Abstract and Introduction
Purpose of review There is direct evidence that the pathogenesis of inflammatory bowel disease (IBD) involves the gastrointestinal microbiota and some evidence that the microbiota might also play a similar role in irritable bowel syndrome (IBS). The aim of this article is to review the emerging evidence for the mechanisms and effectiveness of probiotics in the management of these disorders.
Recent findings The composition of the gastrointestinal microbiota is strongly influenced by factors including age, diet and disease. Probiotics may be effective through their impact on the host gastrointestinal microbiota and promotion of mucosal immunoregulation. Probiotics are considered to be well tolerated, although the quality of studies and health claims has been variable. There are many short-term studies demonstrating the effectiveness of probiotics in IBS, although recommendations should be made for specific strains and for specific symptoms. Within IBD, a number of trials have shown the benefits of a range of probiotics in pouchitis and in ulcerative colitis, although current evidence in Crohn's disease is less promising.
Summary Clearly, some probiotics have considerable potential in the management of IBS and IBD; however, the benefits are strain specific. High-quality trials of probiotics in gastrointestinal disorders as well as laboratory investigations of their mechanism of action are required in order to understand who responds and why.
The gastrointestinal microbiota are a complex and metabolically active ecosystem that play an important role in health and disease. Genotypic sequencing studies have been used to demonstrate that the human gastrointestinal tract can be populated by any of 1000–1150 different species, with individuals harbouring at least 160. Despite this diversity, a core of 18 species was found in all individuals and 57 species were found in 90% of individuals, indicating considerable dominance and interindividual stability of these species across humans.
Many of these bacteria cluster within individuals. In a recent study across four countries, the sequenced metagenomes were shown to fit into three distinct clusters ('enterotypes'), each characterized by variations in numbers of Bacteroides (enterotype 1), Prevotella (enterotype 2) and Ruminococcus (enterotype 3). The abundance of these genera correlated positively or negatively with other genera, indicating a propensity for coexistence or avoidance of other species, respectively. Overall, this describes a microbial ecosystem whose structure is determined, at least in part, by the abundance of species that together contribute to a limited number of preferred compositions.
The composition of the microbiota is strongly influenced by factors including age, disease and diet. In one study, the microbiota of people aged 65–96 years was different from younger adults, with higher Bacteroides and Clostridia cluster IV, as well as some signature sequences that were present only in older people. Numerous diseases have been associated with alterations in the microbiota (dysbiosis), ranging from gastrointestinal disorders such as irritable bowel syndrome (IBS) and inflammatory bowel disease (IBD) to extra-intestinal disorders such as obesity and diabetes. In terms of diet, the impact of food intake on the microbiota is only recently being explored in depth. Habitual long-term diet has been shown to strongly associate with enterotype, with protein/animal fat being associated with enterotype 1 and carbohydrate being associated with enterotype 2. Meanwhile, acute feeding of diets differing in fat and nonstarch polysaccharides alter the microbiota in humans, and this has been examined in detail in gnotobiotic mice in whom manipulation of dietary macronutrients was shown to account for the majority of the change in microbiota.
Approaches to modulating the gastrointestinal microbiota have been investigated as a method of promoting health and in some cases treat disease, in particular the use of probiotic organisms.
Curr Opin Gastroenterol. 2013;29(2):184-189. © 2013 Lippincott Williams & Wilkins