Eating Fibre To Make You Thin?
Summer is on the way, and I’m sure we all want to look our trim best for those beach holidays, if we can drag ourselves away from our research, of course! Joking aside, obesity is a major public health burden, and so huge efforts are being made to promote healthier diets and exercise. Many people baulk at changing their habits, so the dieting industry – notorious for promotion of sham pseudoscience and downright fraud – is rapidly expanding. News of the next wonder diet pill is often rightly filed away under “nonsense”, but the latest collection of headlines does have some scientific backing behind it. So have scientists really discovered a chemical that switches off hunger?
Consumption of dietary carbohydrates – starch and fibre – has been reported to decrease body weight, and the study, by a research consortium lead by scientists at Imperial College London, postulates a simple mechanism to explain this observation. Microbes in the digestive system break down and ferment these carbs and produce acetate – the sour essence of vinegar and dreaded spoiler of oxidized wines – as a major by-product. The researchers used a variety of clever isotopic labelling techniques – scanning for carbon-11 and carbon-13 enriched food introduced into the diets of mice instead of the naturally abundant carbon-12 – to monitor the biodistribution of acetate. Inulin, a carbohydrate found in many fibrous foods, was used to induce acetate production in the mice.
Labelled acetate was found to travel from the colon, across the blood-brain barrier, and into the brain, specifically the hypothalamus, a region known to be involved in appetite regulation. The acetate was then metabolized through the glutamine-glutamate cycle that is known to control the release of neurotransmitters – chemical signals in the brain – which regulate appetite. Additionally, mice fed with large amounts of fermentable fibre ate less food and gained less weight than mice fed with non-fermentable fibre that does not produce acetate in the gut.
Both the Telegraph and the Daily Mail reported the discovery of an appetite-suppressing chemical and immediately re-introduced the old favourite, the cure-all diet pill. The Daily Express takes it too far, however, with the inaccurate headline “Fat pill made to stop dieters feeling hungry”, and were rightly chided for doing so by the NHS Choices website in their analysis of the story. All three newspapers include comments from lead author Prof Gary Frost, but only the Telegraph and the Daily Mail include the precautionary statement:
“The major challenge is to develop an approach that will deliver the amount of acetate needed to suppress appetite but in a form that is acceptable and safe for humans. Acetate is only active for a short amount of time in the body, so if we focused on a purely acetate-based product we would need to find a way to drip feed it and mimic its slow release in the gut.”
For once, the reporting is actually quite reasonable, reflecting the good science behind the headlines.
The research certainly needs to be repeated in humans to confirm that suppressing our own appetite is possible, although a diet high in fibre is already recommended. One final caveat comes in a write-up of the story in Nature magazine. Wiliam Colvers of the University of Alberta expresses concern about the high levels of fibre used in the study, around 11% of the total diet. Colvers suggests an unfortunate side-effect, “the room would be full of mouse farts”, and that the thinner mice may simply have eaten less as they were uncomfortable. So would a pill that made you slimmer but gassier ever be popular? We’ll wait for the human studies to find out!
G. Frost, M. L. Sleeth, M. Sahuri-Arisoylu, B. Lizarbe, S. Cerdan, L. Brody, J. Anastasovska, S. Ghourab, M. Hankir, S. Zhang, D. Carling, J. R. Swann, G. Gibson, A. Viardot, D. Morrison, E. L. Thomas and J. D. Bell (2014). The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. Nature Communications, 5, article number 3611. doi: 10.1038/ncomms4611.