Abstract
Recently in Gut, a coding sucrase-isomaltase (SI) variant (15Phe at single nucleotide polymorphism rs9290264) with 35% reduced disaccharidase activity was reported to increase IBS risk and to correlate with more frequent stools. These observations were not assessed in relation to key dietary factors including carbohydrate (ie, SI substrates) consumption.
Here, we studied two large German population-based cross-sectional cohorts, namely PopGen (n=639; average age 61.4; 44.8% female) and FoCus (n=759; average age 53.0; 58.5% female), with available genotype (genome-wide arrays), dietary (12-month food frequency questionnaire, FFQ), faecal microbiota (16S sequencing) and IBS status (self-reported from questionnaire) data, as previously described in detail.
In a combined age/sex/body mass index (BMI)-adjusted logistic regression analysis of the two data sets, carriers of the 15Phe variant (52.86%) reported IBS significantly more often than non-carriers (3.69% vs 1.84%, respectively; P=0.044, OR=2.04), thus replicating and extending previous findings.1 When taking into account the consumption of SI substrate carbohydrates (polysaccharides and disaccharides; g/day) estimated from FFQ, this association appeared strongest for individuals with lowest intake (not shown). In particular, as illustrated in figure 1, starch was the individual carbohydrate component where the largest difference in IBS prevalence was observed between 15Phe carriers and non-carriers (7.8% vs 1.9%, respectively; P=0.029, OR=4.17). This suggests that 15Phe-driven genetic IBS risk effects may be better detectable in low-carbohydrate consumers (possibly driven by starch intake), where relative differences in SI enzymatic activity might have more pronounced consequences on the presence of symptom-generating undigested carbohydrates in the large bowel (compared with other intake groups, where colonic accumulation of undigested carbohydrates may result from higher intake irrespective of genotype).
Here, we studied two large German population-based cross-sectional cohorts, namely PopGen (n=639; average age 61.4; 44.8% female) and FoCus (n=759; average age 53.0; 58.5% female), with available genotype (genome-wide arrays), dietary (12-month food frequency questionnaire, FFQ), faecal microbiota (16S sequencing) and IBS status (self-reported from questionnaire) data, as previously described in detail.
In a combined age/sex/body mass index (BMI)-adjusted logistic regression analysis of the two data sets, carriers of the 15Phe variant (52.86%) reported IBS significantly more often than non-carriers (3.69% vs 1.84%, respectively; P=0.044, OR=2.04), thus replicating and extending previous findings.1 When taking into account the consumption of SI substrate carbohydrates (polysaccharides and disaccharides; g/day) estimated from FFQ, this association appeared strongest for individuals with lowest intake (not shown). In particular, as illustrated in figure 1, starch was the individual carbohydrate component where the largest difference in IBS prevalence was observed between 15Phe carriers and non-carriers (7.8% vs 1.9%, respectively; P=0.029, OR=4.17). This suggests that 15Phe-driven genetic IBS risk effects may be better detectable in low-carbohydrate consumers (possibly driven by starch intake), where relative differences in SI enzymatic activity might have more pronounced consequences on the presence of symptom-generating undigested carbohydrates in the large bowel (compared with other intake groups, where colonic accumulation of undigested carbohydrates may result from higher intake irrespective of genotype).
| Original language | English |
|---|---|
| Pages (from-to) | 177-178 |
| Number of pages | 2 |
| Journal | Gut |
| Volume | 68 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1 Jan 2019 |
| Externally published | Yes |
Keywords
- carbohydrates
- enteric bacterial microflora
- genetics
- irritable bowel syndrome