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.
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. Published online before print July 9, 2015, doi: 10.1177/0148607115594675JPEN 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.
Results: A 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.