Researchers have yet to fully understand the biological basis of post-traumatic stress disorder. Now, new research investigates the counterintuitive role of stress hormones as a protective factor in PTSD.
Stress hormones include the group of hormones call glucocorticoids and include cortisol. The hormones are considered stress hormones because their levels increase following stress.
Over the past three decades, scientists have learned that the release of cortisol prepared the body to cope with the physical demands of stress.
Researchers have also linked high levels of cortisol to depression and other stress-related disorders, giving rise to the hypothesis that high levels of cortisol on a long-term basis may impair the psychological capacity to cope with stress.
This theory has led to using drugs such as mifepristone as a treatment for depression by blocking glucocorticoid activity.
However, emerging research suggests that, in animal models and in humans, elevating glucocorticoid levels may actually reduce the development of posttraumatic stress disorder or PTSD.
A new study confirmed this hypothesis as Rajnish Rao and colleagues discovered that elevated levels of glucocorticoids at the time of acute stress offers protection against anxiety-like behavior and the delayed enhancing effect of stress.
The study is found in the journal Biological Psychiatry.
“It seems, increasingly, that the ‘trauma’ in posttraumatic stress disorder is the impact of stress on brain structure and function,” commented Dr. John Krystal, Editor of Biological Psychiatry.
“The study by Rao and colleagues provides evidence that glucocorticoids may have protective effects in their animal model that prevent from these changes in synaptic connectivity, potentially shedding light on protective effects of glucocorticoids described in relation to PTSD.”
Senior author Sumantra Chattarji, Ph.D., explained the reasoning behind their work: “First, this work was inspired by a puzzle — counterintuitive clinical reports — that individuals having lower levels of cortisol are more susceptible to developing PTSD and that cortisol treatment in turn reduces the cardinal symptoms of PTSD.
“Second, using a rodent model of acute stress, we were not only able to capture the essence of these clinical reports, but also identify a possible cellular mechanism in the amygdala, the emotional hub of the brain.”
Experts say that the lab results are consistent with clinical reports on the protective effects of glucocorticoids against the development of PTSD symptoms triggered by traumatic stress.
“With the increasing costs and suffering associated with PTSD victims, it is our hope that basic research of the kind reported in this study will help in developing new therapeutic strategies against this debilitating disorder,” concluded Chattarji.