What is atherosclerosis, and how does it develop?
Atherosclerosis is an inflammatory and degenerative disease of the arteries characterized by the accumulation of atherosclerotic plaques in the intima (inner layer) of the arterial walls. These plaques are composed of oxidized lipids, foam cells, smooth muscle cells, fibrin, and calcium. They gradually narrow the arterial lumen and can rupture, triggering acute thrombosis—the mechanism behindmyocardial infarction and stroke. Cardiovascular support supplements are available in the store’s cardiovascular health line.
- Mechanism of formation: endothelial dysfunction (damage to the inner wall caused by hypertension, smoking, oxidized LDL) → infiltration of LDL into the intima → oxidation of LDL → recruitment of monocytes → differentiation into macrophages → phagocytosis of oxidized LDL → foam cells → lipid plaque → fibrosis (fibrous cap) → calcification—a silent process spanning decades
- Distinction fromarteriosclerosis: arteriosclerosis refers to the hardening and loss of elasticity of the arteries due to aging — atherosclerosis specifically refers to the formation of lipid plaques — the two processes often coexist
- Affected arterial regions: coronary arteries (angina, heart attack) — carotid and cerebral arteries (stroke, transient ischemic attack) — arteries of the lower extremities (arteritis — intermittent claudication, critical limb ischemia) — aorta (aneurysm)
Risk factors and diagnosis of atherosclerosis
- Modifiable risk factors: hypercholesterolemia (high LDL—primary lipid factor)— high blood pressure (mechanical damage to the endothelium)—smoking (LDL oxidation, endothelial dysfunction — smoking cessation recommended — Tabac Info Service: 3989) — type 2 diabetes (glycation of vascular proteins) — abdominal obesity — physical inactivity — chronic stress
- Non-modifiable risk factors: age (>50 years in men, >60 years in postmenopausal women) — male gender — family history of early coronary artery disease
- Diagnosis and screening: lipid profile (LDL, HDL, TG) — fasting blood glucose — carotid Doppler ultrasound (measurement of intima-media thickness — early marker) — coronary calcium score (CT scan) — coronary angiography (coronary arteries) — Doppler ultrasound of the lower extremities (peripheral arterial disease) — brain MRI — performed by a physician or cardiologist
Prevention, medical treatment, and natural supplements
These supplements support prevention and help manage risk factors—they do not treat existing plaques and are not a substitute for prescribed medications (statins, antiplatelet agents, antihypertensives). Medical advice is essential before taking any supplements if you are currently undergoing cardiovascular treatment.
- Anti-atherosclerotic diet: Mediterranean diet—reduction of saturated fats (fatty meats, whole-milk dairy products, palm oil) and trans fats—increased soluble fiber (oats, legumes—which bind intestinal cholesterol)—polyphenols (berries, dark chocolate, extra-virgin olive oil) — omega-3 EPA-DHA (fatty fish 2–3 times/week — anti-inflammatory effects on blood vessels, EFSA claim) — salt < 5 g/day
- Physical activity: 150 min/week improves endothelial function, increases HDL, reduces LDL and triglycerides, and normalizes blood pressure
- Statins (prescription only): 30–55% reduction in LDL depending on the compound — documented stabilization and partial regression of plaques — never stop taking them without medical advice
- Omega-3 EPA-DHA: reduces vascular inflammation and triglycerides — 2 to 3 g/day — EFSA claim regarding normal heart function
