LAUSR

76 77 78 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 95 96 97 98 99 100 101 102 103 104 105 106 107 108 109 110 111 112 113 114 115 116 117 Dirritable bowel syndrome, because food is a major inducer of symptoms, and dietary manipulation empowers patients to influence the outcome of their disorder. It is not surprising, therefore, that the arrival of the low FODMAP diet, which is based on sound scientific evidence, has led to its enthusiastic adoption in clinical practice across the world. However, the diet has been criticized in 4 main areas: (1) the strength of the efficacy data, mainly owing to perceived bias in clinical trial design and the lack of realworld placebo-controlled trials; (2) the complexity and difficulty of teaching the diet; (3) safety, especially on the structure of gut microbiota; and (4) longer term efficacy and safety. The article by Staudacher et al in the current edition of Gastroenterology addresses three of these issues. Performance of high-quality, randomized, controlled trials of therapeutic diets is challenging. Theoretically, the standards by which we judge a dietary intervention should be as stringent as those for a pharmacological agent. Critics argue that such standards have not been adequately met for the low FODMAP diet. A gold standard approach for evaluating a therapeutic diet is the provision of all food to recipients in a double-blinded way, as was done in the pivotal study for the low FODMAP diet, with unequivocally positive results. Unfortunately, feeding studies do not mimic real-world clinical practice, where diets are taught by health professionals and implemented by patients. Dietitianled randomized, controlled trials have been conducted where comparator diets have ranged from habitual diet (which lacks the placebo effect of active dietitian-mediated intervention), high FODMAP diet (where potential exacerbation symptoms may exaggerate the efficacy of the low FODMAP diet), or currently administered active diets. All of these studies were designed to primarily address questions (effects on structure and function of gut microbiota, and on metabolomics profiles, and comparison with currently instituted therapies) other than efficacy over placebo. Furthermore, in the pivotal feeding study, the placebo diet was constructed on the basis of a typical intake of FODMAPs in healthy Australians, which proved to be greater than that retrospectively estimated from the participants’ habitual diet. Although the mean difference in oligosaccharide intake of 1.2 g/d was unlikely to induce symptoms, it may have confounding effects on the gut