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Title: Comparison of diets entriched in stearic, oleic and palmitic acids on inflammation, immune response, cardiometabolic risk factors and fecal bile acids concentrations in mildly hypercholesterolemic postmenopausal women - ...

Author
item MENG, HUICUI - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item MATTHAN, NIRUPA - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item WU, DAYONG - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item LI, LIJUN - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item RODRIGUEZ-MORATO, JOSE - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item COHEN, REBECCA - Tufts University
item GALLUCCIO, JEAN - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item DOLNIKOWSKI, GREGORY - Jean Mayer Human Nutrition Research Center On Aging At Tufts University
item LICHTENSTEIN, ALICE - Jean Mayer Human Nutrition Research Center On Aging At Tufts University

Submitted to: The American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/24/2019
Publication Date: 6/10/2019
Citation: Meng, H., Matthan, N.R., Wu, D., Li, L., Rodriguez-Morato, J., Cohen, R., Galluccio, J.M., Dolnikowski, G.G., Lichtenstein, A.H. 2019. Comparison of diets enriched in stearic, oleic and palmitic acids on inflammation, immune response, cardiometabolic risk factors and fecal bile acids concentrations in mildly hypercholesterolemic postmenopausal women - randomized cross-over trial. American Journal of Clinical Nutrition. https://doi.org/10.1093/ajcn/nqz095.
DOI: https://doi.org/10.1093/ajcn/nqz095

Interpretive Summary: Cardiometabolic disorders remain the major causes of mortality and morbidity in the United States and globally, hence, are leading public health challenges. Although positive associations between dietary saturated fatty acid intake and cardiometabolic risk have been documented, some recent reports have questioned the strength of the relationship. A potential source of discrepancies in the available data may be attributable to differential effects of individual saturated fatty acids, particularly stearic acid (18:0), compared to the shorter chain saturated fatty acids, particularly palmitic acid (16:0), and to its metabolic product, oleic acid (18:1), a monounsaturated FA. Our objective was to determine the relative comparability of diets enriched in 16:0, 18:0 and 18:1 on inflammation and coagulation markers, T lymphocyte proliferation/ ex vivo cytokine secretion, plasma cardiometabolic risk factors, and fecal bile acid concentrations. We found that diet enriched 18:0 and 18:1 had similar and more favorable effects on fasting plasma cholesterol profiles than 16:0. Other measures, with one exception, were similar among the fatty acids tested. Unlike 18:1, the hypocholesterolemic effect of 18:0 may be mediated by inhibition of intestinal hydrophobic secondary bile acid synthesis. These findings add to the data suggesting there should be a reassessment of current saturated fatty acid dietary guidance and Nutrient Facts panel labeling.

Technical Abstract: Background: Direct comparisons among saturated fatty acids (SFA) varying in chain length, specifically palmitic acid (16:0) and stearic acid (18:0), relative to the latter's metabolic product, oleic acid (18:1), on cardiometabolic risk factors is limited. Objective: To determine the relative comparability of diets enriched in 16:0, 18:0 and 18:1 on inflammation and coagulation markers, T lymphocyte proliferation/ ex vivo cytokine secretion, plasma cardiometabolic risk factors, and fecal bile acid concentrations. Design: Hypercholesterolemic postmenopausal women (N=20, 64 +/- 7y, BMI 26.4 +/- 3.4kg/m^2, LDL-cholesterol>/=2.8mmol/L) were provided with each of three diets (55%E carbohydrate, 15%E protein, 30%E fat, with about 50% fat contributed by 16:0, 18:0, or 18:1 in each diet; 5 weeks/diet phase) using a randomized cross-over design with 2-week washouts between phases. Outcome measures were assessed at the end of each phase. Results: Fasting LDL-cholesterol and nonHDL-cholesterol concentrations were lower after the 18:0 and 18:1 than 16:0 diet (all P<0.01). Fasting HDL-cholesterol concentrations were lower after the 18:0 than 16:0 and 18:1 diets (P<0.01). The 18:0 diet resulted in lower lithocholic acid (P=0.01) and total secondary bile acids (SBA) concentrations (P=0.04) than 18:1 diet. All other outcome measures were similar among diets. Lithocholic acid concentrations were positively correlated with fasting LDL-cholesterol concentrations (r=0.33; P=0.011). Total SBA, lithocholic acid and deoxycholic acid concentrations were negatively correlated with fasting HDL-cholesterol (r=-0.51 to -0.44; P<0.01) concentrations, and positively correlated with LDL-cholesterol:HDL-cholesterol (r=0.37 to 0.54; P<0.01) ratios. Conclusions: Dietary 18:0 and 18:1 had similar and more favorable effects on fasting LDL-cholesterol and nonHDL-cholesterol concentrations than 16:0. Unlike 18:1, the hypocholesterolemic effect of 18:0 may be mediated by inhibition of intestinal hydrophobic SBA synthesis. These findings add to the data suggesting there should be a reassessment of current SFA dietary guidance and Nutrient Facts panel labeling.