Endometriosis Symptoms, Etiology, and Effects of Lifestyle Changes and Food Habits: A Detailed Literature Review

Endometriosis is a chronic gynecological disorder characterized by the presence of endometrial-like tissue outside the uterine cavity. It affects approximately 10–15% of women of reproductive age and is associated with pelvic pain, dysmenorrhea, dyspareunia, infertility, and reduced quality of life. The pathogenesis of endometriosis is complex and multifactorial, involving hormonal imbalances, genetic predispositions, immunological dysfunctions, environmental exposures, and epigenetic modifications. Lifesty le factors and dietary patterns have emerged as important modulators in the onset and progression of endometriosis. This review aims to synthesize current evidence on the symptoms, etiology, and the role of lifestyle modifications—including physical activi ty, stress management, sleep, smoking, alcohol, and dietary habits—in the prevention and management of endometriosis. The paper highlights both protective and risk-enhancing behaviors and provides perspectives for future interventions.

A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science databases for publications between 2000 and 2025. Keywords included endometriosis, dysmenorrhea, etiology, pathogenesis, lifestyle factors, diet, nutrition, and risk f actors. Both observational and interventional studies were included, with emphasis on systematic reviews, meta -analyses, and well -designed cohort studies. Studies not in English or not directly related to endometriosis were excluded. References were limited to 60 to maintain clarity and avoid redundancy, prioritizing the most relevant and high -quality evidence. Citation style followed the Vancouver system. Definition of Terms Endometriosis: A gynecological condition defined by the presence of functional endometrial -like tissue outside the uterine cavity, often leading to pain and infertility. Dysmenorrhea: Painful menstruation, commonly classified as primary (without pelvic pathology) or secondary (associated with pelvic disease such as endometriosis). Lifestyle factors: Modifiable behaviors including diet, exercise, smoking, alcohol use, sleep, and stress management that influence disease risk and progression. Chemoprevention: The use of natural or synthetic agents, including dietary components, to inhibit, reverse, or slow the development of disease. International Journal for Multidisciplinary Research (IJFMR) E-ISSN: 2582-2160 ● Website: www.ijfmr.com ● Email: [email protected] IJFMR250557155 Volume 7, Issue 5, September-October 2025 2

Endometriosis is a debilitating disorder with significant medical, social, and economic consequences. Globally, it affects approximately 190 million women and adolescent girls of reproductive age, though prevalence varies based on diagnostic methods and population characteristics [1]. Clinical presentation is heterogeneous, ranging from asymptomatic cases to severe pelvic pain, infertility, and systemic manifestations [2]. The economic burden of endometriosis is considerable, with costs associated not only with direct medical care but also loss of productivity, absenteeism, and reduced quality of life [3]. Despite advances in diagnostic techniques, including imaging and mini mally invasive surgery, delayed diagnosis remains common, often extending from 7 to 10 years after symptom onset [4]. The etiology of endometriosis is complex and multifactorial. Several theories —including retrograde menstruation, coelomic metaplasia, stem/progenitor cell involvement, genetic predisposition, immune dysfunction, and hormonal imbalances—have been proposed [5,6]. However, none alone can fully explain the heterogeneity of the disease. Lifestyle and environmental factors, particularly diet, exercise, stress, sleep, and exposure to endocrine-disrupting chemicals, have been recognized as important contributors to risk and disease progression [7,8]. This review provides an in-depth examination of the clinical features, etiology, and the impact of dietary and lifestyle factors on endometriosis, aiming to integrate evidence into actionable insights for both prevention and management. Symptoms and Dysmenorrhea The hallmark symptoms of endometriosis include dysmenorrhea, chronic pelvic pain , dyspareunia, dyschezia, and infertility [9]. Dysmenorrhea is particularly significant, often severe and debilitating, and tends to worsen over time rather than improve as in primary dysmenorrhea [10]. The pain is typically cyclical but may persist throughout the menstrual cycle in advanced cases. Endometriosis-related dysmenorrhea is attributed to excessive production of prostaglandins and cytokines in ectopic endometrial tissue, leading to uterine hypercontractility, ischemia, and heightened pain perception [11]. Chronic inflammation also contribu tes to central sensitization, amplifying pain even in the absence of visible lesions [12]. In addition to dysmenorrhea, other manifestations include fatigue, bloating, gastrointestinal disturbances, and urinary symptoms, which further complicate diagnosis [13]. Infertility, affecting up to 50% of women with endometriosis, is associated with pelv ic adhesions, distorted anatomy, and impaired oocyte and embryo quality [14]. The impact on quality of life is profound, with significant psychological consequences such as anxiety, depression, and reduced social functioning [15]. Dysmenorrhea remains the most reliable clinical indicator of endometriosis and should prompt further di agnostic evaluation when persistent and resistant to conventional therapy. Etiology and Pathogenesis The pathogenesis of endometriosis remains an area of intense investigation, with several interrelated mechanisms proposed: International Journal for Multidisciplinary Research (IJFMR) E-ISSN: 2582-2160 ● Website: www.ijfmr.com ● Email: [email protected] IJFMR250557155 Volume 7, Issue 5, September-October 2025 3 Retrograde Menstruation Theory First proposed by Sampson in 1927, this theory suggests that viable endometrial fragments flow backward through the fallopian tubes into the peritoneal cavity during menstruation, where they implant and proliferate [16]. While retrograde menstruation occur s in up to 90% of women, only a fraction develop endometriosis, indicating that additional factors such as immune dysfunction and genetic predisposition play roles [17]. Coelomic Metaplasia This theory posits that peritoneal mesothelial cells undergo metaplasia into endometrial -like cells under hormonal or inflammatory stimuli. It helps explain rare cases of endometriosis in men receiving estrogen therapy and in women without functional endometrium [18]. Stem/Progenitor Cell Theory Recent evidence supports the role of endometrial stem/progenitor cells with high proliferative capacity in establishing ectopic lesions. Bone marrow-derived stem cells may also contribute to lesion formation [19]. Genetic and Epigenetic Factors Genetic susceptibility plays a role, with studies identifying loci associated with endometriosis risk, including those regulating hormone metabolism and inflammation [20]. Epigenetic modifications, such as DNA methylation and histone acetylation, alter gen e expression in endometriotic tissue, promoting survival and angiogenesis [21]. Hormonal and Immunological Dysregulation Endometriotic lesions are estrogen -dependent and resistant to progesterone, resulting in an estrogen - dominant, pro-inflammatory environment [22]. Immune dysfunction, including impaired natural killer cell activity and increased macrophage infiltration, facilitates lesion survival and progression [23]. Environmental Exposures Endocrine-disrupting chemicals (EDCs), including dioxins, bisphenol A, and phthalates, have been implicated in altering hormone signaling and immune responses, potentially increasing endometriosis risk [24]. The multifactorial nature of endometriosis suggests that genetic predisposition interacts with environmental exposures and lifestyle factors to determine disease onset and severity. Diet and Nutrition in Endometriosis Dietary patterns and nutrient intake significantly influence the risk and severity of endometriosis. Nutrition modulates systemic inflammation, oxidative stress, and hormonal balance —all central mechanisms in endometriosis pathophysiology. Pro-inflammatory Diets Diets rich in red and processed meats, trans fats, and refined carbohydrates are associated with increased risk and severity of endometriosis. Red meat consumption has been linked to elevated estrogen levels, while trans fats promote systemic inflammation [25]. International Journal for Multidisciplinary Research (IJFMR) E-ISSN: 2582-2160 ● Website: www.ijfmr.com ● Email: [email protected] IJFMR250557155 Volume 7, Issue 5, September-October 2025 4 Protective Dietary Components Fruits, vegetables, whole grains, and omega-3 fatty acids exert protective effects. High intake of fruits and green vegetables is associated with reduced risk, likely due to their antioxidant and anti -inflammatory properties [26]. Omega-3 fatty acids, found in fatty fish and flaxseed, reduce prostaglandin synthesis and may alleviate dysmenorrhea [27]. Dairy Products and Vitamin D The role of dairy is controversial, though some studies suggest protective effects attributed to calcium, vitamin D, and anti -inflammatory properties of certain dairy proteins [28]. Vitamin D, through its immunomodulatory role, has been associated with reduced risk and symptom relief [29]. Micronutrients Antioxidant vitamins such as vitamins C and E, as well as trace elements like zinc and selenium, counter oxidative stress and have been linked to improved outcomes [30]. Caffeine and Alcohol High caffeine and alcohol consumption may exacerbate endometriosis by altering estrogen metabolism, though findings remain inconsistent [31]. Dietary Patterns Adherence to Mediterranean dietary patterns—rich in fruits, vegetables, fish, legumes, and olive oil—has been associated with lower risk and improved symptom management [32]. Conversely, Western dietary patterns correlate with higher disease prevalence [33]. Overall, dietary interventions represent a promising, non -invasive strategy to complement conventional treatments and improve quality of life in women with endometriosis. Lifestyle Factors Lifestyle behaviours play a crucial role in modulating endometriosis risk, symptom severity, and overall quality of life. Modifiable factors—including physical activity, smoking, alcohol intake, stress, and sleep patterns—interact with hormonal, immune, and metabolic pathways that underlie the disease process. Physical Activity Regular physical activity exerts beneficial effects by lowering estrogen levels, enhancing immune surveillance, and reducing systemic inflammation [34]. Exercise also improves pelvic blood flow and reduces oxidative stress, which may alleviate dysmenorrhea and chronic pelvic pain [35]. Cohort studies have shown that women engaging in moderate -to-vigorous physical activity experience reduced risk of endometriosis diagnosis and milder symptoms [36]. However, evidence remains mixed, with some studies reporting no significant association, potentially due to variations in exercise intensity, frequency, and individual susceptibility [37]. Smoking Cigarette smoking has complex and somewhat contradictory effects. While smoking is generally associated with reduced estrogen levels, it also induces systemic inflammation, oxidative stress, and International Journal for Multidisciplinary Research (IJFMR) E-ISSN: 2582-2160 ● Website: www.ijfmr.com ● Email: [email protected] IJFMR250557155 Volume 7, Issue 5, September-October 2025 5 vascular dysfunction, which may exacerbate symptoms [38]. Meta -analyses suggest that smoking does not consistently reduce endometriosis risk, and in some cases, it may worsen pelvic pain and disease progression [39]. Alcohol Consumption Alcohol intake has been linked to increased risk of endometriosis in multiple observational studies [40]. Alcohol disrupts estrogen metabolism, raises circulating estradiol levels, and promotes oxidative stress [41]. Women with endometriosis often report w orsening pelvic pain and dysmenorrhea with regular alcohol consumption [42]. Stress and Psychological Health Chronic stress amplifies hypothalamic-pituitary-adrenal (HPA) axis activity, increasing cortisol secretion and impairing immune function [43]. Stress -induced inflammatory pathways may worsen pain and contribute to central sensitization [44]. Women with end ometriosis are at elevated risk for anxiety and depression, conditions that further exacerbate pain perception and reduce treatment adherence [45]. Interventions such as mindfulness, cognitive-behavioural therapy, and yoga have demonstrated benefit in symptom management [46]. Sleep Patterns Sleep disturbances are highly prevalent in women with endometriosis, often related to pain, hormonal imbalances, and psychological distress [47]. Poor sleep exacerbates systemic inflammation, impairs pain regulation, and worsens fatigue [48]. Studies suggest that improving sleep hygiene and treating comorbid insomnia can significantly reduce pain severity and improve quality of life [49]. Obesity and Body Mass Index (BMI) Although endometriosis often occurs in women with normal BMI, obesity may contribute to systemic inflammation, altered estrogen metabolism, and poorer outcomes [50]. Weight management through balanced diet and physical activity may improve symptom control and treatment response.

The interplay between genetic, hormonal, immunological, and environmental factors makes endometriosis a highly complex disease. Lifestyle factors —including diet, exercise, stress management, and sleep — emerge as critical, modifiable determinants that influence disease onset, symptom severity, and quality of life. Evidence suggests that anti -inflammatory diets, regular physical activity, stress reduction, and adequate sleep can improve clinical outcomes, whereas smoking, alcohol consumption, and sedentary behaviour worsen symptoms. The heterogeneity of findings in existing literature highlights methodological limitations, including reliance on self-reported data, small sample sizes, and varying diagnostic criteria. Moreover, cultural and socioeconomic factors affect lifestyle behaviours and access to healthcare, underscoring the need for more diverse and representative research cohorts. Future Directions Future research should focus on: International Journal for Multidisciplinary Research (IJFMR) E-ISSN: 2582-2160 ● Website: www.ijfmr.com ● Email: [email protected] IJFMR250557155 Volume 7, Issue 5, September-October 2025 6 1. Longitudinal Cohort Studies: To clarify causal links between lifestyle factors and endometriosis risk. 2. Randomized Controlled Trials (RCTs): To assess the efficacy of dietary and lifestyle interventions in symptom management. 3. Integrative Approaches : Combining conventional therapies with lifestyle modification, nutrition, and mind-body practices. 4. Personalized Medicine : Identifying subgroups of patients who may benefit most from specific lifestyle interventions based on genetic and epigenetic profiles. 5. Public Health Strategies : Awareness campaigns to educate women and healthcare providers about the role of lifestyle in prevention and management.

Endometriosis remains a major public health concern, significantly impairing women’s reproductive, psychological, and social well -being. While its etiology is multifactorial and not fully understood, evidence increasingly points to the role of modifiable l ifestyle and dietary factors in influencing disease risk and progression. Adoption of anti-inflammatory diets, engagement in regular physical activity, stress management, quality sleep, and avoidance of alcohol and smoking appear beneficial. These strategi es represent low -cost, non -invasive adjuncts to conventional medical and surgical therapies. Future integrative approaches that emphasize patient education and individualized lifestyle interventions may reduce disease burden and improve long-term outcomes.

1. Zondervan KT, Becker CM, Koga K, Missmer SA, Taylor RN, Viganò P. Endometriosis. Nat Rev Dis Primers. 2018;4:9. 2. Johnson NP, Hummelshoj L; World Endometriosis Society Montpellier Consortium. Consensus on current management of endometriosis. Hum Reprod. 2013;28(6):1552-68. 3. Giudice LC. Clinical practice. Endometriosis. N Engl J Med. 2010;362(25):2389-98. 4. Parasar P, Ozcan P, Terry KL. Endometriosis: Epidemiology, Diagnosis and Clinical Management. Curr Obstet Gynecol Rep. 2017;6:34-41. 5. Chapron C, Marcellin L, Borghese B, Santulli P. Rethinking mechanisms, diagnosis and management of endometriosis. Nat Rev Endocrinol. 2019;15(11):666-82. 6. Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertil Steril. 2012;98(3):511-9. 7. Saunders PTK, Horne AW. Endometriosis: etiology, pathobiology, and therapeutic prospects. Cell. 2021;184(11):2807-24. 8. Vercellini P, Viganò P, Somigliana E, Fedele L. Endometriosis: pathogenesis and treatment. Nat Rev Endocrinol. 2014;10(5):261-75. 9. Kennedy S, Bergqvist A, Chapron C, D’Hooghe T, Dunselman G, Greb R, et al. ESHRE guideline for the diagnosis and treatment of endometriosis. Hum Reprod. 2005;20(10):2698-704. 10. Dunselman GAJ, Vermeulen N, Becker C, Calhaz -Jorge C, D’Hooghe T, De Bie B, et al. ESHRE guideline: management of women with endometriosis. Hum Reprod. 2014;29(3):400-12. 11. Missmer SA, Hankinson SE, Spiegelman D, Barbieri RL, Marshall LM, Hunter DJ. Incidence of laparoscopically confirmed endometriosis by demographic, anthropometric, and lifestyle factors. Am J Epidemiol. 2004;160(8):784-96. International Journal for Multidisciplinary Research (IJFMR) E-ISSN: 2582-2160 ● Website: www.ijfmr.com ● Email: [email protected] IJFMR250557155 Volume 7, Issue 5, September-October 2025 7 12. Kvaskoff M, Mahamat-Saleh Y, Farland LV, Shigesi N, Terry KL, Harris HR, et al. Endometriosis and cancer: a systematic review and meta-analysis. Hum Reprod Update. 2021;27(2):393-420. 13. Nnoaham KE, Hummelshoj L, Webster P, d’Hooghe T, de Cicco Nardone F, de Cicco Nardone C, et al. Impact of endometriosis on quality of life and work productivity: a multicenter study across ten countries. Fertil Steril. 2011;96(2):366-73.e8. 14. Moradi M, Parker M, Sneddon A, Lopez V, Ellwood D. Impact of endometriosis on women’s lives: a qualitative study. BMC Womens Health. 2014;14:123. 15. Ballard KD, Lowton K, Wright JT. What’s the delay? A qualitative study of women’s experiences of reaching a diagnosis of endometriosis. Fertil Steril. 2006;86(5):1296-301. 16. Vercellini P, Meana M, Hummelshoj L, Somigliana E, Viganò P, Fedele L. Priorities for endometriosis research: a proposed focus on deep dyspareunia. Reprod Sci. 2011;18(2):114-8. 17. Facchin F, Barbara G, Saita E, Mosconi P, Roberto A, Fedele L, et al. Impact of endometriosis on quality of life and mental health: pelvic pain makes the difference. J Psychosom Obstet Gynaecol. 2015;36(4):135-41. 18. Culley L, Law C, Hudson N, Denny E, Mitchell H, Baumgarten M, et al. The social and psychological impact of endometriosis on women’s lives: a critical narrative review. Hum Reprod Update. 2013;19(6):625-39. 19. Fuldeore MJ, Soliman AM. Prevalence and symptomatic burden of diagnosed endometriosis in the United States: national estimates from a cross -sectional survey of 59,411 women. Gynecol Obstet Invest. 2017;82(5):453-61. 20. Shafrir AL, Farland LV, Shah DK, Harris HR, Kvaskoff M, Zondervan K, et al. Risk for and consequences of endometriosis: a critical epidemiologic review. Best Pract Res Clin Obstet Gynaecol. 2018;51:1-15. 21. Meuleman C, Vandenabeele B, Fieuws S, Spiessens C, Timmerman D, D’Hooghe T. High prevalence of endometriosis in infertile women with normal ovulation and normospermic partners. Fertil Steril. 2009;92(1):68-74. 22. Bulun SE. Endometriosis. N Engl J Med. 2009;360(3):268-79. 23. Sampson JA. Peritoneal endometriosis due to menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol. 1927;14:422-69. 24. Brosens I, Benagiano G. Is neonatal uterine bleeding involved in the pathogenesis of endometriosis as a source of stem cells? Fertil Steril. 2013;100(3):622-3. 25. Burney RO, Talbi S, Hamilton AE, Vo KC, Nyegaard M, Nezhat CR, et al. Gene expression analysis of endometrium reveals progesterone resistance and candidate susceptibility genes in women with endometriosis. Endocrinology. 2007;148(8):3814-26. 26. Guo SW. Epigenetics of endometriosis. Mol Hum Reprod. 2009;15(10):587-607. 27. Smolarz B, Szyłło K, Romanowicz H. Endometriosis: Epidemiology, classification, pathogenesis, treatment and genetics. (Review). Oncol Lett. 2021;22(6):854. 28. Hapangama DK, Kamal AM, Bulmer JN. Estrogen receptor β: the guardian of the endometrium. Hum Reprod Update. 2015;21(2):174-93. 29. Patel BG, Lenk EE, Lebovic DI, Shu Y, Yu J, Taylor RN. Pathogenesis of endometriosis: interaction between endocrine and inflammatory pathways. Best Pract Res Clin Obstet Gynaecol. 2018;50:50-60. 30. Zondervan KT, Becker CM, Missmer SA. Endometriosis. N Engl J Med. 2020;382(13):1244-56. International Journal for Multidisciplinary Research (IJFMR) E-ISSN: 2582-2160 ● Website: www.ijfmr.com ● Email: [email protected] IJFMR250557155 Volume 7, Issue 5, September-October 2025 8 31. Viganò P, Parazzini F, Somigliana E, Vercellini P. Endometriosis: epidemiology and aetiological factors. Best Pract Res Clin Obstet Gynaecol. 2004;18(2):177-200. 32. Harris HR, Costenbader KH, Mu F, Kvaskoff M, Malspeis S, Karlson EW, et al. Endometriosis and the risks of systemic lupus erythematosus and rheumatoid arthritis in women. Ann Rheum Dis. 2016;75(7):1279-84. 33. Vitonis AF, Vincent K, Rahmioglu N, Fassbender A, Buck Louis GM, Hummelshoj L, et al. World Endometriosis Research Foundation Endometriosis Phenome and Biobanking Harmonization Project: II. Clinical and covariate phenotype data collection in endometriosis research. Fertil Steril. 2014;102(5):1223-32. 34. Shan K, Lian F, Zhuo L, Wang Y, Guo J, Zhang R. Dietary patterns and endometriosis risk: a systematic review and meta-analysis. Medicine (Baltimore). 2021;100(22):e26129. 35. Parazzini F, Viganò P, Candiani M, Fedele L. Diet and endometriosis risk: a literature review. Reprod Biomed Online. 2013;26(4):323-36. 36. Harris HR, Chavarro JE, Malspeis S, Willett WC, Missmer SA. Dairy-food, calcium, magnesium, and vitamin D intake and endometriosis risk. Am J Epidemiol. 2013;177(5):420-30. 37. Trabert B, Peters U, De Roos AJ, Scholes D, Holt VL. Diet and risk of endometriosis in a population- based case-control study. Fertil Steril. 2011;96(2):366-73. 38. Yamamoto A, Harris HR, Vitonis AF, Chavarro JE, Missmer SA. A prospective cohort study of meat and fish consumption and endometriosis risk. Am J Obstet Gynecol. 2018;219(2):178.e1-178.e10. 39. Nodler JL, DiBenedetti DB, Carr KR, Sikes CR, Muramoto ML. Dietary supplement use and risk of endometriosis in women: a systematic review. Reprod Biomed Online. 2020;41(1):317-28. 40. Nirgianakis K, Gasparri ML, Radan AP, Villiger A, McKinnon B, Mosimann B, et al. Nutritional and dietary interventions in endometriosis: a systematic review. Reprod Biomed Online. 2022;44(5):779- 804. 41. Santanam N, Kavtaradze N, Murphy A, Dominguez C, Parthasarathy S. Antioxidant supplementation reduces endometriosis-related pelvic pain in humans. Transl Res. 2013;161(3):189-95. 42. Chiaffarino F, Parazzini F, Bertuccio P, Chatenoud L, Ricci E, Bianchi S, et al. Coffee and caffeine intake and risk of endometriosis: a meta-analysis. Eur J Nutr. 2014;53(7):1573-9. 43. Missmer SA, Chavarro JE, Malspeis S, Bertone -Johnson ER, Hornstein MD, Spiegelman D, et al. A prospective study of dietary fat consumption and endometriosis risk. Hum Reprod. 2010;25(6):1528 - 35. 44. Hediger ML, Hartnett HJ, Louis GM. Association of endometriosis with body size and figure. Fertil Steril. 2005;84(5):1366-74. 45. Vitonis AF, Baer HJ, Hankinson SE, Laufer MR, Missmer SA. A prospective study of body size during childhood and early adulthood and the incidence of endometriosis. Epidemiology. 2010;21(3):433-9. 46. Farland LV, Missmer SA, Bijon A, Gusto G, Gelot A, Clavel-Chapelon F, et al. Physical activity and endometriosis risk in women with infertility or pain: evidence from the French E3N cohort. Hum Reprod. 2016;31(2):364-72. 47. Vitonis AF, Hankinson SE, Hornstein MD, Missmer SA. Adult physical activity and endometriosis risk. Epidemiology. 2010;21(6):911-7. 48. Yamamoto A, Harris HR, Vitonis AF, Chavarro JE, Missmer SA. A prospective study of alcohol consumption and risk of endometriosis. Am J Obstet Gynecol. 2019;220(3):262.e1-262.e10. International Journal for Multidisciplinary Research (IJFMR) E-ISSN: 2582-2160 ● Website: www.ijfmr.com ● Email: [email protected] IJFMR250557155 Volume 7, Issue 5, September-October 2025 9 49. Parazzini F, Chiaffarino F, Surace M, Chatenoud L, Cipriani S, Chiantera V, et al. Selected food intake and risk of endometriosis. Hum Reprod. 2004;19(8):1755-9. 50. Vercellini P, Somigliana E, Viganò P, Abbiati A, Barbara G, Crosignani PG. Post -operative endometriosis recurrence: a plea for prevention based on pathogenetic, epidemiological and clinical evidence. Reprod Biomed Online. 2010;21(2):259-65. 51. Bulun SE, Yilmaz BD, Sison C, Miyazaki K, Bernardi L, Liu S, et al. Endometriosis. Endocr Rev. 2019;40(4):1048-79. 52. Kundu S, Wild RA, Unruh D, Poretsky L. Metabolic aspects of endometriosis: a review. Reprod Sci. 2021;28(10):2774-84. 53. Kvaskoff M, Mu F, Terry KL, Harris HR, Poole EM, Farland LV, et al. Endometriosis: a high -risk population for major chronic diseases? Hum Reprod Update. 2015;21(4):500-16. 54. Prescott J, Farland LV, Tobias DK, Gaskins AJ, Spiegelman D, Chavarro JE, et al. A prospective cohort study of endometriosis and subsequent risk of infertility. Hum Reprod. 2016;31(7):1475-82. 55. Morotti M, Vincent K, Becker CM. Mechanisms of pain in endometriosis. Eur J Obstet Gynecol Reprod Biol. 2017;209:8-13. 56. Howard FM. The role of laparoscopy in chronic pelvic pain: promise and pitfalls. Obstet Gynecol Surv. 1993;48(6):357-87. 57. Johnson NP, Hummelshoj L. Consensus on current management of endometriosis. Hum Reprod. 2013;28(6):1552-68. 58. Giudice LC, Kao LC. Endometriosis. Lancet. 2004;364(9447):1789-99. 59. Stratton P, Berkley KJ. Chronic pelvic pain and endometriosis: translational evidence of the relationship and implications. Hum Reprod Update. 2011;17(3):327-46. 60. Vercellini P, Buggio L, Berlanda N, Barbara G, Somigliana E, Bosari S. Estrogen -progestins and progestins for the management of endometriosis. Fertil Steril. 2016;106(7):1552-71.e2.