This comprehensive review delves into the evolving landscape of nutrition's role in Inflammatory Bowel Disease (IBD), while incorporating transformative insights from the recently published American Gastroenterology Association (AGA) clinical practice update (CPU) on diet in IBD. Recent years have witnessed a paradigm shift, recognizing diet not only as an influencer in disease development but also as a disease-modifying factor and treatment avenue for IBD. The AGA CPU endorses a balanced Mediterranean-style diet, emphasizing the need for personalized recommendations tailored to individual patient characteristics, including disease course, surgical history, and pharmacotherapy. The implementation of complex nutritional strategies necessitates the involvement of both gastroenterologists and registered dietitians. Guidance for patients and caregivers is available through organizations such as Crohn's and Colitis Canada and Crohn's and Colitis Foundation. While animal models offer valuable insights, the review underscores their limitations in replicating the complexity of IBD biology observed in humans. It advocates for an exploration of nutrigenomics, utilizing molecular tools to analyze how diet-derived bioactive compounds influence gene expression for precision nutrition insights. Practical challenges in dietary intervention studies, including regional variations and complexities in food handling, require attention for enhanced comparability. Limited data exist on combined dietary and medical therapies, but promising outcomes suggest potential synergies. Precision treatments could develop through an understanding of the function of particular food metabolites in influencing inflammation. The objective of this review is to offer a summary of the present comprehension of diet, serving as both a potential factor contributing to and a therapeutic avenue for IBD. Clinical Trial Registration: This study is not a part of a clinical trial.

Vitamin D is considered as a potential immunomodulator in inflammatory bowel disease development; however, emerging evidence remains inconsistent. We aimed to investigate prospective association between serum vitamin D level and long-term risk of elderly-onset inflammatory bowel disease in a large-scale cohort.

Participants without inflammatory bowel disease at enrollment from the UK Biobank were included. Baseline blood samples were collected and serum 25-hydroxyvitamin D (25(OH)D) levels were measured. Participants were classified as vitamin D deficiency (<50 nmol/L), insufficiency (50-75 nmol/L) or sufficiency (≥75 nmol/L) based on predefined cutoffs. Primary outcome was incident elderly-onset inflammatory bowel disease, including ulcerative colitis and Crohn's disease. Hazard ratio (HR) and 95% confidence intervals (CIs) of related associations were determined using multivariable Cox regression.

Among 357,656 participants (mean age, 57.9±6.9 years), 196,499 (54.9%) and 121,035 (33.8%) had vitamin D deficiency and insufficiency, respectively. During median 13.3 years' follow-up, 1,622 elderly-onset inflammatory bowel disease cases were identified. Compared with vitamin D sufficiency, no associations with vitamin D deficiency (HR=0.91, 95%CI: 0.78-1.07) or insufficiency (HR=0.86, 95%CI: 0.73-1.01) were observed for elderly-onset inflammatory bowel disease. Similarly, no associations with per 10 nmol/L increase of serum 25(OH)D were detected for elderly-onset inflammatory bowel disease (HR=1.00, 95%CI: 0.98-1.03), ulcerative colitis (HR=1.00, 95%CI: 0.97-1.03) or Crohn's disease (HR=1.01, 95%CI: 0.97-1.05). Compared with the lowest quartile, no associations with higher quartiles of serum 25(OH)D were observed for inflammatory bowel disease (HRQ4VSQ1=1.03, 95%CI: 0.89-1.19), ulcerative colitis (HRQ4VSQ1=1.06, 95%CI: 0.90-1.26) or Crohn's disease (HRQ4VSQ1=0.93, 95%CI: 0.73-1.20). Further sensitivity and subgroup analyses demonstrated similar results.

Serum vitamin D level or deficiency status is not associated the development of elderly-onset inflammatory bowel disease, ulcerative colitis or Crohn's disease.

Vitamin D deficiency is common in Paediatric Inflammatory Bowel Disease (PIBD) and has been implicated in disease pathogenesis and disease exacerbation. Current guidelines recommend oral vitamin D supplementation when 25OHD levels are below 50 nmol/L. Supplementation comes in two forms: either a daily supplement of a low dose of vitamin D3 (2000 IU) for several months or a single high dose of oral vitamin D3-termed 'stoss' therapy, with no consensus regarding optimum treatment.

A randomised controlled trial was conducted in children with a prior diagnosis of PIBD with 25OHD deficiency (< 50 nmol/L), comparing 2000 IU oral D3 daily to a stoss protocol (oral D3 dosage 400,000 IU for 3-12 years of age or 800,000 IU for > 12 years). Children were followed for 12 months, with biochemistry (25OHD, calcium, magnesium, phosphate, parathyroid hormone, haemoglobin, haematocrit, platelets, albumin), stool markers (calprotectin, S100A12), anthropometrics (weight, height, body mass index) as well as clinical disease indices (Paediatric Crohn's Disease Activity Index, Paediatric Ulcerative Colitis Activity Index) and medication use collected at 3, 6, 9 and 12 months.

74 children aged 5-18 years completed the study. Both 2000 IU daily and stoss protocol significantly increased 25OHD from baseline values at 3, 6, 9 and 12 months. One patient randomised to stoss protocol had a 25OHD level of 263 nmol/L with normal serum calcium. There was no difference in biochemical, stool or clinical markers between groups at any time point, nor was there any correlation between 25OHD level and calprotectin or 25OHD level and clinical disease activity scores.

Stoss protocol was non-inferior to 2000 IU daily vitamin D3 in raising 25OHD levels at 12 months. There was also no difference between 25OHD levels at 3, 6 and 9 months between groups.

The pandemic of obesity preceded global spread of Inflammatory Bowel diseases by almost 2 decades. A pathogenic relationship has been described between obesity and inflammatory bowel diseases, but Crohn`s disease may be selectively impacted. The role of diet in pathogenesis has also gained significant support in the last few decades. This review explores dietary relationships to account for epidemiological observations. Quantifiable indices for diets have been described including a glycemic index, inflammatory indices and levels of food processing. Meta-analyses have been published which examine each for effects on obesity and co-morbidities as well as Crohn's disease and ulcerative colitis. This review suggests that ultra-processed foods provide the best link between obesity and Crohn's disease explaining epidemiological observations. However, the other 2 types of dietary indices likely contribute to ulcerative colitis as well as to co-morbidities related to both obesity and inflammatory bowel diseases. The term ultra-processed foods cover a large number of additives and extensive work is needed to define individual or combined harmful effects. Furthermore, the interactions among the 3 main indices need clarification in order to precisely apply therapeutic diets to both diseases (obesity and inflammatory bowel disease).

The inhibitory effects of the tumor necrosis factor-α (TNF-α) antibody infliximab (IFX) on colitis are well established. Since IFX dosing is weight-based and associated with various side effects, there is a growing interest in identifying combination therapies that can enhance its efficacy, particularly in overweight inflammatory bowel disease (IBD) patients, to maximize the anti-inflammatory effect while minimizing the required dose. Our research revealed that overweight IBD patients present decreased vitamin D levels in the intestinal epithelium alongside elevated TNF-α levels. In mice fed a high-fat diet (HFD) for four weeks, treatment with the vitamin D analog palicalcitol (PAL) reduced lipid synthesis and TNF-α production in intestinal epithelial cells (IECs). In a 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced experimental colitis model, PAL treatment mitigated TNF-α-induced damage to the intestinal epithelial barrier and reduced the activation of Th1 and Th17 cells in the lamina propria, thereby reducing colitis development in HFD-fed mice. Notably, the combination of IFX and PAL was more effective than IFX alone in treating colitis in these mice. Overall, our findings suggest that vitamin D inhibits TNF-α production by reducing lipid synthesis in IECs, thereby enhancing IFX therapy in overweight IBD patients.

Endometriosis is a prevalent chronic gynaecological disorder, but its cause is still unclear, and both genetic and environmental factors may contribute disease aetiology. Prominent amongst the latter is vitamin D which can be obtained either by the action of sunlight on skin or from dietary sources. Serum levels of the main circulating form of vitamin D, 25-hydroxvitamin D (25(OH)D), have been reported to be inversely correlated with endometriosis, suggesting that vitamin D-deficiency may be a risk factor for the disease. Crucially, the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25(OH)2D) is known to exert many functions beyond its established role in the endocrinology of mineral homoeostasis and prevention of rickets. Several of these extra-skeletal effects of 1,25(OH)2D may impact the risk and progression of endometriosis. The following review details the studies that have assessed associations between vitamin D status/supplementation and endometriosis severity and disease progression, but also describes the mechanistic targets for 1,25(OH)2D in endometriosis with specific reference to immunomodulatory responses and effects on angiogenesis. Endometriosis is an under-reported health issue with poor non-invasive options for diagnosis. Given that vitamin D-deficiency may trigger or exacerbate key pathophysiological responses linked to endometriosis, analysis of vitamin D status in women may provide an alternative risk marker for endometriosis. Treatment options for endometriosis are also limited and the review will also consider whether vitamin D supplementation has a role in the management of endometriosis, either in prevention or treatment.

The incidence of inflammatory bowel disease (IBD) is increasing worldwide. Dietary patterns may be associated with odds of this disease. Although previous reviews have attempted to summarize the evidence in this field, the growing body of investigations prompted us to conduct an updated comprehensive systematic review.

We used the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines to evaluate the association between dietary patterns before disease onset and the risk of IBD. PubMed, SCOPUS, and Web of Science were searched using structured keywords up to November 20, 2023.

Twenty-four publications (13 case-control, 1 nested case-control, and 10 cohort studies) were included in this review. The sample size of these studies ranged from 181 to 482 887 subjects. The findings were inconsistent across the included studies, showing inverse, direct, or no association between different dietary patterns and the risk of IBD.

This review provides comprehensive data on the link between dietary patterns prior to IBD diagnosis and risk of this condition. The explicit finding of present review is the extent gap in our knowledge in this field. Therefore, large-scale, high-quality studies are warranted to improve our understanding of the relationship between dietary patterns and IBD risk.

In Graves' disease (GD), an autoimmune disease, antibodies targeting the thyroid stimulating hormone (TSH) receptor cause the production of excessive amounts of thyroid hormone. A significant association was reported between low 25-hydroxy [25(OH)] vitamin D3 (VitD) levels and various autoimmune disorders. Therefore, this study aimed to investigate the effects of VitD deficiency and replacement therapy on laboratory and clinical parameters in GD patients.

Forty GD patients and 37 healthy controls were included in this study. The GD patients were divided into two groups: the nonreplacement group was administered antithyroid treatment only (n = 18), and the replacement group was administered antithyroid treatment + VitD replacement (n = 22). Clinical and laboratory data of all the participants were compared at the time of diagnosis and 3 months after treatment.

Baseline serum VitD levels in the GD patients were significantly lower than the baseline serum VitD levels in the control group (16.1 ± 9.9 vs. 22.2 ± 8.5 ng/mL, p < 0.005). A significant improvement was observed in the serum VitD levels in the replacement group after three months (14.6 ± 8.3 vs. 40.4 ± 17.2 ng/mL, p < 0.001). A significant increase in the serum TSH levels and a significant decrease in the serum free triiodothyronine (fT3) and free thyroxine (fT4) levels were observed in the replacement and nonreplacement groups at the end of three months. However, there was no significant effect of VitD replacement on the serum TSH, fT3, and fT4 levels. There was no difference in the serum thyroid receptor antibodies levels between the replacement and nonreplacement groups.

Although VitD deficiency was detected in the GD patients, there was no significant accelerating effect of VitD replacement on the thyroid hormone levels. These results need to be confirmed with studies that have larger patient numbers and longer follow-up periods.

This editorial builds on the article by Shakhshir et al. We conducted an overview of evidence-based dietary interventions in adults with inflammatory bowel disease (IBD). In the IBD population, there may be a role for the Mediterranean diet due to its anti-inflammatory effects, long-term sustainability, and role in improving cardiovascular health. In active Crohn's disease, the use of exclusive enteral nutrition, the Crohn's disease exclusion diet, or the specific carbohydrate diet may be used as a short-term adjunct to medical therapy and may improve mucosal healing. The low-FODMAP diet can assist in reducing symptoms for patients without evidence of active bowel inflammation. As interest in nutritional therapy increases amongst clinicians and patients alike, it is integral that dietary therapies are understood and discussed in routine management of patients with IBD as part of holistic care, ideally through a multidisciplinary setting with involvement of experienced dietitians. This serves to improve clinician-patient engagement and reduce complications of IBD including micro and micronutrient deficiencies.

Patients with inflammatory bowel disease (IBD) are more likely to be confirmed with vitamin D deficiency. However, the association between inflammation and vitamin D remains unclear. The purpose of this study was to evaluate the association between inflammation and vitamin D in hospitalized patients with IBD.

All the participants were recruited from one teaching hospital from June 2018 to October 2022. Inflammation was evaluated by serum concentration of C-reactive protein (CRP), using an immunoturbidimetric method at admission. We further divided the participants into five groups based on serum CRP levels: <5, 5-9.9, 10-19.9, 20-39.9, and >40mg/L. Serum 25-hydroxy-vitamin D (25-(OH)-D) was assessed by liquid chromatography tandem mass spectrometry. Addi-tional information, including age, sex, body mass index (BMI), IBD (ulcerative colitis vs. Crohn's disease) subtype, was abstracted from medical records.

This study included 1,989 patients with IBD (average age was 39.4 years, 33.8% of them were women, 1,365 CD and 624 UC patients). The median CRP was 5.49 mg/L (range of quartiles: 1.64~19.5 mg/L) and the prevalence of 25-(OH)-D deficiency was 69.8%. CRP was significantly associated with serum level of 25-(OH)-D. The difference in 25-(OH)-D was -4.28 ng/ml (-5.27 ng/ml, -3.31 ng/ml) between two extremist CRP groups after adjustment of potential covariates (age, sex, BMI, type of IBD, dietary type, season, and lymphocyte count). Subgroup analysis in sex, type of IBD, and age, were similar to the main analysis results.

There was a negative association between CRP levels and vitamin D in hospitalized patients with IBD.

Complementary and integrative health (CIH) approaches are increasingly popular among patients with gastrointestinal (GI) disorders. Whole person health has been identified as an important perspective in integrative health. While complementary approaches have been discussed in the GI literature, the whole person health framework has not yet been incorporated. Whole person health is particularly relevant as we shift to patient-centered care to facilitate holistic healing for this population. The aim of this paper is to apply a conceptualization of whole person health and its relevance in understanding how CIH approaches can be utilized for patients with stress-sensitive GI disorders, such as disorders of gut-brain interaction (DGBI) and inflammatory bowel disease (IBD).

Between July 2023 and December 2023 numerous major databases were reviewed to identify relevant articles for this narrative review. Keywords searched included (but not limited to) complementary alternative medicine, integrative medicine, DGBI, IBD, whole person health, and CIH categories (nutritional, mind-body, psychological). We limited our search to peer-reviewed English language articles. Studies were also cross-referenced to incorporate additional relevant studies.

This narrative review describes how to integrate CIH approaches with whole person health for patients with some of the most common stress-sensitive GI disorders, including DGBIs and IBD. In each section, we highlight how each domain of the whole person health framework (biological, behavioral, social, environmental) can be addressed through CIH approaches: psychological, mind-body practices, and nutritional.

The integration of CIH approaches into the treatment of GI disorders is a growing area of interest that holds promise for enhancing patient outcomes. The two concepts of CIH and whole person health are harmonizing, and their integration serves to support patients who are already using CIH approaches, and providers who can facilitate shared-decision-making and patient-centered care. While not exhaustive, this review demonstrates positive associations between the use of CIH and beneficial outcomes across all whole person health domains for patients with GI disorders.

Oral lichen planus (OLP) is a common, prevalent, immune-mediated, inflammatory disease affecting both the skin and oral mucosa and is considered one of the potentially malignant diseases. Since OLP is regarded as an immunologically mediated disease, some studies suggest the use of vitamin D (VD) for its management as it exhibits immune-modulatory, anti-inflammatory, and antimicrobial properties, as well as anti-proliferative, pro-differentiative, and anti-angiogenic effects. VD has demonstrated a suppressive effect on TH1 pro-inflammatory cytokines, including IFN-γ while augmenting the secretion of anti-inflammatory cytokines. At the same time, VD deficiency is a prevalent public issue. Therefore, the present study aimed to investigate the role of VD as an adjunct to steroids in the management of VD-deficient OLP patients as well as its inhibitory effect on IFN-γ through measurement of salivary and tissue IFN-γ levels in OLP patients.

A total of 40 patients with ulcerative or erythematous OLP, diagnosed according to the World Health Organization's (WHO) modified criteria for OLP, were randomly allocated into one of the two study groups to receive either systemic steroids in addition to VD supplements (Group A) or systemic steroids only (Group B). Blood samples were collected for the measurement of serum VD level (SVDL) using the enzyme-linked immunosorbent assay (ELISA) to involve only patients with VD deficiency or insufficiency (≤ 30 ng/ml). Clinical evaluation of the lesion involved objective signs and subjective symptoms. Also, changes in salivary and tissue INF-γ levels (in pg/mL and pg/mg, respectively) were determined using the ELISA technique. All parameters were measured at baseline and after 4 weeks of treatment. The clinical pharmacy team devised a checklist to record all team interventions. The interventions were categorized into six domains, including drug interactions and/or adverse reactions, medication dose issues, drug selection issues, support with medication history, patient-related concerns, and suggestions for dental medication.

After one month of treatment, a significantly greater number of patients in group A showed complete pain relief and resolution of clinical lesions, as well as a greater number of patients showing a reduction in the clinical severity of lesions than in group B (P = 0.005). Also, there was a statistically significant reduction in average VAS pain scores and clinical scores in group A compared to group B after 1 month of treatment (P = 0.001 and 0.002, respectively). Furthermore, there was a statistically significant greater reduction in salivary and tissue IFN-γ levels in group A than in group B (P ≤ 0.001 and 0.029, respectively) after 1 month of treatment.

Current evidence suggests a significant preventive and therapeutic role for VD as an adjunct to standard therapies indicated for OLP lesions. These protective and therapeutic functions are achieved through the suppressive effect of VD on pro-inflammatory cytokines, particularly IFN-γ. Also, salivary IFN-γ appears to be a valuable prognostic marker for monitoring the progression of OLP. In addition, the inter-professional collaboration between dentists and clinical pharmacists helped to deliver complete, patient-centered primary care and ensured the quality of the medications included in patient kits, thus improving patient treatment and management. Nevertheless, further studies with larger sample sizes, longer follow-ups, and standardized designs may still be needed.

Vitamin D deficiency is common in patients with inflammatory bowel disease (IBD). In this study, we aimed to evaluate the prevalence and risk factors of vitamin D deficiency in a Taiwanese IBD cohort. Vitamin D levels were checked in adult patients with IBD who were treated at Changhua Christian Hospital, a medical center in central Taiwan, from January 2017 to December 2023. The risk factors for vitamin D deficiency were evaluated. 106 adult IBD patients were included, including 20 patients with Crohn's disease and 86 with ulcerative colitis. The median age at diagnosis was 39.2 years. The mean vitamin D level was 22.2 ± 8 ng/mL. Forty-five patients (42.5%) had vitamin D deficiency (vitamin D level < 20 ng/mL). Comparing patients with normal vitamin D levels and those with vitamin D deficiency after multivariate adjustment, female sex and early age at diagnosis were identified as statistically significant risk factors. We found a prevalence of 42.5% of vitamin D deficiency in the Taiwanese IBD population. Understanding this issue is essential for teaching patients and doctors about vitamin D deficiency screening and improving patient outcomes.

Diet is an environmental exposure implicated in the development of inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC). Dietary therapy is also a tool for management of these conditions. Nutrition therapy for IBD has been shown to reduce intestinal inflammation, promote healing, and alleviate symptoms, as well as improve patients' nutrition status. Although the mechanisms of action of most nutrition therapies for IBD are not well understood, the diets are theorized to eliminate triggers for gut dysbiosis and mucosal immune dysfunction associated with the typical Western diet. Exclusive enteral nutrition and the Crohn's disease exclusion diet are increasingly being used as the primary treatment modality for the induction of remission and/or maintenance therapy in children, and in some adults, with CD. Several other diets, such as the Mediterranean diet, anti-inflammatory diet for IBD, and diets excluding gluten, FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols), lactose, or other compounds, may be helpful in symptom management in both CD and UC, though evidence for biochemical efficacy is limited. In this review, we discuss the role of diet components in IBD pathogenesis and examine diets currently used in the management of children and adults with IBD. We also address practical, psychosocial, and cultural considerations for dietary therapy across diverse populations.

Environmental factors play an important role in inflammatory bowel diseases (IBD; Crohn's disease, [CD], ulcerative colitis [UC]). As part of the Crohn's & Colitis Challenges 2024 agenda, the Environmental Triggers workgroup summarized the progress made in the field of environmental impact on IBD since the last Challenges cycle in this document. The workgroup identified 4 unmet gaps in this content area pertaining to 4 broad categories: (1) Epidemiology; (2) Exposomics and environmental measurement; (3) Biologic mechanisms; and (4) Interventions and Implementation. Within epidemiology, the biggest unmet gaps were in the study of environmental factors in understudied populations including racial and ethnic minority groups and in populations witnessing rapid rise in disease incidence globally. The workgroup also identified a lack of robust knowledge of how environmental factors may impact difference stages of the disease and for different disease-related end points. Leveraging existing cohorts and targeted new prospective studies were felt to be an important need for the field. The workgroup identified the limitations of traditional questionnaire-based assessment of environmental exposure and placed high priority on the identification of measurable biomarkers that can quantify cross-sectional and longitudinal environmental exposure. This would, in turn, allow for identifying the biologic mechanisms of influence of environmental factors on IBD and understand the heterogeneity in effect of such influences. Finally, the working group emphasized the importance of generating high-quality data on effective environmental modification on an individual and societal level, and the importance of scalable and sustainable methods to deliver such changes.

Diet is a modifiable risk factor for disease course and data over the past decade have emerged to indicate its role in Crohn's disease (CD) and ulcerative colitis (UC). However, literature is riddled with misinterpretation of data, often leading to unexpected or conflicting results. The key understanding is that causative factors in disease development do not always proceed to an opportunity to change disease course, once established. Here, we discuss the data on dietary influences in three distinct disease states for CD and UC-predisease, active disease and quiescent disease. We appraise the literature for how our dietary recommendations should be shaped to prevent disease development and if or how that differs for CD and UC induction therapy and maintenance therapy. In UC, principles of healthy eating are likely to play a role in all states of disease. Conversely, data linking dietary factors to CD prevention and treatment are paradoxical with the highest quality evidence for CD treatment being exclusive enteral nutrition, a lactose, gluten and fibre-free diet comprising solely of ultraprocessed food-all dietary factors that are not associated or inversely associated with CD prevention. High-quality evidence from dietary trials is much awaited to expand our understanding and ultimately lead our dietary recommendations for targeted patient populations.

Recent data suggest a potential pathophysiological link between inflammatory bowel disease (IBD) and multiple sclerosis (MS), two immune-mediated diseases both of which can have a significant impact on patients' quality of life. In the present manuscript, we investigate the association between IBD and MS in a German cohort of general practice patients. These results may have important implications for the screening and management of patients with IBD, as well as for further research into the pathophysiological mechanisms underlying both disorders.

4,934 individuals with IBD (11,140 with Crohn's disease (CD) and 13,794 with ulcerative colitis (UC)) as well as 24,934 propensity score matched individuals without IBD were identified from the Disease Analyzer database (IQVIA). A subsequent diagnosis of MS was analyzed as a function of IBD using Cox regression models.

After 10 years of follow-up, 0.9% and 0.7% of CD and UC patients but only 0.5% and 0.3% of matched non-IBD pairs were diagnosed with MS, respectively (pCD = 0.002 and pUC < 0.001). Both CD (HR: 2.09; 95% CI 1.28-3.39) and UC (HR: 2.35; 95% CI 1.47-3.78) were significantly associated with a subsequent MS diagnosis. Subgroup analysis revealed that the association between both CD and UC and MS was more pronounced among male patients.

The results of our analysis suggest a notable association between IBD and a subsequent MS diagnosis. These findings warrant further pathophysiological investigation and may have clinical implications for the screening of IBD patients in the future.

We assessed whether early-life diet quality and food intake frequencies were associated with subsequent IBD.

Prospectively recorded 1-year and 3-year questionnaires in children from the All Babies in Southeast Sweden and The Norwegian Mother, Father and Child Cohort Study were used to assess diet quality using a Healthy Eating Index and intake frequency of food groups. IBD was defined as >2 diagnoses in national patient registers. Cox regression yielded HRs adjusted (aHRs) for child's sex, parental IBD, origin, education level and maternal comorbidities. Cohort-specific results were pooled using a random-effects model.

During 1 304 433 person-years of follow-up, we followed 81 280 participants from birth through childhood and adolescence, whereof 307 were diagnosed with IBD. Compared with low diet quality, medium and high diet quality at 1 year of age were associated with a reduced risk of IBD (pooled aHR 0.75 (95% CI=0.58 to 0.98) and 0.75 (95% CI=0.56 to 1.00)). The pooled aHR per increase of category was 0.86 (0.74 to 0.99). Pooled aHR for children 1 year old with high versus low fish intake was 0.70 (95% CI=0.49 to 1.00) for IBD, and showed association with reduced risk of UC (pooled aHR=0.46; 95% CI=0.21, 0.99). Higher vegetable intake at 1 year was associated with a risk reduction in IBD. Intake of sugar-sweetened beverages was associated with an increased risk of IBD. Diet quality at 3 years was not associated with IBD.

In this Scandinavian birth cohort, high diet quality and fish intake in early life were associated with a reduced risk of IBD.

With the increasing age of the general population in developed countries, the management of several chronic diseases becomes more and more complex due to comorbidities. Some, especially inflammatory bowel diseases, formerly believed to belong to the young adult population, have now been recognized as being present at disease onset also in the ageing population, representing medical challenges different from those in the younger population. In the past few years, knowledge on this special older population has increased, changing initial beliefs concerning epidemiology and course of disease. In the present review, we addressed the most recent evidence concerning their current incidence compared with other age groups, their clinical course, potential risk factors for the development of late-onset IBDs, associated diseases, and cancer risk beyond therapy-related neoplasias.

Inflammatory bowel disease (IBD), mainly comprising ulcerative colitis and Crohn's disease, is a group of gradually progressive diseases bringing significant mental anguish and imposes serious economic burdens. Interplay of genetic, environmental, and immunological factors have been implicated in its pathogenesis. Nutrients, as crucial environmental determinants, mainly encompassing carbohydrates, fats, proteins, and micronutrients, are closely related to the pathogenesis and development of IBD. Nutrition is essential for maintaining the dynamic balance of intestinal eco-environments to ensure intestinal barrier and immune homeostasis, while this balance can be disrupted easily by maladjusted nutrition. Research has firmly established that nutrition has the potential to shape the composition and function of gut microbiota to affect the disease course. Unhealthy diet and eating disorders lead to gut microbiota dysbiosis and further destroy the function of intestinal barrier such as the disruption of membrane integrity and increased permeability, thereby triggering intestinal inflammation. Notably, appropriate nutritional interventions, such as the Mediterranean diet, can positively modulate intestinal microecology, which may provide a promising strategy for future IBD prevention. In this review, we provide insights into the interplay between nutrition and gut microbiota and its effects on IBD and present some previously overlooked lines of evidence regarding the role of derived metabolites in IBD processes, such as trimethylamine N-oxide and imidazole propionate. Furthermore, we provide some insights into reducing the risk of onset and exacerbation of IBD by modifying nutrition and discuss several outstanding challenges and opportunities for future study.

Vitamin D deficiency is a risk factor for developing multiple sclerosis (MS). However, the immune effects of vitamin D in people with MS are not well understood. We analyzed transcriptomic datasets generated by RNA sequencing of immune cell subsets (CD4+, CD8+ T cells, B cells, monocytes) from 33 healthy controls and 33 untreated MS cases. We utilized a traditional bioinformatic pipeline and weighted gene co-expression network analysis (WGCNA) to determine genes and pathways correlated with endogenous vitamin D. In controls, CD4+ and CD8+ T cells had 1079 and 1188 genes, respectively, whose expressions were correlated with plasma 25-hydroxyvitamin D level (P < 0.05). Functional enrichment analysis identified association with TNF-alpha and MAPK signaling. In CD4+ T cells of controls, vitamin D level was associated with expression levels of several genes proximal to multiple sclerosis risk loci (P = 0.01). Genes differentially associated with endogenous vitamin D by case-control status were enriched in TNF-alpha signaling via NF-κB. WGCNA suggested a blunted response to vitamin D in cases relative to controls. Collectively, our findings provide further evidence for the immune effects of vitamin D, and demonstrate a differential immune response to vitamin D in cases relative to controls, highlighting a possible mechanism contributing to MS pathophysiology.

Lactose intolerance (LI) and vitamin D deficiency (VDD) have been linked to inflammatory bowel disease (IBD). We conducted an observational study in 192 Chilean IBD patients to investigate the prevalence of a specific gene variant (LCT-13910 CC genotype) associated with LI and the prevalence of VDD/Vitamin D Receptor (VDR) gene variants. Blood samples were analyzed using Illumina's Infinium Global Screening Array. The LCT-13910 CC genotype was found in 61% of IBD patients, similar to Chilean Hispanic controls and lower than Chilean Amerindian controls. The frequency of the LCT-13910-C allele in Chilean IBD patients (0.79) was comparable to the general population and higher than Europeans (0.49). Regarding VDR and VDD variants, in our study, the rs12785878-GG variant was associated with an increased risk of IBD (OR = 2.64, CI = 1.61-4.32; p-value = 0.001). Sixty-one percent of the Chilean IBD cohort have a genetic predisposition to lactose malabsorption, and a significant proportion exhibit genetic variants associated with VDD/VDR. Screening for LI and VDD is crucial in this Latin American IBD population.

Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, are inflammatory diseases of the gastrointestinal tract. The incidence of IBD is increasing in minority populations; however, little is known about the epidemiology and disease characteristics of IBD in Black women.

Our study population included participants in the Black Women's Health Study. Diagnosis of IBD was self-reported through the biennial questionnaires starting at baseline in 1995. We estimated the incidence of IBD according to age and geographic region. A follow-up supplementary questionnaire was also sent to a subset of participants who reported diagnosis of IBD to evaluate the accuracy of self-reported diagnosis and to assess disease characteristics.

Through December 31, 2021, a total of 609 cases of IBD were reported, of which 142 were prevalent at baseline (prevalence, 0.24%), and 467 were incident (crude incidence rate, 33.2/100 000 person-years). The incidence of IBD was highest in the younger than 30 years age group and similar across geographic region. Among the participants who responded to the supplementary questionnaire, 57.1% had confirmed diagnosis of IBD.

In a large prospective cohort of US Black women, we found that the incidence of IBD was similar to previously published estimates in US White women. Future studies should focus on identifying risk factors for IBD in Black individuals in the United States.

Vitamin D possesses immunomodulatory properties and has been implicated in the pathogenesis and severity of inflammatory bowel disease (IBD). Animal studies and emerging epidemiological evidence have demonstrated an association between vitamin D deficiency and worse disease activity. However, the role of vitamin D for the treatment of IBD is unclear.

To evaluate the benefits and harms of vitamin D supplementation as a treatment for IBD.

We used standard, extensive Cochrane search methods. The latest search date was Jun 2023.

We included randomised controlled trials (RCTs) in people of all ages with active or inactive IBD comparing any dose of vitamin D with another dose of vitamin D, another intervention, placebo, or no intervention. We defined doses as: vitamin D (all doses), any-treatment-dose vitamin D (greater than 400 IU/day), high-treatment-dose vitamin D (greater than 1000 IU/day), low-treatment-dose vitamin D (400 IU/day to 1000 IU/day), and supplemental-dose vitamin D (less than 400 IU/day).

We used standard Cochrane methods. Our primary outcomes were 1. clinical response for people with active disease, 2. clinical relapse for people in remission, 3. quality of life, and 4. withdrawals due to adverse events. Our secondary outcomes were 5. disease activity at end of study, 6. normalisation of vitamin D levels at end of study, and 7. total serious adverse events. We used GRADE to assess certainty of evidence for each outcome.

We included 22 RCTs with 1874 participants. Study duration ranged from four to 52 weeks. Ten studies enroled people with Crohn's disease (CD), five enroled people with ulcerative colitis (UC), and seven enroled people with CD and people with UC. Seventeen studies included adults, three included children, and two included both. Four studies enroled people with active disease, six enroled people in remission, and 12 enroled both. We assessed each study for risk of bias across seven individual domains. Five studies were at low risk of bias across all seven domains. Ten studies were at unclear risk of bias in at least one domain but with no areas of high risk of bias. Seven studies were at high risk of bias for blinding of participants and assessors. Vitamin D (all doses) versus placebo or no treatment Thirteen studies compared vitamin D against placebo or no treatment. We could not draw any conclusions on clinical response for UC as the certainty of the evidence was very low (risk ratio (RR) 4.00, 95% confidence interval (CI) 1.51 to 10.57; 1 study, 60 participants). There were no data on CD. There may be fewer clinical relapses for IBD when using vitamin D compared to placebo or no treatment (RR 0.57, 95% CI 0.34 to 0.96; 3 studies, 310 participants). The certainty of the evidence was low. We could not draw any conclusions on quality of life for IBD (standardised mean difference (SMD) -0.13, 95% CI -3.10 to 2.83 (the SMD value indicates a negligent decrease in quality of life, and the corresponding CIs indicate that the effect can range from a large decrease to a large increase in quality of life); 2 studies, 243 participants) or withdrawals due to adverse events for IBD (RR 1.97, 95% CI 0.18 to 21.27; 12 studies, 1251 participants; note 11 studies reported withdrawals but recorded 0 events in both groups. Thus, the RR and CIs were calculated from 1 study rather than 12). The certainty of the evidence was very low. High-treatment-dose vitamin D versus low-treatment-dose vitamin D Five studies compared high treatment vitamin D doses against low treatment vitamin D doses. There were no data on clinical response. There may be no difference in clinical relapse for CD (RR 0.48, 95% CI 0.23 to 1.01; 1 study, 34 participants). The certainty of the evidence was low. We could not draw any conclusions on withdrawals due to adverse events for IBD as the certainty of the evidence was very low (RR 0.89, 95% CI 0.06 to 13.08; 3 studies, 104 participants; note 2 studies reported withdrawals but recorded 0 events in both groups. Thus, the RR and CIs were calculated from 1 study rather than 3). The data on quality of life and disease activity could not be meta-analysed, were of very low certainty, and no conclusions could be drawn. Any-treatment-dose vitamin D versus supplemental-dose vitamin D Four studies compared treatment doses of vitamin D against supplemental doses. There were no data on clinical response and relapse. There were no data on quality of life that could be meta-analysed. We could not draw any conclusions on withdrawals due to adverse events for IBD as the certainty of the evidence was very low (RR 3.09, 95% CI 0.13 to 73.17; 4 studies, 233 participants; note 3 studies reported withdrawals but recorded 0 events in both groups. Thus, the RR and CIs were calculated from 1 study rather than 4).

There may be fewer clinical relapses when comparing vitamin D with placebo, but we cannot draw any conclusions on differences in clinical response, quality of life, or withdrawals, due to very low-certainty evidence. When comparing high and low doses of vitamin D, there were no data for clinical response, but there may be no difference in relapse for CD. We cannot draw conclusions on the other outcomes due to very low certainty evidence. Finally, comparing vitamin D (all doses) to supplemental-dose vitamin D, there were no data on clinical relapse or response, and we could not draw conclusions on other outcomes due to very low certainty evidence or missing data. It is difficult to make any clear recommendations for future research on the basis of the findings of this review. Future studies must be clear on the baseline populations, the purpose of vitamin D treatment, and, therefore, study an appropriate dosing strategy. Stakeholders in the field may wish to reach consensus on such issues prior to new studies.

Crohn's disease (CD) is frequently associated with malnutrition, inflammation and a deficiency of vitamin D (VD) with the relationships between these symptoms being poorly defined. VD is a modulator of the immune system and is associated with the onset of CD and disease activity. The level of serum VD may have potential in the assessment of CD activity. This study aimed to evaluate the relationships between VD, nutritional status and inflammation, and to identify more accurate VD thresholds.

The study included 76 outpatients with CD diagnosed between October 2018 and October 2020 and 76 healthy volunteers. Levels of serum 25(OH)D and nutritional indicators, as well as biochemical and disease activity assessments, were conducted.

Patients with CD and healthy participants were found to differ significantly in their 25(OH)D levels as well in levels of nutritional and inflammatory indicators. The optimal VD cut-off value was found to be 46.81 nmol/L for CD development and 35.32 nmol/L for disease activity. Levels of 25(OH)D were correlated with both nutritional status and inflammation.

The VD level is likely to be a useful additional tool in the evaluation of CD patients and predicting the disease activity and clinical response. The VD level may relate both to the nutritional status and levels of inflammation in CD patients, and disease progression.

Inflammatory Bowel Disease (IBD) is a complex, chronic inflammatory condition affecting the gastrointestinal tract. IBD has been associated with a variety of neurologic manifestations including peripheral nerve involvement, increased risk of thrombotic, demyelinating and events. Furthermore, an evolving association between IBD and neurodegenerative disorders has been recognized, and early data suggests an increased risk of these disorders in patients diagnosed with IBD. The relationship between intestinal inflammatory disease and neuroinflammation is complex, but the bidirectional interaction between the brain-gut-microbiome axis is likely to play an important role in the pathogenesis of these disorders. Identification of common mechanisms and pathways will be key to developing potential therapies. In this review, we discuss the evolving interface between IBD and neurological conditions, with a focus on clinical, mechanistic, and potentially therapeutic implications.

Autophagy, a highly conserved cellular self-degradation pathway, has emerged with novel roles in the realms of immunity and inflammation. Genome-wide association studies have unveiled a correlation between genetic variations in autophagy-related genes and heightened susceptibility to autoimmune and inflammatory diseases. Subsequently, substantial progress has been made in unraveling the intricate involvement of autophagy in immunity and inflammation through functional studies. The autophagy pathway plays a crucial role in both innate and adaptive immunity, encompassing various key functions such as pathogen clearance, antigen processing and presentation, cytokine production, and lymphocyte differentiation and survival. Recent research has identified novel approaches in which the autophagy pathway and its associated proteins modulate the immune response, including noncanonical autophagy. This review provides an overview of the latest advancements in understanding the regulation of immunity and inflammation through autophagy. It summarizes the genetic associations between variants in autophagy-related genes and a range of autoimmune and inflammatory diseases, while also examining studies utilizing transgenic animal models to uncover the in vivo functions of autophagy. Furthermore, the review delves into the mechanisms by which autophagy dysregulation contributes to the development of three common autoimmune and inflammatory diseases and highlights the potential for autophagy-targeted therapies.

Vitamin D has a regulatory role in innate and adaptive immune processes. Previous studies have reported that low pretreatment vitamin D concentrations are associated with primary non-response (PNR) and non-remission to anti-TNF therapy. This study aimed to assess whether pretreatment 25-hydroxyvitamin D concentrations predicted PNR and non-remission to infliximab and adalimumab in patients with active luminal Crohn's disease.

25-Hydroxyvitamin D concentrations were measured in stored baseline samples from 659 infliximab- and 448 adalimumab-treated patients in the Personalised Anti-TNF Therapy in Crohn's disease (PANTS) study. Cut-offs for vitamin D were deficiency <25 nmol/L, insufficiency 25-50 nmol/L, and adequacy/sufficiency >50 nmol/L.

About 17.1% (189/1107; 95% CI, 15.0-19.4) and 47.7% (528/1107; 95% CI, 44.8-50.6) of patients had vitamin D deficiency and insufficiency, respectively. 22.2% (246/1107) of patients were receiving vitamin D supplementation. Multivariable analysis confirmed that sampling during non-summer months, South Asian ethnicity, lower serum albumin concentrations, and non-treatment with vitamin D supplementation were independently associated with lower vitamin D concentrations. Pretreatment vitamin D status did not predict response or remission to anti-TNF therapy at week 14 (infliximab P_pnr = .89, adalimumab P_pnr = .18) or non-remission at week 54 (infliximab P = .13, adalimumab P = .58). Vitamin D deficiency was, however, associated with a longer time to immunogenicity in patients treated with infliximab, but not adalimumab.

Vitamin D deficiency is common in patients with active Crohn's disease. Unlike previous studies, pretreatment vitamin D concentration did not predict PNR to anti-TNF treatment at week 14 or nonremission at week 54.

Vitamin D (VD) deficiency was reported to contribute to the progression of Crohn's disease (CD) and affect the prognosis of CD patients. This study investigated the role of serum VD, body mass index (BMI), and tumor necrosis factor alpha (TNF-α) in the diagnosis of Crohn's disease.

CD patients (n=76) and healthy subjects (n=76) were enrolled between May 2019 and December 2020. The serum 25-hydroxyvitamin D [25(OH)D] levels, BMI, and TNF-α levels, together with other biochemical parameters, were assessed before treatment. The diagnostic efficacy of the single and joint detection of serum 25(OH)D, BMI, and TNF-α was determined using receiver operating characteristic (ROC) curves.

The levels of 25(OH) D, BMI, and nutritional indicators, including hemoglobin, total protein, albumin, and high-density lipoprotein cholesterol, were much lower, and the TNF-α levels were much higher in the CD patients than in the healthy subjects (P<0.05 for all). The areas under the ROC curve for the single detection of 25(OH)D, BMI, and TNF-α were 0.887, 0.896, and 0.838, respectively, with the optimal cutoff values being 20.64 ng/mL, 19.77 kg/m², and 6.85 fmol/mL, respectively. The diagnostic efficacy of the joint detection of 25(OH)D, BMI, and TNF-α was the highest, with an area under the ROC curve of 0.988 (95%CI: 0.968-1.000).

The joint detection of 25(OH)D, TNF-α, and BMI showed high sensitivity, specificity, and accuracy in CD diagnosis; thus, it would be effective for the diagnosis of CD in clinical practice.

Vitamin D (VitD) deficiency has garnered significant attention in contemporary medical research. Although the canonical biological activity of VitD manifests itself mainly in the regulation of calcium-phosphorus metabolism, recent studies show that, thanks to the presence of numerous receptors, VitD may also play an important role in regulating the immune system. VitD deficiency has been demonstrated to impact autoimmune disease, coeliac disease, infections (including respiratory/COVID-19), and patients with cancer. Recent studies also show that VitD plays a significant role in autoimmune thyroid diseases (AITDs). Many studies have shown a correlation between low VitD levels and chronic autoimmune thyroiditis - Hashimoto thyroiditis (HT), Graves' disease (GD), and postpartum thyroiditis (PPT). This review article, therefore, describes the current state of knowledge on the role of VitD in AITDs, including HT, GD, and PTT.

Diet has a key role in the homeostasis of the gut microenvironment, influencing the microbiome, the gut barrier, host immunity and gut physiology. Yet, there is little information on the role of early diet in the onset of inflammatory gastrointestinal disorders later in life, especially in dogs. Therefore, the aim of the present cross-sectional, epidemiological study with longitudinal data, was to explore associations of companion dogs' early life diet style and food items with owner-reported chronic enteropathy (CE) incidence in later life. Food frequency questionnaire data from Finnish companion dogs was analyzed using principal component analysis and logistic regression. We found that feeding a non-processed meat-based diet and giving the dog human meal leftovers and table scraps during puppyhood (2-6 months) and adolescence (6-18 months) were protective against CE later in life. Especially raw bones and cartilage as well as leftovers and table scraps during puppyhood and adolescence, and berries during puppyhood were associated with less CE. In contrast, feeding an ultra-processed carbohydrate-based diet, namely dry dog food or "kibble" during puppyhood and adolescence, and rawhides during puppyhood were significant risk factors for CE later in life.

Evidence for antioxidants, minerals and vitamins in relation to the risk of Crohn's disease (CD) and ulcerative colitis (UC) is limited and inconsistent. This mendelian randomization (MR) study aimed to examine the causal associations of circulating levels of antioxidants, minerals and vitamins with CD and UC.

Single-nucleotide polymorphisms associated with antioxidants (beta-carotene, lycopene and uric acid), minerals (copper, calcium, iron, magnesium, phosphorus, zinc and selenium), and vitamins (folate, vitamins A, B6, B12, C, D, E and K1) were employed as instrumental variables. Genetic associations with CD and UC were extracted from the UK Biobank, the FinnGen study and the International Inflammatory Bowel Disease Genetics Consortium. The inverse variance weighted method and sensitivity analyses were performed.

Genetically predicted higher lycopene (OR = 0.94, 95% CI: 0.91-0.97), vitamins D (OR = 0.65, 95% CI: 0.54-0.79) and K1 (OR = 0.93, 95% CI: 0.90-0.97) levels were inversely associated with CD risk, whereas genetically predicted higher magnesium (OR = 1.53, 95% CI: 1.23-1.90) levels were positively associated with CD risk. Higher levels of genetically predicted lycopene (OR = 0.91, 95% CI: 0.88-0.95), phosphorus (OR = 0.69, 95% CI: 0.58-0.82), selenium (OR = 0.91, 95% CI: 0.85-0.97), zinc (OR = 0.91, 95% CI: 0.89-0.94), folate (OR = 0.71, 95% CI: 0.56-0.92) and vitamin E (OR = 0.78, 95% CI: 0.69-0.88) were associated with reduced UC risk, whereas genetically predicted high levels of calcium (OR = 1.46, 95% CI: 1.22-1.76) and magnesium (OR = 1.24, 95% CI: 1.03-1.49) were associated with increased risk of UC.

Our study provided evidence that circulating levels of antioxidants, minerals and vitamins might be causally linked to the development of IBD.

Nutrition is of paramount importance not only for healthy individuals, but all the more for the ones with pathologies interlinked with the diet. In that light, diet, when used accordingly can act in a protective manner in inflammatory bowel diseases. The interplay of diet and IBD is not thoroughly defined, and guidelines are a work in progress. However, significant knowledge has been gained with regard to foods and nutrients that may exacerbate or alleviate the core symptoms. Patients with IBD restrict from their diet a plethora of foods often arbitrary, thus depriving themselves from valuable constituents. Careful navigation into the newfound field of genetic variants and personalization of diet should be employed with avoidance of the Westernized diet, processed foods and additives, and focus on a holistic approach with a balanced diet rich in bioactive compounds in order to improve the quality of life of these patients and address diet-related deficiencies.

Inflammatory bowel diseases (IBD) are chronic, progressive and relapsing inflammatory disorders of unknown etiology that may cause disability over time. Data from epidemiologic studies indicate that diet may play a role in the risk of developing and the course of IBD. It is known that the group of beneficial bacteria was reduced in the IBD and that the Mediterranean diet (MD)-which is defined as eating habits characterized by high consumption of plant foods, mainly cereals, vegetables, fruit as well as olive oil, and small portions of dairy products, sweets, sugar and meat products-affects gut microbiota, enriching beneficial bacteria, which support gut barrier function and reduce inflammation. Although several studies support different favorable effects of MD on IBD, adherence to MD by IBD patients is generally low, including patients from the Mediterranean Basin. Patients avoid many products which are elements of MD because there cause gastrointestinal symptoms. Patients should be encouraged to have a healthy and well-balanced diet according to individual tolerance of products. A good option seems to be good modified MD, changing hard-to-digest products to easy digest.

This study aimed to examine the environmental factors associated in Iranian patients with inflammatory bowel disease (IBD).

The role of environmental factors in the development of IBD remains uncertain.

In this case-control study, the patients with IBD referred to the Taleghani Hospital, Tehran, Iran, were recruited from 2017 to 2019. Controls were matched by sex. Data were collected using the designed questionnaire and also valid questionnaire such Pittsburgh Sleep Quality Index (PSQI) and Hospital Anxiety and Depression Scale (HADS) for sleep quality and anxiety/depression, respectively. Conditional logistic regression models were used to estimate adjusted odds ratios (ORs).

The study population included 200 individuals: 100 (50%) IBD patients and 100 (50%) controls. Age under 50, marital status, sleep difficulties, vitamin D insufficiency, anxiety/depression, dietary fiber deficit, post-menopausal hormone treatment, oral contraceptives, and antibiotics were all prognostic factors for IBD on the univariate analysis (P< 0.005). In multivariate analysis, the risk of IBD was significantly increased with 50 years (OR: 6.699, 95%CI: 3.271-8.662, P=0.017), abnormal sleep status (OR: 6.383, 95%CI: 3.389-7.19, P=0.001), and using oral contraceptive (OR: 7.426, 95%CI: 5.327-9.865, P=0.001). However, the risk of IBD was significantly decreased with older age (OR: 0.795, 95%CI: 0.697-0.907, P=0.001) and married status (OR: 0.008, 95%CI: 0.001-0.438, P=0.018).

Data suggest that the environmental factors play a significant role in the etiology of IBD and probably on the disease course. While the evidence for some factors is strong, many factors require further supportive data.