D David Wang1, John L Sievenpiper2, Russell J de Souza3, Adrian I Cozma1, Laura Chiavaroli1, Vanessa Ha1, Arash Mirrahimi4, Amanda J Carleton5, Marco Di Buono6, Alexandra L Jenkins7, Lawrence A Leiter8, Thomas M S Wolever8, Joseph Beyene9, Cyril W C Kendall10, David J A Jenkins8. 1. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada; Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, Toronto, ON, Canada. 2. Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, Toronto, ON, Canada; Department of Pathology and Molecular Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada. Electronic address: john.sievenpiper@utoronto.ca. 3. Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, Toronto, ON, Canada; Department Clinical Epidemiology and Biostatistics, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada. 4. Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, Toronto, ON, Canada; School of Medicine, Faculty of Medicine, Queen's University, Kingston, ON, CANADA. 5. Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, Toronto, ON, Canada; Undergraduate Medical Education (MD Program), Faculty of Medicine, University of Toronto, Toronto, ON, Canada. 6. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada. 7. Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, Toronto, ON, Canada. 8. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada; Toronto 3D Knowledge Synthesis and Clinical Trials Unit, Clinical Nutrition and Risk Factor Modification Centre, Toronto, ON, Canada; Keenan Research Center of the Li Ka Shing Knowledge Institute, Toronto, ON, Canada; Division of Endocrinology, St. Michael's Hospital, Toronto, ON, Canada; Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, ON, Canada. 9. Department Clinical Epidemiology and Biostatistics, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada; Population Health Sciences, Research Institute Hospital for Sick Children, Toronto, ON, Canada. 10. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada; Department Clinical Epidemiology and Biostatistics, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada; College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, SK, Canada.
Abstract
BACKGROUND: In the absence of consistent clinical evidence, concerns have been raised that fructose raises postprandial triglycerides. PURPOSE: A systematic review and meta-analysis was conducted to assess the effect of fructose on postprandial triglycerides. DATA SOURCES: Relevant studies were identified from MEDLINE, EMBASE, and Cochrane databases (through September 3, 2013). DATA SELECTION: Relevant clinical trials of ≥ 7-days were included in the analysis. DATA EXTRACTION: Two independent reviewers extracted relevant data with disagreements reconciled by consensus. The Heyland Methodological Quality Score (MQS) assessed study quality. Data were pooled by the generic inverse variance method using random effects models and expressed as standardized mean differences (SMD) with 95% confidence intervals (CI). Heterogeneity was assessed (Cochran Q statistic) and quantified (I(2) statistic). DATA SYNTHESIS: Eligibility criteria were met by 14 isocaloric trials (n = 290), in which fructose was exchanged isocalorically for other carbohydrate in the diet, and two hypercaloric trials (n = 33), in which fructose supplemented the background diet with excess energy from high-dose fructose compared with the background diet alone (without the excess energy). There was no significant effect in the isocaloric trials (SMD: 0.14 [95% CI: -0.02, 0.30]) with evidence of considerable heterogeneity explained by a single trial. Hypercaloric trials, however, showed a significant postprandial triglyceride raising-effect of fructose (SMD: 0.65 [95% CI: 0.30, 1.01]). LIMITATIONS: Most of the available trials were small, short, and of poor quality. Interpretation of the isocaloric trials is complicated by the large influence of a single trial. CONCLUSIONS: Pooled analyses show that fructose in isocaloric exchange for other carbohydrate does not increase postprandial triglycerides, although an effect cannot be excluded under all conditions. Fructose providing excess energy does increase postprandial triglycerides. Larger, longer, and higher-quality trials are needed. PROTOCOL REGISTRATION: ClinicalTrials.gov identifier, NCT01363791.
BACKGROUND: In the absence of consistent clinical evidence, concerns have been raised that fructose raises postprandial triglycerides. PURPOSE: A systematic review and meta-analysis was conducted to assess the effect of fructose on postprandial triglycerides. DATA SOURCES: Relevant studies were identified from MEDLINE, EMBASE, and Cochrane databases (through September 3, 2013). DATA SELECTION: Relevant clinical trials of ≥ 7-days were included in the analysis. DATA EXTRACTION: Two independent reviewers extracted relevant data with disagreements reconciled by consensus. The Heyland Methodological Quality Score (MQS) assessed study quality. Data were pooled by the generic inverse variance method using random effects models and expressed as standardized mean differences (SMD) with 95% confidence intervals (CI). Heterogeneity was assessed (Cochran Q statistic) and quantified (I(2) statistic). DATA SYNTHESIS: Eligibility criteria were met by 14 isocaloric trials (n = 290), in which fructose was exchanged isocalorically for other carbohydrate in the diet, and two hypercaloric trials (n = 33), in which fructose supplemented the background diet with excess energy from high-dose fructose compared with the background diet alone (without the excess energy). There was no significant effect in the isocaloric trials (SMD: 0.14 [95% CI: -0.02, 0.30]) with evidence of considerable heterogeneity explained by a single trial. Hypercaloric trials, however, showed a significant postprandial triglyceride raising-effect of fructose (SMD: 0.65 [95% CI: 0.30, 1.01]). LIMITATIONS: Most of the available trials were small, short, and of poor quality. Interpretation of the isocaloric trials is complicated by the large influence of a single trial. CONCLUSIONS: Pooled analyses show that fructose in isocaloric exchange for other carbohydrate does not increase postprandial triglycerides, although an effect cannot be excluded under all conditions. Fructose providing excess energy does increase postprandial triglycerides. Larger, longer, and higher-quality trials are needed. PROTOCOL REGISTRATION: ClinicalTrials.gov identifier, NCT01363791.
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