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Hypothesis proposes endometriosis as an estrogen-activated autoimmune disease causing pain via immune attack.
For more than a century, endometriosis has been treated as a disease of the pelvis. This paper proposes that endometriosis is instead an estrogen-activated autoimmune disease that develops in two stages: cells placed by a corrupted internal signal and grown under estrogen, then attacked by the body's own immune system once estrogen activates them and they begin to bleed where they cannot drain. It argues that the immune attack — not the volume of tissue — is the source of pain and organ damage, reframing the disease from one of immune failure to one of estrogen-triggered immune attack. It further proposes that because endometriosis is a whole-body disease, it can be detected before surgery by profiling its multi-system signature rather than searching for a single marker. The model is developed from established science and a documented surgical, pathology, and endocrine record spanning fourteen surgeries, including disease recurrence after surgical menopause. Presented as a hypothesis to invite testing and discussion.
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Kaitlyn Stewart (2026) studied this question.
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