Prebiotics and Synbiotics: Dietary Strategies for Improving Gut Health

Janina A. Krumbeck; Maria X. Maldonado-Gomez; Amanda E. Ramer-Tait; Robert W. Hutkins

Disclosures

Curr Opin Gastroenterol. 2016;32(2):110-119. 

In This Article

Prebiotics, the Healthy Gut Microbiota, and the Challenge of Individual Variation

Although several microbial taxa or genera have been suggested as being beneficial to the host (i.e., Bifidobacterium and Lactobacillus spp.[41,42]), there is still no actual definition of what constitutes a healthy gut microbiota.[32,43] One recent study showed that gut microbiota from healthy human hunter gatherers was significantly different from a healthy western cohort, suggesting that the ideal or optimal composition of an individual's gut microbiota depends on the lifestyle of the individual.[44] Although enrichment of specific taxa by diet is possible, the clinical significance of these changes may not be readily apparent. Indeed, organisms not previously recognized as contributing to host heath, including Eubacteria, Faecalibacter, Akkermansia, Ruminococcus, and Roseburia, are known to respond to prebiotics.[5,16,45,46] Finally, several microorganisms categorized previously as detrimental are now recognized as part of the gut 'normobiosis' and may even be beneficial. For example, Clostridia spp. have recently been shown to be beneficial in the attenuation of diseases in models of colitis and allergic diarrhea.[42,47,48]

Significant interindividual variability[49] can also make the outcome of dietary interventions less predictable. Indeed, multiple studies have reported the occurrence of study participants who respond to prebiotics and other dietary treatments (responders), whereas in similar studies, study participants fail to respond (nonresponders) to the same treatments.[14,43,50,51] Responses to dietary interventions likely depend on the taxonomic and functional composition of the gut microbiota. Thus, when a given compound is selectively fermented by a limited number of bacteria (fulfilling the actual definition of prebiotic) the response will depend on the gene content and functionality of the target bacteria before supplementation. The presence of species known to metabolize certain compounds, however, is not a guarantee of a positive response to prebiotic supplementation. For instance, dietary interventions in obese study participants resulted in decreased cholesterol concentrations, but only in individuals with high initial levels of Clostridium sphenoides.[43] Furthermore, Davis et al.[52] showed that a fraction of study participants who had consumed as much as 10 g GOS/day for 3 weeks did not respond to the treatment, even though they harbored bifidobacteria at similar levels as that of responders. The authors suggested that nonresponders may lack specific strains capable of metabolizing GOS.[52]

The ability of a particular species to ferment certain prebiotics is strain specific.[53–55] Thus, GIT environments having a similar taxonomic assembly might differ in functional capabilities and therefore result in different responses to prebiotics interventions. Moreover, although a given strain may have the biochemical and physiological means to transport and metabolize a prebiotic, it must also outcompete other autochthonous members of the microbiota to actually utilize the prebiotic compounds and potentially expand its population.[52] Ultimately, the complexity and individuality of the gut microbiota and the structural complexity of dietary fibers likely contribute to the phenomenon of responders and nonresponders.

As a practical strategy, consumption of fermentable fiber or combinations of prebiotics may enrich for a larger and more diverse population of gut microbes. This strategy could potentially reduce the occurrence of nonresponders. In addition, stimulating a broader spectrum of microorganisms, either directly or via cross-feeding, could also promote greater diversity within the gut ecosystem. High levels of diversity are generally considered important for a functional gut ecosystem.[56] Several human gastrointestinal diseases are associated with reduced microbial diversity and gene richness.[5] In particular, reductions in Firmicutes are frequently described.[57] Reduced diversity has also been reported to have an impact on the production of beneficial metabolites by gut microbes. For example, antibiotic treatments and diarrheal disease are characterized by reduced or altered production of short chain fatty acids.[58,59] In contrast, increased diversity has been associated with an improvement in insulin sensitivity.[60] Furthermore, and perhaps most importantly, the restoration of a diverse gut microbiota is associated with successful treatments for C. difficile infections.[61]

Ultimately, the success of a prebiotic treatment depends on its ability to enhance health or reduce a disease phenotype. Several meta-analyses and systematic reviews of human trials with various prebiotics have been conducted with various end points assessed (Table 2).[62–71] In general, these analyses have shown that commercial prebiotics were effective for some conditions (i.e., constipation and diarrhea), but not others (i.e., cholesterol reduction and eczema).

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