Probiotics and Gut Microbiota Stability

Can dietary microbes promote stability of the gut microbial community? And if so, does this translate into any measurable benefits to human health?

The ideal composition of a healthy gut microbial community is not known. But even in the absence of a known healthy target microbiota, a reasonable argument could be made that helping maintain stability of your own gut microbiota  – either through promotion of resilience so that a potential perturbation has less of an effect, or through facilitating a return of a perturbed microbial community to normal – is a useful characteristic of a probiotic.

Such a function could be brought to bear after correction of some deficiency in a microbial community (as occurs with fecal microbial transplant or other more drastic interventions that impact the microbiota), with the aim of promoting stability of the newly established, healthier community.

Or such a function may be important as we encounter different stresses that can disrupt microbiota throughout life, including antibiotic exposure, psychological stress, onset of some diseases and dietary changes.

Although many randomized, controlled trials have documented that probiotics can benefit human health, we know precious little about the ability of probiotics to promote of stability of gut microbial communities. In 2014, Veiga and coauthors proposed that dietary microbes invoke changes in gut microbiota that ameliorate symptoms through improved homeostasis of gut microbiota.  (See an earlier post on this study.) They hypothesized that this may occur, at least in part, through cross feeding between ingested bacteria and resident ones. Such cross-feeding might be mediated through increased short chain fatty acid production in the colon brought on by consumption of a fermented probiotic milk. Since this same fermented milk improved the symptoms of subjects with irritable bowel syndrome (Agrawal et al. 2008), such facilitation of homeostasis may have beneficial physiological effects as well.