As my regular readers are more than aware, one of my biggest interests is personalized nutrition. In 2003, I started my son, Alex, on the Specific Carbohydrate Diet when his inflammatory bowel disease proved recalcitrant to the array of pharmaceuticals his gastroenterologist prescribed for him. Within a year, his colonoscopy was clear. Thus,I follow the research on this topic as best as I can. And thus, I found a new paper in Gut particularly interesting. Why is it that some people with irritable bowel syndrome (which affects about 15% of the human population) respond beautifully to the FODMAPS (fermentable oligo-, di-, mono-saccharides and polyols) diet while many do not? What differentiates the responders from the non-responders?
To delve into this question, researchers analyzed stool samples from 56 people with IBS and 56 people who lived with those afflicted (but who did not have IBS), all of whom ate their usual diets.[i] Those with IBS were found to have two distinct microbial signatures which the researchers dubbed either “pathogen-like” (IBSP) or “health-like” (IBSH). The IBSH patients had microbiota that were similar to the other member of their household. However, the IBSP subjects had abundant levels of harmful Firmicutes species, including C.difficile, C.sordelli and C. perfringens, and to boot, was very low in beneficial species like Bacteroidetes. Two other interesting findings in the IBSP group: lactic acid bacterial species Streptococcus parasanguinis and Streptococcus timonensis, which are usually found in the mouth, were also abundant. And, the “…bacterial genes for amino acid and carbohydrate metabolism were overexpressed, which may explain the excess of some metabolites that are linked to IBS symptoms…”
In the next part of the study, 41 of these pairs had their stools analyzed after 4 weeks of the low FODMAPS diet. The microbiomes of the household members and those with the IBSH profile remained the same. However, those with the IBSP profile showed marked changes: their microbiota became healthier, with an increase in Bacteroidetes and a drop in Firmicutes species. Plus, the bacterial genes involved in the metabolism of amino acids and carbohydrates were no longer overexpressed.
Interestingly, 3 out of 4 patients with IBS showed symptom improvement on FODMAPS but the clinical response was greater in this with the IBSP profile.
The conclusion then? “…as shown elsewhere, the structure of faecal microbiota might predict the degree of response to restriction of FODMAPs. Second, restricting FODMAPs can correct IBS-associated dysbiosis in the community structure and also in the metabolic pathways, and this correction appears to be maintained even when FODMAPs are reintroduced into the diet with concomitant symptom control.”[ii]
Many questions remain, obviously, including a biggie: what do people with the IBSH profile have IBS symptoms if their microbiota resemble that of healthy individuals?! And what can be done to help them, since they are unlikely to respond dramatically to FODMAPS? Still, I thought this was really very interesting in that, it suggests that there may be a relatively simple and inexpensive way someday of reducing the guess work in picking what treatments, including diet, may be successful for a particular individual: “Reasons behind such heterogeneity of outcomes need to be defined so that the diet can be directed to the candidates more likely to respond or, more importantly, away from those highly likely not to respond.”