Retrograde Menstruation Theory

By RRM Academy Reviewed by Dr. Naomi Whittaker, MD, Board-Certified OBGYN, MIGS, NFPMC, FCI Updated June 17, 2026

The retrograde menstruation theory is the historically dominant explanation for how endometriosis arises: during menstruation, tissue flows backward through the fallopian tubes into the peritoneal cavity, where it implants and establishes disease. The theory was first described by Dr. John Sampson in 1927 and has shaped reproductive medicine's understanding of endometriosis ever since.¹

It remains a leading partial mechanism. Retrograde menstrual flow is common. Studies estimate that 76 to 90 percent of menstruating women experience some degree of retrograde flow, yet most never develop endometriosis.¹ That gap is the first signal that retrograde menstruation cannot be the whole story.

The second signal is geography. The theory can plausibly account for disease on the ovaries and the superficial peritoneal surfaces, where refluxed tissue could reasonably land and implant. It cannot account for endometriosis at sites menstrual reflux cannot reach: the diaphragm, the pleural cavity, the bowel wall at points remote from the pelvic cavity, and other extrapelvic locations.¹

The third signal is developmental. Researchers have documented ectopic endometrial tissue in human female fetuses, examining 101 fetal specimens.² These findings are consistent with an embryologic origin, sometimes called the embryonic rest or Mullerianosis theory, in which primitive endometrial tissue is displaced during organogenesis before menstruation has ever occurred. Retrograde flow cannot explain a disease that begins before birth.

The fourth signal is the rare but documented occurrence of histologically confirmed endometriosis in male patients.³ These cases are uncommon and typically associated with estrogen exposure, but they demonstrate that endometriosis can appear in individuals for whom menstrual reflux is anatomically impossible. The disease is not simply a product of retrograde flow.

Contemporary pathogenesis research reflects this complexity. No single theory fully explains all presentations of endometriosis. The leading competing frameworks include coelomic metaplasia (normal peritoneal or pleural cells transform into endometrial-like tissue), the embryonic rest hypothesis (displaced primitive Mullerian cells persist at ectopic sites from development), stem-cell recruitment (circulating endometrial or bone-marrow-derived stem cells seed distant sites), and lymphovascular spread (endometrial cells travel via lymphatic or blood vessel channels to reach remote anatomic locations).¹ These theories are not mutually exclusive. Different mechanisms may predominate in different disease subtypes or anatomic locations.

What this means clinically is direct. Endometriosis is established, vascularized, progressive disease with a biological origin that varies by patient and by anatomic site. Suppressing menstruation does not remove it. The treatment and surgical specifics are covered in the excision surgery entry and the broader endometriosis overview. The point that matters here: the retrograde menstruation theory alone does not define what the disease is, and framing it primarily as a menstruation problem directs treatment in the wrong direction.

The retrograde menstruation theory persists as a partial explanation. It captures something real about how peritoneal and ovarian disease may arise in many women. But treating it as the complete picture has led to decades of research and clinical practice that framed endometriosis as a menstruation problem rather than a systemic disease with multiple biological origins. That framing has consequences: it directs attention toward suppressing the cycle rather than addressing the disease, and it leaves patients with extrapelvic, deep infiltrating, or atypically-located disease without an adequate explanation for their condition. Understanding the limits of this theory is the starting point for understanding why endometriosis remains widely misdiagnosed and undertreated. For a related condition that shares some disease mechanisms, see adenomyosis.

This content is for educational purposes only and does not constitute medical advice. Consult an RRM clinician or healthcare provider for guidance specific to your situation.