{"paper_id":"25569121-0a83-4d52-b72a-c1133403ef12","body_text":"124\nThis is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International  \n(CC BY-NC-SA 4.0). License (http://creativecommons.org/licenses/by-nc-sa/4.0/)\nREVIEW PAPER\nDOI: https://doi.org/10.5114/pm.2022.116437\nMenopause Rev 2022; 21(2): 124-132\nIntroduction\nEndometriosis is a  chronic inflammatory disorder \ncharacterized by the presence of ectopic endometri-\nal-like glands and stroma, often involving the pelvic \norgans and frequently leading to anatomical distortion \nwithin the pelvis [1, 2]. The prevalence of this disease \nranges between six and ten percent [3], while the in-\ncidence is believed to be above 33% for patients with \nacute pelvic pain [4]. Nevertheless, it is difficult to pre-\ncisely estimate the incidence and prevalence of super -\nficial peritoneal endometriosis because of the absence \nof an accurate non-invasive biomarker [5]. The main \nsymptoms for affected women include chronic pelvic \npain, dysmenorrhea, infertility [6], and deep dyspareu-\nImpact of lifestyle and diet on endometriosis: a fresh look to a busy corner\nNassir Habib1, Giovanni Buzzaccarini2, Gabriele Centini3, Gaby N. Moawad4, Pierre-Francois Ceccaldi5, \nGeorgios Gitas6, Ibrahim Alkatout7, Giuseppe Gullo8, Sanja Terzic9, Zaki Sleiman10\n 1Obstetrics and Gynecology Department, Francois Quesnay Hospital, Mantes-La-Jolie, France \n 2Department of Women’s and Children’s Health, University of Padua, Padova, Italy \n 3Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy \n 4Gynecology Department, George Washington University, Washington, United States of America \n 5Obstetrics and Gynecology Department, Beaujon Teaching Hospital, Clichy and Paris Diderot University, Clichy, France \n 6Department of Obstetrics and Gynecology, Campus Charité Mitte, Charité-Universitätsmedizin Berlin, Berlin, Germany \n 7Department of Obstetrics and Gynecology, University Hospital of Schleswig-Holstein, Kiel, Germany \n 8Azienda Ospedaliera Ospedali Riuniti (AOOR) Villa Sofia Cervello, IVF Public Center, University of Palermo, Palermo, Italy \n 9Department of Medicine, School of Medicine, Nazarbayev University, Nur-Sultan, Kazakhstan \n10Obstetrics and Gynecology Department, Lebanese American University, Beirut, Lebanon\nAbstract \nEndometriosis is a chronic inflammatory disorder with a prevalence of six to ten percent in women of child-\nbearing age. As long as the aetiology of endometriosis is not fully understood and the disease has no definitive \ntreatment, an examination of the environmental factors or interventions that could modify or cure endometriosis \nwould greatly benefit women suffering from this chronic condition. \nThis literature review utilized the electronic databases PubMed, EMBASE, and MEDLINE until February 2021. \nStudies indicate that fish oil may have a positive effect on reducing endometriosis-related pain due to the effects \nof pro-inflammatory prostaglandins derived from omega-3 fatty acids. The same effect was seen with the intro-\nduction of antioxidant vitamins C, D, and E. There is clinical viability of a low fermentable oligo-, di-, and mono-\nsaccharides and polyols diet to successfully reduce the symptoms of patients who suffer from both endometriosis \nand irritable bowel syndrome. Despite the low level of evidence, there are frequent associations between endo-\nmetriosis and gastrointestinal conditions in addition to the influence of various nutritional factors on the disease. \nThe management of endometriosis requires a holistic approach focused on reducing overall inflammation, \nincreasing detoxification, and attenuating troublesome symptoms. A dietician may provide great benefit in the \nmanagement of these patients, especially at younger ages and in early stages. High-level evidence and well-\ndesigned randomized studies are lacking when it comes to studying the effect of lifestyle and dietary intake on \nendometriosis. Inarguably, further research with a more extensive focus is needed.\nKey words: endometriosis, nutrition, lifestyle, chronic pelvic pain, diet.\nnia [7]. However, the management of these symptoms is \nnot standardized, and the disease can recur even after \nproper surgical [8] or pharmacological management [9]. \nIn particular, we can consider surgery as a cytoreductive \ntherapy, which removes the illness. However, endome-\ntriosis can recur. On the other hand, medical therapy \nacts with a suppressive effect on endometriosis. Simi-\nlarly but differently, in the case of medical therapy ces-\nsation, the illness may be reactivated.\nDifferent hypotheses explain the pathogenesis of en - \ndometriosis [10, 11]. The most widely accepted theo-\nry involves retrograde menstruation [7], but the exact \naetiology remains unknown. As long as the aetiology \nof endometriosis is not fully understood and the condi-\ntion has no definitive treatment [12], women suffering \nCorresponding author: \nZaki Sleiman, Obstetrics and Gynecology Department, Lebanese American University, Beirut, Lebanon, \ne-mail: zakinexus@hotmail.com\nSubmitted: 03.01.2022\nAccepted: 22.02.2022\n\nMenopause Review/Przegląd Menopauzalny 21(2) 2022\n125\nfrom this chronic disease may greatly benefit from in-\nsights into environmental factors [13] or interventions \nthat could prevent, modify, or cure endometriosis [14]. \nEndometriosis is a hormone-dependent chronic inflam-\nmatory condition that depends on oestrogen for growth \nand maintenance. Oestrogen is produced by the ova-\nries, skin and fatty tissue, and also could be produced \nlocally by the endometriotic lesions themselves through \na  positive feedback loop between PGE2, aromatase, \noestrogen, and COX-2 [15, 16]. In this scenario, an asso-\nciation has been found between diet and oestrogen-de-\npendent diseases (similar to breast or endometrial can-\ncer). Many dietary and lifestyle modifications can play \na considerable role in symptom minimization [17] and \nmay influence disease severity or progression [18–20]. \nThe purpose of this paper is to review the literature \nto evaluate the impact of environment, lifestyle, and \ndiet on symptom expression and endometriosis pro-\ngression. We also aim to identify a potential diet to help \nwomen with endometriosis control their disease or  \nat least find symptomatic relief. \nMaterial and methods\nA  literature review was conducted using the elec-\ntronic databases PubMed, EMBASE, and MEDLINE \nwith the search terms ‘endometriosis’ (MeSH) and \n‘nutrition’, ‘lifestyle’, ‘diet’, ‘irritable bowel disease’, \n‘physical activity’, ‘weight’, or ‘body mass index’ (BMI).  \nThe review specifically evaluated articles published in \nthe English language until February 2021. Multiple au-\nthors reviewed the papers and independently selected \nthe articles included in this review. \nRisk factors and pathogenesis of endometriosis \nThe incidence of dysmenorrhea has been quoted \nto be as high as 45–90% in developing countries, and \nit is a frequent complaint of women who suffer from \nendometriosis [21, 22], with a  robust potential nega-\ntive impact on the quality of life [23] and psychological \nwellbeing [24]. The combination of dysmenorrhoea and \nunexplained infertility [25] appears to be a significant \npredictor of endometriosis in women suffering from \nthese two concomitant conditions [26, 27], which needs \naccurate differential diagnosis [28]. Early age at men-\narche and shorter menstrual cycles have been consis-\ntently associated with a  higher risk of endometriosis \n[29–31], potentially as a result of an altered hormonal \nmilieu and an increased duration of exposure to retro-\ngrade menstruation. However, with less consistent evi-\ndence, researchers have found that endometriosis may \nbe related to the monthly duration of menses, the reg-\nularity of menstrual cycles, the heaviness of menstrual \nflow, and tampon use [30, 32, 33]. \nAlong with its broad array of risk factors, endo-\nmetriosis has a  multifactorial pathogenesis (Fig. 1). \nThe retrograde menstruation theory can explain the \npathogenesis of endometriosis to a  large extent, but \nnot completely, as the theory notably lacks an expla-\nnation of how endometrial tissue grafts onto the peri-\ntoneum. It is obvious that endometriosis is a complex \nImplantation and growht of pathological \nendometrial fragments\nFig. 1. Pathogenesis and risk factors of endometriosis\nStructural endometrial abnormalities\nImpaired steroid biosynthesis over expression\nNeoangiogenesis, endometrial neurogenesis \nProinflammatory profile in endometrial tissue \nHormones, immune disorders \nInteraction of genetic and hereditary \npredisposition \nEpigenetic inflammatory and environmental factors \n\nMenopause Review/Przegląd Menopauzalny 21(2) 2022\n126\nphenomenon caused by the interaction of genetic and \nhereditary predispositions, epigenetic inflammatory \nand environmental factors, hormones, immune disor -\nders, and certain structural endometrial abnormali-\nties [1, 34–36]. Indeed, impaired steroid biosynthesis \n(e.g., hyperoestrogenism, progesterone resistance, or \naromatase over-expression) increases the endometrial \ninvasive potential associated with neoangiogenesis, en-\ndometrial neurogenesis, and a  pro-inflammatory pro-\nfile in endometrial tissue compared with disease-free \nendometrium. These are examples of pre-existing en-\ndometrial abnormalities that could also promote the \nimplantation and growth of pathological endometrial \nfragments outside the uterine cavity [37]. Meanwhile,  \nit remains uncertain how these mechanisms partici-\npate to create the different phenotypes of endometrio-\nsis, and the potential cross-talk of these elements with  \nthe immune system within the pelvic cavity [38]. \nGenetically, women with a first-degree relative suf-\nfering from endometriosis are six times more likely to \nbe diagnosed with endometriosis compared to the gen-\neral population [26]. Moreover, large studies of twins \nreveal a  heritability of approximately 50% [39, 40]. \nHowever, the identification of genetic factors causing \nthis condition is incomplete, and the current evidence \nsuggests that the likelihood of having a “major gene” \ninvolved in familial endometriosis is low [41–43]. No-\ntably, whole-genome association studies have reported \na  dozen sensitive regions although these regions ac-\ncount for just over four percent of heritability [36]. \nThe involvement of endocrine-disrupting chemi-\ncals in endometriosis remains questionable [44–46]. \nAt present, the evidence of a  direct relation between \nendometriosis and endocrine-disrupting chemicals is \ninconsistent [47]. \nNew recent findings show that the glandular and \nstromal components of endometriosis originate from \ndifferent sources. Moreover, the epithelial component  \nof endometriosis harbours cancer-associated muta-\ntions, compared to the stromal component, which is mu-\ntation-free. These findings suggested that the stroma \nis regenerative, unlike the glands. Additionally, the en-\ndometriotic lesions were found to have epithelial pro-\ngenitors and mesenchymal stem cells. All these insights \nshow that endometriosis is derived from different \nsources and the pathogenetic mechanisms are more \ncomplex than expected [48].\nResults\nPhysical factors \nBirthweight \nScientific advances in medicine have revealed how \nintrauterine exposures impact the embryo or fetus by \ncontinuously reprogramming its development for ex-\ntrauterine life [49, 50]. The relationship between birth \nweight and the risk of developing endometriosis has \nbeen the subject of several studies [29, 51–53]. Extremes \nof birthweight, both low and high, have been found to \nbe associated with a  higher risk of developing endo-\nmetriosis over a  woman’s lifetime (RR = 1.3, 95% CI: \n1.0–1.8) [29, 51]. However, conflicting data exist re-\ngarding prematurity and endometriosis risk, with some \nstudies reporting an increased risk [52–54] and others \nreporting no association [51, 55, 56]. For an accurate in-\nterpretation of the influence of birthweight on the risk \nof endometriosis, it is necessary to restrict analyses to \nterm births, and for studies including preterm neonates \nto adjust for gestational age. \nChildhood, adolescent, and adult weight \nIn the same sense as above, the relationship be-\ntween childhood and adolescent weights and the de-\nvelopment of endometriosis is counterbalanced. Early \nstudies described the current state of being thin and \nunderweight as hallmarks of patients suffering from \nendometriosis, without insight into whether this is \na cause or a consequence of their disease or its symp-\ntoms [30, 33, 57–59]. Regardless of the patient’s age, \ncurrent evidence suggests an inverse relationship be-\ntween BMI and the prevalence of endometriosis [56, \n60–62]. However, the association between obesity and \nendometriosis remains debatable. Some researchers \nhave discovered an elevated incidence of endometri-\nosis in obese women [63] with a correlation between \nthe risk of developing endometriosis and prepubertal \nobesity [64]. Nagle et al. suggested that women who \nreported being overweight at 10 years of age had an \nincreased risk of endometriosis (OR = 2.8; 95% CI: \n1.1–7.5), whereas there was no clear evidence of an \nassociation between relative weight at 16 years of age \nand the risk of endometriosis [64]. Other researchers \nhave reported an inverse relationship between obesity \nand the risk of endometriosis [32, 60, 65–69]. In a me-\nta-analysis, Liu et al. found a significant inverse associ-\nation; the overall analysis revealed a 33% reduction in \nthe risk of endometriosis for each 5 kg/m\n2 increase in \nBMI (RR = 0.67; 95% CI: 0.53–0.84), with statistically \nsignificant heterogeneity across the studies (p < 0.001, \nI = 86.9%) [67]. These contradictory results confirm the \nneed for studies with larger numbers to elucidate the \nreal association between being overweight or obese \nand endometriosis while taking into account metabolic \nand biochemical parameters. \nPhysical activity \nIn view of the inflammatory [70] and oestrogen-de-\npendent profile of the disease [1], the role that physical \nactivity can play in reducing the risk of endometriosis \nseems highly possible on an intuitive level. Current \nevidence suggests that endometriosis symptoms may \nbe reduced by physical activity [62, 71]. However, this \n\nMenopause Review/Przegląd Menopauzalny 21(2) 2022\n127\nassociation is inconsistent [72]. Case-control studies \nhave inconclusively found that patients who exercised \nregularly had fewer symptoms compared to individu-\nals without self-reported regular exercise [58, 73, 74]. \nWhen comparing women with the highest physical \nactivity levels to the lowest, researchers discovered \na non-significant decrease in the reporting of endome-\ntriosis-related symptoms (RR = 0.89, 95% CI: 0.77–1.03) \n[75]. Nevertheless, physical activity may influence en-\ndometriosis symptomatology and progression due to \nits known influence on hormonal levels, such as de-\ncreasing luteal oestrogens [76] and increasing sex hor -\nmone binding globulin levels [77].\nBreastfeeding \nIn a  prospective cohort study of 72,394 women, \nFarland et al. found that breastfeeding was a  protec-\ntive factor for endometriosis-related symptoms among  \nthe 3,296 (4.6%) women who had laparoscopically con-\nfirmed endometriosis [78]. Additionally, the rate of en-\ndometriosis-related symptoms was decreased among \nwomen with at least six months of postpartum breast-\nfeeding. Although the causation behind this correla-\ntion is not fully understood, the present belief is that  \nthe symptomatic relief is due to amenorrhoea [78, 79]. \nDietary factors\nAlcohol consumption \nData are mixed regarding alcohol consumption and \nthe development of endometriosis [68, 71, 80]. Several \nstudies have identified an association between alcohol \nconsumption and symptoms related to endometrio-\nsis, whereas others have not [30, 62, 71, 74, 81–83]. \nStill, the available evidence is not without limitations. \nIn the studies where researchers found an association \nbetween endometriosis and alcohol consumption, it is \ndifficult to ascertain whether the consumption is due \nto the disease or vice versa. At this time, it also remains \nunknown whether different types of alcohol affect this \ndisease differently. \nDiet\nInflammation, oestrogen activity, menstrual regular-\nity, and prostaglandin physiology are important patho-\nphysiologic processes to consider when diagnosing and \ntreating endometriosis [80]. Diet is an integral compo-\nnent of these factors and, as such, consumption likely \nhas a role in the development and progression of this \ndisease. In fact, a recent case-control study found that \nwomen who consume diets with high inflammatory \npotential are significantly more likely to have endome-\ntriosis in comparison to those with less inflammatory \ndiets [84].\nA  prospective cohort study of the Nurses’ Health \nStudy II population found that women who consume \nmore than two servings a day of red meat have a 56% \nhigher risk of endometriosis diagnosis compared to \nthose who consume less than one serving per week \n(95% CI: 1.22–1.99), with the association being high-\nest for those who consume non-processed red meats \n[85]. In contrast, a  case-control study comparing the \nfrequency and consumption per week of selected \nitems in the Iranian diet found the intake of red meat \nto be associated with a  lower risk of endometriosis  \n(OR = 0.61, 95% CI: 0.41–0.91) [86]. Jurkiewicz-Przondzi-\nono et al. highlighted dietary factors that potentially in-\ncrease the risk of developing endometriosis, including \nthe high intake of ham, red meat, and trans-unsatu-\nrated fatty acids [80]. The authors surmised that the \npro-inflammatory profiles of these foods account for \ntheir associations with the disease [80]. \nOmega-6 fatty [87] acids derived from the diet are \nthe precursors of the pro-inflammatory prostaglandins \nPGE2 and PGF2α, which likely increase uterine cramps \nand cause the painful symptoms of endometriosis [88]. \nIn the same review, it was also suggested that antiox-\nidant vitamins (D, E, and B-group vitamins) [89, 90], as \nwell as foods rich in calcium and omega-3 fatty acids, \nmay protect against the development of endometrio-\nsis [80]. In the cohort study by Darling et al. including \n70,617 women (n = 1,383 for the experimental group \nwith confirmed endometriosis and n = 69,234 for the \ncontrol group), the consumption of products rich in vita-\nmins such as folic acid (p = 0.003), vitamin C (p = 0.02), \nand vitamin E (p < 0.0001) was inversely proportional \nto the risk of developing endometriosis [91]. The au-\nthors did not find that endometriosis symptoms were \nmitigated by providing these same vitamins through \ndietary supplements [91]. A  recent double-blind ran-\ndomized placebo-controlled trial examining treatment \nwith vitamin D [92], omega-3 fatty acids, or placebo in \nwomen with surgically confirmed endometriosis and \npelvic pain found that women in both the vitamin D and \nplacebo arms had similarly significant improvements in \npain scores, while those in the omega-3 arm demon-\nstrated lesser improvements [93]. Thus, while pro-in-\nflammatory omega-6 fatty acids may increase endome-\ntriosis-related pain, antioxidant vitamins and omega-3 \nfatty acids may be protective against these symptoms.\nMethylation changes [94], which are a  hallmark  \nof cancers and endometriosis [95], are influenced by di-\netary factors such as folate consumption, calorie intake, \nand polyphenol content. Such compounds tend to bio-\naccumulate in lipids contained particularly in meat, liv-\ner, and dairy products and can also be counted among \nthe risk factors for endometriosis. However, nowhere in \nthe literature is this association reported. \nIn a study of curcumin and its impact on endome-\ntriosis, the authors found that this spice might have \npotential benefits for the prevention and treatment  \nof endometriosis. The benefits from curcumin are believed \n\nMenopause Review/Przegląd Menopauzalny 21(2) 2022\n128\nto be due to its anti-inflammatory, antioxidant, anti-tu-\nmour, and anti-angiogenic profile [96]. However, because \nof the limited studies on this topic and inconsistent data, \nfurther studies are needed to improve the knowledge  \nof the true impact of curcumin on endometriosis.\nFasting \nFasting can help preserve energy levels [97], there-\nby providing the body time to regenerate and heal. In-\ncreased hormonal modulation, reduced inflammation \n[98], and increased stress resistance are ways in which \nfasting may help reduce chronic pain severity. In clinical \npractice, we have found that strategic fasting can help \nreduce symptomatic flares among patients suffering \nfrom symptoms related to endometriosis. We some-\ntimes advise outpatients to eat lightly or to fast prior \nto their menstrual cycles in order to lessen the activity \nof the gastrointestinal (GI) tract, thereby reducing the \nuncomfortable and painful GI symptoms associated \nwith endometriosis. Currently, there are no studies on \nthe role of fasting in the management of endometriosis. \nFODMAPs and irritable bowel syndrome \nIrritable bowel syndrome (IBS) impacts 11.2% of the \npopulation worldwide and significantly affects quality \nof life for many women. The role of diet is very import-\nant in IBS, both in worsening and improving symp-\ntoms for patients suffering from this disorder. The fer -\nmentable oligo-, di-, and mono-saccharides and polyols  \n(FODMAPs) comprise a group of carbohydrates resistant \nto digestion that are found in a broad range of foods. \nFODMAPs play a substantial role in initiating the symp-\ntoms of IBS [96, 99, 100]. Diets low in FODMAPs have \na proven efficacy with a high level of evidence in alleviat-\ning symptoms related to IBS, and as such were adopted \nin the IBS treatment guidelines of the National Institute \nfor Health and Care Excellence and the British Dietetic \nAssociation. Initiating a diet low in FODMAPs requires \nthe expertise of a dietitian or a clinician with the proper \ntraining and experience in this approach [100]. \nPatients who suffer from IBS are often found to \nhave concurrent symptoms of endometriosis. Women \ndiagnosed with endometriosis are two to three times \nmore likely to receive a  concomitant diagnosis of IBS \ncompared to women without endometriosis [96, 101]. \nSchink et al. found a nearly four-fold increase in food \nintolerances in patients with endometriosis compared \nto controls [102]. In addition, Schomacker et al. found \na  higher prevalence of IBS in women diagnosed with \nendometriosis compared to women with no endome-\ntriosis, regardless of whether or not there was endo-\nmetriosis infiltrating the bowel [103]. Interestingly, \na prospective cohort study found that although 52% of \nwomen with confirmed endometriosis had IBS, more \nsevere IBS symptoms were found in patients with low-\ner-stage endometriosis [104].\nIt seems plausible that the association between IBS \nand endometriosis is not only epidemiological but that \nthere are also shared pathophysiological pathways. \nBoth disorders cause similar symptoms for patients \nand are defined by their chronic low-grade inflamma-\ntory state. An awareness of the association between \nIBS and endometriosis is extremely important for the \nmanagement of patients with endometriosis-associat-\ned pelvic pain. While observing a series of 160 women \nwith IBS, Moore et al. reported a  significant improve-\nment in symptoms with the effect of the low-FODMAP \ndiet for patients with IBS and endometriosis compared \nto patients with IBS alone (72% vs. 40%, respectively,  \np = 0.001) [99]. The authors concluded that a low-FOD-\nMAP diet may be beneficial for women suffering from \nsymptoms related to both IBS and endometriosis [99]. \nEvidence suggests using a multidisciplinary approach to \nthe care of patients with GI symptoms related to either \nIBS or endometriosis in order to reach an appropriate \ndiagnosis followed by the correct therapy [105]. \nSoy and phytoestrogens \nThe weak oestrogenic effect of phytoestrogens pres-\nent in soy has been found to be associated with an in-\ncreased risk of oestrogen-dependent diseases [106, 107]. \nIn Japan, soy is commonly consumed and the high \nphytoestrogen intake there has been associated with \nan elevated risk of endometriosis. Liu et al. compared \nthe change of endometrial thickness before and after \nisoflavone supplementation [107]. The authors found  \nthat a  daily isoflavone dose of more than 54  mg per \nday may decrease endometrial thickness in post-meno-\npausal women and produce different effects on popu-\nlations [107]. \nNevertheless, it seems that not all phytoestrogens \nhave the same impact on endometriosis. Some animal \nmodels have indicated that puerarin and genistein, \ntwo phytoestrogens with antineoplastic properties, re-\nduce the burden of endometriotic lesions via inhibiting \naromatase and oestrogen receptor-a  expression and \nreducing oestrogen concentrations [107]. In a  small \ncase series, Chandrareddy et al. found that dietary phy-\ntoestrogens were associated with abnormal uterine \nbleeding in women [108]. Although these women had \na variety of symptoms and pathologies discovered, they \nall had symptomatic improvement when phytoestro-\ngens were withdrawn from their diet [108]. \nGluten-free diet and coeliac disease\nOxidative stress, chronic inflammation, and immu-\nnological disorders are features shared between coeli-\nac disease and endometriosis. The literature is scarce \nregarding the association between these two diseases. \nSantoro et al. investigated this hypothetical associa-\ntion and detected a  higher prevalence of coeliac dis-\nease among women diagnosed with endometriosis, but  \n\nMenopause Review/Przegląd Menopauzalny 21(2) 2022\n129\nthe results were not statistically significant [109]. Caser-\nta et al. reported a case of a woman suffering from en-\ndometriosis with concomitant coeliac disease, where \na gluten-free diet improved her fertility [110]. Marziali \net al. tested the gluten-free diet in 207 symptomatic \nwomen suffering from endometriosis and reported \na  statistically significant improvement in symptoms \nin 75% of the women [111]. Women exposed to a glu-\nten-free diet had a significantly better quality of life in \naddition to improved physical and social functioning  \n(p < 0.005) [110]. Both endometriosis and coeliac \ndisease are associated with chronic inflammation, \nand both present with significant elevations of inter -\nferon-gamma (IFN-γ) and interleukin-6 (IL-6). Thus,  \nthe authors concluded that a gluten-free diet is efficient \nin improving endometriosis symptoms after 12 months \nof treatment and plays an antagonist role by decreasing \nIFN-γ and IL-6 [111]. \nHigh-fat diet \nHigh fat consumption is associated with oxidative \nstress and inflammation – two key features of endome-\ntriosis. Some inflammatory markers, such as IL-6, are \nfound in higher concentrations in women with endo-\nmetriosis, and are increased by specific fatty acid expo-\nsure [112]. In contrast, decreasing oxidative stress us-\ning diets rich in antioxidants may be protective against \nthe progression or development of endometriosis [113]. \nHeard et al. reported an increase in endometriosis le-\nsion development in mouse models after exposure to \na high-fat diet independent of overt obesity and weight \ngain [114]. This association was believed to be due to \npromoted oxidative stress and inflammatory pathways \nprovoked by high-fat diets. Maintaining a healthy diet \nhas considerable health benefits and may also decrease \nthe risk of endometriosis [114, 115]. \nThe missing link: new insights into fertility \noutcomes\nRecent discoveries in micronutrients have made prog-\nress thanks to the pharmaceutical field. In particular, \na great effort has been spent on inositol research. Ino-\nsitols, in the form of myo-inositol and D-inositol, have \nbeen proposed as pharmaceutical agents with a positive \neffect on insulin sensitivity and PCOS women. For this \nreason, their administration is widely accepted and pro-\nposed as adjuvant therapy in women affected by PCOS \nwith difficulty in conceiving [115–120]. Similarly, vitamin \nD has also been proposed as a possible adjuvant for fer-\ntility. However, unlike the inositols, vitamin D excessive \nlevels may play a detrimental role in infertility [121–123].\nConclusions\nThis paper reviewed the impact of different lifestyle \nand dietary factors on the development and severity \nof endometriosis as reported in the literature, empha-\nsizing that this disease is multifactorial with a  con-\ncomitant inflammatory pattern. High-level evidence \nand well-designed randomized studies are lacking \nwhen it comes to studying the effect of these modi-\nfiable risk factors on endometriosis. However, certain \nstudies indicate that fish oil may have a positive effect \non reducing pain due to the effects of the anti-inflam-\nmatory prostaglandins PGE3 and PGE3α derived from \nomega-3 fatty acids. The same effects were seen with \nthe introduction of the antioxidant vitamins C, D, and \nE. Current literature demonstrates that there is clinical \nviability of a  low-FODMAP diet to successfully reduce \nthe symptoms of patients who suffer from both endo-\nmetriosis and IBS. Despite the low level of evidence, \nthere are frequent associations between endometriosis \nand GI conditions in addition to the influence of dif-\nferent nutritional factors on the disease. There is also \nevidence that the adaptation of individualized dietary \nchanges yields statistically significant improvements \nin endometriosis-related symptoms [124]. Thus, there \nmay be great benefit to including a  dietician in the \nmanagement of these patients, especially at younger \nages and in early stages. The management of endome-\ntriosis requires a  holistic approach focused on reduc-\ning overall inflammation, increasing detoxification, and \nattenuating troublesome symptoms. Inarguably, further \nresearch with a more extensive focus is needed.\nDisclosure\nThe authors report no conflict of interest.\nReferences \n1. Vercellini P , Viganò P , Somigliana E, et al. Endometriosis: pathogenesis \nand treatment. Nat Rev Endocrinol 2014; 10: 261-275.\n2. Djokovic D, Pinto P , van Herendael BJ, Laganà AS, Thomas V , Keckstein \nJ. Structured report for dynamic ultrasonography in patients with sus-\npected or known endometriosis: recommendations of the Interna-\ntional Society for Gynecologic Endoscopy (ISGE). Eur J Obstet Gynecol \nReprod Biol 2021; 263: 252-260. \n3. Giudice LC, Kao LC. Endometriosis. 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