Caffeine addiction

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Classification and external resources
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Classification and external resources

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 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] 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 3 times a day for 18 days.[6]

According to the Journal of Caffeine Research, a new study has found that more people are dependent on caffeine causing experts to issue a "caffeine use disorder" warning. The study, coauthored by American University psychology professor Laura Juliano, illustrates the increasing number of individuals who are suffering withdrawal symptoms and their inability to reduce their caffeine consumption, causing the "caffeine use disorder" as a serious condition. Juliano stated in a press release, “There is misconception among professionals and lay people alike that caffeine is not difficult to give up. However, in population-based studies, more than 50 percent of regular caffeine consumers report that they have had difficulty quitting or reducing caffeine use. Through our research, we have observed that people who have been unable to quit or cut back on caffeine on their own would be interested in receiving formal treatment—similar to the outside assistance people can turn to if they want to quit smoking or tobacco use.” Juliano also made the claim that the negative effects from caffeine are often overlooked because it is a "socially acceptable and widely consumed drug that is well integrated into our customs and routines."[7][8][9]

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.[10]

The formal definition of caffeine is Caffeine is defined as a white, crystalline, bitter alkaloid, C 8 H 10 N 4 O 2 , generally derived from coffee and tea. Caffeine has the ability to mimic neurochemicals found in the brains receptors to suppress the chemicals that make someone tired. In addition to consuming large amount of caffeine, abruptly stopping the consumption also can have an effect on the mood. Suddenly quitting caffeine may increase the symptoms of depression, irritability, fatigue and headaches. As the chemicals in the brain are releasing its natural stimulants, the stimulants highly affect muscle contraction. This is why the heart rate is affected as well as blood pressure. People often experience a lack of sleep when they consume caffeine; this is one of the most common and underestimated side effects of caffeine. Caffeine mimics a neurochemical called Adenosine (the more Adenosine the body produces, the sleepier someone feels).


  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 Studeville, George. “Caffeine Addiction Is a Mental Disorder, Doctors Say.” National Geographic. Jan. 15, 2010.
  5. ^ 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
  6. ^ "Caffeine Pharmacology." News Medical.
  7. ^ "Experts Warn Of ‘Caffeine Use Disorder’". CBS DC. 29 January 2014. Retrieved 30 January 2014. 
  8. ^ Smith, Brett (29 January 2014). "Researchers Say ‘Caffeine Use Disorder’ Is A Major Health Concern". Red Orbit. Retrieved 30 January 2014. 
  9. ^ "Do you have caffeine use disorder?". Health 24. 29 January 2014. Retrieved 30 January 2014. 
  10. ^ 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