Abstract P176: Consumption of Sugar-Sweetened Beverages Lowers Lipoprotein(a) Levels in Obese and Overweight Adults: Findings in a Double-Blind Parallel-Arm Study

Abstract

Elevated levels of lipoprotein(a) [Lp(a)] are a genetically regulated, causal, and prevalent risk factor for atherosclerotic cardiovascular disease. A size polymorphism in the apolipoprotein(a) [apo(a)] gene, determined by the number of Kringle (K) repeats, inversely regulates Lp(a) plasma levels. Despite strong genetic regulation, non-genetic factors such as diet influence Lp(a) levels. However, the relationship between Lp(a) level and sugar consumption remains understudied. In this double-blinded parallel arm study, we investigated the effect of consuming glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks on plasma Lp(a) levels in 32 overweight/obese adults. Lp(a) levels were measured using an apo(a) size insensitive ELISA and apo(a) isoform sizes were determined by Western blotting. The mean (SD) age of participants was 54 ± 8 years, 50% were women, and 75% were of European descent. The mean body mass index was 29 ± 3 kg/m 2 and 28% of participants had metabolic syndrome. In all participants, baseline median Lp(a) level was 10.3 mg/dL (IQR: 4, 28 mg/dL). At the end of the 10-week intervention, Lp(a) levels were reduced by an average of -4 mg/dL (-13%) in all participants, by -4 mg/dL (-15%) in the glucose group (n=15) and by -5 mg/dL (-11%) in the fructose group (n=17), respectively. The mean percent changes in Lp(a) levels in the low (≤25 mg/dL) (n=23) vs high (>25 mg/dL) (n=9) baseline Lp(a) groups were similar: -14% (-2 mg/dL) vs -11% (-11 mg/dL), respectively. Notably, the carrier status of an atherogenic small (≤22K repeats) apo(a) size did not substantially impact Lp(a) responses as the mean Lp(a) changes were similar in carriers (-15%) (n=8) vs non-carriers (-13%) (n=24). In conclusion, in overweight/obese adults, consuming sugar-sweetened beverages providing 25% of energy requirements for 10 weeks reduced Lp(a) levels by ~13% independent of apo(a) size variability. The findings suggest that pathways involving carbohydrates and fatty acid metabolism might potentially impact Lp(a) levels. The specific mechanisms underlying the effect of sugar-sweetened beverage consumption to reduce circulating Lp(a) levels warrant further investigation.