Caffeine Abuse And Dependence

As the most widely used psychoactive drug in the world, caffeine has considerable potential for abuse. Its adenosine receptor-mediated effects on the central nervous system serve to establish it as potentially addictive (Gilliland and Bullock, 1984; Nehlig, 1999; Griffiths and Chausmer, 2000), and the well-documented behavioral reinforcing properties of the drug further increase that probability (Griffiths and Chausmer, 2000). Caffeine displays both positive reinforcing characteristics, exemplified by the temporary enhancement of cognitive performance (Ryan et al., 2002), and negative reinforcing attributes, seen in its ability to relieve withdrawal symptoms (Bernstein et al.,

2002). Both the powerful stimulant properties of caffeine and its abuse potential have peaked the interest of many scientists and led to the conduct of extensive research focused on the role of the drug in physiology and behavior, including that involved in psychopathology. As one indication of this escalating empirical effort, a search of Medline reveals a total of 1094 publications between 1971 and 1980, 4743 between 1981 and 1990, and 6476 between 1991 and 2000. By way of comparison, this latter number is higher than those for marijuana (2704), amphetamine (5683), or heroin (2991).

Caffeine Dependence

In the Diagnostic and Statistical Manual of Mental Disorders — Fourth Edition (DSM-IV; American Psychiatric Association, 1994), a diagnosis of substance abuse includes substance-related occupational, interpersonal, social, and psychological consequences. Dependence criteria include tolerance, withdrawal, a strong desire or unsuccessful attempt to stop usage, spending a great deal of time with the drug, using more than intended, use despite knowledge of harm, and foregoing other activities to use. The International Classification of Diseases — Tenth Revision (ICD-10; World Health Organization, 1992) uses the term harmful use instead of abuse and classifies it as a pattern of use that is health-damaging. Its dependence criteria overlap with those in the DSM-IV but also include a "compulsive use" criterion. Despite these formal definitions of the terms abuse and dependence, the terms are often used interchangeably in the literature (Griffiths et al., 1996; Holtzman, 1990).

Epidemiology

Though firm prevalence rates have yet to be established, caffeine dependence has been examined by measuring the endorsement of the DSM-IV dependence criteria (Hughes et al., 1992, 1998; Strain et al., 1994). Hughes et al. (1998) tested 162 random caffeine users and found that the most commonly endorsed criterion was a strong desire or unsuccessful attempt to stop usage. Another investigation employed a structured clinical interview based on the dependence criteria in the DSM and tailored specifically for caffeine (Strain et al., 1994). Results showed that the most frequently endorsed dependence criteria were the presence of withdrawal symptoms and continued use despite psychological or physiological harm. A third study recently investigated the presence of caffeine dependence in a small sample of teenagers. Using the Diagnostic Interview Scale for Children, with substance dependence criteria modified for caffeine use, it was found that withdrawal criteria were met by 77.8% of those consuming caffeine and tolerance criteria by 41.7% of respondents (Bernstein et al., 2002). Based on these and other studies, current estimates suggest prevalence rates ranging from 9 to 30% in caffeine consumers (Griffiths and Chausmer, 2000).

Given these prevalence rates, consider that about 80% of U.S. adults consume an average of 4.2 mg/kg/day of caffeine, equivalent to about four cups of coffee (Denaro et al., 1990), and many consume more than 15 mg/kg/day (Mandel, 2002). Even if the entire population, including noncoffee drinkers, is taken into account, average daily consumption is estimated to be 2.4 mg/kg/day (Chou, 1992; Mandel, 2002). Moreover, even when consumed in moderate amounts, the drug has a half-life of 4 to 5 h (Kaplan et al., 1997). These statistics suggest that there may be a very large number of caffeine-dependent users (Mandel, 2002).

Further evidence comes from the documentation of caffeine abuse in selected populations, including athletes and inpatients. Both professional and amateur athletes frequently consume caffeine, sometimes to the point of abuse, in order to take competitive advantage of its stimulating properties. Among a large sample of Canadian teenagers, for instance, 27% admitted to consuming caffeine to improve their performance in various sports (Melia et al., 1996). Although the drug does tend to enhance performance, particularly during endurance events, deleterious effects, such as precompetition anxiety and psychological dependence, may also be experienced by these athletes as a result of caffeine abuse (Sinclair and Geiger, 2000). In addition to athletes, caffeine abuse in clinical populations has been studied. In a sample of 60 hospital inpatients, MacKay and Rollins (1989) found that 47% consumed more than 750 mg of caffeine per day. It is likely that these patients, if queried, would endorse the diagnostic criteria for a caffeine-related disorder. Though those in an inpatient population may present themselves to a mental health provider complaining primarily of anxiety and depressive symptomatology, these patients often also consume excessive amounts of caffeine (Greden et al., 1978; Rihs et al., 1996).

Caffeine Intoxication

Caffeine intoxication is a syndrome involving psychological and physical distress caused by chronic or acute overconsumption of caffeine, usually in excess of 500 to 600 mg daily (James and Stirling, 1983). It is included in DSM-IV and ICD-10 and appeared in earlier editions of these nomenclatures as caffeinism, a term still used in the literature. The syndrome is often manifested by such somatic complaints as diuresis, tachycardia, and tremulousness, as well as by anxiety (Kendler and Prescott, 1999). Thus, the central nervous system, gastrointestinal system, and cardiovascular system are all affected by excessive caffeine consumption. Caffeinism may be related to an addiction to other licit substances, such as nicotine and alcohol, and to lower academic performance (Bradley and Petree, 1990; Kozlowski et al., 1993).

There is limited research on the treatments available for those with caffeinism. Fox and Rubinoff (1979) used a behavioral method involving self-monitoring and rewards to decrease daily caffeine intake. Baseline data were collected on three coffee drinkers suffering from caffeinism. Participants then switched from brewed to instant coffee, thereby gradually decreasing the amount of caffeine consumed. Treatment goals (decrease baseline level to 600 mg) were developed, and participants then invested $20 in the treatment, with portions of this deposit returned if progress occurred. This behavioral approach was successful in decreasing coffee-drinking behavior by 69%, and an average 67% reduction was maintained at a 10-month follow-up. In a similar treatment, focused on the reduction of caffeine intake to a safe level, James and Stirling (1983) also found significant reductions in caffeine use in a sample of 27 excessive users. Thus, there is some evidence that caffeinism can be effectively treated.

Caffeine and Anxiety Disorders

A substantial body of research has linked caffeine use to anxiety disorders. In fact, evidence suggests that caffeine is not only a contributing factor in anxiety and the anxiety disorders but can also precipitate the onset and exacerbate the symptoms of some of these disorders. Research in this area has centered on panic disorder (PD) and generalized anxiety disorder (GAD), but obsessive-compulsive disorder (OCD), social phobia, and post-traumatic stress disorder (PTSD) have also been addressed. Patients diagnosed with GAD or PD are negatively affected by caffeine. They show hypersensitivity to the drug (Boulenger et al., 1984; Bruce et al., 1992) and exhibit improvement in anxiety symptoms when they abstain from consuming this powerful stimulant (Bruce and Lader, 1989; Bruce et al., 1992). Self-ratings of anxiety also increase in PD patients when caffeine is consumed, and the drug can even trigger panic attacks (Charney et al., 1985; Lee et al., 1988; Bruce, 1990).

Caffeine consumption also impacts other anxiety disorders. Those diagnosed with social phobia also have a hypersensitivity to caffeine, though to a lesser extent than is the case for GAD and PD patients (Nutt et al., 1998; den Boer, 2000). Other studies show that caffeine abuse is common in OCD patients with comorbid major depressive disorder (Perugi et al., 1997). Some evidence suggests that the drug may be involved in the pathogenesis of PTSD (Iancu et al., 1996). In fact, some have proposed that the use of decaffeinated coffee in military settings could reduce the prevalence of anxiety reactions and perhaps of PTSD itself (Iancu et al., 1996). A further indication is the finding of Solursh and Solursh (1994) that reduction in caffeine use results in improvement of sexual functioning in some Vietnam combat veterans diagnosed with chronic PTSD.

A final note on the role of caffeine in anxiety disorders concerns the currency of the available studies. It is notable that most of the studies done to date appear in literature prior to 1990. This earlier literature provides the basic information that caffeine affects patients with anxiety disorders, but much more work is needed to determine the exact nature and extent of that impact. Additional studies in this area would certainly be welcome.

The Role of Caffeine in Other Disorders

Caffeine has also been implicated in a number of other disorders, including depression, schizophrenia, bipolar disorder, eating disorders, ADHD in children, and restless legs syndrome. In depressive patients, caffeine is often used as a self-medication against the depressive mood state, including that seen in seasonal affective disorder (Krauchi et al., 1997; Abbott and Fraser, 1998). Its use is also higher in both clinically depressed patients and adolescents who report a high number of depressive symptoms (Leibenluft et al., 1993; Worthington et al., 1996; Bernstein et al., 2002). One unfortunate side effect of such self-medication with caffeine is that it exacerbates insomnia and parasomnias in many depressed patients, thereby further decreasing quality of life (Neylan, 1995). Thus, any short-term stimulant relief that depressed patients might receive from the use of caffeine may be outweighed by its deleterious effects.

Schizophrenia is also associated with the high levels of caffeine use (Donnelly et al., 1996; Van Ammers et al., 1997). Evidence concerning actual amounts of caffeine intake in this population is largely lacking because use is often neither regulated nor monitored. However, early researchers estimated that between 17 and 71% of schizophrenic inpatients and outpatients use more than 500 mg of caffeine per day (Furlong, 1975; Winstead, 1976), and more recent evidence suggests that 38% of schizophrenics use more than 500 mg per day (Mayo et al., 1993). Not surprisingly, then, members of the general population who score higher on a schizotypy scale also report greater caffeine intake than those who score low (Larrison et al., 1999). One explanation for the substantial use of caffeine in the schizophrenic population is that the adenosine A2A antagonistic effects of the drug may produce an effect similar to increased dopaminergic neurotransmission in the ventral striatum (Ferre, 1997). An alternative suggestion is that caffeine may counteract some negative effects of neuroleptic medications (Kruger, 1996).

Despite the fact that many schizophrenic patients choose to consume caffeine, it is not clear whether the drug has primarily advantageous or deleterious effects on symptoms. In fact, some studies have found caffeine use to increase subjective distress and psychotic symptoms (Hamera et al., 1995; Hyde, 1990; Lucas et al., 1990; Ferre, 1997). Moreover, schizophrenics who are heavy caffeine users appear to need larger doses of antipsychotic medications than do nonusers (Hyde, 1990). Contrary findings show, however, that switching patients to decaffeinated coffee does not produce any amelioration of symptoms (Koczapski et al., 1989). One attempt to explain these discrepancies in results is the suggestion that certain subgroups of schizophrenics may be more highly sensitive to the possible psychotogenic effects of caffeine (Hyde, 1990).

Three final disorders to be considered are eating disorders, ADHD, and restless legs syndrome. Early case reports of excessive caffeine consumption among eating disorder patients (Sours, 1983) have been supported by a few studies showing caffeine abuse by bulimics (Kruger and Braunig, 1995), some suggesting higher levels of caffeine consumption in purgers than in restrictors (Haug et al., 2001). However, other recent research shows that caffeine consumption in these groups is about the same as or less than that of age-matched control samples (Stock et al., 2002). Research with ADHD children shows, not surprisingly, that caffeine may be better than no treatment in decreasing impulsivity, aggression, and both parents' and teachers' perceptions of symptom severity (Leon, 2000). In a second study, caffeine was better than placebo in decreasing hyperactivity and teacher-rated symptom severity and in improving executive functions. However, it was not as effective as methylphenidate and proved to have little or no effect on performance during tests of attention (Riccio et al., 2001). A final disorder is restless legs syndrome. Although there now appears to be a major genetic component in this disorder, perhaps transmitted on an autosomal dominant gene with multifactorial expression (Winkelmann, 2002), emotional and behavioral factors have also been identified. Symptoms of anxiety and depressive disorders, social alienation, and dimin ished cognitive focus have been reported as typical of RLS patients (Kuny, 1991; Aikens et al., 1999; Ulfberg et al., 2001), and caffeine has been implicated (Lutz, 1978; Paulson, 2000). In fact, one recent investigation showed that regular use of nonopioid analgesics, frequently containing caffeine, is a risk factor for RLS and is associated with increases in both psychiatric and medical comorbidity (Leutgeb, 2002).

Psychopharmacological Treatment: Caffeine Interactions

In addition to its observed effects on psychiatric symptomatology, caffeine interacts with some of the medications used to treat psychological disorders. One early investigation showed that caffeine can interfere with the action of benzodiazepines used in treating the anxiety disorders (Greden et al., 1981). More recent work demonstrates that it can increase the risk of clozapine toxicity, such as sedation, seizures, and hypotension (Carrillo et al., 1998; Patton and Beer, 2001), and increase the excretion of lithium, thereby leading to treatment failure in lithium patients (Jefferson, 1988). In a recent review, Patton and Beer (2001) summarized the effects of caffeine on antipsychotics, benzodiazopines, and tricyclic antidepressants. Most commonly, treatment failure and increased risk of toxicity occur through reduced sedative, anxiolytic, or anticonvulsant effects or reduced metabolism of the drug.

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