IBS, whereby certain
DNA changes cause reduced enzymatic activity and inefficient digestion of carbohydrates, thus inducing symptoms like
bloating,
diarrhoea, and
abdominal pain.
In the new study, the Gastrointestinal Genetics team now analysed genetic and health data from over 360,000 individuals in the UK Biobank, and found that individuals with defective sucrase variants were exposed to a significantly higher risk of IBS, while those with isomaltase defects were not affected. At the same time, sucrase defective carriers experienced more severe bowel symptoms, and were more likely to avoid sucrose-rich foods.
“On top of maltose from starch, sucrase has the unique ability to break down sucrose” said senior author Mauro D’Amato, Professor of Medical Genetics at LUM University and Ikerbasque Research Professor at CIC bioGUNE, “and it may be so that this sugar triggers bowel symptoms in individuals with genetic defects associated with reduced sucrase function. This not only contributes to understanding IBS risk in people predisposed to carbohydrate maldigestion, but also supports the idea of tailoring their dietary treatment based on genetics.”
IBS affects millions worldwide, often with unclear pathogenesis and limited treatment options. This study reinforces the importance of digestive enzyme genetics in IBS predisposition, and provides rationale for dietary modifications - such as reducing sucrose intake - in genetically susceptible individuals.
Ref: Domain-specific effects of sucrase-isomaltase genotype in irritable bowel syndrome. Torices L, Bonfiglio F, Esteban-Blanco C, Zamfir-Taranu A, Naim HY, D’Amato M. Gastroenterology. DOI: 10.1053/j.gastro.2025.01.242.
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