David J A Jenkins1, Cyril W C Kendall2, Vladimir Vuksan3, Dorothea Faulkner4, Livia S A Augustin5, Sandra Mitchell4, Christopher Ireland4, Korbua Srichaikul6, Arash Mirrahimi7, Laura Chiavaroli4, Sonia Blanco Mejia4, Stephanie Nishi4, Sandhya Sahye-Pudaruth4, Darshna Patel4, Balachandran Bashyam4, Edward Vidgen5, Russell J de Souza8, John L Sievenpiper9, Judy Coveney5, Robert G Josse10, Lawrence A Leiter10. 1. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaDepartment of Medicine, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaClinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, CanadaDivision of Endocrinology and Metabolism, St. Michael's Hospital, Toronto, ON, CanadaLi Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, ON, Canada nutritionproject@smh.ca. 2. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaClinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, CanadaCollege of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, SK, Canada. 3. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaClinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, CanadaLi Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, ON, Canada. 4. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaClinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, Canada. 5. Clinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, Canada. 6. Clinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, CanadaMedical School, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. 7. Clinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, CanadaSchool of Medicine, Faculty of Health Sciences, Queen's University, Kingston, ON, Canada. 8. Clinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, CanadaDepartment of Clinical Epidemiology and Biostatistics, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada. 9. Clinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, CanadaLi Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, ON, CanadaDepartment of Pathology and Molecular Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada. 10. Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaDepartment of Medicine, Faculty of Medicine, University of Toronto, Toronto, ON, CanadaClinical Nutrition and Risk Factor Modification Center, St. Michael's Hospital, Toronto, ON, CanadaDivision of Endocrinology and Metabolism, St. Michael's Hospital, Toronto, ON, CanadaLi Ka Shing Knowledge Institute of St. Michael's Hospital, Toronto, ON, Canada.
Abstract
OBJECTIVE: Despite their independent cardiovascular disease (CVD) advantages, effects of α-linolenic acid (ALA), monounsaturated fatty acid (MUFA), and low-glycemic-load (GL) diets have not been assessed in combination. We therefore determined the combined effect of ALA, MUFA, and low GL on glycemic control and CVD risk factors in type 2 diabetes. RESEARCH DESIGN AND METHODS: The study was a parallel design, randomized trial wherein each 3-month treatment was conducted in a Canadian academic center between March 2011 and September 2012 and involved 141 participants with type 2 diabetes (HbA1c 6.5%-8.5% [48-69 mmol/mol]) treated with oral antihyperglycemic agents. Participants were provided with dietary advice on either a low-GL diet with ALA and MUFA given as a canola oil-enriched bread supplement (31 g canola oil per 2,000 kcal) (test) or a whole-grain diet with a whole-wheat bread supplement (control). The primary outcome was HbA1c change. Secondary outcomes included calculated Framingham CVD risk score and reactive hyperemia index (RHI) ratio. RESULTS: Seventy-nine percent of the test group and 90% of the control group completed the trial. The test diet reduction in HbA1c units of -0.47% (-5.15 mmol/mol) (95% CI -0.54% to -0.40% [-5.92 to -4.38 mmol/mol]) was greater than that for the control diet (-0.31% [-3.44 mmol/mol] [95% CI -0.38% to -0.25% (-4.17 to -2.71 mmol/mol)], P = 0.002), with the greatest benefit observed in those with higher systolic blood pressure (SBP). Greater reductions were seen in CVD risk score for the test diet, whereas the RHI ratio increased for the control diet. CONCLUSIONS: A canola oil-enriched low-GL diet improved glycemic control in type 2 diabetes, particularly in participants with raised SBP, whereas whole grains improved vascular reactivity.
RCT Entities:
OBJECTIVE: Despite their independent cardiovascular disease (CVD) advantages, effects of α-linolenic acid (ALA), monounsaturated fatty acid (MUFA), and low-glycemic-load (GL) diets have not been assessed in combination. We therefore determined the combined effect of ALA, MUFA, and low GL on glycemic control and CVD risk factors in type 2 diabetes. RESEARCH DESIGN AND METHODS: The study was a parallel design, randomized trial wherein each 3-month treatment was conducted in a Canadian academic center between March 2011 and September 2012 and involved 141 participants with type 2 diabetes (HbA1c 6.5%-8.5% [48-69 mmol/mol]) treated with oral antihyperglycemic agents. Participants were provided with dietary advice on either a low-GL diet with ALA and MUFA given as a canola oil-enriched bread supplement (31 g canola oil per 2,000 kcal) (test) or a whole-grain diet with a whole-wheat bread supplement (control). The primary outcome was HbA1c change. Secondary outcomes included calculated Framingham CVD risk score and reactive hyperemia index (RHI) ratio. RESULTS: Seventy-nine percent of the test group and 90% of the control group completed the trial. The test diet reduction in HbA1c units of -0.47% (-5.15 mmol/mol) (95% CI -0.54% to -0.40% [-5.92 to -4.38 mmol/mol]) was greater than that for the control diet (-0.31% [-3.44 mmol/mol] [95% CI -0.38% to -0.25% (-4.17 to -2.71 mmol/mol)], P = 0.002), with the greatest benefit observed in those with higher systolic blood pressure (SBP). Greater reductions were seen in CVD risk score for the test diet, whereas the RHI ratio increased for the control diet. CONCLUSIONS: A canola oil-enriched low-GL diet improved glycemic control in type 2 diabetes, particularly in participants with raised SBP, whereas whole grains improved vascular reactivity.
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