Testing
Cutting saturated fat raises Lp(a) even as it lowers LDL-C, a diet effect long assumed not to exist, updated review argues (Nutrients 2025)
Original title: Lipoprotein(a) and Effects of Diet: Time for Reassessment
This narrative review by Enkhmaa and Berglund reassesses dietary regulation of Lp(a), long assumed to be governed almost entirely by genetics and unaffected by diet, unlike LDL cholesterol's well-established response to saturated fat (SFA) intake. The authors describe clear evidence that SFA intake affects Lp(a) in the opposite direction to LDL-C: reducing SFA intake raises Lp(a) even as it lowers LDL-C, and the review extends beyond classic SFA-reduction studies to newer clinical trial evidence on increased sugar intake and ketogenic diets. It also examines how apolipoprotein(a) size polymorphism, the major genetic determinant of Lp(a) level, interacts with these dietary effects. The authors note that whether diet also alters Lp(a)'s molecular and lipidomic composition, beyond its concentration, remains unknown, and call for further study of whether diet should become a formal component of elevated Lp(a) management.
Original abstract
Dietary modification is a critical tool in the prevention of cardiovascular disease (CVD). While the role of saturated fat (SFA) intake is well established in affecting LDL cholesterol concentrations, diet impacts on lipoprotein(a) (Lp(a)) have been less studied. Lp(a) is a prevalent, strong, and highly heritable risk factor for CVD and a therapeutic target for CVD risk management. While significant insights have been made into the genetic regulation of Lp(a), our understanding of any metabolic impact on Lp(a) by other factors, including diets, is limited. For many years, Lp(a) was not considered to be subject to dietary regulation, but there is now clear evidence of a dietary impact, in particular variability in SFA intake, on Lp(a) concentrations. The present narrative review aims to provide an updated view on dietary regulation of Lp(a), moving beyond studies testing the effect of reducing SFA intake, to include new evidence from clinical trials on the impact of an increased sugar intake and ketogenic diets. In addition to describing an opposite effect of SFA on Lp(a) and LDL cholesterol concentrations, with a rise in Lp(a) during a reduced SFA intake, this review also provides new data on the role of apolipoprotein(a) size polymorphism, a major genetic regulator of Lp(a) concentrations. Beyond an impact on Lp(a) concentrations, the extent to which diet might impact Lp(a)'s molecular and metabolic properties including its lipidomic composition remains unknown. Taken together, evidence shows the presence of a dietary modulation of Lp(a) beyond its genetic control and points to the need to better understand Lp(a)'s cardiovascular risk factor properties, including metabolomics/lipidomics characteristics. This also raises the issue whether diet should be a component of elevated Lp(a) management, and this needs to be addressed in future studies.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.