Date of Completion

5-8-2014

Embargo Period

5-8-2014

Keywords

metabolic syndrome, fat oxidation, weight-loss, body composition, low-carbohydrate, ketones, insulin, carbohydrate, feeding study

Major Advisor

Jeff S. Volek, Ph.D., R.D.

Associate Advisor

Carl M. Maresh, Ph.D.

Associate Advisor

William J. Kraemer, Ph.D.

Associate Advisor

Maria Luz Fernandez, Ph.D.

Field of Study

Kinesiology

Degree

Doctor of Philosophy

Open Access

Open Access

Abstract

Despite evidence that low-carbohydrate diets (LCD) can improve metabolic syndrome (MetS) characteristics and risk for cardiovascular disease, concerns remain regarding the potential deleterious effects of higher fat intake. If higher fat intake (in the context of lower carbohydrate intake) is accompanied by higher fat oxidation, there would likely be more efficient fat loss and improved health parameters. Our aim was to examine how diets spanning a broad range of carbohydrate levels ranging from very low (<50 g/day) to current dietary guidelines (~350 g/day) affect substrate oxidation patterns and changes in body composition within the same person while keeping caloric and protein intake constant. After an initial 3-wk run-in LCD, 16 adults with MetS (age 44.9 ± 9.9 yr, BMI 37.9 ± 6.3 kg/m2) were fed six sequential moderately hypocaloric 3-wk diets that progressively increased carbohydrate (CHO) (from 47 to 344 g/day) with concomitant decreases in total fat. Body composition was determined by dual-energy X-ray absorptiometry (DXA) and respiratory quotient (RQ), fat oxidation, and resting energy expenditure (REE) were determined by indirect calorimetry after each diet phase. Subjects lost significantly more fat mass (-2.32±1.53 kg) on the free-living LCD phase, but overall fat mass loss was variable between subjects and on average less than expected from the calculated caloric deficit (-8.3±4.5 vs 12.74±15.81 kg, respectively). There was a significant decrease in REE, but no significant change in relative REE (kcals/kg/day). Fat oxidation rates significantly increased when consuming diets with 7% CHO, but decreased to below baseline by the highest CHO phase. RQ decreased on the LCD (0.75±0.04), and increased linearly as CHO increased, up to 0.84 ±0.05. Body mass was significantly correlated with CHO consumption (r=0.49), insulin (r=0.34), fat consumption (r=-0.49) and ketones (r=0.46). These findings suggest that it is difficult to estimate weight loss within an individual, even with a constant caloric deficit, since individuals vary in their substrate oxidation response to reintroduction of dietary carbohydrate. Those who can maintain a higher fat oxidation to a greater extent as carbohydrates are increased (and fat decreased) may possess an enhanced ability for fat loss on higher carbohydrate diets.

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