Caffeine withdrawal increases lithium blood levels

Abstract

Caffeine is a methylxanthine whose primary biological effect is antagonism of the adenosine receptor. Its presence in coffee, tea, chocolate, soda beverages, and many prescription and over-thecounter drugs makes it the most commonly consumed stimulant. Excessive caffeine intake is especially prevalent among psychiatric patients (Furlong 1975; Greden et al 1978). Greden et al (1978) also found that psychiatric inpatients who were heavy users of caffeine scored significantly higher on ratings of depression and anxiety. Lucas et al (1990) found that caffeine increases arousal and has a psychotogenic effect when administered to schizophrenic patients. Apart from the stimulatory effects on anxiety and arousal (Lucas et al 1990; Nehlig et al 1992), the consumption of caffeine might bear some other relevance to psychiatric patients. Methylxanthines increase urine formation in a way similar to that of thiazides (Rall 1991). Thus, caffeine might interfere with the clearance of some psychotropic drugs which are mainly excreted by the kidneys, e.g., lithium. Approximately 95% of lithium ingested is eliminated in the urine (Baldessarini 1991). Nevertheless, studies of caffeine interaction with lithium are scarce and sometimes contradictory. Thomsen and Schou (1968) demonstrated an increase in lithium urinary excretion in six subjects who ingested a single dose of caffeine. The magnitude of the increase in lithium excretion or the decrease in lithium blood levels was not mentioned; however, Bikin et al (1982) demonstrated no significant changes in renal lithium clearance in six coffee-consuming (800 mg/day) subjects