Components that help in anti-atherosclerotic action are substances that can contribute to preventing or slowing the formation of plaques in the arteries. Here are some examples:

• Omega-3 Fatty Acids. Found in fatty fish, flaxseeds, and walnuts, they can reduce inflammation and improve arterial health.
• Dietary Fiber. Found in fruits, vegetables, and whole grains, it helps lower LDL cholesterol.
• Antioxidants. Such as vitamin C, vitamin E, and flavonoids, protect arteries from free radical damage (1).
• Niacin (Vitamin B3). Can help reduce cholesterol and triglycerides in the blood (2).
• Curcumin. The active ingredient in turmeric, known for its anti-inflammatory properties.
• Garlic. Known for its properties that reduce cholesterol and blood pressure.
• Green Tea. Rich in catechins, it can help lower cholesterol and improve arterial health.
• Resveratrol. Found in grapes and red wine, has beneficial effects on arterial health (3).
• Soy. Contains isoflavones that can help lower cholesterol.
• Regular Physical Exercise. Helps improve circulation and lower cholesterol.

Components that can contribute to or exacerbate atherosclerosis include various factors that can increase the risk of plaque formation in the arteries. Here are some examples

• Saturated and Trans Fats. Found in fried foods, packaged snacks, and some animal products, they can increase LDL cholesterol and promote atherosclerosis.
• Refined Sugars. Found in sweets and sugary drinks, can contribute to inflammation and plaque buildup.

• Cigarette Smoking. Can damage the walls of arteries and accelerate plaque formation.
• Alcohol. Excessive consumption can increase the risk of atherosclerosis.
• Sedentary Lifestyle. Lack of physical activity can contribute to plaque buildup in the arteries.
• Obesity. Increases the risk of atherosclerosis due to inflammation and high cholesterol levels.
• Diet Low in Fruits and Vegetables. A diet lacking in antioxidants and fiber can increase the risk of atherosclerosis.
• Chronic Stress. Can contribute to inflammation and plaque buildup.
• High Blood Pressure. Hypertension can damage arteries and promote atherosclerosis.
• Diabetes. Uncontrolled diabetes can accelerate plaque formation due to high blood sugar levels.

The reports  provided on Tiiips website are for informational purposes only and should not replace medical advice. Always consult a healthcare professional before making health-related decisions.

References_____________________________________________________________________

(1) Batty M, Bennett MR, Yu E. The Role of Oxidative Stress in Atherosclerosis. Cells. 2022 Nov 30;11(23):3843. doi: 10.3390/cells11233843. 

Abstract. Atherosclerosis is a chronic inflammatory disease of the vascular system and is the leading cause of cardiovascular diseases worldwide. Excessive generation of reactive oxygen species (ROS) leads to a state of oxidative stress which is a major risk factor for the development and progression of atherosclerosis. ROS are important for maintaining vascular health through their potent signalling properties. However, ROS also activate pro-atherogenic processes such as inflammation, endothelial dysfunction and altered lipid metabolism. As such, considerable efforts have been made to identify and characterise sources of oxidative stress in blood vessels. Major enzymatic sources of vascular ROS include NADPH oxidases, xanthine oxidase, nitric oxide synthases and mitochondrial electron transport chains. The production of ROS is balanced by ROS-scavenging antioxidant systems which may become dysfunctional in disease, contributing to oxidative stress. Changes in the expression and function of ROS sources and antioxidants have been observed in human atherosclerosis while in vitro and in vivo animal models have provided mechanistic insight into their functions. There is considerable interest in utilising antioxidant molecules to balance vascular oxidative stress, yet clinical trials are yet to demonstrate any atheroprotective effects of these molecules. Here we will review the contribution of ROS and oxidative stress to atherosclerosis and will discuss potential strategies to ameliorate these aspects of the disease.

(2) Meyers CD, Kamanna VS, Kashyap ML. Niacin therapy in atherosclerosis. Curr Opin Lipidol. 2004 Dec;15(6):659-65. doi: 10.1097/00041433-200412000-00006. PMID: 15529025.

Abstract. Purpose of review: Well designed, randomized, placebo-controlled studies show that niacin prevents cardiovascular disease and death. Unfortunately, early studies and anecdotal evidence have limited its use by promoting the opinion that niacin is intolerable and contraindicated in diabetes. As evidence mounts that treating multiple lipid risk factors decreases cardiovascular risk, the use of niacin in the treatment of atherosclerosis is experiencing somewhat of a renaissance....Summary: New data indicate that niacin alters lipoprotein metabolism in novel ways, and mediates other beneficial nonlipid changes that may be atheroprotective. This information forms the rationale for the use of niacin in combination with agents possessing complementary mechanisms of action (e.g. statins) for cardiovascular risk reduction beyond that observed with monotherapy. Further research into the specific mechanisms of niacin may identify additional targets for future drug development.

(3) Bonnefont-Rousselot D. Resveratrol and Cardiovascular Diseases. Nutrients. 2016 May 2;8(5):250. doi: 10.3390/nu8050250. PMID: 27144581; PMCID: PMC4882663.

Abstract. The increased incidence of cardiovascular diseases (CVDs) has stimulated research for substances that could improve cardiovascular health. Among them, resveratrol (RES), a polyphenolic compound notably present in grapes and red wine, has been involved in the "French paradox". RES is known for its antioxidant and anti-inflammatory properties and for its ability to upregulate endothelial NO synthase (eNOS). RES was able to scavenge (•)OH/O₂(•-) and peroxyl radicals, which can limit the lipid peroxidation processes. Moreover, in bovine aortic endothelial cells (BAEC) under glucose-induced oxidative stress, RES restored the activity of dimethylargininedimethylaminohydrolase (DDAH), an enzyme that degrades an endogenous inhibitor of eNOS named asymmetric dimethylarginine (ADMA). Thus, RES could improve (•)NO availability and decrease the endothelial dysfunction observed in diabetes. Preclinical studies have made it possible to identify molecular targets (SIRT-1, AMPK, Nrf2, NFκB…); however, there are limited human clinical trials, and difficulties in the interpretation of results arise from the use of high-dose RES supplements in research studies, whereas low RES concentrations are present in red wine. The discussions on potential beneficial effects of RES in CVDs (atherosclerosis, hypertension, stroke, myocardial infarction, heart failure) should compare the results of preclinical studies with those of clinical trials.