Milk fat may lead to bowel diseases by altering gut bacteria: Study
The findings may help explain why immune-related conditions such as colitis have become more prevalent in Western societies in the last half century. Writing in Nature, the team of US-based researchers reveal that consumption of a diet high in saturated milk fats causes a "boom in bad bacteria" in the gut – which in turn leads to increased inflammation and a higher risk of developing bowel conditions for certain people.
"Here we show how the trend in consumption of Western-type diets by many societies can potentially tip the mutualistic balance between host and microbe to a state that favors the onset of disease," said Professor Eugene Chang of the University of Chicago, USA – who led the study.
The research team revealed that concentrated milk fats, that are abundant in processed and confectionery foods, alter the composition of bacteria in the intestines by encouraging the growth of harmful gut microbes. Such changes then disrupt the delicate balance between the microbiota and the immune system, leading to unregulated immune responses that can damage tissues and be difficult to switch off, they said.
"This is the first plausible mechanism showing step-by-step how Western-style diets contribute to the rapid and ongoing increase in the incidence of inflammatory bowel disease," said Chang.
"We know how certain genetic differences can increase the risk for these diseases, but moving from elevated risk to the development of disease seems to require a second event which may be encountered because of our changing lifestyle."
The researchers worked with a mouse model that has many of the characteristics of human IBD.
Chang and his team explained that genetically deleting the immune system modulator molecule interleukin 10 – which acts as a brake on the immune system's response to intestinal bacteria – caused about 20% of mice to develop colitis when fed a low-fat diet or a diet high in polyunsaturated fats.
However when exposed to a diet high in saturated milk fats, the rate of disease development within six months tripled – increasing to more than 60%.
In addition, the onset, severity and extent of colitis were much greater than that observed in mice fed low-fat diets, they said.
The team then set out to find why milk fat triggered inflammation when polyunsaturated fat did not – tracing the answer to the gut microbiome.
Chang revealed that uncommon gut microbe, called Bilophila wadsworthia, was preferentially selected in the presence of milk fat. Previous studies have shown high levels of B. wadsworthia in patients with appendicitis and other intestinal inflammatory disorders, including inflammatory bowel disease.
"That piqued our interest," said Chang. "These pathobionts, which are usually non-abundant, seem to be quite prominent in these diseases."
Indeed, while B. wadsworthia levels were almost undetectable in mice on a low-fat or unsaturated-fat diet, the ‘bad’ bacteria made up about 6% of all gut bacteria in mice fed a high milk-fat diet.
"Unfortunately, these can be harmful bacteria," Chang explained. "Presented with a rich source of sulfur, they bloom, and when they do, they are capable of activating the immune system of genetically prone individuals."
Re-shaping the ecosystem
The lead researchers noted that whilst there is very little that can be done to ‘correct’ genes that predispose individuals to increased risk of developing such inflammatory diseases, one thing that can be done is to try and shift the balance of gut bacteria back to a ‘healthy state’
"In essence, the gut microbiome can be 're-shaped' in sustainable and predictable ways that restore a healthy relationship between host and microbes, without significantly affecting the lifestyles of individuals who are genetically prone to these diseases,” said Chang. “We are testing that right now."
Published online ahead of print, doi: 10.1038/nature11225
“Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitisin Il10−/− mice”
Authors: S. Devkota, Y. Wang, M.W. Musch, V. Leone, H. Fehlner-Peach, A. Nadimpalli, D.A. Antonopoulos, B. Jabri, E.B. Chang