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Summary sheet: Cannabis
Drawing of Cannabis sativa
Chemical Nomenclature
Common names Cannabis, THC, 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 2.5 - 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 THC, 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, visual disconnection, 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.

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]

Long-term cannabis use may be associated with negative cognitive effects such as brain fog, lowered motivation, difficulty learning, and inattention. These effects are typically reversible with tapered use and time off.[13]

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.[14]

The history of cannabis and its usage by humans dates back to at least the third millennium BC in written history, and possibly as far back as the Pre-Pottery Neolithic B (8800–6500 BCE) based on archaeological evidence. For millennia, the plant has been valued for its use for fiber and rope, as food and medicine, and for its psychoactive properties for religious and recreational use.

The earliest restrictions on cannabis were reported in the Islamic world by the 14th century. In the 19th century, it began to be restricted in colonial countries, often associated with racial and class stresses.

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.[6][7]

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.[16][17]


The word cannabis is from Greek κάνναβις (kánnabis) (see Latin cannabis), which was originally Scythian or Thracian.[18] It is related to the Persian kanab, the English canvas and possibly the English hemp (Old English hænep).[18]

Common names

Cannabis has numerous common and street names. The most common ones are: marijuana,[1] weed,[2] pot,[3] grass,[4] hemp,[5], ganja, THC.


Cannabis plants contain a number of different specific compounds at various ratios. Cannabis contains more than 460 compounds;[19] at least 80 of these are cannabinoids,[20][21] chemical compounds that interact with cannabinoid receptors in the brain.[22] The most common cannabinoids are listed below:


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

Phytocannabinoid ← phytocannabinoid acid

Quasi-psychedelic phytocannabinoids

  • Δ-8-THC. Psychoactive, but about half as potent as Δ-9-THC.
    • Decarboxylation: Δ-8-THCA → Δ-8-THC -- only trace amounts exist in cannabis
    • Chemical conversion: CBD + acid 8 h → 50% Δ-8-THC
  • Δ-9-THC (THC). Most abundant psychoactive component of cannabis. Is the standard when comparing THC analogs.
  • Δ-10-THC. Psychoactive, but less potent than Δ-8-THC.
    • Decarboxylation: Δ-10-THCA → Δ-10-THC-- only trace amounts exist in cannabis
    • Chemical conversion: CBD + acid
  • THCH (more info). 25 times more potent than THC.
    • Decarboxylation: THCHA → THCH -- only trace amounts exist in cannabis
    • Chemical conversion: CBDH + acid
  • THCP (more info). 30 times more potent than THC.
    • Biosynthesis: CBGPA → THCPA → THCP[23]
    • Decarboxylation: THCPA → THCP-- only trace amounts exist in cannabis
    • Chemical conversion: CBDP + acid

Quasi-psychedelic phytocannabinoids synthesized through chemical modification

  • AcO-THC (aka THC-O-acetate). 3-5 times more potent than THC.
    • Metabolization: THCAO is a prodrug, meaning it requires metabolization in order to take effect. It metabolically undergoes an activation process of converting to THC through de-acetylation, then THC continues into its own primary metabolites similarly to THC's oral route. Because of this, the onset when smoked can be significantly longer ranging from 20-45 minutes, but not as long as ingesting THC orally in comparison. THCAO through the oral route can also have longer onsets than oral THC due to its extra metabolic processes, with an onset of around 90 minutes.[24]
    • Decarboxylation: Lack of information on decarboxylation, but it can be inferred that it decarboxylates like its normal parent compound since research suggests that heating it at 340°C (644°F) unbinds the acetyl group, releasing toxic ketene gas.[25]
    • Chemical conversion: acetic anhydride + Δ-9-THC/Δ-8-THC → Δ-9-THCAO/Δ-8-THCAO, respectively.[26]

Non-quasi-psychedelic phytocannabinoids, some which can be synthesized to quasi-psychedelic cannabinoids with biosynthesis or chemical conversion (see above)

  • CBD
    • Biosynthesis: CBGA → CBDA → CBD[27]
    • Decarboxylation: CBDA → CBD
    • Chemical conversion: THC + iodine → CBD
  • CBDD
  • CBDH
  • CBDP
    • Biosynthesis: CBGPA → CBDPA → CBDP[28]
    • Decarboxylation: CBDPA → CBDP
  • CBG
    • Despite sounding a lot like THC, THCC is more similar to CBD than it is to THC
    • THCV is non-psychoactive.[29]


The most psychoactive cannabinoid found in the cannabis plant is tetrahydrocannabinol (or delta-9-tetrahydrocannabinol), commonly known as THC.[19] 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.[19] The most studied are THC, CBD and CBN.[30]

CYP2C9 genotype affects THC sensitivity significantly:

Subjects with the *3/*3 genotype had 3-fold higher THC levels in their blood than subjects with the *1/*1 genotype. Those subjects with one copy of each gene (*1/*3) had intermediate THC levels that were about 2-fold higher than subjects with *1/*1.[31]

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.[32] THC also potentiates the effects of the glycine receptors.[33] 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.[34] 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:

Dosage and preparation


"Our results showed an overall increase in potency of illicit cannabis, from approximately 10% in 2009 to approximately 14% in 2019. These results are in agreement with other potency monitoring programs in several European countries."[60]

Math to calculate the quantity needed weed: Desired THC from divided by the THC strength of the strain. For example, if you want to smoke 3 mg (a common dose) from cannabis with 12% THC:

3 mg / 12% = 3/0.12 = 25 mg

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. Because each strain has its own balance of cannabinoids, 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.

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).

Hypothetical phytocannabinoiod differences between C. indica and C. sativa

The effects of sativa may be used for a high, while indica may be used for its sedative effects. Both types are used as medical cannabis.

  • Cannabinoid ratios: On average, Cannabis indica has higher levels of THC compared to CBD, whereas Cannabis sativa has lower levels of THC to CBD.[61] However, huge variability exists within either species. A 2015 study shows the average THC content of the most popular herbal cannabis products in the Netherlands has decreased slightly since 2005.[62]
  • Terpene ratios: Sativa ancestry is associated with farnesene and [ergamotene, while Indica ancestry is associated with myrcene, elemene, and sesquiterpene alcohols.

In 2022, studies found that plants identified as "indica" or "sativa" based on common methods of differentiation (e.g. plant height or leaf shape) are not, in fact, chemically distinguishable, with many identified as "sativa" having cannabinoid ratios predicted of "indica" plants and vice versa. The authors have concluded that the chemical makeup of cannabis plants cannot be reliably determined by simple inspection of the plants' physical characteristics and that the "indica" and "sativa" labels are not informative as to the cannabinoids (or other chemical components) delivered.[63][64]


Common usage

Consumption methods

Cannabis is consumed in many different ways:[72]

  • 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.[73]
  • 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).[74]
  • 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).[75] 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.[76]
  • 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).
  • Tinctures vary from edibles, usually only containing extracted (and potent) THC in liquid form. Tinctures can be taken sublingually, or orally.
  • 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.[77] Oral doses of cannabis are more effective in reducing nausea and vomiting[78].

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.[79]

Toxicity and harm potential


Cannabis is common, and its tolerance is moderate, so intoxication can occur frequently. Frequent use of cannabis with more than 10% THC increased the risk of developing a psychotic disorder. 5% THC provides pain relief as well as intoxication.[80] We recommend you to dilute your cannabis product (see below).

Analysis of data from 901 patients showed that the use of high-potency cannabis (THC content ≥10%) was associated with a modestly increased risk of developing a psychotic disorder compared to never using cannabis.[81]

Street cannabis has an average THC content of 12%,[82] and medical cannabis products have more than 10% THC.[80] We recommend you to weigh and dilute cannabis buds, and hashish, with 3 times more, and 10 times more hemp respectively. Avoid mixing with tobacco to avoid nicotine: Stimulants should be used with caution in combination with [quasi-]psychedelics including cannabis.

Table from the 2010 ISCD study ranking various drugs (legal and illegal) based on statements by drug-harm experts. Cannabis was found to be the eighth overall most dangerous drug.[83]
Radar plot showing relative physical harm, social harm, and dependence of cannabis[84]

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.[85][86]

Cannabis arteritis (CA) is a very rare peripheral vascular disease similar to Buerger's disease.[87]

Cannabis use during brain development (including during pregnancy and adolescence) has been shown to interfere with a variety of neurobiological systems. Meta-analysis following ~5 weeks of abstinence reveals lasting changes in the central executive and default mode networks, which are involved in attention and working memory. The extent of these changes as risk factors is not entirely clear.[88]


A NIH study found that suicide risk is higher with marijuana users than non-users. [89]

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. [90]

Not only that, but another study studied the association between cannabis and suicidality also has correlation.[91]

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,[58] particularly in vulnerable individuals with risk factors for psychotic illnesses (like a past or family history of schizophrenia).[92][93][59]

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.[94] 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."[95]

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,[96] 2.594 mol/kg, about 815.7 grams of THC per kilogram of body weight,[97] and human deaths from overdose are unheard of.[98]

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[99] and in the worst case this can lead to death.[100]

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.[101]

Dependence on cannabis is more common amongst heavy users. Cannabis use can lead to increased tolerance[22][102] and withdrawal symptoms upon stopping usage.[30][103] 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.[104]

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.[105]

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.[106]

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.

  • 2C-T-x
  • 2C-x
  • 5-MeO-xxT
  • Amphetamines - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences
  • aMT
  • Cocaine - Stimulants increase anxiety levels and the risk of thought loops which can lead to negative experiences
  • DMT
  • DOx
  • Lithium - Lithium is commonly prescribed in the treatment of bipolar disorder; however, there is a large body of anecdotal evidence that suggests taking it with cannabinoids can significantly increase the risk of psychosis and seizures. As a result, this combination should be strictly avoided.
  • LSD
  • Mescaline
  • Mushrooms
  • 25x-NBOMe

Legal status

Legal status of cannabis possession for recreational use
  Legal or essentially legal
  Illegal but decriminalized
  Illegal but often unenforced
  No information

For table of countries, see Wikipedia's global cannabis legalization table.

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.[107][108]

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.[109]

See also

External links

Further reading


  1. 1.0 1.1 Marijuana (word), 2022 
  2. 2.0 2.1 Definition of WEED 
  3. 3.0 3.1 Definition of POT 
  4. 4.0 4.1 Definition of GRASS 
  5. 5.0 5.1 Definition of HEMP 
  6. 6.0 6.1 Erowid Cannabis Vault : Legal Status 
  7. 7.0 7.1 WDR-2010 
  8. Russo, E. B. (5 September 2013). Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. Routledge. ISBN 9781136614934. 
  9. El-Alfy, A. T., Ivey, K., Robinson, K., Ahmed, S., Radwan, M., Slade, D., Khan, I., ElSohly, M., Ross, S. (June 2010). "Antidepressant-like effect of Δ9-tetrahydrocannabinol and other cannabinoids isolated from Cannabis sativa L". Pharmacology, biochemistry, and behavior. 95 (4): 434–442. doi:10.1016/j.pbb.2010.03.004. ISSN 0091-3057. 
  10. Fusar-Poli, P., Crippa, J. A., Bhattacharyya, S., Borgwardt, S. J., Allen, P., Martin-Santos, R., Seal, M., Surguladze, S. A., O’Carrol, C., Atakan, Z., Zuardi, A. W., McGuire, P. K. (1 January 2009). "Distinct Effects of Δ9-Tetrahydrocannabinol and Cannabidiol on Neural Activation During Emotional Processing". Archives of General Psychiatry. 66 (1): 95. doi:10.1001/archgenpsychiatry.2008.519. ISSN 0003-990X. 
  11. Booth, M. (30 September 2011). Cannabis: A History. Random House. ISBN 9781409084891. 
  12. Clarke, P. B. (1986). Black paradise: the Rastafarian movement. New Religious Movements Series. Aquarian Pr. ISBN 9780850304282. 
  13. Kevin Hill, MD, and MD Michael Hsu. “Cognitive Effects in Midlife of Long-Term Cannabis Use.” Harvard Health, 14 June 2022,
  14. ElSohly, M. A., ed. (2007). Marijuana and the cannabinoids. Forensic science and medicine. Humana Press. ISBN 9781588294562. 
  16. ElSohly, M. A., Mehmedic, Z., Foster, S., Gon, C., Chandra, S., Church, J. C. (1 April 2016). "Changes in Cannabis Potency Over the Last 2 Decades (1995–2014): Analysis of Current Data in the United States". Biological Psychiatry. 79 (7): 613–619. doi:10.1016/j.biopsych.2016.01.004. ISSN 0006-3223. 
  17. ElSohly, M. A., Mehmedic, Z., Foster, S., Gon, C., Chandra, S., Church, J. C. (1 April 2016). "Changes in Cannabis Potency over the Last Two Decades (1995-2014) - Analysis of Current Data in the United States". Biological psychiatry. 79 (7): 613–619. doi:10.1016/j.biopsych.2016.01.004. ISSN 0006-3223. 
  18. 18.0 18.1 "Online Etymology Dictionary". Retrieved 17 February 2011. 
  19. 19.0 19.1 19.2 Ben Amar, M. (April 2006). "Cannabinoids in medicine: A review of their therapeutic potential". Journal of Ethnopharmacology. 105 (1–2): 1–25. doi:10.1016/j.jep.2006.02.001. ISSN 0378-8741. 
  20. Downer, E. J., Campbell, V. A. (5 August 2009). "Phytocannabinoids, CNS cells and development: A dead issue?: Phytocannabinoids have neurotoxic properties". Drug and Alcohol Review. 29 (1): 91–98. doi:10.1111/j.1465-3362.2009.00102.x. ISSN 0959-5236. 
  21. Burns, T. L., Ineck, J. R. (February 2006). "Cannabinoid Analgesia as a Potential New Therapeutic Option in the Treatment of Chronic Pain". Annals of Pharmacotherapy. 40 (2): 251–260. doi:10.1345/aph.1G217. ISSN 1060-0280. 
  22. 22.0 22.1 22.2 Borgelt, L. M., Franson, K. L., Nussbaum, A. M., Wang, G. S. (February 2013). "The Pharmacologic and Clinical Effects of Medical Cannabis". Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy. 33 (2): 195–209. doi:10.1002/phar.1187. ISSN 0277-0008. 
  24. Cooke, Justin (25 January 2022). "How Are Cannabinoids Metabolized? (CBD, THC, CBG, THC-O, & More)". DailyCBD. 
  29. Abioye, A; Ayodele, O; Marinkovic, A; Patidar, R; Akinwekomi, A; Sanyaolu, A (31 January 2020). "Δ9-Tetrahydrocannabivarin (THCV): a commentary on potential therapeutic benefit for the management of obesity and diabetes". Journal of cannabis research. 2 (1): 6. doi:10.1186/s42238-020-0016-7. PMC 7819335Freely accessible. PMID 33526143. 
  30. 30.0 30.1 Gordon, A. J., Conley, J. W., Gordon, J. M. (14 November 2013). "Medical Consequences of Marijuana Use: A Review of Current Literature". Current Psychiatry Reports. 15 (12): 419. doi:10.1007/s11920-013-0419-7. ISSN 1535-1645. 
  32. Cannabidiol is an allosteric modulator at mu- and delta-opioid receptors
  33. Hejazi, N., Zhou, C., Oz, M., Sun, H., Ye, J. H., Zhang, L. (1 March 2006). "Δ9-Tetrahydrocannabinol and Endogenous Cannabinoid Anandamide Directly Potentiate the Function of Glycine Receptors". Molecular Pharmacology. 69 (3): 991–997. doi:10.1124/mol.105.019174. ISSN 0026-895X. 
  34. Franklin, J. M., Carrasco, G. A. (March 2013). "Cannabinoid receptor agonists upregulate and enhance serotonin 2A (5-HT 2A ) receptor activity via ERK1/2 signaling". Synapse. 67 (3): 145–159. doi:10.1002/syn.21626. ISSN 0887-4476. 
  35. 35.0 35.1 35.2 35.3 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. 
  36. 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. 
  37. Mechoulam, R., ed. (1986). Cannabinoids as therapeutic agents. CRC Press. ISBN 9780849357725. 
  38. 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.
  39. An Overview Of Tetrahydrocannabivarin (THCV), 2013 
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