Most of us experience some sort of trauma during our lifetime, yet only about 25 to 35 percent of people who are exposed to severely disturbing events go on to develop post-traumatic stress disorder (PTSD). According to a new study, a person’s vulnerability to the condition may be determined by their responsiveness to stress hormones, thus offering a potential explanation for this discrepancy.
People with PTSD typically display fear extinction deficits, whereby their conditioned responses to stimuli associated with traumatic events don’t soften over time. Other hallmarks of the condition include a reduction in the volume of the hippocampus – a brain region that plays a key role in memory and emotion – as well as rapid eye movement (REM) sleep disturbances.
Because REM sleep is crucial for memory consolidation, disruptions to this key sleep phase are likely to impede any attempts to overcome one’s trauma. Interestingly, however, studies have also shown that PTSD sufferers tend to have lower levels of glucocorticoids – or stress hormones – such as cortisol.
“There are considerable differences in the levels of glucocorticoids that individuals release to the bloodstream when stressed,” explained study author Carmen Sandi in a statement. “Low glucocorticoid levels are frequently observed in PTSD patients following trauma exposure and were initially suspected to be a consequence of trauma exposure.”
“The possibility that this could be a trait constituting a preexisting PTSD risk factor has been an outstanding open question for many years,” she said. To provide an answer, the study authors conducted experiments on mice that had been genetically engineered to display a blunted response to stress hormones.
Brain scans revealed that these rodents had reduced hippocampi, while recordings of brain activity also revealed deficits in REM sleep. Furthermore, after the mice had been conditioned to associate a noise with receiving an electric shock, mice with dampened cortisol responses were less able to un-learn this association, and continued to freeze in fear whenever they heard the noise.
These findings suggest that fear extinction deficits, hippocampal reductions, and REM disturbances may all be mediated by glucocorticoids, and that people with low levels of these hormones might therefore be more vulnerable to PTSD.
To confirm the robustness of this conclusion, the study authors injected the mice with the stress hormone corticosterone, and found that this ameliorated the animals’ excessive fear and REM disturbances.
The researchers therefore assert that “blunted glucocorticoids were associated with PTSD-related features such as impaired fear extinction, reduced hippocampal volume, and REMS disturbances.” As such, they propose that dampened sensitivity to stress hormones “not only predicts but may also contribute causally to core PTSD symptoms.”
Obviously, these findings will need to be replicated in humans before such hypotheses can be confirmed, although the authors suggest that glucocorticoid treatments may be effective for some people suffering from PTSD.
The study is published in the journal Biological Psychiatry.
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