Put simply: pretty much, yes. If you go to the doctor, and get your “bad cholesterol” (LDL-C) measured, that will predict heart disease risk very well. But the details are a bit more complicated, so let’s go over them.
Low density lipoproteins (LDL) are one of several types of particles that transport fats in the blood. Fats need to be packaged like this since they’re hydrophobic (i.e., they’ll separate out in water), and the blood is mostly water.
The liver releases fats to the bloodstream by packaging them in very-low density lipoproteins (VLDLs) that contain both triglycerides and cholesterol. These VLDLs provide the body with fats, and in the process of delivering those fats, are transformed into LDL.[1]
LDL particles are very widely accepted as being a main cause of atherosclerosis.[2][3] But clinics don’t usually measure LDL particles. Insead, they usually measure the amount of cholesterol contained in LDL particles: LDL-C. Because LDL is very cholesterol-rich, this serves as an excellent proxy for LDL levels in the blood, and thus correlates very well to atherosclerotic risk.
But the blood level of LDL-C alone does not tell the whole story of atherosclerosis.[4]
First, any cholesterol particle with a specific protein called ApoB, including LP(a), remnant particles, and very low density, low density, and intermediate density lipoproteins, can play a role in depositing fats like cholesterol and triglycerides into vessel walls, inducing inflammation, and making atherosclerosis worse.[5] That’s because oxidized particles with ApoB are recognized and taken up by immune cells, which starts building up the fatty streak mentioned above.[6]
Second, preliminary evidence suggests that LDL particles with different densities have differing atherosclerotic potential: small dense LDL particle levels better predict heart disease risk and may be able to cause more damage than large buoyant LDL particles.[7][5]
Next, the inflammatory environment in which LDL-C particles are circulating affects the extent and type of immune activation and fatty acid oxidation, which is necessary for atherosclerotic progression.[8]
Lastly, other components deposited in plaques — oxidized fats, triglycerides, calcium, dead cells, and scar tissue — affect plaque stability and resistance to further damage.[8]
Taken together, LDL particles which are rich in cholesterol play a major role in causing atherosclerosis, but the presence of other factors may determine the extent of that damage.
References
- ^King TCCardiovascular PathologyElsevier's Integrated Pathology.(2007 pp. 169-195)
- ^Ference BA, Ginsberg HN, Graham I, Ray KK, Packard CJ, Bruckert E, Hegele RA, Krauss RM, Raal FJ, Schunkert H, Watts GF, Borén J, Fazio S, Horton JD, Masana L, Nicholls SJ, Nordestgaard BG, van de Sluis B, Taskinen MR, Tokgözoglu L, Landmesser U, Laufs U, Wiklund O, Stock JK, Chapman MJ, Catapano ALLow-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus PanelEur Heart J.(2017 Aug 21)
- ^Goldstein JL, Brown MSA century of cholesterol and coronaries: from plaques to genes to statins.Cell.(2015-Mar-26)
- ^Libby PThe changing landscape of atherosclerosis.Nature.(2021-04)
- ^Shapiro MD, Fazio SApolipoprotein B-containing lipoproteins and atherosclerotic cardiovascular disease.F1000Res.(2017)
- ^Steinberg D, Witztum JLOxidized low-density lipoprotein and atherosclerosis.Arterioscler Thromb Vasc Biol.(2010-Dec)
- ^Ikezaki H, Furusyo N, Yokota Y, Ai M, Asztalos BF, Murata M, Hayashi J, Schaefer EJSmall Dense Low-Density Lipoprotein Cholesterol and Carotid Intimal Medial Thickness Progression.J Atheroscler Thromb.(2020-Oct-01)
- ^Göran K Hansson, Peter LibbyThe immune response in atherosclerosis: a double-edged swordNat Rev Immunol.(2006 Jul)