Childhood Trauma and Endometriosis: What the Research Really Shows

Is childhood trauma linked to endometriosis?

Emerging research suggests a meaningful association between adverse childhood experiences (ACEs) and later endometriosis diagnosis.

But does trauma cause endometriosis?
Or is something more biologically complex happening?

Let’s look at what the research actually shows — and what it doesn’t.

‍

What Is Endometriosis?

Endometriosis is a chronic, estrogen-dependent inflammatory disease in which tissue similar to the uterine lining grows outside the uterus.

It affects approximately 1 in 10 reproductive-age women, girls and those born with a uterus across the world.

It is associated with:

• Chronic pelvic pain
• Dysmenorrhea (painful periods)
• Infertility
• Fatigue
• Endo belly and gastrointestinal symptoms
• Systemic inflammation

Modern research shows endometriosis is not just a gynecological condition.

It involves:

• Immune dysfunction
• Chronic inflammation
• Progesterone resistance
• Estrogen signaling dysregulation
• Neuroangiogenesis (nerve and blood vessel growth)
• Epigenetic changes

This systemic nature is critical when we examine the potential link between childhood trauma and endometriosis.

And when you begin tracking not just pain — but inflammation patterns, stress load, fatigue, and hormone shifts — patterns often emerge that were invisible before. Structured tracking transforms guesswork into insight.

‍

What Large-Scale Studies Show About Trauma and Endometriosis

The Nurses’ Health Study II (2010)

One of the first major studies examining trauma and endometriosis risk found:

• Severe chronic sexual abuse was associated with ~79% increased risk of laparoscopically confirmed endometriosis.
• Severe physical abuse also increased risk.
• Associations were strongest in infertility-associated endometriosis.

This study used surgically confirmed diagnoses — strengthening its validity.

The Swedish Nationwide Cohort Study (2025)

A nationwide study of over one million women found a clear dose–response relationship between adverse childhood experiences and endometriosis diagnosis:

• One adversity → modest increased risk
• Multiple adversities → progressively higher risk
• Violence and sexual abuse showed the strongest associations

Dose–response relationships strengthen the credibility of associations.

But association does not equal causation.

‍

‍

🔎 Direct Answer: Is Childhood Trauma Linked to Endometriosis?

Yes. Large population studies show that women exposed to severe adverse childhood experiences have a higher likelihood of later endometriosis diagnosis. However, these studies are observational and cannot prove that trauma directly causes endometriotic lesions to form.

Researchers believe early-life stress may influence immune, inflammatory, and hormonal systems that are involved in endometriosis development.

🔎 Can Stress Cause Endometriosis?

There is no experimental evidence proving that stress directly causes endometriosis.

However, chronic stress and early-life trauma can alter:

• Immune regulation
• Inflammatory signaling
• Estrogen pathways
• Pain processing systems

Because endometriosis is an inflammatory, immune-mediated, estrogen-dependent disease, stress biology may influence disease progression or symptom severity in susceptible individuals.

‍

‍

Where Stress Biology and Endometriosis Intersect

1️⃣ HPA Axis Dysregulation

Adverse childhood experiences can alter the hypothalamic–pituitary–adrenal (HPA) axis — the body’s stress-response system.

Long-term stress exposure can disrupt cortisol regulation, which plays a major role in immune control.

Dysregulated cortisol patterns can contribute to a pro-inflammatory environment.

Endometriosis lesions thrive in inflammatory conditions.

This creates biological plausibility — not proof — but meaningful overlap.

2️⃣ Immune Dysfunction and Inflammation

Endometriosis involves:

• Impaired immune clearance
• Elevated inflammatory cytokines (IL-6, TNF-α)
• Altered macrophage function

Early-life stress is also associated with increased inflammatory cytokines and long-term pro-inflammatory gene expression.

The overlap between early-life stress and inflammation and endometriosis is one of the strongest biological bridges.

If trauma influences immune tone, and immune tone influences lesion survival, integration matters.

Managing endometriosis therefore requires more than isolated symptom suppression. It requires structured support across inflammatory, immune, hormonal, and nervous system pathways.

3️⃣ Estrogen Signaling Changes

Endometriosis is estrogen-dependent and characterized by:

• Increased local estrogen production
• Progesterone resistance
• Altered estrogen receptor activity

Stress exposure has been shown to influence endocrine signaling and receptor expression.

The nervous system, immune system, and endocrine system are biologically intertwined.

Care plans should reflect that reality.

4️⃣ Epigenetic Imprinting

Both trauma and endometriosis are associated with epigenetic modifications — long-term changes in gene expression.

Epigenetic shifts may influence:

• Inflammatory thresholds
• Hormone responsiveness
• Pain sensitivity

Epigenetics does not mean trauma “creates” disease.

But it may shape biological vulnerability across a lifetime.

5️⃣ Pain Sensitization

Endometriosis is a neuroinflammatory condition.

Lesions contain nerve fibers, and many patients develop central sensitization.

Trauma exposure is also linked to heightened threat detection and altered pain processing.

This overlap may influence symptom severity — even if it does not initiate lesion formation.

‍

Early-life adversity may:

• Alter immune surveillance
• Shift inflammatory baselines
• Modify estrogen signaling
• Prime stress-response pathways

This is not about blame.

It is about systems biology.

And systems biology requires integrated strategy — not fragmented care.

‍

‍

What This Means for Trauma-Informed Endometriosis Care

This research does NOT mean:

• Trauma caused your endometriosis.
• Endometriosis is psychological.
• Nervous system work replaces medical treatment.

It does suggest:

Whole-body conditions require whole-body frameworks.

Trauma-informed endometriosis care may include:

• Nervous system regulation
• Anti-inflammatory lifestyle support
• Hormone and immune system optimization
• Integrated medical care

Not because endometriosis is “in your head.”

But because inflammation, hormones, immune function, and stress biology are interconnected.

‍

Where to Go From Here

If you’re tired of piecing this together alone…

If you’ve sensed there’s more to endometriosis than prescriptions and procedures…

If you want to understand how inflammation, hormones, immune signaling, stress, and pain interact inside your body…

You need more than scattered advice.

You need a structured roadmap.

Inside the Endo45 app, we help you:

• Track symptom patterns
• Monitor hormone signals
• Support nervous system regulation
• Measure progress with your EndoFit™ Score

Because surviving endometriosis was never the end goal.

Thriving is.

If you’re ready to move from uncertainty to strategy — explore Endo45 here.

‍

‍

FAQs

Does childhood trauma increase the risk of endometriosis?

Large observational studies suggest that severe adverse childhood experiences are associated with higher likelihood of later endometriosis diagnosis. However, this does not prove trauma directly causes endometriosis.

Can stress trigger endometriosis flares?

Yes. Stress can increase inflammatory signaling and alter hormone balance, which may exacerbate endometriosis symptoms.

Is endometriosis a psychosomatic condition?

No. Endometriosis is a chronic inflammatory disease with immune and hormonal components. Stress may influence symptoms, but it does not mean the disease is psychological.

Should endometriosis care be trauma-informed?

Many experts believe trauma-informed care can improve patient outcomes by addressing nervous system regulation alongside medical management.

‍

‍

References

1. Missmer SA, Hankinson SE, Spiegelman D, Barbieri RL, Michels KB, Hunter DJ. History of abuse and risk of endometriosis. Human Reproduction. 2010;25(7):1795–1803. doi:10.1093/humrep/deq095
2. Rostvall M, et al. Adverse childhood experiences and the risk of endometriosis—a nationwide cohort study. Human Reproduction. 2025;40(9):1735–1743. doi:10.1093/humrep/deaf101
3. Chen LH, et al. A lifelong impact on endometriosis: Pathophysiology and pharmacological treatment. International Journal of Molecular Sciences. 2023;24(8):7503. doi:10.3390/ijms24087503
4. Taylor HS, Kotlyar AM, Flores VA. Endometriosis is a chronic systemic disease: Clinical challenges and novel innovations. The Lancet. 2021;397(10276):839–852. doi:10.1016/S0140-6736(21)00389-5
5. Lovallo WR, Farag NH, Vincent AS, Thomas TL, Wilson MF. Cortisol responses to mental stress following caffeine intake in men and women. Pharmacology Biochemistry and Behavior. 2006;83(3):441–447. doi:10.1016/j.pbb.2006.03.005
6. Miller GE, Chen E, Parker KJ. Psychological stress in childhood and susceptibility to chronic diseases of aging: Moving toward a model of behavioral and biological mechanisms. Psychological Bulletin. 2011;137(6):959–997. doi:10.1037/a0024768
7. Danese A, Baldwin JR. Hidden wounds? Inflammatory links between childhood trauma and psychopathology. Annual Review of Psychology. 2017;68:517–544. doi:10.1146/annurev-psych-010416-044208
8. Wasada T, Akamine Y, Kato K, Ibayashi H, Nomura Y. Adrenal contribution to circulating estrogens in women. Endocrinologia Japonica. 1978;25(2):123–128. doi:10.1507/endocrj1954.25.123
9. Ma X, Nan F, Liang H, et al. Excessive intake of sugar: An accomplice of inflammation. Frontiers in Immunology. 2022;13:988481. doi:10.3389/fimmu.2022.988481
10. Parazzini F, Cipriani S, Bravi F, Pelucchi C, Chiaffarino F, Viganò P. A metaanalysis on alcohol consumption and risk of endometriosis. American Journal of Obstetrics and Gynecology. 2013;209(2):106.e1–106.e10. doi:10.1016/j.ajog.2013.05.039

This article is based on peer-reviewed research and large-scale population studies. Observational studies demonstrate association but cannot prove direct causation. Readers are encouraged to consult healthcare professionals for individualized medical guidance.