For decades, endometriosis has been described as a gynecological condition in which tissue similar to the lining of the uterus grows outside of the uterus. While this explanation accounts for some symptoms, it does not adequately explain the full biological complexity of the disease. Millions of women experience systemic symptoms including immune dysfunction, neurological pain, organ involvement, and severe inflammatory responses that extend far beyond the reproductive system.
Based on my medical history, surgical findings, metabolic research, and clinical observations, I propose a broader biological framework: endometriosis may originate as a systemic disease involving disruptions in metabolic pathways, immune regulation, hormonal signaling, and lymphatic transport throughout the body.
One pathway that may play a central role in this process involves methionine, an essential amino acid that humans can only obtain through diet. Methionine is fundamental to cellular function because it drives methylation, a biochemical process responsible for regulating DNA expression, detoxification, hormone metabolism, immune activity, and cellular repair.
Methionine metabolism depends on enzymes associated with pathways including the CBS (cystathionine β-synthase) gene, which helps convert methionine into usable biological compounds. When this pathway becomes impaired, methionine may accumulate rather than being properly converted and utilized within the body.
Excess methionine may disrupt normal cellular signaling and interact with hormonal pathways, particularly estrogen-driven growth signals. In this environment, cellular growth may become dysregulated, potentially allowing abnormal endometrial-like tissue to form and persist outside of its normal location.
When methionine metabolism becomes dysregulated, methylation pathways may also be affected. Methylation is essential for activating certain nutrients, vitamins, and medications in the body. If these pathways do not function properly, individuals may struggle to absorb or metabolize nutrients and medications in their standard forms.
This dysfunction may explain why some patients require methylated forms of vitamins or bioavailable nutrients in order for the body to properly process them. It may also contribute to irregular responses to medications, immune instability, and systemic inflammation.
Because methylation pathways influence nearly every biological system—including neurological function, immune signaling, hormone regulation, and cellular repair—disruptions in these pathways may amplify the symptoms associated with endometriosis.
The liver plays a central role in regulating amino acid metabolism and iron storage. When metabolic pathways become disrupted, the body may begin storing excess iron in tissues in the form of compounds such as hemosiderin. Hemosiderin deposits are frequently observed in endometriotic lesions, suggesting that metabolic dysfunction may contribute to the inflammatory tissue environment seen in the disease.
These findings support the possibility that endometriosis is not simply misplaced uterine tissue but may instead represent tissue that has undergone metabolic and inflammatory transformation.
Another biological system that may explain the widespread distribution of endometriosis is the lymphatic system. The lymphatic network functions as both a transport system and an immune surveillance system, moving cells, inflammatory molecules, and metabolic byproducts throughout the body.
If abnormal cells or inflammatory signals enter this network, they may travel through lymphatic pathways and implant in distant tissues. This could explain why endometriosis has been documented in organs far from the uterus, including the lungs, diaphragm, intestines, and nervous system.
The involvement of the lymphatic system may also explain why many patients experience systemic symptoms affecting the immune system, nerves, muscles, and connective tissues.
Endometriosis is strongly associated with infertility. Current estimates suggest the disease is present in approximately 50% of infertility cases. The disease may alter the uterine environment, interfere with implantation, and disrupt early embryonic development.
During the earliest stage of pregnancy, the developing embryo—known as the blastocyst—must successfully implant within a healthy endometrial lining. Chronic inflammation, abnormal tissue growth, immune dysfunction, and metabolic disruption may create an environment that prevents implantation or causes early pregnancy loss.
In severe cases, endometriosis can lead to structural changes, scarring, and damage to reproductive organs that may contribute to infertility or sterilization.
My own medical history illustrates the systemic and life-threatening potential of this disease. After multiple surgeries for endometriosis and adenomyosis, I experienced a catastrophic uterine rupture during pregnancy that resulted in massive internal bleeding.
During this event, my unborn child was exposed to a large volume of maternal blood. Laboratory testing later revealed that his methionine levels were approximately five times higher than normal, likely due to ingestion of maternal blood during the rupture. This observation suggests that elevated methionine levels may have been present within the uterine environment.
While this observation alone does not prove causation, it raises important questions about how metabolic pathways and amino acid regulation may influence reproductive health and disease progression.
Endometriosis is often underestimated in terms of its prevalence and severity. Current global estimates suggest that hundreds of millions of women live with the disease worldwide. Some analyses indicate that when undiagnosed and symptomatic cases are included, the number may approach one in six women during their lifetime.
In advanced cases, endometriosis can cause organs to become fused together through inflammatory scar tissue, leading to bowel obstruction, kidney damage, or other serious complications requiring emergency surgery. In rare situations, delayed diagnosis and treatment have contributed to organ failure and life-threatening outcomes.
These realities demonstrate that endometriosis is not a minor reproductive disorder but a disease capable of affecting multiple organs and biological systems.
Taken together, these observations suggest that endometriosis may be better understood as a systemic disease involving metabolic dysfunction, immune dysregulation, hormonal signaling, and lymphatic transport throughout the body.
If this model proves correct, it could reshape how endometriosis is studied and treated. Future research may focus on metabolic biomarkers, genetic screening, immune regulation, and earlier detection strategies that move beyond the traditional pelvic-only framework.
Endometriosis may not begin in the uterus.
It may begin in the body’s metabolic and immune systems, influencing how cells grow, communicate, and survive throughout the body.
Understanding this origin could transform diagnosis, treatment, and prevention for millions of women worldwide.