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editorial
. 2025 Nov 14;88(1):7–8. doi: 10.1097/MS9.0000000000004321

Linking childhood trauma to endometriosis: evidence and implications for reproductive health screening

Noor Un Nisa Irshad a,*, Muhammad Mudasir Atif a, Muhammad Talha b, Mohammed Hammad Jaber Amin c,*
PMCID: PMC12767943  PMID: 41497146

Dear Editor,

Childhood trauma is exposure to high-stress events that can potentially be traumatic. Such events usually include sexual, emotional, and physical abuse, and emotional and physical neglect by parents or guardians. Exposure to childhood maltreatment, which is commonly measured with instruments such as the Childhood Trauma Questionnaire (CTQ), is associated with increased risk of later mental-health disorders and many chronic diseases[1]. Endometriosis is a chronic inflammatory condition in which tissue similar to that lining the inside of the uterus grows outside of it. Diagnosis typically requires visualization of lesions (usually at laparoscopy) with histological confirmation, and disease extent is commonly classified using the revised ASRM staging system[2]. This includes symptoms of chronic pelvic pain and infertility[3].

Endometriosis affects about 10–15% of women of reproductive age, estimated to be around 190 million worldwide[4]. It is generally a complex, multifactorial condition and has genetic, hormonal, immunological, and environmental influences. Most recently, adverse childhood experiences (ACE) have been highlighted as important factors in the development and progression of endometriosis[3,5]. Endometriosis may reflect hypothalamic-pituitary-adrenal (HPA)-axis dysregulation and related immune/inflammatory changes associated with early-life stress, a plausible but still hypothetical pathway supported primarily by indirect evidence. Observed associations include elevated pro-inflammatory markers (e.g., CRP, IL-6, TNF-α), altered cortisol/HPA-axis dynamics after early adversity, and increased central pain sensitization in endometriosis-associated pain. These findings support hypotheses linking early stress to altered neuro-immune function in some patients with endometriosis, but causality remains unproven, and mechanisms are indirect[6-8].

Practical screening guidance:

  • When to consider trauma inquiry: consider a brief trauma screen for patients presenting with chronic pelvic pain, severe dysmenorrhea, unexplained infertility, or treatment-resistant pelvic pain[1-3,5,6].

  • Brief validated tools, examples for initial screening: Childhood Trauma Questionnaire (CTQ and short forms such as CTQ-SF) (used in endometriosis research)[1]; adverse-childhood-experience (ACE) constructs/questionnaires (e.g., 10-item ACE) or register-based ACE measures[3]; and a short PTSD screen (e.g., PC-PTSD-5) when PTSD is suspected.[1-3]

  • If a screen is positive: assess immediate safety (current abuse, suicidality), use trauma-informed communication, offer referral to mental-health services, and arrange multidisciplinary care linking gynecology with mental-health/pain specialists. Document findings and ensure confidentiality[1,3,5,6].

  • Caveats: screening tools are screening instruments (not diagnostic); positive results require follow-up assessment and appropriate referral. Instruments listed above are supported in the endometriosis literature for research/epidemiology or for demonstrating clinical relevance, but brief-tool validation specifically in endometriosis clinical populations is limited and should be followed by clinical assessment[1-6].

There are emerging studies demonstrating a strong relationship between childhood trauma and the development of endometriosis. One Swedish cohort study, which included about 1.3 million women, found that those women who had experienced childhood abuse were more than twice as likely to develop endometriosis [hazard ratio (HR) = 2.38, 95% confidence interval (CI): 1.89–2.99][5]. The greater the number of traumatic events, the higher the risk, with a 60% higher risk in women with five or more exposures (HR = 1.61, 95% CI: 1.37–1.88). This shows a long-term impact on reproductive and overall health[5]. Furthermore, another study of 8276 women with endometriosis and 240 117 controls revealed a tendency toward a greater prevalence of childhood trauma, emotional, physical, and sexual abuse, among the women with endometriosis[3]. Analyses reported higher prevalence of specific trauma types among cases than controls, for example, emotional/physical abuse affected 8% in cases versus 5% in controls; sexual abuse affected 5% versus 4%. Significantly, women presenting both endometriosis and trauma history report oftentimes severe symptoms and a higher chance of presenting treatment resistance or a later diagnosis due to overlapping pain syndromes[5,7].

Potential confounders, including socioeconomic adversity, comorbid chronic pain and psychiatric disorders, and differential healthcare-seeking or diagnostic access, may partly account for observed associations. In addition, retrospective self-report instruments (e.g., CTQ, ACEs questionnaires) are vulnerable to recall and reporting bias and should be interpreted with caution.

Moreover, most of the studies in this area are observational in nature; several methodological aspects – reporting of self-reported trauma and confounding factors (socioeconomic status and psychiatric conditions) – have to be accounted for while interpreting results. Future studies with more fine-grained data will shed more light on these phenomena.

In conclusion, emerging studies support an association between childhood trauma and endometriosis, suggesting the need to include trauma monitoring in reproductive health care. The patient’s trauma history should be assessed in the context of endometriosis. Coordination among the gynecologist, mental health professional, and primary care provider is also important. Adequate funding and integration of support services are essential for early diagnosis, better outcomes, and a successful public health response[9]. This letter to the editor complies with the TITAN Guidelines 2025 for transparency and integrity in academic publishing[10].

Footnotes

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

Published online 14 November 2025

Contributor Information

Noor Un Nisa Irshad, Email: noorunnisairsad@gmail.com.

Muhammad Mudasir Atif, Email: musassiratifgammy@gmail.com.

Muhammad Talha, Email: mtem276@gmail.com.

Mohammed Hammad Jaber Amin, Email: mohammesjaber123@gmail.com.

Ethical approval

Not applicable.

Consent

Not applicable.

Sources of funding

The authors declare that no funds, grants, or other support were received during the preparation of this manuscript.

Author contributions

Conceptualization: N.u.n.I., M.M.A. Writing – original draft preparation: N.u.n.I., M.M.A., M.T., M.H.J.A. Writing – review and editing: N.u.n.I., M.M.A., M.T., M.H.J.A. All authors have reviewed the final version of the manuscript.

Conflicts of interest disclosure

The authors declare that they have no conflict of interest.

Guarantor

Mohammed Hammad Jaber Amin and Noor un nisa Irshad.

Research registration unique identifying number (UIN)

Not applicable.

Peer and provenance statement

None.

Data availability statement

Not applicable.

References

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

Not applicable.


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