Inflammatory bowel disease (IBD) is a chronic disease that is associated with aspects of brain anatomy and activity. In this preliminary MRI study, we investigated differences in brain structure and in functional connectivity (FC) of brain regions in 35 participants with Crohn's disease (CD) and 21 healthy controls (HC). Voxel-based morphometry (VBM) analysis was performed to contrast CD and HC structural images. Region of interest (ROI) analyses were run to assess FC for resting-state network nodes. Independent component analysis (ICA) identified whole brain differences in FC associated with resting-state networks. Though no structural differences were found, ROI analyses showed increased FC between the frontoparietal (FP) network and salience network (SN), and decreased FC between nodes of the default mode network (DMN). ICA results revealed changes involving cerebellar (CER), visual (VIS), and SN components. Differences in FC associated with sex were observed for both ROI analysis and ICA. Taken together, these changes are consistent with an influence of CD on the brain and serve to direct future research hypotheses.
Abstract Background We aimed to investigate (1) the stability of inflammatory aspects of diet over 1 year among persons with inflammatory bowel disease (IBD) and (2) the impact of change in diet on changes in inflammation and IBD symptoms over 1 year. Methods Participants were recruited to the Manitoba Living with IBD Study and completed the Harvard Food Frequency Questionnaire (FFQ). The Dietary Inflammatory Index (DII) and the Empirical Dietary Inflammatory Index (EDII) were used to calculate the inflammatory potential of the diet. Inflammation was measured by fecal calprotectin (≥250 µg/g). Symptoms were measured by the IBD Symptom Inventory (IBDSI). All measures were obtained at baseline and 1 year. Dietary Inflammatory Index and Empirical Dietary Inflammatory Index scores >0 and <0 reflect pro- and anti-inflammatory diet, respectively. Variance components analyses were used to describe diet stability. Associations between changes in diet and changes in active inflammation and symptoms were assessed using ordinal logistic regression and multilevel linear regression modeling. Results One hundred thirty-five participants (66% CD) were included. Approximately one third of the variance in EDII (36%) and DII (33%) scores was explained by changes in diet over time. Each unit increase in the change in EDII (baseline to follow-up) was associated with a greater odds of FCAL, indicating active inflammation (>250 µg/g; odds ratio, 3.1; 95% confidence interval [CI], 1.02–9.93; P = 0.04) and with a rise in IBDSI of 6.7 (95% CI, 1.0–12.4; P = 0.022; theoretical IBDSI range, 0–81). There was no association between changes in DII and changes in FCAL or IBDSI. Conclusion The EDII, but not the DII, may have utility to identify the inflammatory potential of diet. This inflammatory potential can contribute to inflammation and/or disease symptoms in persons with IBD.
Abstract Background In this matched case‐control longitudinal study among people living with inflammatory bowel disease (IBD), we investigated beliefs about what triggers a flare. Methods Adults with confirmed IBD and active disease within 2 years were enrolled in the Manitoba Living with IBD Study and followed biweekly with online surveys for 1 year. The 7‐point IBD Symptom Change Indicator was used for participant identification of a flare. Flare cases were matched to non‐flare controls by sex and disease type. Members of each matched pair completed supplementary information on diet changes and psychological functioning in the previous 2 weeks and provided stool samples to assess fecal calprotectin (FCAL). Results Of 128 enrolled participants, 95 matched flare/non‐flare pairs were created. Those reporting a flare were more likely to have elevated FCAL (51% vs 34% among non‐flares, P = 0.043). Although 61% of study participants believed at baseline that a food may trigger flares, and 25% of those in a flare believed that a food may have triggered their current flare, there was no difference in consumption of assessed foods between flares and non‐flares in the previous 2 weeks. Patients with flares were more likely to be having difficulties in emotional state than controls (40% vs 18%, P = 0.001) and more likely to be stressed or worried (64% vs 33%, P = 0.001). Conclusion Although a majority of individuals with IBD believe that specific foods trigger their disease flares, this was not supported by the current findings. Recent psychological functioning was associated with self‐reported IBD flare.
As the importance of the brain-gut axis in the pathobiology of inflammatory bowel disease (IBD) continues to evolve, a greater understanding of brain structure and functional connectivity (FC) is necessary. In this magnetic resonance imaging (MRI) study, we investigated differences in brain structure and in FC of brain regions in 111 participants with IBD (76 ulcerative colitis (UC) and 35 Crohn's disease (CD)) and 74 healthy controls (HC). Significant differences between IBD and HC were observed in the three analyses used (voxel based morphometry, region-of-interest, and independent component analysis) in brain regions of the default mode, cerebellar, and visual networks. Significant differences between IBD subtypes (UC, CD) were found. The results of the current study establish that a relationship between brain functional connectivity and the brain-gut axis exists in IBD.
Persons with IBD and their clinicians often use the term ‘flare’ to refer to a presumed disease worsening. Instruments used to identify a patient-defined IBD flare are limited. A case-control design was used to assess the relationship between a 7-point indicator used to identify an IBD flare and alternative measures of disease activity and quality of life: fecal calprotectin (FCAL), a 2-point self-report scale defining IBD as inactive/active, a newly developed symptom index score (SIBDSI), and the short form IBDQ (SIBDQ). Persons aged 18–75 living in Manitoba with a confirmed IBD diagnosis (n=71) were surveyed biweekly for 26 weeks (98% response rate), and provided periodic stool samples. A patient-defined IBD flare was identified using a score of 6 or 7 on the 7-point indicator; a dynamic measure assessing change in symptoms over time. Participants with self-defined flares were systematically matched to controls (participants who had never reported a flare) based on survey week, sex, and disease type. We compared the prevalence of active IBD symptoms using the SIBDSI and the SIBDQ. We also compared SIBDSI and SIBDQ scores for both flares and controls at the time of and two weeks prior to the reported flare, to determine if the patient-identified flare reflected a change in symptom activity. A FCAL level ≥ 150 was indicative of intestinal inflammation. 38% of participants reported at least one IBD flare during the study period. 97.2% of persons reporting a flare described having active IBD compared with 32.4% of controls (p<0.001). 94.4% of persons reporting a flare vs 38.2% of controls had an SIBDSI score above the cut-off of 14 for CD; 13 for UC (p<0.001). The mean SIBDSI score was significantly different in flares versus controls (31.1 ± 12.0 vs 11.9 ± 7.5, p<0.001), as was the mean SIBDQ score (44.3 ± 9.1 vs 57.0 ± 9.1, p<0.001). There was a greater change in SIBDSI and SIBDQ scores among flares than among controls, comparing two weeks prior and the time of the reported flare (SIBDSI Δ=8.61 ± 8.37 vs 0.27 ± 3.94; SIBDQ Δ=6.22 ± 5.27 vs 0.45 ± 3.36; p<0.001 for both. Participants in the flare group were no more likely than matched controls to have an elevated FCAL (52.9% vs. 47.1%, p=0.825) at the time of the reported flare. The presence of a self-reported flare was associated with higher levels of symptom activity and lower health related quality of life. Changes in symptoms and quality of life concurrent with the report of a flare, provided confirmation of the patient experience. While FCAL levels did not differentiate those reporting a flare from those not, scores were elevated for approximately half of both groups, suggesting inflammation does not consistently translate to symptoms. CIHR
