INTERVALS OF A PLANT-BASED, LOW-CALORIE DIET IMPROVE CLINICAL SYMPTOMS COMPARED WITH USUAL DIET IN PATIENTS INITIATING ADVANCED THERAPIES FOR MODERATE-TO-SEVERE ULCERATIVE COLITIS

Introduction: Diet plays an important role in ulcerative colitis (UC) yet there are no studies examining the role of diet as adjunctive therapy to medication. The aim of our study was to determine whether two 5-day intervals of a low-calorie plant-based diet (PB diet) that mimics fasting, improves clinical response to medications by week 8 in patients with active UC.
Methods: Adult patients with UC starting a new advanced therapy (as second or third-line drug) were included. All patients had active disease (simple clinical colitis activity index (SCCAI) (>2)). Patients with diet restrictions or comorbidities (e.g., diabetes) were excluded. Patients could be on baseline steroids or mesalamines. Participants were randomly assigned to Arm 1 (2 intervals of the PB diet + standard medical therapy for 8 weeks) or Arm 2 (low residue control diet + standard medical therapy for 8 weeks) in a 1:1 randomization; Figure 1. Patients on the PB diet were given commercially available fasting mimicking diet kits. Day one of the diet provided ~1,090 kcal (10% protein, 56% fat, 34% carbs), while days two through five provided only 725 kcal (9% protein, 44% fat, 47% carbs). We added low calorie snacks and made small adjustments to foods based on tolerance, keeping stable % of macronutrients. Diet and adherence were assessed at baseline and during intervention using validated indices. Both arms received the same number of phone calls. The SCCAI was completed at baseline and week 8. Our primary outcome was decrease in SCCAI at week 8. Blood and stool were collected. An independent student’s t-test was performed to evaluate our primary outcome.
Results:
A total of 83 patients were screened and 32 agreed to participate. 24 patients completed the study: 19 were on tofacitinib, two on upadacitinib, two on infliximab and one on risankizumab. 10 patients were randomized to the PB diet and 14 to the control diet. A Shapiro-Wilk’s test revealed a normal distribution of our primary outcome. The mean baseline SCCAI for the PB diet was 7.73 (SD 3.97) compared to 7.47 (SD 2.23) for the control arm. 50% of those in the PB diet had a clinical response by week 8 compared to 30.7% in the placebo arm (defined as a decrease in SCCAI by 3) (p<.05). The mean decrease in SCCAI for the PB diet was 4.4 (SD 3.32) compared to 1.61 (SD 2.43) for the control arm (p=0.037), Figure 2. Similarly, when examining differences in response among patients treated only with JAK inhibitors, a similar trend in SCCAI between the PB diet and control arm was observed (p=.06). Fecal calprotectin as well as diet predictors of response to therapy will be determined.
Conclusion:
Our pilot study indicates that intermittent low-calorie, PB diets may enhance response to induction medical therapy among patients with active UC. It also suggests that even short, defined intervals of diet therapy may provide benefit in UC.