What causes endometriosis?
Endometriosis is a chronic inflammatory disease in which uterine lining-like tissue grows outside the uterine cavity. Despite intensive research, the exact cause is still not clearly understood. The current scientific view is based on a multifactorial explanatory model.
|
Influencing factor |
Role in disease development |
|
Retrograde Menstruation |
Backflow of menstrual blood through the fallopian tubes into the abdominal cavity – basic model of the disease. |
|
Genetic predisposition |
Increased risk with family clustering – several risk genes discussed. |
|
Immunological factors |
Dysregulation of the body's immune defense prevents breakdown of displaced cells. |
|
Hormonal influences |
Estrogen dominance promotes the growth of endometriosis lesions. |
|
Inflammatory processes |
Chronic inflammatory reactions lead to pain and tissue changes. |
|
Embryonic cell remnants |
Theory of Müllerian residual cells – Maldevelopment in the urogenital tract. |
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Stem cells & metaplasia |
Connective tissue differentiates incorrectly into endometrium-like tissue. |
|
Environmental factors (e.g., dioxins) |
Hormone-active substances could trigger epigenetic changes. |
Endometriosis is a complex disease whose causes lie in an interplay of several biological and environmental factors. Current research emphasizes the relevance of a personalized, interdisciplinary approach for diagnosis and therapy – especially in therapy-resistant or advanced cases. The development cannot always be explained individually – early diagnosis and consistent treatment are important.

The most common theories on the development of endometriosis
Several scientific theories exist to explain the development of endometriosis. However, no single theory can fully explain all manifestations. Therefore, a multifactorial mechanism is currently assumed. The main theories are:
|
Theory |
Description |
Significance |
|
Retrograde Menstruation |
Menstrual blood flows backward through the fallopian tubes into the abdominal cavity and "plants" uterine lining-like cells there. |
Widespread, but does not explain all cases – e.g., not in women without menstruation. |
|
Metaplasia theory |
Peritoneal cells transform into endometrium-like tissue under certain stimuli. |
Could explain occurrence in unusual locations (e.g., lungs). |
|
Embryonic residual cells |
Remnants of embryonic tissue later develop into endometriosis lesions. |
Relevance especially in endometriosis in childhood or outside the pelvis. |
|
Lymphatic and Bloodstream Spread |
Endometrial cells reach distant body sites via blood or lymph vessels. |
Could explain distant lesions (e.g., in the lungs). |
|
Immune Theory |
A disturbed immune defense prevents the elimination of displaced cells. |
Could explain chronic inflammatory processes and persistence. |
|
Genetic factors |
Increased occurrence in affected families suggests a hereditary component. |
No single gene identified, but familial clustering is documented. |
These theories are not seen as mutually exclusive but complement each other. Most likely, each affected individual has a unique combination of hormonal, immunological, genetic, and external factors playing a role.
Genetics, Hormones, Environment: The Complex Causes of Endometriosis
The causes of endometriosis are considered multifactorial. This means: There is no the one Not a single cause, but a complex interplay of multiple influencing factors. Three particularly relevant areas are increasingly coming into focus in research:

Genetic factors
Studies show that endometriosis occurs more frequently in families. Daughters and sisters of affected individuals have up to six times higher risk. Several genetic risk loci have been identified, which are linked to immune regulation and hormone metabolism, among others. However, there is no single "endometriosis gene."
Hormonal influences
Endometriosis is an estrogen-dependent condition. Increased local estrogen production in endometriosis lesions promotes their growth and activity. At the same time, those affected often show reduced progesterone sensitivity – leading to disrupted hormonal regulation ("progesterone resistance").
Environmental Factors
Exposure to environmental toxins – such as dioxins, plasticizers (e.g., BPA), or polychlorinated biphenyls (PCBs) – is being discussed. These substances can act hormonally ("endocrine disruptors") and promote the growth of endometrium-like lesions in animal models. The evidence in humans is not yet conclusive but is becoming increasingly relevant.
The development of endometriosis likely results from a combination of genetic predisposition, hormonal dysregulation, and environmental exposure. Added to this are immunological changes and individual risk factors such as early menarche or certain surgeries. Current research increasingly focuses on this systemic interplay.
Endometriosis Causes: What Those Affected Should Know
The exact causes of endometriosis are not yet fully understood, but current findings suggest an interplay of several factors:
- Genetics: Clustering in affected families, increased susceptibility due to inherited risk genes.
- Hormones: Estrogen dominance and a reduced progesterone response promote the growth of endometrial lesions.
- Immune system: Malfunctions prevent the removal of displaced uterine lining.
- Environmental factors: Hormone-active pollutants such as dioxins or plasticizers are suspected of promoting endometriosis.
- Retrograde Menstruation: Backflow of menstrual blood through the fallopian tubes into the abdominal cavity – possibly a trigger.
Since many of these factors interact, the disease varies greatly from person to person. Early education about possible causes helps those affected to take symptoms seriously and seek targeted medical advice.
Can stress trigger endometriosis?
Stress is not considered a direct cause of endometriosis, but it can significantly influence the disease. Chronic stress intensifies inflammatory processes, weakens the immune system, and can worsen hormonal imbalances – factors that can promote the progression of endometriosis. Additionally, stress increases pain perception and contributes to chronicity. Conscious stress management is therefore an important part of symptom-oriented therapy.
Why do I get exactly endometriosis?
Why a particular woman develops endometriosis usually cannot be clearly determined. Research suspects an interplay of genetic predisposition, hormonal influences, immune defense disorders, and environmental factors. Early first menstruation, heavy or long periods, and family history also increase the risk. Ultimately, it is a multifactorial disease – not a result of personal behavior or avoidable causes.
Research into the causes of endometriosis: An overview for those affected - Connection between endometriosis and autoimmune diseases
Scientific studies increasingly show a notable coincidence between endometriosis and certain autoimmune diseases. Particularly common are Hashimoto's thyroiditis, systemic lupus erythematosus, rheumatoid arthritis, Sjögren's syndrome or multiple sclerosis in endometriosis patients. This increased comorbidity suggests an immunological contributing cause in the pathogenesis of endometriosis.
A central research topic is impaired immune system function: Normally, cells that appear outside the uterus would be recognized and eliminated by immunological mechanisms. However, in endometriosis, this apparently does not succeed – on the contrary, the faulty immune system tolerated or supported even the implantation and survival of the displaced endometrium-like cells.
Possible immunological mechanisms:
|
Immunopathological factor |
Significance in endometriosis |
|
Reduced NK cell activity |
Less killing of misplaced cells |
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Increased macrophage activity |
Chronic inflammatory reaction in the peritoneal cavity |
|
Altered cytokine profile |
Promotion of the growth of endometriotic lesions |
|
Autoantibodies |
Evidence of systemic autoimmune reactions |
|
T-cell dysregulation |
Lack of immunological defense against ectopic tissue |
Particularly striking is the high level of pro-inflammatory cytokines (e.g., IL-1β, IL-6, TNF-α) in the peritoneum of endometriosis patients. These molecules not only promote local inflammation but also act systemically – which many of the nonspecific symptoms which could explain symptoms like fatigue, joint pain, or migraine.
Importance for practice:
- Diagnostics: The immunological connection suggests specifically looking for autoimmune comorbidities in endometriosis patients – especially in cases of systemic symptoms.
- Therapy: Immunomodulatory measures – e.g., anti-inflammatory diet, stress reduction, or new immunologically active drugs – could play an even greater role in the future.
- Research: The distinction between autoimmune and autoinflammatory components is not yet fully clarified. It is suspected that endometriosis represents more of a mixed form of chronic inflammatory disease with autoimmune involvement.
Endometriosis is not only a hormonally induced but also an immunologically mediated disease. The overlap with autoimmune diseases underlines the systemic nature of the pathology and opens new therapeutic perspectives, especially in the area of immunoregulatory approaches.
Are environmental toxins a cause of endometriosis?
The suspicion that Environmental toxins A growing number of studies support that environmental toxins could be involved in the development of endometriosis – even though a clear causal relationship has not yet been definitively proven. The focus is on Endocrine disruptors, i.e., chemical substances that can disrupt hormonal balance.
Possible environmental risk factors:
|
Substance class |
Examples |
Possible mechanism of action |
|
Dioxins and PCBs |
Industrial emissions, contaminated food |
Interference with estrogen metabolism, immune modulation |
|
Bisphenol A (BPA) |
Plastics, canned food, thermal paper |
Estrogen-like effect, pro-inflammatory |
|
Phthalates (plasticizers) |
Cosmetics, plastic packaging |
Changes in gene expression in the uterus |
|
Pesticides (e.g., organochlorine compounds) |
Agriculture, residues in food |
Hormone-active effects, possible DNA damage |
What does the research say?
- Animal models show that dioxin exposure can promote the development of endometriosis-like lesions.
- In Epidemiological studies higher BPA and phthalate levels have been detected in the blood or urine of endometriosis patients.
- However, the connection is Multifactorial: Environmental toxins may not act alone but in combination with genetic or immunological factors.
Relevance for those affected
- Avoidance of hormone-active substances in cosmetics, food, and household products can be recommended as a precautionary measure.
- Organic products, glass instead of plastic, and critical handling of industrially processed products can potentially reduce personal risk – the benefit is not yet confirmed.
Environmental toxins – especially hormone-active chemicals – are reasonably suspected to increase the risk of endometriosis. Whether they act as a sole cause or merely as a contributing factor in the complex causative framework is still under research. Nevertheless, conscious handling of potential pollutants in everyday life is worthwhile.
New insights into the pathogenesis of endometriosis
The new scientific findings shift endometriosis from a purely gynecological to a systemic, immunologically influenced diseaseThis increases hope for Targeted, personalized therapies – and in the future also less invasive diagnostic methods.
|
New insight |
Significance for pathogenesis |
Clinical perspective |
|
Microbiome changes (e.g., Fusobacteria) |
Local inflammation and immune dysfunction |
Potential stool test for diagnosis |
|
Epigenetics & microRNA |
Altered regulation of gene expression |
Blood-based biomarkers possible |
|
Neuroinvasion |
Direct nerve damage caused by lesions |
Explanation for severe, therapy-resistant pain |
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Chronic inflammation |
Sustained immune activation |
New targets for immunomodulatory therapies |
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Neovascularization |
Ensuring lesion survival |
Target for vessel-inhibiting agents |