Date

June 2010

Document Type

Thesis

Degree Name

M.S.

Institution

Oregon Health & Science University

Abstract

Background: Low-carbohydrate diets are used successfully for weight loss but may induce a state of heightened inflammation due to their high fat content. However, little research has explored the impact of low- and high-carbohydrate diets on circulating fatty acid and inflammatory marker concentrations. Objective: A secondary analysis of data obtained from the Energy Balance Study was used to determine whether changes in circulating concentrations of fatty acids and inflammatory markers were different after six weeks of low- or high-carbohydrate dietary intervention in obese adults. Relationships between changes in fatty acid and inflammatory marker concentrations were also determined within groups. Methodology: Twenty-three obese, but otherwise healthy adults participated in a randomized controlled feeding study. Participants consumed a standard diet for three weeks and then either an ad libitum low- (n=10) or high- (n=13) carbohydrate diet for six weeks. Fasting blood samples collected at the end of the second and ninth weeks of dietary intervention were analyzed for concentrations of saturated, omega-6 (n-6) and omega-3 (n-3) fatty acids, Creactive protein (CRP) and interleukin-6 (IL-6). Wilcoxon signed-rank tests and rank sum tests were used to determine whether differences in the change from baseline of each variable were significant, within and between groups, respectively. Changes from baseline, adjusted for baseline values and weight loss, were compared between groups using robust regression analyses. Spearman correlation analyses were used to determine relationships between the change in concentrations of fatty acids and the change in concentrations of inflammatory markers within groups after adjusting for weight loss. Results: Subjects in the low-carbohydrate diet group lost -5 ± 3 kg and subjects in the high-carbohydrate diet group lost -3 ± 2 kg with the low-carbohydrate diet group losing more weight than the high-carbohydrate diet group (p=0.05). Plasma saturated fatty acid concentrations were significantly lower after the low- and high-carbohydrate dietary interventions than before but the changes from baseline were not different between groups (p=0.6). Plasma n-6 fatty acid concentrations were not significantly different from baseline after the low- and high-carbohydrate diet interventions and change from baseline was similar between the two diet groups (p=0.4). Plasma n-3 fatty acid concentration was higher after the high-carbohydrate diet intervention (p=0.02) but not after the low carbohydrate diet intervention; however changes from baseline between groups were not different (p=0.2). As a result, the n-6/n-3 fatty acid concentration ratio was lower after the high-carbohydrate diet intervention but not the low carbohydrate diet intervention (p<0.01). There were no differences in the change in inflammatory marker concentrations between groups. When mean plasma fatty acid and inflammatory marker concentrations were adjusted for baseline values and weight loss the only comparison that was significant between groups was the plasma n-6/n-3 fatty acid ratio (p=0.02); the plasma n-6/n-3 fatty acid ratio was lower in the high-carbohydrate diet group than the low-carbohydrate diet group. The change in plasma concentrations of saturated fatty acids was positively correlated with the change in concentrations of CRP in the high-carbohydrate diet group (p=0.01), but not the low-carbohydrate diet group (p=0.4). The change in plasma concentrations of n-3 fatty acids was negatively correlated with the change in concentrations of CRP (p=0.05) in the low-carbohydrate diet group, but not the high-carbohydrate diet group (p=0.2). Conclusions: During active weight loss, changes in circulating concentrations of saturated, n-6 and n-3 fatty acids, and IL-6 and CRP were similar between groups despite extreme differences in the macronutrient content of the low- and high-carbohydrate diets. These results are different from what we anticipated, as we hypothesized that the low-carbohydrate diet would heighten inflammation. Although a randomized, well controlled feeding study was used to test these hypotheses, the study was not powered, a priori, to detect differences in our outcome variables. Therefore, our results should be interpreted with caution due to the high risk of a type II error (β=0.37) that may have produced results showing no differences, when differences actually existed. To confirm the results described here, additional studies with larger sample sizes that are powered to detect differences in changes in plasma fatty acid and inflammatory marker concentrations after low- and high-carbohydrate dietary interventions should be performed. Funding: This research was funded by grants from the National Center for Complementary and Alternative Medicine (R21-AT002753) and the National Center for Research Resources (UL1 RR024140), a component of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research.

Identifier

doi:10.6083/M46H4FD4

Division

Graduate Programs in Human Nutrition

School

School of Medicine

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