Impact of Sexual Assault on Circulating Gonadal Hormones Levels in Premenopausal Women with PTSD

Introduction: According to the Office on Women's Health at the U.S. Department of Health, being physically or sexually assaulted are the most common cause of posttraumatic stress disorder (PTSD) in women. An emerging hypothesis is that there is a bidirectional relationship between gonadal hormones and PTSD in women, particularly estrogen. Therefore, the present study aimed to investigate the effects of PTSD on circulating levels of estradiol (E2) and progesterone (P4). We hypothesized that women with PTSD (PTSD+, n=45) would present with lower levels of E2 and P4 compared to trauma-exposed controls without PTSD (PTSD-, n=47); and that among PTSD+, women who had experienced sexual assault (n=20) would further show a decrease in E2 and P4. Methods: Our participants were already clinically diagnosed with PTSD prior to enrollment in the study. We collected demographics and blood samples to quantify serum E2 and P4 levels using the quantitative sandwich enzyme-linked immunoassay technique (ELISA). Blood samples were centrifuged at 4 degrees Celsius and 3000 rpm for 15 minutes after clotting. Next, the serum was pipetted into cryovials and stored at -80 degrees Celsius until ELISA testing. We log-transformed (log 10 ) E2 and P4 due to non-normal distribution. Results: PTSD+ were older and had higher BMI. As hypothesized, we found lower levels of logE2 in PTSD+ compared to PTSD- females (1.4±0.4 vs 1.6±0.4 pg/mL, p=0.022). However, P4 levels were comparable between the two groups. Our analysis further revealed that women who had experienced sexual assault had lower logE2 (1.2±0.6 vs 1.6±0.5 pg/mL, p=0.015) and logP4 (-0.32±0.5 vs 0.02±0.6 pg/mL, p=0.045) compared to women who did not. Conclusion: These findings suggest that PTSD, particularly stemming from sexual assault, may lower serum levels of E2 and P4 and potentially inhibit their physiologically protective effects in women before menopause. NIH K01 K01HL161027, NIH R03 R03HL174817, UMN CTSI (UL1TR002494) This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.