Obesity and functional gastrointestinal disorders: What is the link?

Functional gastrointestinal disorders (FGIDs), or disorders of gut-brain interaction (DGBI), are one of the most common GI disorders globally, with an estimated prevalence of almost 40% globally.1 Although there are some 33 disorders that make up FGIDs, the most prevalent conditions include functional dyspepsia (FD), irritable bowel syndrome (IBS), and functional constipation (FC). The pathophysiology of FGIDs is complex, involving gut-brain axis dysregulation, visceral hypersensitivity, gastrointestinal dysmotility, low grade intestinal inflammation, gut dysbiosis, and psychological disorders.2 They are one of the most common conditions managed in gastroenterology clinics and often lead to increased healthcare utilization.3 Epidemiologically, several factors have been shown to be associated with FGIDs including gender, age, ethnicity, genetics, geographical location and diet.4 Obesity, defined as a body mass index (BMI) of > 30 kg/m2, is yet another factor that has been linked with FGIDs. In a population-based study, Guo et al. found that IBS was significantly related to the metabolic syndrome and elevated triglycerides among 1096 Japanese subjects.5 In a recent systematic review of 348 studies, Zia et al. found that obesity (in addition to gender, psychological disorders, stress, poor sleep, and somatic symptoms) was identified as a risk factor for IBS and abdominal pain-related DGBI.6 Furthermore, some studies have reported that chronic GI symptoms (which may include FGIDs) among morbidly obese patients do improve after undergoing weight-loss surgery.7 So how does obesity cause FGIDs? In this issue of the journal, Yanping et al. postulate that obesity may lead to FGIDS, particularly IBS, by increasing visceral hypersensitivity.8 Visceral hypersensitivity is one of the pathophysiological mechanisms involved in generating symptoms in IBS, mainly by having a lower pain threshold to bowel distension or an increased sensitivity to normal intestinal function.2 The authors suggest that obesity may be involved in hyperexcitability of primary visceral afferent fibers at the intestinal level and enhanced perception of the intestinal signal in the brain. Through low-grade, chronic inflammation, obesity is thought to mediate the effects of sensitizing the gut via an increased intestinal permeability, gut microbiota variation, and vitamin D insufficiency. Although the hypothesis suggested by Wu et al. are plausible, there are some inconsistencies in the association of obesity or an increased BMI with FGIDs. In a large European population-based study exploring BMI with various FGIDs among 35 447 adults, FD was associated with being underweight while the risk of functional diarrhea increased with BMI in females. Other associations were insignificant.9 This observation was similarly observed in a primary care study of 1002 Asian adults, whereby a low BMI (< 18 kg/m2) and anxiety were found to be associated with FD, while no other FGIDs were associated with BMI.10 Hence, since obesity seems to be associated with some FGIDs (IBS in particular) and not others, it is uncertain if the causal mechanism is via visceral hypersensitivity alone. Another possibility, as the authors suggest, is that it is not an increased BMI per se but abdominal/visceral adiposity that leads to FGIDs via chronic low-grade inflammation and its sequelae.11 Both obesity and FGIDs share certain similar pathophysiological mechanisms, such as chronic low-grade inflammation, changes in intestinal permeability, endocrine abnormalities, and an altered gut microbiome.2, 12 However, cause and effect between obesity and FGIDs cannot be easily disentangled. Further studies exploring pathophysiological mechanisms between different FGIDs and abdominal/visceral adiposity are still required, before the link can be confidently ascertained.