Nocturnal deterioration of pulmonary function in asthmatic patients is a well-recognized and well-documented phenomenon. The mechanism of this "morning dip," however, remains uncertain. Although the circadian rhythms of body temperature, corticosteroid, catecholamine, histamine, and opiate peptide levels, and even sleep itself have been shown to be in phase with the diurnal variation in asthma, a causal relationship has yet to be established. Increased nighttime bronchial reactivity to histamine, acetylcholine, and house dust allergen have been demonstrated. In general, continuous treatment with theophylline, beta-adrenergic agonists, or corticosteroids attenuates the degree of morning dip but does not completely eliminate the circadian rhythm of asthma. The significance of nocturnal asthma is emphasized by the observation that asthma deaths occur more frequently during nighttime hours and are often preceded by large daily swings in peak expiratory flow. Further studies examining the etiology and treatment of nocturnal asthma are needed.