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Summary sheet: Cannabis
Drawing of Cannabis sativa
Chemical Nomenclature
Common names Cannabis, Marijuana, Weed, Pot, Mary Jane, Grass, Herb, Green, Bud, Tree. More names.
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold 0.4 mg (THC)
Light 0.4 - 2 mg (THC)
Common 2 - 4 mg (THC)
Strong 4 - 10 mg (THC)
Heavy 10 mg + (THC)
Total 2.3 - 5 hours
Onset 0.1 - 10 minutes
Come up 5 - 10 minutes
Peak 15 - 45 minutes
Offset 3 - 4 hours
After effects 45 - 180 minutes
Threshold 1 mg (THC)
Light 2.5 - 5 mg (THC)
Common 5 - 10 mg (THC)
Strong 10 - 25 mg (THC)
Heavy 25 mg + (THC)
Total 4 - 10 hours
Onset 20 - 60 minutes
Come up 30 - 60 minutes
Peak 1 - 2 hours
Offset 4 - 6 hours
After effects 6 - 12 hours

Total 3 - 7 hours
Onset 1 - 10 minutes
Come up 15 - 30 minutes
Peak 30 - 60 minutes
Offset 4 - 6 hours

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.


Cannabis (also known as marijuana,[1] weed,[2] pot,[3], grass,[4] hemp,[5] and many others) is a preparation of the cannabis plant that produces psychoactive effects when consumed (via smoking, vaporizing, or ingestion). It is the most used illicit substance in the world.[6][7] The mechanism of action is binding activity at cannabinoid receptors distributed throughout the body.[citation needed]

The principal psychoactive constituent of cannabis is tetrahydrocannabinol (THC), which makes up one of 483 known compounds in the plant,[8] including at least 84 other cannabinoids such as cannabidiol (CBD), cannabinol (CBN), tetrahydrocannabivarin (THCV),[9][10] and cannabigerol (CBG). At least three species are recognized: Cannabis sativa, Cannabis indica, and Cannabis ruderalis.[citation needed]

The earliest recorded uses of cannabis date from the 3rd millennium BC.[11] In modern times, cannabis is used for recreational or medicinal and religious or spiritual purposes.[12] It played a central role in the 1960s youth counterculture movement and is associated with the art and music of this era.[citation needed]

Subjective effects include sedation, appetite enhancement, immersion enhancement, creativity enhancement, increased sense of humor, increased music appreciation, and euphoria. The effects can vary widely depending on dose, strain & form, tolerance, and set and setting. Notably, it can either strongly suppress or enhance anxiety depending on the individual and situation.

Lower doses are associated with relaxing effects similar to a depressant. Higher doses are associated with mild-to-moderate hallucinogenic effects such as visual hallucinations, conceptual thinking and time distortion, as well as a greater risk of anxiety, paranoia, and delusions (generally more prevalent with sativa strains).

Cannabis is considered to have low to moderate abuse potential.[citation needed] Chronic use is associated with escalating tolerance and psychological dependence in some individuals.[citation needed] It has very low physical toxicity and is essentially impossible to physically overdose on. However, it is capable of exacerbating certain mental health symptoms like delusions or psychosis in predisposed individuals (see this section).[citation needed]

It is highly advised to use harm reduction practices if using this substance.

History and culture

The genus cannabis is indigenous to central Asia and the Indian subcontinent.[13] Tombs in China reveal humans were smoking cannabis 2500 years ago.[14]

Since the early 20th century, cannabis has been subject to legal restrictions with the possession, use, and sale of cannabis preparations containing psychoactive cannabinoids currently illegal in most countries. However, there is a recent growing trend towards decriminalization and legalization, with the sale of cannabis made legal in some US states and Canada.

In 2004, the U.N. estimated that global consumption patterns of cannabis indicated that approximately 4% of the adult world population (162 million people) used cannabis annually and that approximately 0.6% (22.5 million) of people used cannabis daily.[15] According to the United Nations, it is the most used illicit drug in the world.[16][17]

Potency trends

The potency of illicit cannabis plant material has consistently increased over time since 1995 from ~4% in 1995 to ~12% in 2014. The cannabidiol content has decreased on average from ~.28% in 2001 to <.15% in 2014, resulting in a change in the ratio of Δ9-tetrahydrocannabinol to cannabidiol from 14 times in 1995 to ~80 times in 2014.[18][19]


The word cannabis is from Greek κάνναβις (kánnabis) (see Latin cannabis),[20] which was originally Scythian or Thracian.[21] It is related to the Persian kanab, the English canvas and possibly the English hemp (Old English hænep).[21]

Common names

Cannabis has numerous common and street names. The most common ones are: marijuana,[22] weed,[23] pot,[24], grass,[25] hemp,[26], ganja.


Cannabis plants contain a number of different specific compounds at various ratios. Cannabis contains more than 460 compounds;[27] at least 80 of these are cannabinoids,[28][29] chemical compounds that interact with cannabinoid receptors in the brain.[30] The most common cannabinoids are listed below:


Upon heating, cannabinoid acids decarboxylate to give their psychoactive cannabinoid.

Phytocannabinoid ← acid

  • CBC (cannabichromene) ← CBCA (cannabichromenic acid)
  • CBCV (cannabichromevarin) ← CBCVA (cannabichromevarinic acid)
  • CBD (cannabidiol) ← CBDA (cannabidiolic acid)
  • CBDP (Cannabidiphorol) ← CBDPA (Cannabidiphorolic acid)
  • CBDV (cannabidivarin) ← CBDVA (cannabidivarinic acid)
  • CBE (cannabielsoin) ← CBEA (cannabielsoin acid)
  • CBG (cannabigerol) ← CBGA (cannabigerolic acid)
  • CBGM (cannabigerol monomethyl ether) ← CBGAM (cannabigerolic acid monomethyl ether)
  • CBGV (cannabigerovarin) ← CBGVA (cannabigerovarinic acid)
  • CBL (cannabicyclol) ← CBLA (cannabicyclolic acid)
  • CBN (cannabinol) ← CBNA (cannabinolic acid)
  • CBT (cannabicitran) ← CBTA (cannabicitranic acid)
  • CBV (cannabivarin) ← CBVA (cannabivarinic acid)
  • delta-8-THC (delta-8-tetrahydrocannabinol) ← delta-8-THCA (delta-8-tetrahydrocannabinolic acid)
  • THC (tetrahydrocannabinol) ← THCA (tetrahydrocannabinolic acid)
  • THCC (tetrahydrocannabiorcol) ← THCCA (tetrahydrocannabiorcolic acid)
  • THCP (tetrahydrocannabiphorol) ← THCPA (tetrahydrocannabiphorolic acid)
  • THCV (tetrahydrocannabivarin) ← THCVA (tetrahydrocannabivarinic acid)


The most psychoactive cannabinoid found in the cannabis plant is tetrahydrocannabinol (or delta-9-tetrahydrocannabinol), commonly known as THC.[31] Other cannabinoids include delta-8-tetrahydrocannabinol, cannabidiol (CBD), cannabinol (CBN), cannabicyclol (CBL), cannabichromene (CBC) and cannabigerol (CBG); they have less psychotropic effects than THC, but may play a role in the overall effect of cannabis.[32] The most studied are THC, CBD and CBN.[33]

The entourage effect is a proposed mechanism by which compounds present in cannabis which are largely non-psychoactive by themselves modulate the overall psychoactive effects of the plant (these resulting principally from the action of the main psychoactive component of cannabis, tetrahydrocannabinol (THC)).

THC appears to alter mood and cognition through its agonist actions on the CB1 receptors, which inhibit a secondary messenger system (adenylate cyclase) in a dose dependent manner. Via CB1 activation, THC indirectly increases dopamine release and produces psychotropic effects.

Cannabidiol acts as an allosteric modulator of the mu and delta opioid receptors.[34] THC also potentiates the effects of the glycine receptors.[35] However, the role of these interactions and how they result in the cannabis high remains subject to on-going scientific investigation.

Drugs that activate the CB1 and CB2 receptors are known to upregulate and enhance 5-HT2A receptor activity.[36] The ERK1/ERK2 signaling pathway has been shown to mediate this effect, but the exact biochemical mechanism is unknown. This upregulation and enhancement of the 5-HT2A receptor is why cannabis potentiates the effects of psychedelic drugs and can cause psychedelic effects in very high doses.

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects

Visual effects

Cognitive effects

Auditory effects

Multi-sensory effects

Combination effects

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:

Strains and forms


Types of cannabis

Sativa and indica are the two major types of cannabis plants which can mix together to create hybrid strains. Each strain has its own range of effects on the body and mind, resulting in a wide range of medicinal benefits.

Indica plants typically grow short and wide compared to sativa plants which grow tall and thin. Indica plants are better suited for indoor growing because of their short growth and sativa plants are better suited for outdoor growing because some strains can reach over 25 ft. in height.

The high produced from smoking indica bud is a strong physical "body high" that will make one sleepy or sedated and provides a deep relaxation feeling compared to a sativa high, which is known to be more energetic and uplifting.

Marijuana strains range from pure sativas to pure indicas with hybrid strains consisting of both indica and sativa (for example, 30% indica – 70% sativa, 50% – 50% combinations, or 80% indica – 20% sativa). Because sativa and indica buds have very different medicinal benefits and effects, certain strains can be targeted to better treat specific illnesses.


Common usage

Consumption methods

Cannabis is consumed in many different ways:[70]

  • Smoking typically involves inhaling vaporized cannabinoids ("smoke") from small pipes, bongs (portable versions of hookahs with water chamber), paper-wrapped joints, tobacco-leaf-wrapped blunts, and other items.[71]
  • Vaporizers heat herbal cannabis to 165–190 °C (329–374 °F), causing the active ingredients to evaporate into a vapor without burning the plant material (the boiling point of THC is 157 °C (315 °F) at 760 mmHg pressure).[72]
  • Cannabis tea contains relatively small concentrations of THC because THC is an oil (lipophilic) and is only slightly water-soluble (with a solubility of 2.8 mg per liter).[73] Cannabis tea is made by first adding a saturated fat to hot water (e.g., cream or any milk except skim) with a small amount of cannabis.[74]
  • Edibles are cannabis added as an ingredient to one of a variety of foods.
  • Sublingual/buccal consumption typically involves the absorption of cannabinoids through the membranes inside the mouth (usually through a candy or tincture).
  • Tincture
  • Topical consumption typically involves the use of either a cream or lip balm containing cannabinoids absorbed through the skin.

Preparation methods

Preparation methods for this compound within our tutorial index include:

Medical use

Cannabis is an emerging treatment option for those suffering from many serious diseases, including cancer. Due to its pain relieving, nausea suppressing effects, cannabis can be useful for those undergoing radiation therapy and chemotherapy.[75] Oral doses of cannabis are more effective in reducing nausea and vomiting[76].

In addition to the anti-nausea effects, the appetite enhancement effects of cannabis can combine with the antiemetic effects and make it more likely that the patient will gain or maintain weight through cancer treatment.[77]

Toxicity and harm potential


This toxicity and harm potential section is a stub.

As a result, it may contain incomplete or even dangerously wrong information! You can help by expanding upon or correcting it.
Note: Always conduct independent research and use harm reduction practices if using this substance.

Radar plot showing relative physical harm, social harm, and dependence of cannabis[78]

Despite its reputation for being a benign substance, it is important to be aware that cannabis use is associated with distinct risks. Acute adverse effects include anxiety, hyperemesis syndrome, impaired coordination and judgment, suicidal ideations/tendencies, and psychotic symptoms.

It is strongly advised to use harm reduction practices if using this substance.

Cannabinoid hyperemesis syndrome (CHS) is recurrent nausea, vomiting, and stomach cramp that sometimes occurs due to prolonged, high-dose cannabis use.[79][80]

Cannabis arteritis (CA) is a very rare peripheral vascular disease similar to Buerger's disease.[81]


A NIH study found that suicide risk is higher with marijuana users than non-users. [82]

On the other hand, the largest study as of 2018 in association with cannabis use and the risk of suicide, there was no found evidence between the two. This study shows that it is unlikely a risk factor for suicide, either directly or as a consequence of use. [83]

Not only that, but another study studied the association between cannabis and suicidality also has correlation.[84]

The main takeaway from these studies and more is that while suicide risk may be higher with people who use cannabis, cannabis is unlikely the cause or an additional significant factor.

Psychosis risk

The prolonged usage of THC and other cannabinoids may increase one's disposition to mental illness and psychosis,[85] particularly in vulnerable individuals with risk factors for psychotic illnesses (like a past or family history of schizophrenia).[86][87][88]

Individuals with a personal or family history of mental illness, particularly psychotic disorders like schizophrenia, should not use cannabis without the advice of a qualified mental health practitioner.

Lethal dosage

No fatal overdoses associated with cannabis use have been reported as of 2010.[89] A review published in the British Journal of Psychiatry in February 2001 said that "no deaths directly due to acute cannabis use have ever been reported."[90]

THC, the principal psychoactive constituent of the cannabis plant, has extremely low physiological toxicity and the amount that can enter the body through the consumption of cannabis plants poses no threat of death. In lab animal tests, scientists have had much difficulty administering a dose of THC that is high enough to be lethal. The dose of THC needed to kill 50% of tested rodents is very high,[91] 2.594 mol/kg, about 815.7 grams of THC per kilogram of body weight,[92] and human deaths from overdose are unheard of.[93]

At present, it is estimated that the LD50 of cannabis is around 1:20,000 or 1:40,000. This means that, in order to induce death, a cannabis smoker would have to consume 20,000 to 40,000 times as much cannabis as is contained in one cannabis cigarette. A user would theoretically have to smoke nearly 1,500 pounds of cannabis within about 15 minutes to induce a lethal response.

It is worth noting that the rare condition Cannabinoid Hyperemesis Syndrome (CHS) can cause ongoing nausea, vomiting and severe dehydration which can lead to renal failure[94] and in the worst case this can lead to death.[95]

Dependence and abuse potential

Cannabis is moderately habit-forming. Research has shown the overall dependence potential for cannabis to be less than that for caffeine, tobacco, alcohol, cocaine or heroin, but higher than that for psilocybin, mescaline, or LSD.[96]

Dependence on cannabis is more common amongst heavy users. Cannabis use can lead to increased tolerance[97][98] and withdrawal symptoms upon stopping usage.[99][100][101] Prolonged cannabis usage requires the user to consume higher doses of the substance to achieve a common desirable effect, and reinforce the body's metabolic systems for synthesizing and eliminating it more efficiently.[102]

Tolerance to many of the effects of cannabis develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 1 - 2 weeks for the tolerance to be reduced to half and 2 - 3 weeks to be back at baseline (in the absence of further consumption). THC has been detected in heavy cannabis users after 77 days of drug abstinence.[103]

Cannabis exhibits cross-tolerance with all cannabinoids, meaning that all cannabinoids will have a reduced effect for a period of time upon using cannabis. The mechanisms that create this tolerance to THC are thought to involve changes in cannabinoid receptor function.

One study found that about 1 in 10 users of cannabis may develop dependence characterized by the occurrence of a withdrawal syndrome after abstinence. This withdrawal syndrome was found to peak 2-3 days after quitting and is mostly complete by 1 week; however, sleep disturbances and vivid dreams may persist for 2-3 weeks.[104]

Dangerous interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

Legal status

Map showing cannabis laws worldwide
  Legal or essentially legal
  Illegal but decriminalized
  Illegal but often unenforced
  No information

United Nations

The legality of cannabis for medical and recreational use varies by country, in terms of its possession, distribution, and cultivation, and (in regards to medical) how it can be consumed and what medical conditions it can be used for. These policies in most countries are regulated by the United Nations Single Convention on Narcotic Drugs that was ratified in 1961, along with the 1971 Convention on Psychotropic Substances and the 1988 Convention against Illicit Traffic in Narcotic Drugs and Psychotropic Substances.[105][106]

Rescheduling proposals

The World Health Organization (WHO) is calling for whole-plant marijuana, as well as cannabis resin, to be removed from Schedule IV—the most restrictive category of a 1961 drug convention signed by countries from around the world.[107]

Sweden: Tetrahydrocannabinol is a controlled substance under the 1971 Convention on Psychotropic Substances[106]. However, it has been approved for medical use by the Swedish Medical Products Agency[108], in the form of an oral solution sold under the brand name Sativex.[109][110]

See also

External links

Further reading


  8. Ethan B Russo (2013). Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. Routledge. p. 28. ISBN 978-1-136-61493-4. |
  9. Antidepressant-like effect of ?9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L ( / NCBI) |
  10. Distinct Effects of ?9-Tetrahydrocannabinol and Cannabidiol on Neural Activation During Emotional Processing |
  11. Martin Booth (2003). Cannabis: A History. Transworld. p. 36. ISBN 978-1-4090-8489-1.
  12. Clarke, Peter B. (1986). Black Paradise: The Rastafarian Movement. New Religious Movements Series. Wellingborough: The Aquarian Press. ISBN 978-0-85030-428-2
  13. A. ElSohly, Mahmoud (2007). Marijuana and the Cannabinoids. Humana Press. p. 8. ISBN 1-58829-456-0. Retrieved 2 May 2011.
  20. "cannabis" OED Online. July 2009. Oxford University Press. 2009. [1]
  21. 21.0 21.1 "Online Etymology Dictionary". Retrieved 17 February 2011. 
  27. Cannabinoids in medicine: A review of their therapeutic potential |
  28. Phytocannabinoids, CNS cells and development: A dead issue? |
  29. Cannabinoid Analgesia as a Potential New Therapeutic Option in the Treatment of Chronic Pain |
  30. The Pharmacologic and Clinical Effects of Medical Cannabis |
  31. Cannabinoids in medicine: A review of their therapeutic potential |
  32. Cannabinoids in medicine: A review of their therapeutic potential |
  33. Medical Consequences of Marijuana Use: A Review of Current Literature |
  34. Cannabidiol is an allosteric modulator at mu- and delta-opioid receptors
  35. 9-Tetrahydrocannabinol and Endogenous Cannabinoid Anandamide Directly Potentiate the Function of Glycine Receptors |
  36. Franklin JM, Carrasco GA. Cannabinoid receptor agonists upregulate and enhance serotonin 2A (5-HT(2A)) receptor activity via ERK1/2 signaling. Synapse. 2012;67(3):145-59.
  37. 37.0 37.1 37.2 37.3 Robson, P. (2001). "Therapeutic aspects of cannabis and cannabinoids". The British Journal of Psychiatry. 178 (2): 107–115. doi:10.1192/bjp.178.2.107. ISSN 0007-1250. 
  38. Mechoulam, Raphael; Parker, Linda A.; Gallily, Ruth (2002). "Cannabidiol: An Overview of Some Pharmacological Aspects". The Journal of Clinical Pharmacology. 42 (S1): 11S–19S. doi:10.1002/j.1552-4604.2002.tb05998.x. ISSN 0091-2700. 
  39. Mechoulam, R. (1984). Cannabinoids as therapeutic agents. Boca Raton, FL: CRC Press. ISBN 0-8493-5772-1.
  40. Investigating the Neuroendocrine and Behavioral Controls of Cannabis-Induced Feeding Behavior. JF Davis, PQ Choi, J Kunze, P Wahl, Washington State University Pullman, WA, USA. Presented July 2018, Society for the Study of Ingestive Behavior, Bonita Springs, FL.
  41. Tetrahydrocannabivarin (THCV): A Cannabinoid Fighting Obesity |
  42. Wong, MM; Craun, EA; Bravo, AJ; Pearson, MR; Protective Strategies Study, Team. (August 2019). "Insomnia symptoms, cannabis protective behavioral strategies, and hazardous cannabis use among U.S. college students". Experimental and clinical psychopharmacology. 27 (4): 309–317. doi:10.1037/pha0000273. PMID 30907602. 
  43. The Pharmacologic and Clinical Effects of Medical Cannabis |;jsessionid=1E004D7B7E2B5CA792E75A6E83EEC59C.f03t01
  44. The Therapeutic Potential of Cannabis and Cannabinoids |
  45. Systematic Review and Meta-analysis of Cannabis Treatment for Chronic Pain |
  46. Cannabinoids for treatment of chronic non-cancer pain; a systematic review of randomized trials |
  47. Yazulla, S (September 2008). "Endocannabinoids in the retina: from marijuana to neuroprotection". Progress in retinal and eye research. 27 (5): 501–26. doi:10.1016/j.preteyeres.2008.07.002. PMID 18725316. 
  48. Charlotte Figi: The Girl Who is Changing Medical Marijuana Laws Across America |
  49. On the frontier of medical pot to treat boy's epilepsy |
  50. Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy ( / NCBI) |
  51. Cannabidiol displays antiepileptiform and antiseizure properties in vitro and in vivo. ( / NCBI) |
  52. An electrophysiological analysis of the anticonvulsant action of cannabidiol on limbic seizures in conscious rats. ( / NCBI) |
  53. Δ⁹-Tetrahydrocannabivarin suppresses in vitro epileptiform and in vivo seizure activity in adult rats. ( / NCBI) |
  54. Cannabinoids: Defending the Epileptic Brain ( / NCBI) |
  55. Is Marijuana an Effective Treatment for Glaucoma? |
  56. Cardiovascular Effects of Cannabis |
  58. Lac, A; Luk, JW (February 2018). "Testing the Amotivational Syndrome: Marijuana Use Longitudinally Predicts Lower Self-Efficacy Even After Controlling for Demographics, Personality, and Alcohol and Cigarette Use". Prevention science : the official journal of the Society for Prevention Research. 19 (2): 117–126. doi:10.1007/s11121-017-0811-3. PMID 28620722. 
  59. Feinberg, I., Jones, R, Walker JM, Cavness, C, March, J. (1975). Effects of high dosage delta-9-tetrahydrocannabinol on sleep patterns in man. Clin Parmacol Ther. 1975; 17(4):458-66.
  61. Causal association between cannabis and psychosis: examination of the evidence - The British Journal of Psychiatry Jan 2004, 184 (2) 110-117 |
  62. A Teenager With Agitation: Higher Than She Should Have Climbed - Pediatric Emergency Care: June 2010 - Volume 26 - Issue 6 - pp 462-465 |
  63. High Times in Ag Science: Marijuana More Potent Than Ever |
  66. EMCDDA (2008). "A cannabis reader: global issues and local experiences". Monograph Series. 8 (1).  European Monitoring Centre for Drugs and Drug Addiction, Lisbon, doi:10.2810/13807
  67. (PDF)  Missing or empty |title= (help)
  69. Gloss, D (October 2015). "An Overview of Products and Bias in Research". Neurotherapeutics. 12 (4): 731–4. doi:10.1007/s13311-015-0370-x. PMC 4604179Freely accessible. PMID 26202343. 
  70. The Cultural/Subcultural Contexts of Marijuana Use at the Turn of the Twenty-First Century |
  71. Allan Tasman; Jerald Kay; Jeffrey A. Lieberman; Michael B. First, Mario Maj (2011). Psychiatry. John Wiley & Sons. p. 9. ISBN 978-1-119-96540-4. |
  72. Cannabis and Cannabis Extracts: Greater Than the Sum of Their Parts? |
  73. Dronabinol |
  74. Marijuana medical handbook |
  76. "Antiemetic Effect of Delta-9-Tetrahydrocannabinol in Patients Receiving Cancer Chemotherapy" Stephen E. Sallan, M.D., Norman E. Zinberg, M.D., and Emil Frei, III, M.D. DOI: 10.1056/NEJM197510162931603
  77. American College of Physicians. Supporting Research into the Therapeutic Role of Marijuana. Philadelphia: American College of Physicians; 2008: Position Paper. (Available from American College of Physicians, 190 N. Independence Mall West, Philadelphia, PA19106.)
  78. Development of a rational scale to assess the harm of drugs of potential misuse (ScienceDirect) |
  79. Sorensen, Cecilia J.; DeSanto, Kristen; Borgelt, Laura; Phillips, Kristina T.; Monte, Andrew A. (20 December 2016). "Cannabinoid Hyperemesis Syndrome: Diagnosis, Pathophysiology, and Treatment—a Systematic Review". Journal of Medical Toxicology. 13 (1): 71–87. doi:10.1007/s13181-016-0595-z. PMC 5330965Freely accessible. PMID 28000146. 
  80. DeVuono, Marieka; Parker, Linda (2020). "Cannabinoid Hyperemesis Syndrome: A Review of Potential Mechanisms". Cannabis and Cannabinoid Research. 5: 132–144. doi:10.1089/can.2019.0059. 
  81. El Omri, N; Eljaoudi, R; Mekouar, F; Jira, M; Sekkach, Y; Amezyane, T; Ghafir, D (2017). "Cannabis arteritis". The Pan African medical journal. 26: 53. doi:10.11604/pamj.2017.26.53.11694. PMID 28451030. 
  85. Causal association between cannabis and psychosis: examination of the evidence - The British Journal of Psychiatry Jan 2004, 184 (2) 110-117 |
  86. Every-Palmer, S. Synthetic cannabinoid use and psychosis: an explorative study. Journal of Drug and Alcohol Dependence 2011.
  87. “Spice” Girls: Synthetic Cannabinoid Intoxication - The Journal of Emergency Medicine Volume 40, Issue 3, March 2011, Pages 296–299 (ScienceDirect) |
  88. A Teenager With Agitation: Higher Than She Should Have Climbed - Pediatric Emergency Care: June 2010 - Volume 26 - Issue 6 - pp 462-465 |
  89. Does cannabis use increase the risk of death? Systematic review of epidemiological evidence on adverse effects of cannabis use |
  90. Pharmacology and effects of cannabis: a brief review |
  91. Adverse effects of cannabis |
  93. Tetrahydrocannabinols in clinical and forensic toxicology ( / NCBI) |
  94. Cannabinoid Hyperemesis Syndrome |
  95. Cannabinoid Hyperemesis Syndrome: Reports of Fatal Cases |
  96. Lopez-Quintero C, Pérez de los Cobos J, Hasin DS, et al.: Probability and predictors of transition from first use to dependence on nicotine, alcohol, cannabis, and cocaine: results of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). Drug Alcohol Depend 2011; 115: 120–30 |
  97. The Pharmacologic and Clinical Effects of Medical Cannabis |
  98. The Effect of Cannabis Compared with Alcohol on Driving |
  99. Medical Consequences of Marijuana Use: A Review of Current Literature |
  100. State of the Art Treatments for Cannabis Dependence (ScienceDirect) |
  101. Cannabinoid tolerance and dependence |
  102. MARIJUANA AND MEDICINE Assessing the Science Base |
  104. Winstock AR, Ford C, Witton J. Assessment and management of cannabis use disorders in primary care. BMJ. 2010;340:c1571. PubMed doi:10.1136/bmj.c1571
  105. Habibi, Roojin; Hoffman, Steven J. (March 2018). "Legalizing Cannabis Violates the UN Drug Control Treaties, But Progressive Countries Like Canada Have Options". Ottawa Law Review. 49 (2). Retrieved 22 July 2018. 
  106. 106.0 106.1 Bewley-Taylor, David; Jelsma, Martin; Rolles, Steve; Walsh, John (June 2016). "Cannabis regulation and the UN drug treaties" (PDF). Retrieved 22 July 2018. 
  108. Sativex SPC. Sativex is approved for use in Sweden, Denmark, Canada, New Zealand, Spain, Germany and other EU countries.
  110. Sativex is prescribed for some adult patients with moderate to severe spasticity caused by multiple sclerosis, if other medications have proven to be insufficient in relieving the patient of symptoms.