Caffeine dependence

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Caffeine dependence
Classification and external resources
ICD-10F15.2
 
  (Redirected from Caffeine addiction)
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Caffeine dependence
Classification and external resources
ICD-10F15.2
Addiction glossary[1][2]
addiction – a state characterized by compulsive engagement in rewarding stimuli, despite adverse consequences
reinforcing stimuli – stimuli that increase the probability of repeating behaviors paired with them
rewarding stimuli – stimuli that the brain interprets as intrinsically positive or as something to be approached
addictive drug – a drug that is both rewarding and reinforcing
addictive behavior – a behavior that is both rewarding and reinforcing
sensitization – an amplified response to a stimulus resulting from repeated exposure to it
drug tolerance – the diminishing effect of a drug resulting from repeated administration at a given dose
drug sensitization or reverse tolerance – the escalating effect of a drug resulting from repeated administration at a given dose
drug dependence – an adaptive state associated with a withdrawal syndrome upon cessation of repeated drug intake
physical dependence – dependence that involves physical–somatic withdrawal symptoms (e.g., fatigue)
psychological dependence – dependence that involves emotional–motivational withdrawal symptoms (e.g., dysphoria and anhedonia)
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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 cocaine and the substituted amphetamines. Caffeine blocks adenosine receptors A and A2A.[3] Adenosine is a by-product of cellular activity, and stimulation of adenosine receptors produces 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.

Dependence[edit]

Mild physical dependence can result from excessive caffeine intake.[4] Caffeine addiction, or a pathological and compulsive form of use, has never been documented in humans.[4]

Studies have 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] Professor Roland Griffiths, a professor of neurology at John Hopkins in Baltimore 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]

References[edit]

  1. ^ 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. pp. 364–375. ISBN 9780071481274. 
  2. ^ Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues Clin Neurosci 15 (4): 431–443. PMC 3898681. PMID 24459410. DESPITE THE IMPORTANCE OF NUMEROUS PSYCHOSOCIAL FACTORS, AT ITS CORE, DRUG ADDICTION INVOLVES A BIOLOGICAL PROCESS: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement 
  3. ^ Fisone, G, Borgkvist A, Usiello A (2004): Caffeine as a psychomotor stimulant: Mechanism of Action. Cellular and Molecular Life Sciences 61:857-872
  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