Diet and Irritable Bowel Syndrome

Anusha Thomas; Eamonn M.M. Quigley


Curr Opin Gastroenterol. 2015;31(2):166-171. 

In This Article

Abstract and Introduction


Purpose of review Those who suffer from irritable bowel syndrome (IBS) have long reported the frequent precipitation of their symptoms in relation to food ingestion and have often been convinced that certain foods were especially problematic. However, until very recently, research on the responses to food or individual dietary constituents, in IBS, has been scarce. This review addresses recent literature on diet and IBS.

Recent findings The complexity of food–symptom interactions in IBS is being revealed in recent and ongoing research. Such studies have revealed the variable effects of fibre in IBS and the susceptibility of IBS individuals to the ingestion of poorly digested and absorbed carbohydrates. The latter has led to the widespread adoption of the low-fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) diet. Less certain is the role of another widely adopted dietary strategy, gluten restriction. Diet–microbe interactions are critical to the homeostasis of the gut microbiome in health and may well be disturbed in disease; enthusiasm continues, therefore, for the use of probiotics in IBS.

Summary Food is a common precipitant of symptoms in IBS and recent research has focused on the role(s) of individual dietary constituents in IBS and on fibre, FODMAPs, gluten and probiotics, in particular. Each may have a role in certain IBS sufferers.


Irritable bowel syndrome (IBS) is a chronic functional gastrointestinal disorder characterized by abdominal pain or discomfort associated with abnormal bowel habit in the absence of any currently detectable structural, physiological or biochemical abnormalities of the gastrointestinal tract. In the absence of a reliable or a validated biomarker, IBS is defined on the basis of symptoms according to one of several diagnostic systems. Most common amongst these are the Rome criteria, which have now gone through three iterations; pending the outcome of the fourth set of such deliberations, Rome III diagnostic criteria remain the benchmark for the diagnosis of IBS in clinical research. According to Rome III, IBS is defined by the presence of 'recurrent abdominal pain or discomfort for at least 3 days per month in the past 3 months, associated with 2 or more of the following: improvement with defecation, onset associated with a change in the frequency of stool or onset associated with a change in the form or appearance of stool'.[1] Bloating, distension and fatigue are also commonly featured in IBS and overlap with other functional gastrointestinal disorders is the rule rather than the exception. IBS symptoms are common in the general population and, in a minority of sufferers, exert a significant negative impact on quality of life, work, education and family life. Consequently, IBS is responsible for imparting considerable morbidity as well as a significant economic burden, throughout the world and in Western society, in particular.[2–5] Despite these costs to society and the individual and decades of clinical and laboratory investigations into the pathophysiology of IBS, our understanding of IBS remains incomplete and its treatment, therefore, somewhat unsatisfactory.[6] IBS is undoubtedly a heterogeneous disorder and may, indeed, encompass a number of distinct entities. It comes as no surprise, therefore, that over the years a number of factors have been proposed as relevant to the etiopathogenesis of IBS and its various symptoms. Over the years, these have ranged from genetics to gut dysmotility, visceral hypersensitivity, altered brain processing of visceral signals and abnormal psycho-neuro-endocrine and hypothalamic-pituitary-adrenal responses.[7,8] Along the way, the frequent association of IBS with anxiety and depression has often led to the latter acting as confounding variables in IBS research. In an attempt to introduce some uniformity to the field, the paradigm of the brain-gut axis emerged as a unifying concept,[9] with various manifestations and/or presentations of IBS being seen to locate themselves on one or other point along this axis. Accordingly, in some individuals, their symptoms may be largely of central origin, in others, more peripheral/gut-located factors may predominate. Indeed, of late, research in IBS has to a significant extent focused more on a number of putative peripheral factors, and progress in this area has been facilitated by advances in our understanding of the enteric nervous system, the gut microbiome, mucosal immune responses, epithelial barrier function and epithelial secretory mechanisms. Indeed, abnormalities in the gut microbiome,[10,11] the host immune response, the epithelial barrier, intestinal secretion,[12] as well as systemic immune mediators[13] have been variably identified in IBS individuals, subgroups thereof or experimental models, and novel therapeutic strategies developed accordingly. Unfortunately, few of these have, as yet, led to effective and targeted treatment strategies for IBS sufferers.[14] Most recently, and belatedly, the important role of the ubiquitous interloper into the gastrointestinal environment, food, has begun to be recognized and serious research efforts devoted to understanding its role in IBS and to the development of dietary approaches to the management of IBS.