Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Clinical: Approaches · Group therapy · Techniques · Types of problem · Areas of specialism · Taxonomies · Therapeutic issues · Modes of delivery · Model translation project · Personal experiences ·

Classification and external resources
ICD-10 F15

Caffeine is a commonplace CNS 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 flavouring agent.

Caffeine's mechanism of action is somewhat different from that of many other addictive drugs, such as cocaine or the 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]


Physical and psychological addiction can result from excessive caffeine intake. 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.[4] Griffiths strongly believes that caffeine withdrawal should be classified as a psychological disorder.[4] Through his research, withdrawals occurred within 12 to 24 hours after stopping caffeine intake and could last as long as nine days. [5]


Taking over 300 mg (approximately 3 cups of espresso) of caffeine daily over a long period of time may overstimulate the nervous system and produce nervousness, a flushed face, muscle twitching, irregular and/or rapid heart beat (tachycardia), and rambling thoughts and speech. [citation needed]

Caffeine intoxication is a mental disorder in the ICD-10 and the DSM-IV.


A single cup of coffee can reduce cerebral blood flow by 30%,[6] resulting in the widening of blood vessels in the tissues outside the brain in preterm infants.[2]

Behavioral effectsEdit

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.[7]

See alsoEdit


  1. 1.0 1.1 Fisone, G, Borgkovist A, Usiello A (2004): Caffeine as a psychomotor stimulant: Mechanism of Action. Cellular and Molecular Life Sciences 61:857-872
  2. 2.0 2.1 Nehlig A, Daval J-L, Debry G (1992): Caffeine and the central nervous system: Mechansisms of action, biochemical, metabolic, and psychostimulant effects. Brain Research Reviews 17: 139-170.
  3. Eskenazi B (1993): Caffeine during pregnancy: Grounds for concern? Journal of the American Medical Association 270:2973-2974
  4. 4.0 4.1 Studeville, George. “Caffeine Addiction Is a Mental Disorder, Doctors Say.” National Geographic. Jan. 15, 2010.
  5. Griffiths R, Juliano (2004): Psychopharmacology; A Critical Review of Caffeine Withdrawal; Sept. 21, 2004
  6. Hoecker C, Nelle M, Poeschl J, Beedgen B. Linderkamp O (2002): Caffeine impairs cerebral and intestinal blood flow velocity in preterm infant. Pediatrics 109: 784-787.
  7. Wesentsten NJ, Belenky G, Kautz Ma, Thorne DR, Reichardt RM, Balkin TJ (2002): Maintaining alertness and performance during sleep deprivation: Modafinil versus caffeine. Psychopharmacology 159:238-247


  • Burchfield, C. Hedges, D. Mind, Brain and Drug: An Introduction to Psychopharmacology 2006, Pearson Education, Inc., pp. 144–146
This page uses Creative Commons Licensed content from Wikipedia (view authors).

Ad blocker interference detected!

Wikia is a free-to-use site that makes money from advertising. We have a modified experience for viewers using ad blockers

Wikia is not accessible if you’ve made further modifications. Remove the custom ad blocker rule(s) and the page will load as expected.