Abstract MP42: Reduction in Dietary Transfat Intake is Associated with Improved Lipid Particle Number in a Primary Prevention Population

Abstract

Background: Recent public policy has focused on elimination of dietary transfats. The extent to which changes in transfat intake correlate with changes in cardiovascular disease (CVD) risk in real world settings is not established. Lipid Particle Number (LPN) is a novel marker of CVD risk and data from the Framingham Offspring Study indicate a doubling of CVD risk among those with LPN values in the highest versus lowest quartile. The purpose of this study was to determine if a decrease in transfat intake is associated with a decrease in LPN in a free living population at risk of CVD. Methods: This was a 1 year follow-up study of family members (n = 400, 33% male, 36% racial/ethnic minority, mean age 48 +/- 13) of patients hospitalized with CVD who participated in a 1 year NHLBI sponsored randomized controlled primary prevention lifestyle intervention trial and had complete dietary data and LPN measures at baseline and 1 year. Transfat (% of total kilocalories per day) was assessed by the validated Block Food Frequency Questionnaire and LPN (nmol/L) was measured at a central lab using NMR spectroscopy at baseline and 1 year. Traditional CVD risk factors and potential confounders were assessed by trained research personnel using standardized measures and questionnaires. Change in transfat as a percentage of total diet and mean absolute change in LPN at 1 year was assessed using multivariate adjusted linear regression models. Results: Over 1 year 57% (n = 226) of the study population decreased their transfat intake which did not vary significantly by group assignment. There was a significant positive correlation between baseline dietary transfat intake and LPN (p = 0.04). At baseline higher mean LPN was also associated with male sex (p < 0.001), overweight/obesity (≥ 25 kg/m 2 , p < 0.001), waist size (men ≥ 40 inches, women ≥ 35 inches, p < 0.001), HgA1c (≥ 6.5%, p = 0.003), and current smoking (p = 0.01). Over 1 year, for every 1 percent change in transfat intake there was a 27 nmol/L change in LPN (p = 0.04). The association between the change in transfat intake and change in LPN was independent of baseline predictors, confounders, and group assignment (p = 0.03). Conclusion: In a free living population at risk of CVD, a reduction in transfat intake over 1 year was significantly associated with a reduction in LPN. These data suggest how improved LPN may be one potential mechanism by which elimination of transfat may confer CVD benefit, and provide insight into the potential for a decrease in transfat intake to decrease the burden of CVD.