Irritable Bowel Syndrome (IBS) a common functional disorder of the gastrointestinal (GI) tract. Several factors are implicated in its pathogenesis. In recent times, gut “dysbiosis,” i.e. an upsetting of the balance of the gut bacterial population, has joined the list.
IBS typically manifests as recurrent episodes of abdominal pain, accompanied by a change in bowel habits. It is present in 12% of the general population and can have a significant negative impact on the sufferer’s productivity and quality of life. Annually, IBS costs the US health system over $30 billion.
The gut microbiome is made up of a diverse community of about 100 trillion microorganisms: mostly bacteria, but also viruses, fungi, and others. Studies have demonstrated more than 2,000 different species of bacteria from 12 phyla. 93.5% of the species are from four dominant phyla: Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria.
An imbalance in these gut bacterial communities, i.e. gut “dysbiosis” is thought to lead to the activation of the gut immune system and potential low-grade inflammation. This, in turn, affects several other factors downstream, leading to the onset of IBS.
This line of thought is supported by evidence showing a dramatically increased risk of IBS following a bout with acute gastroenteritis. Such “post-infection IBS” is the result of a perfect storm, combining a range of infectious triggers and susceptibility factors present in an individual. This is further supported by demonstrated differences in the composition of the gut microbiome in IBS patients vs healthy controls.
A recent study employed a “molecular fingerprinting technique” to discover a gut microbiome “signature” which accompanied a severe form of IBS. A great reduction in the diversity and richness of the gut microbiota of IBS patients has been observed along with a significant increase in the harmful bacteria and a decrease in the beneficial bacterial groups. What remains unknown at this point is whether small intestine bacterial overgrowth is a cause or consequence of IBS or both.
Microbiome-based treatments for IBS:
Prebiotics are indigestible complex sugars (oligosaccharides and polysaccharides—fructooligosaccharides or galactooligosaccharides (GOS)—) that promote the growth or activity (or both) of bacteria that impart a health benefit for the host. Early work demonstrated that selected prebiotics promoted the growth of potentially beneficial bifidobacteria while inhibiting the growth of potentially harmful Bacteroides, Clostridia, or Coliforms.
Prebiotics “feed” the intestinal microbiota. Their degradation products, short-chain fatty acids, are released into blood circulation. As a result, they affect not only the gastrointestinal tract but also other, more distant organs.
As prebiotics have health benefits, plus production and storage advantages over probiotics, they are promising candidates to promote gut health as a replacement or in association with probiotics.
Probiotics are live or attenuated microorganisms, usually bacteria or yeast, that are beneficial to the host’s digestive system in particular. They alter gut microbial communities in a manner that ultimately imparts a health benefit to the host. In the context of IBS, probiotics have been suggested to decrease visceral hypersensitivity or bring about an anti-inflammatory effect. A recent study demonstrated efficacy in IBS patients towards the improvement of global symptoms, abdominal pain, bloating, and flatulence.
In addition, IBS patients often suffer from depression or anxiety, and recent studies suggest that IBS and depression share abnormalities in pathophysiology. These include dysbiosis, altered intestinal permeability, and gut immune activation.
A number of studies have reported the beneficial effects of probiotics on these psychological symptoms. Such “psychobiotics” present an interesting avenue for future research.
All in all, once we know more about the varied situations representing abnormal gut conditions, we will be better able to understand what comprises a “healthy” microbiome.