Psychology Wiki

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)

Tetrahydrocannabinol chemical structure

IUPAC name
CAS number
ATC code


Chemical formula {{{chemical_formula}}}
Molecular weight 314.4636
Bioavailability 10–35% (inhalation), 6–20% (oral)[1]
Metabolism mostly hepatic by CYP2C[1]
Elimination half-life 1.6–59 h,[1] 25–36 h (orally administered dronabinol)
Excretion 65–80% (feces), 20–35% (urine) as acid metabolites[1]
Pregnancy category C
Legal status Schedule I and III (US)
Routes of administration orally, smoked (or vaporized)

Tetrahydrocannabinol (/ˌtɛtrəˌhdrɵkəˈnæbɨnɔːl/ Template:Respell or /ˌtɛtrəˌhdrɵkəˈnæbɨnɒl/ Template:Respell;[2] THC), or more precisely its main isomer (−)-trans-Δ9-tetrahydrocannabinol ((6aR,10aR)-delta-9-tetrahydrocannabinol), is the principal psychoactive constituent (or cannabinoid) of the cannabis plant. First isolated in 1964, in its pure form, by Israeli scientists Raphael Mechoulam, Yechiel Gaoni and colleagues at the Hebrew University of Jerusalem,[3][4][5] it is a glassy solid when cold, and becomes viscous and sticky if warmed. A pharmaceutical formulation of (−)-trans-Δ9-tetrahydrocannabinol, known by its INN dronabinol, is available by prescription in the U.S. and Canada under the brand name Marinol. An aromatic terpenoid, THC has a very low solubility in water, but good solubility in most organic solvents, specifically lipids and alcohols.[6]

Like most pharmacologically-active secondary metabolites of plants, THC in cannabis is assumed to be involved in self-defense, perhaps against herbivores.[7] THC also possesses high UV-B (280–315 nm) absorption properties, which, it has been speculated, could protect the plant from harmful UV radiation exposure.[8][9][10]

Tetrahydrocannabinol with double bond isomers and their stereoisomers is one of only three cannabinoids scheduled by Convention on Psychotropic Substances (the other two are dimethylheptylpyran and parahexyl). Note that cannabis as a plant is scheduled by Single Convention on Narcotic Drugs (Schedule I and IV).


The pharmacological actions of THC result from its partial agonist activity at the cannabinoid receptor CB1 (Ki=10nM[11]), located mainly in the central nervous system, and the CB2 receptor (Ki=24nM[12]), mainly expressed in cells of the immune system.[13] The psychoactive effects of THC are primarily mediated by its activation of CB1G-protein coupled receptors, which result in a decrease in the concentration of the second messenger molecule cAMP through inhibition of adenylate cyclase.[14]

The presence of these specialized cannabinoid receptors in the brain led researchers to the discovery of endocannabinoids, such as anandamide and 2-arachidonoyl glyceride (2-AG). THC targets receptors in a manner far less selective than endocannabinoid molecules released during retrograde signaling, as the drug has a relatively low cannabinoid receptor efficacy and affinity. In populations of low cannabinoid receptor density, THC may act to antagonize endogenous agonists that possess greater receptor efficacy.[15] THC is a lipophilic molecule and may bind non-specifically to a variety of receptors in the brain and body, such as adipose tissue. For a review of the mechanisms behind endocannabinoid synaptic transmission, see the endocannabinoid system.

Several studies have suggested that THC also has an anticholinesterase action[16][17] which may implicate it as a potential treatment for Alzheimer's and Myasthenia Gravis.


THC has mild to moderate analgesic effects, and cannabis can be used to treat pain by altering transmitter release on dorsal root ganglion of the spinal cord and in the periaqueductal gray.[14] Other effects include relaxation, alteration of visual, auditory, and olfactory senses, fatigue, and appetite stimulation. THC has marked antiemetic properties, and may also reduce aggression in certain subjects.[18]

Due to its partial agonistic activity, THC appears to result in greater downregulation of cannabinoid receptors than endocannabinoids, further limiting its efficacy over other cannabinoids. While tolerance may limit the maximal effects of certain drugs, evidence suggests that tolerance develops irregularly for different effects with greater resistance for primary over side-effects, and may actually serve to enhance the drug's therapeutic window.[15] However, this form of tolerance appears to be irregular throughout mouse brain areas and warrants future research.

THC reduces mouse male fertility in vivo, by inhibiting ATP production in sperm.[19]

THC, as well as other cannabinoids that contain a phenol group, possesses mild antioxidant activity sufficient to protect neurons against oxidative stress, such as that produced by glutamate-induced excitotoxicity.[13]

Appetite and taste

It has long been known that, in humans, cannabis increases appetite and consumption of food. The mechanism for appetite stimulation in subjects is believed to result from activity in the gastro-hypothalamic axis. CB1 activity in the hunger centers in the hypothalamus increases the palatability of food when levels of a hunger hormone ghrelin increase prior to consuming a meal. After chyme is passed into the duodenum, signaling hormones such as cholecystokinin and leptin are released, causing reduction in gastric emptying and transmission of satiety signals to the hypothalamus. Cannabinoid activity is reduced through the satiety signals induced by leptin release.

Based on the connection between palatable food and stimulation of dopamine (DA) transmission in the shell of the nucleus accumbens (NAc), it has been suggested that cannabis does not only stimulate taste, but possibly the hedonic value of food. A taste-reactivity paradigm in mice was used to investigate the influence of THC on DA release in the NAc upon application of sucrose or quinine solutions. THC application was found to enhance DA release in the NAc from sucrose, but not quinine, in a dose-dependent manner. This effect was enhanced with sweeter solution, which correlated with an increase the researchers' hedonic-behavior assessment as well. The mechanism behind this effect was elucidated by application of rimonabant, a CB1 receptor inverse agonist, known to reduce intake of food or sweet solutions. However, the same DA enhancement effect was not found upon repeated application of sucrose, suggesting that the DA response undergoes habituation.[20] The inconsistency between DA habituation and enduring appetite observed after THC application suggests that cannabis-induced appetite stimulation is not only mediated by enhanced pleasure from platable food, but through THC stimulation of another appetitive response as well.


The effects of the drug can be suppressed by the CB1 receptor antagonist rimonabant (SR141716A) as well as opioid receptor antagonists (opioid blockers) naloxone and naloxonazine.[21] The α7 nicotinic receptor antagonist methyllycaconitine can block self-administration of THC in rates comparable to the effects of varenicline on nicotine administration.[22]


7 double bond isomers and their 30 stereoisomers
Dibenzopyran numbering Monoterpenoid numbering Number of stereoisomers Natural occurrence Convention on Psychotropic Substances Schedule Structure
Short name Chiral centers Full name Short name Chiral centers
Δ6a,7-tetrahydrocannabinol 9 and 10a 8,9,10,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol Δ4-tetrahydrocannabinol 1 and 3 4 No Schedule I 150px
Δ7-tetrahydrocannabinol 6a, 9 and 10a 6a,9,10,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol Δ5-tetrahydrocannabinol 1, 3 and 4 8 No Schedule I 150px
Δ8-tetrahydrocannabinol 6a and 10a 6a,7,10,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol Δ6-tetrahydrocannabinol 3 and 4 4 Yes Schedule I 150px
Δ9,11-tetrahydrocannabinol 6a and 10a 6a,7,8,9,10,10a-hexahydro-6,6-dimethyl-9-methylene-3-pentyl-6H-dibenzo[b,d]pyran-1-ol Δ1,7-tetrahydrocannabinol 3 and 4 4 No Schedule I 150px
Δ9-tetrahydrocannabinol 6a and 10a 6a,7,8,10a-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol Δ1-tetrahydrocannabinol 3 and 4 4 Yes Schedule II 150px
Δ10-tetrahydrocannabinol 6a and 9 6a,7,8,9-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol Δ2-tetrahydrocannabinol 1 and 4 4 No Schedule I 150px
Δ6a,10a-tetrahydrocannabinol 9 7,8,9,10-tetrahydro-6,6,9-trimethyl-3-pentyl-6H-dibenzo[b,d]pyran-1-ol Δ3-tetrahydrocannabinol 1 2 No Schedule I 150px
4 stereoisomers of Δ9-tetrahydrocannabinol
Names Description Natural occurrence Structure
(−)-trans-Δ9-tetrahydrocannabinol (6aR,10aR)-Δ9-tetrahydrocannabinol levorotary trans Yes 150px
(−)-cis-Δ9-tetrahydrocannabinol (6aS,10aR)-Δ9-tetrahydrocannabinol levorotary cis Yes 150px
(+)-trans-Δ9-tetrahydrocannabinol (6aS,10aS)-Δ9-tetrahydrocannabinol dextrorotary trans No 150px
(+)-cis-Δ9-tetrahydrocannabinol (6aR,10aS)-Δ9-tetrahydrocannabinol dextrorotary cis No 150px

Note that 6H-dibenzo[b,d]pyran-1-ol is the same as 6H-benzo[c]chromen-1-ol.

See also: Cannabidiol#Isomerism, John C. Leffingwell Chirality & Bioactivity I.: Pharmacology, 2003.


3D rendering of the THC molecule

File:White widow.jpg

A hybrid Cannabis strain (White Widow) flower coated with trichomes, which contain more THC than any other part of the plant

File:Trichomes on a Cannabis Sativa Flower.jpg

Closeup of THC-filled trichomes on a Cannabis sativa leaf

There has never been a documented human fatality solely from overdosing on tetrahydrocannabinol or cannabis in its natural form,[23] though the synthetic THC pill "Marinol" was cited by the FDA as being responsible for 4 deaths between January 1, 1997 and June 30, 2005.[24] Information about THC's toxicity is primarily based on results from animal studies. The toxicity depends on the route of administration and the laboratory animal. Absorption is limited by serum lipids, which can become saturated with THC, mitigating toxicity.[25]


The discovery of THC was first described in "Isolation, structure and partial synthesis of an active constituent of hashish", published in the Journal of the American Chemical Society in 1964.[3] Research was also published in the academic journal Science, with "Marijuana chemistry" by Raphael Mechoulam in June 1970,[26] followed by "Chemical basis of hashish activity" in August 1970.[27] In the latter, the team of researchers from Hebrew University Pharmacy School and Tel Aviv University Medical School experimented on monkeys to isolate the active compounds in hashish. Their results provided evidence that, except for tetrahydrocannabinol, no other major active compounds were present in hashish.

Studies in humans

Evidence suggests that THC helps alleviate symptoms suffered both by AIDS patients, and by cancer patients undergoing chemotherapy, by increasing appetite and decreasing nausea.[28][29][30][31] It has also been shown to assist some glaucoma patients by reducing pressure within the eye, and is used in the form of cannabis by a number of multiple sclerosis patients, who use it to alleviate neuropathic pain and spasticity. The National Multiple Sclerosis Society is currently supporting further research into these uses.[32] Studies in humans have been limited by federal and state laws criminalizing marijuana.

In August 2009 a phase IV clinical trial by the Hadassah Medical Center in Jerusalem, Israel started to investigate the effects of THC on post-traumatic stress disorders.[33]

Dronabinol's usefulness as a treatment for Tourette syndrome cannot be determined until/unless longer controlled studies on larger samples are undertaken.[34][35][36]

Research on THC has shown that the cannabinoid receptors are responsible for mediated inhibition of dopamine release in the retina.[37]

In a 1981 double-blind, placebo-controlled study, oral THC was given to Multiple Sclerosis patients. A decrease in spasticity was shown when compared with placebo.[38] In a 1983 single-blind, placebo-controlled study, decreased tremor occurred in 1/4 of Multiple Sclerosis patients.[39]

Several studies have been conducted with spinal injury patients and THC. Decreased tremor occurred in 2/5 patients in a 1986 double-blind, placebo-controlled crossover study.[40] THC was shown to decrease spasticity and pain in a 1990 double-blind, placebo-controlled study.[41]

Studies in animals and in vitro

There is evidence to suggest THC can prevent Alzheimer's Disease in an animal model by preventing the inflammation caused by microglia cells which are activated by binding of amyloid protein.[42]

In 2006, researchers from Scripps Research Institute, using both computer modeling and biochemical assays, found THC "may provide an improved therapeutic for Alzheimer's disease" that would treat "both the symptoms and progression" of the disease. THC, they found, inhibits the formation of amyloid plaque (the primary marker for Alzheimer's disease). The authors concluded that their research offered "convincing evidence that THC possesses remarkable inhibitory qualities."[43] THC was found to be "considerably more effective" than two of the leading Alzheimer's drugs on the market, donepezil and tacrine.[44]

THC may also be an effective cancer treatment, with studies showing tumor size reduction in mice conducted in 1975[45] and 2007,[46] as well as in a pilot study in humans with glioblastoma multiforme (a type of brain cancer).[47] THC has also been found to attenuate conditioned retching and sickness, experimentally verifying anecdotal reports that THC alleviates nausea and vomiting when undergoing chemotherapy.[48]

A two-year study in which rats and mice were force-fed tetrahydrocannabinol dissolved in corn oil showed reduced body mass, enhanced survival rates, and decreased tumor incidences in several sites, mainly organs under hormonal control. It also caused testicular atrophy and uterine and ovarian hypoplasia, as well as hyperactivity and convulsions immediately after administration, of which the onset and frequency were dose related.[49]

Research in rats indicates that THC prevents hydroperoxide-induced oxidative damage as well as or better than other antioxidants in a chemical (Fenton reaction) system and neuronal cultures.[50] In mice low doses of Δ9-THC reduces the progression of atherosclerosis.[51]

Research has also shown that past claims of brain damage from cannabis use fail to hold up to the scientific method.[52] Instead, recent studies with synthetic cannabinoids show that activation of CB1 receptors can facilitate neurogenesis,[53] as well as neuroprotection,[54] and can even help prevent natural neural degradation from neurodegenerative diseases such as MS, Parkinson's, and Alzheimer's. This, along with research into the CB2 receptor (throughout the immune system), has given the case for medical marijuana more support.[55][56] THC is both a CB1 and CB2 agonist.[57]

Scientific studies indicating side-effects

Conceivable long-term ill effects of THC on humans are disputed but not improbable, yet its status as an illegal drug in most countries can make research difficult, for instance in the United States where the National Institute on Drug Abuse was the only legal source of cannabis for researchers until it recently became legalized in Colorado and Washington.[58]

Some studies claim a variety of negative effects associated with long-term use, including short-term memory loss.[59][60] Using positron emission tomography (PET), one study reports altered memory-related brain function (23% better memory for the cannabis users in recalling the end of a list of things to remember, but 19% worse memory for cannabis users in recalling the middle of a list of things to remember) in chronic daily cannabis users.[61]

Some studies have suggested that cannabis 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.[62] Other studies have made similar associations, especially in individuals predisposed to psychosis prior to cannabis use.[63] A 2005 paper from the Dunedin study suggested an increased risk in the development of psychosis linked to polymorphisms in the COMT gene.[64] However, a more recent study cast doubt on the proposed connection between this gene and the effects of cannabis on the development of psychosis.[65]

A 2008 German review reported that cannabis was a causal factor in some cases of schizophrenia and stressed the need for better education among the public due to increasingly relaxed access to cannabis.[66] Though cannabis use has increased dramatically in several countries over the past few decades, the rates of psychosis and schizophrenia have not generally increased, casting some doubt over whether the drug can cause cases that would not otherwise have occurred.[67]

Conversely, research from 2007 reported a correlation between cannabis use and increased cognitive function in schizophrenic patients.[68]

A 2008 National Institutes of Health study of 19 chronic heavy marijuana users with cardiac and cerebral abnormalities (averaging 28g to 272g (1 to 9+ oz) weekly) and 24 controls found elevated levels of apolipoprotein C-III (apoC-III) in the chronic smokers.[69] An increase in apoC-III levels induces the development of hypertriglyceridemia.

A 2008 study by the University of Melbourne of 15 heavy marijuana users (consuming at least 5 marijuana cigarettes daily for on average 20 years) and 16 controls found an average size difference for the smokers in the hippocampus (12 percent smaller) and the amygdala (7 percent smaller).[70] It has been suggested that such effects can be reversed with long term abstinence.[71]

A 2008 study at Karolinska Institute suggested that young rats treated with THC received an increased motivation for drug use, heroin in the study, under conditions of stress.[72][73]

A study of around 1000 people in New Zealand found that starting cannabis below the age of 18, when the brain is undergoing major development, induces a 8 point IQ drop on average. This effect was not fully reverted after stopping cannabis use. However, starting cannabis older seems to be safer.[74]

Opinions and statistical observations indicating side-effects

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."[75] In other words, THC and other active substances of cannabis may accentuate symptoms in people already predisposed, but likely don't cause psychotic disorders on their own. However, a French review from 2009 came to a conclusion that cannabis use, particularly that before age 15, was a factor in the development of schizophrenic disorders.[76]

A 2009 study found that there was a high prevalence of cannabis in the toxicological analysis of homicide (22%) and suicide victims (11%) in Australia.[77] In a similar study from Sweden it was also found that suicide victims had a significantly higher use of cannabis, but the authors found that "this was explained by markers of psychological and behavioral problems."[78]


File:THC biosynthesis.png

Biosynthesis of THC

In the cannabis plant, THC occurs mainly as tetrahydrocannabinolic acid (THCA, 2-COOH-THC). Geranyl pyrophosphate and olivetolic acid react, catalysed by an enzyme to produce cannabigerolic acid,[79] which is cyclized by the enzyme THC acid synthase to give THCA. Over time, or when heated, THCA is decarboxylated producing THC. The pathway for THCA biosynthesis is similar to that which produces the bitter acid humulone in hops.[80][81]

Natural occurrence

Main article: Medical_cannabis#Difference between C. indica and C. sativa

Cannabis indica may have a CBD:THC ratio 4–5 times that of Cannabis sativa.


THC is metabolized mainly to 11-OH-THC by the body. This metabolite is still psychoactive and is further oxidized to 11-nor-9-carboxy-THC (THC-COOH). In humans and animals, more than 100 metabolites could be identified, but 11-OH-THC and THC-COOH are the dominating metabolites. Metabolism occurs mainly in the liver by cytochrome P450 enzymes CYP2C9, CYP2C19, and CYP3A4.[82] More than 55% of THC is excreted in the feces and ~20% in the urine. The main metabolite in urine is the ester of glucuronic acid and THC-COOH and free THC-COOH. In the feces, mainly 11-OH-THC was detected.[83]

Detection in body fluids

THC, 11-OH-THC and THC-COOH can be detected and quantitated in blood, urine, hair, oral fluid or sweat using a combination of immunoassay and chromatographic techniques as part of a drug use testing program or in a forensic investigation of a traffic or other criminal offense or suspicious death.[84][85][86]


Dronabinol is the INN for a pure isomer of THC, (–)-trans9-tetrahydrocannabinol, which is the main isomer found in cannabis.[87] It is sold as Marinol (a registered trademark of Solvay Pharmaceuticals). Dronabinol is also marketed, sold, and distributed by PAR Pharmaceutical Companies under the terms of a license and distribution agreement with SVC pharma LP, an affiliate of Rhodes Technologies. Synthesized THC may be generally referred to as dronabinol. It is available as a prescription drug (under Marinol[88]) in several countries including the United States and Germany. In the United States, Marinol is a Schedule III drug, available by prescription, considered to be non-narcotic and to have a low risk of physical or mental dependence. Efforts to get cannabis rescheduled as analogous to Marinol have not succeeded thus far, though a 2002 petition has been accepted by the DEA. As a result of the rescheduling of Marinol from Schedule II to Schedule III, refills are now permitted for this substance. Marinol has been approved by the U.S. Food and Drug Administration (FDA) in the treatment of anorexia in AIDS patients, as well as for refractory nausea and vomiting of patients undergoing chemotherapy, which can remain in the body for up to 5 years, which has raised much controversy as to why natural THC is still a schedule I drug.[89]

An analog of dronabinol, nabilone, is available commercially in Canada under the trade name Cesamet, manufactured by Valeant Pharmaceuticals. Cesamet has also received FDA approval and began marketing in the U.S. in 2006; it is a Schedule II drug.[citation needed]

In April 2005, Canadian authorities approved the marketing of Sativex, a mouth spray for multiple sclerosis patients, who can use it to alleviate neuropathic pain and spasticity. Sativex contains tetrahydrocannabinol together with cannabidiol and is a preparation of whole cannabis rather than individual cannabinoids. It is marketed in Canada by GW Pharmaceuticals, being the first cannabis-based prescription drug in the world (in modern times). In addition, Sativex received European regulatory approval in 2010.[90]

Comparisons to medical marijuana

Main article: Medical marijuana

While there has never been a documented human fatality from overdosing on tetrahydrocannabinol or cannabis in its natural form,[91] Marinol can lead to death.[92]

Female cannabis plants contain more than 60 cannabinoids, including cannabidiol (CBD), thought to be the major anticonvulsant that helps multiple sclerosis patients;[93] and cannabichromene (CBC), an anti-inflammatory which may contribute to the pain-killing effect of cannabis.[94]

It takes over one hour for Marinol to reach full systemic effect,[95] compared to seconds or minutes for smoked or vaporized cannabis.[96] Some patients accustomed to inhaling just enough cannabis smoke to manage symptoms have complained of too-intense intoxication from Marinol's predetermined dosages. Many patients have said that Marinol produces a more acute psychedelic effect than cannabis, and it has been speculated that this disparity can be explained by the moderating effect of the many non-THC cannabinoids present in cannabis. For that reason, alternative THC-containing medications based on botanical extracts of the cannabis plant such as nabiximols are being developed. Mark Kleiman, director of the Drug Policy Analysis Program at UCLA's School of Public Affairs said of Marinol, "It wasn't any fun and made the user feel bad, so it could be approved without any fear that it would penetrate the recreational market, and then used as a club with which to beat back the advocates of whole cannabis as a medicine.".[97] United States federal law currently registers dronabinol as a Schedule III controlled substance, but all other cannabinoids remain Schedule I, excepting synthetics like nabilone.[98]

Regulatory history

Since at least 1986, the trend has been for THC in general, and especially the Marinol preparation, to be downgraded to less and less stringently-controlled schedules of controlled substances, in the U.S. and throughout the rest of the world.

On July 13, 1986, the Drug Enforcement Administration (DEA) issued a Final Rule and Statement of Policy authorizing the "Rescheduling of Synthetic Dronabinol in Sesame Oil and Encapsulated in Soft Gelatin Capsules From Schedule I to Schedule II" (DEA 51 FR 17476-78). This permitted medical use of Marinol, albeit with the severe restrictions associated with Schedule II status. For instance, refills of Marinol prescriptions were not permitted. At its 1045th meeting, on April 29, 1991, the Commission on Narcotic Drugs, in accordance with article 2, paragraphs 5 and 6, of the Convention on Psychotropic Substances, decided that Δ9-tetrahydrocannabinol (also referred to as Δ9-THC) and its stereochemical variants should be transferred from Schedule I to Schedule II of that Convention. This released Marinol from the restrictions imposed by Article 7 of the Convention (See also United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic Substances).[citation needed]

An article published in the April–June 1998 issue of the Journal of Psychoactive Drugs found that "Healthcare professionals have detected no indication of scrip-chasing or doctor-shopping among the patients for whom they have prescribed dronabinol". The authors state that Marinol has a low potential for abuse.[99]

In 1999, Marinol was rescheduled from Schedule II to III of the Controlled Substances Act, reflecting a finding that THC had a potential for abuse less than that of cocaine and heroin. This rescheduling constituted part of the argument for a 2002 petition for removal of cannabis from Schedule I of the Controlled Substances Act, in which petitioner Jon Gettman noted, "Cannabis is a natural source of dronabinol (THC), the ingredient of Marinol, a Schedule III drug. There are no grounds to schedule cannabis in a more restrictive schedule than Marinol".[100]

At its 33rd meeting, in 2003, the World Health Organization Expert Committee on Drug Dependence recommended transferring THC to Schedule IV of the Convention, citing its medical uses and low abuse potential.[101]

See also



  1. 1.0 1.1 1.2 1.3 Grotenhermen F (2003). Pharmacokinetics and pharmacodynamics of cannabinoids. Clin Pharmacokinet 42 (4): 327–60.
  2. Dictionary Reference: tetrahydrocannabinol: /ˌtɛtrəˌhdrəkəˈnæbəˌnɔːl/, /-ˌnɒl/
  3. 3.0 3.1 (1964). Isolation, structure and partial synthesis of an active constituent of hashish. Journal of the American Chemical Society 86 (8): 1646–1647.
  4. Interview with the winner of the first ECNP Lifetime Achievement Award: Raphael Mechoulam, Israel February 2007
  5. (2007). Cannabinoids: A Secret History. Chemical Heritage Newsmagazine 25 (2).
  6. Garrett, Edward R., C. Anthony Hunt (July 1974). Physicochemical properties, solubility, and protein binding of Δ9 -tetrahydrocannabinol. J. Pharm. Sci. 63 (7): 1056–64.
  7. Pate, David W. (1994). Chemical ecology of Cannabis. Journal of the International Hemp Association 1 (29): 32–37.
  8. Pate, David W. (1983). Possible role of ultraviolet radiation in evolution of Cannabis chemotypes. Economic Botany 37 (4): 396–405.
  9. (1987). Photochemical decomposition of cannabidiol in its resin base. Phytochemistry 26 (4): 1216–1217.
  10. (1987). UV-B radiation effects on photosynthesis, growth and cannabinoid production of two Cannabis sativa chemotypes. Photochemistry and Photobiology 46 (2): 201–206.
  11. PDSP Database - UNC. URL accessed on 11 June 2013.
  12. PDSP Database - UNC. URL accessed on 11 June 2013.
  13. 13.0 13.1 PMID 16570099 (PMID 16570099)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  14. 14.0 14.1 PMID 11316486 (PMID 11316486)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  15. 15.0 15.1 PMID 17828291 (PMID 17828291)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  16. Brown, Hugh (1972). Possible anticholinesterase-like effects of trans(−)δ8 and -δ9tetrahydrocannabinol as observed in the general motor activity of mice. Psychopharmacologia 27 (2): 111–6.
  17. Eubanks, Lisa M., et al. (2006). A Molecular Link Between the Active Component of Marijuana and Alzheimer's Disease Pathology. Molecular Pharmaceutics 3 (6): 773–7.
  18. Hoaken (2003). Drugs of abuse and the elicitation of human aggressive behavior. Addictive Behaviors 28: 1533–1554.
  19. PMID 21615727 (PMID 21615727)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  20. PMID 22063718 (PMID 22063718)
    Citation will be completed automatically in a few minutes. Jump the queue or expand by hand
  21. (2004). Marijuana and cannabinoid regulation of brain reward circuits. British Journal of Pharmacology 143 (2): 227–34.
  22. Solinas, M., et al. (2007). Nicotinic 7 Receptors as a New Target for Treatment of Cannabis Abuse. Journal of Neuroscience 27 (21): 5615–20.
  23. (2002). Cannabinoid analgesia. Pharmacology & Therapeutics 95 (2): 127–35.
  24. Deaths from Marijuana v. 17 FDA-Approved Drugs. (PDF) URL accessed on 2011-02-03.
  25. Erowid Cannabis Vault : THC Material Safety Data Sheet. URL accessed on 2011-04-20.
  26. (1970). Marihuana Chemistry. Science 168 (3936): 1159–1165.
  27. (1970). Chemical Basis of Hashish Activity. Science 169 (3945): 611–612.
  28. Cannabis and Cannabinoids – National Cancer Institute
  29. Haney M (2007). Dronabinol and marijuana in HIV-positive marijuana smokers. Caloric intake, mood, and sleep. Journal of Acquired Immune Deficiency Syndromes 45 (5): 545–54.
  30. Abrams DI, Hilton JF, Leiser RJ, Shade SB, Elbeik TA, Aweeka FT, Benowitz NL, Bredt BM, Kosel B, Aberg JA, Deeks SG, Mitchell TF, Mulligan K, Bacchetti P, McCune JM, Schambelan M. (2003). Short-term effects of cannabinoids in patients with HIV-1 infection: a randomized, placebo-controlled clinical trial. Annals of Internal Medicine 139 (4): 258–66.
  31. Grotenhermen, Franjo (2002). "Review of Therapeutic Effects" Cannabis and Cannabinoids: Pharmacology, Toxicology and Therapeutic Potential, New York City: Haworth Press.
  32. Marijuana (Cannabis). National Multiple Sclerosis Society. URL accessed on 2009-09-05.
  33. NCT00965809
  34. Müller-Vahl, K. R., et al. (2002). Treatment of Tourette's Syndrome with Δ9-Tetrahydrocannabinol (THC): A Randomized Crossover Trial. Pharmacopsychiatry 35 (2): 57–61.
  35. Muller-Vahl, Kirsten R., et al. (2003). Delta 9-Tetrahydrocannabinol (THC) is Effective in the Treatment of Tics in Tourette Syndrome. The Journal of Clinical Psychiatry 64 (4): 459–65.
  36. Müller-Vahl, Kirsten R., et al. (2003). Treatment of Tourette Syndrome with Delta-9-Tetrahydrocannabinol (Δ9-THC): No Influence on Neuropsychological Performance. Neuropsychopharmacology 28 (2): 384–8.
  37. (1996). Cannabinoid receptor-mediated inhibition of dopamine release in the retina. Naunyn-Schmiedeberg's archives of pharmacology 354 (6): 791–5.
  38. Petro, DJ, Ellenberg C. (1981). Treatment of human spasticity with delta-9 tetrahydrocannabinol.. Journal of Clinical Pharmacology 36: 189–261.
  39. Clifford, DB (1983). Tetrahydrocannabinol for tremor in multiple sclerosis.. Annals of Neurology 13(6): 669–671.
  40. Hannigan, WC, Destree R, Truong XT. (1986). The effect of delta-9-THC on human spasticity. Clinical Pharmacology and Therapeutics 39: 198.
  41. HMaurer, M, Henn V, Dittrich A, Hofmann A. (1990). Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double-blind trial.. European Archives of Psychiatry and Clinical Neuroscience. 240: 1–4.
  42. Ramirez, B. G., et al. (2005). Prevention of Alzheimer's Disease Pathology by Cannabinoids: Neuroprotection Mediated by Blockade of Microglial Activation. Journal of Neuroscience 25 (8): 1904–13.
  43. Eubanks, Lisa M., et al. (2006). A Molecular Link Between the Active Component of Marijuana and Alzheimer's Disease Pathology. Molecular Pharmaceutics 3 (6): 773–7.
  44. News Release
  45. Munson, AE, et al. (1975). Antineoplastic activity of cannabinoids. Journal of the National Cancer Institute 55 (3): 597–602.
  46. (2007). Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 27 (3): 339–46.
  47. Guzmán, M, et al. (2006). A pilot clinical study of Δ9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme. British Journal of Cancer 95 (2): 197–203.
  48. Kemp, Stephen W.P. (2001). The effect of detla-9-tetrahydrocannabinol (THC) on lithium-induced sickness reactions in both rats (Rattus norvegicus) and the house musk shrew (Suncus murinus) (M.A. thesis) Wilfrid Laurier University
  49. Chan, P, et al. (1996). Toxicity and Carcinogenicity of Δ9-Tetrahydrocannabinol in Fischer Rats and B6C3F1 Mice. Fundamental and Applied Toxicology 30 (1): 109–17.
  50. (1998). Cannabidiol and (−)Δ9-tetrahydrocannabinol are neuroprotective antioxidants. Proceedings of the National Academy of Sciences 95 (14): 8268–73.
  51. Steffens, Sabine, et al. (2005). Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice. Nature 434 (7034): 782–6.
  52. Grant, Igor et al. (2003). Non-acute (residual) neurocognitive effects of cannabis use: A meta-analytic study. Journal of the International Neuropsychological Society 9 (5).
  53. Jiang, W., et al. (2005). Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects. Journal of Clinical Investigation 115 (11): 3104–3116.
  54. (2005). Cannabinoids: Between Neuroprotection and Neurotoxicity. Current Drug Targets - CNS & Neurological Disorders 4 (6): 677–684.
  55. Correa, Fernando, et al. (2005). The Role of Cannabinoid System on Immune Modulation: Therapeutic Implications on CNS Inflammation. Mini Reviews in Medicinal Chemistry 5 (7): 671–675.
  56. Fernández-Ruiz, Javier, et al. (2007). Cannabinoid CB2 receptor: a new target for controlling neural cell survival?. Trends in Pharmacological Sciences 28 (1): 39–45.
  57. Pertwee, Roger G (2010). Cannabinoid Receptor Ligands. Tocris. URL accessed on 2011-04-20.
  58. Medical Marijuana
  59. (2009). Does cannabis use affect prospective memory in young adults?. Journal of Psychopharmacology 24 (2): 241–6.
  60. Indlekofer, F, et al. (2008). Reduced memory and attention performance in a population-based sample of young adults with a moderate lifetime use of cannabis, ecstasy and alcohol. Journal of Psychopharmacology 23 (5): 495–509.
  61. Block, R, et al. (2002). Effects of frequent marijuana use on memory-related regional cerebral blood flow. Pharmacology Biochemistry and Behavior 72: 237–50.
  62. Moore, Theresa HM, et al. (2007). Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. The Lancet 370 (9584): 319–28.
  63. Henquet, C., et al. (2005). Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. BMJ 330 (7481): 11–0.
  64. Caspi, A, et al. (2005). Moderation of the Effect of Adolescent-Onset Cannabis Use on Adult Psychosis by a Functional Polymorphism in the Catechol-O-Methyltransferase Gene: Longitudinal Evidence of a Gene X Environment Interaction. Biological Psychiatry 57 (10): 1117–27.
  65. Zammit, S., et al. (2007). Genotype effects of CHRNA7, CNR1 and COMT in schizophrenia: interactions with tobacco and cannabis use. The British Journal of Psychiatry 191 (5): 402–7.
  66. (2008). Cannabis and Schizophrenia: new findings in an old debate. Neuropsychiatrie : Klinik, Diagnostik, Therapie und Rehabilitation : Organ der Gesellschaft Osterreichischer Nervenarzte und Psychiater 22 (4): 223–9.
  67. Degenhardt L, Hall W, Lynskey M (2001). Comorbidity between cannabis use and psychosis: Modelling some possible relationships (PDF), Sydney: National Drug and Alcohol Research Centre. URL accessed 2006-08-19.
  68. (2007). The neuropsychological correlates of cannabis use in schizophrenia: Lifetime abuse/dependence, frequency of use, and recency of use. Schizophrenia Research 96 (1–3): 169–184.
  69. Jayanthi, S, et al. (2008). Heavy marijuana users show increased serum apolipoprotein C-III levels: evidence from proteomic analyses. Molecular Psychiatry 15 (1): 101–112.
  70. Yucel, M., et al. (2008). Regional Brain Abnormalities Associated With Long-term Heavy Cannabis Use. Archives of General Psychiatry 65 (6): 694–701.
  71. (2006). Marijuana use is associated with a reorganized visual-attention network and cerebellar hypoactivation. Brain 129 (5): 1096–1112.
  72. Ellgren, Maria (9 February 2007). Neurobiological effects of early life cannabis exposure in relation to the gateway hypothesis (in English and Swedish).Template:Page needed
  73. (2006). Adolescent Cannabis Exposure Alters Opiate Intake and Opioid Limbic Neuronal Populations in Adult Rats. Neuropsychopharmacology 32 (3): 607–615.
  74. BBC News - Young cannabis smokers run risk of lower IQ, report claims
  75. (2004). Causal association between cannabis and psychosis: examination of the evidence. The British Journal of Psychiatry 184 (2): 110–117.
  76. (2009). Le cannabis est-il un facteur de vulnérabilité des troubles schizophrènes ?. Archives de Pédiatrie 16 (9): 1302–5.
  77. (2009). Drugs and violent death: comparative toxicology of homicide and non-substance toxicity suicide victims. Addiction 104 (6): 1000–1005.
  78. Price, C., et al. (2009). Cannabis and suicide: longitudinal study. The British Journal of Psychiatry 195 (6): 492–497.
  79. (1998). Prenylation of olivetolate by a hemp transferase yields cannabigerolic acid, the precursor of tetrahydrocannabinol. FEBS Letters 427 (2): 283–5.
  80. Marks, M. D., et al. (2009). Identification of candidate genes affecting Δ9-tetrahydrocannabinol biosynthesis in Cannabis sativa. Journal of Experimental Botany 60 (13): 3715–26.
  81. Baker PB, Taylor BJ, Gough TA. (Jun 1981). The tetrahydrocannabinol and tetrahydrocannabinolic acid content of cannabis products. J Pharm Pharmacol. 33 (6): 369–72.
  82. Watanabe K, Yamaori S, Funahashi T, Kimura T, Yamamoto I (March 2007). Cytochrome P450 enzymes involved in the metabolism of tetrahydrocannabinols and cannabinol by human hepatic microsomes. Life Science 80 (15): 1415–9.
  83. (2005). Pharmacokinetics and Metabolism of the Plant Cannabinoids, Δ9-Tetrahydrocannibinol, Cannabidiol and Cannabinol. Cannabinoids 168 (168): 657–90.
  84. Schwilke, E. W., et al. (2009). Δ9-Tetrahydrocannabinol (THC), 11-Hydroxy-THC, and 11-Nor-9-carboxy-THC Plasma Pharmacokinetics during and after Continuous High-Dose Oral THC. Clinical Chemistry 55 (12): 2180–2189.
  85. Röhrich, J, et al. (2010). Concentrations of Δ9-Tetrahydrocannabinol and 11-Nor-9-Carboxytetrahydrocannabinol in Blood and Urine After Passive Exposure to Cannabis Smoke in a Coffee Shop. Journal of Analytical Toxicology 34 (4): 196–203.
  86. (2011) Disposition of Toxic Drugs and Chemicals in Man, 9th, 1644–8, Seal Beach, CA: Biomedical Publications.
  87. List of psychotropic substances under international control. (PDF) URL accessed on 2011-04-20.Template:Page needed
  88. Marinol - the Legal Medical Use for the Marijuana Plant. Drug Enforcement Administration. URL accessed on 2011-04-20.
  89. Eustice, Carol Medicinal Marijuana: A Continuing Controversy. URL accessed on 2011-04-20.
  90. Sativex Oromucosal Spray. URL accessed on 2012-02-01.
  91. - Pharmacology & Therapeutics - Cannabinoid analgesia
  93. Pickens, JT (1981). Sedative activity of cannabis in relation to its delta'-trans-tetrahydrocannabinol and cannabidiol content. British Journal of Pharmacology 72 (4): 649–56.
  94. (2006). Cannabinoid Analgesia as a Potential New Therapeutic Option in the Treatment of Chronic Pain. Annals of Pharmacotherapy 40 (2): 251–260.
  95. MARINOL (dronabinol) capsule drug label/data at Daily Med from U.S. National Library of Medicine, National Institutes of Health.
  96. McKim, William A (2002). Drugs and Behavior: An Introduction to Behavioral Pharmacology, 5th, Prentice Hall.
  97. includeonly>Greenberg, Gary. "Respectable Reefer", Mother Jones, 2005-11-01. Retrieved on 8 April 2010.
  98. Government eases restrictions on pot derivative | Online Athens
  99. (1998). Abuse potential of dronabinol (Marinol). Journal of Psychoactive Drugs 30 (2): 187–96.Template:Better source
  100. Petition to Reschedule Cannabis (Marijuana). Coalition for Rescheduling Cannabis.Template:Better source
  101. WHO Expert Committee on Drug Dependence.

Further reading

External links

Cannabinoids edit

{Anandamide} {CBD} {CBDV} {CBN} {CBV} {CP 55,940} {HU-210} {Nabilone} {Rimonabant} {THC} {THCV} {WIN 55,212-2} {URB597}

Template:Cannabis Template:Drug use Template:Euphoriants

[edit]Psychedelic tryptamines

α,N,N-TMT, 2,N,N-TMT, 5,N,N-TMT, 4-Acetoxy-DMT 4-Acetoxy-DET, 4-Acetoxy-DIPT, 4-HO-5-MeO-DMT, α-ET, α-MT, Baeocystin, Bufotenin, DET, DIPT, DMT, DPT, EIPT, Ethocin, Ethocybin, Miprocin, Iprocin, MET, MIPT, 5-Me-MIPT 5-MeO-α-ET, 5-MeO-α-MT, 5-MeO-DALT, 5-MeO-DET, 5-MeO-DIPT, 5-MeO-DMT, 5-MeO-DPT, 5-MeO-MIPT, 5-MeO-2,N,N-TMT, Norbaeocystin, Psilocin, Psilocybin


Template:Antiemetics and antinauseants Template:Orexigenics Template:Ancient anaesthesia-footer

This page uses Creative Commons Licensed content from Wikipedia (view authors).