What is atherosclerosis?
Atherosclerosis refers to the buildup of fatty plaque on the interior lining of the arteries — the medium- and large-sized blood vessels that carry nutrients and oxygen to tissues throughout the body. The formation of these plaques damage the inside surface of the arteries and leads to more plaque buildup, inflammation, artery hardening and narrowing, and an increased risk of clotting.[1] Severe plaque buildup leads to a wide range of diseases, including coronary artery disease, carotid artery disease (blockage of the arteries feeding into the brain), and peripheral arterial disease (blockage of arteries in the arms, legs, or pelvis).[2]
Atherosclerosis should not be confused with arteriosclerosis, which is a broader term referring to general thickening and stiffening of blood vessels of all sizes; atherosclerosis is a specific kind of arteriosclerosis. [1]
What are the main signs and symptoms of atherosclerosis?
Atherosclerosis can be visualized using a process called angiography. While this is one of the better methods for assessing atherosclerosis, it’s not usually used for routine screening since it’s invasive.[3] Other less invasive methods can be used to assess atherosclerosis, including coronary calcium scans that measure calcium buildup inside heart arteries (less invasive, but involves radiation exposure) and the ankle-brachial test (noninvasive; mainly relates to atherosclerosis in the peripheral arteries, but atherosclerosis in the periphery is correlated with atherosclerosis elsewhere in the body[3]), as well as ultrasonography.[4]
Atherosclerosis is usually symptomless until it starts causing other atherosclerotic cardiovascular diseases like coronary artery disease.[5]
How is atherosclerosis diagnosed?
Preclinical atherosclerosis isn’t usually diagnosed directly through imaging or the other measurements mentioned above. However, once it manifests clinically, it may be caught during imaging or through the criteria for the clinical diseases it leads to (e.g., peripheral artery disease). Atherosclerosis may also be presumed on the basis of risk factors such as biomarkers like high blood pressure or LDL-C, demographics like age, or behaviors like smoking.
What are some of the main medical treatments for atherosclerosis?
Medical treatment options depend on the type of clinical disease and how far it’s progressed.
If a person doesn’t have clinical disease yet, then the main medical treatments usually target the major risk factors of high cholesterol and high blood pressure using drugs like statins and antihypertensives as spelled out in major guidelines.[6]
Medical treatment is often added on top of lifestyle changes, since lifestyle plays a large role in atherosclerosis. The major lifestyle recommendations are discussed more fully below.
Have any supplements been studied for atherosclerosis?
Yes, although exactly which supplements qualify depends on whether you count studies involving markers tightly related to atherosclerosis like LDL-C or only count studies that measure atherosclerosis more directly. A lot more studies have looked at biomarkers related to atherosclerosis than direct measurements. However, since a lot of studies have examined biomarkers like LDL-C and blood-pressure that are firmly established to actually cause atherosclerosis, the evidence base isn’t too bad.
A very incomplete list of supplements examined for impact on atherosclerosis or its biomarkers include:[7]
How could diet affect atherosclerosis?
Diet plays a huge role in atherosclerosis through impacting many of its associated risk factors, such as obesity, high cholesterol, high blood-pressure, and diabetes. Recent guidelines cite strong evidence that weight loss in people with overweight or obesity can reduce atherosclerotic disease risk. There’s also strong evidence that a diet high in fruits and vegetables, legumes, nuts, whole grains, and fish can reduce the risk for diseases caused by atherosclerosis. Weaker evidence suggests that swapping out saturated fat with mono- or polyunsaturated fats and minimizing processed meats and refined carbohydrates can also help.[6]
Are there any other treatments for atherosclerosis?
The biggest lifestyle change that can impact atherosclerosis is quitting smoking[8]. Getting aerobic exercise is also extremely important. To reduce atherosclerotic risk, people should ideally perform at least 150 minutes of moderate-intensity aerobic activity, 75 minutes of vigorous-intensity aerobic activity, or a combination of the two each week.[6] A rule of thumb to measure intensity is the talk test: moderate aerobic activity makes it hard to sing but not to talk, whereas it’s hard to say more than a few words at a time during vigorous aerobic exercise.
What causes atherosclerosis?
Atherosclerosis starts with damage to the interior lining of medium and large arteries, which often occurs in arteries that are under high pressure and tension, a process that can start in childhood.[9] This damage leads to the fats — which are mostly in the form of low density lipoprotein (LDL), but can also be carried by other apolipoprotein B-containing lipoproteins[10] — being trapped in the interior arterial lining. The more such lipoproteins there are, the more that can get trapped. The fats then get oxidized, which attracts white blood cells — mainly macrophages — to try to clean up the mess. However, when there’s a lot of fat to clean up, the macrophages overdo it and transform into foam cells, which is one of the main ingredients of atherosclerotic plaque formation.
Examine Database: Atherosclerosis
Research FeedRead all studies
In this post hoc analysis of a randomized controlled trial, supplementation with macular carotenoids (lutein, zeaxanthin, and meso-zeaxanthin) reduced some markers of inflammation and serum levels of oxidized LDL. However, several limitations reduce our confidence in the result.
Frequently asked questions
Atherosclerosis refers to the buildup of fatty plaque on the interior lining of the arteries — the medium- and large-sized blood vessels that carry nutrients and oxygen to tissues throughout the body. The formation of these plaques damage the inside surface of the arteries and leads to more plaque buildup, inflammation, artery hardening and narrowing, and an increased risk of clotting.[1] Severe plaque buildup leads to a wide range of diseases, including coronary artery disease, carotid artery disease (blockage of the arteries feeding into the brain), and peripheral arterial disease (blockage of arteries in the arms, legs, or pelvis).[2]
Atherosclerosis should not be confused with arteriosclerosis, which is a broader term referring to general thickening and stiffening of blood vessels of all sizes; atherosclerosis is a specific kind of arteriosclerosis. [1]
Atherosclerosis can be visualized using a process called angiography. While this is one of the better methods for assessing atherosclerosis, it’s not usually used for routine screening since it’s invasive.[3] Other less invasive methods can be used to assess atherosclerosis, including coronary calcium scans that measure calcium buildup inside heart arteries (less invasive, but involves radiation exposure) and the ankle-brachial test (noninvasive; mainly relates to atherosclerosis in the peripheral arteries, but atherosclerosis in the periphery is correlated with atherosclerosis elsewhere in the body[3]), as well as ultrasonography.[4]
Atherosclerosis is usually symptomless until it starts causing other atherosclerotic cardiovascular diseases like coronary artery disease.[5]
Preclinical atherosclerosis isn’t usually diagnosed directly through imaging or the other measurements mentioned above. However, once it manifests clinically, it may be caught during imaging or through the criteria for the clinical diseases it leads to (e.g., peripheral artery disease). Atherosclerosis may also be presumed on the basis of risk factors such as biomarkers like high blood pressure or LDL-C, demographics like age, or behaviors like smoking.
Medical treatment options depend on the type of clinical disease and how far it’s progressed.
If a person doesn’t have clinical disease yet, then the main medical treatments usually target the major risk factors of high cholesterol and high blood pressure using drugs like statins and antihypertensives as spelled out in major guidelines.[6]
Medical treatment is often added on top of lifestyle changes, since lifestyle plays a large role in atherosclerosis. The major lifestyle recommendations are discussed more fully below.
Yes, although exactly which supplements qualify depends on whether you count studies involving markers tightly related to atherosclerosis like LDL-C or only count studies that measure atherosclerosis more directly. A lot more studies have looked at biomarkers related to atherosclerosis than direct measurements. However, since a lot of studies have examined biomarkers like LDL-C and blood-pressure that are firmly established to actually cause atherosclerosis, the evidence base isn’t too bad.
A very incomplete list of supplements examined for impact on atherosclerosis or its biomarkers include:[7]
Diet plays a huge role in atherosclerosis through impacting many of its associated risk factors, such as obesity, high cholesterol, high blood-pressure, and diabetes. Recent guidelines cite strong evidence that weight loss in people with overweight or obesity can reduce atherosclerotic disease risk. There’s also strong evidence that a diet high in fruits and vegetables, legumes, nuts, whole grains, and fish can reduce the risk for diseases caused by atherosclerosis. Weaker evidence suggests that swapping out saturated fat with mono- or polyunsaturated fats and minimizing processed meats and refined carbohydrates can also help.[6]
Atherosclerosis has long been considered to be a progressive, irreversible condition; once it starts, there is no way to reverse — or so we thought. Evidence from animal and human studies using drugs has made it clear that atherosclerosis can actually be reversed to some degree.[19] There’s also some evidence from studies that image blood vessels have shown that atherosclerosis can be reversed by diet and lifestyle interventions to some extent as well, although the evidence is more confounded since most of the evidence looks at combined, complex lifestyle interventions.[20] For example, a holistic lifestyle and plant-based diet intervention showed reversal of blocked arteries.[21] Also, an olive oil-rich Mediterranean diet was able to reduce the thickness of artery plaque among people with coronary artery disease.[22]
Weight loss is well-established to prevent atherosclerosis,[6] but weight loss has lackluster effects on reversing established atherosclerosis in people with type 2 diabetes.[23] Overall, it looks like adopting a healthy dietary pattern may either slow or possibly reverse the narrowing of arteries due to atherosclerosis, particularly in early stages of plaque formation[24], and these effects are enhanced alongside lifestyle changes like exercising, stress management, and quitting smoking.
The biggest lifestyle change that can impact atherosclerosis is quitting smoking[8]. Getting aerobic exercise is also extremely important. To reduce atherosclerotic risk, people should ideally perform at least 150 minutes of moderate-intensity aerobic activity, 75 minutes of vigorous-intensity aerobic activity, or a combination of the two each week.[6] A rule of thumb to measure intensity is the talk test: moderate aerobic activity makes it hard to sing but not to talk, whereas it’s hard to say more than a few words at a time during vigorous aerobic exercise.
Atherosclerosis starts with damage to the interior lining of medium and large arteries, which often occurs in arteries that are under high pressure and tension, a process that can start in childhood.[9] This damage leads to the fats — which are mostly in the form of low density lipoprotein (LDL), but can also be carried by other apolipoprotein B-containing lipoproteins[10] — being trapped in the interior arterial lining. The more such lipoproteins there are, the more that can get trapped. The fats then get oxidized, which attracts white blood cells — mainly macrophages — to try to clean up the mess. However, when there’s a lot of fat to clean up, the macrophages overdo it and transform into foam cells, which is one of the main ingredients of atherosclerotic plaque formation.
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.[11]
LDL particles are very widely accepted as being a main cause of atherosclerosis.[12][13] 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.[14]
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.[15] That’s because oxidized particles with ApoB are recognized and taken up by immune cells, which starts building up the fatty streak mentioned above.[16]
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.[17][15]
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.[18]
Lastly, other components deposited in plaques — oxidized fats, triglycerides, calcium, dead cells, and scar tissue — affect plaque stability and resistance to further damage.[18]
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
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- ^MedlinePlus: Atherosclerosis
- ^StatPearls: atherosclerosis
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- ^Donna K Arnett, Roger S Blumenthal, Michelle A Albert, Andrew B Buroker, Zachary D Goldberger, Ellen J Hahn, Cheryl Dennison Himmelfarb, Amit Khera, Donald Lloyd-Jones, J William McEvoy, Erin D Michos, Michael D Miedema, Daniel Muñoz, Sidney C Smith Jr, Salim S Virani, Kim A Williams Sr, Joseph Yeboah, Boback Ziaeian2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice GuidelinesCirculation.(2019 Sep 10)
- ^Joe W E Moss, Dipak P RamjiNutraceutical therapies for atherosclerosisNat Rev Cardiol.(2016 Sep)
- ^Gaemperli O, Liga R, Bhamra-Ariza P, Rimoldi ONicotine addiction and coronary artery disease: impact of cessation interventions.Curr Pharm Des.(2010)
- ^Newman WP, Freedman DS, Voors AW, Gard PD, Srinivasan SR, Cresanta JL, Williamson GD, Webber LS, Berenson GSRelation of serum lipoprotein levels and systolic blood pressure to early atherosclerosis. The Bogalusa Heart Study.N Engl J Med.(1986-Jan-16)
- ^Jan Borén, M John Chapman, Ronald M Krauss, Chris J Packard, Jacob F Bentzon, Christoph J Binder, Mat J Daemen, Linda L Demer, Robert A Hegele, Stephen J Nicholls, Børge G Nordestgaard, Gerald F Watts, Eric Bruckert, Sergio Fazio, Brian A Ference, Ian Graham, Jay D Horton, Ulf Landmesser, Ulrich Laufs, Luis Masana, Gerard Pasterkamp, Frederick J Raal, Kausik K Ray, Heribert Schunkert, Marja-Riitta Taskinen, Bart van de Sluis, Olov Wiklund, Lale Tokgozoglu, Alberico L Catapano, Henry N GinsbergLow-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus PanelEur Heart J.(2020 Jun 21)
- ^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)
- ^Goldberg IJ, Sharma G, Fisher EAAtherosclerosis: Making a U Turn.Annu Rev Med.(2020-01-27)
- ^Parsons C, Agasthi P, Mookadam F, Arsanjani RReversal of coronary atherosclerosis: Role of life style and medical management.Trends Cardiovasc Med.(2018-11)
- ^Gupta SK, Sawhney RC, Rai L, Chavan VD, Dani S, Arora RC, Selvamurthy W, Chopra HK, Nanda NCRegression of coronary atherosclerosis through healthy lifestyle in coronary artery disease patients--Mount Abu Open Heart TrialIndian Heart J.(2011 Sep-Oct)
- ^Jimenez-Torres J, Alcalá-Diaz JF, Torres-Peña JD, Gutierrez-Mariscal FM, Leon-Acuña A, Gómez-Luna P, Fernández-Gandara C, Quintana-Navarro GM, Fernandez-Garcia JC, Perez-Martinez P, Ordovas JM, Delgado-Lista J, Yubero-Serrano EM, Lopez-Miranda JMediterranean Diet Reduces Atherosclerosis Progression in Coronary Heart Disease: An Analysis of the CORDIOPREV Randomized Controlled Trial.Stroke.(2021-11)
- ^, Wing RR, Bolin P, Brancati FL, Bray GA, Clark JM, Coday M, Crow RS, Curtis JM, Egan CM, Espeland MA, Evans M, Foreyt JP, Ghazarian S, Gregg EW, Harrison B, Hazuda HP, Hill JO, Horton ES, Hubbard VS, Jakicic JM, Jeffery RW, Johnson KC, Kahn SE, Kitabchi AE, Knowler WC, Lewis CE, Maschak-Carey BJ, Montez MG, Murillo A, Nathan DM, Patricio J, Peters A, Pi-Sunyer X, Pownall H, Reboussin D, Regensteiner JG, Rickman AD, Ryan DH, Safford M, Wadden TA, Wagenknecht LE, West DS, Williamson DF, Yanovski SZCardiovascular effects of intensive lifestyle intervention in type 2 diabetes.N Engl J Med.(2013-Jul-11)
- ^Raitakari O, Pahkala K, Magnussen CGPrevention of atherosclerosis from childhood.Nat Rev Cardiol.(2022-08)
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- High-density lipoprotein (HDL) - AIM-HIGH Investigators, Boden WE, Probstfield JL, Anderson T, Chaitman BR, Desvignes-Nickens P, Koprowicz K, McBride R, Teo K, Weintraub WNiacin in patients with low HDL cholesterol levels receiving intensive statin therapyN Engl J Med.(2011 Dec 15)
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