World Library  
Flag as Inappropriate
Email this Article

Cocaine dependence

Article Id: WHEBN0014079207
Reproduction Date:

Title: Cocaine dependence  
Author: World Heritage Encyclopedia
Language: English
Subject: Alcoholism, Warren Boyd, Comedown (drugs), Substance dependence, Cocaine
Collection: Cocaine, Substance Dependence
Publisher: World Heritage Encyclopedia

Cocaine dependence

Cocaine dependence
Classification and external resources
ICD-10 F14.2
ICD-9 304.2
eMedicine med/3116
MeSH D019970

Cocaine dependence (or addiction) is a psychological desire to use cocaine regularly. Cocaine overdose may result in cardiovascular and brain damage such as constricting blood vessels in the brain, causing strokes and constricting arteries in the heart, causing heart attacks[1] specifically in the central nervous system.

The use of cocaine creates euphoria and high amounts of energy much like caffeine. If taken in large unsafe doses, it is possible to cause mood swings, paranoia, insomnia, psychosis, high blood pressure, tachycardia, panic attacks, cognitive impairments and drastic changes in personality.

The symptoms of cocaine withdrawal (also known as comedown or crash) range from moderate to severe: dysphoria, depression, anxiety, psychological and physical weakness, pain and compulsive craving.

Historically, the addiction was known as cocainism.[2]


  • Signs and symptoms 1
  • Risk 2
  • Mechanism 3
  • Treatment 4
    • Withdrawal symptoms 4.1
    • Therapy 4.2
    • Medications 4.3
  • Epidemiology 5
  • See also 6
  • Notes 7
  • References 8

Signs and symptoms

Cocaine is a powerful stimulant known to make users feel energetic, happy, talkative, etc. In time, negative side effects include increased body temperature, irregular or rapid heart rate, high blood pressure, increased risk of heart attacks, strokes and even sudden death from cardiac arrest.[3] Many habitual abusers develop a transient manic-like condition similar to amphetamine psychosis and schizophrenia, whose symptoms include aggression, severe paranoia, and tactile hallucinations including the feeling of insects under the skin (formication), also known as Formication"coke bugs", during binges.[4]


According to a study of 1081 US residents aged over 11 years who had used cocaine for the first time within 24 months prior to assessment, the risk of becoming cocaine-dependent within 2 years of first use (recent-onset) is 5-6%; after 10 years, it increases to 15-16%. These are the aggregate rates for all types of use considered, i.e., smoking, snorting, injecting. Among recent-onset users, the relative rates are higher for smoking (3.4 times) and much higher for injecting. They also vary, based on other characteristics, such as sex: among recent-onset users, women are 3.3 times more likely to become addicted, compared with men; age: among recent-onset users, those who started using at ages 12 or 13 were 4 times as likely to become addicted, compared with those who started between ages 18 and 20.[5][6]

However, a study of non-deviant[nb 1] users in Amsterdam found "relative absence of destructive and compulsive use patterns over a ten year period" and concluded that cocaine users can and do exercise control. "Our respondents applied two basic types of controls to themselves: 1) restricting use to certain situations and to emotional states in which cocaine's effects would be most positive, and 2) limiting mode of ingestion to snorting of modest amounts of cocaine, staying below 2.5 grams a week for some, and below 0.5 grams a week for most. Nevertheless, those whose use level exceeded 2.5 grams a week all returned to lower levels."[7]


It is speculated that cocaine's intense addictive properties stem partially from its DAT-blocking effects (in particular, increasing the dopaminergic transmission from ventral tegmental area neurons). However, a study has shown that mice with no dopamine transporters still exhibit the rewarding effects of cocaine administration.[8] Later work demonstrated that a combined DAT/SERT knockout eliminated the rewarding effects.[9]

Signaling cascade in the nucleus accumbens that results in psychostimulant addiction

This diagram depicts the signaling events in the brain's reward center that are induced by chronic high-dose exposure to psychostimulants that increase the concentration of synaptic dopamine, like amphetamine, methylphenidate, phenethylamine, and cocaine. Following presynaptic dopamine and glutamate co-release by such psychostimulants, postsynaptic receptors for these neurotransmitters trigger internal signaling events through a cAMP pathway and calcium-dependent pathway that ultimately result in increased CREB phosphorylation.[10][11] Phosphorylated CREB increases levels of ΔFosB, which in turn represses the c-fos gene with the help of corepressors.[11] A highly stable (phosphorylated) form of ΔFosB, one that persists in neurons for one or two months, slowly accumulates following repeated exposure to stimulants through this process.[12][13] ΔFosB functions as "one of the master control proteins" that produces addiction-related structural changes in the brain, and upon sufficient accumulation, with the help of its downstream targets (e.g., nuclear factor kappa B), it induces an addictive state.[12][13]


A study published in May 2008, in the journal Molecular Psychiatry, detailed the effect of long-term cocaine intake on the amount and activity of thousands of proteins in monkeys. The researchers used "proteomic" technology, which enables the simultaneous analysis of thousands of proteins, to compare the "proteome" (all proteins expressed at a given time) between a group of monkeys that self-administered cocaine and a group that did not receive the drug. The study provides a comprehensive assessment of biochemical changes occurring in the cocaine-addicted brain. The profound changes in structure, metabolism and signaling of neurons may explain why relapse occurs and why it is difficult to reverse these changes after the drug use is discontinued.[14]

On 14 February 2011, two Swiss psychologists, Dr. Francois Crespo and Dr. Sylvie Petitjean, published two years of trials and research which demonstrates that gambling along with psychotherapy is the best method to break the cocaine addiction cycle. According to Dr. Crespo - "After cocaine is used, it activates the reward center inside the brain. The brain released euphoric hormones and neurotransmitters such as dopamine, oxytocin and adrenaline which act as a mood enhancer. The same occurs with gambling: the brain perceives a reward from winning or the potential of a reward. The reward causes intense moments of happiness, which compensate for the desire to use cocaine". Further research is being conducted on long term relapse rates.[15][16]

Withdrawal symptoms

After taking cocaine on a regular basis, some users will become addicted. When the drug is discontinued immediately, the user will experience what has come to be known as a "crash" along with a number of other cocaine withdrawal symptoms, including paranoia, depression, exhaustion, anxiety, itching, mood swings, irritability, fatigue, insomnia, an intense craving for more cocaine, and in some cases nausea and vomiting. Some cocaine users also report having similar symptoms to schizophrenia patients and feel that their mind is lost. Some users also report formication: a feeling of a crawling sensation on the skin also known as "coke bugs". These symptoms can last for weeks or, in some cases, months. Even after most withdrawal symptoms dissipate most users feel the need to continue using the drug; this feeling can last for years and may peak during times of stress. About 30-40% of cocaine addicts will turn to other substances such as medication and alcohol after giving up cocaine. There are various medications on the market to ease cocaine withdrawal symptoms.[17]


Twelve-step programs such as Cocaine Anonymous (modeled on Alcoholics Anonymous) have been widely used to help those with cocaine addiction. Cognitive Behavioral Therapy (CBT) combined with Motivational Therapy (MT) have proven to be more helpful than 12 step programs in treating cocaine dependency.[18] However, both these approaches have a fairly low success rate. Cocaine vaccines are in clinical trials that will limit the rewarding effects from cocaine.[19] The National Institutes of Health of US, particularly National Institute on Drug Abuse (NIDA) is researching modafinil, a narcolepsy drug and mild stimulant, as a potential cocaine treatment. Ibogaine has been under investigation as a treatment for cocaine dependency-and is used in clinics in Mexico, the Netherlands and Canada, but cannot be used legally in the USA. Non pharmacological treatments such as acupuncture[20][21] and hypnosis[22][23] have been explored, but without conclusive results. Cocaine addiction continues to be the most difficult to manage behind heroin.[24][25]


Medications that have been investigated include acetylcysteine,[26][27][28] baclofen,[29][30] bupropion,[31] vanoxerine,[32] and vigabatrin.[29] Kim Janda has been working for years on a vaccination that would cure cocaine addiction.[33]


In the United States, cocaine use results in about 5,000 to 6,000 deaths annually.[34]

See also

  • SB-277011-A - a dopamine D3 receptor antagonist, used in the study of cocaine addiction. Where cocaine reduces the threshold for brain electrical self-stimulation in rats, an indication of cocaine's rewarding effects, SB-277011-A completely reverses this effect.


  1. ^ The study's authors stated that they wanted to know which effects and consequences of cocaine use would become visible with persons who are mainstream citizens or as close to that social stratum as possible


  1. ^ Cocaine Use and Its Effects
  2. ^ Medical herald. 1891. p. 79. Retrieved 16 June 2011. 
  3. ^ Walsh, Karen (October 2010). "Teen Cocaine Use". 
  4. ^ Gawin, F.H. (1991). "Cocaine addiction: Psychology and neurophysiology".  
  5. ^ Tierney, John. "The Rational Choices of Crack Addicts". New York Times. Retrieved 16 September 2013. 
  6. ^ O'Brien MS, Anthony JC (2005). "Risk of becoming cocaine dependent: epidemiological estimates for the United States, 2000–2001.". Neuropsychopharmacology 30 (5): 1006–1018.  
  7. ^ Cohen, Peter; Sas, Arjan (1994). Cocaine use in Amsterdam in non deviant subcultures. Addiction Research, Vol. 2, No. 1, pp. 71-94.
  8. ^ Sora, I; Wichems, C; Takahashi, N; Li, XF; Zeng, Z; Revay, R; Lesch, KP; Murphy, DL; Uhl, GR (23 June 1998). "Cocaine reward models: Conditioned place preference can be established in dopamine- and in serotonin-transporter knockout mice". Proc. Natl. Acad. Sci. U.S.A. 95 (13): 7600–7704.  
  9. ^ Sora, I.; Hall, FS; Andrews, AM; Itokawa, M; Li, XF; Wei, HB; Wichems, C; Lesch, KP et al. (April 2001). "Molecular mechanisms of cocaine reward: Combined dopamine and serotonin transporter knockouts eliminate cocaine place preference". Proc. Natl. Acad. Sci. U.S.A. 98 (9): 5300–5.  
  10. ^ Kanehisa Laboratories (10 October 2014). "Amphetamine – Homo sapiens (human)". KEGG Pathway. Retrieved 31 October 2014. 
  11. ^ a b Renthal W, Nestler EJ (2009). "Chromatin regulation in drug addiction and depression". Dialogues Clin. Neurosci. 11 (3): 257–268.  
  12. ^ a b Robison AJ, Nestler EJ (November 2011). "Transcriptional and epigenetic mechanisms of addiction". Nat. Rev. Neurosci. 12 (11): 623–637.  
  13. ^ a b Nestler EJ (December 2012). "Transcriptional mechanisms of drug addiction". Clin. Psychopharmacol. Neurosci. 10 (3): 136–143.  
  14. ^ Newswise: Research Reveals Molecular Fingerprint of Cocaine Addiction
  15. ^ Der Standard: Stimulus to stimulus in the race (in German)
  16. ^ BlackJack Champ News: Swiss docs prove gambling cure for cocaine users
  17. ^ Cocaine withdrawal Symptoms Resource
  18. ^ "Cognitive behavioural therapy reduced cocaine abuse compared with 12 step facilitation". 17 January 2008. Retrieved 25 August 2012. 
  19. ^ "Baylor Doctors are Working on Cocaine Vaccine". 17 January 2008. Retrieved 11 September 2008. 
  20. ^ Margolin, Arthur et al. (2 January 2002). "Acupuncture for the treatment of cocaine addiction: A randomized controlled trial". The Journal of the American Medical Association 287 (1). 
  21. ^ Otto, Katharine C.; Quinn, Colin; Sung, Yung-Fong (Spring 1998). "Auricular acupuncture as an adjunctive treatment for cocaine addiction: A pilot study". The American Journal on Addictions 7 (2): 164–170.  
  22. ^ Page, R.A.; Handleya, G.W. (1993). "The use of hypnosis in cocaine addiction". American Journal of Clinical Hypnosis 36 (2): 120–123.  
  23. ^ Potter, Greg (2004). "Intensive therapy: Utilizing hypnosis in the treatment of substance abuse disorders". American Journal of Clinical Hypnosis 47 (1): 21–28.  
  24. ^ Schaler, Jeffrey A. (September–October 1991). "Drugs and free will". Society 28 (6): 42–49.  
  25. ^ Barbara, John; Morrison, June (January 1975). "If addiction is incurable, why do we try to cure it?: A comparison of control methods in the U.K. and the U.S". Crime & Delinquency 21 (1): 28–33.  
  26. ^ Mardikian PN, LaRowe SD, Hedden S, Kalivas PW, Malcolm RJ (March 2007). "An open-label trial of N-acetylcysteine for the treatment of cocaine dependence: a pilot study". Prog. Neuropsychopharmacol. Biol. Psychiatry 31 (2): 389–94.  
  27. ^ LaRowe SD, Myrick H, Hedden S et al. (July 2007). "Is cocaine desire reduced by N-acetylcysteine?". Am J Psychiatry 164 (7): 1115–7.  
  28. ^ Gass JT, Olive MF (January 2008). "Glutamatergic substrates of drug addiction and alcoholism". Biochem. Pharmacol. 75 (1): 218–65.  
  29. ^ a b Karila L, Gorelick D, Weinstein A et al. (May 2008). "New treatments for cocaine dependence: a focused review". Int. J. Neuropsychopharmacol. 11 (3): 425–38.  
  30. ^ Ling W, Shoptaw S, Majewska D (May 1998). "Baclofen as a cocaine anti-craving medication: a preliminary clinical study". Neuropsychopharmacology 18 (5): 403–4.  
  31. ^ Margolin A, Kosten TR, Avants SK et al. (December 1995). "A multicenter trial of bupropion for cocaine dependence in methadone-maintained patients". Drug Alcohol Depend 40 (2): 125–31.  
  32. ^ Cherstniakova SA, Bi D, Fuller DR, Mojsiak JZ, Collins JM, Cantilena LR (September 2001). "Metabolism of vanoxerine, 1-[2-[bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl)piperazine, by human cytochrome P450 enzymes". Drug Metab. Dispos. 29 (9): 1216–20.  
  33. ^ Douglas Quenqua (3 October 2011). "An Addiction Vaccine, Tantalizingly Close".  
  34. ^ "Unintentional Drug Poisoning in the United States". Center for Disease Control. 
This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from World eBook Library are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.