The analgesic syndrome, comprising renal disease, hypertension, peptic ulcer, anaemia and recurrent headache, accounts for wide-spread morbidity and mortality especially in Queensland and New South Wales. Epidemiological and clinical evidence gathered from many Western societies implicates unsupervised consumption of compound analgesic preparations, particularly those containing phenacetin, in the causation of the majority of cases. Laboratory experiments so far have failed to produce an entirely satisfactory model of clinical analgesic nephropathy. In small animals, papillary necrosis results from prolonged feeding with large doses of aspirin and a number of other anti-inflammatory agents more readily than when phenacetin, paracetamol or phenazone is given alone. The apparently conflicting deductive and experimental data may be reconciled if, as indicated by preliminary observations, salicylates enhance the toxicity of phenacetin derivatives. In planning a programme of prevention for the analgesic syndrome, the central aetiological role of non-narcotic drug dependency must be recognized. As the analgesics to which addiction commonly occurs are the compound powders and tablets, or those containing a stimulant, these preparations should be available only in circumstances where their use can be monitored. Suspected unsupervised and unwarranted consumption of analgesics should be checked by urinary testing for drug metabolites. Because the underlying problem of analgesic dependency is behavioural and environmental in origin rather than medical, the physician must combine forces with the social engineer to devise a definitive solution for this condition.