New insights into cortisol levels in PTSD

The article “Relationship of cortisol, norepinephrine, and epinephrine levels with war-induced posttraumatic stress disorder in fathers and their offspring” by Yahyavi et al.¹ provided interesting data on the neuroendocrinology of post-traumatic stress disorder (PTSD). The mechanisms that underlie the associations of cortisol levels with traumatic exposures and PTSD are still not well understood and, as stated by the authors, findings are far from consistent.

Similarly to the findings of Yahyavi et al., in a sample of individuals exposed to trauma during the preceding 5 years, patients with PTSD had neither an increase nor a decrease in mean urinary cortisol levels.² Conversely, in a recently published study, Wingenfeld et al.³ reported decreased cortisol values in outpatients with PTSD recruited from two Veterans Affairs medical centers. Furthermore, researchers have reported lower cortisol levels in the acute aftermath of trauma in patients who later developed PTSD.⁴

It seems that inadequate glucocorticoid release following stress not only delays recovery by disrupting biological homeostasis in the short run but can also interfere with the processing or interpretation of stressful information, resulting in long-term disruptions in memory integration.⁵ Consistent with these findings is the fact that a single dose of hydrocortisone administered in the acute aftermath of trauma produced recovery while promoting enhanced synaptic plasticity and connectivity in the secondary prevention of PTSD.⁵ In this sense, it remains unclear whether deregulation of the HPA axis, leading to low peritraumatic levels of cortisol, endures post-traumatically.

Another critical issue in this matter has to do with changes in cortisol levels secondary to pharmacological treatment of PTSD (e.g., sertraline), an important aspect not addressed by the authors.⁶ Finally, it is worth mentioning that PTSD is characterized by the presence of four symptom clusters (intrusion, avoidance, negative alterations in cognitions and mood, and alterations in arousal and reactivity) instead of the three mentioned in the paper.

References

• ¹
  Yahyavi ST, Zarghami M, Naghshvar F, Danesh A. Relationship of cortisol, norepinephrine, and epinephrine levels with war-induced posttraumatic stress disorder in fathers and their offspring. Rev Bras Psiquiatr. 2015;37:93-8.
• ²
  Young EA, Breslau N. Cortisol and catecholamines in posttraumatic stress disorder: an epidemiologic community study. Arch Gen Psychiatry. 2004;61:394-401.
• ³
  Wingenfeld K, Whooley MA, Neylan TC, Otte C, Cohen BE. Effect of current and lifetime posttraumatic stress disorder on 24-h urinary catecholamines and cortisol: results from the Mind Your Heart Study. Psychoneuroendocrinology. 2015;52:83-91.
• ⁴
  Witteveen AB, Huizink AC, Slottje P, Bramsen I, Smid T, van der Ploeg HM. Associations of cortisol with posttraumatic stress symptoms and negative life events: a study of police officers and firefighters. Psychoneuroendocrinology. 2010;35:1113-8.
• ⁵
  Zohar J, Yahalom H, Kozlovsky N, Cwikel-Hamzany S, Matar MA, Kaplan Z, et al. High dose hydrocortisone immediately after trauma may alter the trajectory of PTSD: interplay between clinical and animal studies. Eur Neuropsychopharmacol. 2011;21:796-809.
• ⁶
  Pacella ML, Feeny N, Zoellner L, Delahanty DL. The impact of PTSD treatment on the cortisol awakening response. Depress Anxiety. 2014;31:862-9.

Publication Dates

• Publication in this collection
  June 2016

History

• Received
  11 Aug 2015
• Accepted
  12 Feb 2016