Date Published: June 09, 2013
Publisher: Blackwell Publishing Ltd
Author(s): C H Wilder-Smith, A Materna, C Wermelinger, J Schuler.
The association of fructose and lactose intolerance and malabsorption with the symptoms of different functional gastrointestinal disorders (FGID) remains unclear.
To investigate the prevalence of fructose and lactose intolerance (symptom induction) and malabsorption and their association with clinical gastrointestinal (GI) as well as non-GI symptoms in FGID and the outcome of dietary intervention.
Fructose and lactose intolerance (defined by positive symptom index) and malabsorption (defined by increased hydrogen/methane) were determined in 1372 FGID patients in a single centre using breath testing. Results were correlated with clinical symptoms in different FGID Rome III subgroups. The effectiveness of a targeted saccharide-reduced diet was assessed after 6–8 weeks.
Intolerance prevalence across all FGIDs was 60% to fructose, 51% to lactose and 33% to both. Malabsorption occurred in 45%, 32% and 16% respectively. There were no differences in intolerance or malabsorption prevalence between FGID subgroups. FGID symptoms correlated with symptoms evoked during testing (r = 0.35–0.61. P < 0.0001), but not with malabsorption. Non-GI symptoms occurred more commonly in patients with intolerances. Methane breath levels were not associated with constipation using several cut-off thresholds. Adequate symptom relief was achieved in >80% of intolerant patients, irrespective of malabsorption.
Fructose and lactose intolerances are common in FGID and associated with increased non-GI symptoms, but not with specific FGID subtypes. Symptoms experienced during breath testing, but not malabsorption, correlate with FGID symptoms. Effective symptom relief with dietary adaptation is not associated with malabsorption. Mechanisms relating to the generation of GI and non-GI symptoms due to lactose and fructose in FGID need to be explored further.
Adverse reactions to food are common in the population and are claimed by up to 67% of individuals with Functional Gastrointestinal Disorders (FGID).1 They form part of the Rome III definition of Functional Dyspepsia (FD), and are frequent in Irritable Bowel Syndrome (IBS).2 Food hypersensitivity is often difficult to confirm, but avoidance of specific foods often diminishes symptoms. Possible underlying mechanisms include nutrient maldigestion or malabsorption, chemical or mechanical hypersensitivity, changes in gastrointestinal motility, the enteric microbiome, and immune and psychological responses. Reliable tests are lacking for several of these mechanisms and results may be ambiguous, for example, for tests of malabsorption and allergy. However, there has been recent progress, both in more refined test methodology and in interventional studies.3, 4 Although carbohydrate intolerances, defined as symptoms associated with their ingestion, are probably not the cause of most FGID, the reduced consumption of fermentable saccharides in patients with malabsorption results in symptom relief superior to most pharmaceutical treatments.5, 6 However, the significance of carbohydrate-related symptoms and of malabsorption in FGID remains unclear, as do the optimal diagnostic techniques.7 Furthermore, the common association of GI intolerances with non-GI reactions in FGID remains unexplained.
All successive patients referred to our gastroenterology practice by general practitioners between January 2008 and May 2011 for evaluation of FGID were eligible for inclusion in this prospective study, except those with evidence of organic disease, which was assessed by routine haematology and biochemistry blood testing and also stool testing for calprotectin and pancreas elastase determined in two stool samples in all patients. Parasite and bacterial stool cultures were performed if clinically indicated. Upper and lower endoscopies with biopsies were required in patients older than 40 years or in patients with diarrhoea or faecal blood.8 Coeliac disease was excluded by antitranglutaminase antibodies or duodenal biopsies. One consultant gastroenterologist (CWS) performed all the medical and dietary history taking and physical examinations. The dietary history included two sections: an open question requesting a listing of avoided and poorly tolerated foods and then a specific list of the main fructose, fructooligosaccharide, galactosaccharide, lactose and sorbitol-containing foods as well as the 10 commonest food allergies in Europe. In addition, skin rashes, urticaria, rhinitis, headache, imperative defaecatory urge, changes in stool consistency related to mealtimes were documented. All patients completed a standardised questionnaire, which included the specific questions for classification of GI symptoms into FGID groups according to the Rome III criteria and additional questions regarding allergies, childhood and family history, central nervous, musculoskeletal and cardiac system symptoms, and the use of polyol-containing sweets and chewing gum. Patients were classified into FGID subgroups according to the Rome III criteria.9 The most prominent FGID was chosen for classifying each patient. The study was performed in accordance with the Helsinki Declaration of 1975 as revised in 1983.
Patient characteristics are shown in Table 1. Seventy-six per cent of the 1372 patients were of Northern European and 19% of Mediterranean European Caucasian descent. Of these patients, the following subgroups were defined according to the Rome III criteria: Irritable Bowel Syndrome (n = 212), comprised of IBS with constipation (IBS-c, n = 37), IBS with diarrhoea (IBS-d, n = 67), IBS with alternating constipation and diarrhoea (IBS-m, n = 94) and IBS unclassified (IBS-u, n = 14), Functional Dyspepsia(n = 606), comprised of FD with postprandial distress (FD-ppd, n = 368) and FD with epigastric pain syndrome (FD-eps, n = 238), and Functional Bloating (n = 109).
Both fructose and lactose intolerance as shown by breath testing were common in this large group of FGID patients, one third of whom had an overlap of both intolerances. The important question is whether intolerances are an underlying mechanism or an epiphenomenon in FGID. The prevalence of intolerances was similar across all major types of FGID, except IBS-C. As the different FGID phenotypes were not related to distinct distributions of the intolerances, a causal relationship between FGID and the intolerances would have to be explained by divergent host responses to the saccharide ingestion. Such potential host factors include the enteric microbiome, intestinal permeability, nervous system and immune responses, all of which are interrelated and differ between FGID and controls.20–24 Hypersensitivity to distension and to ingested nutrients has been shown in different FGID, but we are not aware of comparisons between subgroups, except in IBS-C, where fermentation processes may be influenced by a prolonged transit time.16, 25–31
Guarantor of the article: Clive H. Wilder-Smith.