16, 21 October 2008 (UTC)

Herbivores

How does THC protect the plant from herbivores? Does it taste bad or something? Simultaneous movement (talk) 00:28, 22 October 2008 (UTC)

I removed the paragraph, there is no evidence or scientific article supporting this statement. If someone can find a good scientific reference, please put it back. -- Panoramix303 (talk) 20:35, 22 October 2008 (UTC)

I have added the reworded sentences about the role of THC in the plant back in. Self-defense as well as UV protection have been widely discussed in the scientific literature. Both roles have never been proven (how would you do that?) and I hope the current version makes that clearer. It should be relatively easy to reference this if somebody seriously questions the current formulation. Cacycle (talk) 03:04, 23 October 2008 (UTC)

Pate, David W. Possible role of ultraviolet radiation in evolution of Cannabis chemotypes. Economic Botany 37 (4): 396-405 (1983)

Pate, David W. Chemical ecology of Cannabis. Journal of the International Hemp Association 1 (2): 29, 32-37 (1994) 121.200.212.105 (talk · contribs) 06:07, 26 October 2008

That's fine, but you can't just add it to the lead without some explanation in the body of the article. This is a fascinating topic that should be explained in detail. To address the original poster's question, Simultaneous movement, "short-term memory loss in herbivores...reduce[s] repeated attacks."[2] Speculative, but it makes sense. Viriditas (talk) 12:14, 12 November 2009 (UTC)

THC "neurotoxic" - THC and brain cell death, DNA destruction:

http://www.jneurosci.org/cgi/reprint/18/14/5322.pdf:

Marijuana consumption elicits diverse physiological and psychological effects in humans, including memory loss. Here we report that D9-tetrahydrocannabinol (THC), the major psychoactive component of marijuana, is toxic for hippocampal neurons. Treatment of cultured neurons or hippocampal slices with THC caused shrinkage of neuronal cell bodies and nuclei as well as genomic DNA strand breaks, hallmarks of neuronal apoptosis. Neuron death induced by THC was inhibited by nonsteroidal anti-inflammatory drugs, including indomethacin and aspirin, as well as vitamin E and other antioxidants. Furthermore, treatment of neurons with THC stimulated a significant increase in the release of arachidonic acid. We hypothesize that THC neurotoxicity is attributable to activation of the prostanoid synthesis pathway and generation of free radicals by cyclooxygenase. These data suggest that some of the memory deficits caused by cannabinoids may be caused by THC neurotoxicity.

The apoptosis is apparently what makes it a good anti-cancer agent, the not-psychoactive-on-its-own cannabinoid CBD does the same thing, however this is destructive to the brain by the same mode of action (which is why it is also destructive to cancer). I also once heard there was a DNA test to see if one ever in their life has taken marijuana (rather than a drug test just to see if it is in ones system), I wonder if this relates to the "genomic DNA strand breaks" mentioned in this neuroscience article. It certainly makes THC seem very neurotoxic, even when compared to methamphetamine, etc. 67.5.157.237 (talk) —Preceding undated comment was added at 12:38, 25 October 2008 (UTC).

In science the significance of single publications for real life problems is usually rather low - that is the reason why we strongly prefer secondary sources (i.e. review articles) that put findings into context over primary sources as references in Wikipedia articles (see Wikipedia:No original research#Primary, secondary and tertiary sources. These findings have not been reproduced in ten years as far as I can see - suggesting that something was funky with this study - and their conclusions are purely speculative. Cacycle (talk) 16:54, 25 October 2008 (UTC)

I don't think a chemical can be both neuroprotective and neurotoxic. I removed a statement relating to this "study" on the Aspirin page months ago.--Metalhead94 (talk) 20:06, 26 October 2008 (UTC)

There is no reason why a compound can not be neuroprotective and -toxic at the same time. It is just a question of the specific cell system used, the receptor reserve and so on. Please leave the statement in the article, there is more than just one evidence that THC has a dual role in neurotoxicity. -- Panoramix303 (talk) 06:01, 27 October 2008 (UTC)

I think Panoramix303 has an anti-marijuana POV. The article now does not even indicate that THC is neuroprotective. Andre (talk) 19:22, 27 October 2008 (UTC)

Actually, it does mention the possibility with a citation. We must only comment on other users actions, not their motivations... unless they become disruptive, in which cases it may be prudent to discuss POV or COI issues. NJGW (talk) 19:28, 27 October 2008 (UTC)

I saw the bit about neuroprotection with synthetic CB1, but there's no out and out statement using the term "neuroprotective" as there was before. I was merely trying to point out that this user seems to be trying to compensate for a perceived pro-cannabis POV and in doing so is perhaps creating an anti-cannabis one. Andre (talk) 20:50, 27 October 2008 (UTC)

That's an issue we can address... I think the article is mostly NPOV right now. Does anybody feel that there are POV issues in the present article? NJGW (talk) 21:18, 27 October 2008 (UTC)

The article states that THC is an antioxidant and neuroprotective. The reason I removed the sentence about antioxidative properties from the first paragraph is that it is one of the minor properties of THC. I certainly don't have an anticannabinoid bias, I just have a bias towards balanced approaches. There were several problems in the article as discussed above, e.g. the LD50 section. If parts of an article are not very credible than readers might not believe other more important issues. THC is an agonist of the CB1 receptor, the most abundant GCPR in the brain, therefore it will have plenty of effects, good and bad. We should just try to make the article more appealing to readers not familiar with the topic, e.g. telling a story and not just connecting single sentences about the effects of THC. -- Panoramix303 (talk) 19:02, 28 October 2008 (UTC)

Soluble in butane???

Hexane I can believe, but since butane is a gas at normal temperatures and pressures this is either nonsense or needs clarification. Was pentane intended, or liquid butane under pressure, or below its boiling point? Xarqi (talk) 00:44, 8 December 2008 (UTC)

It is true, hemp can be extracted with butane which has a boiling point of −0.5 °C. Liquid butane will start evaporating, thereby cooling the liquid to a constant −0.5 °C. It is a somewhat wasteful process when done ghetto style without recovering the butane. It has been reported to give a superior extract without much chlorophyll. Cacycle (talk) 01:43, 8 December 2008 (UTC)

Does it cause psychosis or not?

Someone want to resolve the conflict between this:

"Research has also shown that past claims of brain damage from cannabis use fail to hold up to the scientific method.[33] Instead, recent studies with synthetic cannabinoids show that activation of CB1 receptors can facilitate neurogenesis,[34] as well as neuroprotection[35], and can even help prevent natural neural degradation from neurodegenerative diseases such as MS, Parkinson's, and Alzheimer's."

and this:

"Some studies have suggested that marijuana users have a greater risk of developing psychosis than non-users. This risk is most pronounced in cases with an existing risk of psychotic disorder.[40] Other studies have made similar associations, especially in individuals predisposed to psychosis prior to cannabis use.[41] A literature review on the subject concluded that "Cannabis use appears to be neither a sufficient nor a necessary cause for psychosis. It is a component cause, part of a complex constellation of factors leading to psychosis."[42] Recent research has also shown a correlation between cannabis use and increased cognitive function in schizophrenic patients.[43]"

It seems the fact that these 2 viewpoints are contradictory needs to be highlighted. Also the last sentence of the second paragraph contradicts the rest of the paragraph. *Note: psychosis is the major symptom of schizophrenia.* Does someone else want to elaborate and highlight the differences between these studies? Is it really both neuroprotective/neurogenerative (against MS, Parkinson's, Alzheimer's, Schizophrenia) *and* a factor leading to psychosis. Anyone want to research and cite how that would be possible? 76.24.169.192 (talk) 04:14, 20 August 2009 (UTC)

Verification on solubility in water

Can someone verify THC's solubility in water? The reference it cites is a dead link. Falcon8765 (talk) 04:39, 20 August 2009 (UTC)

Is THC an alcohol?

Is THC an alcohol? cannabinol ends with ol and THC has an OH in it. I guess it just seems awkward to refer to THC as an alcohol.

THC is a phenol. If the OH is connected to an aromatic system the OH becomes a phenolic OH, not alcoholic OH. Panoramix303 (talk) 05:50, 24 August 2009 (UTC)

As phenols are a subclass of alcohols one could say that THC is an alcohol (also notice the -ol in phenol...). But phenolic OH groups have indeed somewhat different properties compared to "normal" (aliphatic) alcohols. Hope that helps... Cacycle (talk) 19:05, 24 August 2009 (UTC)

Routes

Why does it have a ? Shouldn't it be oral, inhalation and intravenous?Tdinatale (talk) 13:32, 28 August 2009 (UTC)

Intravenous is kind of difficult, I saw reports in the scientific literature for intravenous THC formulations but no report about human use. Panoramix303 (talk) 13:36, 28 August 2009 (UTC)

Solubility given in mg/L or mg/mL?

Both units and also two different temperatures are present in the article. This makes no sense to me. Bobber0001 (talk) 08:29, 17 November 2009 (UTC)

Fixed it. The mg/mL unit is added by the ChemBox automatically. It is now correct. Panoramix303 (talk) 20:05, 17 November 2009 (UTC)

dont have any facts

I saw a PBS special on THC, that we have receptor sites where our brains make a chemical that helps us forget and this chemical closly resembles THC thats why we are able to accept it.(thc) Yes i know i could have done more research and got this statement perfect but i will let someone else do the research and take the cred for it. This can be verified her papers were announced on the program —Preceding unsigned comment added by 76.110.84.17 (talk) 00:01, 25 December 2009 (UTC)

A link to the clinical study was added but you can also do it yourself. If you need help, leave me a message my page.Panoramix303 (talk) 17:49, 25 December 2009 (UTC)

Correction

"In August 2009 a phase IV clinical trial by the Hadassah Medical Center in Jerusalem, Israel was started to investigate the effects of THC on post-traumatic stress disorders in women."

According to the link given the study is open to both men and women, though there are additional restrictions for women (pregnancy exclusion). —Preceding unsigned comment added by 99.224.163.104 (talk) 00:36, 25 February 2010 (UTC)

Thanks! I removed it, now it is neutral. Panoramix303 (talk) 06:49, 25 February 2010 (UTC)

I don't see THC as being a deterrent to consuming cannabis (the article claims that it may be a deterrent to herbivorous consumption. I would rather say that the THC is more of propagation inducer, evolutionarily. —Preceding unsigned comment added by Scottyglenncornog (talk • contribs) 05:12, 11 April 2010 (UTC)

Actually I think the purpose of THC is a protective chemical against Ultraviolet light, which is why exposing a plant to more UV light increases its THC content.Fireemblem555 (talk) 20:40, 30 April 2010 (UTC)

PLEASE

Let me ask you to please try to make this article as accurate as possible please, cannabis use is destroying the life of someone I love... I guess this is important to me as to anyone with the same problem. I know, by the way, many people with the same problem... thank you —Preceding unsigned comment added by 190.97.59.157 (talk) 22:35, 25 November 2010 (UTC)

in what way is it inaccurate? 92.24.198.205 (talk) 17:31, 27 November 2010 (UTC)

Original Research, or Not?

I am a cancer patient. I recently got a prescription for dronabinol, which I filled. I can say how much it cost at a Walmart pharmacy. But since I can't cite a reference, I can see how it could be argued that the price information constituted original research. On the other hand, the pricing information is verifiable, by simply calling a pharmacy and asking. One needs no prescription to do that.

Is the pricing original research or not?

Aziscohos (talk) 21:11, 8 February 2011 (UTC) — Preceding unsigned comment added by Aziscohos (talk • contribs) 14:47, 8 February 2011 (UTC)

I'd like to know.... FranklinP77 (talk) 18:49, 13 February 2011 (UTC)

error regarding dopamine

Recent research out of London seems to contradict the notion that THC precipitates dopamine production.

http://www.ncbi.nlm.nih.gov/pubmed/19539765

CONCLUSION: In the largest study of its kind so far, we have shown that recreational cannabis users do not release significant amounts of dopamine from an oral THC dose equivalent to a standard cannabis cigarette. This result challenges current models of striatal dopamine release as the mechanism mediating cannabis as risk factor for schizophrenia.

Editing this stuff into the article is way over my head. Could someone make the correction please?

HB681g (talk) 02:10, 12 March 2011 (UTC)

Addiction

While it seems to be common knowledge that marijuana is not physically addictive, there have been reports of an acute withdrawal syndrome after cessation of chronic heavy marijuana use. This constitutes a form of physical addiction, and is possible evidence that THC may be slightly addictive also. —Preceding unsigned comment added by 96.245.60.157 (talk) 00:15, 16 March 2011 (UTC)

And the source of these reports is...? The fact of the matter is: The sentence was removed because a mental addiction was implied with no proof other than a generic statement that can be applied to anything. There are individuals addicted to things like shopping and video games whom can suffer an acute withdrawal when the cycle is broken. Does that constitute possible evidence of a physical addiction?--96.2.39.19 (talk) 08:36, 16 March 2011 (UTC)

LD50 Implications

Given the rat LD50 value for inhaled THC of 42 mg/kg, the LD50 of a 70 kg mammal would likely be near 2940 mg. Assuming high quality marijuana is 20% THC, the LD50 of marijuana should be 14700 mg, or 14.7 grams. Granted, this does not account deviation in LD50 values among species and the effects of other phytocannabinoids, regardless, I feel the "estimates" assuming hundreds of pounds must be smoked to overdose are dangerous and a fabrication, at least until somebody can cite the grounds by which they make these estimates. —Preceding unsigned comment added by 96.245.60.157 (talk) 00:37, 16 March 2011 (UTC)

"at least until somebody can cite the grounds by which they make these estimates." Isn't that already done? The estimate given in the Toxicity section (and a followup comment related to this same idea) has a footnote pointing to a specific reference that whoever-added-this-to-the-article claims supports the statement. So you can begin to answer your own question--look up that ref. Or if you cannot access the full article, you can read at least its free abstract to see if it seems likely to support this sort of statement. You can also consider the general quality of the ref itself, per reliable-source standards. DMacks (talk) 08:57, 16 March 2011 (UTC)

Rats are not humans, nor are they any other mammal but rats. Its unsafe to assume that the LD50 of a substance for one creature at one weight can be used as a formula for all mammals. Assuming that 14.7 grams of marijuana would be unsafe, I would have died last summer when I shared a 28.5 gram joint of 24% (laboratory proven) marijuana with a friend. Its not even certain that 14.7 grams of marijuana would kill a 70 kg rat. You're right. Assumptions, especially those based on incomplete research (such as not even reading the entire wikipedia entry) are dangerous. You, too, can make assumptions. Don't you ever forget that -James Randi--96.2.39.19 (talk) 23:26, 16 March 2011 (UTC)

Regardless, all I was trying to prove with that estimate was that the reference saying thousands of pounds would have to be smoked is dangerous and isn't supported by any evidence in the article this page cites. In addition, anecdotes really don't mean anything. —Preceding unsigned comment added by 96.245.60.157 (talk) 13:24, 19 March 2011 (UTC)

I have to agree, the reference which suggests it would take 1500 pounds of marijuana to kill the average person is not valid in this case. It comes from a peer reviewed journal which is discussing the legal issue of marijuana and is not an experiment of any kind to explicitly determine the LD50 value for humans, nor does it contain any other relevant scientific data. The quote in the paper is made by DEA administrative-law judge Francis Young from 1988 and not from any scientific findings within the paper. In the article it actually states that it is an estimate and in fact there is no reference cited in that paper that indicates where this information came from. What we do know is that the LD50 for rats is around 600-1200 mg/kg (ingested). If you take the higher estimation of 1200 mg/kg and factor in an 80 kg person you are looking at approximately 1 kg (2.2 lbs) of cannabis with a THC % of 10% (I used the low end). I am not saying humans metabolize all things exactly the same as rats but its within reason. That's why research is done with rats. The point is it is more on the order of a few pounds NOT 1500! This reference should be removed, it is just a misrepresentation of a quote in a scientific journal that was manipulated to fit someones argument. For those wanting the context of the quote I will paste it below: In 1988, after two years of hearings, DEA administrative-law judge Francis Young recommended shifting marijuana to Schedule II on the grounds that it was safe and had a “currently accepted medical use in treatment.”19 Specifically, Judge Young found that “marijuana, in its natural form, is one of the safest therapeutically active substances known to man. . . . At present it is estimated that marijuana's LD-50 [median lethal dose] is around 1:20,000 or 1:40,000. In layman's terms . . . a smoker would theoretically have to consume 20,000 to 40,000 times as much marijuana as is contained in one marijuana cigarette . . . nearly 1500 pounds of marijuana within about fifteen minutes to induce a lethal response.” As for medical use, the judge concluded, among other things, that marijuana “has a currently accepted medical use in treatment in the United States for nausea and vomiting resulting from chemotherapy treatments.”19 The administrator of the DEA rejected Young's recommendation, on the basis that there was no scientific evidence showing that marijuana was better than other approved drugs for any specific medical condition. Further attempts to get the courts to reclassify marijuana have been unsuccessful.--Jeremy —Preceding unsigned comment added by 205.193.94.40 (talk) 19:39, 28 April 2011 (UTC)

"One estimate of THC's LD50 for humans indicates that about 1,500 pounds (680 kg) of cannabis would have to be smoked within 14 minutes.[22] This estimate is supported by studies which indicate that the effective dose of THC is at least 1000 times lower than the estimated lethal dose (a "therapeutic ratio" of 1000:1). This is much higher than alcohol (therapeutic ratio 10:1), cocaine (15:1), or heroin (6:1).[23]"

This needs to stop being added again, for the above reason. Also, it is contradictory: If the therapeutic ratio of THC is 1000:1 and an active dose is .5 grams, 500 grams would be a lethal dose, which is about 1.1 pounds. Not 15,000. The study cited does NOT support the claim of Francis Young, and the study is not compliant with more accurate (inhalation route of administration rather than IV/oral) studies regarding THC's median lethal dose. I'm adding a disputed tag to the toxicity section. — Preceding unsigned comment added by 68.238.244.186 (talk) 02:59, 28 July 2011 (UTC)

12/6/2011 Edits

Before I began editing, these pages were a jumbled mess of confused science and faux-science that had clearly been compiled by recreational marijuana users with minimal understand of how solid research is conducted or reported. Most of the sections were written independently and did not read cohesively when considered by page; as such much of my efforts were spent cleaning up the inconsistencies, miscitations, and straight up fallacies that littered each topic discussed. In addition, I added more citations from appropriate and current research and reorganized the pages so that they are presented in a more digestable format. In summary, these pages on endocannabinoid receptors were not lacking attention before my edits, but had rather received too much attention from people who just did not know what they were talking about. I have simplified, clarified, and expounded where appropriate with the intention of creating a more cohesive and through product. The extent of these edits are subtle, but were based on eight research pages that I read dealing with the topics I addressed Wyliea (talk) 01:52, 7 December 2011 (UTC)

Since this is a "talk" page

I'm "in medicine" and just can't get on the bus with the marijuana people. I mean, weed may have it's benefits (so does heroin) but as you've stated above, the recreational users have bastardized the literature with anecdotal testimonial "facts."

My big one is that if indeed this is a credible treatment, would you give your 10 year old cancer patient/child of your own a refer and teach him how to "fire up?" "No Johnny. You've got to inhale it deeply and hold it into your lungs. Watch how daddy does it..." Blondesareeasy (talk)Thanks for playing. —Preceding undated comment added 22:36, 1 February 2012 (UTC).

Your argument is based on the logical fallacy "Reduction to Absurdity." By your logic, Johnny wouldn't get the 'birds-n-bees lecture'; he would watch live demonstrations of safe-sex and then perform supervised demonstrations to prove the lesson was learned.

This article is about Delta-9 Tetrahydrocannabinol, which is only one of the cannibinoids extracted or synthetically produced to provide an effective treatment for cancer patients. Based on the article, nabilone (marketed as Cesamet in the USA) would be the preferred method of treatment and is a fast-acting mouth spray. It seems unlikely any doctor would prescribe lung-damaging treatments if a safer, equally-effective and less hazardous alternative were available. Though it does seem strange that 10-12% of children in school get dosed with amphetamines to 'cure' them of their intolerance to sitting in a chair seven hours a day like 'normal' children know to do.

You want to talk about anecdotal evidence? How about the 'studies' relating violent crime to illegal substances? If they weren't illegal there'd be no need to visit criminals. That's basically the definition of statistical entrapment. There will always be higher incidence of violence in black-markets. The police and politicians know this, but the conclusions of the studies provide misdirection away from 100%-correlated causal factor.

My only concern in this matter is the perversion of logic, reasoning and argumentation. Ritual suicide by alcohol and tobacco: OK, cannabis: NO WAY. Manufactured in China: OK, cigar from Cuba: NO WAY. These are trivial examples.

Jason Singer (talk) 03:09, 6 February 2012 (UTC)

See but thats the issue right there. No one disputes the notion of "ritual suicide by alcohol and tobacco". What a specious analogy that is! The message that alcohol and tobacco are deadly is replayed 24x7x365. The issue is, as we inch towards legalization, that THC is being presented as a cancer curing miracle drug that has *never* in human history *harmed anyone*. And to the one-issue legalization zealots, *nothing* can convince them different and *nothing* else matters beyond smoking pot. Any evidence that there might be anything negative at all about pot is aggressively rejected. Why is that this does not trip your "perversion of logic, reasoning and argumentation" sensor? — Preceding unsigned comment added by 70.15.134.116 (talk) 22:24, 3 January 2014 (UTC)

I find it quite ironic that, in the United States, marijuana is a schedule 1 substance meaning, among other things, that it has no medical benefits. However, marinol is marketed as a medical evaluation of marijuana to assist in medical conditions and actually has a medical value, and is hence a schedule 3 substance. Why is it that if the primary substance has no medicinal value at all, but a product which is basically just THC, the assumed primary ingredient in marijuana (the primary substance), does have medical value. Where's the logic in that? Styk0n (talk) 08:30, 12 November 2012 (UTC)

"Talk page" refers to conversation about the article itself and how to improve it, not debate about the subject of the article. If you feel the article as it stands misrepresents THC, gather your sources and make edits. 184.182.183.82 (talk) 16:38, 21 May 2013 (UTC)

Boiling point of THC

The old wikipedia page got the number 157C somehow. Looking this up doesn't seem to find any real sources. So I've removed that number and placed a number given to me by the Royal Society of Chemistry from their analytic database. This other page also uses this number so I figure that should be a good start. http://en.wikipedia.org/wiki/Cannabis_(drug) LegacyWeapon (talk) 18:07, 11 March 2012 (UTC)

I looked at the ChemSpider source you cited, and I cannot find the value you reported (199.14 °C at unspecified pressure so assuming 1 atm) anywhere on it. For example, looking in the Properties section, I don't see a boiling-point in the "experimental" tab. In the various "predicted" tabs, I do see:

"390.448 °C at 760 mmHg" for ACD/Labs

"407.23" and "200 @ 0.02 mm Hg deg C" EPISuite

Those are all pretty far off of 199 °C at 1 atm. Conversely, the previous 157 °C value at 1 atm is exactly what ref it had listed says. That ref has a data table that notes "values obtained from various sources, primarily Buckingham, 1992; Guenther, 1948; Parry, 1918; and Mechoulam (personal communication, April 2001)." Because I was unable to verify your value, I reverted back to the previous. Would be useful to find the underlying source for the 157 value, expecially since it is so different from the predicted results. But predicted values are only of limited reliability, especially since not reported in an actual peer-reviewed source, so I think we're stuck with either 157 or maybe nothing (per lack of close agreement among sources). DMacks (talk) 18:31, 11 March 2012 (UTC)

That other page states "the boiling point of THC is 390.4 °F (199.1 °C) at 760 mmHg pressure", cited to the chemspider source. Notice the 390.4 value...perhaps the editor who wrote the wikipedia content just misread the units when reporting it? I'm tagging that value there as a point of concern. DMacks (talk) 18:43, 11 March 2012 (UTC)

1/2/2013 Edits

Shouldn't its legal status be updated to include 2012 election changes of medical and recreation cannabis, or not because cannabis s. is not thc. — Preceding unsigned comment added by 76.180.166.44 (talk) 01:46, 6 January 2013 (UTC)

I don't think that makes the difference. Even if it's only "cannabis" that is now legal and not "THC", it would still be relevant to this article. So go ahead and add it in there. Charles35 (talk) 02:46, 6 January 2013 (UTC)

Vaporization point (and boiling point)

I plan to build a vaporizer (for experiments with my pet animals), does anybody know the vaporization point? 95.112.162.127 (talk) 08:39, 6 April 2013 (UTC)

365 °F MidnightRequestLine (talk) 16:10, 6 April 2013 (UTC)

IUPAC NAME IS INCORRECT

Gentlemen I would like to bring to your attention that the stereochemical identities for the IUPAC name for THC are incorrect. The two chiral centers should have "R" as their stereochemical identity not "S". Solving the chirality for the two chiral centers in the structure also shows "R" not "S". This needs to be fixed right away. This is Dr. Mark A Olson of Texas A&M University Corpus Christi, assistant professor of chemistry. I was alerted by my students to this error and verified it. Please see that it is corrected. — Preceding unsigned comment added by 64.71.89.15 (talk) 00:36, 24 April 2013 (UTC)  Done

"Trade off alcohol for marijuana"

I have come upon many persons, sadly consumed by alcoholism. but in the trade off have found marijuana as an alternative to alcohol. From ongoing research can can prove to be a less destructive and possibly healthier alternative for these persons suffering through alcoholism. — Preceding unsigned comment added by 74.105.80.14 (talk) 05:56, 28 December 2013 (UTC)

Copyright violation

I removed links to a journal article hosted at badgerlawyer.com, but Meteor sandwich yum reinstated them. How is this not copyright violation? Alexbrn ^{talk|contribs|COI} 06:10, 12 January 2014 (UTC)

Hi. That was a mistake. I wasn't watching edit history. Can you elaborate (on why they're a CV), please? meteor_sandwich_yum (talk) 06:19, 12 January 2014 (UTC)

Because the article has copyright of the publisher. This is an illicit copy (unless there is something demonstrating otherwise - which I can't see). Alexbrn ^{talk|contribs|COI} 06:24, 12 January 2014 (UTC)

(Add) it's http://dx.doi.org/10.1097/01.ftd.0000197091.07807.22 (indexed as PMID 16628124). Alexbrn ^{talk|contribs|COI} 06:30, 12 January 2014 (UTC)

Hmmm... they didn't claim for this to be their own work, but accredited it properly to the original publisher. Still copyright violation? They gave enough detail for someone to reasonably trace the work back to its author.

I don't have anything against just going with the primary source, it's just that this makes me curious. I'm reverting article addition after I post this for safety. meteor_sandwich_yum (talk) 06:43, 12 January 2014 (UTC)

Nevermind. Subscription-only content I was linking to. Thanks. meteor_sandwich_yum (talk) 06:51, 12 January 2014 (UTC)

Yes it was only the link that concerned me - which you've now fixed. Alexbrn ^{talk|contribs|COI} 09:07, 12 January 2014 (UTC)

Resolved

Third party v. MEDREF tag

Meteor sandwich yum removed the MEDREF tag and replaced it with a third-party tag,[3] which I have reverted. In edit summary, s/he mentions we have "plenty of data", which is not the concern with incorrect medical sourcing. The article uses primary sources (which can be cherry-picked to present a POV) when there are numerous secondary reviews available that are compliant with MEDRS. To avoid original research on Wikipedia, we prefer secondary sources to primary-- it's not an issue of "third-party", rather overuse of primary sources rather than secondary reviews. SandyGeorgia (Talk) 13:49, 12 January 2014 (UTC)

Touché. I retract my action, tag names are deceiving. Medref, at first glance, sounds like it means we need more studies, not better studies. The Coalition for Rescheduling Cannabis is obviously a party with a COI here, but cherry-picking is much more predominant. Even one meta-analysis seems to uphold the POV-pushing: "Research has also shown that past claims of brain damage from cannabis use fail to hold up to the scientific method..."

It's sort of a 'gray area' for this — do you believe cherry-picking might be a more representative tag? This issue can also be seen as sociopolitical, not just biological. As a side note, I notice the talk page doesn't include a "part of the scope of WikiProject Medicine" banner. meteor_sandwich_yum (talk) 14:29, 12 January 2014 (UTC)

I don't know that "cherry picking" is a more representative tag (well, I wasn't aware of the existence of such a tag), but considering the purpose of a tag is to get the article fixed, the way to fix it is by consulting secondary reviews compliant with MEDRS, and removing the primary sources-- so I think the MEDREF tag is correct.

The talk page should have a WPMED project banner, but regardless, medical and health-related content anywhere on Wikipedia should conform to MEDRS, whether or not the talk page is tagged (and Pharmacology covers it, see MEDRS). SandyGeorgia (Talk) 14:34, 12 January 2014 (UTC)

Added it to WikiProject Medicine, by the way. meteor_sandwich_yum (talk) 22:59, 1 February 2014 (UTC)

Resolved

Mouse male fertility

Meteor sandwich yum, regarding the weird statement from a primary source on mouse male fertility that you tagged, if you have time to examine the reviews at Cannabis in pregnancy, you might find the information to rewrite whatever that line was hoping to say. I only got to a rough-in at the pregnancy article, but I seem to recall seeing that kind of info in some of those secondary reviews. If you do find something there, it would be better to write it there, and then have this article link to the pregnancy article. There is a huge problem with duplication of text across all of the {{cannabis}} articles, so reproduction/fertility text might be better placed there. SandyGeorgia (Talk) 06:35, 15 January 2014 (UTC)

Thanks. Will look into it — I hope to resolve some of these issues and not just tag-bomb, by the way. meteor_sandwich_yum (talk) 06:37, 15 January 2014 (UTC)

When you start seeing how much there is to be done, you may find you have to tag-bomb just to know what remains to be done! SandyGeorgia (Talk) 06:47, 15 January 2014 (UTC)

Thanks meteor_sandwich_yum (talk) 17:27, 15 January 2014 (UTC)

Meteor, with respect to the duplicate and poorly sourced content everywhere in this suite, the additional difficulty at this article is sorting out which sources discuss specifically THC, versus other cannabinoids. Have fun here :) SandyGeorgia (Talk) 17:37, 15 January 2014 (UTC)

Organizational guideline

... at Wikipedia:MEDMOS#Drugs, medications and devices. SandyGeorgia (Talk) 17:40, 15 January 2014 (UTC)

Human study, January 2013

Of interest?

Pot for Sleep Front Psychiatry. 2013 Jan 22;4:1. doi: 10.3389/fpsyt.2013.00001. PMID: 23346060 eCollection 2013.

Proof of concept trial of dronabinol in obstructive sleep apnea.

Prasad B, Radulovacki MG, Carley DW.

Abstract on the use of Marijuana derivative as treatment for OSA

Study Objective: Animal data suggest that Δ(9)-TetraHydroCannabinol (Δ(9)THC) stabilizes autonomic output during sleep, reduces spontaneous sleep-disordered breathing, and blocks serotonin-induced exacerbation of sleep apnea. On this basis, we examined the safety, tolerability, and efficacy of dronabinol (Δ(9)THC), an exogenous Cannabinoid type 1 and type 2 (CB1 and CB2) receptor agonist in patients with Obstructive Sleep Apnea (OSA).

Design and Setting:

....etc.

--Hordaland (talk) 23:15, 16 January 2014 (UTC)

Hmmm... Review study, within the last 2 years, sample size of 17. Mentioned conflict-of-interest, but what concerns me more is that fact that it's so preliminary. To quote (emphasis mine):

Conclusion: Dronabinol treatment is safe and well-tolerated in OSA patients at doses of 2.5–10 mg daily and significantly reduces AHI [Apnea Hypopnea Index] in the short-term. These findings should be confirmed in a larger study in order to identify sub-populations with OSA that may benefit from cannabimimetic pharmacologic therapy.

A sample size of 17 is way too small to state this as a demonstrated effect, only good for a pilot study. Also, I believe this is self-published? I can't find any reviews of it anywhere. Furthermore, it would further the pro-marijuana bias in this article.

If this were a meta-analysis with a larger population and we needed expansion on the biomedical effects of THC, possibly. This seems more appropriate as a concept treatment for obstructive sleep apnea than for a description of dronabinol.

My vote is no. Interesting article, however. meteor_sandwich_yum (talk) 13:14, 27 January 2014 (UTC)

Just read these above. I don't care about pot, for or against, but to say that a sample size of 17 is way too small to state effect, is a complete mis-understanding of scientific studies, and I suggest a new person is assigned to this page who has a background in scientific methodology. Don't know about this study, but the statistical methods used in peer-reviewed studies have been developed by experts, over decades, to adjust for smaller sample size. More importantly, the experts who are the peer-reviewers of a published study, decided it had significance enough to publish it. A Wikipedia editor, deciding that he/she is more qualified and better informed on the specific study, than the expert scientists who reviewed the paper, and deemed it had significance, is why Wikipedia is not a real encyclopedia.

. — Preceding unsigned comment added by Two Wrongs (talk • contribs) 14:05, 14 August 2014 (UTC)

Marinol, Cannabis, and Mortality

The FDA's Adverse Events Reporting system cannot be used to make the claim that "While cannabis is not known to cause death, Marinol was cited by the FDA as being responsible for 5 deaths (4 direct and 1 indirectly involved) between January 1, 1997 and June 30, 2005.[96]" Neither deaths caused by Marinol nor the safety of cannabis is established by the cited source.

According to the FDA, as quoted in the cited source: "For any given report there is no certainty that the suspected drug caused the reaction. This is because physicians are encouraged to report suspected reactions. The event may have been related to the underlying disease forwhich the drug was given to concurrent drugs being taken or may have occurred by chance at the same time the suspected drug was taken." How can this possibly be used as support for the statement "Marinol was cited by the FDA as being responsible for 5 deaths"?

Furthermore, the fact that these reports are collected by FDA does not change the fact that they are case reports. Per WP:MEDRS, they cannot be used to support any healthcare related statement. "Case reports, whether in the popular press or a peer reviewed medical journal, are a form of anecdote and generally fall below the minimum requirements of reliable medical sources."

Cannabis has been associated with sudden cardiac death in many literature case reports that are of equal quality to the source cited here. There's not much point in listing them, however, as case reports are not suitable sources for health related content, whehter they deal with the safety of marinol or that of cannabis. Formerly 98 (talk) 09:55, 11 March 2014 (UTC)

Total and complete bullshit. The statement that "there is no certainty that the suspected drug caused the reaction" is a standard scientific disclaimer. Yes, there is no certainty when it comes to any of this, and yet, high doses of Marinol kill people while high doses of cannabis do not. Cannabis has not been associated with sudden cardiac death anywhere, and anyone who claims it has is full of crap. If that were true, college campuses would be mortuaries. Those kids smoke until they fall asleep on their couches with Cheetos-stained fingers. Nobody dies of heart attacks. They die from drinking too much legal alcohol and legal caffeinated drinks and smoking legal tobacco. Seriously? Keep fucking that chicken and keep drinking what's left of that Kool-Aid, because pretty soon the cat's gonna be out of the bag, and you'll be the last one standing. Nobody is buying the propaganda anymore and pretty soon, you guys are gonna be out of a job. It's only a matter of time now. It's over guy, pack it up and go home. Viriditas (talk) 10:12, 11 March 2014 (UTC)

Actually, I withdraw part of my statement above. There are MEDRS compliant sources showing an increased risk of MI in the first hour after smoking a joint, published in no lesser source than the Lancet. http://www.ncbi.nlm.nih.gov/pubmed/21353301. This should probably be added to the article. Formerly 98 (talk) 13:18, 11 March 2014 (UTC)

Now you are clearly trolling. Cannabis comes at the very bottom, after traffic exposure (7.4%), physical exertion (6.2%), alcohol (5.0%), coffee (5.0%), a difference of 30 μg/m3 in PM10 (4.8%), negative emotions (3.9%), anger (3.1%), heavy meal (2.7%), positive emotions (2.4%), sexual activity (2.2%), cocaine use (0.9%), marijuana smoking (0.8%) and respiratory infections (0.6%). Viriditas (talk) 23:44, 11 March 2014 (UTC)

Thats for overall attibutable cases in the population. Everyone is exposed to air pollution, but only a few smoke dope. The risk to those who do smoke is ranked pretty high. Formerly 98 (talk) 00:11, 12 March 2014 (UTC)

Pretty high? You mean like the risk you take when walking across a crowded street or driving a car? You'll need to quantify this risk. I predict it is close to nonexistent in reality. Otherwise, why aren't we seeing it in epidemiological reports and records? Maybe because it doesn't exist? Let's look at the United States. We've got 19 million cannabis smokers as of 2013. Does the predicted risk match what we are seeing in emergency rooms? No, what we see in emergency rooms is the result of legal prescription drugs, legal alcohol, and legal tobacco use. Where is the rise in MI due to cannabis use? After all, cannabis is being used more than ever now. People should be dropping dead like flies from MI. Where's the evidence? Viriditas (talk) 00:26, 12 March 2014 (UTC)

The evidence is in the paper I cited and half a dozen others like it. "High" as in the 3rd largest of 12 trigger factors identified at the individual level. Which is actually pretty amazing given that while the entire population is exposed to factors like air pollution, the fraction of the population that smokes pot is mostly young and has a relatively low baseline risk.

Cannabis consumption is also associated with increased risk of stroke: http://www.ncbi.nlm.nih.gov/pubmed/23850313Formerly 98 (talk) 10:50, 12 March 2014 (UTC)

Your so-called "evidence" is pure bunk. Give it up. Viriditas (talk) 19:56, 12 March 2014 (UTC)

I see no evidence at all. 19 million Americans use cannabis daily, yet there is no reported incidence of MI in those users. Where's the evidence? Viriditas (talk) 19:48, 12 March 2014 (UTC)

Do you have any objections to the actual sources or are you merely going to object based on your own intuition? Second Quantization (talk) 08:51, 12 March 2014 (UTC)

You call yourself a skeptic, but that's obviously false. There's no evidence that cannabis causes MI on a statistically significant basis. You're content to cite political propaganda as fact, but I'm not. Please don't call yourself a skeptic anymore, as you are denigrating the term. Viriditas (talk) 19:48, 12 March 2014 (UTC)

Edit looks good. Related papers [4][5][6] which are well cited. Related and well cited paper about K2: [7]. The article should mention the general effects of THC on the cardiovascular system, some of which the linked article provides,

"It is well known that marijuana has pathophysiological effects on the cardiovascular system. The physiologic effects of THC are mediated by stimulation of the sympathetic nervous system through release of norepinephrine9 and also by parasympathetic blockade. THC has been shown to increase cardiac output by as much as 30%.10 Marijuana use can increase the heart rate from 20% to 100% in a dose-dependent manner, which leads to increased oxygen demands on the myocardium. Heart-rate increases start in the first 10 minutes after smoking and last up to 3 hours.11,–,16 Smoking marijuana also leads to an increase in carboxyhemoglobin levels, which results in a decrease in oxygen-carrying capacity."

Second Quantization (talk) 08:50, 12 March 2014 (UTC)

And yet no evidence whatsoever that any one of 19 million American cannabis users has ever been admitted to the hospital for MI due to their cannabis use. None. But you'll continue to cite sources sans evidence that use the unscientific fear-mongering term "marijuana" instead of the medical term "cannabis" because those NIDA dollars have to keep rolling in and the DEA must meet their quota. Pure fucking nonsense. You're no skeptic, that's for sure. This entire nonsense has been completely debunked by a cardiologist. You have lost your "skeptic" rights. Viriditas (talk) 19:53, 12 March 2014 (UTC)

Get that peer reviewed then come back to me. I have no interest in your American politics, stick to the topic. Second Quantization (talk) 23:47, 12 March 2014 (UTC)

An argument from authority as a response? No true skeptic would say that.  :). Peer review, as in the political process which publishes anti-cannabis propaganda on a daily basis based on small sample sizes but won't allow pro-cannabis studies based on large sample sizes to see the light of day? You mean that broken, biased process which serves the interests of the government and the pharmaceutical companies, but not the interests of the public and patients? Is that what you mean? Viriditas (talk) 02:01, 13 March 2014 (UTC)

Using peer reviewed articles is standard on wikipedia, it's not about being a skeptic or not. Where is your evidence that any of your conspiratorial claims are true? I'm disinclined to listen to somehow claim that scientific peer review is a "political process which publishes anti-cannabis propaganda on a daily basis based on small sample sizes but won't allow pro-cannabis studies based on large sample sizes to see the light of day". It sounds like pure conspiratorial reasoning. Second Quantization (talk) 09:19, 13 March 2014 (UTC)

The cannabis literature is more than 90% negative and chock full of false assumptions, half-truths, and scaremongering because it is funded by first and foremost by drug "abuse' and drug control and prevention programs, and this starts at the United Nations and works its way down. You seem to be blissfully unaware of the political bias inherent in the medical literature. Positive research can't get published and positive studies can't get funded, and researchers who are studying positive effects can't get cannabis to use from the government. You seem to be the very last person in the world to be aware of this historical fact. Someone is vastly ignorant in this discussion, and it isn't me. I would really appreciate it if you would stop referring to yourself as a "skeptic" because you are pure believer in anti-cannabis studies that lack any semblance of scientific knowledge about cannabis. You're starting to make skeptics look like fundamentalists who believe anything the "authorities" tell them to believe. At what point did you stop critically evaluating the medical literature and start accepting it without question? Because that was the point when you stopped being a skeptic. Viriditas (talk) 10:51, 13 March 2014 (UTC)

Oh I see. I'm not thinking critically because I didn't accept your unsubstianted claims of a mass conspiracy. My mistake, Second Quantization (talk) 12:02, 13 March 2014 (UTC)

How about NIDA saying they don't fund pro-cannabis research? How about cannabis researchers who say they can't study or publish positive research because the government won't let them? Don't let little things like facts get in the way of reality. You seem to be ignorant about a great deal. Viriditas (talk) 12:54, 13 March 2014 (UTC)

[8] is not funded by NIDA. [9] not funded by NIDA. [10] not funded by NIDA. [11] not funded by NIDA. You also didn't back up your initial claim that NIDA said "they don't fund pro-cannabis research". Second Quantization (talk) 13:50, 13 March 2014 (UTC)

You were more than willing to go to the mat to defend the idea that Marinol causes fatalities based on half a dozen case reports , but faced with greater evidence (a larger number of case reports and some actual controlled studies) supporting a link of cannabis to CV events, suddenly its all a conspiracy. I think you should cool it.Formerly 98 (talk) 21:31, 12 March 2014 (UTC)

Marinol has killed people, and its warnings are well known.[12] Yet, it is offered by pharmaceutical companies with the help of the FDA as an alternative to cannabis, which has been proven to be safer and more efficacious than Marinol. This is not an idea nor a conspiracy, it is proven historical fact suported by actual medical evidence. On the other hand, once cannabis starts gaining grounds for legalization, it's suddenly, out of the blue dangerous and harmful. Sorry, we're not buying the usual round of bullshit. Sell your pharmaceutical snake oil elsewhere. As Dr. Rehman clearly shows, the notion the original findings are based on a 2001 paper that "studied heart attacks in 3882 patients, of whom only 3.2% used cannabis and only 9 patients had used cannabis within an hour of the heart attack. The 4.8 fold risk determination was therefore based on this tiny sample of 9 patients". We see this continual misuse of sources and data again and again in the cannabis literature, all to justify the drug war and the continuing persecution of cannabis users by the medical-prison-judicial-industrial-complex. It's bullshit, and I've called you out on it. You can call it a conspiracy all you want. The fact of the matter is, there are 19 million cannabis users in the US alone who aren't suffering from heart attacks or strokes, diseases which have a strong genetic risk factor. For some reason you can't explain, the emergency rooms and hospitals in the United States aren't filled with cannabis users suffering from heart disease and strokes. Can you explain that? Or will you just cite another debunked study pointing to a sample size of 9 patients who drank alcohol, smoked tobacco, and consumed caffeinated drinks, and whose genetic risk factors for heart attacks and strokes were not determined? Surely, the college campus clinics should be teeming with students having strokes and heart attacks? Why aren't they? Instead we see legal pharmaceutical drugs killing 23,000 people alone in 2010, while 26,000 died from legal alcohol in that year alone. Where are all the bodies of the dead cannabis users and why are you hiding them? Could it be that they don't exist and you are promoting propaganda? Viriditas (talk) 21:56, 12 March 2014 (UTC)

WP:SOAPBOX Wikipedia is not a soapbox. If you think the Sources don't meet WP:RS then provide an argument. If they conflict with the sources you find reliable that doesn't mean they are actually unreliable by wp:rs standards. There's room for pro-pot, anti-pot, and people who don't actually care to edit here if they follow wikipedia policy. There's no point in incivility.Serialjoepsycho (talk) 23:43, 12 March 2014 (UTC)

No, we don't know Marinol has killed people. All we have is a FIA document from the FDA stating that people who were taking Marinol died, but the cause of death is undetermined. Its a spontaneous reporting system. People come to the hospital, tell the nurse what drugs they are taking, and some of them die. If they are taking a legal drug, they likely tell their doctor and if the doctor thinks there is the slightest chance the drug played a role in the death, they report it to FDA. If the patient is taking illegal drugs, they probably don't tell the doctor. So those who die from cardiac arrest in the hour after smoking a doobie don't get reported to AERS. And since AERS is designed to capture side effects of Rx drugs, even if the doctor knew the patient was smoking pot an hour before having an MI, most wouldn't think to report it to FDA. Its not an FDA regulated drug.

We have several controlled studies saying that stroke and MI are increased in the aftermath of cannabis consumption. You ask why people aren't dropping like flies as if everyone in the country personally knowing several who died was the minimal threshold for demonstration of harm. Did you know anyone who died of a heart attack while taking Vioxx? It killed 25,000 in 10 years on the market. Do you know anyone who had a heart attack on Premarin? It was the biggest selling drug in the US for a decade, and probably killed 50,000 or so. Spread across a few million people, several thousand unecessary deaths a year are easy to miss. Up until the early 1960's, many cigarette ads featured physicians recommending an after dinner smoke to improve digestion. You don't have to have half the population dying each year to have a real problem. And you won't necessarily catch on without the type of epidemiological studies that I cited in the article.

Somebody is using this article to try to pump a product with very limited medical benefits and well-established risks as a cure-all. I'll be cleaning it up over the next few weeks to remove material that is not properly sourced with MEDRS compliant citations. Formerly 98 (talk) 23:54, 12 March 2014 (UTC)

In other words, you have no good evidence that cannabis causes these health problems, but you feel confident that adding weak associative studies based on small sample sizes and poorly controlled subjects is acceptable. I believe the MEDRS guideline says the opposite. Furthermore, I do know people who have died from the legal pharmaceutical drugs you've mentioned, some of them quite famous. However, I believe the legal settlement prevents people from talking about it, which is why you haven't heard much about it. Your argument from ignorance stinks. The fact that there is a well funded and organized effort to demonize cannabis is a documented fact, and the twisted data and contorted study results prove it. Viriditas (talk) 02:10, 13 March 2014 (UTC)

Just because a paper is nominally MEDRS compliant doesn't mean it is reliable or intelligent, let alone that it should be used. View the link that Viriditas posted in his "bunk" statement above. The study on MI risk centered on a mere 9 people for their big claim, and the authors of the stroke paper didn't do any of the work needed to prove it was cannabis and not any of the other drugs their subjects were taking. So really, these papers are no good for anything beyond the pointlessly generic statement "some potheads have had heart attacks and strokes". Just because they managed to get through peer review doesn't mean we have to accept their conclusions at face value. If we were reading multiple reviews of this work that supported the same conclusion, I might change my mind. As far as the FDA statement goes, most likely every drug in existence has been in the system of someone who recently had a heart attack and died. It's an issue so generic it's not worth reporting in an encyclopedia. Someguy1221 (talk) 02:31, 13 March 2014 (UTC)

I would be weary of using the FDA source if the other sources themselves are weak.Serialjoepsycho (talk) 05:04, 13 March 2014 (UTC)

Someguy, who is using the study from 2001 that viriditas addresed? The one I have linked to is from 2011. Viriditas dismissed all the studies by attacking one and his linked "debunking" only addressed one of the studies mentioned by Wolff while ignoring all other evidence they claim. If he focussed on backing up his claims which he has made rather than going on the offensive perhaps he would actually convince people. The papers I provided are highly cited, if they are highly cited, but poorly done, then the citation trail should show objections in the literature. This will not satisfy Viri, though, because he has claimed there is a conspiracy to exclude pro-cannabis studies. Second Quantization (talk) 09:24, 13 March 2014 (UTC)

Your very own 2011 paper is the one using the 2001 paper. That's where they got their data (they did not collect their own). The conclusions are overreaching in both cases. And I did read the studies. The 2011 work from the Lancet simply accepts the marijuana data at face value, and that data came from a rather small sample. It's a study of literally just 124 people who smoke pot and had heart attacks (incidentally 84 of them were tobacco addicts, 53 were obese, 37 had high blood pressure, and 15 had a history of chest pain). Their groundbreaking conclusion is based on the fact that 9 of these 124 individuals had their heart attack within one hour of smoking a joint (two of them were also snorting coke at the same time). All this speaks to is the fact that the investigators found a group of very unhealthy potheads, and some of them had heart attacks soon after smoking a joint. If these guys are anything like the potheads I knew in college, a significant chunk of the day is "soon after smoking a joint". This study is the sole basis of the claim you are attempting to cite from the 2011 paper. Someguy1221 (talk) 09:33, 13 March 2014 (UTC)

Someguy, I already know that the 2011 paper I have found cites the 2001 one. That is what I said. Read what I wrote. Now read the rest of it: " his linked "debunking" only addressed one of the studies mentioned by Wolff while ignoring all other evidence they claim". You have ignored that again and focussed on the one study and used your original research to try and debunk it. Saying that all the papers are just based on this is directly contradicted by what they say, the 2011 one for example is a study on 48 patients. Saying the Mittleman paper is "a study of literally just 124 people who smoke pot" is misleading. No it's not, it's a study of 3882 patients, 124 of which smoked cannabis. The significance of this effect is determined by statistical methods, not by ad-hoc reasoning (in part informed by your personal experiences about your friends) about what you think is significant. Second Quantization (talk) 10:28, 13 March 2014 (UTC)

The studies you cite are worthless. I can find dozens of hard cases showing the harm caused by meth, cocaine, heroin, alcohol, and tobacco, and I can visit every major hospital and pull people out of their beds and point to them and say, see, here's your proof. Meanwhile, there isn't a single person you can point to, not one, that is currently in a medical facility suffering from a stroke or heart problems caused by cannabis. But you'll continue to claim like a fundamentalist religious believer, that there are, and we should take your word for it because the study claims it might be possible. Yeah, and unicorns might be possible too. Are you practicing skepticism or religion here? Because you are spouting off theoretical religious belief, not science. Viriditas (talk) 10:56, 13 March 2014 (UTC)

Again with the rhetoric. The link between smoking and lung cancer was not uncovered immediately despite a rise in lung cancer in the 30s. There were no beds you could pull up and say, here's your definitive proof. Causal links are difficult to substantiate. It was uncovered through studies looking at the stats. I don't recall ever saying to take my word for anything, nor dictating what people should believe. Rather what I have done is highlight some well cited peer reviewed papers, and then endured a barrage of abuse from you instead of a polite discussion. I have no firm views on this topic and I am in favour of legalisation, but this perhaps does not fit with your ideology. Second Quantization (talk) 11:59, 13 March 2014 (UTC)

Unbelievable. You actually appear to be ignorant of the most demonstrable medical conspiracy of the 20th century, namely the tobacco conspiracy, which sought to promote industry-friendly medical "science" for 100 years while covering up and playing down the health consequences. The link between tobacco and cancer was first hypothesized as a carcinogen in 1898, with the first animal experiments finally producing demonstrable evidence for the link in the 1930s. The scientific consensus for lung cancer from tobacco first formed in the 1950s. Because of the constant "doubt is our product" propaganda from the tobacco industry, the public did not fully become cognizant of the risk until thirty years after the science was solid. And throughout this last century, tobacco industry funded studies appeared in peer-reviewed journals without proper disclosure, twisting and distorting the science at every possible level. Surely you must know this. Viriditas (talk) 12:15, 13 March 2014 (UTC)

It's actually kind of interesting that Second Quantization posted about this on WT:MED, because I remember seeing a bunch of news stories about how two men had died from marijuana. The stories are based on this study (note that the men apparently had underlying conditions, so it wasn't entirely caused by the marijuana; nevertheless, this demonstrates that its ability to increase peoples' heart rate is not entirely benign). Jinkinson talk to me 12:09, 13 March 2014 (UTC)

Debunked. You guys are just not on your game this week. "Cannabis has been known to cause death when laced with other substances, by triggering a heart condition or by causing respiratory cancers. But whether it can be directly lethal has remained unclear. A 2011 report from the UK Department of Health says no cases of fatal overdose have been associated with cannabis."[13] And yet, the guy who says cannabis killed these people admits they don't know how it could trigger arrhythmias and posits "unknown channelopathies that increase the risk of cardiac conditions triggered by the drug". Sounds like unicorns to me. Viriditas (talk) 12:24, 13 March 2014 (UTC)

Overdose is not the only way to die from something. Dying because cannabis smoke triggered your asthma is still dying "from cannabis use", but it's not an overdose. Dying from an allergic reaction is still dying, but not from an overdose. Dying because it slightly changes the viscosity of your blood, so you ended up with a stroke, is still dying from cannabis use. Overdose is a very specific pharmacological mechanism. Most people who die from tobacco and alcohol use don't die of overdoses, either. In fact, tobacco overdose from smoking is almost unheard of. WhatamIdoing (talk) 15:28, 13 March 2014 (UTC)

• Viriditas, I'm aware of the tobacco denialist claims. Why would you assume I'm not? But they aren't relevant to what I am saying. My point is that it was not a matter of pulling up beds and pointing at lung cancer victims. The studies and links took years of work: [14] and weren't trivially obvious. The consensus wasn't established till the 1950's. As far as I am aware the denialists did not subvert the scientific consensus except in the political arena. You have already acknowledged the peer reviewed literature is not favourable towards your position. You are cherry picking newspapers and blogs that agree with you and claiming that since the newspaper contains criticism it is inherently valid and automatically constitutes a debunking. This is exactly the same thing you have done before in other scientific topic areas. Second Quantization (talk) 12:31, 13 March 2014 (UTC)
  • You are gravely misinformed. The denialists not only subverted the scientific consensus, they fought it successfully in the halls of academia and in the peer reviewed journals. Proctor writes: "Tobacco industry sponsorship has been corrosive of honest intellectual inquiry on a scale that is difficult to comprehend. Tobacco expertise for many years was dominated by the industry...Entire scientific societies have been formed to sabotage the science showing harms of one kind or another, and several scientific journals owe their existence to the industry's need for "friendly research". The industry is not just corrupting academia; they are also creating it...collaboration with the tobacco industry is one of the most deadly abuses of scholarly integrity in modern history..." Viriditas (talk) 12:51, 13 March 2014 (UTC)

Viriditas, an internet news blog is not a suitable source for health related content on Wikipedia. See WP:MEDRS. You cannot use non-MEDRS sources to say that more reliable sources are false. What you are doing is cherry picking some sources which support your own opinion and ignoring the fact that they are terrible sources. Wikipedia follows the views published in reliable sources, not the opinions of editors. If you want to promote other views, suggest you find a platform other than Wikipedia to do it. Get it peer reviewed and published, or write a textbook chapter, otherwise your opinion does not hold any weight against these sources. This is a non-issue. Lesion (talk) 12:33, 13 March 2014 (UTC)

Actually, you are the one who needs to read MEDRS, since the use of sources here violates WP:MEDSCI. I have never once argued that an "internet news blog" should be used anywhere, I have merely shown that the claims that are being made are not only controversial, but disputed, and lack good evidence. Per WP:MEDSCI they should be removed immediately or qualified. There is absolutely no consensus that cannabis causes strokes or heart attacks. None. And you have conveniently ignored the very policy you came here to remind me about. I seem to know it better than you do. Viriditas (talk) 12:51, 13 March 2014 (UTC)

For those, such as Viriditas, who are looking for more details on the proposed mechanism by which cannabis could kill, I point you to this study, which states, "the possibility of a sudden increase in parasympathetic tone and parasympathetic activity may lead to an asystolic arrest which may be a cause of sudden death." Jinkinson talk to me 12:46, 13 March 2014 (UTC)

And there's absolutely no scientific consensus that cannabis causes such deaths, and there remains no evidence to support it. Per WP:MEDSCI, we should not be portraying it as undisputed fact as is being done here. Clearly, the real people cherry picking and promoting a singular POV are the ones who keep adding this material. Viriditas (talk) 12:51, 13 March 2014 (UTC)

I find it hard to believe that papers such as this one can adequately control for tobacco consumption. Despite this concern, this paper concludes: "cannabis-related stroke is not a myth, and a likely mechanism of stroke in most cannabis users is the presence of reversible MIS induced by this drug. The reality of the relationship between cannabis and stroke is, however, complex because other confounding factors have to be considered (ie, lifestyle and genetic factors)."

In any case, our task in Wikipedia is not to decide if the evidence supports a causal link, but to report the findings of reliable sources. Note that we should be referring to secondary sources such as review papers, not case series or letters that refute case series. Axl ¤ [Talk] 12:54, 13 March 2014 (UTC)

"... should be referring to secondary sources such as review papers", sounds good. Do you have any suggested secondary sources? Second Quantization (talk) 13:02, 13 March 2014 (UTC)

Agree with the above. Our role is to report the findings of reliable sources. "Reliable sources" is clearly defined by MEDRS. Arguing about whether results published in reliable sources are "valid", especially from within the context of conspiracy theories, is a valid topic for those who want to start their own blog, but is not within the scope of Wikipedia.

BTW, I cannot find any statement supporting the claim "Absorption is limited by serum lipids, which can become saturated with THC, mitigating toxicity" in the cited reference. In fact, the word "lipid" does not seem to appear within the cited doc. Unless someone can point out something I missed or provide an alternative MEDRS compliant reference, that statement needs to be removed from the article.

Formerly 98 (talk) 14:35, 13 March 2014 (UTC)

PMID 21353301, mentioned above, is a meta analysis, which is (by definition) a secondary source. In fact, it is a type of secondary source that MEDRS prizes highly. WhatamIdoing (talk) 15:28, 13 March 2014 (UTC)

The two papers that I mentioned (Desbois and Wolff) are suitable papers.

I have searched for suitable sources. Each paper seems to fall into one of two camps: "causal link shown", or "causal link possible".

Clear causal link

• Desbois
• Mallaret
• Jones
• Greydanus
• Singla
• Aryana
• Moussouttas
• Ghuran

Possible link

• Wolff
• Thomas
• Singh
• Thanvi
• Prescrire
• Grotenhermen

The papers that describe a causal link indicate that events are rare, and typically occur in people with pre-existing disease/risk factors. I did not find any papers that deny the possibility of a causal link. Axl ¤ [Talk] 15:07, 13 March 2014 (UTC)