Caffeine dependence

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Caffeine dependence
Classification and external resources
ICD-10 F15.2

Caffeine is a commonplace central nervous system stimulant drug which occurs in nature as part of the coffee, tea, yerba mate and some other plants. It is also an additive in many consumer products, most notably beverages advertised as energy drinks. Caffeine is also added to sodas such as Coca-Cola and Pepsi, where, on the ingredients listing, it is designated as a flavoring agent.

Caffeine's mechanism of action is somewhat different from that of many other drugs of abuse, such as cocaine or the substituted amphetamines. Caffeine antagonizes, or blocks, adenosine receptors. Adenosine is a by-product of cellular activity, and the adenosine receptors play a role in producing feelings of tiredness and the need to sleep. Caffeine's ability to block these receptors means the levels of the body's natural stimulants, dopamine and norepinephrine continue at higher levels. While the drug is active, adenosine site antagonization increases, as do levels of neurotransmitters.

Caffeine's mechanism of action[edit]

Caffeine's stimulative effects hail from both a reduction in the obstruction produced by adenosine and a constraint of neuronal activity.[1] There are four known adenosine receptors; A1 and A2A are the two subtypes that caffeine (theoretically) antagonizes. Adenosine A1 receptors are presynaptic and reside in many areas of the brain, including the cerebral cortex and hippocampus, where they inhibit the release of dopamine, glutamate, and acetylcholine.[1] Caffeine antagonizes benzodiazepines as well, though it is weaker than that of the adenosine receptors. Caffeine can interfere with the effects of concurrently consumed benzodiazepines.[2]

The half-life in adults ranges from 3.5–6 hours and varies with age. Pregnancy also affects the half-life; by the end of pregnancy, it increases to ten hours. Caffeine's half-life is longer in the fetus, as it lacks liver enzymes CYP1A2 and CYP1A1 to metabolize it.[3]

Dependence[edit]

Mild physical dependence can result from excessive caffeine intake.[4] Caffeine addiction, or a pathological and compulsive form of use, has been documented in humans.[4]

In an interview, Roland Griffiths, a professor in the departments of psychiatry and neuroscience at the Johns Hopkins School of Medicine, said that studies had demonstrated that people who take in a minimum of 100 mg of caffeine per day (about the amount in one cup of coffee) can acquire a physical dependence that would trigger withdrawal symptoms that include headaches, muscle pain and stiffness, lethargy, nausea, vomiting, depressed mood, and marked irritability.[5] Griffiths strongly believes that caffeine withdrawal should be classified as a psychological disorder.[5] Through his research, withdrawals occurred within 12–24 hours after stopping caffeine intake and could last as long as nine days.[6] Continued exposure to caffeine will lead the body to create more adenosine receptors in the central nervous system which makes it more sensitive to the effects of adenosine in two ways. Firstly, it will reduce the stimulatory effects of caffeine by increasing tolerance. Secondly, it will increase the withdrawal symptoms of caffeine as the body will be more sensitive to the effects of adenosine once caffeine intake stops. Caffeine tolerance develops very quickly. Tolerance to the sleep disruption effects of caffeine were seen after consumption of 400 mg of caffeine 3 times a day for 7 days, whereas complete tolerance was observed after consumption of 300 mg taken 3 times a day for 18 days.[7]

Behavioral effects[edit]

Caffeine has been shown to be as effective as modafinil in adults who were awake for more than 54 hours in maintaining cognitive alertness. However, it has the potential to promote anxiety, especially in young adults.[8]

References[edit]

  1. ^ a b Fisone, G, Borgkvist A, Usiello A (2004): Caffeine as a psychomotor stimulant: Mechanism of Action. Cellular and Molecular Life Sciences 61:857-872
  2. ^ Nehlig, A.; Daval, J. L.; Debry, G. R. (1992). "Caffeine and the central nervous system: Mechanisms of action, biochemical, metabolic and psychostimulant effects". Brain Research Reviews 17 (2): 139–170. doi:10.1016/0165-0173(92)90012-B. PMID 1356551.  edit
  3. ^ Eskenazi, B. (1993). "Caffeine During Pregnancy: Grounds for Concern?". JAMA: the Journal of the American Medical Association 270 (24): 2973–2974. doi:10.1001/jama.1993.03510240085039.  edit
  4. ^ a b Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 375. ISBN 9780071481274. "Long-term caffeine use can lead to mild physical dependence. A withdrawal syndrome characterized by drowsiness, irritability, and headache typically lasts no longer than a day. True compulsive use of caffeine has not been documented." 
  5. ^ a b Studeville, George. “Caffeine Addiction Is a Mental Disorder, Doctors Say.” National Geographic. Jan. 15, 2010. http://news.nationalgeographic.com/news/2005/01/0119_050119_ngm_caffeine.html
  6. ^ Juliano, L. M.; Griffiths, R. R. (2004). "A critical review of caffeine withdrawal: Empirical validation of symptoms and signs, incidence, severity, and associated features". Psychopharmacology 176 (1): 1–29. doi:10.1007/s00213-004-2000-x. PMID 15448977.  edit
  7. ^ "Caffeine Pharmacology." News Medical. http://www.news-medical.net/health/Caffeine-Pharmacology.aspx
  8. ^ Wesensten, N.; Belenky, G.; Kautz, M. A.; Thorne, D. R.; Reichardt, R. M.; Balkin, T. J. (2001). "Maintaining alertness and performance during sleep deprivation: Modafinil versus caffeine". Psychopharmacology 159 (3): 238–247. doi:10.1007/s002130100916. PMID 11862356.  edit