There was a time, and not so long ago, when lack of dietary fibre was considered to be cause of most ailments of modern civilisation. Dennis Burkitt (remember him?) had, like so many young doctors of his generation, had gone to Africa. He not only described Burkitt’s lymphoma, a facial tumour that afflicted children in Uganda and was caused by a virus, but he also observed the inhabitants of that country, most of whom lived in scattered rural villages, had few of the diseases that afflicted western city dwellers. Obesity, heart attacks, strokes, diabetes, gallstones, coeliac disease, arthritis, cancer of the colon, diverticulae disease and of course IBS were rare in Uganda.
I remember hearing him talk. He showed a slide of a hot air balloon and declared that his method of doing research was to float over the savannah and observe the big picture rather than peer down a microscope in the laboratory. Burkitt was an epidemiologist. He observed that faecal output in Uganda was about twice as bulky as the ‘British Standard Stool’ and the diet of the rural African was more plant based and contained much more ‘roughage’ or dietary fibre.
Inspired by missionary zeal, Burkitt returned to England and preached the gospel of the good life enriched by dietary fibre to all who would listen to him. Many did. His observations launched a whole fibrous raft of research into the role of diet in common diseases, food companies fell over themselves to market high fibre cereals and a muesli belt stretched across home counties from Berkhamsted to Tunbridge Wells. Gastroenterologist Ken Heaton down the M4 at Bristol advised that breakfast was the most important meal of the day and its benefit could be gauged by his Bristol stool scale. Thirty years on, stool gazers still puzzle over how many lumps constitute a 1 or 2 on the chart and whether it matters.
The Bran Wagon trundled on for about twenty years before the wheel finally came off. Academic nutritionists turned their attention to the larger amounts of fat and sugar that people on a fibre depleted diet consumed and papers from gastroenterologist, Dr Peter Whorwell in Manchester showed that putting people on a fibre rich diet, especially one that contained insoluble fibre, gave people with IBS more bloating and pain. Overnight it seemed, the fibre hypothesis was abandoned and doctors who all too recently sent their IBS patients home with bags of bran or bottles of prune juice, now advised removing fibre from the diet, although most still retained a fibre rich diet for constipation. Then in 2006, Peter Gibson and his colleagues showed that diets low in poorly absorbed simple and complex sugars (FODMAPs), low molecular components of fibre, could reduce symptoms of bloating, pain and diarrhea.
But fashions across the World Wide Web change all too quickly. Research never stands still. No sooner than one hypothesis seems established than scientists and commentators are chipping away to undermine it. As revelations about the colonic microbiome leap-frog each other month by month, the fibre hypothesis is again under scrutiny. Evidence from studies conducted in mice suggest that short chain fatty acids generated by the fermentation of poorly absorbed plant based foods make the gut less leaky to pro-inflammatory bacterial lipopolysaccharide. Thus we might expect that people on a diet rich in unabsorbed plant foods (dietary fibre) would reconstitute their beneficial bacteria, generate short chain fatty acids and in time suffer less from gut symptoms.
So where does this leave the low FODMAP diet? Well, although excluding the intake of rapidly fermented carbohydrate reduces the production of gas and symptoms of bloating, pain and diarrhea in people with a sensitive gut, could over-zealous prescription of the low FODMAP diet could also deplete the colon of the beneficial bacteria, such as bifidobacteria spp, bacteroides spp and Akkermansii that generate short chain fatty acids and suppress colonic inflammation? Recent papers that might be the case. If so, maintaining people on a low FODMAP diet could risk prolonging the gut sensitivity so that they have to remain on the diet. In other words the treatment may help the symptoms but could prolong the disease? The battle against the symptoms may be won for a time, but the war against IBS lost. Treating mice with fructo-oligosaccharides, the same sugars that are deleted in a low FODMAP diet restored bifidobacteria and short chain fatty acids and reduced leakiness and inflammation.
So what is the answer? Could it be to adopt a pragmatic approach and restrict (but not exclude) rapidly fermented FODMAPs during flare ups of IBS in much the same way as one might take a cough syrup to calm a sore throat, but to increase these when you are feeling better, all the while maintaining a good intake of more slowly fermented longer chain polysaccharides to maintain colonic integrity and calm inflammation? The difficulty there lies in the fact that many of the same plants that contain the rapidly fermented fructo-oligosaccharides also contain longer chain fructo-polysaccharides.