{"paper_id":"fd66c269-0b00-4529-9b0a-27b7347c1237","body_text":"npj | women's health Review\nhttps://doi.org/10.1038/s44294-026-00133-y\nState of the science and research\nopportunities on dietary patterns in\nendometriosis and uterine fibroids\nCheck for updates\nTrina M. Fresco1,L i s aM .T u s s i n g - H u m p h r e y s1,S a g eJ .K i m2, Mary Dawn Koenig3, Saria Lofton4,\nPamela Pearson3 &V a n e s s aM .O d d o1\nEndometriosis and fibroids are prevalent uterine conditions. Mechanisms for both conditions —\nimmune dysfunction, in flammation, and sex hormone dysfunction —are plausibly in fluenced by diet.\nHere, we review the epidemiology and pathophysiology, and synthesize evidence on dietary patterns,\nendometriosis and uterine fibroid prevalence, risk, and symptomology. The evidence (12 studies)\nsuggests that low-quality diets (ultra-processed) are associated with higher rates of both conditions,\nand high-quality diets are associated with lower symptom burden.\nAt least 10% of reproductive-age females experience endometriosis\nglobally, while uterine fibroids impact up to 70 –80% of females during\ntheir lifetime 1,2. Non-Hispanic (NH) Black, Hispanic, Asian American,\nand socioeconomically disadvantaged women experience a dis-\nproportionate burden of disease, delayed diagnosis patterns, and\ngreater symptom severity, which likely re flects underlying structural\ninequities in exposure to risk factors, access, and care\n3–8. Structural and\nindividual-level exposures, including dietary patterns 9,10, can in fluence\nbiological mechanisms that contri bute to the onset, progression, and\nseverity of endometriosis and uterine fibroids. Despite the high pre-\nvalence of endometriosis and uterine fibroids, and plausible associa-\ntions with the underlying mechanisms contributing to these diseases,\nthe diet-related determinants of both conditions remain\nunderstudied\n11. This paper reviews the pathophysiology of endome-\ntriosis and uterine fibroids and then examines the current evidence on\ndietary patterns in relation to those conditions, to better understand\nthese relationships and identify research gaps.\nEpidemiology of endometriosis\nEndometriosis affects an estimated 6.5 million women in the United States\n(U.S.)\n12. While reports indicate that NH-White women in the U.S. have a\nhigher prevalence of endometriosis compared to NH-Black and Hispanic\nwomen, data from a systematic review indicate that the lower prevalence\namong racially minoritized women is more consistent with underdiagnosis\nor diagnostic delay, rather than a true difference in prevalence\n3. It is likely\nthat women residing in under-resourced communities have greater barriers\nto specialty care, which may contribute to the lower prevalence observed\namong minoritized women in the U.S.\n5,13.\nPathophysiology of endometriosis . Endometriosis is the ectopic\nimplantation of endometrial glands and connective tissue outside the\nuterus, initially identified as implants and later as lesions, as abnormally\nimplanted cells proliferate\n1,14. Progression involves interrelated\nmechanisms such as immune dysfunction, in flammation, and dysregu-\nlation of sex hormones 15,16. Immune dysfunction occurs when ectopic\nendometrial tissue evades apoptosis, and the peritoneal cavity contains\nelevated levels of immune cells, both of which allow implants to survive\nand proliferate\n16. Chronic in flammation then emerges when immune\nresponses become overactive, dysregulated, and sustained, promoting\nadhesion formation, which may connect pelvic organs, distort pelvic\nanatomy, and contribute to infertility and chronic pain\n14. Sex hormone\ndysregulation occurs when progesterone-mediated suppression of\nestrogen receptor alpha (Er α) becomes impaired, leading to unopposed\nand excessive circulating estradiol (E2) activity that drives cellular pro-\nliferation and the growth of ectopic endometrial implants, lesions, and\npotentially adhesions\n16. Elevated peritoneal E2 further activates immune\ncells, creating a feedback loop between a pro-in flammatory cycle and\nlesion growth14.\nSymptomology and diagnosis of endometriosis . Symptomology and\nseverity do not necessarily correlate with endometriosis subtypes or\npathological stage, and up to 25% of women present as asymptomatic\n15,17.\nThe predominant symptom is pain, driven by immune cell activation and\ninflammation\n14, which may present acutely1 and often correlates with the\nlocation and extent of ectopic implants, lesions, and adhesions 14. Other\ncommon symptoms include infertility, impacts on quality of life (QoL)\ndue to depression and fatigue attributable to chronic pain,\n1Department of Kinesiology and Nutrition, University of Illinois Chicago, Chicago, IL, USA. 2Division of Health Policy and Administration, University of Illinois\nChicago, Chicago, IL, USA. 3Department of Human Development Nursing Science, University of Illinois Chicago, Chicago, IL, USA. 4Department of Population\nHealth Nursing Science, University of Illinois Chicago, Chicago, IL, USA. e-mail: voddo@uic.edu\nnpj Women's Health |            (2026) 4:12 1\n1234567890():,;\n1234567890():,;\n\ngastrointestinal symptoms, and pain during defecation (dyschezia),\nmenstruation (dysmenorrhea), intercourse (dyspareunia), and urination\n(dysuria)\n1. Diagnosis is often delayed, given the variation of sympto-\nmology and overlap with other conditions 14, and con firmation is only\npossible through histological analysis of biopsy samples obtained during\nsurgery2. However, in some cases, transvaginal ultrasound visualizes\novarian endometrioma and, less commonly, deeply in filtrating endo-\nmetriotic tissue2.\nEpidemiology of uterine fibroids\nThe estimated prevalence of uterine fibroids in the U.S. is wide-ranging\n(~5–69%)18. By age 50, uterine fibroids affect up to 70% of NH-White\nwomen and more than 80% of NH-Black women19,20. Disparities also exist in\nthe prevalence of uterine fibroids; a 2014 population-based study utilizing\ndata from a healthcare system in Seattle found that NH-Black women had\nthe highest prevalence of uterine fibroids (18.5%), followed by Native\nAmerican (11.9%), Asian/Native Hawaiian/Pacific Islander (11.5%), His-\npanic (11.1%), and NH-White women (10.3%)21. Further, a recent narrative\nreview by Evans et al.8 reported that lower educational attainment and low\nincome were associated with uterinefibroid incidence.\nUterine fibroid pathophysiology . Uterine fibroids are benign, mono-\nclonal smooth muscle tumors of the myometrium, characterized by size,\nuterine location, and extracellular matrix components, including col-\nlagen, fibronectin, and proteoglycans\n22,23. Growth patterns vary; tumors\nenlarge during estrogen- and progesterone-dominant states such as\npregnancy, and regress after menopause23. As with endometriosis, uterine\nfibroid progression is shaped by immune dysfunction, inflammation, and\nsex hormone dysregulation 23,24. Elevated pro-in flammatory cytokines in\nuterine fibroid tissue suggest that immune activation contributes to\ndisease progression25. Chronic inflammation and oxidative stress create a\nmicroenvironment conducive to tumor formation 24. Sex hormone dys-\nregulation arises as E2 promotes cell proliferation and inhibits apoptosis,\nand progesterone stimulates extracellular matrix deposition, contribut-\ning to tumor size and stiffness\n23. Local E2 production within uterine\nfibroid tissue further exacerbates tumor progression 23.\nSymptomology and diagnosis of uterine fibroids. Clinically, these\npathophysiological processes result in a wide spectrum of symptoms 20,22,\nwith variation in the size, number, and location of the tumors, as well as\nindividual hormonal and inflammatory responses\n20. While some women\nremain asymptomatic, others experience pelvic pain and menorrhagia\n(heavy menstrual bleeding), which can lead to fatigue, dizziness, physical\nlimitations, and lower QoL\n22. Uterine fibroids also contribute to infertility\nand pregnancy complications, signaling the disruption of uterine\nanatomy\n20,22. In some cases, large fibroid size produces bulk symptoms\nand increased abdominal girth, pressure, bloating, and other gastro-\nintestinal symptoms\n26. Given symptom heterogeneity and overlap with\nother conditions, accurate diagnosis is essential for effective\nmanagement2.\nDietary patterns and endometriosis and uterinefibroids\nA low-quality diet is characterized by increased intake of high-fat dairy,\nsodium, processed and ultra-processed foods, red and processed meats,\nrefined carbohydrates, added sugars, and saturated and trans-fats\n15.I nt h e\nU.S., ~72% of daily energy intake comes from alcohol, cereals, dairy pro-\nducts, refined sugars, and refined vegetable oils\n27. Individuals who consume\na low-quality diet are more likely to experience adverse metabolic outcomes,\nincluding obesity, type 2 diabetes, and hyperlipidemia, all of which can\namplify inflammation and E2 concentrations that can increase the risk of\nendometriosis and uterinefibroids\n15,19,28–31.\nIn contrast, a high-quality diet, characterized as a diet rich in anti-\ninflammatory and antioxidant nutrients such as fruits, vegetables, and\nhealthy fats, may support uterine health via sex hormone and immune\nregulation\n1,32–37. Moreover, diets high in fiber aid in sex hormone (E2)\nmetabolism and excretion through the digestive system14, and are inversely\ncorrelated with urinary estrogen32,38,39.\nPrior reviews have focused on individual food groups and macro- and\nmicronutrients with respect to uterine health14,23,24,40–44; however, nutrients\nand foods are not consumed in isolati on. Thus, below we explore the lit-\nerature on dietary patterns in relation to endometriosis and uterinefibroid\n(see Table 1)32–37,45–48 incidence/prevalence and symptomology.\nResults\nEndometriosis\nWe retrieved 11 studies from six countries, which employedfive different\nstudy designs to examine the relationship between dietary patterns and\nendometriosis from 2012 to 2025. Twelve dietary patterns, organized by\nlow-quality and high-quality, were examined for their association with at\nleast one of five endometriosis-related outcomes, including endometriosis\nincidence/prevalence, gastrointestinal health, pain perception (dyschezia,\ndysmenorrhea, dyspareunia, dysuria, and non-menstrual pelvic pain), and\nQoL. The studies included 25–81,997 participants.\nLow-quality dietary patterns . An estrogen-associated dietary pattern\nwas established using reduced rank regression in a subsample of par-\nticipants from the Nurses ’ Health Study II\n49. The dietary pattern\nincluding cream soup, alcohol, red meat, pizza, and nuts was positively\nassociated with luteal E2 levels, which is associated with breast\ncancer\n32,49,50. The estrogen-associated dietary pattern and endometriosis\ndiagnosis were tested in 2024 also in the Nurses ’ Health Study II cohort,\nand the authors reported a significantly lower risk for the fourth (hazard\nratio [HR]: 0.85; 95% CI: 0.76 –0.93) and fifth quintiles (HR: 0.82; 95%\nCI: 0.74 –0.91) versus the first32.T h e s efindings are contrary to expec-\ntations, given the positive correlation with higher luteal estrogen, and\nmay indicate that exogenous estrogen exposure is not relevant to disease\nrisk\n32.\nAp r o - i nflammatory diet, de fined via an algorithmic assessment\nnamed the Dietary Inflammatory Index (DII), can be used to quantify the\ninflammatory potential of a person’sd i e t ;ah i g h e rD I Is c o r er eflects greater\npro-inflammatory potential33.W ei d e n t ified two studies that investigated a\npro-inflammatory diet pattern using a data-driven approach32 and DII51,52 in\nrelation to endometriosis incidence/prevalence32,33. In the Nurses ’ Health\nStudy II, a higher pro-inflammatory diet was associated with a higher risk of\nendometriosis diagnosis for the third (HR: 1.15; 95% CI: 1.04 –1.28) and\nfourth (HR: 1.20; 95% CI: 1.08–1.33) versus the first quintile32. In a cross-\nsectional analysis using data from the U.S. NHANES (1999–2006), Liu et al.\nreported that individuals in the highest DII tertile (versus lowest) had a 57%\nhigher odds of endometriosis (95% CI: 1.14–2.17)33. These studies suggest\nthat a pro-in flammatory diet pattern, characterized by higher intakes of\nrefined carbohydrates, added sugars, saturated and trans fats, processed\nmeats, and lower intakes of fiber and antioxidant-rich foods, was con-\nsistently associated with a greater likelihood of endometriosis. This aligns\nwith a key mechanistic pathway in which excessive proin flammatory\ncytokines may amplify peritoneal immune dysfunction, creating a feedback\nloop with sex hormone dysregulationand lesion growth that is associated\nwith increased risk of endometriosis\n15,32,33,52,53.\nA Western dietary pattern is characterized by high-fat dairy, fried\nfoods, red and processed meats, processed foods, sugar-sweetened bev-\nerages, sweets and desserts, and lower intake of fruits, nuts, vegetables, and\nwhole grains\n27,32. Using principal component analysis to de fine diet, one\nU.S.-based prospective cohort study found that consuming a Western\ndietary pattern was associated with a higher risk of a laparoscopically\nconfirmed endometriosis (15% and 27% higher for the fourth and fifth\nquintiles, respectively, versus thefirst)\n32.T h e s efindings align with evidence\nthat a Western dietary pattern is associated with diminished immune\nfunction, which upregulates proinflammatory signaling, heightens inflam-\nmatory activity, and sex hormone dysregulation, including higher E2 levels\nand lower sex hormone binding globulin levels, consistent with greater\nconsumption of red meat and eggs\n27,30,32,54,55.\nhttps://doi.org/10.1038/s44294-026-00133-y Review\nnpj Women's Health |            (2026) 4:12 2\n\nTable 1 | Dietary patterns, endometriosis, and uterine fibroids\nDietary pattern(s) Author; country of\nparticipants\nStudy design Participants Outcomes of interest Key findings: ↑ for statistically signi ficant\npositive associations, ↓ for statistically\nsignificant inverse associations, and — for no\nsignificant result\nEndometriosis:\n1. AHEI-2010/Harvard\nHealthy Eating Plate\n2. DASH\n3. Estrogen-associated\npattern\n4. Pro-inflammatory pattern\n5. Prudent diet\n6. Western diet\nDougan et al. (2024); U.S32. Prospective\ncohort study\n N = 81,997\n Premenopausal\n Age: 25–42 years\nEndometriosis incidence 1. AHEI-2010: ↓\n2. DASH: —\n3. Estrogen-associated pattern: ↓\n4. Pro-inflammatory pattern: ↑\n5. Prudent diet: —\n6. Western diet: ↑\nAlternative Healthy\nEating Index\nGhoreishy et al. (2025);\nIran64\nCase-control study  N = 313\n Age: 18–49 years\nEndometriosis prevalence ↓\nEndometriosis diet van Haaps et al. (2023);\nNetherlands48\nCross-\nsectional study\n N = 211\n Age: ≥ 18 years old\nEndometriosis-related QoL: daily functioning,\nphysical functioning, psychological functioning,\nquality of life, social participation, and spiritual\nfunctioning\n↓ (reverse measured)\n1. Endometriosis diet\n2. Low-FODMAP\nvan Haaps et al. (2023);\nNetherlands47\nNon-randomized\ninterventional trial\n N = 72\n Mean age:\nEndometriosis diet (39.1 y)\nLow-FODMAP diet (36.9 y)\n Control group (37.6 y)\n Presence of endometriosis-\nrelated pain symptoms (VAS-\nscore ≥3, 0–10 cm)\nEndometriosis-related symptoms:\n1.\nPain perception: bloating, chronic pelvic pain,\ndeep dyspareunia, dysmenorrhea, dysuria,\ntiredness\n2. GI health\n3. QoL: children, emotional wellbeing, infertility,\nmedical profession, pain, powerlessness, self-\nimage, sexual intercourse, social support,\ntreatment, and work life\nEndometriosis diet:\n1. Pain perception: bloating ↓\n2. GI Health: —\n3. QoL: 2 out of 11 domains (social support and\nmedical profession) ↓\nLow-FODMAP:\n1. Pain perception: deep dyspareunia ↓\n2. GI Health: —\n3. QoL: 1 out of 11 domains ↓\nLow-FODMAP Keukens et al. (2025);\nNetherlands35\nSingle-arm,\ninterventional trial\n N = 47\n Age: ≥18 years old\n Presence of debilitating GI\nsymptoms\nEndometriosis-related symptoms:\n1.\nGI symptoms: constipation and bloating\n2. QoL: children, emotional wellbeing, infertility,\nmedical profession, pain, powerlessness, self-\nimage, sexual intercourse, social support,\ntreatment, and work life\n1. GI symptoms: constipation ↓, and bloating —\n2. QoL: 7 of 11 ↓\nLow-FODMAP (first\nphase only)\nVarney et al. (2024);\nAustralia\n36\nCrossover\nfeeding trial\n N = 40\n Age: 18 years to menopause\n Presence of poorly managed GI\nsymptoms\n Low-FODMAP diet = < 5 g/day\nFODMAPs\n Control condition = 20 g/day\nFODMAPs\nEndometriosis-related symptoms:\n1. GI symptoms\n2. Overall health-related QoL\n,\n1. GI symptoms: ↓\n2. QoL: overall health-related QoL ↓\nGluten-free diet Marziali et al. (2012); Italy 45 Pre-post\ninterventional trial\n N = 330\n Age: 18–40 years\n Presence of pain symptoms\nEndometriosis-related pain perception:\ndysmenorrhea, deep dyspareunia, and non-\nmenstrual pelvic pain\n↓\nMCT-modified ketogenic diet Naeini et al. ( 2025); Iran37 Randomized\ncontrolled trial\n N = 50\n Age: 25–35 years\n Presence of pain symptoms\nEndometriosis-related pain perception: dyschezia,\ndyspareunia, and pelvic pain\nPelvic pain: —\nDyschezia or dyspareunia: —\nMediterranean diet Cirillo et al. (2023); Italy 34 Interventional trial  N = 35\n Reproductive-aged women\nEndometriosis-related pain perception: dyschezia,\ndyspareunia, dysuria, and non-menstrual pelvic pain\nAt 3 months, pain perception in all domains: ↓\nAt 6 months, dyspareunia ↓ and dyschezia ↓\nhttps://doi.org/10.1038/s44294-026-00133-y Review\nnpj Women's Health |            (2026) 4:12 3\n\nTable 1 (continued) | Dietary patterns, endometriosis, and uterine fibroids\nDietary pattern(s) Author; country of\nparticipants\nStudy design Participants Outcomes of interest Key findings: ↑ for statistically signi ficant\npositive associations, ↓ for statistically\nsignificant inverse associations, and — for no\nsignificant result\nMIND diet Noormohammadi et al.\n(2025); Iran46\nCase-control study  N = 313\n Age: 18–49 years\nEndometriosis prevalence ↓\nPro-inflammatory diet Liu et al. (2023); U.S 33. Cross-\nsectional study\n N = 3410\n Median age [IQR]: 40.0 years\n[32.0, 47.0]\nEndometriosis prevalence ↑\nUterine fibroids:\nVegetarian diet Lee et al. (2022); Taiwan 74 Prospective\ncohort study\n N = 1997\n Premenopausal women with\ncomplete data\n Age: 30–59 years\nUterine fibroids prevalence —\nSummarizes the dietary patterns, study characteristics, participant demographics, outcomes of interest, and direction of associations across the literature included in this review. Symbols indicate statistically significant positive associations (↑), inverse associations (↓), or\nnull findings (—).\nAcronyms:\nAHEI-2010: Alternative Healthy Eating Index-2010.\nDASH: Dietary Approaches to Stop Hypertension.\nEHP-30: Endometriosis Health Pro file-30 is a quality of life (QoL) assessment tool, range 0 –100, 0 = best possible health status.\nGI Health: gastrointestinal health.\nIQR: interquartile range (25th –75th percentiles).\nLow-FODMAP: fermentable oligosaccharides, disaccharides, monosaccharides, and polyols.\nMCT-modified ketogenic diet: Medium-Chain Triglyceride (MCT)-modi fied ketogenic diet.\nMIND diet: Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet.\nQoL: quality of life measured using ‘My Positive Health’, a non-validated tool for endometriosis QoL, scale 0 –10, 10 = best possible health status.\nhttps://doi.org/10.1038/s44294-026-00133-y Review\nnpj Women's Health |            (2026) 4:12 4\n\nHigh-quality dietary patterns . The Dietary Approaches to Stop\nHypertension (DASH) diet was developed to treat hypertension 56 and\nincludes low-fat/fat-free dairy products, beans, nuts, and vegetable oils,\nwhile limiting foods high in saturated fat (e.g., full-fat dairy), tropical oils\n(e.g., coconut, palm), sodium to 1500 mg/day, sugar-sweetened bev-\nerages, and sweets\n56,57. We identi fied one prospective cohort study\ninvestigating adherence to the DASH diet and endometriosis incidence32.\nNo statistically signi ficant association was observed between those\nquintiles of the DASH eating pattern and endometriosis 32. The findings\nwere contrary to hypotheses, given that a DASH diet is associated with\nlower inflammation and improved metabolic health\n58.\nThe endometriosis diet is an avoidance dietary pattern, popular among\nwomen experiencing pain in the Netherlands 48. In general, the pattern\nrecommends avoidance of red meat, gluten, cow’s milk, sugars, nutrients\nhigh in estrogen (e.g., soy), and limiting caffeine to 200 mg/day47,48.E v i d e n c e\nconsists of one cross-sectional study and one non-randomized interven-\ntional trial with a control group. In t he cross-sectional study, higher QoL\nscores (range 0 –10, 10=most positive health) across six domains were\nreported among participants who adhered to the endometriosis diet (versus\nnot)48. In the interventional trial, the d iet was associated with lower pain\nperception from bloating (mean difference [MD]: −0.99; 95% CI: −1.94,\n−0.04), and lower scores for 2 of 11 Q oL domains (social support MD:\n−15.47; 95% CI: −23.89, −7.06, medical profession MD:−18.71; 95% CI:\n−32.79, −4.63) [range 0–100, 0 = best possible health status], compared to\ncontrols47. Given the absence of a standardized approach to following the\ndiet, the existing studies do not provide suf ficient evidence to propose a\nspecific mechanistic pathway to support the improved symptoms47.\nA gluten-free diet restricts gluten, a protein found in barley, malts, rye,\nand wheat (e.g., pasta, bread) 59,60.W ei d e n t ified a single-arm, pre-post\ninterventional trial that examined the association between a gluten-free diet\nand pain perception for dysmenorrhea, deep dyspareunia, and non-\nmenstrual pelvic pain. Marziali et al. found that adhering to a gluten-free\ndiet was associated with lower pain perception among 75% of patients, while\n25% reported no change, and no patient reported higher pain perception\n45.\nGluten avoidance may reduce intestinal permeability, which in turn may\nlower immune activation\n61 and the cytokine-driven nociceptive pain sig-\nnaling in endometriosis62.\nThe Alternative Healthy Eating Index (AHEI) quantifies adherence to\nthe Harvard Healthy Eating Plate (HHEP)63.I nt h eA H E I ,c o n s u m p t i o no f\nalcohol, sweetened beverages, long-chain fatty acids, polyunsaturated fatty\nacids, trans fats, fruits, red and processed meats, sodium, and vegetables is\nscored from 0–10 (none to optimal consumption, respectively, score range:\n0–110)\n32.W ei d e n t ified two studies that examined the AHEI and the like-\nlihood of endometriosis32,64. One prospective cohort study found that a\nhigher AHEI-2010 score was associated with a lower risk of endometriosis\n(HR: 0.87; 95% CI: 0.78 –0.96) in the fifth versus first quintile\n32.Ac a s e -\ncontrol study observed that each one-unit increase in the AHEI score was\nassociated with 19% lower odds of endometriosis (95% CI: 0.78–0.88)\n64.T h e\nprotective effect of the HHEP32 is likely linked to two mechanisms. First,\nattenuation of inflammatory burden, achieved through lower circulating\ninflammatory markers as a result of the antioxidant-rich foods characteristic\nof higher AHEI scores 64. The second mechanism is the facilitation of\nestrogen metabolism; as Fung et al. report, higher AHEI scores were asso-\nciated with lower E2 and higher sex hormone-binding globulin levels, a\nhormone which binds and inactivates estrogens\n55.\nThe low-FODMAP (fermentable oli gosaccharides, disaccharides,\nmonosaccharides and polyols) diet eli minates short-chain carbohydrate\nfoods, which are poorly absorbed by the small intestine and can result in\ngastrointestinal symptoms\n35,65. The second phase reintroduces foods indi-\nvidually to determine tolerance, and phase three maintains the personalized\nplan, including tolerated high-FODMAPs 35,66.H i g h - F O D M A Pf o o d s\ninclude asparagus, cauliflower, mango, nectarines, cow and soy milk, most\nlegumes, some seafood, wheat bread, honey, and cashews67.W ei n c l u d e d\nthree studies: one crossover feeding t rial, one non-randomized interven-\ntional trial with a control group, and on e single-arm, interventional trial,\nwhich examined the association o f a low-FODMAP dietary pattern on\ngastrointestinal health, QoL, and pain perception 35,36,47. In the crossover\nfeeding study by Varney et al., a low-FODMAP diet (<5 g/day FODMAPs)\nwas associated with a decrease in gastrointestinal symptoms among 60% of\nparticipants compared to only 26% of participants who consumed the\ncontrol condition (20 g/day FODMAPs), both modeled on the Australian\ndietary guidelines\n36. In the non-randomized interventional trial by van\nHaaps et al., there was no improvement in GI health following the diet47.T h e\nsingle-arm, interventional trial by Keukens et al. reported lower constipation\nscores (7.0 at baseline and 5.0 at di et completion) following the low-\nFODMAP diet, with no statistically signi ficant association reported for\nbloating35. Related to QoL, Varney et al. reported improvement from\nbaseline (median: 55.6; 95% CI: 48.0, 62.0) for participants on the low-\nFODMAP diet (median: 45.3; 95%; CI:29.6, 50.9) compared to the control\ncondition (median: 47.1; 95% CI: 37.8, 56.7), although the results did not\nreach statistical significance based on the trial’sap r i o r ip - v a l u eo f0 . 0 136.v a n\nHaaps et al. reported a lower score in one out of 11 domains observed (MD:\n17.14; 95% CI: -31.27, -3.00) compared to controls\n47. Keukens et al. reported\nlower scores in 7 of 11 domains, compared to baseline ( p\nvalues≤ 0.001–0.04)35. The non-randomized interventional trial by van\nHaaps et al. was the only study to examine pain perception, and reported\nsignificantly lower scores for deep dyspareunia, one of the six domains\nassessed (MD:−1.15; 95% CI: −2.2, −0.10)\n47.B e n efits of a low-FODMAP\ndiet may re flect the reduction of fermentable carbohydrate load, which\ndecreases intestinal distension and limits immune activation in the gut 68.\nFermentable carbohydrates can also have positive health benefits and sup-\nport immune balance; therefore, restriction and reintroduction should be\nindividualized69.\nThe Medium-Chain Triglyceride (MCT)-modified ketogenic dietary\npattern focuses on high-fat and protein foods, and low-carbohydrate intake\nwith the addition of MCTs as a fat source37,70. In a randomized controlled\ntrial, Naeini et al. tested a 70–80% fat, 15–20% protein, and 5–10% carbo-\nhydrate diet supplemented with 500 ml of MCT oil over three days, every\nthree weeks for the 12-week intervention as adjunct therapy to traditional\ntreatment with an oral contraceptive pill\n37. Women were randomized by\nendometriosis stage (I or II) and diet (MCT-modi fied ketogenic diet or\ncontrol diet), then assessed for dyschezia, dyspareunia, and pelvic pain36.\nThere was no statistically significant effect on these domains between par-\nticipants randomized to the MCT-modi fied ketogenic diet group when\ncomparing mean differences to the control group37. Within-group differ-\nences were examined, and a decrease i n all pain perception domains was\nobserved in both groups. While this study did not observe an association\nbetween groups, the MCT-modified ketogenic diet can increase ketone body\nproduction, which is associated with lower systemic inflammation in other\ncontexts\n37,70.\nA Mediterranean dietary pattern is characterized by high intake of\nbeans, minimally refined breads and cereals, fruits, nuts, olive oil as the main\nfat, seeds, and vegetables; moderate consumption of dairy, eggs,fish, poultry,\nand red wine; and low consumption of red meat 71. One Italian-based\ninterventional trial examined the association of consuming a Mediterranean\ndiet and pain perception 34. Cirillo et al. observed lower pain perception\nscores in all domains compared to baseline; dyschezia, dyspareunia, dysuria,\nand non-menstrual pelvic pain at three months, with continued lowering of\nscores in two domains (dyspareunia and dyschezia) after six months of\nfollowing the diet\n34. It is possible that thefiber, antioxidants, and healthy fats\ncharacteristic of a Mediterranean diet support immune regulation, reduce\ninflammatory activity, and promote sex hormone metabolism through\nimproved fecal excretion of excess estrogen and increased sex hormone\nbinding globulin production\n34,71,72.\nResearchers combined the Mediterranean and DASH diets to promote\nbrain health for Alzheimer ’s patients, resulting in an anti-in flammatory\npattern low in fat and sodium, high in fiber, with an avoidance of pro-\ninflammatory foods such as butter, fried foods, red meat, and sweets known\nas the Mediterranean-DASH Intervention for Neurodegenerative Delay\n(MIND) Diet\n46. In one case-control study from Iran, with each one-unit\nhttps://doi.org/10.1038/s44294-026-00133-y Review\nnpj Women's Health |            (2026) 4:12 5\n\nincrease in MIND score, there was a 47% lower odds of endometriosis (odds\nratio [OR]: 0.53; 95% CI: 0.42 –0.67)46.T h i sfinding is consistent with the\nbiological plausibility described above for the Mediterranean diet; moreover,\nfeatures of the MIND diet further enhance potential results, as the DASH\naddition is even stricter in its restriction of red meats and high-fat inflam-\nmatory food items, which directly correlate to sex hormone\nhomeostasis\n34,46,58,71.\nA prudent diet is characterizedby higher intake of legumes,fish, fruit,\nvegetables, and whole grains, and lower intake of high-fat dairy, fried foods,\nred and processed meat, processed foods, sugar-sweetened beverages,\nsweets, and desserts\n32,73. In a U.S. prospective cohort, principal component\nanalysis was used to de fine the prudent diet, and the pattern was not\nassociated with reduced risk of endometriosis 32.T h i sfinding was unex-\npected, as Chandler et al. observed metabolic signatures associated with the\nFig. 1 | PRISMA flow diagram for dietary patterns and endometriosis study\nselection. Illustrates the identification, screening, and inclusion of studies evaluating\ndietary patterns in relation to endometriosis conducted in Covidence. Two duplicate\nrecords were removed before screening, titles and abstracts were reviewed for\nrelevance, and a review of full texts assessed eligibility. Acronym: PRISMA: preferred\nreporting items for systematic reviews and meta-analysis\nhttps://doi.org/10.1038/s44294-026-00133-y Review\nnpj Women's Health |            (2026) 4:12 6\n\nprudent dietary pattern consistent with anti-inflammatory and antioxidant\nproperties73.F u r t h e r ,h i g hfiber in this diet may plausibly have sex hormone-\nregulating benefits as described earlier72,73.\nUterine fibroids\nThe search yielded one Taiwanese study that analyzed adherence to a\nvegetarian dietary pattern with uterine fibroid prevalence from 202274.A\nvegetarian diet ( https://www.nal.usda.gov/human-nutrition-and-food-\nsafety/vegetarian-nutrition) is typically characterized by plant-based\nfoods, including fruits, beans and pea s, grains, nuts, and vegetables, and\ngenerally excludes animal products such as meat, poultry, and seafood. The\nstudy utilized a national biobank database with demographic and lifestyle\ninformation, and matched participant info to their disease diagnosis\nthrough the national health insurance research database\n74.T h e r ew a sn o\nFig. 2 | PRISMA flow diagram for dietary patterns and uterine fibroids study\nselection. Depicts the identi fication, screening, and inclusion of studies evaluating\ndietary patterns in relation to uterine fibroids conducted in Covidence. One\nduplicate record was removed prior to screening, title and abstracts were reviewed\nfor relevance, and a review of full texts evaluated eligibility. Acronym: PRISMA:\npreferred reporting items for systematic reviews and meta-analysis.\nhttps://doi.org/10.1038/s44294-026-00133-y Review\nnpj Women's Health |            (2026) 4:12 7\n\nstatistically significant association between self-reported vegetarian diet\nadherence and fibroids prevalence (OR: 1.09; 95% CI: 0.77–1.55)74.W h i l e\nBarnard et al. state that a vegetarian diet is associated with sex hormone\nmetabolism driven by elevated levels of sex hormone binding globulin\n75,a n d\nthere are many health benefits associated with the pattern76, a vegetarian diet\nis not inherently higher quality and can include low-quality processed foods.\nFor example, Hargreaves et al. identified over 10 patterns ( e.g., lactovege-\ntarian, semi-vegetarian)\n77, and the Academy of Nutrition and Dietetics notes\nthat vegetarian diets may reduce intakeof certain nutrients, and underscores\nthe need to follow nutritional guidelines to avoid deficiencies78.\nDiscussion\nWe identified 11 studies examining dietary patterns and endometriosis, and\none study examining dietary patterns and uterinefibroids. This indicates a\npaucity of studies examining the role of dietary patterns in these all-too-\ncommon uterine health conditions. This was surprising, given the diet ’s\nrelationship to inflammation, metabolic health, and obesity, all of which\ncontribute to the development and severity of both conditions.\nOf the five observational studies identified, associations were mixed.\nDiets with higher in flammatory potential (e.g., Western diet) were asso-\nciated with a higher likelihood of endometriosis32, whereas higher adherence\nto dietary patterns deemed high-quality (e.g., HHEP/AHEI) was associated\nwith a lower likelihood32,46,64. Common limitations included selection and\nrecall bias, measurement error, residual or unmeasured confounding, and\ntemporality limitations32,33,46,48,64,74.I nt h eu t e r i n efibroids study, there was a\nlack of strati fication of vegetarian status by age, a limitation given the\npotential variation in disease prevalence with menopausal status74.\nSix interventional studies also showed mixed results. Avoidance\npatterns (e.g., gluten-free) reported better QoL and lower pain\nperception\n35,45,47. Similarly, the low-FODMAP trials consistently\nimproved QoL and lower pain perception 35,36,47. A Mediterranean diet\nintervention had minimal effects on pain 34. There are several limitations\nto the interventional trials, incl uding heterogeneity and mostly non-\nrandomization, with small samples, short follow-up, and variable\nprotocols. Further limitations include participant diet self-selection in\nthe van Haaps study\n47, unassessed effectiveness of blinding in the\nVarney crossover feeding trial 36, and very narrow age inclusion criteria\nwith a high drop-out rate in the only randomized controlled trial 37.\nNotably, there was no dietary pattern-focused interventional trial\namong women with uterine fibroids.\nThe existing evidence reviewed begins to suggest that high-quality\ndietary patterns rich in antioxidants and anti-inflammatory compounds are\nassociated with a lower prevalence and symptom severity of endometriosis;\nconversely, some low-quality dietary patterns may be associated with higher\nprevalence and more severe symptomology. However, research on uterine\nfibroids remains extremely limited, while endometriosis findings offer a\nconceptual framework for future research.\nQualitative analysis is necessary to center the perspectives of women\nliving with endometriosis and uterinefibroids, and the clinicians who care\nfor them. Through interviews and focus groups studies should examine 1)\npatient thoughts and interest in dietary interventions to manage symptoms,\n2) patient perceptions of feasibility and acceptability of following a dietary\npattern, and 3) clinician views on implementing dietary strategies in the\ncontext of clinical care.\nRigorously designed randomized controlled trials are needed to\nunderstand what dietary patterns positively affect symptoms and the QoL of\nwomen suffering from endometriosis and uterinefibroids.\nFuture studies must recruit partici pants representative of national\nracial, ethnic, and socioeconomic populations with intentional inclusion of\nmulticultural women. Stratification by insurance status may further clarify\nhow access to, and navigation across the continuum of endometriosis and\nuterine fibroid care intersect with structural, upstream exposures, and\nindividual behavior to shape diagnosis, progression, treatment, and out-\ncomes. This approach would provide a more comprehensive understanding\nof the modi fiable factors that shape uterine health in the U.S. to inform\npolicy, prevention, and equitable delivery of food as medicine in clinical\npractice.\nMethods\nIn this review, we used the following search terms to assess the current\nresearch available for dietary patterns and 1) endometriosis and 2) uterine\nfibroids solely in PubMed: ( “diet” [mesh] OR diet *[tiab]) AND (Endo-\nmetriosis[tiab] OR “endometriosis” [MeSH]) and ( “diet” [mesh] OR\ndiet*[tiab]) AND (Leiomyoma[tiab] ORfibroid*[tiab]), see Figs.1–2.T h e\ninclusion criteria for both searches included English-language, peer-\nreviewed studies of women aged 18 –64, in any geography/publication\nyear. The search for dietary patterns and endometriosis yielded 413 studies,\nof which two duplicates were removed, 308 were irrelevant per title/abstract\nscreening, 92 were excluded in full-text review, and 11 were extracted.\nDietary patterns and uterine fibroids generated 178 studies, of which one\nduplicate was removed, 150 were irrelevant per title and abstract screening,\n27 were excluded in full-text review, and one study was extracted. Screening\nand extraction were conducted by a single reviewer utilizing a pre-\ndesigned form.\nData availability\nNo datasets were generated or analysed during the current study.\nCode availability\nNot applicable.\nReceived: 17 September 2025; Accepted: 6 February 2026;\nReferences\n1. Abulughod, N., Valakas, S. & El-Assaad, F. Dietary and nutritional\ninterventions for the management of endometriosis. Nutrients 16,\n3988, https://doi.org/10.3390/nu16233988 (2024).\n2. Durnell Schuiling, K., Fried, E. M. & Likis, F. E. 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Diet. 125,\n831–846.e2 (2025).\nAcknowledgements\nWe are grateful to Amelia Brunskill, Associate Professor and Liaison\nLibrarian at the University of Illinois Chicago, for her guidance in developing\nthe literature search strategy.\nAuthor contributions\nT.M.F., L.M.T.-H., and V.M.O. conceived the idea for the paper; T.M.F.\nconducted the search and screening, extracted data, synthesized evidence,\nand drafted the manuscript; T.M.F., L.M.T.-H., and V.M.O. critically revised the\nmanuscript; S.J.K., M.D.K., and P.P. provided feedback; T.M.F., L.M.T.-H.,\nM.D.K., S.L., P.P., and V.M.O. approved thefinal version of the manuscript.\nCompeting interests\nThe authors declare no competing interests.\nAdditional information\nCorrespondenceand requests for materials should be addressed to\nVanessa M. 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If material\nis not included in the article’s Creative Commons licence and your intended\nuse is not permitted by statutory regulation or exceeds the permitted use,\nyou will need to obtain permission directly from the copyright holder. To\nview a copy of this licence, visit http://creativecommons.org/licenses/by-\nnc-nd/4.0/\n.\n© The Author(s) 2026\nhttps://doi.org/10.1038/s44294-026-00133-y Review\nnpj Women's Health |            (2026) 4:12 10","source_license":"CC0","license_restricted":false}