Abstract
Post-traumatic stress disorder (PTSD) only develops after exposure to a traumatic event in some individuals. PTSD can be chronic and debilitating, and is associated with co-morbidities such as depression, substance use, and cardiometabolic disorders. One of the most important pathophysiological mechanisms underlying the development of PTSD and its subsequent maintenance is a dysfunctional hypothalamic–pituitary–adrenal (HPA) axis. The corticotrophin-releasing hormone, cortisol, glucocorticoid receptor (GR), and their respective genes are some of the mediators of PTSD’s pathophysiology. Several treatments are available, including medication and psychotherapies, although their success rate is limited. Some pharmacological therapies based on the HPA axis are currently being tested in clinical trials and changes in HPA axis biomarkers have been found to occur in response not only to pharmacological treatments, but also to psychotherapy—including the epigenetic modification of the GR gene. Psychotherapies are considered to be the first line treatments for PTSD in some guidelines, even though they are effective for some, but not for all patients with PTSD. This review aims to address how knowledge of the HPA axis-related genetic makeup can inform and predict the outcomes of psychotherapeutic treatments.
Highlights
Post-traumatic stress disorder (PTSD) is a trauma- and stressor-related disorder which can only develop after the experience of a major traumatic event (TE) [1]
In this paper we aim to review the extant knowledge regarding the interplay between the HPA axis regulatory genes and psychotherapeutic interventions for patients with PTSD, by taking into account the previously-reported HPA axis-related G × E interactions involved in PTSD pathophysiology, as well as the interactions between the genetic makeup and psychotherapy and the urgent need to improve patients’ psychotherapeutic outcomes
Cortisol serves several functions, including mobilisation of energy to cope with the aversive stimuli, memory processing, immune system modulation, the termination of the response by active feedback processes, repressing all unnecessary activity—such as growth (emergency mode: when a person is faced with a traumatic event (TE) GCs inactivate all non-essential activities for survival [46])
Summary
Post-traumatic stress disorder (PTSD) is a trauma- and stressor-related disorder which can only develop after the experience of a major traumatic event (TE) [1]. SNPs in the GR and FKBP5 genes and FKBP5 epigenomic alterations predict psychotherapeutic outcomes [33,35,36] Another ten genes, including a gene related with stress vulnerability (ZFP57), have been recently associated with psychotherapeutic outcomes in a longitudinal study of genome-wide DNA methylation levels [34]. In this paper we aim to review the extant knowledge regarding the interplay between the HPA axis regulatory genes and psychotherapeutic interventions for patients with PTSD, by taking into account the previously-reported HPA axis-related G × E interactions involved in PTSD pathophysiology, as well as the interactions between the genetic makeup and psychotherapy and the urgent need to improve patients’ psychotherapeutic outcomes
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