Abstract

Reduction in dietary saturated fatty acids (SFA) intake results in a significant clinically meaningful lowering of LDL-C across ethnicities. In contrast, the role of dietary SFA reduction in modulating emerging risk factors for cardiovascular disease (CVD) in different ethnic groups remains poorly understood. An elevated level of lipoprotein(a) [Lp(a)], an independent casual risk factor for CVD, disproportionally affects African Americans. In this study, we assessed the responses in Lp(a) to dietary SFA reduction specifically in African Americans (N=166) enrolled in GET-READI (The Gene-Environment Trial on Response in African Americans to Dietary Intervention), a randomized controlled feeding trial. Men and women with above optimal LDL-C were fed two diets in a random order for five weeks each: (1) the average American diet (AAD) (37% total fat: 16% SFA), and (2) a diet similar to the Dietary Approaches to Stop Hypertension (DASH) combination diet (25% total fat: 6% SFA). The mean age of participants was 33 years (range: 18-64 years), 70% were women, the mean BMI was 28.4 kg/m 2 and LDL-C was 116 mg/dL. At the end the 5-week intervention period with the DASH diet, compared with the end of the AAD diet, LDL-C was significantly reduced (mean change: -12.4 mg/dL, p <0.0001), as were the levels of total cholesterol (-16.6 mg/dL, p <0.0001), HDL-C (-5 mg/dL, p <0.0001), apoA-1 (-8.7 mg/dL, p <0.0001) and apoB-100 (-5.7 mg/dL, p <0.0001). In contrast, Lp(a) levels were significantly increased following the DASH diet compared to AAD (from a median value of 44 mg/dL with AAD to 58 mg/dL with DASH; mean change: +11.2 mg/dL, p <0.0001). As LDL-C measurements typically include Lp(a)-cholesterol, the “true” LDL-C decrease is estimated at -16 mg/dL, i.e., an underestimation by about 30%. In conclusion, in a large cohort of African Americans, an ethnic group with a high burden of elevated Lp(a), reductions in SFA intake significantly increased Lp(a) while reducing LDL-C. These findings suggest that dietary SFA reduction exerted an opposing effect on the circulating levels of two highly-atherogenic lipoproteins. Future studies are warranted to elucidate mechanism(s) underlying the SFA reduction-induced increase in Lp(a) and its role in CVD risk across population groups.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call