on May 28, 2026
Cardiovascular diseases are still today the leading cause of mortality and disability in industrialized countries. According to estimates by the World Health Organization (WHO), they cause over 17 million deaths worldwide every year, a number destined to increase in the coming decades. Among the main modifiable risk factors, dyslipidemia stands out, a condition characterized by alterations in blood lipid levels, particularly cholesterol and triglycerides.
Alterations in lipid metabolism are extremely widespread in the adult population and are associated with a significant increase in the risk of atherosclerosis, ischemic heart disease, myocardial infarction, and stroke. In Italy, it is estimated that dyslipidemias affect about 15-20% of the population, often in association with other metabolic conditions such as obesity, arterial hypertension, diabetes mellitus, and metabolic syndrome.
What is cholesterol?
Cholesterol is a lipid molecule essential for cellular life. Although it is frequently considered exclusively as a cardiovascular risk factor, cholesterol performs numerous fundamental biological functions.
It is an essential structural component of cell membranes, contributes to membrane fluidity and stability, and is involved in cell growth and division processes. Furthermore, it is the precursor of vitamin D, bile acids, and steroid hormones produced by the adrenal glands and gonads, such as cortisol, aldosterone, testosterone, and estrogens.
In the nervous system, cholesterol is particularly abundant in the myelin sheath, the structure that coats nerve fibers and allows for the proper transmission of electrical impulses.
From a chemical point of view, cholesterol is insoluble in water; for this reason, it is transported in the blood through particles called lipoproteins.
HDL, LDL, and VLDL: the different forms of cholesterol transport
Lipoproteins are mainly distinguished into:
- HDL (High Density Lipoproteins), commonly referred to as “good cholesterol”
- LDL (Low Density Lipoproteins), considered the main atherogenic carrier
- VLDL (Very Low Density Lipoproteins), rich in triglycerides
HDL perform a protective function because they remove excess cholesterol from peripheral tissues and return it to the liver through the so-called “reverse cholesterol transport.”
LDL, on the other hand, transport cholesterol from the liver to peripheral tissues. When present in excess, they can infiltrate the vascular wall, undergo oxidative processes, and promote the formation of atherosclerotic plaque.
The progressive accumulation of lipids and inflammatory cells in the arterial wall represents the main biological mechanism underlying atherosclerosis and its cardiovascular complications.
Cholesterol biosynthesis and metabolic regulation
The liver is the main organ involved in the synthesis and metabolism of cholesterol. In adults, daily endogenous production is estimated to be between 1 and 2 grams, while the dietary contribution is generally lower.
The key enzyme in cholesterol biosynthesis is HMG-CoA reductase, present in the endoplasmic reticulum of hepatocytes.
Its activity is regulated by numerous metabolic and hormonal factors. High intracellular concentrations of cholesterol inhibit the enzyme through a negative feedback system, limiting the synthesis of new cholesterol.
Some hormones also influence this process:
- insulin stimulates the endogenous synthesis of cholesterol;
- glucagon inhibits it;
- estrogens and thyroid hormones further modulate lipid metabolism.
Saturated fatty acids can increase hepatic cholesterol synthesis and negatively alter the plasma lipid profile.
Dyslipidemias and cardiovascular risk
Increased plasma LDL represents one of the main modifiable cardiovascular risk factors. Numerous epidemiological studies have shown a direct correlation between high LDL-cholesterol levels and an increased incidence of myocardial infarction and ischemic heart disease.
International guidelines generally recommend total cholesterol values below 200 mg/dL, while therapeutic targets for LDL-cholesterol are adjusted based on individual cardiovascular risk.
Cardiovascular risk increases especially when:
- LDL levels are high;
- HDL levels are low;
- arterial hypertension, visceral obesity, diabetes, or insulin resistance coexist;
- low-grade chronic inflammation is present.
Oxidized LDL also plays an important role in vascular endothelial activation and the inflammatory response, promoting the progression of atherosclerotic plaque.
Diet, lifestyle, and cholesterol control
The approach to dyslipidemias cannot be limited exclusively to pharmacological therapy. Diet, physical activity, and metabolic control are fundamental tools in cardiovascular prevention.
The Biomolecular diet, rich in plant fiber, monounsaturated fatty acids, polyphenols, and omega-3s, has shown favorable effects on the lipid profile and overall cardiovascular risk.
Weight loss, reduced consumption of saturated fats and refined sugars, and regular physical activity also contribute to the improvement of lipid metabolism.
In some selected cases, nutraceutical supplements containing phytosterols, fermented red rice, berberine, omega-3s, or natural antioxidants may be used, always under the supervision of a healthcare professional.
Conclusions
Cholesterol should not be considered simply an “enemy”, but a biologically essential molecule whose metabolic balance is fundamental to the health of the organism.
Dyslipidemias, however, represent an important cardiovascular risk factor, especially when associated with other metabolic alterations. Understanding the mechanisms of cholesterol synthesis, transport, and regulation allows for a more conscious approach to cardiovascular prevention.
The integrated management of lifestyle, diet, and metabolic risk factors remains one of the most effective tools for reducing the incidence of cardiovascular disease in the population.
Bibliographic references
- World Health Organization. Cardiovascular diseases (CVDs). WHO Fact Sheets.
- Ference BA et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. Eur Heart J. 2017.
- Libby P. Inflammation in atherosclerosis. Nature. 2002.
- Grundy SM et al. 2018 AHA/ACC Guideline on the Management of Blood Cholesterol.
- Goldstein JL, Brown MS. A century of cholesterol and coronaries. Cell. 2015.
- Ross R. Atherosclerosis: an inflammatory disease. N Engl J Med. 1999.
- Ridker PM et al. Inflammation, C-reactive protein, and cardiovascular disease. Circulation. 2003.
- Estruch R et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013.
- Brown MS, Goldstein JL. The SREBP pathway: regulation of cholesterol metabolism. Cell. 1997.
- Gylling H et al. Plant sterols and plant stanols in the management of dyslipidaemia. Eur Heart J. 2014.
