This is an unofficial archive of PsychonautWiki as of 2025-08-11T15:14:44Z. Content on this page may be outdated, incomplete, or inaccurate. Please refer to the original page for the most up-to-date information.
[[File:Cannabis Plant.jpg|250px|thumbnail|right|A flowering [[cannabis]] plant, the most common source of cannabinoids.]]
[[File:Cannabis Plant.jpg|250px|thumbnail|right|A flowering [[cannabis]] plant, the most common source of cannabinoids.]]
[[File:USMC-100201-M-3762C-001.jpg|250px|thumbnail|right|A bag of Spice brand herbal incense. This contains [[Synthetic cannabinoid|synthetic cannabinoids]] which produce a similar effect to that of [[cannabis]].]]
[[File:USMC-100201-M-3762C-001.jpg|250px|thumbnail|right|A bag of Spice brand herbal incense. This contains [[Synthetic cannabinoid|synthetic cannabinoids]] which produce a similar effect to that of [[cannabis]].]]
'''Cannabinoids''' are a class of diverse chemical compounds that act on cannabinoid receptors on cells that repress neurotransmitter release in the brain. These receptor proteins include the endocannabinoids (produced naturally in the body by humans and animals),<ref>The endocannabinoid system as an emerging target of pharmacotherapy (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/16968947</ref> the phytocannabinoids (found in [[cannabis]] and some other plants), and [[synthetic cannabinoids]] (manufactured chemically). The most notable cannabinoid is the phytocannabinoid [[∆9-tetrahydrocannabinol]] (THC), the primary psychoactive compound of cannabis.<ref>The endocannabinoid system: drug targets, lead compounds, and potential therapeutic applications (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/16078824</ref><ref>Pertwee, Roger, ed. (2005). Cannabinoids. Springer-Verlag. p. 2. ISBN 3-540-22565-X.</ref> Cannabidiol (CBD) is another major constituent of the plant, representing up to 40% in extracts of the plant resin.<ref>http://www.unodc.org/unodc/en/data-and-analysis/bulletin/bulletin_1962-01-01_3_page005.html</ref> There are at least 85 different cannabinoids isolated from cannabis which exhibit varied effects.<ref>http://www.unodc.org/unodc/en/data-and-analysis/bulletin/bulletin_1962-01-01_3_page005.html</ref>
A '''cannabinoid''' is one of a class of diverse chemical compounds that act on cannabinoid receptors on cells that alter neurotransmitter functioning in the brain. These receptor proteins include the endocannabinoids (produced naturally in the body by humans and animals),<ref name="Pacher2006">{{cite journal | vauthors=((Pacher, P.)), ((Bátkai, S.)), ((Kunos, G.)) | journal=Pharmacological Reviews | title=The endocannabinoid system as an emerging target of pharmacotherapy | volume=58 | issue=3 | pages=389–462 | date= September 2006 | issn=0031-6997 | doi=10.1124/pr.58.3.2}}</ref> the phytocannabinoids (found in [[cannabis]] and some other plants), and [[synthetic cannabinoids]] (manufactured chemically).
Synthetic cannabinoids encompass a variety of distinct chemical classes: the classical cannabinoids structurally related to [[THC]]; the nonclassical cannabinoids (cannabimimetics) including the aminoalkylindoles, 1,5-diarylpyrazoles, quinolines, and arylsulphonamides; and eicosanoids related to the endocannabinoids.<ref>The endocannabinoid system: drug targets, lead compounds, and potential therapeutic applications (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/16078824</ref><ref>Pertwee, Roger, ed. (2005). Cannabinoids. Springer-Verlag. p. 2. ISBN 3-540-22565-X.</ref>
The most notable cannabinoid is the phytocannabinoid [[∆9-tetrahydrocannabinol]] (THC), the primary psychoactive compound of cannabis.<ref name="Lambert2005">{{cite journal | vauthors=((Lambert, D. M.)), ((Fowler, C. J.)) | journal=Journal of Medicinal Chemistry | title=The endocannabinoid system: drug targets, lead compounds, and potential therapeutic applications | volume=48 | issue=16 | pages=5059–5087 | date=11 August 2005 | issn=0022-2623 | doi=10.1021/jm058183t}}
</ref><ref name="Abood2005">{{cite book | veditors=((Abood, M. E.)), ((Pertwee, R. G.)) | date= 2005 | title=Cannabinoids | publisher=Springer | series=Handbook of experimental pharmacology | isbn=9783540225652}}</ref> Cannabidiol (CBD) is another major constituent of the plant, representing up to 40% in extracts of the plant resin.<ref>{{Citation | title=UNODC - Bulletin on Narcotics - 1962 Issue 3 - 004 | url=//www.unodc.org/unodc/en/data-and-analysis/bulletin/bulletin_1962-01-01_3_page005.html}}</ref> There are at least 85 different cannabinoids isolated from cannabis which exhibit varied effects.
Synthetic cannabinoids encompass a variety of distinct chemical classes: the classical cannabinoids structurally related to [[THC]]; the nonclassical cannabinoids (cannabimimetics) including the aminoalkylindoles, 1,5-diarylpyrazoles, quinolines, and arylsulphonamides; and eicosanoids related to the endocannabinoids.<ref name="Lambert2005"/><ref name="Abood2005"/>
==Cannabinoid receptors==
==Cannabinoid receptors==
Before the 1980s, it was often speculated that cannabinoids produced their physiological and behavioral effects via nonspecific interactions instead of interacting with specific receptors directly. The discovery of the first cannabinoid receptors in the 1980s helped to resolve this debate. These receptors are common in animals and have been found in mammals, birds, fish, and reptiles. At present, there are two known types of cannabinoid receptors, termed CB1 and CB2,<ref>The endocannabinoid system as an emerging target of pharmacotherapy (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/16968947</ref> with mounting evidence of more.<ref>Evidence for novel cannabinoid receptors | The human brain has more cannabinoid receptors than any other G protein-coupled receptor (GPCR) type.</ref><ref>Boron, Walter F.; Boulpaep, Emile L., eds. (2009). Medical Physiology: A Cellular and Molecular Approach. Saunders. p. 331. ISBN 978-1-4160-3115-4. </ref> However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
Before the 1980s, it was often speculated that cannabinoids produced their physiological and behavioral effects via nonspecific interactions instead of interacting with specific receptors directly. The discovery of the first cannabinoid receptors in the 1980s helped to resolve this debate. These receptors are common in animals and have been found in mammals, birds, fish, and reptiles. At present, there are two known types of cannabinoid receptors, termed CB1 and CB2,<ref name="Pacher2006"/> with mounting evidence of more.<ref>{{cite journal | vauthors=((Begg, M.)), ((Pacher, P.)), ((Batkai, S.)), ((Oseihyiaman, D.)), ((Offertaler, L.)), ((Mo, F.)), ((Liu, J.)), ((Kunos, G.)) | journal=Pharmacology & Therapeutics | title=Evidence for novel cannabinoid receptors | volume=106 | issue=2 | pages=133–145 | date= May 2005 | url=https://linkinghub.elsevier.com/retrieve/pii/S0163725804002013 | issn=01637258 | doi=10.1016/j.pharmthera.2004.11.005}}</ref><ref>{{cite book | veditors=((Boron, W. F.)), ((Boulpaep, E. L.)) | date= 2009 | title=Medical physiology: a cellular and molecular approach | publisher=Saunders/Elsevier | edition=2nd ed., International ed | isbn=9781416031154}}</ref> However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
===Cannabinoid receptor type 1===
===Cannabinoid receptor type 1===
CB1 receptors are found primarily in the brain, more specifically in the basal ganglia and in the limbic system (including the hippocampus).<ref>The endocannabinoid system as an emerging target of pharmacotherapy (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/16968947 </ref> They are also found in the cerebellum and in both male and female reproductive systems. CB1 receptors are absent in the medulla oblongata, the part of the brain stem responsible for respiratory and cardiovascular functions. Thus, there is not the risk of respiratory or cardiovascular failure that can be produced by some drugs. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis. However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
CB1 receptors are found primarily in the brain, more specifically in the basal ganglia and in the limbic system (including the hippocampus).<ref name="Pacher2006"/> They are also found in the cerebellum and in both male and female reproductive systems. CB1 receptors are absent in the medulla oblongata, the part of the brain stem responsible for respiratory and cardiovascular functions. Thus, there is not the risk of respiratory or cardiovascular failure that can be produced by some drugs. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis. However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
===Cannabinoid receptor type 2===
===Cannabinoid receptor type 2===
CB2 receptors are predominantly found in the immune system, or immune-derived cells<ref>Is lipid signaling through cannabinoid 2 receptors part of a protective system? (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/21295074</ref> with the greatest density in the spleen. While found only in the peripheral nervous system, a report does indicate that CB2 is expressed by a subpopulation of microglia in the human cerebellum.<ref>Cannabinoid CB2 receptors are expressed by perivascular microglial cells in the human brain: an immunohistochemical study (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/15266552</ref> CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.<ref>Is lipid signaling through cannabinoid 2 receptors part of a protective system? (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/21295074</ref> However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
CB2 receptors are predominantly found in the immune system, or immune-derived cells<ref name="Pacher2011">{{cite journal | vauthors=((Pacher, P.)), ((Mechoulam, R.)) | journal=Progress in Lipid Research | title=Is lipid signaling through cannabinoid 2 receptors part of a protective system? | volume=50 | issue=2 | pages=193–211 | date= April 2011 | issn=1873-2194 | doi=10.1016/j.plipres.2011.01.001}}</ref> with the greatest density in the spleen. While found only in the peripheral nervous system, a report does indicate that CB2 is expressed by a subpopulation of microglia in the human cerebellum.<ref>{{cite journal | vauthors=((Núñez, E.)), ((Benito, C.)), ((Pazos, M. R.)), ((Barbachano, A.)), ((Fajardo, O.)), ((González, S.)), ((Tolón, R. M.)), ((Romero, J.)) | journal=Synapse (New York, N.Y.) | title=Cannabinoid CB2 receptors are expressed by perivascular microglial cells in the human brain: an immunohistochemical study | volume=53 | issue=4 | pages=208–213 | date=15 September 2004 | issn=0887-4476 | doi=10.1002/syn.20050}}</ref> CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.<ref name="Pacher2011"/> However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
==Subjective effects==
==Subjective effects==
The effects listed below are based upon the [[subjective effects index]] and personal experiences of [[PsychonautWiki]] [[Special:TopUsers|contributors]]. The listed effects will rarely (if ever) occur all at once, but heavier dosages will increase the chances and are more likely to induce a full range of effects.
{{Preamble/SubjectiveEffects}}
===Physical effects===
{{effects/base
|{{effects/physical|
*'''[[Sedation|Sedation]]''' - Although certain strains of cannabinoids present mild encouraged [[Stimulation|stimulation]] at low to moderate doses, for the most part the effects on the user's energy levels are primarily sedating. This encourages one to relax, but can, however, be suppressed by simply forcing oneself to engage in physical activities.
*'''[[Sedation|Sedation]]''' - Although certain strains of cannabinoids present mild encouraged [[Stimulation|stimulation]] at low to moderate doses, for the most part the effects on the user's energy levels are primarily sedating. This encourages one to relax, but can, however, be suppressed by simply forcing oneself to engage in physical activities.
*'''[[Motor control loss|Motor control loss]]''' - This substance causes a partial to moderate suppression of motor control which intensifies proportional to dosage but rarely results in a complete inability to walk and perform basic movements.
*'''[[Motor control loss|Motor control loss]]''' - These substances cause a partial to moderate suppression of motor control which intensifies proportional to dosage but rarely results in a complete inability to walk and perform basic movements.
*'''[[Appetite enhancement|Appetite enhancement]]''' - The feeling of increased appetite following the use of cannabinoids has been documented for hundreds of years<ref>Mechoulam, R. (1984). Cannabinoids as therapeutic agents. Boca Raton, FL: CRC Press. ISBN 0-8493-5772-1.</ref> and is known colloquially as "the munchies" in popular American and United Kingdom culture. Clinical studies and survey data have found that cannabis increases food enjoyment and interest in food.<ref>How Marijuana Works | http://science.howstuffworks.com/marijuana4.htm</ref> This is thought to be due to the way in which endocannabinoids in the hypothalamus activate cannabinoid receptors that are responsible for maintaining food intake.<ref>How Marijuana Works | http://science.howstuffworks.com/marijuana4.htm</ref>
*'''[[Appetite enhancement|Appetite enhancement]]''' - The feeling of increased appetite following the use of cannabinoids has been documented for hundreds of years<ref>{{cite book | veditors=((Mechoulam, R.)) | date= 1986 | title=Cannabinoids as therapeutic agents | publisher=CRC Press | isbn=9780849357725}}</ref> and is known colloquially as "the munchies" in popular American and United Kingdom culture. Clinical studies and survey data have found that cannabis increases food enjoyment and interest in food.<ref>{{Citation | year=2001 | title=How Marijuana Works | url=https://science.howstuffworks.com/marijuana.htm}}</ref> This is thought to be due to the way in which endocannabinoids in the hypothalamus activate cannabinoid receptors that are responsible for maintaining food intake.
*'''[[Nausea suppression|Nausea suppression]]''' - Cannabis is effective for suppressing nausea induced by both general illness and substances. It is considered an effective treatment for chemotherapy-induced nausea and vomiting (CINV)<ref>The Pharmacologic and Clinical Effects of Medical Cannabis | http://onlinelibrary.wiley.com/doi/10.1002/phar.1187/abstract;jsessionid=1E004D7B7E2B5CA792E75A6E83EEC59C.f03t01</ref> and is a reasonable option in those who do not improve following preferential treatment.<ref>The Therapeutic Potential of Cannabis and Cannabinoids | http://www.aerzteblatt.de/int/archive/article?id=127603</ref>
*'''[[Nausea suppression|Nausea suppression]]''' - Cannabis is effective for suppressing nausea induced by both general illness and substances. It is considered an effective treatment for chemotherapy-induced nausea and vomiting (CINV)<ref>{{cite journal | vauthors=((Borgelt, L. M.)), ((Franson, K. L.)), ((Nussbaum, A. M.)), ((Wang, G. S.)) | journal=Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy | title=The Pharmacologic and Clinical Effects of Medical Cannabis | volume=33 | issue=2 | pages=195–209 | date= February 2013 | url=https://onlinelibrary.wiley.com/doi/10.1002/phar.1187 | issn=02770008 | doi=10.1002/phar.1187}}</ref> and is a reasonable option in those who do not improve following preferential treatment.<ref>{{Citation | vauthors=((Ärzteblatt, D. Ä. G., Redaktion Deutsches)) | title=The Therapeutic Potential of Cannabis and Cannabinoids (23.07.2012) | url=https://www.aerzteblatt.de/int/archive/article?id=127603}}</ref>
*'''[[Dehydration|Dehydration]]'''
*'''[[Dehydration|Dehydration]]'''
*'''[[Vasodilation|Vasodilation]]''' - THC decreases blood pressure which dilates the blood vessels and increases blood flow throughout the body. The arteries in the eyeball expand from the decreased blood pressure. Studies in the 1970s showed marijuana, when smoked or eaten, effectively lowers intraocular pressure by about 25%, as much as standard medications.<ref>Cardiovascular Effects of Cannabis | http://www.idmu.co.uk/canncardio.htm</ref> These enlarged arteries often produce a bloodshot red eye effect. It is precisely this effect on the human eye that makes cannabinoids an effective medicine for glaucoma.<ref>Is Marijuana an Effective Treatment for Glaucoma? | http://medicalmarijuana.procon.org/view.answers.php?questionID=000140</ref>
*'''[[Vasodilation|Vasodilation]]''' - THC decreases blood pressure which dilates the blood vessels and increases blood flow throughout the body. The arteries in the eyeball expand from the decreased blood pressure. Studies in the 1970s showed marijuana, when smoked or eaten, effectively lowers intraocular pressure by about 25%, as much as standard medications.<ref>Cardiovascular Effects of Cannabis | http://www.idmu.co.uk/canncardio.htm</ref> These enlarged arteries often produce a bloodshot red eye effect. It is precisely this effect on the human eye that makes cannabinoids an effective medicine for glaucoma.<ref>{{Citation | title=Is Marijuana an Effective Treatment for Glaucoma? - Medical Marijuana - ProCon.org | url=https://medicalmarijuana.procon.org/questions/is-marijuana-an-effective-treatment-for-glaucoma/}}</ref>
*'''[[Pain relief|Pain relief]]''' - This substance has been reported as being useful for treating certain headaches and chronic pain, including pain caused by neuropathy and possibly fibromyalgia and rheumatoid arthritis.<ref>Systematic Review and Meta-analysis of cannabinoids Treatment for Chronic Pain | http://onlinelibrary.wiley.com/doi/10.1111/j.1526-4637.2009.00703.x/abstract</ref><ref>Cannabinoids for treatment of chronic non-cancer pain; a systematic review of randomized trials | http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2125.2011.03970.x/abstract</ref>
*'''[[Pain relief|Pain relief]]''' - This substance has been reported as being useful for treating certain headaches and chronic pain, including pain caused by neuropathy and possibly fibromyalgia and rheumatoid arthritis.<ref>{{cite journal | vauthors=((Martín-Sánchez, E.)), ((Furukawa, T. A.)), ((Taylor, J.)), ((Martin, J. L. R.)) | journal=Pain Medicine | title=Systematic Review and Meta-analysis of Cannabis Treatment for Chronic Pain | volume=10 | issue=8 | pages=1353–1368 | date= November 2009 | url=https://academic.oup.com/painmedicine/article-lookup/doi/10.1111/j.1526-4637.2009.00703.x | issn=1526-2375 | doi=10.1111/j.1526-4637.2009.00703.x}}</ref><ref>{{cite journal | vauthors=((Lynch, M. E.)), ((Campbell, F.)) | journal=British Journal of Clinical Pharmacology | title=Cannabinoids for treatment of chronic non-cancer pain; a systematic review of randomized trials: Cannabinoids for pain | volume=72 | issue=5 | pages=735–744 | date= November 2011 | url=https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2125.2011.03970.x | issn=03065251 | doi=10.1111/j.1365-2125.2011.03970.x}}</ref>
*'''[[Perception of increased weight|Perception of increased weight]]''' ''or'' '''[[Perception of decreased weight|Perception of decreased weight]]''' - Depending on the specific cannabinoid, one can find themselves with a body which can feel either physically heavier or lighter than it usually would in a manner that is entirely dependent upon dosage.
*'''[[Perception of increased weight|Perception of increased weight]]''' ''or'' '''[[Perception of decreased weight|Perception of decreased weight]]''' - Depending on the specific cannabinoid, one can find themselves with a body which can feel either physically heavier or lighter than it usually would in a manner that is entirely dependent upon dosage.
*'''[[Changes in gravity|Changes in gravity]]''' - At extremely high doses, many users report a feeling of being pulled backwards across vast distances at powerful speeds. This sensation progressively increases in intensity and eventually becomes unbearable if one leans backwards or lies down but usually disappears altogether once the user sits up or leans forward.
*'''[[Changes in gravity|Changes in gravity]]''' - At extremely high doses, many users report a feeling of being pulled backwards across vast distances at powerful speeds. This sensation progressively increases in intensity and eventually becomes unbearable if one leans backwards or lies down but usually disappears altogether once the user sits up or leans forward.
*'''[[Geometry]]''' - Certain cannabinoids are capable of inconsistently inducing mild to intense psychedelic geometry at high doses. Within many users who also regularly use psychedelics, however, they are capable of inducing these consistently in a visual style which seems to be an averaged out depiction of all the psychedelics one has used within the past. These rarely extend beyond level 4 and are considered to be mild, fine, small and zoomed out (but often well-defined).
*'''[[Internal hallucinations]]
}}
|{{effects/cognitive|
*'''[[Anxiety]]''' - Certain cannabinoids induce anxiety consistently; however, all cannabinoids are capable of inducing anxiety at high doses or with chronic administration.
*'''[[Conceptual thinking]]'''
*'''[[Conceptual thinking]]'''
*'''[[Emotion enhancement]]''' - The most prominent cognitive component of the cannabinoid experience is the way in which it enhances the emotions one is already feeling proportional to dosage. This can result in euphoria, extreme laughter, and increased immersion within tasks and activities or it can result in anxiety or paranoia depending on the user's current state of mind.
*'''[[Effect::Feelings of impending doom]]'''
*'''[[Mindfulness]]'''
*'''[[Mindfulness]]'''
*'''[[Emotion enhancement]]''' - The most prominent cognitive component of the cannabinoid experience is the way in which it enhances the emotions one is already feeling proportional to dosage. This can result in euphoria, extreme laughter, and increased immersion within tasks and activities or it can result in anxiety or paranoia depending on the user's current state of mind.
*'''[[Novelty enhancement]]''' - This effect is most notable when high levels of [[THCV]] are present.
*'''[[Information processing suppression]]'''
*'''[[Increased music appreciation]]'''
*'''[[Anxiety]]''' - Certain canabinoids induce anxiety consistently; however, all cannabinoids are capable of inducing anxiety at high doses or with chronic administration.
*'''[[analysis suppression]]'''
*'''[[Paranoia]]''' - Certain cannabinoids induce paranoia consistently and all cannabinoids are capable of inducing paranoia at high doses or with chronic administration.
*'''[[Paranoia]]''' - Certain cannabinoids induce paranoia consistently and all cannabinoids are capable of inducing paranoia at high doses or with chronic administration.
*'''[[Effect::Feelings of impending doom]]'''
*'''[[Sleepiness]]'''
*'''[[Thought connectivity]]'''
*'''[[Thought deceleration]]'''
===Visual effects===
}}
*'''[[Colour enhancement]]'''
*'''[[Visual acuity suppression]]'''
*'''[[Geometry]]''' - Certain cannabinoids are capable of inconsistently inducing mild to intense psychedelic geometry at high doses. Within many users who also regularly use psychedelics, however, it is capable of inducing these consistently in a visual style which seems to be an averaged out depiction of all the psychedelics one has used within the past. These rarely extend beyond level 4 and are considered to be mild, fine, small and zoomed out (but often well-defined).
===Auditory effects===
{{effects/auditory|
*'''[[Auditory enhancement|Enhancements]]'''
*'''[[Auditory enhancement|Enhancements]]'''
}}
}}
==Phytocannabinoids==
==Phytocannabinoids==
[[File:Phyto cannabinoids infograph.jpg|thumbnail|200px|Comparison of phytocannabinoids]]
[[File:Phyto cannabinoids infograph.jpg|thumbnail|200px|Comparison of phytocannabinoids]]
Phytocannabinoids can be defined as any plant-derived natural product capable of either directly interacting with cannabinoid receptors or sharing chemical similarity with cannabinoids or both.
Phytocannabinoids can be defined as any plant-derived natural product capable of either directly interacting with cannabinoid receptors or sharing chemical similarity with cannabinoids or both. The [https://en.wikipedia.org/wiki/Entourage_effect 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]]
*[[CBD]]
{{Phytocannabinoids}}
*[[CBN]]
*[[CBG]] (Cannabigerol)
*[[CBC]] (Cannabichromene)
*[[CBL]] (Cannabicyclol)
*[[CBV]] (Cannabivarin)
*[[THCV]] (Tetrahydrocannabivarin)
*[[CBDV]] (Cannabidivarin)
*[[CBCV]] (Cannabichromevarin)
*[[CBGV]] (Cannabigerovarin)
*[[CBGM]] (Cannabigerol Monomethyl Ether)
====Plant sources====
====Plant sources====
*[[Cannabis]]
*[[Cannabis]]
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===Toxicity and harm potential===
===Toxicity and harm potential===
{{Main|Synthetic cannabinoid#Toxicity and harm potential}}
{{Main|Synthetic cannabinoid#Toxicity and harm potential}}
Unlike [[cannabis]], there have been multiple deaths<ref name="death1">Brents, L. K.; Reichard, E. E.; Zimmerman, S. M.; Moran, J. H.; Fantegrossi, W. E.; Prather, P. L. (2011). "Phase I hydroxylated metabolites of the K2 synthetic cannabinoid JWH-018 retain in vitro and in vivo cannabinoid 1 receptor affinity and activity". PLoS ONE 6 (7) (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/21755008</ref><ref name="death2">Coroner: Lamar Jack ingested chemical found in fake marijuana before he died (IndependentMail.com) | https://web.archive.org/web/20131009101212/http://www.independentmail.com/news/2011/oct/15/coroner-lamar-jack-ingested-chemical-found-fake-ma/</ref><ref name="death3"> Coffman, K. (6 September 2013). "Colorado probes three deaths possibly linked to synthetic marijuana". Reuters (Denver). | http://www.reuters.com/article/us-usa-colorado-spice-idUSBRE98516A20130906</ref><ref name="death4">Perspectives of drugs: synthetic cannabinoids in Europe (European Monitoring Centre for Drugs and Drug Addiction | http://www.emcdda.europa.eu/topics/pods/synthetic-cannabinoids</ref><ref name="death5">Westin AA, Frost J, Brede WR, Gundersen PO, Einvik S, Aarset H, Slørdal L. “Sudden Cardiac Death Following Use of the Synthetic Cannabinoid MDMB-CHMICA”. J Anal Toxicol. 2016 Jan 19;40(1):86-7. | https://www.erowid.org/references/refs_view.php?ID=8961</ref><ref name="death6">Adamowicz P. “Fatal intoxication with synthetic cannabinoid MDMB-CHMICA”. Forensic Sci Int. 2016 Mar;. | https://www.erowid.org/references/refs_view.php?ID=8963</ref><ref name="death7">Synthetic Cannabinoid–Related Illnesses and Deaths | http://www.nejm.org/doi/full/10.1056/NEJMp1505328</ref> associated with the repeated abuse of synthetic cannabinoids as well as serious side effects resulting from its long-term use.<ref> Vardakou, I; Pistos, C; Spiliopoulou, Ch (2010). "Spice drugs as a new trend: Mode of action, identification and legislation". Toxicology Letters 197 (3): 157–62. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/20566335</ref><ref> Auwärter, V.; et al. (2009). "'Spice' and other herbal blends: harmless incense or cannabinoid designer drugs?". Journal of mass spectrometry : JMS 44 (5) | http://onlinelibrary.wiley.com/doi/10.1002/jms.1558/abstract</ref><ref>Toxicological Findings of Synthetic Cannabinoids in Recreational Users | http://jat.oxfordjournals.org/content/37/8/534.full</ref> Therefore, it is strongly discouraged to take this substance for extended periods of time or in excessive doses. Compared to cannabis and its active cannabinoid THC, the adverse effects are often much more severe and can include [[high blood pressure]], [[increased heart rate]], heart attacks,<ref>Mir, A; Obafemi, A; Young, A; Kane, C (December 2011). "Myocardial infarction associated with use of the synthetic cannabinoid k2.". Pediatrics 128 (6) | http://pediatrics.aappublications.org/content/pediatrics/early/2011/11/04/peds.2010-3823.full.pdf</ref><ref>Acute myocardial infarction, associated with the use of a synthetic adamantyl-cannabinoid: a case report (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4715335/</ref> agitation,<ref name="teen">A Teenager With Agitation: Higher Than She Should Have Climbed - Pediatric Emergency Care: June 2010 - Volume 26 - Issue 6 - pp 462-465 | http://journals.lww.com/pec-online/Abstract/2010/06000/A_Teenager_With_Agitation__Higher_Than_She_Should.16.aspx</ref> [[nausea|vomiting]],<ref>T. "Extreme Nausea, Incoherent: An Experience with JWH-018 (ID 84443)". Erowid.org. Oct 12, 2010. erowid.org/exp/84443 | https://www.erowid.org/experiences/exp.php?ID=84443</ref><ref>Exdrugaddict. "Playing With Fire: An Experience with Spice (ID 90178)". Erowid.org. Dec 16, 2013. erowid.org/exp/90178 | https://www.erowid.org/experiences/exp.php?ID=90178</ref><ref>Boss Lok. "Non-Allergic Adverse Reaction: An Experience with Spice and Synthetic Cannabinoids ('Drill') (ID 85853)". Erowid.org. Oct 12, 2010. erowid.org/exp/85853 | https://www.erowid.org/experiences/exp.php?ID=85853</ref> [[external hallucinations|hallucinations]],<ref> Jeanna Bryner (March 3, 2010). "Fake Weed, Real Drug: K2 Causing hallucinations in Teens". LiveScience. | http://www.livescience.com/6149-fake-weed-real-drug-k2-causing-hallucinations-teens.html</ref> [[psychosis|psychosis]],<ref> Every-Palmer, S (2010). "Warning: Legal synthetic cannabinoid-receptor agonists such as JWH-018 may precipitate psychosis in vulnerable individuals". Addiction 105 (10): 1859–60. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/20840203</ref><ref name="british">Causal association between cannabis and psychosis: examination of the evidence - The British Journal of Psychiatry Jan 2004, 184 (2) 110-117 | http://bjp.rcpsych.org/content/184/2/110.short</ref><ref name="teen">A Teenager With Agitation: Higher Than She Should Have Climbed - Pediatric Emergency Care: June 2010 - Volume 26 - Issue 6 - pp 462-465 | http://journals.lww.com/pec-online/Abstract/2010/06000/A_Teenager_With_Agitation__Higher_Than_She_Should.16.aspx</ref><ref name="muller"> Müller, H.; Sperling, W.; Köhrmann, M.; Huttner, H.; Kornhuber, J.; Maler, J. (2010). "The synthetic cannabinoid Spice as a trigger for an acute exacerbation of cannabis induced recurrent psychotic episodes". Schizophrenia Research 118 (1–3) (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/20056392</ref> [[seizures]],<ref>Thisisntover. "Most Insane Hour of My Life: experience with JWH-018 (ID 85936)". Erowid.org. Oct 1, 2010. erowid.org/exp/85936 | http://www.erowid.org/experiences/exp.php?ID=85936</ref><ref>Michael C. "The Night My Brain Caved: experience with AM-2201 (ID 92954)". Erowid.org. Sep 18, 2012. erowid.org/exp/92954 | https://www.erowid.org/experiences/exp.php?ID=92954</ref><ref>Steve. "Next-Night Seizures: experience with Products - Spice and Synthetic Cannabinoids ('Apocalypse'?) (ID 89290)". Erowid.org. Feb 3, 2011. erowid.org/exp/89290 | https://www.erowid.org/experiences/exp.php?ID=89290</ref> and convulsions<ref>ilovethagreenery. "Should've Called Poison Control Bro: An Experience with Products - Spice and Synthetic Cannabinoids ('Diamond Dove') & Alcohol (ID 92698)". Erowid.org. Jan 6, 2012. erowid.org/exp/92698 | https://www.erowid.org/experiences/exp.php?ID=88807 | https://www.erowid.org/experiences/exp.php?ID=88807</ref><ref> Schneir, AB; Baumbacher, T (December 13, 2011). "Convulsions Associated with the Use of a Synthetic Cannabinoid Product.". Journal of Medical Toxicology 8 (1): 62–4 (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/22160733</ref> as well as many others. Sixteen cases of acute kidney injury resulting from synthetic cannabinoid abuse have been reported.<ref>Acute Kidney Injury Associated with Synthetic Cannabinoid Use — Multiple States, 2012 (Centers for Disease Control and Prevention) | http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6206a1.htm</ref> [[JWH-018]] has also been associated with strokes in two healthy adults.<ref>Ischemic stroke after use of the synthetic marijuana "spice". (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/24212384</ref>
Unlike [[cannabis]], there have been multiple deaths<ref name="death1">{{cite journal | vauthors=((Brents, L. K.)), ((Reichard, E. E.)), ((Zimmerman, S. M.)), ((Moran, J. H.)), ((Fantegrossi, W. E.)), ((Prather, P. L.)) | journal=PloS One | title=Phase I hydroxylated metabolites of the K2 synthetic cannabinoid JWH-018 retain in vitro and in vivo cannabinoid 1 receptor affinity and activity | volume=6 | issue=7 | pages=e21917 | date= 2011 | issn=1932-6203 | doi=10.1371/journal.pone.0021917}}</ref><ref name="death2">{{Citation | year=2013 | title=Coroner: Lamar Jack ingested chemical found in fake marijuana before he died » Anderson Independent Mail | url=https://web.archive.org/web/20131009101212/http://www.independentmail.com/news/2011/oct/15/coroner-lamar-jack-ingested-chemical-found-fake-ma/}}</ref><ref name="death3">{{Citation | year=2013 | title=Colorado probes three deaths possibly linked to synthetic marijuana | url=https://www.reuters.com/article/us-usa-colorado-spice-idUSBRE98516A20130906}}</ref><ref name="death4">{{Citation | title=Synthetic cannabinoids in Europe | url=https://www.emcdda.europa.eu/topics/pods/synthetic-cannabinoids}}</ref><ref name="death5">{{cite journal | vauthors=((Westin, A. A.)), ((Frost, J.)), ((Brede, W. R.)), ((Gundersen, P. O. M.)), ((Einvik, S.)), ((Aarset, H.)), ((Slørdal, L.)) | journal=Journal of Analytical Toxicology | title=Sudden Cardiac Death Following Use of the Synthetic Cannabinoid MDMB-CHMICA | pages=bkv110 | date=9 September 2015 | url=https://academic.oup.com/jat/article-lookup/doi/10.1093/jat/bkv110 | issn=0146-4760 | doi=10.1093/jat/bkv110}}</ref><ref name="death6">{{cite journal | vauthors=((Adamowicz, P.)) | journal=Forensic Science International | title=Fatal intoxication with synthetic cannabinoid MDMB-CHMICA | volume=261 | pages=e5–e10 | date= April 2016 | url=https://linkinghub.elsevier.com/retrieve/pii/S0379073816300469 | issn=03790738 | doi=10.1016/j.forsciint.2016.02.024}}</ref><ref name="death7">{{cite journal | vauthors=((Trecki, J.)), ((Gerona, R. R.)), ((Schwartz, M. D.)) | journal=New England Journal of Medicine | title=Synthetic Cannabinoid–Related Illnesses and Deaths | volume=373 | issue=2 | pages=103–107 | date=9 July 2015 | url=https://doi.org/10.1056/NEJMp1505328 | issn=0028-4793 | doi=10.1056/NEJMp1505328}}</ref> associated with the repeated abuse of synthetic cannabinoids as well as serious side effects resulting from its long-term use.<ref>{{cite journal | vauthors=((Vardakou, I.)), ((Pistos, C.)), ((Spiliopoulou, C.)) | journal=Toxicology Letters | title=Spice drugs as a new trend: mode of action, identification and legislation | volume=197 | issue=3 | pages=157–162 | date=1 September 2010 | issn=1879-3169 | doi=10.1016/j.toxlet.2010.06.002}}</ref><ref>{{cite journal | vauthors=((Auwärter, V.)), ((Dresen, S.)), ((Weinmann, W.)), ((Müller, M.)), ((Pütz, M.)), ((Ferreirós, N.)) | journal=Journal of Mass Spectrometry | title=‘Spice’ and other herbal blends: harmless incense or cannabinoid designer drugs? | volume=44 | issue=5 | pages=832–837 | date= May 2009 | url=https://onlinelibrary.wiley.com/doi/10.1002/jms.1558 | issn=10765174 | doi=10.1002/jms.1558}}</ref><ref>{{cite journal | vauthors=((Kronstrand, R.)), ((Roman, M.)), ((Andersson, M.)), ((Eklund, A.)) | journal=Journal of Analytical Toxicology | title=Toxicological Findings of Synthetic Cannabinoids in Recreational Users | volume=37 | issue=8 | pages=534–541 | date=1 October 2013 | url=https://academic.oup.com/jat/article-lookup/doi/10.1093/jat/bkt068 | issn=0146-4760 | doi=10.1093/jat/bkt068}}</ref> Therefore, it is strongly discouraged to take this substance for extended periods of time or in excessive doses. Compared to cannabis and its active cannabinoid THC, the adverse effects are often much more severe and can include [[high blood pressure]], [[increased heart rate]], heart attacks,<ref>{{cite journal | vauthors=((Mir, A.)), ((Obafemi, A.)), ((Young, A.)), ((Kane, C.)) | journal=Pediatrics | title=Myocardial Infarction Associated With Use of the Synthetic Cannabinoid K2 | volume=128 | issue=6 | pages=e1622–e1627 | date=1 December 2011 | url=https://publications.aap.org/pediatrics/article/128/6/e1622/31047/Myocardial-Infarction-Associated-With-Use-of-the | issn=0031-4005 | doi=10.1542/peds.2010-3823}}</ref><ref>{{cite journal | vauthors=((McIlroy, G.)), ((Ford, L.)), ((Khan, J. M.)) | journal=BMC Pharmacology & Toxicology | title=Acute myocardial infarction, associated with the use of a synthetic adamantyl-cannabinoid: a case report | volume=17 | pages=2 | date=16 January 2016 | url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4715335/ | issn=2050-6511 | doi=10.1186/s40360-016-0045-1}}</ref> agitation,<ref name="teen">{{cite journal | vauthors=((Vearrier, D.)), ((Osterhoudt, K. C.)) | journal=Pediatric Emergency Care | title=A Teenager With Agitation: Higher Than She Should Have Climbed | volume=26 | issue=6 | pages=462–465 | date= June 2010 | url=http://journals.lww.com/00006565-201006000-00016 | issn=0749-5161 | doi=10.1097/PEC.0b013e3181e4f416}}</ref> [[nausea|vomiting]],<ref>{{Citation | title=JWH-018 - Erowid Exp - “Extreme Nausea, Incoherent” | url=https://www.erowid.org/experiences/exp.php?ID=84443}}</ref><ref>{{Citation | title=Spice - Erowid Exp - “Playing With Fire” | url=https://www.erowid.org/experiences/exp.php?ID=90178}}</ref><ref>{{Citation | title=Spice and Synthetic Cannabinoids ('Drill’) - Erowid Exp - “Non-Allergic Adverse Reaction” | url=https://www.erowid.org/experiences/exp.php?ID=85853}}</ref> [[external hallucinations|hallucinations]],<ref>{{Citation | vauthors=((published, J. B.)) | year=2010 | title=Fake Weed, Real Drug: K2 Causing Hallucinations in Teens | url=https://www.livescience.com/6149-fake-weed-real-drug-k2-causing-hallucinations-teens.html}}</ref> [[psychosis|psychosis]],<ref>{{cite journal | vauthors=((Every-Palmer, S.)) | journal=Addiction (Abingdon, England) | title=Warning: legal synthetic cannabinoid-receptor agonists such as JWH-018 may precipitate psychosis in vulnerable individuals | volume=105 | issue=10 | pages=1859–1860 | date= October 2010 | issn=1360-0443 | doi=10.1111/j.1360-0443.2010.03119.x}}</ref><ref name="british">{{cite journal | vauthors=((Arseneault, L.)), ((Cannon, M.)), ((Witton, J.)), ((Murray, R. M.)) | journal=The British Journal of Psychiatry | title=Causal association between cannabis and psychosis: examination of the evidence | volume=184 | issue=2 | pages=110–117 | date= February 2004 | url=https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/causal-association-between-cannabis-and-psychosis-examination-of-the-evidence/71BA37D16485F186CE7B6B785E5B69A4 | issn=0007-1250 | doi=10.1192/bjp.184.2.110}}</ref><ref name="teen"/><ref name="muller">{{cite journal | vauthors=((Müller, H.)), ((Sperling, W.)), ((Köhrmann, M.)), ((Huttner, H. B.)), ((Kornhuber, J.)), ((Maler, J.-M.)) | journal=Schizophrenia Research | title=The synthetic cannabinoid Spice as a trigger for an acute exacerbation of cannabis induced recurrent psychotic episodes | volume=118 | issue=1–3 | pages=309–310 | date= May 2010 | issn=1573-2509 | doi=10.1016/j.schres.2009.12.001}}</ref> [[seizures]],<ref>{{Citation | title=JWH-018 - Erowid Exp - “Most Insane Hour of My Life” | url=https://www.erowid.org/experiences/exp.php?ID=85936}}</ref><ref>{{Citation | title=AM-2201 - Erowid Exp - “The Night My Brain Caved” | url=https://www.erowid.org/experiences/exp.php?ID=92954}}</ref><ref>{{Citation | title=Products - Spice and Synthetic Cannabinoids (“Apocalypse”?) - Erowid Exp - “Next-Night Seizures” | url=https://www.erowid.org/experiences/exp.php?ID=89290}}</ref> and convulsions<ref>{{Citation | title=Products - Spice and Synthetic Cannabinoids ('Smiley Dog’) - Erowid Exp - “Never Again” | url=https://www.erowid.org/experiences/exp.php?ID=88807}}</ref><ref>{{cite journal | vauthors=((Schneir, A. B.)), ((Baumbacher, T.)) | journal=Journal of Medical Toxicology: Official Journal of the American College of Medical Toxicology | title=Convulsions associated with the use of a synthetic cannabinoid product | volume=8 | issue=1 | pages=62–64 | date= March 2012 | issn=1937-6995 | doi=10.1007/s13181-011-0182-2}}</ref> as well as many others. Sixteen cases of acute kidney injury resulting from synthetic cannabinoid abuse have been reported.<ref>{{Citation | title=Acute Kidney Injury Associated with Synthetic Cannabinoid Use — Multiple States, 2012 | url=https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6206a1.htm}}</ref> [[JWH-018]] has also been associated with strokes in two healthy adults.<ref>{{cite journal | vauthors=((Freeman, M. J.)), ((Rose, D. Z.)), ((Myers, M. A.)), ((Gooch, C. L.)), ((Bozeman, A. C.)), ((Burgin, W. S.)) | journal=Neurology | title=Ischemic stroke after use of the synthetic marijuana “spice” | volume=81 | issue=24 | pages=2090–2093 | date=10 December 2013 | issn=1526-632X | doi=10.1212/01.wnl.0000437297.05570.a2}}</ref>
It should be noted that pre-mixed, branded blends (like Spice and K2) are more dangerous than pure powder because the specific chemicals and dosages are usually unlisted as well as the potential of inconsistent areas of dense powder, leading to an overdose. As synthetic cannabinoids are active in the milligram range (with below 5mg being a common dose), it is important to [[Dosage|use proper precautions when dosing]] to avoid a negative experience.
It should be noted that pre-mixed, branded blends (like Spice and K2) are more dangerous than pure powder because the specific chemicals and dosages are usually unlisted as well as the potential of inconsistent areas of dense powder, leading to an overdose. As synthetic cannabinoids are active in the milligram range (with below 5mg being a common dose), it is important to [[Dosage|use proper precautions when dosing]] to avoid a negative experience.
Like [[THC]], prolonged usage of synthetic [[cannabinoids]] may increase one's disposition to mental illness and psychosis<ref name="british">Causal association between cannabis and psychosis: examination of the evidence - The British Journal of Psychiatry Jan 2004, 184 (2) 110-117 | http://bjp.rcpsych.org/content/184/2/110.short</ref>, particularly in vulnerable individuals with risk factors for psychotic illnesses (like a past or family history of schizophrenia).<ref>Every-Palmer, S. Synthetic cannabinoid use and psychosis: an explorative study. Journal of Drug and Alcohol Dependence 2011. | https://www.researchgate.net/publication/49831304_Every-Palmer_S_Synthetic_cannabinoid_JWH-018_and_psychosis_An_explorative_study</ref><ref>“Spice” Girls: Synthetic Cannabinoid Intoxication - The Journal of Emergency Medicine Volume 40, Issue 3, March 2011, Pages 296–299 (ScienceDirect) | http://www.sciencedirect.com/science/article/pii/S0736467910008802</ref><ref name="teen">A Teenager With Agitation: Higher Than She Should Have Climbed - Pediatric Emergency Care: June 2010 - Volume 26 - Issue 6 - pp 462-465 | http://journals.lww.com/pec-online/Abstract/2010/06000/A_Teenager_With_Agitation__Higher_Than_She_Should.16.aspx</ref> It is recommended that individuals with risk factors for psychotic disorders not use synthetic cannabinoids.<ref> Every-Palmer, S (September 1, 2011). "Synthetic cannabinoid JWH-018 and psychosis: an explorative study.". Drug and Alcohol Dependence 117 (2-3): 152–7 (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/21316162</ref>
Like [[THC]], prolonged usage of synthetic [[cannabinoids]] may increase one's disposition to mental illness and psychosis<ref name="british"/>, particularly in vulnerable individuals with risk factors for psychotic illnesses (like a past or family history of schizophrenia).<ref>{{cite journal | vauthors=((Every-Palmer, S.)) | journal=Drug and Alcohol Dependence | title=Synthetic cannabinoid JWH-018 and psychosis: An explorative study | volume=117 | issue=2–3 | pages=152–157 | date= September 2011 | url=https://linkinghub.elsevier.com/retrieve/pii/S0376871611000639 | issn=03768716 | doi=10.1016/j.drugalcdep.2011.01.012}}</ref><ref>{{cite journal | vauthors=((Schneir, A. B.)), ((Cullen, J.)), ((Ly, B. T.)) | journal=The Journal of Emergency Medicine | title=“Spice” Girls: Synthetic Cannabinoid Intoxication | volume=40 | issue=3 | pages=296–299 | date=1 March 2011 | url=https://www.sciencedirect.com/science/article/pii/S0736467910008802 | issn=0736-4679 | doi=10.1016/j.jemermed.2010.10.014}}</ref><ref name="teen"/> It is recommended that individuals with risk factors for psychotic disorders not use synthetic cannabinoids.<ref>{{cite journal | vauthors=((Every-Palmer, S.)) | journal=Drug and Alcohol Dependence | title=Synthetic cannabinoid JWH-018 and psychosis: an explorative study | volume=117 | issue=2–3 | pages=152–157 | date=1 September 2011 | issn=1879-0046 | doi=10.1016/j.drugalcdep.2011.01.012}}</ref>
Although there is no valid data on the toxicity of synthetic cannabinoids so far, there is concern that the naphthalene group found in THJ-018 and some other [[synthetic cannabinoids]] may be toxic or carcinogenic.<ref>Naphthalene - United States Environmental Protection Agency | http://www.epa.gov/ttn/atw/hlthef/naphthal.html</ref><ref>Toxicity and metabolism of methylnaphthalenes: comparison with naphthalene and 1-nitronaphthalene. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/19464565</ref><ref>Synthetic cannabinoids in herbal products (United Nations Office on Drugs and Crime) | https://www.unodc.org/documents/scientific/Synthetic_Cannabinoids.pdf</ref><ref>HAMILTON MORRIS: NAPTHALENE IS SO OVER | http://hamiltonmorris.blogspot.co.uk/2010/06/napthalene-is-so-over.html</ref>
Although there is no valid data on the toxicity of synthetic cannabinoids so far, there is concern that the naphthalene group found in THJ-018 and some other [[synthetic cannabinoids]] may be toxic or carcinogenic.<ref>Naphthalene - United States Environmental Protection Agency | http://www.epa.gov/ttn/atw/hlthef/naphthal.html</ref><ref>{{cite journal | vauthors=((Lin, C. Y.)), ((Wheelock, A. M.)), ((Morin, D.)), ((Baldwin, R. M.)), ((Lee, M. G.)), ((Taff, A.)), ((Plopper, C.)), ((Buckpitt, A.)), ((Rohde, A.)) | journal=Toxicology | title=Toxicity and metabolism of methylnaphthalenes: comparison with naphthalene and 1-nitronaphthalene | volume=260 | issue=1–3 | pages=16–27 | date=16 June 2009 | issn=1879-3185 | doi=10.1016/j.tox.2009.03.002}}</ref><ref>Synthetic cannabinoids in herbal products (United Nations Office on Drugs and Crime) | https://www.unodc.org/documents/scientific/Synthetic_Cannabinoids.pdf</ref><ref>{{Citation | vauthors=((Morris, H.)) | year=2010 | title=HAMILTON MORRIS?: NAPTHALENE IS SO OVER | url=http://hamiltonmorris.blogspot.com/2010/06/napthalene-is-so-over.html}}</ref>
It is strongly recommended that one use [[responsible drug use|harm reduction practices]] when using these drugs.
It is strongly recommended that one use [[responsible drug use|harm reduction practices]] when using these drugs.
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Please be aware that pre-mixed, branded blends are unreliable as they often fail to list the constituents and dosages. Many people have been hospitalised or suffered negative symptoms believing they are comparable to cannabis in potency and effects. This is not the case, and they should be avoided in favour of pure analytical samples where possible.
Please be aware that pre-mixed, branded blends are unreliable as they often fail to list the constituents and dosages. Many people have been hospitalised or suffered negative symptoms believing they are comparable to cannabis in potency and effects. This is not the case, and they should be avoided in favour of pure analytical samples where possible.
====Naphthoylindole family====
===Indazolecarboxamides===
*[[5F-AKB48]]
*[[AB-CHMINACA]]
*[[AB-FUBINACA]]
===Indolecarboxamides===
*[[APICA]]
*[[STS-135]]
*[[MDMB-CHMICA]]
===Indolecarboxylates===
*[[5F-PB-22]]
*[[BB-22]]
===Naphthoylindoles===
*[[AM-2201]]
*[[JWH-018]]
*[[JWH-073]]
*[[JWH-073]]
*[[JWH-018]]
*[[JWH-122]]
*[[JWH-122]]
*[[JWH-250]]
===Naphthoylindazoles===
*[[THJ-018]]
*[[THJ-018]]
*[[THJ-2201]]
*[[THJ-2201]]
====5F family====
===Tetramethylcyclopropanoylindoles===
*[[5F-AKB48]]
*[[5F-PB-22]]
*[[5F-UR-144]]
*[[AM-2201]] (5F-JWH-018)
*[[STS-135]]
====Pentylindole family====
*[[UR-144]]
*[[UR-144]]
*[[5F-UR-144]]
====Comprehensive List====
====Comprehensive List====
For a comprehensive list of known [[synthetic cannabinoid]] derivatives, [https://www.reddit.com/r/Drugs/wiki/cannabinoids /r/Drugs/wiki] has published a respectable directory of names and links to further information.
For a comprehensive list of known [[synthetic cannabinoid]] derivatives, [https://www.reddit.com/r/Drugs/wiki/cannabinoids /r/Drugs/wiki] has published a respectable directory of names and links to further information.
A flowering cannabis plant, the most common source of cannabinoids.A bag of Spice brand herbal incense. This contains synthetic cannabinoids which produce a similar effect to that of cannabis.
A cannabinoid is one of a class of diverse chemical compounds that act on cannabinoid receptors on cells that alter neurotransmitter functioning in the brain. These receptor proteins include the endocannabinoids (produced naturally in the body by humans and animals),[1] the phytocannabinoids (found in cannabis and some other plants), and synthetic cannabinoids (manufactured chemically).
The most notable cannabinoid is the phytocannabinoid ∆9-tetrahydrocannabinol (THC), the primary psychoactive compound of cannabis.[2][3] Cannabidiol (CBD) is another major constituent of the plant, representing up to 40% in extracts of the plant resin.[4] There are at least 85 different cannabinoids isolated from cannabis which exhibit varied effects.
Synthetic cannabinoids encompass a variety of distinct chemical classes: the classical cannabinoids structurally related to THC; the nonclassical cannabinoids (cannabimimetics) including the aminoalkylindoles, 1,5-diarylpyrazoles, quinolines, and arylsulphonamides; and eicosanoids related to the endocannabinoids.[2][3]
Before the 1980s, it was often speculated that cannabinoids produced their physiological and behavioral effects via nonspecific interactions instead of interacting with specific receptors directly. The discovery of the first cannabinoid receptors in the 1980s helped to resolve this debate. These receptors are common in animals and have been found in mammals, birds, fish, and reptiles. At present, there are two known types of cannabinoid receptors, termed CB1 and CB2,[1] with mounting evidence of more.[5][6] However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
Cannabinoid receptor type 1
CB1 receptors are found primarily in the brain, more specifically in the basal ganglia and in the limbic system (including the hippocampus).[1] They are also found in the cerebellum and in both male and female reproductive systems. CB1 receptors are absent in the medulla oblongata, the part of the brain stem responsible for respiratory and cardiovascular functions. Thus, there is not the risk of respiratory or cardiovascular failure that can be produced by some drugs. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis. However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
Cannabinoid receptor type 2
CB2 receptors are predominantly found in the immune system, or immune-derived cells[7] with the greatest density in the spleen. While found only in the peripheral nervous system, a report does indicate that CB2 is expressed by a subpopulation of microglia in the human cerebellum.[8] CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.[7] However, the role of these interactions and how they result in the cannabinoid high experience continues to remain elusive.
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 PsychonautWikicontributors. 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
Sedation - Although certain strains of cannabinoids present mild encouraged stimulation at low to moderate doses, for the most part the effects on the user's energy levels are primarily sedating. This encourages one to relax, but can, however, be suppressed by simply forcing oneself to engage in physical activities.
Motor control loss - These substances cause a partial to moderate suppression of motor control which intensifies proportional to dosage but rarely results in a complete inability to walk and perform basic movements.
Appetite enhancement - The feeling of increased appetite following the use of cannabinoids has been documented for hundreds of years[9] and is known colloquially as "the munchies" in popular American and United Kingdom culture. Clinical studies and survey data have found that cannabis increases food enjoyment and interest in food.[10] This is thought to be due to the way in which endocannabinoids in the hypothalamus activate cannabinoid receptors that are responsible for maintaining food intake.
Nausea suppression - Cannabis is effective for suppressing nausea induced by both general illness and substances. It is considered an effective treatment for chemotherapy-induced nausea and vomiting (CINV)[11] and is a reasonable option in those who do not improve following preferential treatment.[12]
Vasodilation - THC decreases blood pressure which dilates the blood vessels and increases blood flow throughout the body. The arteries in the eyeball expand from the decreased blood pressure. Studies in the 1970s showed marijuana, when smoked or eaten, effectively lowers intraocular pressure by about 25%, as much as standard medications.[13] These enlarged arteries often produce a bloodshot red eye effect. It is precisely this effect on the human eye that makes cannabinoids an effective medicine for glaucoma.[14]
Pain relief - This substance has been reported as being useful for treating certain headaches and chronic pain, including pain caused by neuropathy and possibly fibromyalgia and rheumatoid arthritis.[15][16]
Perception of increased weightorPerception of decreased weight - Depending on the specific cannabinoid, one can find themselves with a body which can feel either physically heavier or lighter than it usually would in a manner that is entirely dependent upon dosage.
Changes in gravity - At extremely high doses, many users report a feeling of being pulled backwards across vast distances at powerful speeds. This sensation progressively increases in intensity and eventually becomes unbearable if one leans backwards or lies down but usually disappears altogether once the user sits up or leans forward.
Geometry - Certain cannabinoids are capable of inconsistently inducing mild to intense psychedelic geometry at high doses. Within many users who also regularly use psychedelics, however, they are capable of inducing these consistently in a visual style which seems to be an averaged out depiction of all the psychedelics one has used within the past. These rarely extend beyond level 4 and are considered to be mild, fine, small and zoomed out (but often well-defined).
Anxiety - Certain cannabinoids induce anxiety consistently; however, all cannabinoids are capable of inducing anxiety at high doses or with chronic administration.
Emotion enhancement - The most prominent cognitive component of the cannabinoid experience is the way in which it enhances the emotions one is already feeling proportional to dosage. This can result in euphoria, extreme laughter, and increased immersion within tasks and activities or it can result in anxiety or paranoia depending on the user's current state of mind.
Paranoia - Certain cannabinoids induce paranoia consistently and all cannabinoids are capable of inducing paranoia at high doses or with chronic administration.
Phytocannabinoids can be defined as any plant-derived natural product capable of either directly interacting with cannabinoid receptors or sharing chemical similarity with cannabinoids or both. 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)).
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
Decarboxylation: THCA (more info) → THC -- The decarboxylation of this compound by heat is essential for the psychoactive effect of smoked cannabis, and depends on conversion of the enol to a keto group when the alpha carbon is protonated.
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.[18]
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.[19]
Chemical conversion: acetic anhydride + Δ-9-THC/Δ-8-THC → Δ-9-THCAO/Δ-8-THCAO, respectively.[20]
Non-quasi-psychedelic phytocannabinoids, some which can be synthesized to quasi-psychedelic cannabinoids with biosynthesis or chemical conversion (see above)
Synthetic cannabinoids are any artificial compound which is functionally similar to Δ9-tetrahydrocannabinol (THC), the active principle of cannabis. Like THC, they bind to the same cannabinoid receptors in the brain and are often sold as legal alternatives.
Unlike cannabis, there have been multiple deaths[24][25][26][27][28][29][30] associated with the repeated abuse of synthetic cannabinoids as well as serious side effects resulting from its long-term use.[31][32][33] Therefore, it is strongly discouraged to take this substance for extended periods of time or in excessive doses. Compared to cannabis and its active cannabinoid THC, the adverse effects are often much more severe and can include high blood pressure, increased heart rate, heart attacks,[34][35] agitation,[36]vomiting,[37][38][39]hallucinations,[40]psychosis,[41][42][36][43]seizures,[44][45][46] and convulsions[47][48] as well as many others. Sixteen cases of acute kidney injury resulting from synthetic cannabinoid abuse have been reported.[49]JWH-018 has also been associated with strokes in two healthy adults.[50]
It should be noted that pre-mixed, branded blends (like Spice and K2) are more dangerous than pure powder because the specific chemicals and dosages are usually unlisted as well as the potential of inconsistent areas of dense powder, leading to an overdose. As synthetic cannabinoids are active in the milligram range (with below 5mg being a common dose), it is important to use proper precautions when dosing to avoid a negative experience.
Like THC, prolonged usage of synthetic cannabinoids may increase one's disposition to mental illness and psychosis[42], particularly in vulnerable individuals with risk factors for psychotic illnesses (like a past or family history of schizophrenia).[51][52][36] It is recommended that individuals with risk factors for psychotic disorders not use synthetic cannabinoids.[53]
Although there is no valid data on the toxicity of synthetic cannabinoids so far, there is concern that the naphthalene group found in THJ-018 and some other synthetic cannabinoids may be toxic or carcinogenic.[54][55][56][57]
Please be aware that pre-mixed, branded blends are unreliable as they often fail to list the constituents and dosages. Many people have been hospitalised or suffered negative symptoms believing they are comparable to cannabis in potency and effects. This is not the case, and they should be avoided in favour of pure analytical samples where possible.
For a comprehensive list of known synthetic cannabinoid derivatives, /r/Drugs/wiki has published a respectable directory of names and links to further information.
↑ 1.01.11.2Pacher, P., Bátkai, S., Kunos, G. (September 2006). "The endocannabinoid system as an emerging target of pharmacotherapy". Pharmacological Reviews. 58 (3): 389–462. doi:10.1124/pr.58.3.2. ISSN0031-6997.
↑ 2.02.1Lambert, D. M., Fowler, C. J. (11 August 2005). "The endocannabinoid system: drug targets, lead compounds, and potential therapeutic applications". Journal of Medicinal Chemistry. 48 (16): 5059–5087. doi:10.1021/jm058183t. ISSN0022-2623.
↑ 3.03.1Abood, M. E., Pertwee, R. G., eds. (2005). Cannabinoids. Handbook of experimental pharmacology. Springer. ISBN9783540225652.
↑Boron, W. F., Boulpaep, E. L., eds. (2009). Medical physiology: a cellular and molecular approach (2nd ed., International ed ed.). Saunders/Elsevier. ISBN9781416031154.CS1 maint: Extra text (link)
↑ 7.07.1Pacher, P., Mechoulam, R. (April 2011). "Is lipid signaling through cannabinoid 2 receptors part of a protective system?". Progress in Lipid Research. 50 (2): 193–211. doi:10.1016/j.plipres.2011.01.001. ISSN1873-2194.
↑Núñez, E., Benito, C., Pazos, M. R., Barbachano, A., Fajardo, O., González, S., Tolón, R. M., Romero, J. (15 September 2004). "Cannabinoid CB2 receptors are expressed by perivascular microglial cells in the human brain: an immunohistochemical study". Synapse (New York, N.Y.). 53 (4): 208–213. doi:10.1002/syn.20050. ISSN0887-4476.
↑Mechoulam, R., ed. (1986). Cannabinoids as therapeutic agents. CRC Press. ISBN9780849357725.
↑Brents, L. K., Reichard, E. E., Zimmerman, S. M., Moran, J. H., Fantegrossi, W. E., Prather, P. L. (2011). "Phase I hydroxylated metabolites of the K2 synthetic cannabinoid JWH-018 retain in vitro and in vivo cannabinoid 1 receptor affinity and activity". PloS One. 6 (7): e21917. doi:10.1371/journal.pone.0021917. ISSN1932-6203.
↑Vardakou, I., Pistos, C., Spiliopoulou, C. (1 September 2010). "Spice drugs as a new trend: mode of action, identification and legislation". Toxicology Letters. 197 (3): 157–162. doi:10.1016/j.toxlet.2010.06.002. ISSN1879-3169.
↑Müller, H., Sperling, W., Köhrmann, M., Huttner, H. B., Kornhuber, J., Maler, J.-M. (May 2010). "The synthetic cannabinoid Spice as a trigger for an acute exacerbation of cannabis induced recurrent psychotic episodes". Schizophrenia Research. 118 (1–3): 309–310. doi:10.1016/j.schres.2009.12.001. ISSN1573-2509.
↑Schneir, A. B., Baumbacher, T. (March 2012). "Convulsions associated with the use of a synthetic cannabinoid product". Journal of Medical Toxicology: Official Journal of the American College of Medical Toxicology. 8 (1): 62–64. doi:10.1007/s13181-011-0182-2. ISSN1937-6995.
↑Freeman, M. J., Rose, D. Z., Myers, M. A., Gooch, C. L., Bozeman, A. C., Burgin, W. S. (10 December 2013). "Ischemic stroke after use of the synthetic marijuana "spice"". Neurology. 81 (24): 2090–2093. doi:10.1212/01.wnl.0000437297.05570.a2. ISSN1526-632X.
↑Every-Palmer, S. (1 September 2011). "Synthetic cannabinoid JWH-018 and psychosis: an explorative study". Drug and Alcohol Dependence. 117 (2–3): 152–157. doi:10.1016/j.drugalcdep.2011.01.012. ISSN1879-0046.
↑Lin, C. Y., Wheelock, A. M., Morin, D., Baldwin, R. M., Lee, M. G., Taff, A., Plopper, C., Buckpitt, A., Rohde, A. (16 June 2009). "Toxicity and metabolism of methylnaphthalenes: comparison with naphthalene and 1-nitronaphthalene". Toxicology. 260 (1–3): 16–27. doi:10.1016/j.tox.2009.03.002. ISSN1879-3185.
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