A large number of consumed dietary sources contain caffeine, such as coffee, tea, cocoa beverages, chocolate drinks, and soft drinks. The caffeine content in each of these food items ranges from 2 to 7mg for150ml of cocoa to 40 to 180mg for 150ml of coffee, but the worldwide daily consumption is estimated between 70 to 76mg.

By contrast, caffeine consumption in several European countries and the US surpasses those numbers by a large margin, and for example in the US daily consumption is estimated between 210 to 238mg (note: those numbers were taken from studies done in the early to mid-1980s, and thus they are probably much higher in this new millennium).

Caffeine is absorbed in the gastrointestinal tract within 45 minutes after ingestion, but absorption is not complete when it is taken as coffee. Its half-life is similar across young and elderly individuals, estimated between 2.5 and 4.5 hours.


Adenosine is a naturally occurring intercellular messenger whose many functions have neuroprotective effects on the brain. One such function is that of a homeostatic regulator that matches the rate of energy consumption with the rate of energy supply. In other words, when energy output exceeds the supply of energy fuel, adenosine is naturally released to slow down or halt new chemical reactions, which for example occurs with high body temperature, seizures (i.e., has anticonvulsant effects), or with the generation of free radicals.  It is also a vasodilator that promotes the autoregulation of the cerebral blood flow under both normal and abnormal conditions (i.e., ischemia). Adenosine accomplishes all those functions by way of inhibiting the release of excitatory neurotransmitters (i.e., a chemical messengers) and other neuromodulators, thereby halting the initiation of a particular response. Thus, adenosine has been associated with several normal and pathological processes such as sleep, arousal, neuroprotection, and epilepsy.

By contrast, caffeine blocks adenosine by binding to its receptors in the brain, which thwarts its inhibitory effects and stimulates the initiation of a response. Therefore, by ingesting caffeine we are essentially overriding a natural process by which the brain conserves energy. The therapeutic or adverse effects of caffeine will vary considerably depending upon whether it is administered chronically or acutely, and for example there is evidence that chronic caffeine intake may have neuroprotective effects. On the other hand, the adverse effects may include anxiety, hypertension, and withdrawal symptoms. For example, caffeine overuse and dependency occurs after large amounts are consumed over an extended period of time.


There is evidence that at low doses (e.g., 20-200mg), caffeine produces positive subjective effects, which include feeling energetic, alert, able to focus, and even a desire to socialize. On the other hand, caffeine has been associated with increased anxiety and panic attacks at higher doses. For example, a study reported that psychiatric outpatients who consumed more than 1000mg of caffeine per day had symptoms of generalized anxiety disorder in addition to their primary psychiatric diagnosis. Alternatively, panic disorder individuals are extremely sensitive to the arousing effects of caffeine at even low doses.  

Furthermore, the relationship between caffeine intake and other psychiatric diagnoses have also been, and for example high caffeine consumption reportedly exacerbates symptoms of schizophrenia. More importantly, there are reports indicating that caffeine-intoxicated people might have been misdiagnosed, as such a condition could mimic other psychopathologies like panic disorder, generalized anxiety disorder, bipolar disorder, or even schizophrenia.


Reports indicate that a dose of caffeine equivalent to one cup of coffee taken before bedtime increases sleep latency (i.e., it takes longer to fall asleep) and decreases sleep quality. It is however important to note that caffeine interacts with a modulatory mechanism in sleep regulation rather than with brain circuits involved in the regulation of sleep, as suggested by the fact that some people do not exhibit sleep problems despite regularly consuming caffeine in the evening. In addition, it is clear that the action of caffeine on sleep is related to adenosine as it is an endogenous sleep promoter.


Caffeine appears to have protective effects against cognitive decline, but it may have neurotoxic effects in Parkinson’s and Huntington’s disease. It is also ill-advised in epilepsy and promotes headaches while alleviating migraine headaches.


Fredholm BB, Bättig K, Holmén J, Nehlig A, Zvartau EE. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev. 1999 Mar;51(1):83-133. PMID: 10049999.

Ribeiro JA, Sebastião AM. Caffeine and adenosine. J Alzheimers Dis. 2010;20 Suppl 1:S3-15. doi: 10.3233/JAD-2010-1379. PMID: 20164566.

Dunwiddie TV, Masino SA. The role and regulation of adenosine in the central nervous system. Annu Rev Neurosci. 2001;24:31-55. doi: 10.1146/annurev.neuro.24.1.31. PMID: 11283304.


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