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Summary sheet: Delta-8-THC

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Delta-8-tetrahydrocannabinol (also known as Delta-8-THC and Δ-8-THC) is an isomer of Delta-9-tetrahydrocannabinol (also known as Delta-9-THC and Δ-9-THC). The effects of Delta-8-THC are nearly identical to those of Delta-9-THC, but slightly less potent.

History and culture

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In 1941 Roger Adams and associates from the University of Illinois published the partial synthesis of Delta-8-THC.[1] By 1965 Raphael Mechoulam had completed the total synthesis of Delta-8-THC. Delta-8-THC didn't receive any further attention until 2018 when the Agriculture Improvement Act of 2018 was passed and a loophole was discovered in the act which allowed for the creation of Delta-8-THC "legally". Delta-8-THC use skyrocketed in many states where Marijuana remained illegal and in states where it was legal, consumption still increased as a result of the lack of regulation of Delta-8-THC.



This chemistry section is incomplete.

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The only difference between Delta-8-THC and Delta-9-THC is the movement of a double bond.


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This pharmacology section is incomplete.

You can help by adding to it.

The pharmacology of Delta-8-THC is nearly identical to that of Delta-9-THC. Delta-8-THC was shown to have a slower onset and a shorter duration. Onset varied from 30 to 90 minutes and peak effects were observed between 2-1/2 to 3-1/2 hours.[2]


Physical effects

Visual effects


Cognitive effects

Auditory effects

Multi-sensory effects

Combination effects

Experience reports

There are currently 0 experience reports which describe the effects of this substance in our experience index.

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Toxicity and harm potential


This toxicity and harm potential section is a stub.

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

Radar plot showing relative physical harm, social harm, and dependence of cannabis[29]

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.[30][31]

Cannabis arteritis (CA) is a very rare peripheral vascular disease similar to Buerger's disease.[32]


A NIH study found that suicide risk is higher with marijuana users than non-users. [33]

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. [34]

Not only that, but another study studied the association between cannabis and suicidality also has correlation.[35]

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,[36] particularly in vulnerable individuals with risk factors for psychotic illnesses (like a past or family history of schizophrenia).[37][38][39]

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.[40] 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."[41]

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,[42] 2.594 mol/kg, about 815.7 grams of THC per kilogram of body weight,[43] and human deaths from overdose are unheard of.[44]

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[45] and in the worst case this can lead to death.[46]

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.[47]

Dependence on cannabis is more common amongst heavy users. Cannabis use can lead to increased tolerance[48][49] and withdrawal symptoms upon stopping usage.[50][51][52] 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.[53]

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.[54]

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.[55]

Dangerous interactions

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

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

Legal status


This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

  • United States: Delta-8-THC is unregulated and is available without a prescription.

See also

External links

(List along order below)

  1. Adams, R., Cain, C. K., McPhee, W. D., & Wearn, R. B. (1941). Structure of cannabidiol. xii. isomerization to tetrahydrocannabinols1. Journal of the American Chemical Society, 63(8), 2209–2213.
  2. Hollister, L. E., & Gillespie, H. K. (1973). Delta-8- and delta-9-tetrahydrocannabinol; comparison in man by oral and Intravenous Administration. Clinical Pharmacology & Therapeutics, 14(3), 353–357.
  3. 3.0 3.1 3.2 3.3 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. 
  4. 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. 
  5. Mechoulam, R. (1984). Cannabinoids as therapeutic agents. Boca Raton, FL: CRC Press. ISBN 0-8493-5772-1.
  6. 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.
  7. Tetrahydrocannabivarin (THCV): A Cannabinoid Fighting Obesity |
  8. Wong, MM; Craun, EA; Bravo, AJ; Pearson, MR; Protective Strategies Study, Team. (August 2019). "Insomnia symptoms, cannabis protective behavioral strategies, and hazardous cannabis use among U.S. college students". Experimental and clinical psychopharmacology. 27 (4): 309–317. doi:10.1037/pha0000273. PMID 30907602. 
  9. The Pharmacologic and Clinical Effects of Medical Cannabis |;jsessionid=1E004D7B7E2B5CA792E75A6E83EEC59C.f03t01
  10. The Therapeutic Potential of Cannabis and Cannabinoids |
  11. Systematic Review and Meta-analysis of Cannabis Treatment for Chronic Pain |
  12. Cannabinoids for treatment of chronic non-cancer pain; a systematic review of randomized trials |
  13. Yazulla, S (September 2008). "Endocannabinoids in the retina: from marijuana to neuroprotection". Progress in retinal and eye research. 27 (5): 501–26. doi:10.1016/j.preteyeres.2008.07.002. PMID 18725316. 
  14. Charlotte Figi: The Girl Who is Changing Medical Marijuana Laws Across America |
  15. On the frontier of medical pot to treat boy's epilepsy |
  16. Report of a parent survey of cannabidiol-enriched cannabis use in pediatric treatment-resistant epilepsy ( / NCBI) |
  17. Cannabidiol displays antiepileptiform and antiseizure properties in vitro and in vivo. ( / NCBI) |
  18. An electrophysiological analysis of the anticonvulsant action of cannabidiol on limbic seizures in conscious rats. ( / NCBI) |
  19. Δ⁹-Tetrahydrocannabivarin suppresses in vitro epileptiform and in vivo seizure activity in adult rats. ( / NCBI) |
  20. Cannabinoids: Defending the Epileptic Brain ( / NCBI) |
  21. Is Marijuana an Effective Treatment for Glaucoma? |
  22. Cardiovascular Effects of Cannabis |
  24. Lac, A; Luk, JW (February 2018). "Testing the Amotivational Syndrome: Marijuana Use Longitudinally Predicts Lower Self-Efficacy Even After Controlling for Demographics, Personality, and Alcohol and Cigarette Use". Prevention science : the official journal of the Society for Prevention Research. 19 (2): 117–126. doi:10.1007/s11121-017-0811-3. PMID 28620722. 
  25. Feinberg, I., Jones, R, Walker JM, Cavness, C, March, J. (1975). Effects of high dosage delta-9-tetrahydrocannabinol on sleep patterns in man. Clin Parmacol Ther. 1975; 17(4):458-66.
  27. Causal association between cannabis and psychosis: examination of the evidence - The British Journal of Psychiatry Jan 2004, 184 (2) 110-117 |
  28. A Teenager With Agitation: Higher Than She Should Have Climbed - Pediatric Emergency Care: June 2010 - Volume 26 - Issue 6 - pp 462-465 |
  29. Development of a rational scale to assess the harm of drugs of potential misuse (ScienceDirect) |
  30. Sorensen, Cecilia J.; DeSanto, Kristen; Borgelt, Laura; Phillips, Kristina T.; Monte, Andrew A. (20 December 2016). "Cannabinoid Hyperemesis Syndrome: Diagnosis, Pathophysiology, and Treatment—a Systematic Review". Journal of Medical Toxicology. 13 (1): 71–87. doi:10.1007/s13181-016-0595-z. PMC 5330965Freely accessible. PMID 28000146. 
  31. DeVuono, Marieka; Parker, Linda (2020). "Cannabinoid Hyperemesis Syndrome: A Review of Potential Mechanisms". Cannabis and Cannabinoid Research. 5: 132–144. doi:10.1089/can.2019.0059. 
  32. El Omri, N; Eljaoudi, R; Mekouar, F; Jira, M; Sekkach, Y; Amezyane, T; Ghafir, D (2017). "Cannabis arteritis". The Pan African medical journal. 26: 53. doi:10.11604/pamj.2017.26.53.11694. PMID 28451030. 
  36. Causal association between cannabis and psychosis: examination of the evidence - The British Journal of Psychiatry Jan 2004, 184 (2) 110-117 |
  37. Every-Palmer, S. Synthetic cannabinoid use and psychosis: an explorative study. Journal of Drug and Alcohol Dependence 2011.
  38. “Spice” Girls: Synthetic Cannabinoid Intoxication - The Journal of Emergency Medicine Volume 40, Issue 3, March 2011, Pages 296–299 (ScienceDirect) |
  39. A Teenager With Agitation: Higher Than She Should Have Climbed - Pediatric Emergency Care: June 2010 - Volume 26 - Issue 6 - pp 462-465 |
  40. Does cannabis use increase the risk of death? Systematic review of epidemiological evidence on adverse effects of cannabis use |
  41. Pharmacology and effects of cannabis: a brief review |
  42. Adverse effects of cannabis |
  44. Tetrahydrocannabinols in clinical and forensic toxicology ( / NCBI) |
  45. Cannabinoid Hyperemesis Syndrome |
  46. Cannabinoid Hyperemesis Syndrome: Reports of Fatal Cases |
  47. Lopez-Quintero C, Pérez de los Cobos J, Hasin DS, et al.: Probability and predictors of transition from first use to dependence on nicotine, alcohol, cannabis, and cocaine: results of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). Drug Alcohol Depend 2011; 115: 120–30 |
  48. The Pharmacologic and Clinical Effects of Medical Cannabis |
  49. The Effect of Cannabis Compared with Alcohol on Driving |
  50. Medical Consequences of Marijuana Use: A Review of Current Literature |
  51. State of the Art Treatments for Cannabis Dependence (ScienceDirect) |
  52. Cannabinoid tolerance and dependence |
  53. MARIJUANA AND MEDICINE Assessing the Science Base |
  55. Winstock AR, Ford C, Witton J. Assessment and management of cannabis use disorders in primary care. BMJ. 2010;340:c1571. PubMed doi:10.1136/bmj.c1571