Obesity is thriving in a culture of high fat and sugar-laden lifestyles that characterize the Western world. Concern grows to suggest that these innovations are altering the genetic compositions and metabolic activities of the human gut microbiome. The rate and extent to which gut bacteria reproduce in response to dietary change remains unknown.
Still, recent research results, published in Nature by a Harvard team of scientists, suggests that changing dietary compositions for a short period of time alters the microbial community structure and the differentiation in microbial gene expression. Namely, adopting either a meat or plant-centric diet strongly influences the subsequent flora.
The animal-based diet was shown to increase the abundance and activity of Bilophila wadsworthia, supporting “a link between dietary fat, bile acids and the outgrowth of microorganisms capable of triggering inflammatory bowel disease.” Thus, it appears the adaptability of the microbiome potentially facilitates the diverse range of human dietary lifestyles.
Furthermore, an animal-based diet changed the microbiota in a way that could promote infection with enteric disease. Other recent experiments have illustrated that high fat diets increase the secondary bile acid DCA, which also enhances the risk of developing liver cancer. Elevated DCA levels contribute to microbial disturbances on meat-heavy diets, with this bile acid appearing to inhibit many other bacterial phyla.
Moreover, mouse models show that growth of B.wadsworthia can cause inflammatory bowel disease, by inflaming intestinal tissue. In mice, growth appears to be stimulated by bile acids that are secreted after consuming the saturated fats in milk. Other research shows that high-fat diets in humans promotes growth of B.wadsworthia as well.
The animal-based diet significantly increased faecal bile acid concentrations, as well as enhancing the abundance of microbial DNA and RNA encoding enzymes responsible for sulphur metabolism. Taken together, these findings support the hypothesis that diet-induced changes to the gut microbiota may contribute to the onset of inflammatory bowel disease.