The effect of stress on salivary cortisol in panic disorder patients

Various findings suggest the possibility of an abnormal cortisol response to CRH in panic disorder patients, which raises the question of whether such patients might also produce an abnormal cortisol response to stress. The purpose of the present study was to use salivary cortisol measurement in assessing differences in response to novelty/mild stress situations between panic disorder subjects and controls.

Subjects were recruited by means of posters and subsequently screened for suitability as controls or panic subjects. Twenty-four panic disorder (PD) sufferers and 15 panic-free control subjects were tested on a range of psychometric and physiological measures, at both the start and the end of the experiment. Subjects were tested at the beginning for state anxiety, salivary cortisol, heart rate, and blood pressure, and these tests were repeated at the end of the session (which had been designed to promote reassurance).

The state anxiety scores (STAI) showed a reduction in anxiety level over the test period, and there was a corresponding fall in both blood pressure and heart rate for both groups. Cortisol levels also fell over the course of the interview in the control group, but in the PD group cortisol levels showed no such reduction. In addition, there was a significant difference in the levels of cortisol at the start of the session between the two groups (PD group lower).

These data indicate a possible alteration in cortisol responsiveness to stress/novelty situations in PD subjects. This was considered to be consistent with previous suggestions of HPA axis dysregulation in PD patients, although our research indicates unresponsiveness rather than responsiveness to be a factor to be considered for future investigation.

Our results suggest that not all subjects suffering PD may benefit from stress reduction therapies as a first choice of treatment for their panic attacks. The existence of nocturnal panic attacks (considering sleep as a combination of mental and physical relaxation), in the absence of nightmares, as well as the induction of panic attacks during relaxation support this view.

Apart from the difficulty in accessing sufficient symptomatic subjects, the induction of higher levels of stress could be useful for confirmation of these results. However, this requires specialist support in case of subjects developing panic attacks during the experiments, which was not available during the present study.

Twenty-four panic disorder (PD) sufferers and 15 panic-free control subjects were tested on a range of psychometric and physiological measures, at both the start and the end of an experimental session. Subjects were tested at the beginning for state anxiety, salivary cortisol, heart rate, and blood pressure, and these tests were repeated at the end of the session. The state anxiety scores (STAI) showed a reduction in anxiety level over the test period for both groups, and there was a corresponding fall in both blood pressure and heart rate. Cortisol levels also fell over the course of the session in the control group, but in the PD group cortisol levels showed no such reduction. In addition, there was a significant difference in the levels of cortisol at the start of the session between the two groups (PD group lower). These data indicate a possible alteration in cortisol responsiveness to stress/novelty situations in PD subjects. This was considered to be consistent with previous suggestions of HPA axis dysregulation in PD patients, although our research indicates unresponsiveness rather than responsiveness to be a factor to be considered for future investigation.