Cortisol and Subjective Stress Responses to Acute Psychosocial Stress in Fibromyalgia Patients and Control Participants

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Hypothalamic-pituitary-adrenal axis dysfunction may play a role in fibromyalgia (FM) pathogenesis but it remains understudied in this disorder. Furthermore, early childhood adversities (ECA) are common in FM, but whether they moderate stress reactivity is unknown. Hence, we investigated cortisol and subjective responses to acute psychosocial stress in FM and controls, while adjusting for ECA.


Twenty-seven female FM patients and 24 age-matched female controls were recruited in a tertiary care center and through advertisements, respectively. The Childhood Trauma Questionnaire was used to measure ECA history. Salivary cortisol levels and subjective stress ratings were measured at multiple time points before and after the Trier Social Stress Test (TSST) was administered.


Significant main effects of group [F(1,43) = 7.04, p = .011, lower in FM] and ECA [F(1,43) = 5.18, p = .028, higher in participants with ECA] were found for cortisol responses. When excluding controls with ECA (n = 5), a significant group-by-time interaction was found [F(6,39) = 2.60, p = .032], driven by a blunted response to the stressor in FM compared with controls (p = .037). For subjective stress responses, a significant main effect of group [F(1,45) = 10.69, p = .002, higher in FM] and a trend toward a group-by-time interaction effect [F(6,45) = 2.05, p = .078, higher in FM 30 minutes before and 30 and 75 minutes after the TSST, and impaired recovery (difference immediately after – 30 minutes after the TSST) in FM] were found.


Blunted cortisol responsivity to the TSST was observed in FM patients compared with controls without ECA. FM patients had higher subjective stress levels compared with controls, particularly at baseline and during recovery from the TSST. In FM patients, ECA history was not associated with cortisol or subjective stress levels or with responsivity to the TSST. Future research should investigate the mechanisms underlying hypothalamic-pituitary-adrenal axis dysregulation in FM.

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