What Causes Endometriosis? Theories, Risk Factors, and What We Know

What causes endometriosis? The honest answer: we don’t fully know yet. But decades of research have produced four overlapping explanatory models that together paint an increasingly clear picture. This article covers the leading theories, the real risk factors, and — equally important — what does not cause endometriosis.

For the bigger picture see What is Endometriosis?. For symptoms Endometriosis Symptoms. If you suspect you might be affected, the free symptom screener is a useful starting point.

The four leading explanatory theories

No single theory fully explains endometriosis. Current research views it as a multifactorial disease where multiple mechanisms interact.

1. Retrograde menstruation

The oldest and most-cited theory, first formulated by John Sampson in 1927: during menstruation, some menstrual blood flows backward through the fallopian tubes into the pelvic cavity, where endometrial cells can implant. The catch: retrograde menstruation happens in about 90% of menstruating people — but only a fraction develop endometriosis. So Sampson’s theory is part of the story, not the whole one. Other factors must play a role for retrograde menstruation to actually become endometriosis.

2. Genetic predisposition

Endometriosis runs in families. If your mother, sister, or aunt has endometriosis, your risk is 5 to 7 times higher. Twin studies estimate the genetic component at roughly 50%. But there’s no single “endometriosis gene” — instead, multiple gene variants are involved that influence inflammatory responses, immune function, and hormone receptors. Recent genome-wide association studies (GWAS) have identified over 40 gene regions linked to endometriosis risk. More in Is Endometriosis Genetic?

3. Immune system dysfunction

A healthy immune system should recognize and clear stray endometrial cells. Research shows people with endometriosis often have altered immune responses — less effective clearing of cells that don’t belong, and an increased tendency toward chronic inflammation. This immune dysregulation explains why endometriotic lesions don’t just survive but actively grow, form blood vessels, and activate pain pathways.

4. Hormonal influences

Estrogen is the fuel of endometriosis. It drives the growth of lesions and their cyclical activity. This is why most treatments aim to lower estrogen or block its effect (see Endometriosis Treatment). There’s also evidence of “estrogen resistance” in the normal endometrium of people with endometriosis — the tissue responds differently to hormonal shifts than it does in healthy controls.

Other mechanisms under research

• Stem cell theory: certain stem cells might transform into endometrial-like tissue even outside the uterus
• Embryonic remnant theory: endometriosis-like cells could exist from the embryonic stage and be activated later by hormones — explains rare cases like endometriosis in trans men or pre-pubertal individuals
• Lymphatic and hematogenous spread: endometrial cells might travel via lymph and blood vessels to distant sites — explains rare cases of endometriosis in lung or diaphragm
• Environmental factors: studies show possible links to endocrine disruptors (e.g., dioxins, certain pesticides). Evidence is not conclusive but actively researched

Risk factors — who’s more likely to develop endometriosis?

Risk factors don’t cause endometriosis — they mean risk is statistically elevated.

• Family history of endometriosis (5-7-fold increased risk)
• Early menarche (first period before age 11)
• Short cycles (under 27 days)
• Heavy or long periods
• Nulliparity (never having given birth) or late first birth
• Anatomical abnormalities that obstruct menstrual flow (e.g., obstructive Müllerian anomalies)
• Low BMI is statistically slightly associated (cause vs. consequence is unclear)

What does NOT cause endometriosis

The most important information in this article: stress, lifestyle, poor diet, or “toxic thinking” are not causes of endometriosis. If anyone suggests otherwise — whether in a doctor’s office, wellness forums, or from well-meaning relatives — they are medically wrong.

What these factors can do: influence symptoms. Stress can amplify pain perception. Anti-inflammatory diet can bring relief to some. But this is symptom management, not cause treatment.

This clarification matters because many people with endometriosis spend years being told their disease is “self-inflicted” — through too much stress, too much work, or too little self-care. That’s not just false; it’s dangerous because it delays real medical treatment.

Frequently asked questions

Can sex cause endometriosis?

No. Endometriosis is not caused by sex — not by frequency, not by timing. These myths are widespread but medically unfounded. Endometriosis is a hormonally and genetically driven chronic disease that develops independently of sexual activity.

Does the pill cause endometriosis?

No — the opposite. The combined pill (especially used continuously) is a treatment for endometriosis. It can suppress symptoms but doesn’t worsen the underlying disease. If symptoms appear after stopping the pill, they were previously masked — not caused by the pill.

Can tampons cause endometriosis?

No. There is no scientific evidence linking tampon use to endometriosis. The theory that tampons amplify retrograde menstruation has also been refuted.

Is endometriosis a Western lifestyle disease?

No. Endometriosis occurs worldwide in all populations. Higher reported rates in wealthier countries reflect better diagnostic access — not actually higher disease rates. In countries with limited gynecological care, endometriosis is massively underdiagnosed.

If endometriosis is genetic, can I prevent it?

Currently no known prevention of endometriosis itself. What you can do: watch for symptoms early, ask explicitly about family history, keep a symptom diary, and seek prompt medical evaluation for debilitating symptoms. Early recognition significantly changes the disease course.

Sources

1. Zondervan KT, Becker CM, Missmer SA. Endometriosis. N Engl J Med 2020;382:1244–1256.
2. Sampson JA. Peritoneal endometriosis due to the menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol 1927;14:422–469.
3. Rahmioglu N et al. The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions. Nat Genet 2023;55:423–436.
4. ESHRE. Endometriosis Guideline. 2022.