Caffeine is the most widely consumed behaviorally active substance in the world. Almost all caffeine comes from dietary sources (beverages and food), most of it from coffee and tea. Acute and, especially, chronic caffeine intake appear to have only minor negative consequences on health. For this reason and because few caffeine users report loss of control over their caffeine intake, governmental regulatory agencies impose no restrictions on the use of caffeine. Ordinary caffeine use has generally not been considered to be a case of drug abuse, and is indeed not so classified in DSM-IV (Diagnostic and Statistical Manual of Mental Disorder).3 However, some years ago it was pointed out that caffeine may be a potential drug of abuse (see Gilliland and Bullock, 1984), and more recently caffeine has been described as “a model drug of abuse” (Holtzman, 1990) and the possibility that caffeine abuse, dependence, and withdrawal should be added to diagnostic manuals has been seriously considered (Hughes et al., 1992b; Strain et al., 1994; Pickworth, 1995; Hughes et al., 1998) In the present review we discuss the evidence regarding caffeine and dependence in light of increasing knowledge regarding the actions of caffeine on specific neuronal brain substrates. Because the use of caffeine is probably related to its diverse effects on several brain functions, these are also briefly presented. Even though we have attempted to cover many of the aspects that are relevant to this complex issue, we are aware of several omissions and we also realize that the complex—often somewhat contradictory—literature lends itself to more than one interpretation.
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