Food for Thought: Studies of Food Intake and IBS and DGBI

In the first article by Jaafari et al, the authors identified four predominant food cluster patterns from 54,127 participants from 26 countries who completed online questionnaires. The highest prevalence of IBS was associated with cluster A (including Egypt, Brazil, and Colombia) and the lowest with cluster D from several Asian countries. Cluster A dietary pattern was “rich in FODMAPs.” Cluster D participants reported the highest frequencies of fish, rice and tofu consumption and lowest milk consumption (which could be due to higher rates of lactose intolerance). The limitations from this study include the reliance on a questionnaire, the small number of foods surveyed (10), and cultural differences in reporting symptoms.

The study by Mikhael-Moussa et al examined carbohydrate malabsorption, based on breath testing, in patients diagnosed with disorders of gut-brain interaction (DGBI). Patients completed questionnaires as well.

Key findings:

  • Among the 301 patients with DGBI included in our analysis, 178 (59.1%) had carbohydrate intolerance
  • Carbohydrate-intolerant patients were significantly more likely to be female (P value < 0.001), to have 2 or more DGBI (P value = 0.001) to have lactose maldigestion (P value< 0.001) and fructose malabsorption (P value = 0.023), higher irritable bowel syndrome and somatic symptom severity, and lower quality of life (P value < 0.001) compared with patients without carbohydrate intolerance

Discussion:

  • There are multiple potential reasons why certain foods can contribute to GI symptoms including malabsorption, gastrointestinal mobility, alterations in intestinal microbiota, intestinal distention, fluid accumulation, and localized IgE-dependent reactions (noted with confocal laser endomicroscopy).
  • “Carbohydrate-reduced diets have been found effective in reducing symptoms in patients, regardless of the presence of maldigestion/malabsorption”

My take: Dietary triggers are important for the majority of patients with IBS. In this study, patients with documented carbohydrate malabsorption had increased severity of their symptoms.

Related blog posts:

The Science Behind IBS Dietary Interventions

A succinct review (BE Lacy. Clin Gastroenterol Hepatol 2015; 13: 1899-1906) reviews the topic of dietary interventions for irritable bowel syndrome (IBS).

Here are some of the points:

  • “True food allergies are present in 1% to 4% of the US population, but are not more prevalent in IBS patients.”
  • One study found that “more than 1 in 4 patients with self-reported NCGS [nonceliac gluten sensitivity] actually fulfill the diagnosis.”  In other words, most patients with self-reported NCGS do not have NCGS.
  • “The prevalence of lactase deficiency is similar, or slightly higher, in IBS patients compared with healthy subjects; however, the self-reporting of symptoms attributed to lactose intolerance is not reliable.”
  • Potential mechanisms of food triggering GI symptoms were discussed, including intestinal permeability, visceral hypersensitivity, small intestine bacterial overgrowth, and gut microbiome.

Another article which covers the same topic: PR Gibson et al. Gastroenterol 2015; 148: 1158-74.

 

Disaccharidase Deficiencies in Recurrent Abdominal Pain

Question for pediatric gastroenterologists (first poll I’ve placed in this blog): Do you think disaccharidases are needed routinely for patients with abdominal pain in the absence of bloating, or diarrhea?

A recent report indicated a high rate of disaccharidase deficiencies among children with recurrent abdominal pain. Here’s the abstract link: Disaccharidase Deficiencies in Children With Chronic Abdominal Pain (K El-Chammas, SE Williams, A Miranda. JPEN J Parenter Enteral Nutr July 9, 2015 0148607115594675).  Thanks to Kipp Ellsworth for this reference.

Here’s an excerpt:

Data on disaccharidase activity and histology of endoscopic biopsies were collected retrospectively. Only patients with normal histology were included in the study.

ResultsA total of 203 pediatric patients with CAP were included. The mean (SD) age was 11.5 (3.1) years, and 32.5% were male. The percentages of abnormally low disaccharidase levels using the standard laboratory cutoffs were lactase, 37%; sucrase, 21%; glucoamylase, 25%; and palatinase, 8%. Thirty-nine percent of the patients with low lactase also had low sucrase, and 67% of the patients with low sucrase had low lactase…Also, no association was found between stool consistency, stool frequency, or location of pain and low disaccharidase activity.

My take: I am highly skeptical regarding these findings–see Twyman’s Law | gutsandgrowth. For sucrase deficiency, for example, this report represents an extraordinarily high rate of deficiency compared with previous reports. In addition, there are numerous errors which can occur in the handling of tissue specimens.  With regard to lactase deficiency, of course, this is common but having lactose intolerance does not prove causality with regard to abdominal pain.  Many physicians encourage families to see if there is a link between milk ingestion and GI symptoms to help determine if lactose intolerance is a likely contributor to stomach pain (before endoscopy). Stomach pain in the absence of milk ingestion is not due to lactose intolerance.

Before accepting these high rates, improved methodology (eg. control group and duplicating results) would be helpful.

Related blog postCongenital Sucrase Isomaltase Deficiency