{"paper_id":"b0ff42da-5e9b-4542-a948-6259fb1db991","body_text":"41\nMałgorzata Maria Radowicka 1, Damian Warzecha2,3\nCite as: Radowicka MM, Warzecha D: Endometriosis and diet – can anti-inflammatory foods alleviate symptoms? Pediatr Med Rodz 2025; 21 (1): 41–45\n© 2025 Medical Communication Sp. z o.o. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License \n(CC BY-NC-ND). Reproduction is permitted for personal, educational, non-commercial use, provided that the original article is in whole, unmodified, and properly cited.\nAuthors: Radowicka MM, Warzecha D. Proofreading by ENSKA Agnieszka Kosarzycka.\nReceived: 11.03.2025\nAccepted: 21.03.2025\nPublished: 18.04.2025\nEndometriosis and diet – can anti-inflammatory foods alleviate symptoms?\nEndometrioza i dieta – czy produkty przeciwzapalne mogą łagodzić objawy?\n1 Faculty of Medicine, Academy of Silesia, Katowice, Poland\n2 Faculty of Medicine, University of Warsaw, Warsaw, Poland\n3 Department of Obstetrics and Gynaecology, Southern Hospital, Warsaw, Poland\nCorrespondence: Małgorzata Maria Radowicka, Faculty of Medicine, Academy of Silesia, Rolna 43, 40-555 Katowice, Poland, e-mail: m.radowicka@gmail.com\n1 Wydział Medyczny, Akademia Śląska, Katowice, Polska\n2 Wydział Medyczny, Uniwersytet Warszawski, Warszawa, Polska\n3 Oddział Ginekologii i Położnictwa, Warszawski Szpital Południowy, Warszawa, Polska\nAdres do korespondencji: Małgorzata Maria Radowicka, Wydział Medyczny, Akademia Śląska, Rolna 43, 40-555 Katowice, e-mail: m.radowicka@gmail.com\n https://doi.org/10.15557/PiMR.2025.0004\nORCID iDs\n1. Małgorzata Maria Radowicka   https://orcid.org/0000-0002-4050-5236\n2. Damian Warzecha   https://orcid.org/0000-0002-2822-4896\n \nEndometriosis is a chronic, oestrogen-dependent inflammatory disease characterised by the implantation of endometrial \ntissue outside the uterine cavity. Pathogenetic factors include immune system dysfunction, angiogenesis disturbances, \nhormonal imbalance, and genetic predisposition. Key roles are played by activated macrophages and pro-inflammatory \ncytokines (IL-1, IL-6, TNF-α), as well as an altered Th1/Th2 lymphocyte balance and reduced NK cell activity. Endometriosis \nsignificantly reduces the quality of life for patients, affecting their physical, mental, and social well-being. According to the \nEuropean Society of Human Reproduction and Embryology recommendations, endometriosis treatment should be multi-\nfaceted, incorporating hormonal therapy and non-pharmacological methods such as dietary adjustments. Increasing research \nconfirms the positive impact of an anti-inflammatory diet on reducing inflammation and alleviating endometriosis symptoms. \nSuch a diet focuses on consuming foods rich in omega-3 polyunsaturated fatty acids, polyphenols, and terpenes, which have \nanti-inflammatory and antioxidant properties. The mechanisms of its action include modulating gut microbiota, reducing \ninflammatory markers (C-reactive protein, IL-6, TNF-α), and regulating oxidative stress. Studies show that women following \nan anti-inflammatory diet for at least three months experience reduced levels of inflammatory markers and relief from pain \nsymptoms. Key dietary components, such as eicosapentaenoic and docosahexaenoic acids, work by inhibiting arachidonic \nacid metabolism and synthesising pro-resolving mediators, thereby reducing the production of pro-inflammatory cytokines. \nPolyphenols and terpenes affect cell signalling pathways and reduce the expression of pro-inflammatory genes. In conclusion, \nan anti-inflammatory diet is a promising adjunct to endometriosis therapy, helping to reduce inflammation and improving \npatients’ quality of life. However, further research is needed to determine optimal dietary components and their dosages.\nKeywords: endometriosis, anti-inflammatory diet, pain, endometriosis treatment\nEndometrioza to przewlekła, estrogenozależna choroba zapalna charakteryzująca się implantacją tkanki endometrium poza \njamą macicy. Do czynników patogenetycznych zalicza się dysfunkcję układu odpornościowego, zaburzenia angiogenezy \ni równowagi hormonalnej oraz predyspozycje genetyczne. Główną rolę odgrywają tu m.in. aktywowane makrofagi i cytokiny \nprozapalne (IL-1, IL-6, TNF-α), a także zaburzona równowaga limfocytów Th1/Th2 i obniżona aktywność komórek NK. \nEndometrioza znacząco obniża jakość życia, wpływając na zdrowie fizyczne, psychiczne i społeczne pacjentek. Zgodnie \nz zaleceniami European Society of Human Reproduction and Embryology leczenie endometriozy powinno być wielotorowe \ni obejmować terapię hormonalną oraz metody niefarmakologiczne, takie jak zmiana nawyków żywieniowych. Coraz więcej \nbadań potwierdza korzystny wpływ diety przeciwzapalnej na zmniejszenie stanu zapalnego i łagodzenie objawów \nendometriozy. Dieta ta bazuje na spożywaniu produktów bogatych w wielonienasycone kwasy tłuszczowe omega-3, polifenole \ni terpeny, które wykazują właściwości przeciwzapalne i antyoksydacyjne. Mechanizmy jej działania obejmują m.in. modulację \nmikrobioty jelitowej, zmniejszenie stężenia markerów zapalnych (białka C-reaktywnego, IL-6, TNF-α) i regulację stresu \nAbstract\nStreszczenie\n\nMałgorzata Maria Radowicka, Damian Warzecha\n42\nDOI: 10.15557/PiMR.2025.0004\nPEDIATR MED RODZ  Vol. 21 No. 1, p. 41–45\noksydacyjnego. Badania wskazują, że u kobiet stosujących dietę przeciwzapalną przez co najmniej 3 miesiące obserwuje się \nzmniejszenie stężenia markerów zapalnych i złagodzenie dolegliwości bólowych. Główne składniki diety, takie jak kwas \neikozapentaenowy i dokozaheksaenowy, działają poprzez hamowanie metabolizmu kwasu arachidonowego i syntezę \nmediatorów proresolucyjnych, co przyczynia się do zmniejszenia produkcji cytokin prozapalnych. Z kolei polifenole i terpeny \nwpływają na szlaki sygnalizacyjne komórek i zmniejszają ekspresję genów prozapalnych. Podsumowując, dieta przeciwzapalna \nstanowi obiecujące uzupełnienie terapii endometriozy, wspierając redukcję stanu zapalnego i poprawiając jakość życia \npacjentek. Wymaga jednak dalszych badań, aby ustalić optymalne składniki i dawki.\nSłowa kluczowe: endometrioza, dieta przeciwzapalna, ból, leczenie endometriozy\n \nE\nndometriosis is an oestrogen-dependent, progres -\nsive chronic disease with an inflammatory basis, in \nwhich endometrial cells implant outside the uterine \ncavity. According to World Health Organization data, en -\ndometriosis affects approximately 190 million women of \nreproductive age. However, due to still imperfect diagnos -\ntic methods, it is estimated that the actual prevalence may \nbe significantly higher(1). The disease was first described in \n1690 by Daniel Shroen, while Karl von Rokitansky authored \nthe first reports on the pathogenesis of endometriosis in \n1860(2). Despite over 150 years of knowledge about the dis -\nease, its aetiology remains unclear. Furthermore, it is still \nnot understood why some women experience the classic \nsymptoms of endometriosis, while others, despite signifi -\ncant pelvic changes, experience neither pain nor issues with \nconceiving. Moreover, the time from the onset of symptoms \nto diagnosis remains lengthy, averaging 5–12 years (3).\nEndometriosis significantly affects women’s physical health. \nThe National Health Service lists it among the 20 most \npainful diseases globally (4). It often leads to prolonged ab -\nsences from work or school, creating an economic burden. \nThe disease profoundly impacts women’s mental and emo-\ntional well-being, social activity, and sexual relationships. \nResearch has shown that endometriosis can reduce the \nquality of life to a degree similar to cancer (5).\nOne of the pathomechanisms of endometriosis is a chron -\nic inflammatory process linked to immune system dys -\nfunction, which varies in severity depending on the disease \nstage(6). Macrophages play a crucial role in identifying for -\neign cells and presenting them to T lymphocytes. Women \nwith endometriosis exhibit an increased number of acti -\nvated macrophages in the peritoneal cavity, which have re-\nduced phagocytic capabilities. Proinflammatory cytokines, \nsuch as interleukin (IL) 1, IL-6, IL-8, and tumour necrosis \nfactor-alpha (TNF-α), are also produced in higher concen-\ntrations. Additionally, macrophages in the peritoneal cavity \nof women with endometriosis show increased expression of \ncyclooxygenase-2 (COX-2), leading to elevated prostaglan-\ndin secretion. Increased cytokine release and decreased an-\nti-inflammatory factor production contribute to both the \nde novo development and progression of endometriosis(6,7).\nAnother critical mechanism in the pathogenesis of endome-\ntriosis is the disrupted balance between helper T lympho -\ncytes type 1 (Th1) and type 2 (Th2). Th1 lymphocytes are \nresponsible for cytokine production and promoting cellular \nimmune responses, while Th2 lymphocytes regulate cyto -\nkine secretion to support B cell differentiation and humor -\nal responses. Studies indicate that Th2 lymphocyte activity \npredominates in women with endometriosis(8).\nWomen with endometriosis also exhibit reduced activity of \nnatural killer (NK) cells, which are crucial for natural cyto-\ntoxicity. NK cell dysfunction limits their ability to eliminate \nendometrial elements from the peritoneal cavity, which en-\nter through retrograde menstrual flow, allowing endometri-\nal cell implantation outside the uterus(9).\nAngiogenesis plays a vital role in the development of ecto -\npic endometrium, especially in the microenvironment of \nthe peritoneal cavity. This process is accompanied by the \nformation of nerve fibres, which contribute to pain in pa -\ntients. Vascular endothelial growth factor (VEGF) is re -\nsponsible for the formation and growth of new blood \nvessels. Elevated VEGF levels have been found in the peri -\ntoneal fluid of women with endometriosis, with levels cor-\nrelating positively with disease severity(10).\nTreatment for endometriosis depends on the symptoms \nand a woman’s reproductive plans. Hormonal therapy is the \ncornerstone of treatment, aiming to alleviate pain and slow \ndisease progression. According to the European Society of \nHuman Reproduction and Embryology (ESHRE) guide -\nlines, endometriosis treatment should be multi-faceted, \nencompassing hormonal therapy alongside non-pharma -\ncological methods. These methods include dietary adjust -\nments, regular physical activity, physiotherapy, and psy -\nchotherapy. Surgical intervention, once considered the \ngold standard for diagnosing endometriosis, is no longer \nviewed as a first-line approach. Surgery should be undertak-\nen only after a careful assessment of the benefits and risks, \nand when conservative treatment is ineffective(11).\nEmerging evidence highlights the positive role of dietary \nchanges in managing endometriosis. An anti-inflamma -\ntory diet helps reduce systemic chronic inflammation. \nStudies show that 76% of women adopt non-pharmacolog-\nical methods to manage symptoms after being diagnosed \nwith endometriosis, with almost half (44%) modifying their \ndietary habits(12). Another study found that 55.5% of wom-\nen experienced reduced pain due to conscious food choices.  \nDietary factors can influence the development and pro -\ngression of endometriosis by regulating steroid hormone \n\nEndometriosis and diet – can anti-inflammatory foods alleviate symptoms?\n43\nDOI: 10.15557/PiMR.2025.0004\nPEDIATR MED RODZ  Vol. 21 No. 1, p. 41–45\nmetabolism, the menstrual cycle, inflammation, oxidative \nstress, and muscle contractions(13). This article aims to dis -\ncuss the principles of an anti-inflammatory diet and review \nresearch findings on its impact on the disease.\nDietary interventions in chronic pain patients have been \nshown to reduce intestinal barrier permeability by lowering \nthe production of pro-inflammatory mediators, prevent -\ning harmful metabolites from entering the bloodstream. \nMoreover, consuming anti-inflammatory foods appears \nto improve the quality of life (14).\nDietary habits depend, among other factors, on geograph -\nical location. The typical Western diet is characterised \nby high consumption of saturated fats, refined carbohy -\ndrates, red meat, salt, and sugary beverages. This diet pro -\nmotes excessive production of pro-inflammatory mediators \nwhile reducing anti-inflammatory mediators, including an-\ntioxidants. The Western diet has been shown to negative -\nly impact chronic diseases, such as cardiovascular diseases, \ndiabetes, gastrointestinal disorders, immune system dys -\nfunction, and endometriosis (14,15) . Geographical and so -\nciodemographic factors also influence the prevalence of \nendometriosis (16).\nThe principles of the anti-inflammatory diet were first in -\ntroduced in 1995 by Barry Sears in “The Zone Diet” , with \na revised version appearing in 2015. The diet’s concept is \nbased on macronutrient proportions and their effect on in-\nsulin and cortisol levels. Various types of anti-inflammato-\nry diets exist, such as the Nordic diet, the Okinawa diet, and \nthe Mediterranean diet(17).\nTwo studies analysed the relationship between green vege-\ntable and fruit consumption, measured in servings per week \nor day, and the risk of endometriosis(18,19). An inverse rela-\ntionship was observed between the consumption of green \nvegetables and fruits and the risk of endometriosis. Data \nwere analysed based on the number of servings per week. \nSignificant risk reduction was noted with high consumption \nof green vegetables (odds ratio, OR 0.3; 95% confidence in-\nterval, 95% CI 0.2–0.5; p = 0.0001) and fresh fruits (OR 0.6; \n95% CI 0.4–0.8; p = 0.002). These relationships remained \nconsistent even after adjusting for confounding factors(18).\nIn a case-control study by Trabert et al., the role of a diet \nrich in green vegetables and fruits was analysed similarly \nto the Italian study, considering daily servings. Increased \ndaily fruit servings were associated with a higher disease \nrisk (two or more servings per day compared to one or few-\ner: OR 1.5; 95% CI 1.2–2.3; p = 0.04), while no association \nwith vegetable consumption was found(19).\nInterestingly, vegetables (particularly green ones) contain \nfolic acid, methionine, and vitamin B6, which are associat-\ned with “nutritional genomics” . A group of nutrients known \nas lipotropic, including methionine, choline, folic acid, and \nvitamin B6, plays a key role in this context. These nutrients \ncan influence the human genome by altering gene expres -\nsion or their products and affecting DNA methylation(20).\nThe primary components of an anti-inflammatory diet \nare polyunsaturated fatty acids, phenolic compounds, and \nterpenes/terpenoids. Omega-3 PUFAs exhibit immuno -\nmodulatory and anti-inflammatory effects. Their mech -\nanism of action is complex. Prostaglandins and leukotri -\nenes, produced from arachidonic acid (AA), a member of \nthe omega-6 fatty acids, have pro-inflammatory effects. \nOmega-3 fatty acids – eicosapentaenoic acid (EPA) and doc-\nosahexaenoic acid (DHA) – demonstrate a range of anti-in-\nflammatory actions. Increasing EPA and DHA levels in the \nmembranes of cells involved in the inflammatory process \nimpacts the physical properties of these membranes and \nthe formation of signalling platforms called lipid rafts. EPA \nand DHA disrupt arachidonic acid metabolism. EPA gen -\nerates weaker (less pro-inflammatory) analogues, and both \nEPA and DHA are substrates for the synthesis of resolvins, \nprotectins, neuroprotectins, and maresins, which are spe -\ncialised pro-resolving mediators. By affecting early mem -\nbrane signals and the profile of lipid mediators produced, \nEPA and DHA alter intra- and intercellular signalling. This \nleads to modified patterns of gene expression and protein \nproduction within cells, resulting in reduced production of \ninflammatory cytokines, chemokines, adhesion molecules, \nproteases, and enzymes. The anti-inflammatory effects of \nEPA and DHA are significant for both the prevention and \ntreatment of inflammatory conditions. It has been shown \nthat increasing EPA and DHA intake inhibits arachidon -\nic acid metabolism and reduces the expression of COX-2  \ngenes and proteins(21). Studies have observed decreased pro-\nduction of series-2 prostaglandins (e.g. PGE2) and series-4 \nleukotrienes by inflammatory cells following EPA and DHA \nsupplementation for several weeks to months. In these stud-\nies, a dose-dependent effect on PGE 2 production was ob -\nserved, with an EPA intake of 1.35 g/day for three months \nbeing insufficient to inhibit PGE 2, while 2.7 g/day signif -\nicantly reduced PGE 2 production. This suggests that the \nthreshold for EPA ’s anti-inflammatory effect lies between \n1.35 and 2.7 g/day (22).\nPhenolic compounds are a large, heterogeneous group of \nmolecules widely distributed in nature. Polyphenols are \nfound in many plants, fruits (particularly berries), tea, \nand cocoa, and possess anti-inflammatory and antioxi -\ndant properties. They have been shown to influence cellu -\nlar signalling pathways, such as NF-κB, thereby reducing \nthe expression of pro-inflammatory cytokines. Additionally, \nsome polyphenols, such as resveratrol and quercetin, act as \nAMPK activators, promoting anti-inflammatory respons -\nes and improving metabolism. Research indicates that con-\nsuming polyphenol-rich foods is associated with a reduced \nrisk of cardiovascular diseases, type 2 diabetes, and overall \ninflammation. However, due to limited clear scientific evi -\ndence, establishing reference intake norms for polyphenols \nis challenging. Some studies suggest that total flavonoid  \nintake above 500 mg/day offers health benefits(23).\nTerpenes and terpenoids, a large group of compounds pri -\nmarily derived from the secondary metabolism of plants, \nhave demonstrated anti-inflammatory properties both in vi-\ntro and in vivo  by regulating pro-inflammatory mediators \n\nMałgorzata Maria Radowicka, Damian Warzecha\n44\nDOI: 10.15557/PiMR.2025.0004\nPEDIATR MED RODZ  Vol. 21 No. 1, p. 41–45\nand transcription factors, disrupting signalling pathways, \nand reducing oxidative stress(24).\nCurrent literature suggests that following an anti-inflamma-\ntory diet for at least three months can significantly reduce \ninflammatory marker levels, thereby alleviating pain symp-\ntoms in women with endometriosis(14). This phenomenon is \ncomplex and involves several mechanisms.\nOne such mechanism is the modulation of gut microbio -\nta by an anti-inflammatory diet. The human gut contains \ntrillions of microorganisms that play crucial roles in diges-\ntion, immune function, and neurotransmitter production. \nDietary components, especially polyphenols and fibre, can \nsignificantly influence the composition and function of gut \nmicrobiota. A plant-rich diet promotes microbiota diversity, \nwhich is highly beneficial for health. Through the produc -\ntion of short-chain fatty acids, gut microbiota positively af-\nfects nervous system function by reducing symptoms such \nas fatigue, low mood, stress sensitivity, and cognitive dys -\nfunction. Enriching the diet with prebiotics (e.g. ferment -\nable fibre) and probiotics can further help reduce inflam -\nmation and improve intestinal barrier integrity. Dysbiosis, \nor microbial imbalance, is associated with chronic inflam -\nmatory diseases(25).\nAnother mechanism of action for an anti-inflammatory diet \ninvolves the modulation of inflammatory pathways. Dietary \ncomponents can either exacerbate or reduce inflamma -\ntion by lowering levels of inflammatory markers, including \nC-reactive protein (CRP), IL-6, and TNF-α(26).\nA third key mechanism is the regulation of oxidative stress, \ndefined as an imbalance between free radicals and anti -\noxidants. Antioxidants are compounds that help neutral -\nise harmful free radicals in the body, preventing cellular \ndamage. They are categorised into two main types: exog -\nenous and endogenous antioxidants. Exogenous antioxi -\ndants, such as vitamins, minerals, and polyphenols, cannot \nbe synthesised by the body in sufficient quantities and must \nbe supplied through diet. Endogenous antioxidants, such \nas superoxide dismutase (SOD), glutathione, and ubiqui -\nnol, are produced within the body. Many components of an \nanti-inflammatory diet, including vitamins C and E, carot -\nenoids, and polyphenols, act as antioxidants, directly neu -\ntralising harmful free radicals(27).\nThe effectiveness of an anti-inflammatory diet can be as -\nsessed by monitoring three key markers:\n1. lipid stress – a TG/HDL ratio (in mg/dL) <1 indicates \ngood insulin sensitivity;\n2. inflammatory stress – an AA/EPA ratio in the range of \n1.5–3 maintains inflammatory balance;\n3. glycaemic stress – HbA1c levels between 4.9–5.1% reflect \nproper carbohydrate metabolism regulation(28).\nNot all dietary patterns are strictly pro- or anti-inflamma -\ntory. Classifying a specific dietary pattern can be facilitat -\ned using the empirical Dietary Inflammatory Index (DII). \nThe DII was created to analyse the overall dietary pattern \nin relation to plasma markers of inflammation and to de -\ntermine the inflammatory potential of diets. Developed \nbased on global literature from 1950 to 2010, the DII incor-\nporates 1,943 articles and 45 selected dietary components. \nThe authors of the DII assessed the relationship between \ndietary products/components and inflammatory markers  \n(IL-1β, IL-4, IL-6, IL-10, TNF-α, and CRP). They deter -\nmined whether the 45 individual dietary components in -\ncreased (+1), decreased (−1), or had no effect (0) on these \ninflammatory markers. The DII can be used for initial as -\nsessment of the inflammatory contribution of a patient’s \ncurrent diet and to monitor dietary changes over time(29).\nDISCUSSION\nVarious biological mechanisms have been proposed to ex -\nplain the influence of dietary factors on the risk of develop-\ning endometriosis. However, available epidemiological data \nand observational studies do not always consistently sup -\nport these hypotheses. Due to the limited number of scien-\ntific studies, this report provides a detailed overview of the \nresults from several available studies to highlight even mi -\nnor effects that could serve as a foundation for further re -\nsearch, emphasising the need for additional analyses.\nHormonal therapy remains the cornerstone of endometri-\nosis treatment. Implementing non-pharmacological treat -\nment methods, including an anti-inflammatory diet, signifi-\ncantly improves the effectiveness of therapy. However, there \nis a group of patients for whom hormonal therapy cannot \nbe applied – for example, women trying to conceive, those \nwith contraindications to hormonal treatment, or those \nwho refuse hormonal therapy. For these women, the cor -\nnerstone of care will be the implementation of non-phar -\nmacological methods of pain reduction, with the anti-in -\nflammatory diet playing a key role.\nIt is important to note that endometriosis is a multi-stage \ncondition, beginning with the initial development of the \ndisease, followed by proliferation, vascularisation, and \nperitoneal invasion of endometrial lesions, all accompa -\nnied by an inflammatory response. Various dietary compo-\nnents may have varying effects at specific stages of disease \nprogression. Future research should aim to separately anal-\nyse the impact of diet on both the development of endome-\ntriosis and its clinical consequences.\nCONCLUSIONS\nIn summary, endometriosis is an oestrogen-dependent, \nchronic, and progressive disease. Its pathomechanism in -\nvolves chronic inflammation and immune system dysfunc-\ntion. Treatment is primarily based on hormonal therapy, \nbut non-pharmacological methods, including an anti-in -\nflammatory diet, are playing an increasingly important role. \nThe key components of an anti-inflammatory diet include \nPUFAs, phenolic compounds, and terpenes/terpenoids. \nA diet rich in these substances helps regulate oxidative \nstress and inflammation, positively affecting gut microbi -\nota and immune system function as early as three months \n\nEndometriosis and diet – can anti-inflammatory foods alleviate symptoms?\n45\nDOI: 10.15557/PiMR.2025.0004\nPEDIATR MED RODZ  Vol. 21 No. 1, p. 41–45\nafter implementation. Further research is needed to explore \nthe effects of diet on the different stages of endometriosis \ndevelopment and the need for personalised therapy.\nConflict of interest\nThe authors do not report any financial or personal connections with \nother persons or organisations which might negatively affect the content \nof this publication and/or claim authorship rights to this publication.\nAuthor contribution\nOriginal concept of study; collection, recording and/or compilation of \ndata; analysis and interpretation of data: MMR. Writing of manuscript; \ncritical review of manuscript; final approval of manuscript: MMR, DW .\nReferences\n1. World Health Organization: Endometriosis [Internet]. World \nHealth Organization, Geneva 2021. Available from: https://www.\nwho.int/ [cited: 10 January 2025].\n2. Rokitansky C: Ueber Uterusdrüsen-Neubildung in Uterus- und \nOvarial-Sarcomen. Z Ges Ärzte Wien 1860; 16: 577–581.\n3. De Corte P , Klinghardt M, von Stockum et al.: Time to diagnose \nendometriosis: current status, challenges and regional character-\nistics – a systematic literature review. BJOG 2025; 132: 118–130.\n4. National Health Service: Endometriosis [Internet]. National \nHealth Service, London 2022. Available from: https://www.nhs.\nuk/ [cited: 10 January 2025].\n5. Ruszała M, Dłuski DF , Winkler I et al.: The state of health and \nthe quality of life in women suffering from endometriosis. J Clin \nMed 2022; 11: 2059.\n6. Burney RO, Giudice LC: Pathogenesis and pathophysiology of \nendometriosis. Fertil Steril 2012; 98: 511–519.\n7. Lebovic DI, Mueller MD, Taylor RN: Immunobiology of endo-\nmetriosis. Fertil Steril 2001; 75: 1–10.\n8. Podgaec S, Abrao MS, Dias JA Jr et al.: Endometriosis: an inflam-\nmatory disease with a Th2 immune response component. Hum \nReprod 2007; 22: 1373–1379.\n9. Reis JL, Rosa NN, Ângelo-Dias M et al.: Natural killer cell recep-\ntors and endometriosis: a systematic review. Int J Mol Sci 2022; \n24: 331.\n10. Smolarz B, Szaflik T, Romanowicz H et al.: Analysis of VEGF , \nIGF1/2 and the long noncoding RNA (lncRNA) H19 expression \nin Polish women with endometriosis. Int J Mol Sci 2024; 25: 5271.\n11. Becker CM, Bokor A, Heikinheimo O et al.: ESHRE guideline: \nendometriosis. Hum Reprod Open 2022; 2022: hoac009.\n12. Armour M, Sinclair J, Chalmers KJ et al.: Self-management strat-\negies amongst Australian women with endometriosis: a nation-\nal online survey. BMC Complement Altern Med 2019; 19: 17.\n13. Krabbenborg I, de Roos N, van der Grinten P et al.: Diet quality \nand perceived effects of dietary changes in Dutch endometriosis \npatients: an observational study. Reprod Biomed Online 2021; \n43: 952–961.\n14. Parazzini F , Viganò P , Candiani M et al.: Diet and endometriosis \nrisk: a literature review. Reprod Biomed Online 2013; 26: 323–336.\n15. Clemente-Suárez VJ, Beltrán-Velasco AI, Redondo-Flórez L  \net al.: Global impacts of western diet and its effects on metabo-\nlism and health: a narrative review. Nutrients 2023; 15: 2749.\n16. Moradi Y , Shams-Beyranvand M, Khateri S et al.: A systematic \nreview on the prevalence of endometriosis in women. Indian  \nJ Med Res 2021; 154: 446–454. \n17. Alesi S, Villani A, Matzioris E et al.: Anti-inflammatory diets in \nfertility: an evidence review. Nutrients 2022; 14: 3914.\n18. Parazzini F , Chiaffarino F , Surace M et al.: Selected food intake \nand risk of endometriosis. Hum Reprod 2004: 19; 1755–1759.\n19. Trabert B, Peters U, De Roos AJ et al.: Diet and risk of endome-\ntriosis in a population-based case-control study. Br J Nutr 2011; \n105: 459–467.\n20. McCabe DC, Caudill MA: DNA methylation, genomic silencing, \nand links to nutrition and cancer. Nutr Rev 2005; 63: 183–195.\n21. Calder PC: Omega-3 polyunsaturated fatty acids and inflamma-\ntory processes: nutrition or pharmacology? Br J Clin Pharmacol \n2013; 75: 645–662.\n22. Rees D, Miles EA, Banerjee T et al.: Dose-related effects of eicos-\napentaenoic acid on innate immune function in healthy humans: \na comparison of young and older men. Am J Clin Nutr 2006; 83: \n331–342.\n23. Ponzo V , Goitre I, Fadda M et al.: Dietary flavonoid intake and \ncardiovascular risk: a population-based cohort study. J Transl \nMed 2015; 13: 218.\n24. Guimarães AG, Serafini MR, Quintans-Júnior LJ: Terpenes and \nderivatives as a new perspective for pain treatment: a patent \nreview. Expert Opin Ther Pat 2014; 24: 243–265.\n25. Koh A, De Vadder F , Kovatcheva-Datchary P et al.: From dietary \nfiber to host physiology: short-chain fatty acids as key bacterial \nmetabolites. Cell 2016; 165: 1332–1345.\n26. Badimon L, Chagas P , Chiva-Blanch G: Diet and cardiovascular \ndisease: effects of foods and nutrients in classical and emerging \ncardiovascular risk factors. Curr Med Chem 2019; 26: 3639–3651.\n27. Poljsak B, Šuput D, Milisav I: Achieving the balance between \nROS and antioxidants: when to use the synthetic antioxidants. \nOxid Med Cell Longev 2013; 2013: 956792.\n28. Sears B, Saha AK: Dietary control of inflammation and resolu-\ntion. Front Nutr 2021; 8: 709435.\n29. Shivappa N, Steck SE, Hurley TG et al.: Designing and develop-\ning a literature-derived, population-based dietary inflammatory \nindex. Public Health Nutr 2014; 17: 1689–1696.","source_license":"CC0","license_restricted":false}