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Fiber Intake and Plasminogen Activator Inhibitor-1 in Type 2 Diabetes: Look AHEAD (Action for Health in Diabetes) Trial Findings at Baseline and Year 1

Published:August 15, 2014DOI:https://doi.org/10.1016/j.jand.2014.06.357

      Abstract

      Plasminogen activator inhibitor 1 (PAI-1) is elevated in obese individuals with type 2 diabetes and may contribute, independently of traditional factors, to increased cardiovascular disease risk. Fiber intake may decrease PAI-1 levels. We examined the associations of fiber intake and its changes with PAI-1 before and during an intensive lifestyle intervention (ILI) for weight loss in 1,701 Look AHEAD (Action for Health in Diabetes) participants with dietary, fitness, and PAI-1 data at baseline and 1 year. Look AHEAD was a randomized cardiovascular disease trial in 5,145 overweight/obese patients with type 2 diabetes, comparing ILI (goal of ≥7% reduction in baseline weight) with a control arm of diabetes support and education. ILI participants were encouraged to consume vegetables, fruits, and grain products low in sugar and fat. At baseline, median fiber intake was 17.9 g/day. Each 8.3 g/day higher fiber intake was associated with a 9.2% lower PAI-1 level (P=0.008); this association persisted after weight and fitness adjustments (P=0.03). Higher baseline intake of fruit (P=0.019) and high-fiber grain and cereal (P=0.029) were related to lower PAI-1 levels. Although successful in improving weight and physical fitness at 1 year, the ILI in Look AHEAD resulted in small increases in fiber intake (4.1 g/day, compared with –2.35 g/day with diabetes support and education) that were not related to PAI-1 change (P=0.34). Only 31.3% of ILI participants (39.8% of women, 19.1% of men) met daily fiber intake recommendations. Increasing fiber intake in overweight/obese individuals with diabetes interested in weight loss is challenging. Future studies evaluating changes in fiber consumption during weight loss interventions are warranted.

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      Biography

      L. M. Belalcazar is an associate professor, Department of Medicine, University of Texas Medical Branch, Galveston.

      Biography

      A. M. Anderson is a biostatistician, Department of Biostatistical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC.

      Biography

      J. Rushing is a biostatistician, Department of Biostatistical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC.

      Biography

      W. Lang is an assistant professor, Department of Biostatistical Sciences, Wake Forest University School of Medicine, Winston-Salem, NC.

      Biography

      M. Z. Vitolins is a professor, Department of Epidemiology and Prevention, Wake Forest University School of Medicine, Winston-Salem, NC.

      Biography

      D. C. Schwenke is a research professor, College of Nursing and Health Innovation, Arizona State University, Phoenix.

      Biography

      S. M. Haffner is retired; at the time of the study, he was a professor, Department of Medicine, University of Texas Health Science Center, San Antonio.

      Biography

      H. Yatsuya is a professor, Department of Public Health, Fujita Health University, Toyoake, Japan.

      Biography

      R. Reeves is retired; at the time of the study, she was an assistant professor, Department of Medicine, Baylor College of Medicine, Houston, TX.

      Biography

      F. X. Pi-Sunyer is a professor, Department of Medicine, Columbia University, St Luke’s–Roosevelt Hospital, New York, NY.

      Biography

      R. P. Tracy is a professor, Department of Pathology, University of Vermont, Burlington.

      Biography

      C. M. Ballantyne is a professor, Department of Medicine, Baylor College of Medicine, Houston, TX, and Center for Cardiovascular Disease Prevention, Methodist De Bakey Heart and Vascular Center, Houston, TX.