Atherosclerosis
Atherosclerosis is the buildup of lipid-rich plaque on arteries’ interior lining. While symptomless early on, it can lead to artery blockage and increased clot formation, which can cause a wide range of serious diseases, most commonly coronary heart disease and stroke. Lifestyle factors, such as poor diet, little exercise, and smoking, can be integral in the progression of atherosclerosis and its associated diseases.
Atherosclerosis falls under theCardiovascular Healthcategory.The Examine Database covers Berberine,Folic Acid (Vitamin B9), and 10 other interventions.
Last Updated:October 13, 2024
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]
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.
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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.
What was studied?
The effect of supplementation with macular carotenoids (lutein, zeaxanthin, and meso-zeaxanthin) on inflammation and lipid oxidation.
Macular carotenoids are pigment molecules found in leafy green vegetables, some other vegetables, and egg yolks.[1] They get their name because they are concentrated into the macula, a section of the eye with the highest concentration of photoreceptor cells.
The outcomes were serum levels of various inflammatory cytokines (interleukin 6 or IL-6, interleukin 1-beta or IL-1β, and tumor necrosis factor-α or TNF-α), and oxidized LDL (OxLDL; a form of low-density lipoprotein that has been modified from its natural state via oxidation).
Who was studied?
80 adults without known health conditions (average age of 45; 42 men, 38 women; average BMI of 27).
How was it studied?
A 6-month randomized controlled trial (RCT) (the carotenoid-omega bioavailability study[2]( was conducted — this study was a post hoc (not initially planned) analysis of that RCT.
The participants took either a macular carotenoid supplement or a placebo containing sunflower oil. The macular carotenoid supplement consisted of lutein (L; 10 mg), zeaxanthin (Z; 2 mg), and meso-zeaxanthin (MZ; 10 mg). However, given the fat-soluble nature of carotenoids and the initial RCT’s goal of evaluating the supplement formulation on its bioavailability, the macular carotenoids were administered in 3 different forms for different proportions of the participants in the treatment group:
- 49% received the macular carotenoids suspended in sunflower oil.
- 35% received the macular carotenoids suspended in omega-3 fatty acids (430 mg DHA and 90 mg EPA).
- 16% received the macular carotenoids as micromicelles (i.e., tiny stable droplets that can mix well with water for improved solubility and absorption).
Blood samples were collected before and after the intervention (i.e., at 0 and 6 months). Dietary intakes were not monitored, but macular carotenoid intake was measured using an unspecified questionnaire to ensure no change/minimal change in intake over the study period.
For analysis purposes, the participants who took any form of the supplement were considered as the treatment group (66 participants) and were compared to the placebo group (14 participants).
What were the results?
The treatment group had higher serum concentrations of all macular carotenoids and lower levels of IL-1β] (large effect size), TNF-α (large effect size), and OxLDL (large effect size), compared to the placebo group.
The authors reported that the post hoc analysis showed no differences in the changes observed among the different supplement forms, but these data were not shown.
At baseline, the treatment group had higher levels of IL-1β (35% higher than the placebo group) and TNF-α (32% higher than the placebo group) and higher BMIs (3 points higher than the placebo group), although the differences for BMI and TNF-α weren’t statistically significant).
The big picture
Macular carotenoids (L, Z, and MZ) are stored at high concentrations in the central region of the retina (i.e., macula). These carotenoids protect the eye from light-induced oxidative damage by acting as blue-light filters and antioxidants.[3] Although preclinical (i.e., “test tube”) and observational studies support the antioxidant and anti-inflammatory potential of carotenoids, RCTs don’t always demonstrate the same positive results.[4][3]
In a 2019 systematic review, almost all of the 15 preclinical studies included showed positive effects of L on atherosclerosis risk factors and inflammatory cytokines.[5] However, a 2022 meta-analysis of RCTs found that although L and Z reduced C-reactive protein, they had clear no effect on IL-6 and TNF-α.[6]
This discrepancy could be attributed to various factors, such as different doses used, different tissues assessed in preclinical vs. human studies, and a lack of consideration of factors that can influence both carotenoid status and inflammation (e.g., age, sex, diet, and exercise).[7] This is also partially why dietary recommendations have not formally been assigned.[8] The summarized study is a testament to the complexity of supplemental antioxidants and health outcomes because it appears to be the first RCT to evaluate the effect of macular carotenoids on oxLDL, motivated by positive findings from preclinical studies,[9][10], but there are several aspects that complicate the interpretation of the results.
Oxidized LDL appears to be an indicator of atherosclerosis and cardiovascular disease (CVD) risk, but the mechanisms underlying its role are still theoretical. Circulating oxLDL has also been associated with all stages of atherosclerosis, and it is suggested as a useful tool for CVD prediction (although whether it provides any predictive power beyond LDL itself remains unclear).[11] A role of oxLDL in the atherosclerosis process is fairly well characterized; one of the main stages of atherosclerosis is the formation of foam cells that start to build up in the artery walls, eventually forming plaques that restrict blood flow or cause a blood clot if they break off from the artery wall.[12] When the body’s immune cells see oxLDL as a threat, they package it up, turning themselves into foam cells as they become filled with fatty deposits.[13] This process can also cause inflammation, turning into a vicious cycle (e.g., producing more oxLDL).
How oxidized LDL contributes to atherosclerosis
A 2023 meta-analysis of 3 observational studies reported that participants with CVD — specifically in the context of long-term inflammatory conditions — had increased levels of oxLDL.[14] However, whether oxLDL (in the context of CVD pathophysiology) can be reliably modified is still uncertain because it’s difficult to test in humans, and RCTs haven't been able to consistently target oxidative stress or oxLDL. As a result, whether lowering oxLDL will reduce the risk of CVD remains an untested hypothesis.[15][16][17]
Despite the confusing evidence, macular carotenoids seem to have the potential to prevent LDL oxidation. Macular carotenoids share many of the same transporters with cholesterol, LDL, and oxLDL, and they also are packaged into LDL for distribution throughout the body.[18][19][20] Within LDL, the carotenoids appear to be well positioned to prevent its oxidation.[21] Eating one egg per day for 4 weeks increased blood L and Z concentrations (L and Z are what give the yolk its yellow color), without changing total cholesterol or LDL concentrations, but decreased markers of LDL oxidation.[22]
Although some limited evidence suggests that carotenoids in general can reduce inflammation,[4] the relatively inconsistent effects from macular carotenoids on inflammatory cytokines in most available RCTs,[6] along with the higher baseline levels in the treatment group, give us reason to cautiously consider the decreases in IL-1β and TNF-α. The authors also mentioned that interindividual variability in inflammation status may explain the baseline differences observed, but this — in combination with the absence of adjustments for multiple comparisons — can decrease the reliability of the result and increase the risk of false positives.[23]
Another limitation is that the treatment group not only received different carotenoid supplement forms, but each carotenoid supplement also had different carotenoid concentrations than those claimed on the label.[2] The sunflower-based supplement contained 25 to 31 mg of carotenoids, the omega-3-based supplement contained 25 mg, and the micromicellarized supplement contained 23 mg. Although these differences lacked statistical significance, which may explain why the authors combined the participants who were taking any active supplement into a single treatment group, there was no adjustment for multiple comparisons in the initial study either. Moreover, the individual levels of Z and MZ were higher in the micromicellarized supplement compared to the other supplement forms. This complicates the interpretation of the result because we don’t know whether a different treatment component, the dose of carotenoids, or both was driving the changes observed.
There is reason to believe that the omega-3-based and micromicellarized supplements may have added to or enhanced any benefits from the macular carotenoids. Omega-3s appear to reduce inflammation and lipid oxidation on their own. Supplementation with omega-3s (1.25–2.5 grams/day) has been shown to reduce inflammatory markers, including IL-6 and TNF-α, in various participant populations (e.g., people without known health conditions, pregnant women with obesity)[24][25][26][27] Prescription forms of omega-3s have demonstrated decreases in oxLDL in participants with type 2 diabetes[28] or high levels of inflammation.[29] Micellarization has improved absorption of the macular carotenoids, specifically Z and MZ, compared to other supplement forms.[2] This means that if Z and MZ are indeed having an effect on inflammation and oxidative stress, this supplement form may have a larger effect in comparison to the others.
Overall, mostly preclinical evidence supports supplementation with macular carotenoids for reduced inflammation and lipid oxidation, but the complexity of factors involved (e.g., other dietary components, lifestyle, disease processes), a limited understanding of their interactions, and conflicting RCT evidence reduce our confidence in the benefits of macular carotenoids for cardiovascular disease risk.
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What was studied?
The effect of supplementation with nuts on blood lipids and inflammatory biomarkers in the context of atherosclerotic cardiovascular disease.
The following outcomes were assessed:
- Blood lipids: total cholesterol, LDL cholesterol, VLDL cholesterol, HDL cholesterol, triglycerides, the ratio of total cholesterol to HDL cholesterol, the ratio of LDL cholesterol to HDL cholesterol, non-HDL cholesterol, and the atherogenic index (the ratio of non-HDL cholesterol to HDL cholesterol)
- Inflammatory biomarkers: C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), and interleukin 10 (IL-10)
How was it studied?
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What was studied?
The association between the presence of microplastics and nanoplastics (MNPs) in atherosclerotic plaques and cardiovascular events (heart attack or stroke) or death.
How was it studied?
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Background
Physical activity dramatically reduces the risk for cardiovascular disease (CVD) morbidity and mortality. However, some studies have found that athletes who participate in high amounts of exercise may have elevated levels of coronary artery calcification (CAC) — an established risk factor for CVD — but these associations need to be confirmed with longitudinal data.[49]
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Background
Vitamin A plays an important role in regulating the immune system. Deficiencies can cause problems with cytotoxic and regulatory T-cells. Since imbalance in the levels and function of cytotoxic and regulatory T-cells, in particular, have been implicated in a number of autoimmune diseases, researchers explored the effect of vitamin A on cytokines when supplemented by people with autoimmune diseases.
The study
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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.
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.
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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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- Atherosclerotic Signs - Koscielny J, Klüssendorf D, Latza R, Schmitt R, Radtke H, Siegel G, Kiesewetter HThe antiatherosclerotic effect of Allium sativumAtherosclerosis.(1999 May)
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- Pulse Wave Velocity - Katayoshi T, Uehata S, Nakashima N, Nakajo T, Kitajima N, Kageyama M, Tsuji-Naito KNicotinamide adenine dinucleotide metabolism and arterial stiffness after long-term nicotinamide mononucleotide supplementation: a randomized, double-blind, placebo-controlled trial.Sci Rep.(2023-Feb-16)