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Review Deciphering the diet-inflammatory bowel disease relationship: knowledge gaps and future perspectives
Arshdeep Singh1orcid, Arshia Bhardwaj1orcid, Vandana Midha2orcid, Ajit Sood1orcid

DOI: https://doi.org/10.5217/ir.2025.00278
Published online: March 4, 2026

1Department of Gastroenterology, Dayanand Medical College and Hospital, Ludhiana, India

2Department of Internal Medicine, Dayanand Medical College and Hospital, Ludhiana, India

Correspondence to Ajit Sood, Department of Gastroenterology, Dayanand Medical College, Tagore Nagar, Ludhiana, Punjab 141001, India. E-mail: dr_ajit_sood@dmch.edu
• Received: November 5, 2025   • Revised: December 23, 2025   • Accepted: December 28, 2025

© 2026 Korean Association for the Study of Intestinal Diseases.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Diet is increasingly recognized not as a passive exposure but as a dynamic determinant of inflammatory bowel disease (IBD) pathogenesis, progression, and treatment response. This review article redefines diet as a multidimensional modifier acting through complex interactions with genetics, microbiota, intestinal barrier function, and environmental exposures. Beyond nutrient composition, we highlight how age, sex, habitual diet, cooking methods, contaminants, and lifestyle collectively shape disease trajectories. We also identify key research priorities: incorporation of long-term, mechanistically anchored trials; development of digital, biomarker-informed dietary assessment tools; and integration of polygenic, microbial, and metabolic data to inform individualized therapy. Emerging evidence also calls for culturally tailored and patient-centered frameworks that ensure real-world adherence and equity in dietary interventions. Reframing diet as a biological, behavioral, and environmental nexus shifts it from the periphery to the forefront of IBD care, transforming it from a confounder in research to a therapeutic frontier in clinical practice.
  • Keywords: Dietary patterns; Gastrointestinal microbiome; Inflammation; Inflammatory bowel diseases; Nutrition assessment
Diet is increasingly being recognized as a multifaceted determinant in the pathogenesis, clinical course, treatment, and potential prevention of inflammatory bowel disease (IBD) [1]. Over the past two decades, dietary exposures have emerged not only as modifiable environmental risk factors but also as therapeutic targets of growing scientific and clinical relevance [2]. Epidemiological studies consistently link Westernized dietary patterns, characterized by high intake of saturated fats, refined sugars, and ultra-processed foods, with an increased incidence of IBD. Conversely, dietary patterns enriched in fruits, vegetables, fiber, and omega-3 fatty acids have been associated with potential protective effects. Yet, these associations are neither definitive nor uniform across populations [3]. Dietary exposures are complex and dynamic, shaped by cultural practices, cooking methods, socioeconomic determinants, and food availability [4]. Equally critical are the intricate interactions of diet with host factors, including age, genetics, the gut microbiome, intestinal barrier integrity, and immune regulation [5,6]. These complexities highlight the need to consider diet not as a single, isolated exposure but as an integral modifier of disease. Given these intricacies, there is a pressing need to refine conceptual and methodological frameworks for studying diet in IBD. The following sections outline perspectives on mechanistic insights and central themes for advancing diet-based research and interventions in IBD.
References for this review were identified through a comprehensive search of PubMed, Embase and Scopus databases using the search terms “diet,” “nutrition,” “dietary pattern,” “microbiome,” “intestinal barrier,” and “inflammatory bowel disease” (including “ulcerative colitis” and “Crohn’s disease”) for articles published between January 2000 and August 2025. Additional references were obtained from manual searches of bibliographies of relevant articles and the authors’ personal reference archives. Only articles published in English were considered. Preference was given to original research articles, systematic reviews, meta-analyses, and landmark mechanistic studies that contributed to understanding the role of diet in the pathogenesis, modulation, and management of IBD. Studies examining diet-microbiota interactions, host genetic and metabolic modifiers, and the influence of environmental and lifestyle factors were prioritized. The final reference list was compiled based on the originality, methodological rigor, and relevance of each article to the central themes of this review, including mechanistic insights, current knowledge gaps, and emerging frameworks for precision nutrition in IBD.
Diet is a central regulator of gut homeostasis through coordinated effects on the gut microbiota, intestinal epithelium, immune system, and neuroimmune networks. Habitual dietary patterns shape microbial diversity and stability, influencing the production of key metabolites such as short-chain fatty acids (SCFAs), secondary bile acids, and indoles. SCFAs, particularly butyrate, support epithelial energy metabolism, reinforce tight junctions, maintain the mucus barrier, and preserve a hypoxic luminal environment favorable to barrier function [7]. Diet also modulates immune homeostasis by promoting regulatory T-cell differentiation, interleukin (IL)-10 signaling, and aryl hydrocarbon receptor–dependent IL-22 production, thereby enhancing mucosal tolerance and epithelial repair [8]. In parallel, dietary inputs influence mitochondrial function, oxidative stress responses, and metabolic programming of epithelial and immune cells [9,10]. Diet-microbiota interactions further affect the enteric nervous system, shaping motility and neuroimmune communication [11].
Diet influences the development and progression of IBD through two interrelated but distinct mechanistic pathways: direct effects on host epithelial and immune function and indirect effects mediated through alterations in the gut microbiota and its metabolic outputs (Table 1) [12]. While these pathways are biologically interconnected, distinguishing them conceptually enhances mechanistic clarity and provides a framework for understanding how specific dietary components and patterns contribute to intestinal inflammation.
1. Direct Dietary Effects on the Intestinal Epithelium and Immune System
Dietary fiber increases SCFA production, which supports epithelial proliferation, tight junction stability, mucus secretion, and immune homeostasis [13,14]. Similarly, amino acids generate bioactive metabolites that reinforce barrier function [15]. Conversely, excessive protein intake can be detrimental as toxic metabolites such as ammonia, phenols, and hydrogen sulfide, can impair epithelial function and potentially exacerbate colitis [16,17]. Refined carbohydrates and simple sugars also compromise barrier integrity [18,19]. Experimental data suggest that fructose reduces expression of tight junction proteins (occludin, ZO-1) and antimicrobial peptides [20]. Primary bile acids such as cholic acid, chenodeoxycholic acid, and ursodeoxycholic acid help maintain epithelial integrity and regulate immune responses through activation of bile acid receptors, including farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) [21-23]. High dietary salt intake has been shown to directly modulate host immunity by reducing regulatory T cell populations and promoting pro-inflammatory Th17 (T helper 17) responses [24]. These observations highlight that diet can directly shape epithelial barrier resilience and immune balance, independent of microbial intermediates.
2. Dietary Effects Mediated by Microbiota and Microbial Metabolites
Dietary fiber exerts a protective effect on the gut microbiota by selectively enriching saccharolytic and SCFA-producing bacteria, including Faecalibacterium prausnitzii, Roseburia, and Bifidobacterium, while suppressing the overgrowth of pathobionts and enhancing microbial diversity [25-28]. High-fat diets reshape microbial composition by reducing beneficial taxa such as Akkermansia muciniphila, enriching sulfate-reducing bacteria, and promoting expansion of Bilophila wadsworthia, a pathobiont linked to bile acid-driven inflammation and barrier disruption [29,30]. Dietary modulation of bile acid pools represents another key microbiota-mediated mechanism. Microbial conversion of primary bile acids into secondary bile acids, such as deoxycholic acid and lithocholic acid, can exert detergent-like toxicity, disrupt junctional proteins, induce epithelial apoptosis, and promote inflammation when present in excess [21-23]. In addition, food additives—particularly emulsifiers such as carboxymethylcellulose and polysorbate-80—have been shown in animal models to alter the structure of the microbial community, promote bacterial encroachment into the mucus layer, and induce chronic low-grade inflammation [46]. Excessive intake of refined sugars and simple carbohydrates reduces microbial diversity, decreases SCFA-producing taxa, and promotes the expansion of facultative anaerobes, including members of Proteobacteria [36,37]. Dietary modulation of indole signaling is another microbiota-mediated pathway linking diet to intestinal homeostasis and inflammation. Indoles are produced from dietary tryptophan by gut bacteria (e.g., Lactobacillus, Clostridium, Bacteroides), with plant-based, fiber-rich diets enhancing—and Westernized diets reducing—their production. Microbiota-derived indoles activate the aryl hydrocarbon receptor on epithelial and immune cells, strengthening barrier integrity via tight junction and IL-22–mediated antimicrobial responses while promoting mucosal immune tolerance through regulation of innate lymphoid cells and regulatory T cells [47,48].
Together, these mechanistic insights underscore the biological plausibility of diet as a modulator of intestinal inflammation in IBD. However, translating these pathways into clinically actionable knowledge remains challenging. These challenges directly lead into the key gaps that persist in our understanding of diet-IBD relationships.
1. CD and UC Are Not the Same
Crohn’s disease (CD) and ulcerative colitis (UC) differ in their pathophysiology, anatomical involvement, and interactions with diet [49]. Dietary influences appear more pronounced in CD, where early-life exposures such as low fiber intake and early formula feeding, along with consumption of processed foods and emulsifiers, have been associated with increased disease risk and progression [49-51]. Dietary interventions in CD, including exclusive enteral nutrition (EEN) and the Crohn’s disease exclusion diet (CDED), administered with or without partial enteral nutrition (PEN), have demonstrated efficacy in inducing clinical remission [52-55]. Accordingly, the European Crohn’s and Colitis Organisation (ECCO) recommends EEN as an induction therapy for patients with mild-to-moderate CD [56]. A systematic review of 14 studies involving 564 participants demonstrated that PEN combined with CDED achieved the highest clinical remission rates and superior tolerability compared with PEN alone or EEN [57]. Other solid food-based dietary approaches, such as the Mediterranean diet and symptom-guided or reduced refined carbohydrate diets, have also shown potential benefit, although the supporting evidence is limited by small sample sizes and methodological heterogeneity [57,58]. Reflecting this therapeutic relevance, recent ECCO guidelines emphasize that all patients with CD should have access to specialized dietary advice, particularly during disease flares [56].
In contrast, dietary risk factors and therapeutic effects in UC are less consistent and more heterogeneous [59]. Observational studies have not shown a clear overall association between pro-inflammatory diets and UC risk, with discrepant findings across study designs. The total dietary fiber intake does not appear to be significantly associated with disease risk [60]. Interventional studies suggest that dietary modification may improve symptoms, quality of life, and inflammatory markers—particularly in active disease—but effects on sustained clinical remission remain inconsistent [61,62]. Combined Mediterranean and low-fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (low-FODMAP) diets, with or without PEN, have been associated with reductions in disease activity indices, high-sensitivity C-reactive protein, fecal calprotectin, and favorable modulation of the gut microbiota, alongside improvements in quality of life [63]. Current consensus-based guidance for UC emphasizes reducing saturated fats, red and processed meats, and food additives, while increasing intake of omega-3 fatty acids, tryptophan, pectin, and resistant starch. However, despite encouraging symptomatic benefits, consistent translation into durable clinical remission remains uncertain [62,64,65].
Taken together, the available evidence indicates that although dietary risk factors have been investigated in both CD and UC, findings are more robust and actionable in CD. In CD, diet-based interventions can induce remission and serve as effective primary or adjunctive therapies, whereas in UC, dietary strategies currently function mainly as supportive measures that ameliorate symptoms, inflammatory burden, and quality of life rather than as reliable disease-modifying treatments. These divergent responses highlight the importance of phenotype-specific dietary approaches that reflect the distinct biological and immunological underpinnings of CD and UC.
2. Age-Related Modifiers
Age is a key determinant of dietary exposures and eating behaviors, influencing both nutritional quality and disease susceptibility, and may partly explain age-specific epidemiological patterns observed in IBD [66]. In infancy and early childhood, dietary intake is largely dictated by breastfeeding or formula feeding, followed by caregiver-directed complementary feeding. Adolescence and young adulthood are characterized by greater dietary autonomy, often accompanied by higher consumption of ultra-processed foods, fast foods, and sugar-sweetened beverages—patterns that coincide with the peak incidence of IBD. In contrast, middle-aged adults generally adopt more structured and balanced diets, shaped by occupational demands, family responsibilities, and increasing health awareness. In older adults, dietary diversity often declines due to physiological, medical, and social constraints, including reduced appetite, altered taste and smell, dental issues, polypharmacy, limited mobility, cognitive decline, and social isolation, leading to more monotonous habitual diets.
Ageing is also associated with structural and functional changes in the gastrointestinal tract, including increased intestinal permeability, altered motility, small intestinal bacterial overgrowth, and chronic low-grade inflammation (“inflammaging”), all of which modify diet-microbiota-host interactions [67,68]. Microbial diversity generally declines with age, alongside shifts in key taxa and weakening of protective mechanisms such as gastric acid secretion, bile flow, mucus production, and antimicrobial peptide activity.
From an epidemiological perspective, these patterns may partly account for the high incidence of IBD among young adults, in contrast to the relatively lower incidence observed in elderly populations, despite an overall rise in prevalence attributable to improved survival. Consequently, age groups should not be considered homogeneous in dietary IBD research, and age-specific dietary exposures must be accounted for in risk assessment and intervention design.
3. Sex and Hormonal Differences
Sex-specific hormonal and metabolic profiles modulate nutrient handling, gut physiology, and IBD susceptibility [69,70]. Estrogen and progesterone in women have been shown to enhance epithelial barrier integrity, reduce endoplasmic reticulum stress, and suppress pro-inflammatory cytokine production, effects that are complemented by sex-related differences in gut microbial composition. In contrast, testosterone is associated with distinct microbial signatures and metabolic effects in men and women, reflecting complex hormone–microbiota interactions [71]. Sex differences also extend to energy metabolism and adipose tissue distribution. Women typically exhibit lower basal fat and protein oxidation and differential amino acid metabolism, whereas men accumulate more visceral adiposity and display higher postprandial free fatty acid flux [72]. These metabolic and microbial differences influence epithelial barrier function and immune activation, shaping diet-microbiome interactions relevant to IBD pathogenesis. Incorporating sex-specific biological differences into dietary research and therapeutic strategies is therefore essential for personalized and mechanistically informed IBD care.
4. Host Genetics
Genetic predisposition shapes individual responses to dietary exposures [73,74]. Polygenic risk variants can modify inflammatory responses to specific nutrients [75]. Polygenic risk scores, which integrate the cumulative burden of both risk and protective alleles, help explain why two individuals with similar diets may have divergent outcomes. For example, FUT2 secretor status has been linked to differences in gut microbial composition and mucosal glycosylation, where protective alleles may support a more favorable microbial environment despite exposure to pro-inflammatory diets [76]. Similarly, variants in genes such as HNF4A, which regulates epithelial barrier function, or IL23R, which modulates immune signaling, may reduce inflammatory responses triggered by dietary antigens [77,78]. Thus, while a diet high in processed foods, emulsifiers, or saturated fats may accelerate dysbiosis and mucosal injury in genetically susceptible individuals, those with protective variants may preserve epithelial integrity and immune balance, remaining resilient. Genetic background also interacts with metabolic phenotype to influence the fermentation of dietary nutrients by the gut microbiota [79-81]. This interaction determines not only the efficiency of nutrient utilization but also the spectrum of microbial metabolites produced [82]. Importantly, these metabolic outputs are also influenced by sex-specific hormonal milieu. Such genotype-phenotype-diet interactions may therefore contribute to inter-individual variability in susceptibility to colonic inflammation and disease behavior.
5. Habitual Diet Needs Characterization
The effects of diet on the gut microbiota and intestinal epithelial barrier are inherently transient unless dietary exposures are sustained over time. Consequently, habitual dietary intake represents a critical determinant in both the design and interpretation of dietary intervention studies. The physiological, metabolic, and inflammatory consequences of diet are shaped not only by individual nutrients but also by the habitual combinations in which foods are consumed, as nutrients are rarely ingested in isolation. Long-term dietary patterns, therefore, exert cumulative effects on microbial composition, immune regulation, and epithelial barrier integrity, providing a more ecologically valid reflection of real-world eating behaviors [83,84]. For example, habitual consumption of vegetables alongside red meat may attenuate the pro-inflammatory effects of meat through fiber, polyphenols, and micronutrients that favorably modulate the gut microbiota and immune responses, whereas regular intake of red meat in combination with refined carbohydrates may synergistically promote dysbiosis, impair barrier function, and amplify inflammatory pathways. Accordingly, systematic assessment of habitual dietary patterns allows classification into pro- or anti-inflammatory profiles and offers a more mechanistic and integrative understanding of diet-gut interactions than analyses focused on isolated dietary components. However, it is also important to recognize that habitual diet may also be heterogeneous and shaped by multiple contextual factors, including cultural practices, geographic region, socioeconomic status, religious beliefs, and access to healthcare and nutritional counselling [85]. This variability further extends to food processing techniques, additive exposure, cooking methods, and meal timing. In the context of IBD, this heterogeneity is further compounded by frequent experimentation with exclusion diets, alternative eating patterns, and clinician-recommended modifications, resulting in substantial inter- and intra-individual variability over time. Collectively, these sources of heterogeneity limit comparability across studies and contribute to inconsistent or conflicting findings.
6. Cooking Methods
Cooking and food preparation methods modify nutrient availability and metabolic impact. To illustrate, consider the example of boiled potatoes and fries. Both originate from the same raw ingredient, yet differences in cooking techniques yield distinct biochemical and physiological effects. Boiling potatoes preserves heat-sensitive nutrients and resistant starch, promoting SCFA production, whereas frying generates advanced glycation end products, increases fat content, and may favor pro-inflammatory gut microbiota [86,87]. Thus, even identical raw ingredients can exert markedly different physiological and gut-related effects depending on preparation. Careful consideration and characterization of the mode of food preparation is hence critical when evaluating diet-microbiome interactions, as foods that appear superficially similar may elicit divergent biochemical and physiological effects.
7. Lifestyle
Lifestyle behaviors, including physical activity levels, interact with dietary patterns to influence gut health. Regular physical activity has been linked to increased microbial diversity and the abundance of Bifidobacterium and Lactobacillus [88]. Conversely, a sedentary lifestyle can lead to reduced microbial diversity and an overrepresentation of pro-inflammatory taxa, potentially increasing the risk of IBD. Additionally, eating patterns, including meal timing, frequency, and context, significantly influence gut physiology. Overeating or late-night snacking can disrupt circadian rhythms of the gastrointestinal tract, impair gastric emptying, and alter hormone secretion, including ghrelin and leptin [89,90]. Irregular meal spacing has been associated with altered gut microbiota composition and decreased microbial diversity [91]. Brain-gut interactions further modulate digestive efficiency. Distracted eating, such as watching television or using digital devices, can impair sensory perception, reduce mastication efficiency, and modify postprandial hormonal responses, thereby affecting nutrient absorption and satiety signaling [92-94]. Also, regular consumption of meals outside the home, even when selecting ostensibly “healthy” options, introduces variability in cooking methods, processing, salt, sugar, and additive content, which can influence the gut microbial activity and intestinal barrier integrity.
8. Environmental Contaminants
Dietary exposures are increasingly shaped by environmental contaminants and chemical adulterants. Pollutants, including organic compounds, heavy metals, and pesticides, can accumulate in food, promoting systemic inflammation. The widespread use of pesticides has contributed to intensified food production; however, exposure to specific pesticides has been associated with an elevated risk of IBD [95,96]. While dietary recommendations for IBD often advocate a shift from a Western diet to a Mediterranean dietary pattern, evidence from a randomized controlled trial indicates that transitioning to a Mediterranean diet can be associated with increased exposure to insecticides, organophosphates, and pyrethroids [97]. Thus, even with adoption of a nutritionally favorable dietary pattern, concomitant pesticide exposure may attenuate its health benefits. Food adulteration represents an additional concern; for example, turmeric/curcumin products in Bangladesh have been reported to contain lead, thereby compromising nutritional safety [98]. Chronic exposure to such contaminants can modulate gut health, influence disease susceptibility, and potentially alter disease progression.
9. Drug-Diet Interactions
Pharmacologic therapies in IBD, including corticosteroids, immunosuppressants, biologics, and small molecules, can indirectly influence the gut microbiota and modulate host-microbe interactions with dietary substrates through their effects on immune signaling and epithelial barrier integrity. This interplay generates complex, bidirectional interactions in which specific nutrients may potentiate or attenuate drug effects, while pharmacologic agents may in turn alter the host response to dietary components [99,100].
10. Functional Attributes of Dietary Components
Dietary composition, particularly high intake of sugar, salt, and ultra-processed foods, has been consistently associated with adverse outcomes. However, notable paradoxes challenge simplistic assumptions regarding processed foods. Enteral nutrition therapies, including EEN and PEN, are highly processed formulations yet demonstrate therapeutic benefits, especially in CD. These processed formulations are designed to optimize nutrient composition, reduce dietary antigens, and modulate the gut microbiome in a manner that suppresses inflammation. This contrast indicates that the health impact of processed foods is context-dependent, influenced by nutrient quality, bioactive components, and the physiological goals of the intervention. Additionally, these observations suggest that labelling foods simply as “processed” may be overly reductive. Instead, the functional and compositional attributes, such as macronutrient balance, fiber content, micronutrient adequacy, and absence of harmful additives, determine the net effect on gut health and disease risk.
11. Patient Preferences and Socio-Cultural Impacts
The implementation and effectiveness of dietary interventions in IBD are influenced by patient preferences and socio-cultural factors. Adherence remains the cornerstone of success of dietary interventions and is shaped by a complex interplay of taste preferences, habitual food patterns, socioeconomic status, and cultural or religious beliefs. These determinants not only influence dietary acceptance but also affect the sustainability and real-world applicability of interventions [4,101,102]. Despite a global nutrition transition that has led to partial homogenization of food cultures, distinct regional dietary identities persist. These regional variations present additional challenges to the universal application of dietary strategies. The Mediterranean and CDED require adaptation for vegetarian populations. In contrast, plant-based and anti-inflammatory diets align more closely with Asian dietary traditions but necessitate dietary counselling to ensure adequate protein, iron, and vitamin B12 intake [103,104]. Religion, a fundamental element of culture, further shapes dietary behavior through prescribed food restrictions and fasting practices, thereby influencing nutritional outcomes and intervention feasibility. Therefore, the design of dietary interventions in IBD should incorporate culturally sensitive, economically feasible, and locally tailored frameworks, as these considerations are essential for enhancing patient adherence and ultimately optimizing therapeutic outcomes.
1. Lack of Long-Term Studies
Despite increasing interest in dietary interventions for IBD, there remains a notable paucity of long-term studies evaluating their efficacy, safety, and sustainability. Most existing studies assessing induction of remission have follow-up periods of 4 to 24 weeks, whereas studies evaluating maintenance of remission typically span 1–2 years [58]. While these medium-term studies provide preliminary insights into the potential benefits of specific dietary approaches, they are insufficient to address critical questions regarding sustained effects and long-term feasibility. Dietary interventions represent a continuous exposure that must be maintained over the lifespan to exert meaningful influence on disease trajectory. Short- to medium-term studies cannot fully capture the cumulative impact of diet on relapse rates, nutritional status, gut microbiome composition, or systemic inflammatory processes. Moreover, adherence to dietary interventions is often heterogeneous, yet compliance is infrequently assessed in a systematic manner. Equally important, the outcomes following withdrawal of dietary interventions are poorly reported, leaving the durability of observed benefits uncertain. There is a clear need for well-designed, long-term studies that not only evaluate clinical endpoints but also systematically monitor patient adherence, nutritional adequacy, and quality of life. Incorporating mechanistic analyses, including gut microbiota profiling and metabolomics, will be essential to elucidate the pathways through which dietary exposures modulate disease pathophysiology.
2. Lack of Comparator Diets
In studies assessing dietary interventions for IBD, a major methodological limitation is the lack of a standardized “Western diet” control arm. The Western diet is widely implicated in promoting gut dysbiosis and inflammation. However, when dietary interventions, such as the Mediterranean diet, specific carbohydrate diet, or low-FODMAP diets, are compared directly against each other without this common reference point, it becomes unclear whether observed outcomes reflect true therapeutic benefit, differential efficacy, or simply the absence of harm [105]. In such cases, the statement that “the compared diets were equally effective or equally ineffective” highlights an interpretive gap rather than true equivalence.
3. Limitations of Dietary Assessment Tools
A comprehensive understanding of diet-gut interactions in IBD requires not only the acknowledgment of contextual factors influencing dietary exposures but also the development of precise and multidimensional tools to assess them. Environmental, cultural, socioeconomic, and behavioral determinants shape dietary habits; however, these subtleties are rarely captured by conventional dietary assessment methodologies [106]. Existing instruments, such as food frequency questionnaires and short-term dietary recalls, were originally developed for use in general populations and often fail to adequately reflect the complex, disease-specific dietary behaviors observed in IBD. These self-reported tools are susceptible to recall bias and frequently overlook critical modifiers, including methods of food processing, combinations of food items, portion sizes, meal timing, and temporal variations linked to disease activity or treatment phases [107]. This heterogeneity is amplified by variability in food processing, additive exposure, and nutrient composition. Also, their limited assessment windows restrict the evaluation of long-term dietary patterns and cumulative nutritional exposures. Many studies also inadequately adjust for key confounders such as age, total caloric intake, comorbid conditions, and sex-specific factors. Furthermore, while mechanistic insights into diet-barrier interactions have predominantly emerged from preclinical studies, robust clinical evidence substantiating barrier modulation through dietary interventions in IBD remains scarce.
4. IBD-Specific Sources of Bias
Dietary influences on IBD encompass a broad spectrum of effects, which can differ depending on the stage of disease. It is important to distinguish between factors that contribute to the risk of disease onset and those that affect disease exacerbation or progression. Factors influencing disease onset are those that may predispose an otherwise healthy individual to develop IBD. These include habitual dietary patterns. In contrast, factors affecting disease exacerbation pertain to triggers that influence the course of disease in patients who already have IBD. These may include specific foods, dietary additives, or patterns that provoke inflammation, alter gut microbial activity, or compromise barrier function, leading to flares or symptom worsening. It is therefore important that the diet studies in IBD clearly differentiate these two contexts to guide targeted nutritional strategies for prevention and disease management.
Despite extensive patient-reported data, the specific dietary triggers that precipitate flares in IBD remain incompletely understood. Surveys and studies examining dietary beliefs among patients commonly identify foods such as spicy items, high-fat or fried foods, dairy, red and processed meats, sugary drinks, alcohol, and certain high-fiber foods (including raw vegetables, nuts, seeds, and legumes) as potential exacerbating factors [108]. However, the scientific basis for these associations remains unclear, and in many cases, these attributions reflect patient perceptions rather than rigorously established causal relationships.
Another challenge in elucidating diet-IBD relationships is the influence of disease activity on dietary behavior, which introduces a risk of reverse causality. During disease flares, patients frequently modify or restrict their diet in an effort to alleviate symptoms such as abdominal pain, diarrhea, and bloating [109]. As a result, observed associations between dietary patterns and disease outcomes may reflect symptom-driven dietary changes rather than true causal effects of diet on disease activity. This limitation is particularly relevant in observational studies, where dietary intake is often assessed after disease onset and/or during periods of active inflammation. Furthermore, symptom-related food avoidance may vary between CD and UC, across disease phenotypes, and within the same individual over time, further complicating interpretation of exposure-outcome relationships. Inadequate consideration of disease activity, timing of dietary assessment, and prior dietary modifications may therefore lead to spurious associations or underestimation of beneficial dietary effects, hindering the ability to distinguish habitual dietary patterns from reactive dietary behavior. In addition, under-reporting of dietary intake may be more pronounced among patients with active IBD. Individuals may inadvertently forget, omit, or deliberately under-report foods consumed irregularly or in small quantities. Foods perceived as socially undesirable or “unhealthy” are also more likely to be selectively under-reported. Such differential reporting can introduce systematic bias into dietary assessments. Beyond general nutritional epidemiology challenges, evaluation of diet in IBD is also likely to be affected by medication use (e.g., corticosteroids, biologics), prior surgeries, and psychosocial factors such as anxiety around food. These factors can independently influence appetite, metabolism, and dietary choices, confounding observed associations between diet and outcomes. Failure to account for these IBD-specific biases may obscure true dietary effects.
Addressing the complexities of the role of diet in IBD requires a comprehensive, multi-pronged approach that integrates robust study design, advanced methodological tools, technological innovation, and patient-centered strategies (Fig. 1). A critical first step involves recognizing and evaluating beyond nutrient composition and dietary patterns to include host-specific variables such as age, sex, genetics, and disease phenotype, lifestyle factors (e.g., physical activity, sleep, circadian alignment), cooking practices and level of food processing. Environmental safety factors, including exposure to contaminants and food adulterants, should also be considered. While each of these factors independently associates with the risk of IBD development, their combined influence is not merely additive; rather, the effect of each factor is modified by complex interactions within the overall biological and environmental context (Fig. 2). Integrating digital, biological, and situational data sources is likely to offer a more comprehensive view of dietary exposures. This requires enhancing the dietary assessment methods. Smartphone-based food logs, photographic meal tracking, and ecological momentary assessments can provide real-time monitoring with minimal recall bias [110-112]. When combined with wearable sensors, these tools contextualize dietary intake within broader lifestyle behaviors, including activity, sleep, and stress patterns [113,114]. Objective biomarkers, such as metabolomic, lipidomic, and isotopic tracers, along with Absorption, Distribution, Metabolism, and Elimination (ADME)-based pharmacokinetic frameworks, can further enhance precision by reflecting actual nutrient absorption, metabolism, and host-microbiota interactions [115-119]. Coupling these measurements with multi-omic datasets (microbiome, transcriptome, epigenome, metabolome) will also enable mechanistic insights into how diet modulates mucosal inflammation and disease activity.
Long-term, pragmatic clinical trials are equally essential. Many existing dietary studies are short-term, limiting their ability to evaluate sustainability, nutritional adequacy, quality of life, or patient-reported outcomes. Trials with extended follow-up, systematic adherence monitoring, and adaptive designs that incorporate early mechanistic readouts, such as SCFA production, microbiome shifts, and epithelial barrier markers, can refine interventions iteratively. Comparing dietary interventions against region-specific pro-inflammatory diets, defined and validated through national dietary surveys and inflammatory indices, is essential for generating meaningful and interpretable cross-intervention outcomes. Personalized dietary interventions represent the next frontier in the management of IBD. Integrating factors such as disease phenotype, age, sex, genetic background, and habitual dietary patterns enables the implementation of precision nutrition strategies tailored to individual biological profiles rather than population-level averages. The incorporation of polygenic risk scores, microbial signatures, and metabolic phenotyping may further refine dietary prescriptions, enhancing efficacy while minimizing unnecessary dietary restrictions [119,120]. Accordingly, individuals with pro-inflammatory dietary patterns may derive the greatest benefit from targeted modulation, whereas those adhering to balanced diets may require only subtle adjustments to sustain remission.
Patient-centered implementation is essential for the real-world success of dietary interventions in IBD. Effective strategies must account for taste preferences, cultural practices, socioeconomic factors, and dietary habits, including vegetarian or vegan patterns. Aligning interventions with local dietary norms and ethical or religious considerations enhances both adherence and ecological validity [101]. Additionally, participatory meal planning and co-design of interventions can improve both feasibility and long-term sustainability. Finally, interdisciplinary collaboration is fundamental. Bringing together gastroenterologists, dietitians, microbiologists, geneticists, behavioral scientists, and technologists allows a holistic evaluation of diet-IBD interactions, bridging mechanistic understanding with practical implementation to optimize therapeutic outcomes. Fig. 3 illustrates the proposed conceptual evolution of approaches to studying diet in IBD, representing a continuum that progresses from simplistic analyses integrating dietary factors, the microbiome, and the immune system to a comprehensive, holistic framework that enables precision nutrition.
Diet cannot be implicated in the pathogenesis of IBD in isolation as it is unlikely to act as a direct causative factor, but it exerts a significant modulatory influence through its intricate interactions with host genetics, gut microbiota, immune signaling, and other environmental exposures. The influence of diet on disease activity and mucosal healing also appears to vary with age, sex, and habitual dietary practices. Therefore, rather than serving as a passive background variable, diet represents a dynamic determinant that shapes disease susceptibility, progression, and response to therapy. Understanding the diet-gut axis in IBD thus necessitates an integrative, systems-level perspective that unites epidemiology, mechanistic biology, and clinical nutrition. Future research must move beyond descriptive associations toward informed, data-driven frameworks that capture the complexity of real-world dietary exposures. Harmonizing digital dietary tracking, biomarker-based measures, and contextual variables will be key to decoding how diet functions as both a trigger and a therapeutic tool. Precision nutrition, tailored to individual genetic and microbial signatures, represents the most promising direction for advancing personalized care in IBD.

Funding Source

The authors received no financial support for the research, authorship, and/or publication of this article.

Conflict of Interest

Sood A has received honoraria for speaker events from Pfizer India and Takeda India and serves on the editorial board of this journal. He was not involved in the peer review, evaluation, or decision-making process for this manuscript. The other authors declare no conflicts of interest.

Data Availability Statement

Data sharing is not applicable to this article as no new data were created or analyzed in this study.

Author Contributions

Conceptualization: Singh A, Sood A. Data curation: Singh A, Bhardwaj A. Investigation: Sood A. Methodology: Singh A, Midha V, Sood A. Resources: Singh A, Bhardwaj A, Sood A. Supervision: Sood A. Validation: Singh A, Bhardwaj A, Midha V, Sood A. Visualization: Singh A, Bhardwaj A, Midha V, Sood A. Writing–original draft: Singh A. Writing–review & editing: Singh A, Bhardwaj A, Midha V, Sood A. Approval of final manuscript: all authors.

Fig. 1.
Challenges and potential solutions in addressing the complexities of comprehensively evaluating the role of diet in inflammatory bowel disease.
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Fig. 2.
Multifactorial determinants influencing dietary assessment and inflammatory bowel disease (IBD) risk. This figure presents a conceptual overview of the multiple, interrelated factors that influence how diet is assessed and interpreted in IBD. Individual rows depict key domains each represented along a gradient from lower (yellow) to higher (red) potential influence or risk. (A) Dietary patterns, ranging from early-life feeding to processed food exposure to balanced and traditional diets. (B) Cooking practices, including boiling, steaming, frying, grilling, and high-temperature methods that may alter nutrient composition and food-derived bioactives. (C) Physical activity spectrum, from active lifestyles to sedentary behavior. (D) Disease-related factors, including IBD phenotype, disease extent, medications, and complications, which modify dietary tolerance and interpretation. (E) Age across the life course, reflecting developmental, hormonal, and physiological differences in dietary response. (F) Sex-related differences, encompassing biological and hormonal influences on immune responses and metabolism. (G) Genetic susceptibility, illustrating the spectrum from low to high inherited risk affecting host-diet-microbiome interactions. Rather than acting in isolation, these factors overlap and interact in real-world settings. When considered together, these highlight the complex, context-dependent, and synergistic nature of diet-IBD relationships, highlighting why simplistic, single-factor models are insufficient to capture true dietary effects in IBD.
ir-2025-00278f2.jpg
Fig. 3.
Conceptual continuum in approaches to studying diet in inflammatory bowel disease (IBD). The figure depicts the progression from simplistic models focusing on linear interactions between diet, the gut microbiome, and immune responses to a holistic precision nutrition framework. Along this continuum, key host modifiers—including age, sex, and genetic susceptibility—are incorporated. At the holistic end, all elements of the simplistic model are considered together with host modifiers within an integrated system that supports precision nutrition, incorporating improved dietary assessment, personalized interventions, and ongoing monitoring and feedback, while accounting for disease phenotype, adherence, and multidisciplinary care.
ir-2025-00278f3.jpg
Table 1.
Dietary Components and Their Host-Direct and Microbiota-Mediated Effects Relevant to Inflammatory Bowel Disease
Dietary component Direct effects on host Microbiota-mediated effects Evidence Alignment with dietary patterns
Dietary fiber [25-28] Strengthens tight junctions; increases mucus production; reduces epithelial permeability; promotes anti-inflammatory immune signaling Increases microbial diversity; enriches SCFA (butyrate)–producing taxa; promotes Treg differentiation and epithelial energy metabolism Animal studies, human cohort studies, mechanistic studies Emphasized in Mediterranean and plant-based diets; variable in SCD; selectively emphasized in CDED
High-fat diet [29,31] Disrupts barrier integrity; increases epithelial stress and endotoxemia; activates innate immune pathways Reduces microbial diversity; increases bile-tolerant pathobionts (e.g., Bilophila); alters bile acid profiles leading to Th1/Th17 skewing Animal studies, human observational data Prominent in Westernized diets; discouraged in Mediterranean, plant-based, SCD, and CDED
Red/Processed meat [32] Increases epithelial oxidative stress; generates toxic luminal metabolites; promotes pro-inflammatory immune activation Enhances proteolytic fermentation; increases hydrogen sulfide (H2S) and ammonia; expands pro-inflammatory taxa Animal studies, human clinical trials and epidemiologic data, mechanistic studies Characteristic of Westernized diets; limited in Mediterranean diets; restricted in CDED
Lean meat (fish, poultry) [32] Neutral effects on epithelial barrier; lower oxidative stress compared with red meat Reduced proteolytic fermentation; fewer toxic microbial metabolites compared with red meat Animal studies, human clinical trials and epidemiologic data, mechanistic studies Core protein sources in Mediterranean diet (fish, poultry); allowed in CDED; permitted in SCD
Plant protein [33] Supports immune homeostasis and epithelial healing Preferential saccharolytic fermentation; increased SCFA production; reduced harmful proteolytic metabolites Moderate evidence (cohort studies and mechanistic data) Emphasized in Mediterranean and plant-based diets; encouraged in CDED; variably limited in SCD depending on source
Plant-based diet [34,35] Improves epithelial repair; reduces mucosal inflammation; enhances barrier function Increases bacterial diversity; increases SCFA production; reduces pathobionts; promotes favorable immune–microbe interactions Human clinical trials and observational studies Core principle of plant-based diets; strong alignment with Mediterranean diet; partial overlap with CDED
Sugar (refined) [36,37] Increases intestinal permeability; induces epithelial stress; promotes low-grade inflammation Reduces microbial diversity; decreases SCFA production; promotes dysbiosis and expansion of facultative anaerobes Animal studies, human epidemiologic data, mechanistic studies Abundant in Westernized diets; restricted in Mediterranean, plant-based, SCD, and CDED
Salt (high sodium) [38,39] Promotes Th17 polarization; disrupts epithelial immune balance; reduces tight junction protein expression; decreases goblet cell mucopolysaccharide production Reduces beneficial taxa (e.g., Lactobacillus); alters Firmicutes/Bacteroidetes ratio; amplifies pro-inflammatory immune responses Animal studies, mechanistic studies Common in Westernized diets; limited in Mediterranean, plant-based, and CDED
Artificial sweeteners [40,41] Disrupt epithelial tight junctions and signaling; induce immune dysregulation Promote dysbiosis; alter microbial metabolites; impair glucose tolerance via microbiota Animal studies, mechanistic studies, human epidemiologic data Common in Westernized diets; excluded in SCD and CDED; discouraged in Mediterranean diet
Food additives and emulsifiers [42-45] Disrupt mucus layer; increase epithelial permeability; activate innate immune responses Promote mucolytic bacteria; induce bacterial encroachment; enhance inflammatory signaling; promote growth of adherent-invasive Escherichia coli Animal studies, mechanistic studies, human epidemiologic data, human clinical trials Abundant in ultra-processed foods; excluded in SCD and CDED; minimized in Mediterranean diet

SCFA, short-chain fatty acid; Treg, regulatory T cell; SCD, specific carbohydrate diet; CDED, Crohn’s disease exclusion diet; Th1/Th17, T helper 1/T helper 17 cells.

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      Deciphering the diet-inflammatory bowel disease relationship: knowledge gaps and future perspectives
      Image Image Image
      Fig. 1. Challenges and potential solutions in addressing the complexities of comprehensively evaluating the role of diet in inflammatory bowel disease.
      Fig. 2. Multifactorial determinants influencing dietary assessment and inflammatory bowel disease (IBD) risk. This figure presents a conceptual overview of the multiple, interrelated factors that influence how diet is assessed and interpreted in IBD. Individual rows depict key domains each represented along a gradient from lower (yellow) to higher (red) potential influence or risk. (A) Dietary patterns, ranging from early-life feeding to processed food exposure to balanced and traditional diets. (B) Cooking practices, including boiling, steaming, frying, grilling, and high-temperature methods that may alter nutrient composition and food-derived bioactives. (C) Physical activity spectrum, from active lifestyles to sedentary behavior. (D) Disease-related factors, including IBD phenotype, disease extent, medications, and complications, which modify dietary tolerance and interpretation. (E) Age across the life course, reflecting developmental, hormonal, and physiological differences in dietary response. (F) Sex-related differences, encompassing biological and hormonal influences on immune responses and metabolism. (G) Genetic susceptibility, illustrating the spectrum from low to high inherited risk affecting host-diet-microbiome interactions. Rather than acting in isolation, these factors overlap and interact in real-world settings. When considered together, these highlight the complex, context-dependent, and synergistic nature of diet-IBD relationships, highlighting why simplistic, single-factor models are insufficient to capture true dietary effects in IBD.
      Fig. 3. Conceptual continuum in approaches to studying diet in inflammatory bowel disease (IBD). The figure depicts the progression from simplistic models focusing on linear interactions between diet, the gut microbiome, and immune responses to a holistic precision nutrition framework. Along this continuum, key host modifiers—including age, sex, and genetic susceptibility—are incorporated. At the holistic end, all elements of the simplistic model are considered together with host modifiers within an integrated system that supports precision nutrition, incorporating improved dietary assessment, personalized interventions, and ongoing monitoring and feedback, while accounting for disease phenotype, adherence, and multidisciplinary care.

      Fig. 1.

      Fig. 2.

      Fig. 3.

      Deciphering the diet-inflammatory bowel disease relationship: knowledge gaps and future perspectives
      Dietary component Direct effects on host Microbiota-mediated effects Evidence Alignment with dietary patterns
      Dietary fiber [25-28] Strengthens tight junctions; increases mucus production; reduces epithelial permeability; promotes anti-inflammatory immune signaling Increases microbial diversity; enriches SCFA (butyrate)–producing taxa; promotes Treg differentiation and epithelial energy metabolism Animal studies, human cohort studies, mechanistic studies Emphasized in Mediterranean and plant-based diets; variable in SCD; selectively emphasized in CDED
      High-fat diet [29,31] Disrupts barrier integrity; increases epithelial stress and endotoxemia; activates innate immune pathways Reduces microbial diversity; increases bile-tolerant pathobionts (e.g., Bilophila); alters bile acid profiles leading to Th1/Th17 skewing Animal studies, human observational data Prominent in Westernized diets; discouraged in Mediterranean, plant-based, SCD, and CDED
      Red/Processed meat [32] Increases epithelial oxidative stress; generates toxic luminal metabolites; promotes pro-inflammatory immune activation Enhances proteolytic fermentation; increases hydrogen sulfide (H2S) and ammonia; expands pro-inflammatory taxa Animal studies, human clinical trials and epidemiologic data, mechanistic studies Characteristic of Westernized diets; limited in Mediterranean diets; restricted in CDED
      Lean meat (fish, poultry) [32] Neutral effects on epithelial barrier; lower oxidative stress compared with red meat Reduced proteolytic fermentation; fewer toxic microbial metabolites compared with red meat Animal studies, human clinical trials and epidemiologic data, mechanistic studies Core protein sources in Mediterranean diet (fish, poultry); allowed in CDED; permitted in SCD
      Plant protein [33] Supports immune homeostasis and epithelial healing Preferential saccharolytic fermentation; increased SCFA production; reduced harmful proteolytic metabolites Moderate evidence (cohort studies and mechanistic data) Emphasized in Mediterranean and plant-based diets; encouraged in CDED; variably limited in SCD depending on source
      Plant-based diet [34,35] Improves epithelial repair; reduces mucosal inflammation; enhances barrier function Increases bacterial diversity; increases SCFA production; reduces pathobionts; promotes favorable immune–microbe interactions Human clinical trials and observational studies Core principle of plant-based diets; strong alignment with Mediterranean diet; partial overlap with CDED
      Sugar (refined) [36,37] Increases intestinal permeability; induces epithelial stress; promotes low-grade inflammation Reduces microbial diversity; decreases SCFA production; promotes dysbiosis and expansion of facultative anaerobes Animal studies, human epidemiologic data, mechanistic studies Abundant in Westernized diets; restricted in Mediterranean, plant-based, SCD, and CDED
      Salt (high sodium) [38,39] Promotes Th17 polarization; disrupts epithelial immune balance; reduces tight junction protein expression; decreases goblet cell mucopolysaccharide production Reduces beneficial taxa (e.g., Lactobacillus); alters Firmicutes/Bacteroidetes ratio; amplifies pro-inflammatory immune responses Animal studies, mechanistic studies Common in Westernized diets; limited in Mediterranean, plant-based, and CDED
      Artificial sweeteners [40,41] Disrupt epithelial tight junctions and signaling; induce immune dysregulation Promote dysbiosis; alter microbial metabolites; impair glucose tolerance via microbiota Animal studies, mechanistic studies, human epidemiologic data Common in Westernized diets; excluded in SCD and CDED; discouraged in Mediterranean diet
      Food additives and emulsifiers [42-45] Disrupt mucus layer; increase epithelial permeability; activate innate immune responses Promote mucolytic bacteria; induce bacterial encroachment; enhance inflammatory signaling; promote growth of adherent-invasive Escherichia coli Animal studies, mechanistic studies, human epidemiologic data, human clinical trials Abundant in ultra-processed foods; excluded in SCD and CDED; minimized in Mediterranean diet
      Table 1. Dietary Components and Their Host-Direct and Microbiota-Mediated Effects Relevant to Inflammatory Bowel Disease

      SCFA, short-chain fatty acid; Treg, regulatory T cell; SCD, specific carbohydrate diet; CDED, Crohn’s disease exclusion diet; Th1/Th17, T helper 1/T helper 17 cells.

      Table 1.

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