Unveiling the Bidirectional Relationship on the Effect of Gut Microbiota and Female Infertility: A Narrative Review

Alteration of the gut microbiome is also found to influence thyroid health, a study by Liu et al. identified Intestinimonas (OR = 1.120, p  = 0.014) and Ruminiclostridium5 (OR = 1.189, p  = 0.011) as risk taxa for hypothyroidism, whereas Bifidobacterium (OR = 0.877, p  = 0.011), Lachnospiraceae UCG008 (OR = 0.87, p  = 0.002), Actinobacteria (OR = 0.827, p  = 0.001), and Verrucomicrobia (OR = 0.876, p  = 0.012) were protective; also increased levels of class Negativicutes (OR = 1.039, p  = 0.048), family Christensenellaceae (OR = 1.065, p  = 0.030), genera Eubacterium ruminantium group (OR = 1.057, p  = 0.042) and Ruminococcaceae UCG005 (OR = 1.047, p  = 0.025), and decreased abundance of Akkermansia (OR = 0.954, p  = 0.029) were said to be causally associated with hypothyroidism [ 37 ]. While focusing only on broad bacterial groups and studying mainly one population limits the comparability, still, this study highlights a possible link between gut bacteria and thyroid and since thyroid hormones are said to regulate numerous reproductive processes, including ovarian folliculogenesis and endometrial receptivity [ 38 ], dysbiosis affecting thyroid health, may in turn impact fertility highlighting that the gut–thyroid–reproductive axis as a promising area for future research.

Srijanjali Balagoni: writing – original draft, writing – review and editing, visualization, investigation, validation, methodology, conceptualization, data analysis, supervision, project administration. D. Grace Evelyne: writing – original draft, writing – review and editing, visualization, investigation, validation, methodology, conceptualization, data analysis, supervision, project administration. Aswathy Mathews: resources, writing – original draft, writing – review and editing. Rohit Rao Dugyala: resources, writing – original draft, writing – review and editing. Medhansh Biradar: writing – original draft, writing – review and editing, resources. Vodela Deekshith: writing – review and editing, resources, image generation. Anika Goe l : writing – original draft, writing – review and editing, project administration, resources. Amogh Verma: writing – original draft, writing – review and editing, visualization, investigation, validation, methodology, conceptualization, data analysis, supervision, project administration.

Ovulation is a crucial aspect of the female reproductive cycle; any derangement in it can lead to anovulatory or oligo‐ovulatory cycles, which are among the causes of female infertility. Alterations in the gut microbiome are said to influence these cycles via several mechanisms, one of which is the estrobolome. The term estrobolome is defined as a set of bacterial genes that can metabolize estrogen. These secrete β ‐glucuronidase enzymes [ 39 ]. This converts estrogen from bound form to unbound form [ 40 ]. This affects estrogen recycling, leading to dysregulated reproductive cycles [ 41 ]. Apart from them, it causes obesity, metabolic syndrome, and PCOS [ 42 ]. Elevated levels of the β ‐glucuronidase‐producing bacteria are said to increase the circulating levels of estrogen in the body, which leads to the growth of ectopic endometriotic foci and breast cancer [ 43 ]. Further, derangement in gut microbiome could also lead to the formation of SCFAs and LPS, which modulate the levels of LH [ 21 ], affecting the reproductive cycle. A Prospective study conducted by Sasaki et al. to determine whether the gut microbiome was associated with the ovulatory cycle in women experiencing normogonadotropic anovulation. Where two groups, those with irregular menstrual cycles and those with normal cycles, were analyzed. A significant difference ( p  < 0.05) in 28 bacterial taxa was found between the two, with the former group having an abundance of Prevotella rich species, Clostridiales , Ruminococcus , and Lachnospiraceae (butyrate‐producing bacteria), which was said to influence SCFA metabolism as well as hormonal regulation, suggesting its relation with ovulatory function [ 44 ].

Ethical approval was not required for this review as per the policies of our institution. The Institutional Review Board waived the need for approval in accordance with the institutional guidelines for review articles.

Lifestyle interventions, including health behavior modifications, have shown effects in improving weight and enhancing natural pregnancy rates, but they have not reliably led to better live birth outcomes or birth weights. The current medical evidence on the impact of preconception counseling and lifestyle interventions remains limited. Management strategies to restore the gut microbiome from a disrupted microbiome in maintaining host health must be addressed. Some of the modifiable factors, such as diet, physical activity, stress management, and environmental exposures, play important roles in reproductive health. Observational and interventional studies suggest that weight loss in overweight and obese women is associated with higher rates of natural conception (OR = 1.87; 95% CI: 1.24–2.81; p  = 0.003) [ 59 , 61 ]. However, these associations have not translated consistently into improved assisted reproductive technology (ART) outcomes, reduced pregnancy complications, or higher live birth rates [ 60 ]. This suggests that lifestyle changes, even though beneficial, may be insufficient in cases of established infertility. Psychological conditions, support systems, and health literacy also strongly influence intervention success. Some barriers, such as time, emotional stress, inconsistent medical advice, lack of family support, and reduced access to personalized care, limit real‐world applicability [ 61 ]. While preconception counseling is said to be helpful, variability in program design and delivery highlights the need for standardized and accessible models [ 62 ]. Psychological stress has been identified as both a cause and a consequence of infertility, contributing to hormonal disruptions, ovulatory irregularities, and suboptimal ART (Assisted Reproductive Technology) outcomes [ 63 ]. This bidirectional relationship forms a feedback loop in which infertility aggravates stress, and stress further impairs fertility. This highlights the necessity of integrated care models that address both psychological and reproductive health in women undergoing fertility treatments or ART. The alteration of female microbiota, particularly the composition and stability of vaginal and endometrial microbiomes, has profound implications for fertility. A Lactobacillus ‐dominant vaginal microbiome, especially involving Lactobacillus crispatus , has been associated with improved ART outcomes, enhanced reproductive growth, and reduced miscarriage risks. Women with L. crispatus ‐dominant vaginal microbiota had higher clinical pregnancy rates (41.2% vs. 22.2%) and lower early miscarriage rates (15% vs. 50%; p  = 0.011) compared with women dominated by other Lactobacillus species, suggesting a protective role in early pregnancy [ 62 , 64 ]. In contrast, dysbiosis, an imbalance in the microbiome, is associated with implantation failure, endometrial inflammation, and early pregnancy loss [ 63 ]. In many instances, vaginal dysbiosis and disturbed colonies remain asymptomatic, complicating diagnosis and treatment. This causes a clinical challenge where subclinical microbial imbalances may persist undetected, undermining fertility without clear symptoms and ultimately reducing reproductive potential [ 63 ]. Awareness of the microbiome's role in fertility has been increasing, but management of subclinical dysbiosis remains limited. Current guidelines focus mostly on symptomatic infections and lack protocols for subclinical imbalances. Key research gaps include developing standardized screening and sequencing methods, conducting RCTs to identify effective probiotic strains, doses, and delivery methods, and studying microbiome–reproductive tract interactions. Prospective studies linking microbiome modulation to ART outcomes are also needed [ 59 , 62 ]. Looking ahead, fertility care is expected to become more personalized and integrative, addressing lifestyle, diet, microbial health, and emotional well‐being. Priorities include standardizing microbiome analysis with reliable biomarkers, screening for subclinical dysbiosis in women undergoing ART, and optimizing probiotic treatments through targeted strains and dosing. Expanding lifestyle interventions to include partners and families, along with mental health support, will be essential. In addition, holistic exposome mapping should clarify how environment, diet, stress, and microbiota interact to shape fertility [ 64 ]. The factors influencing female fertility, the interaction of lifestyle, stress, environmental exposures, and microbiome health, require a comprehensive and dynamic approach. Evidence‐based interventions addressing these factors can improve reproductive medicine, leading to an understanding of mechanisms and preparing effective strategies. A systematic review and meta‐analysis involving non‐pregnant women of childbearing age who intend to conceive, including their male partners. Exclusion criteria included participants with BMI < 18 kg/m², genetic disorders in either partner, and trials focused solely on alcohol/smoking cessation, micronutrient supplementation, or diabetes control. Principal outcomes included anthropometric, fertility, obstetric, and fetal results, along with quality and bias assessments [ 65 ]. The meta‐analysis of 1802 articles and eight studies showed that lifestyle interventions in overweight and obese subfertile women resulted in significant weight loss (mean difference −3.48 kg, 95% CI: −4.29 to −2.67, p  < 0.00001) and improved natural conception rates. However, no significant effects (OR = 1.88, 95% CI: 0.63–5.58, p  = 0.26) were observed on ART outcomes or live birth rates. Variability in intervention design and moderate‐to‐high attrition bias suggest that more standardized, rigorous trials are needed [ 62 , 65 ]. Most included studies involved only overweight or obese women, with few male participants; wide variation in intervention duration and design limited comparability. High attrition bias in several studies reduced the reliability. While lifestyle interventions, particularly weight loss, appear beneficial for natural conception, more research is needed to identify effective components and best practices across populations regarding barriers and enablers to a healthy lifestyle in people with infertility [ 66 ]. Various barriers, including emotional distress, inconsistent guidance, and time constraints, complicate infertility‐related lifestyle management. Self‐management skill development and mental health support are essential for success [ 67 ]. Diet, exercise, stress management, etc., also play a role. Diets rich in omega‐3s, fiber, and antioxidants have been linked with better fertility outcomes. Environmental toxins may affect fertility, especially in ART settings. By approaching these factors, future interventions (Table  2 ) may improve reproductive outcomes and promote holistic well‐being [ 65 , 68 , 70 , 71 ]. Summary of lifestyle factors, barriers, and research gaps in female fertility. Note: This table consolidates findings from major reviews and studies exploring the impact of lifestyle and microbiome‐related factors on female fertility outcomes. It outlines each study's design, sample characteristics, principal findings, identified barriers or challenges, and proposed gaps or directions for future research. Abbreviations: BMI, body mass index; n , sample size; RCTs, randomized controlled trial.

The interplay of hormonal, metabolic, environmental, and inflammatory factors is said to have an important role in female fertility. Studies suggest that a dietary approach, including the use of probiotics and ketogenic diets, influences reproductive health by modulating gut microbiota, supporting metabolic function, and reducing inflammation [ 45 , 46 ]. Thus, the effects of the ketogenic diet and probiotics on female fertility, particularly on PCOS, ovulatory disorders, immune programming, and endometrial health, are said to have a bidirectional relationship with gut microbiota, making this an important investigation (Figure  2 ). Microbiome modulation strategies in female infertility [ 47 , 48 , 49 ]. Schematic representation of microbiome modulation strategies in female infertility. Probiotic supplementation increases Lactobacillus abundance and SCFA levels while reducing LPS and β‐glucuronidase, leading to decreased inflammation, lower FAI, and improved ovulation. Ketogenic diet reduces insulin resistance, androgens, and inflammation, enhancing oocyte quality and menstrual regularity. Mediterranean or low–GI diet improves antioxidant status, gut diversity, and reproductive outcomes. Collectively, these interventions restore microbial balance, normalize estrogen metabolism, and enhance endometrial receptivity. Research gaps include small sample sizes, lack of probiotic standardization, and uncertain long‐term outcomes. FAI, free androgen index; GI, glycemic index; LPS, lipopolysaccharides; SCFA, short‐chain fatty acids; SHBG, sex hormone‐binding globulin. [Created using Biorender.com ] Different mechanisms through which probiotics cause beneficial effects on female reproductive health include hormonal regulation, reduction of oxidative stress, inflammation, and modulation of the gut microbiome. Studies also suggest that probiotics can increase sex hormone‐binding globulin (SHBG) and lower the free androgen index (FAI), thus contributing to hyperandrogenism in PCOS [ 50 , 51 ]. They may also increase the levels of nitric oxide (NO) and decrease malondialdehyde (MDA), which are markers linked to oxidative and inflammatory stress, thus supporting reproductive cell protection [ 50 , 52 ]. Further, probiotics help restore microbial balance in PCOS by increasing beneficial taxa, improving insulin sensitivity, and attenuating systemic inflammation, with short‐chain fatty acids (SCFAs), endotoxin regulation (e.g., LPS), and β ‐glucuronidase activity acting as intermediary pathways [ 53 , 54 ]. A meta‐analysis of 13 studies including 855 women with PCOS reported that a probiotic diet is associated with increased SHBG, NO, and also reductions in FAI and MDA [ 40 ]. Although probiotics help in improving menstrual regularity and ovarian function, their influence on testosterone levels and hirsutism management remains inconclusive [ 50 , 55 ]. Very low carbohydrate and high fat intake constitute the ketogenic diet. It influences fertility by regulating body weight, increasing insulin sensitivity, reducing free radicals, and promoting hormonal balance. This diet also aids in rapid weight loss and reduces hyperinsulinemia, key factors of PCOS‐associated anovulation [ 47 , 48 ]. By lowering insulin, it decreases ovarian androgen production, thereby improving ovulatory function [ 48 , 49 ]. It also leads to decreased inflammatory markers, thereby enhancing endometrial receptivity to hormones and the integrity of uterine layers [ 56 ]. A retrospective study having a sample size of 30 found that 100% of PCOS women on a ketogenic diet had regular menstrual cycles, with a 55.6% pregnancy rate among those seeking conception (38.5% vs. 100%, p  = 0.036) [ 48 ]. Another case series with a small sample size of four females reported spontaneous pregnancies in two women with PCOS after 6 months of a protein‐sparing modified fast (PSMF), a variant of the ketogenic diet [ 49 ]. Apart from them, altered reproductive tract microbiota, including reduced Lactobacillus , had a significant (Weighted Mean Difference (WMD) = −0.47 kg/m²; 95% CI −0.87 to −0.06; p  = 0.02) association with endometriosis and PCOS [ 57 , 58 ]. Dietary interventions influence microbiome, indicating a bidirectional link between diet and fertility. Probiotics enhance Lactobacillus dominance, increasing endometrial sensitivity [ 59 ]. They may also alter the gut microbial composition, but long‐standing effects on fertility require further investigation [ 60 ]. Diets that play an important role in improving gut microbiome include the Mediterranean diet, vegetarian diet, and low glycemic index (GI) diets. Diets that are rich in monounsaturated fats, fiber, and antioxidants may support ovulation and metabolic health [ 61 , 62 ]. They also improve metabolic health and reduce PCOS‐associated inflammation, though evidence on direct fertility outcomes is limited [ 63 ]. High glycemic index diets are said to adversely affect ovulation by exacerbating insulin resistance [ 45 , 61 ]. Current evidence suggests that probiotics and ketogenic diets positively influence female fertility, especially in PCOS, by developing hormonal balance, metabolic health, and enriched gut microbiota composition. However, larger randomized controlled trials are needed to define optimal probiotic strains and diet protocols [ 48 , 50 ]. Evaluation of the safety and efficacy of the ketogenic diet in reproductive‐aged women is another future direction of research [ 49 ]. Finding the microbiome‐associated mechanisms linked to diet and fertility outcomes is also of significance [ 53 , 58 ]. Combining dietary changes along with conventional fertility treatment practices offers a promising supportive strategy for improving reproductive health in women with metabolic, hormonal, and inflammatory disorders.

The human body contains millions of microorganisms that live in symbiosis with the host. Each organ in the body has a niche of microbes, which are considered commensals, that help in maintaining the host's overall fitness and well‐being. When this homeostasis of microbiota is disrupted, it is referred to as “Dysbiosis” [ 5 ]. Similarly, the gut consists of commensal organisms like Firmicutes, Bacteroidetes, Actinobacteria, Fusobacteria, Verrucomicrobia , and Proteobacteria [ 6 ]. An imbalance of these flora could lead to dysbiosis of the gut, which causes various subclinical manifestations (Figure  1 ). A clear understanding of important commensal gut bacteria and their mechanisms in dysbiosis is essential for comprehending their role in infertility. Alterations in microbial abundance (Table  1 ) (↑ increase, ↓ decrease) are linked to immune dysregulation, disruption of the mucosal barrier, and disturbances in hormonal homeostasis. These microbial shifts play a key role in understanding their link with infertility [ 7 , 8 , 9 , 10 , 11 , 12 , 13 ]. A study by Marcos et al. demonstrated this emerging connection between gut dysbiosis and infertility; they reported that infertile women exhibited alterations in both the gastrointestinal tract (GIT) and the female reproductive tract (FRT) microbiota. Specifically, the fecal microbiota of infertile participants showed a reduction in α‐diversity ( p  < 0.05) and distinct clustering in beta diversity (PERMANOVA, p  < 0.01) compared to fertile controls. Though limited by its observational design and lack of reported mean ± SD values for α‐diversity, the taxonomic profiling revealed an increased proinflammatory taxa and reduced beneficial taxa ( p  < 0.05). Most importantly, a positive correlation was identified between Streptococcus in the gut and Enterobacteriaceae in the endometrial microbiome ( r  = 0.62, p  < 0.01), which indicates a potential cross‐talk despite the absence of direct microbial exchange between the GIT and FRT [ 5 ]. Pathophysiological map of dysbiosis‐induced infertility [ 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 ]. Pathophysiological map of dysbiosis‐induced infertility. Normal physiology involves balanced microbiota (Firmicutes, Bacteroidetes, Actinobacteria), SCFA production, and stable estrogen metabolism, maintaining mucosal barrier integrity and HPG axis regulation. Dysbiosis reduces microbial diversity and increases Prevotella and Proteobacteria, elevating LPS and β‐glucuronidase, resulting in immune activation (↑ IL‐6, TNF‐α, NF‐κB) and systemic inflammation. Endocrine disruption decreases GnRH and LH pulse amplitude, leading to anovulation, PCOS, endometriosis, and implantation failure. GnRH, gonadotropin‐releasing hormone; IL, interleukin; LH, luteinizing hormone; LPS, lipopolysaccharides; NF‐κB, nuclear factor kappa‐light‐chain‐enhancer of activated B cells; PCOS, polycystic ovary syndrome; SCFA, short‐chain fatty acids; TNF‐α, tumor necrosis factor‐alpha. [Created using Biorender.com ] Key studies linking the female gut and genital microbiota to dysbiosis and immune function. Note: This table summarizes key studies (review and observational) exploring the interplay between gut and genital microbiota in females, thus highlighting how microbial dysbiosis influences immune function and inflammatory states across different conditions. Abbreviations: ↑/increase, indicates an elevated abundance or activity of the microbiota; ↓/decrease, indicates a reduced abundance or activity of the microbiota; → , indicates association with or leads to; 16S rRNA, 16S ribosomal ribonucleic acid; BV, Bacterial vaginosis; GUS, β‐ glucuronidase; LPS, lipopolysaccharide; spp., species (plural).

Written informed consent to participate in this study was not applicable. This review article did not involve the recruitment or participation of human subjects.

The authors have nothing to report.

This article offers a narrative review after use of databases like PubMed, Scopus, Cochrane Library, and Google Scholar applying search terms such as “gut dysbiosis”, “female infertility”, “gut–brain axis”, “reproductive health”, “estrobolome”, “polycystic ovary syndrome (PCOS)”, and “endometriosis”. Eligible studies published between January 2007 and April 2025, consisting of systematic reviews and meta‐analyses, observational, experimental, interventional designs, and RCTs that determined the role of gut microbiota, its metabolites, and how dysbiosis affects reproductive function, are included due to their relevance in addressing research gaps on fertility outcomes. Studies lacking measurable outcomes, non‐research articles, and grey literature were excluded. No original statistical analysis was performed by the authors, as this is a narrative review, and all reported odds ratios, p values, and other statistical measures were taken directly from the cited studies. Much of the current evidence is from observational, small‐scale, or animal studies, and the use of different methodologies limits generalizability. Larger interventional studies are required to find this causality.

Grammarly and ChatGPT were used for language and stylistic refinement. These tools had no involvement in study design, data analysis, interpretation, or content development. All intellectual contributions and scientific interpretations are the sole work of the authors, who take full responsibility for the accuracy, originality, and integrity of the manuscript.

About 8%–13% of women are affected by PCOS worldwide every year, and it is one of the most common metabolic and endocrine disorders with a strong correlation with modern‐day lifestyle [ 14 ]. Emerging studies like Insenser et al. suggest that dysbiosis contributes not only to infertility in general but also to prevalent reproductive disorders like Endometriosis and PCOS. They report a reduced α‐diversity among the PCOS patients compared with healthy controls (Shannon index, p  = 0.03) [ 15 ]. Hassan et al. further highlighted enrichment of gut bacteria including Bifidobacterium, Collinsella , and Paraprevotella compared to controls, Paraprevotella abundance also showed positive associations with disturbed plasma glucose levels ( β  = 0.00077, p  = 0.0014), waist circumference ( β  = 0.00073, p  = 0.0010), and body weight ( β  = 0.00070, p  = 0.002) suggesting the influence of dysbiosis on metabolic traits of PCOS [ 16 ] While the studies indicate a consistent link between specific gut microbiota and PCOS, variations in microbiome sampling techniques and diversity indices affect comparability between the studies. Additionally, about 190 million women who are in their reproductive age group are affected by endometriosis every year, and there is a delay in accurate diagnosis, predisposing affected patients to the long‐term risks associated with the disorder [ 17 ]. Subclinical mechanisms like dysbiosis further aggravate its progression. Colonetti et al. reported the association between dysbiosis and endometriosis, showing elevation of Actinobacteria , Firmicutes , Proteobacteria , and Verrucomicrobia in women with endometriosis compared to controls (gut microbiota SMD = −0.28, 95% CI: −0.70 to 0.14, p  = 0.19), while Lactobacillaceae being decreased (vaginal microbiota SMD = −0.68, 95% CI: −1.72 to 0.35, p  = 0.19). Specific taxa like Enterobacteriaceae , Streptococcus , and Escherichia coli were found to be elevated across various microbiome sites in endometriosis cohorts [ 18 ], indicating the importance of looking deeper into examining specific microbial taxa and their metabolic roles rather than relying solely on broad diversity indices. Larger, longitudinal studies with standardized protocols are needed to validate these associations.

Gut dysbiosis may contribute to female infertility through effects on hormonal signaling, immune regulation, estrogen metabolism, inflammation, and endometrial receptivity. Current evidence links altered gut and reproductive tract microbiota with polycystic ovary syndrome, endometriosis, ovulatory dysfunction, pregnancy complications, and thyroid‐related reproductive disturbances. Probiotics, dietary modification, weight management, and lifestyle interventions appear promising as supportive strategies, but their clinical role remains uncertain because existing studies vary in design, microbiome assessment, intervention protocols, and fertility outcomes. Future longitudinal studies and randomized controlled trials should clarify causal pathways and determine whether targeted microbiome modulation can improve ovulation, implantation, pregnancy, and live birth outcomes.

Apart from its influence on reproductive disorders, the gut microbiome is also said to influence every organ in the body, one such influence is on the bidirectional link of the gut–brain axis (GBA) connecting the central nervous system (CNS) and GIT [ 19 ]. These connections can be neuronal, endocrine, immune, or humoral [ 20 ]. The gut bacteria produce short‐chain fatty acids (SCFA), which stimulate the release of signaling molecules (brain gut peptides) from the GIT, like the GLP‐1, Ghrelin, and YY peptide [ 21 ]. Among them, Ghrelin regulates the hypothalamic regulatory nucleus and luteinizing hormone secretion (LH), causing delays in its release and pulse intensity, inhibiting excessive LH surges [ 22 ]. In an RCT by Kluge et al., Ghrelin administration significantly suppressed the number of LH pulses, as it decreased from 5.46 ± 1.33 mIU/min·mL(placebo) to 4.01 ± 1.37 mIU/min·mLl(ghrelin) ( p  = 0.007). Though these findings are consistent with ghrelin having an inhibitory effect on LH, however inclusion of healthy women ( n  = 6) limits the generalizability to infertile populations, and also the role of dysbiosis in ghrelin‐mediated LH surge remains inconclusive, as exogenous ghrelin was administered [ 23 ]. In chronic cases of gut dysbiosis, due to the release of SCFAs, there is stimulation of the hypothalamic‐pituitary‐adrenal (HPA) axis via brain‐gut peptides, leading to increased cortisol levels. While elevated levels of cortisol are shown to cause impaired signaling of GnRH neurons and the pituitary gonadotrophs, the direct relation between dysbiosis and GBA, thus impacting infertility, requires further exploration [ 24 , 25 ]. Dysbiosis can even act as a contributing factor for pain and inflammation, especially in disorders like endometriosis [ 26 ]. An altered gut microbiome is often associated with an increase in gram‐negative bacteria, causing elevation of lipopolysaccharides (LPS) [ 27 ], which aggravate pain via nociceptive receptors and inflammation via release of proinflammatory cytokines like IL‐1, 8, 33, NF‐κB, and TNF‐α, especially in the progressive states of endometriosis [ 28 , 29 ]. These cytokines activate a protective inflammatory reflex via (afferent nerves) [ 30 ]. Consequently, an imbalance of the gut microbiome may result in the dysregulation of this vagus nerve‐mediated inflammatory reflex, contributing to inflammatory disorders like endometriosis, infertility, and chronic pain [ 26 , 31 ]. Further research is required to clearly establish the role of the vagus nerve in modulating inflammation, specifically in the context of disorders causing infertility.

Infertility in women is often overlooked, and it deeply affects them physically, mentally, and emotionally. A qualitative study by Hasanpoor‐Azghdy et al. revealed that there were devastating effects on the mental health of women suffering from infertility [ 1 ]. According to the WHO, infertility is classified as either primary or secondary. Primary infertility refers to those who never attained pregnancy, and secondary infertility applies to those who have at least one prior pregnancy [ 2 ]. Globally, around 2% of women aged 20–44 were never able to have a live birth (primary infertility), and around 11% were unable to have an additional birth (secondary infertility). The prevalence rates of infertility range from 7.3% to 9.1% in women of 15–34 years of age and it has increased to 25% in women aged 35–40 years, higher rates of infertility are observed in Eastern Europe, North Africa, and the Middle East [ 3 ] and the causes of infertility can be multifactorial including ovulatory failures, PCOS, endometriosis, menstrual irregularities, and endocrine abnormalities (like thyroid, estrogen imbalance etc.) [ 4 ]. While the biological factors are well documented, emerging research suggests gut dysbiosis can be a potential contributor to female infertility. In this review, an attempt is made to understand this relation.

The lead author, Amogh Verma, affirms that this manuscript is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned (and, if relevant, registered) have been explained.

The authors declare no conflicts of interest.