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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 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
Caffeine's stimulative effects hail from both a reduction in the obstruction produced by adenosine and a constraint of neuronal activity. 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. 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.
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.
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. Griffiths strongly believes that caffeine withdrawal should be classified as a psychological disorder. Through his research, withdrawals occurred within 12–24 hours after stopping caffeine intake and could last as long as nine days. 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.
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.
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