Many people with Crohn’s disease (CD) or Ulcerative Colitis (UC) avoid dairy out of fear that it will cause uncomfortable symptoms, such as excess gas, abdominal cramping, and diarrhea. However, not every person with CD or UC is actually lactose maldigester or lactose intolerant, so avoiding all dairy may not be a good option. It could even be counterproductive, because dairy is an excellent source of calcium. This is a particularly important nutrient for people with Crohn’s disease, as certain drug treatments and malabsorption may cause a calcium deficiency. This literature review was performed to extract data on lactose maldigestion prevalence in IBD.
Dairy restrictions may adversely affect disease outcome
Among 1022 articles evaluated, 17 were included in meta-analysis. Lactose maldigestion in inflammatory bowel disease seems to be determined by ethnicity in most cases of UC and CD. Intolerance symptoms depend on several parameters besides lactose maldigestion. The study also indicates that dairy foods may protect against IBD. Nutritional consequences of dairy restrictions might therefore impact adversely on bone and colonic complications. Even if someone with IBD is lactose intolerant, it’s also possible to safely consume certain dairy products that contain very little lactose or can digest it. These include fermented dairy products like yogurt.
The authors conclude that further work is needed to evaluate the role of dairy foods in IBD as well on methods to avoid their restriction.
Source: Andrew Szilagyi et al., Nutrition Journal 2016; 15 :67.
Although a specific diet is not thought to play a role in causing ulcerative colitis, some changes to your diet can help control the condition.
For example, you may find it useful to:
- eat small meals – eating 5 or 6 smaller meals a day, rather than 3 main meals, may help control your symptoms
- drink plenty of fluids – it’s easy to become dehydrated when you have ulcerative colitis, as you can lose a lot of fluid through diarrhoea; water is the best source of fluids, and you should avoid caffeine and alcohol, as these will make your diarrhoea worse, and fizzy drinks, which can cause flatulence (gas)
- take food supplements – ask your GP or gastroenterologist if you need food supplements, as you might not be getting enough vitamins and minerals in your diet
Keep a food diary
Keeping a food diary that documents what you eat can also be helpful.
You may find you can tolerate some foods while others make your symptoms worse.
By keeping a record of what and when you eat, you should be able to identify problem foods and eliminate them from your diet.
But you should not eliminate entire food groups (such as dairy products) from your diet without speaking to your care team, as you may not get enough of certain vitamins and minerals.
If you want to try a new food, it’s best to only try 1 type a day because it’s then easier to spot foods that cause problems.
Temporarily eating a low-residue or low-fibre diet can sometimes help improve symptoms of ulcerative colitis during a flare-up.
These diets are designed to reduce the amount and frequency of the stools you pass.
Examples of foods that can be eaten as part of a low-residue diet include:
- white bread
- refined (non-wholegrain) breakfast cereals, such as cornflakes
- white rice, refined (low-fibre) pasta and noodles
- cooked vegetables (but not the peel, seeds or stalks)
- lean meat and fish
If you’re considering trying a low-residue diet, make sure you talk to your care team first.
This is the largest survey analyzing patient-reported data about the prevalence of a gluten free diet in a Western IBD population. In this Internet based cohort nearly 20% of all patients reported having tried a GFD and 8% were currently attempting a GFD. This is a significantly higher percentage than the current GFD prevalence of 0.5% among individuals without celiac disease in the USA.5 More than half of the patients reported symptom improvement and nearly 40% fewer flare-ups of IBD while being on a GFD. This observation suggests that in a subgroup of IBD patients, gluten may cause intestinal (diarrhea, bloating, abdominal pain) and extraintestinal (fatigue, nausea) symptoms. Similar effects of a GFD have been described in patients with irritable bowel syndrome (IBS) indicating a potential trigger effect of gluten containing foods in gluten susceptible patients.9–11
NCGS is defined by the exclusion of celiac disease including negative celiac serologies and/or normal intestinal architecture and negative immunoglobulin (Ig)E-mediated allergy tests to wheat. Additionally, to meet criteria for NCGS, the clinical symptomatology of IBS type of symptoms has to improve after gluten withdrawal and worsen after the ingestion of gluten. A specific reaction to gluten in patients with NCGS is currently debated.12 Biesiekierski et al recently showed that gluten by itself might be not the culprit for the IBS type symptoms in patients with previously diagnosed NCGS, but rather the intake of low-fermentable, poorly absorbed, short-chain carbohydrates (fermentable, oligo-, di-, monosaccharides, and polyols; FODMAPs) may be responsible for these effects.13 Also, gluten does not elicit an inflammatory response in the duodenum in patients with NCGS.14 The diagnosis of NCGS was reported by nearly 5% of the respondents in our survey. Thus far studies in patients with IBD investigating inflammatory responses to gluten in duodenal or colonic biopsies have not been performed. Theoretically gluten could create a pro-inflammatory environment in the intestine, leading to more frequent disease flares and the need for more intensified therapies, similar to patients with IBD and concurrent celiac disease.15 However, we cannot exclude that a GFD leads to a significant reduction of dietary FODMAPs, which as shown by Biesiekierski et al., leads to an improvement of the GI symptoms of the patients.13 Of note, an exploratory study has demonstrated that dietary reduction of FODMAPs leads to significant amelioration of symptoms including abdominal pain, bloating, gas and diarrhea in patients with IBD.16
Those patients maintaining a GFD at the time period of the survey were asked to fill out a recently validated 7-item Celiac Dietary Adherence Test.8 The additive scores of this test reflect the adherence to a GFD and correlate highly with a standardized dietician evaluation and appear to outperform serological testing. However, the test does not quantify the amount of gluten intake, but rather points to the likelihood of gluten contamination. More than 40% of the respondents were strictly maintaining to a GFD, whereas roughly 25% of the patients were found to be fair or poorly adherent. Intriguingly, of all clinical symptoms, only fatigue improved significantly with good adherence. Fatigue in the absence of iron deficiency anemia is a leading symptom in many patients with IBD.17 It is possible that fatigue conversely influenced adherence in our cohort, but coincidently, the worsening of fatigue was also the most significant finding in a gluten challenge study conducted in patients with NCGS.9
The class II MHC haplotype HLA-DQ2 and HLA-DQ8 are present in almost all CD patients and interestingly can be also found in 50% of patients, who are improving on a gluten free diet, which is higher than can be expected in the general population.6 Studies in patients with irritable bowel syndrome with predominantly diarrhea (IBS-D) have also shown, that carrier of HLA-DQ2 respond favorably to a gluten free diet. In fact in 60% of the patients with IBS-D HLA-DQ2 positivity, but no signs of overt celiac disease (negative TTG antibodies and no signs of active celiac disease on biopsies obtained in the duodenum), symptoms such as diarrhea and bloating improved on a 6 months gluten free diet compared to only 12% in patients without HLA-DQ2 positivity.18 As it is speculated in patients with NCGS, gluten might have a direct impact on intestinal barrier function and the mucosal immune system in IBD patients with the HLA-DQ-2 or DQ 8 genotype.19 In a recent study by Vazquez-Roque et al the small intestinal permeability was significantly increased in IBS-D patients with HLA-DQ2 or 8 positivity on a gluten containing diet (GCD), but this was not the case in HLA-DQ 2 and 8 negative patients.11 Also RNA expressions of several proteins associated with the epithelial barrier in the in colonic mucosa (zonula occludens-1, occludin and claudin) were generally lower in participants on a GCD compared to participants on a GFD. However, diet-associated changes of RNA expression reached only statistical significance in study participants, who were found to have a HLA-DQ 2 or 8 positive status. HLA-DQ2 or DQ8 is not found in higher frequencies in IBD patients, but it would be fascinating to evaluate the associations of these haplotypes with the response to a gluten free diet in IBD patients in prospective studies.20 Moreover the degree of intestinal inflammation in non-celiac IBD patients could be influenced by the recently identified non-gluten α-amylase / tryptase inhibitors (ATIs), which can be found in wheat and related cereals. These ATI are strong activators of the innate immune response via the Toll-like receptor 4, leading to the upregulation of pro-inflammatory cytokines in vitro and in vivo.21
Patient-reported data based from the CCFA partners cohort have several limitations as outlined recently.22 CCFA-Partners is a volunteer sample of patients and thus the above-described findings may not reflect similar diet habits in all IBD patients. To address the possibility of selection bias within the sample completing the GFD questionnaire, we compared the characteristics of those who completed the questionnaire to those of the CCFA Partners cohort in general and found no clinical significant differences. Since the study was based on a single questionnaire without collecting blood samples, we did not rule out occult celiac disease with serologic tissue-transglutaminase testing neither could we determine the HLA DQ2 or DQ 8 status. Previous studies have shown that the prevalence of celiac disease in patients with IBD is comparable to the prevalence in the non-IBD population.15, 23 The finding that 0.6% of patients reported to be diagnosed with celiac disease is comparable to the currently reported 0.7% prevalence of celiac disease (including diagnosed and undiagnosed cases) in the United States.24 Currently the majority of celiac disease patients in the USA are undiagnosed, but since IBD patients suffer from similar GI-symptoms as many celiac disease patients, it is very likely that in the setting of the diagnostic work-up for IBD, concurrent celiac disease is diagnosed either by serologic testing or by endoscopy.
In conclusion, the high prevalence of a GFD in the CCFA Partners cohort strongly suggests a potential role of this diet in the adjunctive therapeutic management of subgroups of IBD patients. Testing GFD in clinical practice in patients with significant intestinal symptoms, which are not solely explained by the degree of intestinal inflammation, has the potential to be a safe and highly efficient therapeutic approach following appropriate testing for celiac disease. Further research into investigating possible mechanisms of gluten-mediated worsening of intestinal inflammation in susceptible IBD patients is also warranted.