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Endometriosis is a chronic, inflammatory disease that can cause debilitating pelvic and period pain and is often associated with infertility as well. It affects roughly 10% (190 million) of reproductive age women globally. The rate is likely to be much higher among Asian and South Asian women. Conventional medicine focuses on hormone treatments, GnRH agonists, and excision surgery to treat this condition. This paper focuses on reviewing current published literature that provides alternative holistic approaches to controlling inflammation that drives this condition. A holistic and integrative approach improves quality of life significantly in women affected by endometriosis. Diet and lifestyle approaches that focus on organic/pastured whole foods, low toxin and xenoestrogen exposure, reduced stress, increased Omega 3 and antioxidant consumption, and avoidance of gluten, corn, dairy, and sugar have been shown to be integral to reducing symptoms as well as bringing about hormone balance and a sustained pain-free life. Combining the dietary aspects with lifestyle modifications like yoga, meditation, strength training, water therapy, sauna, etc., has been shown to be extremely effective in detoxing the estrogen pathways and thereby bringing harmony in women suffering from endometriosis. These alternative approaches help practitioners to empower women to take care of themselves through a natural and holistic approach.

Key Points Endometriosis is characterized by the presence of ectopic endometrium causing pain, infertility or lesion progression; it affects ∼5% of women of reproductive age, with a prevalence peak between 25 years and 35 years of age Interaction of the number and amount of menstrual flows with genetic and environmental factors seems to determine the likelihood of development as well as the phenotypic manifestation of the disease Although pain can be managed via pharmacological inhibition of ovulation and menstruation, lesions are not eradicated; surgery is generally associated with pain relief, but its benefit is often temporary Medical therapy for infertility is inefficacious, whereas laparoscopic elimination of endometriotic lesions and adnexal adhesions increases the chances of conception moderately; in vitro fertilization is a valid alternative to surgery Endometriosis is associated with a 50% increase in the risk of ovarian cancer; preventive interventions are possible, but screening of patients with endometriosis for ovarian cancer is presently not justified Primary prevention of endometriosis is not currently feasible; treatment should be tailored to fit individual needs, and a shared decision-making approach between patient and clinician is encouraged Endometriosis is a chronic inflammatory disease affecting around 5% of reproductive age women, often causing pelvic pain and infertility. This Review addresses current knowledge on the pathogenesis of the condition, medical, surgical and potential new treatments, the role of assisted reproduction, prevention of recurrences, and the association with ovarian cancer. Endometriosis is defined as the presence of endometrial-type mucosa outside the uterine cavity. Of the proposed pathogenic theories (retrograde menstruation, coelomic metaplasia and Müllerian remnants), none explain all the different types of endometriosis. According to the most convincing model, the retrograde menstruation hypothesis, endometrial fragments reaching the pelvis via transtubal retrograde flow, implant onto the peritoneum and abdominal organs, proliferate and cause chronic inflammation with formation of adhesions. The number and amount of menstrual flows together with genetic and environmental factors determines the degree of phenotypic expression of the disease. Endometriosis is estrogen-dependent, manifests during reproductive years and is associated with pain and infertility. Dysmenorrhoea, deep dyspareunia, dyschezia and dysuria are the most frequently reported symptoms. Standard diagnosis is carried out by direct visualization and histologic examination of lesions. Pain can be treated by excising peritoneal implants, deep nodules and ovarian cysts, or inducing lesion suppression by abolishing ovulation and menstruation through hormonal manipulation with progestins, oral contraceptives and gonadotropin-releasing hormone agonists. Medical therapy is symptomatic, not cytoreductive; surgery is associated with high recurrence rates. Although lesion eradication is considered a fertility-enhancing procedure, the benefit on reproductive performance is moderate. Assisted reproductive technologies constitute a valid alternative. Endometriosis is associated with a 50% increase in the risk of epithelial ovarian cancer, but preventive interventions are feasible.

About 10% of reproductive-age women have endometriosis. Symptoms can include severe pain, dysmenorrhea, dyspareunia, dysuria, infertility, and fatigue. The pathogenesis is unclear. Hormonal therapy controls symptoms in some women; others require surgery, which may not be effective.

Endometriosis is a common disease affecting 5–10% of women of reproductive age globally. However, despite its prevalence, diagnosis is typically delayed by years, misdiagnosis is common, and delivery of effective therapy is prolonged. Identification and prompt treatment of endometriosis are essential and facilitated by accurate clinical diagnosis. Endometriosis is classically defined as a chronic, gynaecological disease characterised by endometrial-like tissue present outside of the uterus and is thought to arise by retrograde menstruation. However, this description is outdated and no longer reflects the true scope and manifestations of the disease. The clinical presentation is varied, the presence of pelvic lesions is heterogeneous, and the manifestations of the disease outside of the female reproductive tract remain poorly understood. Endometriosis is now considered a systemic disease rather than a disease predominantly affecting the pelvis. Endometriosis affects metabolism in liver and adipose tissue, leads to systemic inflammation, and alters gene expression in the brain that causes pain sensitisation and mood disorders. The full effect of the disease is not fully recognised and goes far beyond the pelvis. Recognition of the full scope of the disease will facilitate clinical diagnosis and allow for more comprehensive treatment than currently available. Progestins and low-dose oral contraceptives are unsuccessful in a third of symptomatic women globally, probably as a result of progesterone resistance. Oral gonadotropin-releasing hormone (GnRH) antagonists constitute an effective and tolerable therapeutic alternative when first-line medications do not work. The development of GnRH antagonists has resulted in oral drugs that have fewer side-effects than other therapies and has allowed for rapid movement between treatments to optimise and personalise endometriosis care. In this Review, we discuss the latest understanding of endometriosis as a systemic disease with multiple manifestations outside the parameters of classic gynaecological disease.

Endometriosis is a complex gynecological disorder characterized by endometrial-like tissue growing outside the uterus, leading to chronic pain, infertility, and reduced quality of life. Its pathophysiology involves genetic, epigenetic, immune, and molecular factors. Theories such as retrograde menstruation, coelomic metaplasia, and stem cell involvement explain lesion formation. Endometrial mesenchymal stem cells (eMSCs) and epithelial progenitors (eEPs) contribute to lesion establishment by adhering to peritoneal surfaces, proliferating, and differentiating into ectopic tissue. Aberrant adhesion molecules, inflammatory cytokines, and molecular pathways like PI3K/Akt and Wnt/β-catenin drive proliferation, angiogenesis, and resistance to apoptosis. Elevated estrogen levels and progesterone resistance further promote lesion growth and immune evasion. Immune dysfunction, including altered macrophage activity and reduced natural killer (NK) cell function, contributes to inflammation and lesion persistence. Pain is linked to prostaglandin E2 (PGE2) and nerve infiltration, emphasizing the need for targeted pain management. Current therapies, such as GnRH agonists, suppress ovarian hormone production but face limitations in long-term efficacy and side effects. Integrating molecular insights into clinical practice may advance diagnostics and treatment, with emerging approaches focusing on molecular pathways, immune modulation, and hormonal regulation for more effective, personalized therapies. Future research should unravel the complex mechanisms driving endometriosis to improve patient outcomes.

Abstract Estrogen receptor beta (ER[beta], encoded by ESR2 gene) and cytochrome P450 aromatase (encoded by CYP19A1 gene) play critical roles in endometriosis, and the levels of insulin-like growth factor-I (IGF-I) in the peritoneal fluid are significantly higher in patients with endometriosis compared with those in normal women. However, the effects and mechanisms of IGF-I on ER[beta] and aromatase expression remain to be fully elucidated. In this study, human endometriotic stromal cells (ESCs) and endometrial cells (EMs) derived from ovarian endometriomas and eutopic endometrial tissues. ESCs were cultured with IGF-I, signal pathway inhibitors, and siRNAs. ER[beta] and aromatase expression were measured by real-time PCR and Western, respectively. The binding of c-Jun and CREB to the ESR2 and CYP19A1 promoters was assessed by chromatin immunoprecipitation assay. Animal experiments were performed in a xenograft mouse model. Levels of IGF-I mRNA in ESCs were markedly higher than those in EMs. IGF-I upregulated ER[beta] and aromatase expression in ESCs after stimulation of the IGF1R/PI3K/AKT pathway. Following IGF-I treatment, a marked increase in c-Jun and CREB phosphorylation occurred, enhancing binding to the ESR2 and CYP19A1 promoters. An IGF1R inhibitor in vivo reduced IGF-I-induced endometriosis graft growth and ER[beta] and aromatase expression. In conclusion, this is the first report to describe a mechanistic analysis of ER[beta] and aromatase expression regulated by IGF-I in ESCs. Moreover, an IGF1R inhibitor impeded ectopic lesion growth in nude mice. These findings suggest that an inhibitor of IGF1R might have therapeutic potential as an antiendometriotic drug. Key messages Level of IGF-I mRNA in ESCs is markedly higher than that in EMs. IGF-I up-regulates ER[beta] and aromatase expression via IGF1R/PI3K/AKT pathway. C-Jun and CREB are recruited to ESR2 or CYP19A1 promoter by IGF-I stimulation. IGF-1R inhibitors in vivo impede the growth of ectopic lesions in nude mice.

Endometriosis is a hormone-dependent, chronic inflammatory condition that affects 5–10% of reproductive-aged women. It is a complex disorder characterized by the growth of endometrial-like tissue outside the uterus, which can cause chronic pelvic pain and infertility. Despite its prevalence, the underlying molecular mechanisms of this disease remain poorly understood. Current treatment options are limited and focus mainly on suppressing lesion activity rather than eliminating it entirely. Although endometriosis is generally considered a benign condition, substantial evidence suggests that it increases the risk of developing specific subtypes of ovarian cancer. The discovery of cancer driver mutations in endometriotic lesions indicates that endometriosis may share molecular pathways with cancer. Moreover, the application of single-cell and spatial genomics, along with the development of organoid models, has started to illuminate the molecular mechanisms underlying disease etiology. This review aims to summarize the key genetic mutations and alterations that drive the development and progression of endometriosis to malignancy. We also review the significant recent advances in the understanding of the molecular basis of the disorder, as well as novel approaches and in vitro models that offer new avenues for improving our understanding of disease pathology and for developing new targeted therapies.