Effects of Manipulating Dietary Carbohydrate and Fat on Circulating Saturated Fatty Acid Composition

Dietary recommendations by public health organizations promote intakes high in carbohydrates and low in saturated fat (SFA) largely based on the belief that dietary SFA raises plasma cholesterol. While plasma SFA contributes to the risk of metabolic syndrome, diabetes, and cardiovascular disease, the evidence linking dietary SFA to these diseases is substantially weak. An association does exist between high carbohydrate intakes and elevations in plasma SFA, but the amount and individual variability of one’s ability to process dietary carbohydrate has yet to be explored under highly controlled conditions. The primary purpose was to investigate the hypothesis that levels of carbohydrate in the diet are more influential than dietary SFA on circulating SFA and cardio-metabolic risk with an additional aim to explore individual variability. Fourteen overweight men and women with metabolic syndrome were monitored for 21 weeks. After a 3-week run-in low carbohydrate diet, subjects were fed six 3-week diets that incrementally increased in carbohydrate and decreased fat. Plasma fatty acids, lipoproteins, and traditional clinical markers of cardiovascular disease were evaluated after each phase. Plasma triglyceride and cholesteryl ester SFA decreased or remained unchanged despite a two-fold increase in dietary SFA as subjects transitioned from habitual diets to the lowest carbohydrate diet. As carbohydrates progressively increased and SFA decreased, total circulating SFA remained the same or increased, with significant variability between participants. 16:1n-7, a marker of de novo lipogenesis, dramatically and uniformly reduced as carbohydrate intake decreased and rose as carbohydrates increased. Despite continued weight loss, reductions in dietary fat and increases in carbohydrate resulted in fluctuations of total cholesterol, LDL-C, HDL-C but all maintained improvements from baseline. TAG reduced during ChoI and increased after subsequent phases. Insulin sensitivity improved with carbohydrate restriction but gradually returned to near-baseline levels as carbohydrates were reintroduced. Despite similar relative dietary input, degrees of weight loss varied among participants. High SFA intakes do not contribute to accumulation of blood SFA and chronic disease risk when carbohydrate intake is limited. However, decreasing dietary SFA and increasing carbohydrate is associated with a fatty acid profile more indicative of increased de novo lipogenesis and increased disease risk