The role of childhood abuse in HPA-axis reactivity in Social Anxiety Disorder: A pilot study

• Published in: Biological psychology 2010, Vol.83 (1), p.1-6
• Main Authors: Elzinga, Bernet M., Spinhoven, Philip, Berretty, Ed, de Jong, Paula, Roelofs, Karin
• Format: Article
• Language: English
• Subjects: Adult; Adult and adolescent clinical studies; Adult Survivors of Child Abuse - psychology; Analysis of Variance; Anxiety Disorders - complications; Anxiety disorders. Neuroses; Behavioral psychophysiology; Biological and medical sciences; Blood Pressure - physiology; Child; Childhood abuse; Cortisol; Female; Fundamental and applied biological sciences. Psychology; HPA-axis; Humans; Hydrocortisone - metabolism; Hypothalamo-Hypophyseal System - metabolism; Hypothalamo-Hypophyseal System - physiopathology; Male; Medical sciences; Middle Aged; Phobia; Pilot Projects; Pituitary-Adrenal System - metabolism; Pituitary-Adrenal System - physiopathology; Post-traumatic Stress Disorder; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Psychopathology. Psychiatry; Saliva - metabolism; Social Phobia; Stress; Stress, Psychological - complications; Surveys and Questionnaires; Time Factors; Victimology; Young Adult
• ISSN: 0301-0511; 1873-6246
• DOI: 10.1016/j.biopsycho.2009.09.006

Studies on depression have found that childhood abuse (CA) is associated with a persistent sensitization of the hypothalamic–pituitary–adrenal (HPA)-axis to stress in adulthood. So far, it is unknown whether this HPA-axis sensitization is specific to depression, or whether this is a more general outcome associated with CA in patients with mood and anxiety disorders. The aim of this study was to investigate whether CA is associated with enhanced cortisol reactivity to psychosocial stress in Social Anxiety Disorder (SAD). Salivary cortisol levels before, during, and after exposure to psychosocial stress (i.e., Trier Social Stress Task, TSST) in SAD patients with a history of childhood abuse (SAD + CA, n = 9) were compared to cortisol levels in SAD patients without a history of childhood abuse (SAD − CA, n = 9), patients with PTSD related to childhood abuse ( n = 16), and healthy controls without a history of childhood abuse ( n = 16). Analyses showed that the SAD + CA group had a strongly increased cortisol reactivity (mean peak: 17.5 ± 1.9 nmol/l) compared to SAD − CA (mean peak: 9.0 ± 1.1 nmol/l), PTSD (mean peak: 9.0 ± 1.1 nmol/l) and healthy controls (mean peak: 9.6 ± 1.4 nmol/l), whereas baseline cortisol levels did not differ. The enhanced increase in the SAD + CA group was not explained by stronger anxiety in response to the TSST. Consistent with the findings in depression, these results show for the first time that childhood abuse is also associated with strongly increased cortisol reactivity in SAD. When replicated in a larger sample, these findings may have important implications for the treatment of SAD.