Cannabis use disorder

Cannabis use disorder
Classification and external resources
Specialty psychiatry
ICD10 F12
ICD9-CM 304.3

Cannabis use disorder (CUD), also known as cannabis addiction or marijuana addiction, is defined in the fifth revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) and ICD-10 published by World Health Organization as the continued use of cannabis despite clinically significant impairment, ranging from mild to severe.[1]

Signs and symptoms[edit]

Marijuana use and abuse has symptoms that affect behavior, physical, cognitive, and psychosocial aspects of a person’s life. Symptoms include agitation, bloodshot eyes, challenges in problem solving, and paranoia.[2]

Cannabis use is associated with comorbid mental health problems, such as mood and anxiety disorders, and discontinuing cannabis use is difficult for some users.[3] Psychiatric comorbidities are often present in dependent cannabis users including a range of personality disorders.[4]

The use of cannabis at a young age such as the teenage years, can have serious impacts on depression and anxiety in youth and later in life.[5] There is evidence that cannabis use during adolescence, at a time when the brain is still developing, may have deleterious effects on neural development and later cognitive functioning.[6] The brain is not completely developed until a person reaches the age range of 22-27. Excessive use of marijuana can cause harm to this development.[7]. Based on an annual survey data 7 percent of high school seniors that smoke daily function at a lower rate in school than students that do not.[8] The sedating and anxiolytic properties of THC in some users might make the use of cannabis an attempt to self-medicate personality or psychiatric disorders.[9]


Prolonged marijuana use produces both pharmacokinetic changes (how the drug is absorbed, distributed, metabolized, and excreted) and pharmacodynamic changes (how the drug interacts with target cells) to the body. These changes require the user to consume higher doses of the drug to achieve a common desirable effect (known as a higher tolerance), reinforcing the body’s metabolic systems for eliminating the drug more efficiently[10] and further downregulating cannabinoid receptors in the brain.[11] These effects compound themselves in that the chronic user must consume more frequently to overcome the accelerated clearance, and higher doses to overcome the blunted response to receptor activation.

Cannabis users have shown decreased reactivity to dopamine, suggesting a possible link to a dampening of the reward system of the brain and an increase in negative emotionality and addiction severity.[12]

Cannabis users can develop tolerance to the effects of THC. Tolerance to the behavioral and psychological effects of THC has been demonstrated in adolescent humans and animals.[13][14] The mechanisms that create this tolerance to THC are thought to involve changes in cannabinoid receptor function.[13]

According to the National Cannabis Prevention and Information Centre in Australia, a sign of cannabis dependence is that an individual spends noticeably more time than the average recreational user recovering from the use of or obtaining cannabis. For some, using cannabis becomes a substantial and disruptive part of an individual’s life and he or she may exhibit difficulties in meeting personal obligations or participating in important life activities, preferring to use cannabis instead. People who are cannabis dependent have the inability to stop or decrease using cannabis on their own.[15]

Marijuana addiction is more common among heavy users. Marijuana use can lead to increased tolerance[16][17] and, in some users, withdrawal symptoms when trying to stop.[18][3]


Cannabis withdrawal symptoms can occur in one half of patients in treatment for cannabis use disorders. These symptoms include dysphoria (anxiety, irritability, depression, restlessness), disturbed sleep, gastrointestinal symptoms, and decreased appetite. Most symptoms begin during the first week of abstinence and resolve after a few weeks.[3] The withdrawal symptoms are usually not severe, even after heavy use.[19]


Cannabis addiction is often due to prolonged and increasing use of the drug. Increasing the strength of the cannabis taken and an increasing use of more effective methods of delivery often increase the progression of cannabis dependency. It can also be caused by being prone to becoming addicted to substances, which can either be genetically or environmentally acquired.[20]

Risk factors[edit]

Certain factors are considered to heighten the risk of developing cannabis dependence and longitudinal studies over a number of years have enabled researchers to track aspects of social and psychological development concurrently with cannabis use. Increasing evidence is being shown for the elevation of associated problems by the frequency and age at which cannabis is used, with young and frequent users being at most risk.[21]

The main factors in Australia, for example, related to a heightened risk for developing problems with cannabis use include frequent use at a young age; personal maladjustment; emotional distress; poor parenting; school drop-out; affiliation with drug-using peers; moving away from home at an early age; daily cigarette smoking; and ready access to cannabis. The researchers concluded there is emerging evidence that positive experiences to early cannabis use are a significant predictor of late dependence and that genetic predisposition plays a role in the development of problematic use.[22]

High risk groups[edit]

A number of groups have been identified as being at greater risk of developing cannabis dependence and, in Australia, for example, have been found to include adolescent populations, Aboriginal and Torres Strait Islanders and people suffering from mental health conditions.[6]


Young people are at greater risk of developing cannabis dependency because of the association between early initiation into substance use and subsequent problems such as dependence, and the risks associated with using cannabis at a developmentally vulnerable age.[6]


Cannabis use disorder is recognized in the fifth version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5),[23] which added cannabis withdrawal as a new condition.[24]

Some healthcare facilities have been known to diagnose patients with Cannabis Use Disorder, even when the patient does not exhibit or experience any of the criteria for the disorder, simply on the basis that the patient uses cannabis in any manner. Patients receiving this false diagnosis have, in some cases, been denied insurance benefits and employment as a result of the false diagnosis, leaving the healthcare facilities vulnerable to legal action.


Clinicians differentiate between casual users who have difficulty with drug screens, and daily heavy users, to a chronic user who uses multiple times a day.[9]


Psychological intervention includes cognitive behavioral therapy (CBT), motivational enhancement therapy (MET), contingency management (CM), supportive-expressive psychotherapy (SEP), family and systems interventions, and twelve-step programs.[3]

Evaluations of Marijuana Anonymous programs, modelled on the 12-step lines of Alcoholics Anonymous and Narcotics Anonymous, have shown small beneficial effects for general drug use reduction.

In 2006, the Wisconsin Initiative to Promote Healthy Lifestyles implemented a program that helps primary care physicians identify and address marijuana use problems in patients.[25]

Barriers to treatment[edit]

Research that looks at barriers to cannabis treatment frequently cites a lack of interest in treatment, lack of motivation and knowledge of treatment facilities, an overall lack of facilities, costs associated with treatment, difficulty meeting program eligibility criteria and transport difficulties.[26][27][28]

Treatment for dependency[edit]

In the US, as of 2013, cannabis is the most commonly identified illicit substance used by people admitted to treatment facilities.[16] Demand for treatment for cannabis use disorder increased internationally between 1995 and 2002.[29] In the United States, the average adult who seeks treatment has consumed cannabis for over 10 years almost daily and has attempted to quit six or more times.[30]

No medications have been found effective for cannabis dependence as of 2014,[31] but psychotherapeutic models hold promise.[3]

Treatment options for cannabis dependence are far fewer than for opiate or alcohol dependence. Most treatment falls into the categories of psychological or psychotherapeutic, intervention, pharmacological intervention or treatment through peer support and environmental approaches.[22] Screening and brief intervention sessions can be given in a variety of settings, particularly at doctor’s surgeries, which is of importance as most cannabis users seeking help will do so from their general practitioner rather than a drug treatment service agency.[32]

The most commonly accessed forms of treatment in Australia are 12-step programmes, physicians, rehabilitation programmes, and detox services, with inpatient and outpatient services equally accessed.[33] In the EU approximately 20% of all primary admissions and 29% of all new drug clients in 2005, had primary cannabis problems. And in all countries that reported data between 1999–2005 the number of people seeking treatment for cannabis use increased.[34]


As of 2012, there is no medication that has been proven effective for treating cannabis use disorder; research is focused on three treatment approaches: agonist substitution, antagonist, and modulation of other neurotransmitter systems.[3] Dronabinol is an agonist that is legally available; in some cases and trials, it reduced symptoms of withdrawal and reduced cannabis use.[3] Entacapone was well-tolerated and decreased cannabis cravings in a trial on a small number of patients.[3] Acetylcysteine (NAC) decreased cannabis use and craving in a trial.[3] Atomoxetine in a small study showed no significant change in cannabis use, and most patients experienced adverse events.[3] Buspirone shows promise as a treatment for dependence; trials show it reducing cravings, irritability and depression.[3] Divalproex in a small study was poorly tolerated and did not show a significant reduction in cannabis use among subjects.[3]


Cannabis is one of the most widely used drugs in the world. In the United States, between 42%[18] and 49%[35] of people have used cannabis, an estimated 9% of those who use cannabis develop dependence.[36][31] 34.8% of Australians aged 14 years and over have used cannabis one or more times in their life.[37] In the U.S., cannabis is the most commonly identified illicit substance used by people admitted to treatment facilities.[3] Most of these people were referred there by the criminal justice system. 16% of admittees either went on their own, or were referred by family or friends.[38]

There is a high prevalence of cannabis use in the US.[3] Cannabis dependence develops in 9% users, significantly less than that of heroin, cocaine, alcohol, and prescribed anxiolytics,[39] but slightly higher than that for psilocybin, mescaline, or LSD.[36] Of those who use cannabis daily, 10–20% develop dependence.[16]


Columbia University, in collaboration with the National Institute on Drug Abuse (NIDA), is undertaking a clinical trial that looks at the effects of combined medication on cannabis dependency, to see if lofexidine in combination with dronabinol is superior to placebo in achieving abstinence, reducing cannabis use and reducing withdrawal in cannabis-dependent patients seeking treatment for their marijuana use.[40] Men and women between the ages of 18–60 who met DSM-IV criteria for current marijuana dependence were enrolled in a 12-week trial that started in January 2010.

Georgotas & Zeidenberg (1979) conducted an experiment where they gave an average daily dose of 210 mg of tetrahydrocannabinol (THC), the ingredient in cannabis which is responsible for its psychological effects,[41] to a group of volunteers over a 4-week period. After the test ended, the subjects were found to be “irritable, uncooperative, resistant and at times hostile,” and many of the patients experienced insomnia. These effects were likely due to withdrawal from the drug and lasted about 3 weeks after the experiment.[42]

A 2014 Cochrane Collaboration review found insufficient data to evaluate the effectiveness of gabapentin and acetylcysteine in the treatment of cannabis dependence and that it warrants further investigation.[31]

See also[edit]


  1. ^ National Institute on Drug Abuse (2014), The Science of Drug Abuse and Addiction: The Basics
  2. ^ “Cannabis Symptoms”. Timberline Knolls. Retrieved 7 May 2018.
  3. ^ a b c d e f g h i j k l m n Danovitch I, Gorelick DA (June 2012). “State of the art treatments for cannabis dependence”. Psychiatr. Clin. North Am. (Review). 35 (2): 309–26. doi:10.1016/j.psc.2012.03.003. PMC 3371269. PMID 22640758.
  4. ^ Dervaux, Alain (December 2012). “Cannabis: Use and dependence”. La Presse Médicale.
  5. ^ NCPIC. “Cannabis and young people | NCPIC”. Archived from the original on 9 March 2016. Retrieved 30 September 2016.
  6. ^ a b c McLaren, J, Mattick, R P., Cannabis in Australia Use, supply, harms, and responses Monograph series No. 57 Report prepared for: Drug Strategy Branch Australian Government Department of Health and Ageing. National Drug and Alcohol Research Centre University of New South Wales, Australia.
  7. ^ “Excessive use of Cannabis”. Centers for Disease Control and Prevention. Retrieved 7 May 2018.
  8. ^ E.B., Robertson. “Information on Cannabis Addiction”. National Institute on Drug Abuse. Retrieved 7 May 2018.
  9. ^ a b Clinical Textbook of Addictive Disorders, Marijuana, David McDowell, page 169, Published by Guilford Press, 2005 ISBN 1-59385-174-X.
  10. ^ J.E. Joy; S. J. Watson, Jr.; J.A. Benson, Jr (1999). Marijuana and Medicine: Assessing The Science Base. Washington, D.C.: National Academy of Sciences Press. ISBN 0-585-05800-8.
  11. ^ Hirvonen, J; Goodwin, R S; Li, C-T; Terry, G E; Zoghbi, S S; Morse, C; Pike, V W; Volkow, N D; Huestis, M A; Innis, R B (2011). “Reversible and regionally selective downregulation of brain cannabinoid CB1 receptors in chronic daily cannabis smokers”. Molecular Psychiatry. 17 (6): 642–649. doi:10.1038/mp.2011.82. ISSN 1359-4184. PMC 3223558. PMID 21747398.
  12. ^ Madras, B. K. (2014). “Dopamine challenge reveals neuroadaptive changes in marijuana abusers”. Proceedings of the National Academy of Sciences. 111 (33): 11915–11916. doi:10.1073/pnas.1412314111. ISSN 0027-8424. PMC 4143049. PMID 25114244.
  13. ^ a b Gonzalez, S; Cebeira, M; Fernandez-Ruiz, J (June 2005). “Cannabinoid tolerance and dependence: A review of studies in laboratory animals”. Pharmacology Biochemistry and Behavior. 81 (2): 300–318. doi:10.1016/j.pbb.2005.01.028.
  14. ^ Maldonado, R.; Berrendero, F.; Ozaita, A.; Robledo, P. (May 2011). “Neurochemical basis of cannabis addiction”. Neuroscience. 181: 1–17. doi:10.1016/j.neuroscience.2011.02.035.
  15. ^ “Alcohol vs Cannabis 2015”. National Cannabis Prevention and Information. Retrieved 17 April 2015.
  16. ^ a b c Borgelt LM, Franson KL, Nussbaum AM, Wang GS (February 2013). “The pharmacologic and clinical effects of medical cannabis”. Pharmacotherapy (Review). 33 (2): 195–209. doi:10.1002/phar.1187. PMID 23386598.
  17. ^ Sewell RA, Poling J, Sofuoglu M (2009). “The effect of cannabis compared with alcohol on driving”. Am J Addict (Review). 18 (3): 185–93. doi:10.1080/10550490902786934. PMC 2722956. PMID 19340636.
  18. ^ a b Gordon AJ, Conley JW, Gordon JM (December 2013). “Medical consequences of marijuana use: a review of current literature”. Curr Psychiatry Rep (Review). 15 (12): 419. doi:10.1007/s11920-013-0419-7. PMID 24234874.
  19. ^
  20. ^ Coffey1, Carlin2, Lynskey3, Li4, Patton5, Carolyn1, John B.2, Michael3, Ning4, George C.5 (1 April 2003). “Adolescent precursors of cannabis addiction: Findings from the Victorian Adolescent Health Cohort Study”. The British Journal of Psychiatry. 182: 330–336. doi:10.1192/bjp.182.4.330. Retrieved 17 April 2015.
  21. ^ “DrugFacts: Marijuana”. National Institute on Drug Abuse. Retrieved 20 July 2015.
  22. ^ a b Copeland, J, Gerber, S, Swift, W. Evidence-based answers to cannabis questions a review of the literatureNational Drug and Alcohol Research Centre University of New South Wales A report prepared for the Australian National Council on Drugs, December 2004
  23. ^ “Proposed Revision | APA DSM-5”. Retrieved 2011-04-20.
  24. ^ “DSM-5 Now Categorizes Substance Use Disorder in a Single Continuum” (PDF). American Psychiatric Association. 17 May 2013. Retrieved 12 December 2013.
  25. ^ “With Support From Collaborative, Primary Care Practices Identify and Address Behavioral Health Issues, Reducing Binge Drinking, Marijuana Use, and Depression Symptoms”. Agency for Healthcare Research and Quality. 2013-05-08. Retrieved 2013-05-10.
  26. ^ Treloar, C.; Holt, M. (2006). “Deficit models and divergent philosophies: Service providers’ perspectives on barriers and incentives to drug treatment”. Drugs: Education prevention and policy. 13 (4): 367–382. doi:10.1080/09687630600761444.
  27. ^ Treloar, C., Abelson, J., Cao, W., Brener, L., Kippax, S., Schultz, L., Schultz, M., & Bath, N. (2004). Barriers and incentives to treatment for illicit drug users(Monograph Series 53). Canberra: Department of Health and Ageing, National Drug Strategy.
  28. ^ Gates, P., Taplin, S., Copeland, J., swift, W., Martin G. (2008) Barriers and Facilitators to Cannabis TreatmentNational Cannabis Prevention and Information Centre, University of New South Wales, Sydney
  29. ^ Substance Abuse and Mental Health Services Administration, Office of Applied Studies. (2003). Emergency department trends from the drug abuse warning network, final estimates 1995–2002, DAWN Series: D-24, DHHS Publication No. (SMA) 03-3780.
  30. ^ Budney, Alan J.; Roffman, Roger; Stephens, Robert S.; Walker, Denise (December 2007). “Marijuana Dependence and Its Treatment”. Addiction Science & Clinical Practice. 4 (1): 4–16. doi:10.1151/ascp07414. ISSN 1940-0632. PMC 2797098. PMID 18292704.
  31. ^ a b c Marshall, K; Gowing, L; Ali, R; Le Foll, B (17 December 2014). “Pharmacotherapies for cannabis dependence”. The Cochrane Database of Systematic Reviews. 12: CD008940. doi:10.1002/14651858.CD008940.pub2. PMC 4297244. PMID 25515775.
  32. ^ Degenhardt, L., Hall, W. and Lynskey, M. (2000a) Cannabis use and mental health among Australian adults: Findings from the National Survey of Mental Health and Well-being. NDARC Technical Report No. 98 Sydney, National Drug and Alcohol Research Centre, University of New South Wales.
  33. ^ Copeland J, Swift W (April 2009). “Cannabis use disorder: epidemiology and management”. Int Rev Psychiatry (Review). 21 (2): 96–103. doi:10.1080/09540260902782745. PMID 19367503.
  34. ^ EMCDDA (2007). Annual report 2007: The state of the drugs problem in Europe. Luxembourg: Office for Official Publications of the European Communities
  35. ^
  36. ^ a b Budney, AJ; Roffman, R; Stephens, RS; Walker, D (Dec 2007). “Marijuana dependence and its treatment”. Addiction science & clinical practice. 4 (1): 4–16. doi:10.1151/ascp07414. PMC 2797098. PMID 18292704.
  37. ^ “Drug Info”. Australian Drug Foundation. Archived from the original on 25 April 2011.
  38. ^ “Treatment Episode Data Set (TEDS)2001 – 2011. National Admissions to Substance Abuse Treatment Services” (PDF). Substance Abuse and Mental Health Services Administration. Retrieved 17 April 2015.
  39. ^ Wilkie G, Sakr B, Rizack T (March 2016). “Medical Marijuana Use in Oncology: A Review”. JAMA Oncology. doi:10.1001/jamaoncol.2016.0155. PMID 26986677.
  40. ^ “US National Institute of Health”. Retrieved 2011-04-20.
  41. ^ Bradford, Alina (2015). “Live Science”. What is THC (tetrahydrocannabinol)?. Retrieved 17 April 2015.
  42. ^ Johns, Andrew (1 February 2001). “Psychiatric effects of cannabis”. The British Journal of Psychiatry. 178: 116–122. doi:10.1192/bjp.178.2.116. Retrieved 17 April 2015.