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Association of 1-y changes in diet pattern with cardiovascular disease risk factors and adipokines: results from the 1-y randomized Oslo Diet and Exercise Study

¹ From the Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN (DRJ); the Department of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Norway (DRJ, MHR-A, and CAD); the Department of Human Nutrition, Wageningen University, Wageningen, Netherlands (DS); and the Department of Sports Medicine, Norwegian School of Sport Sciences, Oslo, Norway (SAA).

² Supported by grants from the Freia Chocolade Fabriks Medical Foundation, the Direktør Johan Throne Holst Foundation for Nutrition Research, the Norwegian Foundation for Health and Rehabilitation, the Research Council of Norway, the Norwegian Health Association (The Norwegian Council on Cardiovascular Diseases), the Swedish Research Council (K2007-54X-09894-16-3), the Novo Nordisk Foundation, and the Swedish Strategic Foundation. DS was a visiting scholar at the University of Minnesota supported by Stichting Dr. Hendrik Muller's Vaderlandsch Fonds and De Fundatie van de Vrijvrouwe van Renswoude.

³ Reprints not available. Address correspondence to DR Jacobs Jr, University of Minnesota, Division of Epidemiology, School of Public Health, 1300 South 2nd Street, Suite 300, Minneapolis, MN 55454, E-mail: jacobs{at}epi.umn.edu.

Background: We hypothesized that favorable changes in dietary patterns would lead to a reduction in body size and an improvement in metabolic status.

Objective: The objective was to study changes in diet patterns relative to changes in body size, blood pressure, and circulating concentrations of lipids, glucose, insulin, adiponectin, and other cytokines in the context of a 1-y randomized intervention study.

Design: For 1 y, 187 men aged 45 ± 2 y, 50% of whom met the criteria of the metabolic syndrome, were randomly assigned to a diet protocol (n = 45), an exercise protocol (n = 48), a protocol of diet plus exercise (n = 58), or a control protocol (n = 36). A previously defined a priori diet score was created by summing tertile rankings of 35 food group variables; a higher score generally reflected recommended dietary changes in the trial (mean ± SD at baseline: 31 ± 6.5; range: 15–47).

Results: Over the study year, the diet score increased by 2 ± 5.5 in both diet groups, with a decrease of an equivalent amount in the exercise and control groups. The weight change was –3.5 ± 0.6 kg/10-point change in diet score (P < 0.0001), similarly within each intervention group, independently of the change in energy intake or baseline age and smoking status. Weight change was attenuated but remained significant after adjustment for intervention group and percentage body fat. Subjects with an increased diet score had more favorable changes in other body size variables, systolic blood pressure, and blood lipid, glucose, insulin, and adiponectin concentrations. Change in diet score was unrelated to resistin and several cytokines.

Conclusion: The change toward a more favorable diet pattern was associated with improved body size and metabolic profile.

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