An Autoimmune Protocol Diet Improves Patient-Reported Quality of Life in Inflammatory Bowel Disease.

BACKGROUND: Prior studies suggest dietary modification may improve clinical response or remission rates in patients with inflammatory bowel disease (IBD). Our aim was to examine whether an autoimmune protocol diet improves quality of life in patients with active Crohn disease (CD) and ulcerative colitis (UC). METHODS: We conducted an uncontrolled clinical trial of the autoimmune protocol diet in adult patients with active IBD (Harvey-Bradshaw Index ≥ 5 for CD or partial Mayo score ≥ 3 for UC, and erosions/ulcers on endoscopy and/or elevated fecal calprotectin). The dietary intervention consisted of a 6-week elimination phase, followed by a 5-week maintenance phase. Short Inflammatory Bowel Disease Questionnaire (SIBDQ) was completed at baseline, and weeks 3, 6, 9, and 11. RESULTS: The final cohort included 6 UC and 9 CD participants. Mean SIBDQ score improved significantly from baseline (46.5) to weeks 3 (54.0, P = 0.02), 6 (53.3, P = 0.02), 9 (62.0, P = 0.03), and 11 (60.5, P = 0.05). Among participants completing all 5 surveys, mean SIBDQ increased from 46.5 to 61.5 by week 11 (P = 0.03). By week 3, participants experienced significant improvements in bowel movement frequency (36%, P = 0.04), stress (28%, P = 0.01), and ability to perform leisure/sport activities (29%, P = 0.02). Effects were not significantly different between CD and UC participants. CONCLUSIONS: Dietary modification can improve quality of life as early as week 3 in patients with active IBD. Larger randomized controlled trials are needed to examine dietary interventions in IBD.

Implementing Dietary Modifications and Assessing Nutritional Adequacy of Diets for Inflammatory Bowel Disease.

Guidelines for dietary recommendations and nutritional therapy for patients with inflammatory bowel disease (IBD) are lacking, and patients are moving toward popular defined diets for relief of symptoms and inflammation. However, many proposed diets involve elimination of specific foods or food groups and may exacerbate or inadequately replete micronutrient deficiencies that are prevalent in patients with IBD at baseline. Further, limited data are available to guide clinicians on the use of dietary protocols for IBD. This article reviews dietary risk factors for IBD and common beliefs about diet among patients with IBD, and how these aspects may inform general dietary recommendations for this patient population. Additionally, this article reviews dietary interventions used in the management of active IBD, with a focus on whole food diet-based therapies rather than enteral or parenteral nutrition, as well as their nutritional adequacy. This article also highlights various dietary concepts and approaches among patients with IBD, along with the potential for nutritional inadequacy of popular defined diets for IBD. Partnerships with registered dietitians are needed to guide patients with IBD in nutrition and dietary intervention. Larger randomized studies are needed to support evidence-based dietary recommendations for IBD.

The Autoimmune Protocol Diet Modifies Intestinal RNA Expression in Inflammatory Bowel Disease.

Researchers from the Scripps Clinic in La Jolla, CA recently looked at gene expression to better understand the role that diet plays in inflammatory bowel disease. Their findings suggest that diet may help modify inflammatory pathways in people with ulcerative colitis.

Plasma 25-Hydroxyvitamin D, Vitamin D Binding Protein, and Risk of Colorectal Cancer in the Nurses' Health Study.

Total circulating 25-hydroxyvitamin D [25(OH)D)] has been associated with lower risk of colorectal cancer. The physiologic mechanism, however, may be more directly related to the free or bioavailable fraction of 25(OH)D, which is influenced by levels of vitamin D binding protein (VDBP). We assessed the association of prediagnosis total, free, and bioavailable 25(OH)D and VDBP with colorectal cancer risk among predominantly white women in the Nurses' Health Study (NHS) who provided a blood specimen in 1989-1990. We documented 378 cases of colorectal cancer through 2011 and matched them to 689 controls according to age and time of blood draw. We genotyped two common polymorphisms in the gene coding VDBP and calculated free and bioavailable 25(OH)D levels based on total 25(OH)D, VDBP, albumin, and their estimated genotype-specific binding affinities. Total 25(OH)D was associated with lower colorectal cancer risk (P for trend = 0.01). Compared with women in the lowest quintile of total 25(OH)D, those in the highest quintile had a multivariable-adjusted odds ratio (OR) for colorectal cancer of 0.54 [95% confidence interval (CI), 0.33-0.87]. Comparing extreme quintiles, we did not find any significant association with risk of colorectal cancer for VDBP (OR, 0.98; 95% CI, 0.65-1.47), free 25(OH)D (OR, 0.71; 95% CI, 0.46-1.10), or bioavailable 25(OH)D (OR, 0.92; 95% CI, 0.60-1.42). In conclusion, prediagnosis levels of total, but not free or bioavailable 25(OH)D, were associated with lower colorectal cancer risk. Although our findings support an inverse association of vitamin D with colorectal cancer, this association does not appear to be due to the unbound or bioavailable fraction of circulating vitamin D. Cancer Prev Res; 9(8); 664-72. ©2016 AACR.

Vitamin D Supplementation Modulates T Cell-Mediated Immunity in Humans: Results from a Randomized Control Trial.

CONTEXT: Although studies have linked vitamin D deficiency with immune-mediated diseases, data demonstrating a direct effect on T-cell function are sparse. OBJECTIVE: Our objective was to determine whether oral vitamin D3 influences T-cell activation in humans with vitamin D deficiency. DESIGN: This was a single-center ancillary study within Vitamin D Therapy in Individuals at High Risk of Hypertension, a double-blind, multicenter, randomized controlled trial. SETTING: This study was undertaken in a single academic medical center. PARTICIPANTS: Adults with vitamin D deficiency and untreated pre- or early stage I hypertension were included. INTERVENTION: In Vitamin D Therapy in Individuals at High Risk of Hypertension, participants were randomized to either low- (400 IU daily) or high- (4000 IU daily) dose oral vitamin D3 for 6 months. In this ancillary study of 38 patients, we measured CD4+ T-cell activation estimated by intracellular ATP release after stimulation of whole blood with plant lectin phytohemagglutinin collected at baseline (pretreatment) and 2-month follow-up. MAIN OUTCOME MEASURE: Determining whether ATP level changes were significantly different between treatment groups was the main outcome measure. RESULTS: Treatment with 4000 IU of vitamin D3 decreased intracellular CD4+ ATP release by 95.5 ng/ml (interquartile range, -219.5 to 105.8). In contrast, 400 IU of vitamin D3 decreased intracellular CD4+ ATP release by 0.5 ng/ml (interquartile range, -69.2 to 148.5). In a proportional odds model, high-dose vitamin D3 was more likely than low-dose vitamin D3 to decrease CD4+ ATP release (odds ratio, 3.43; 95% confidence interval, 1.06-1.11). CONCLUSIONS: In this ancillary study of a randomized controlled trial, we found that high-dose vitamin D3 significantly reduced CD4+ T-cell activation compared to low-dose vitamin D3, providing human evidence that vitamin D can influence cell-mediated immunity.

Cost-effectiveness analysis of chromoendoscopy for colorectal cancer surveillance in patients with ulcerative colitis.

BACKGROUND: Recent studies report that the risk of colorectal cancer (CRC) among patients with ulcerative colitis (UC) may be lower than previously estimated. Although white-light endoscopy (WLE) with random biopsies is recommended for dysplasia detection in patients with UC, several studies reported increased detection of dysplasia by chromoendoscopy. OBJECTIVE: To analyze the cost effectiveness of chromoendoscopy relative to WLE or no endoscopy for CRC surveillance in patients with UC. DESIGN: Decision-analytic state-transition (Markov) model with Monte Carlo simulation. SETTING: To simulate the clinical course of chronic UC, we estimated dysplasia and CRC incidence and progression, endoscopic test characteristics, stage-specific mortality rates, and costs from published literature and Medicare reimbursement data. PATIENTS: Patients from a population-based age distribution with ulcerative colitis for ≥8 years. INTERVENTION: We compared 3 different strategies at various surveillance intervals: chromoendoscopy with targeted biopsies, WLE with random biopsies, and no surveillance. The robustness of the model was assessed by using probabilistic sensitivity analysis. One-way sensitivity analyses were performed to evaluate individual variables, and 3-dimensional analysis was used to examine the effects of varying screening intervals. MAIN OUTCOME MEASUREMENTS: Incremental cost-effectiveness ratio (ICER). RESULTS: Chromoendoscopy was found to be more effective and less costly than WLE at all surveillance intervals. However, compared with no surveillance, chromoendoscopy was cost effective only at surveillance intervals of at least 7 years, with an ICER of $77,176. Chromoendoscopy was the most cost effective strategy at sensitivity levels >0.23 for dysplasia detection and cost <$2200, regardless of the level of sensitivity of WLE for dysplasia detection. The estimated population lifetime risk of developing CRC ranged from 2.5% (annual chromoendoscopy) to 5.9% (chromoendoscopy every 10 years). LIMITATIONS: Estimates used for the model are based on best available data in the literature. CONCLUSION: Chromoendoscopy is both more effective and less costly than WLE and becomes cost effective relative to no surveillance when performed at intervals of ≥7 years.

Pretreatment 25-hydroxyvitamin D levels and durability of anti-tumor necrosis factor-α therapy in inflammatory bowel diseases.

INTRODUCTION: Emerging evidence supports an immunologic role for 25-hydroxyvitamin D (25(OH)D) in inflammatory bowel disease (IBD). Here we examined if pretreatment vitamin D status influences durability of anti-tumor necrosis factor (TNF)-α therapy in patients with Crohn's disease (CD) or ulcerative colitis (UC). METHODS: All IBD patients who had plasma 25(OH)D level checked <3 months prior to initiating anti-TNF-α therapy were included in this retrospective single-center cohort study. Our main predictor variable was insufficient plasma 25(OH)D (<30 ng/mL). Cox proportional hazards model adjusting for potential confounders was used to identify the independent effect of pretreatment vitamin D on biologic treatment cessation. RESULTS: Our study included 101 IBD patients (74 CD; median disease duration 9 years). The median index 25(OH)D level was 27 ng/mL (interquartile range, 20-33 ng/mL). One-third of the patients had prior exposure to anti-TNF-α therapy. On multivariate analysis, patients with insufficient vitamin D demonstrated earlier cessation of anti-TNF-α therapy (hazard ratio [HR], 2.13; 95% confidence interval [CI], 1.03-4.39; P = .04). This effect was significant in patients who stopped treatment for loss of response (HR, 3.49; 95% CI, 1.34-9.09) and stronger for CD (HR, 2.38; 95% CI, 0.95-5.99) than UC (P = NS). CONCLUSIONS: Our findings suggest that vitamin D levels may influence durability of anti-TNF-α induction and maintenance therapy. Larger cohort studies and clinical trials of supplemental vitamin D use with disease activity as an end point may be warranted.