High Daily Fructose Intake Induces Intestinal Carriers: A Maladaptive Response

Abstract

Purpose: Polymers of fructose are important prebiotics promoting lactic acid bacteria, yet monosaccharide fructose is associated with obesity and some illnesses. Little exists on whether colonic adaptation occurs with regular fructose consumption. We undertook this study to evaluate effects of fructose on symptoms, physiologic response and microbial flora. Methods: 45 healthy subjects (20M, 25F) undertook a 50g fructose challenge. Breath hydrogen for 4.5 hr (TBH2, hydrogenmeter EC 60 Bedfont), symptom score on a 4 point likert scale and fecal bacteria (N38) (total anaerobes, bifidobacteria and lactobacilli by quantitative culture) were measured. A 3 day diet recall questionnaire was used to asses average daily pretest fructose intake. All 26 fructose intolerant (57.8%) subjects were assigned either 30 g fructose intake BID for 2 weeks (16, group F) or were controls (10 group C1). Subjects returned for repetiton of tests. 10 fructose assigned subjects also returned 2 weeks later off fructose (group C) and a third set of tests were repeated (excluding stool). Paired t, unpaired t and Pearson correlations were carried out where appropriate. Significance was accepted at p<0.05. ClinTrials.gov NCT00775567. Results: Compared to test 1, no symptomatic improvement occurred in test 2 for (F) or (C1), nor in test 3 for group (C). Total breath hydrogen decreased significantly in group (C) (delta H2, 97.3±128sd ppm, p=0.04). After excluding a single outlier in group (F), there was also a significant test 2 decrease in total BH2 (delta101±169sd ppm,p=0.036). Comparison of TBH2 between (F) and (C1) was also significant p=0.003. In C1, BH2 change was insignificant (delta-57.7±222sd ppm, p=0.48). There were no discernable effects of fructose intake on bifidobacteria or lactobacilli in test 2 within (change in test2-testl) or between (test 2 only) groups (F) or (C1) or in test 1 in subjects consuming less than 20g fructose daily. In a small set (N5) of subjects in test 1 consuming >20g/d fructose, there was a weak inverse correlation with these bacteria p<0.1>0.05 (prebiotic effect should be positive). Conclusion: Failure to improve symptoms and to impact on fecal bacteria while reducing breath hydrogen after intake of large doses of fructose suggest that the possible mechanism is via induction of fructose carriers. This induction is still evident at 2 weeks. Bacterial adaptation has different observable features. This maladaptive process should lead to proscription of prolonged intake of high doses of monosaccharide fructose.