Dr Paul Moayyedi is a professor in the Division of Gastroenterology at McMaster University, Richard Hunt/AstraZeneca Chair in Gastroenterology, and the inaugural assistant dean of research.
Can the gut microbiota lead to diseases (eg, cirrhosis or obesity)?
Paul Moayyedi, BSc, MB ChB, PhD, MPH: That is an interesting question for which, again, I do not have a definitive answer. There has been some interesting animal work suggesting that gut flora in mice is important to developing obesity. So, you take flora from an obese mouse and it makes a lean mouse more obese, and you can show that the energy absorption is more efficient in those with fat microbiota. I have to say in humans it is yet to be proven.
Yes, there have been microbiome studies looking at obese versus healthy individuals, but of course the diet is very different, the lifestyle is very different, so any differences could be cause or effect. And to date, changing the microbiome has not led to a change in weight. There has been the occasional positive probiotic study, but there is nothing dramatic being seen here. There are randomized trials ongoing in fecal transplants and we will see if that makes a difference, but I think it is far from proven that gut microbiome is highly important in our weight gain, whereas clearly the more calories you eat, the less exercise you do, the more you are likely to gain weight. It is not the only answer, but clearly that is important. The role the microbiota has to play, I feel we have less understanding of how important that is, but it is still an interesting area to explore and hopefully in a few years we will have a better answer to what that position is.
Having said all of that, does the microbiome play an enabling factor in developing, say, alcoholic cirrhosis? The answer is we do not know. Randomized trials are looking to see if they can change the colonic flora, but mainly to reduce the complications of cirrhosis rather than to stop it happening in the first place, which is a whole area that is ripe for research.