12 Investigations into the relationship between emotional stress and asthma have a long and complicated history. Stemming from patient reports and clinician observations that asthma exacerbations were sometimes preceded by emotional reactions or severe stress, a series of empirical investigations was initiated in the 1960s. Study results were inconsistent, with some apparently methodologically rigorous studies showing relationships between emotional arousal and lung function changes, while others were unable to demonstrate such effects [1]. In the face of this confusing picture, a number of reviews have attempted to integrate data from the field, and in so doing have proposed pathways and mechanisms to explain how emotions or stress could affect asthma [1][2][3][4]. From the beginning, this area of research has been plagued by the paradox wherein the typical physiological reaction to emotional arousal was the opposite of physiological events associated with bronchoconstriction. The paper by LAUBE et al. [5] in the current issue of the European Respiratory Journal, which describes careful testing of a hypothesis generated by a theoretical model, represents another step forward in this tortuous process of investigation. Although the authors9 hypothesis was not supported, the specifics of the unexpected results of the study provide another piece of the puzzle, and so contribute to a revision and refinement of the working model for investigating the interaction of stress and asthma.The most important aspect of the results reported by LAUBE et al. [5] was the failure of the data to support the hypothesis; in fact, the results were the opposite of what was expected. The authors hypothesised that the pulmonary response to allergen exposure in individuals with allergic asthma would be potentiated by emotional arousal elicited by a stress interview. Instead, lung function testing showed less airway obstruction in response to allergens during stress visits than during nonstress, control visits. This suggested that the pulmonary response was attenuated rather than potentiated by the emotional stressor. Importantly, the results were consistent with one side of the paradox that has puzzled investigators from the beginning. It is well known (and is also documented in the study by LAUBE et al. [5]) that emotional arousal is accompanied by sympathetic activation, which is physiologically associated with bronchodilation. This contrasts with clinical observations and lore that have focused on emotions as precipitants of asthma attacks, which by their nature involve bronchoconstriction. In fact, in the study by LAUBE et al.[5], the results were consistent with the common sense view that emotional arousal should help to keep the airways open, rather than contribute to their constriction. Therefore, while the actual changes in pulmonary function may be clinically insignificant, the demonstration of statistically significant attenuation of effects under these conditions contributes to the big picture as scientists struggle to underst...