Genetics
In a 10-week RCT, sugar-sweetened beverages lowered Lp(a) by 13% in overweight adults, independent of apo(a) size (J Lipid Res 2024)
Original title: Lipoprotein(a) and diet: consuming sugar-sweetened beverages lowers lipoprotein(a) levels in obese and overweight adults
In a double-blind, parallel-arm randomised controlled trial, 32 overweight or obese adults (mean age 54 years, 50% women, 75% of European descent) consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Lp(a) fell by an average of 13.2% plus/minus 4.3% across all participants (P = 0.005), with reductions of 15.3% in the glucose group (P = 0.07) and 11.3% in the fructose group (P = 0.02), with no significant difference between sugar types. The relative Lp(a) reduction was similar regardless of baseline Lp(a) level or apolipoprotein(a) size polymorphism (carriers versus non-carriers of an atherogenic small, 22 Kringle repeats or fewer, apo(a) isoform), while LDL cholesterol rose over the same period, moving in the opposite direction to Lp(a). This RCT shows that sugar-sweetened beverage consumption lowers Lp(a) independent of genetically determined apo(a) size, a counterintuitive dietary effect opposite to its impact on LDL-C and triglycerides, pointing to a distinct metabolic pathway governing Lp(a).
Original abstract
Lipoprotein(a) [Lp(a)] contributes to cardiovascular disease risk. A genetically determined size polymorphism in apolipoprotein(a) [apo(a)], determined by the number of Kringle (K) repeats, inversely regulates Lp(a) levels. Nongenetic factors including dietary saturated fat influence Lp(a) levels. However, less is known about the effects of carbohydrates including dietary sugars. In this double-blind, parallel arm study among 32 overweight/obese adults, we investigated the effect of consuming glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks on Lp(a) level and assessed the role of the apo(a) size polymorphism. The mean (±SD) age of participants was 54 ± 8 years, 50% were women, and 75% were of European descent. Following the 10-week intervention, Lp(a) level was reduced by an average (±SEM) of -13.2% ± 4.3% in all participants (P = 0.005); -15.3% ± 7.8% in the 15 participants who consumed glucose (P = 0.07); and -11.3% ± 4.5% in the 17 participants who consumed fructose (P = 0.02), without any significant difference in the effect between the two sugar groups. Relative changes in Lp(a) levels were similar across subgroups of lower versus higher baseline Lp(a) level or carrier versus noncarrier of an atherogenic small (≤22K) apo(a) size. In contrast, LDL-C increased. In conclusion, in older, overweight/obese adults, consuming sugar-sweetened beverages reduced Lp(a) levels by ∼13% independently of apo(a) size variability and the type of sugar consumed. The Lp(a) response was opposite to that of LDL-C and triglyceride concentrations. These findings suggest that metabolic pathways might impact Lp(a) levels.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.