Caffeine dependence
Overview
Caffeine is a commonplace CNS stimulant drug, occurring both in nature as part of the coffee, tea and yerba mate plants, and as an additive in many consumer products, most notably beverages advertised as energy drinks (such as Red Bull). However, caffeine is also added to sodas such as Coca-Cola and Pepsi; on the ingredients listing, it is designated as a flavouring agent.
Although its mechanism of action is somewhat different to that of cocaine or the amphetamines, for example, it nonetheless creates a similar pattern of dependence. It is believed that this is due to the (albeit indirect) manipulation of dopamine and norepinephrine levels in the brain and body, which in turn are caused by antagonism of adenosine receptors. Whilst the drug is active, antagonism of adenosine sites increases - as do levels of neurotransmitters. Conversely, when the drug wears off the brain will, in severe enough cases, release less than the usual level of neurotransmitters, in order to compensate for depletion. Due to this effect, users of caffeine will often be tempted to re-dose in order to avoid the "crash".
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Caffeine's mechanism of action
Caffeine provides stimulative effects because it reduces the obstruction produced by adenosine and neuronal activity is constrained.[1] A₁ and A₂ₐ are the two subtypes of which caffeine is thought to antagonize from the four known adenosine receptors. Adenosine A₁ receptors are presynaptic and are found in many areas of the brain, including the cerebral cortex and hippocampus, where the release of dopamine, glutamate, and acetylcholine release is inhibited.[1] Benzodiazepine receptors are antagonized as well, though this antagonism brought on by caffeine is weaker compared to 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 (age is an independent variable) and if the person is pregnant. By the end of pregnancy, its half life increases to ten hours for the pregnant woman. Caffeine's half-life is longer in the fetus due to it lacking the liver enzymes CYP1A2 and CYP1A1 to metabolize it.[3]
Addiction
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 the studies had demonstrated that people who take in a minimum of one hundred milligrams of caffeine per day (about the amount in half a 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, but could last as long as nine days and caffeine consumers are more apt to consume to waive off the withdrawal symptoms instead of to enjoy the product.[5]
Intoxication
Taking over 300 mg of caffeine daily over a long period of time will overstimulate the nervous system and produce nervousness, a flushed face, muscle twitching, irregular and/or rapid heart beat (tacchycardia), rambling thoughts and speech. [citation needed]
Headaches
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 effects
Caffeine has been shown to be as effective as modafinil in adults who were awake for a little more than 54 hours in maintaining cognitive alertness. However, it has the potential to promote anxiety, especially in young adults.[7]
References
- ^ a b Fisone, G, Borgkovist A, Usiello A (2004): Caffeine as a pyschomotor stimulant: Mechanism of Action. Cellular and Molecular Life Sciences 61:857-872
- ^ a b Nehlig A, Daval J-L, Debry G (1992): Caffeine and the central nervous system: Mechansisms of action, biochemical, metabolic, and pyschostimulant effects. Brain Research Reviews 17: 139-170.
- ^ Eskenazi B (1993): Caffeine during pregnancy: Grounds for concern? Journal of the American Medical Association 270:2973-2974
- ^ 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
- ^ Griffiths R, Juliano (2004): Psychopharmacology; A Critical Review of Caffeine Withdrawal; Sept. 21, 2004
- ^ 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.
- ^ Wesentsten NJ, Belenky G, Kautz Ma, Thorne DR, Reichardt RM, Balkin TJ (2002): Maintaining alertness and performance during sleep deprivation: Modafinil versus caffeine. Pyschopharmacology 159:238-247
(Thanks mostly in part to Burchfield, C. Hedges, D. Mind, Brain and Drug: An Introduction to Psychopharmacology 2006, Pearson Education, Inc., pp. 144–146, & Professor James Epps, Ph.D. at USFP