Caffeine: The forgotten variable

Although the majority of the population regularly consume caffeine, there are wide variations between individuals in both daily intake and susceptibility to caffeine's effects. These differences are at least partially genetically determined, possibly via variations in adenosine receptors or caffeine metabolism. Caffeine toxicity is well recognized. Tolerance of its effects and withdrawal symptoms have also been described. Both DSM and ICD-10 recognize caffeine as a potential drug of abuse. Caffeine can induce anxiety, exacerbate psychotic symptoms in some patients with schizophrenia and cause insomnia. It can complicate the management Of depression by increasing lithium clearance and can also increase seizure length during ECT. Caffeine can inhibit the metabolism of sonic psychotropic drugs such as clozapine through the competitive inhibition Of CYP1A2. Potent inhibitors of CYP1A2 such as fluvoxamine can precipitate caffeine toxicity. Enquiries about caffeine consumption should be made in all patients who have apparently treatment-refractory illness, or seem unusually sensitive to, or tolerant of, psychotropic drugs.