Research from the University of Cincinnati College of Medicine suggests a specific stress hormone pattern may signal vulnerability to post-traumatic stress disorder — at least in female animal models — and could help explain why women are diagnosed with PTSD at roughly twice the rate of men.
The study, recently published in the journal Frontiers in Cellular Neuroscience , identified a potential biomarker of PTSD susceptibility that could eventually guide more targeted intervention. Corresponding author James Herman, PhD ; first author Emily Devine; and colleagues led the work.
Not everyone who experiences trauma develops PTSD. Some people appear more vulnerable, and scientists have long sought to understand why.
“We're trying to figure out why some people are susceptible to PTSD and others are resilient,” said Herman, a professor and co-chair of the Department of Biomedical Sciences. “One of the key questions is whether the way a person's body responds to stress can predict PTSD behavioral dysfunction.”
What did the UC PTSD study discover about stress hormones?
Researchers exposed both male and female animal models to a mild stressor and measured stress hormone levels in their blood. Researchers then exposed the animals to a more intense stress model to induce PTSD-like behavioral changes.
Weeks later, the animals underwent behavioral testing that measured anxiety, fear learning and fear extinction, or the ability to “unlearn” a fear response.
In females, those with a stronger hormonal reaction to the mild stressor were significantly more likely to develop PTSD-like deficits after the prolonged stressor, including increased anxiety, impaired fear extinction and enhanced reinstatement of fear. Specifically, low resting corticosterone combined with a higher stress-evoked spike predicted the worst outcomes — a measurable biological signature that may identify at-risk individuals before trauma occurs.
“PTSD patients lose the ability to extinguish their fear,” said Herman, who is also director of UC’s Neurobiology Research Center and associate director of UC’s Gardner Neuroscience Institute . “They are too good at remembering factors associated with negative events.”
In males, stress reactivity did not predict outcomes in the same way, confirming that stress hormone dynamics operate differently across sexes.
“This tells us that the way stress is processed is different in males and females,” said Herman.
How could the findings help humans in the future?
The findings raise the possibility that a simple stress provocation test could one day serve as a clinical biomarker for PTSD risk and point toward early interventions.
“If we can identify people whose physiological stress response puts them at risk, we may be able to intervene earlier,” Herman said. “There may be ways to block the stress response during the post-exposure period.” He added that therapeutic approaches and future drug development could reduce the likelihood of developing lasting stress deficits after trauma.
Herman cautions that the research is preclinical and that the hormone pattern is a candidate biomarker, not a diagnostic test. Next, the team must determine whether similar patterns appear in women who have experienced trauma and whether they predict who goes on to develop PTSD.
“We want to understand what is happening in the brains of susceptible females that distinguishes them from resilient females and from males,” he said. “Can we use that knowledge of their brain circuitry to develop better treatments?”
Research collaborators include Devine, a neuroscience graduate student in Herman’s lab, along with others from UC: James B. Chambers, Taylorae Dunn, Ava Musarra, Sophie Porter, Christine E. Moore, Marissa Smail, Nawshaba Nawreen and Ben A. Packard.
The U.S. Department of Veterans Affairs partially funded the study.
Frontiers in Cellular Neuroscience
Experimental study
Animals
Glucocorticoid dynamics predict susceptibility and resilience to traumatic stress in male and female rats
8-Oct-2026