Fats and health

Edited by Doctor Francesco Casillo

Before going further and in detail on the inter-lipid differences and their effects on the cardiovascular system, it is good to clarify immediately what are the medical reasons that have now promoted a nutritional regimen with a "controlled-limited" consumption of fats (more correctly: "lipids").
The reason for so much concern about lipid supply lies in its "potential" atherogenic effects. Atherosclerosis is a degenerative process of the vascular endothelium (inner wall of the blood vessel).
The main responsible for the arterogenic process are the cells of the immune system and the lipid material, primarily cholesterol.
The initial response to a degeneration of arterial endothelial cells is the increased adherence of Monocytes and T-Lymphocytes towards the affected area.
The protein by-products of Monocytes and Lymphocytes, called Cytokines, mediate the arterogenic process through their chemotactic attraction of the phagocytic cells towards the affected area.
In parallel to this, the exposure to high serum levels of LDL (bad cholesterol) and its subsequent deposition and oxidation, further increases the inflammatory process in progress. This process is given by the increased uptake of LDL by phagocytic cells which in turn are called "Foam Cells" due to their altered lipid content. The lipid material in the phenotyped form of "Foam Cells" can thus infiltrate inside the vascular endothelium, and the more the lipid material accumulates, the more the lumen of the blood vessels involved in this process becomes occluded.

The lipid material that is deposited is called Atheromatous Plaque 1.

In Fig.A the possible events involved in the atherogenesis process2

The native LDL [(N) LDL] penetrates inside the arterial Intimate Tunnel and here it is oxidized [(O) LDL] to then be phagocytosed by macrophages which become Foam Cells with a high lipid content. Oxidized LDL [(O) LDL] is also cyto-toxic for endothelial cells, whereby degenerative processes (EI) are triggered at the expense of the endothelium, with consequent recall of platelet material.
The platelet material releases Growth Factors (PDGFs) that stimulate the proliferation of smooth muscle cells, which in turn can engulf the LDL (O) via endocytosis and also become Foam Cells. ).
The macrophages activated by the phagocytosis of the oxidized LDL, in turn release other macrophages (or monocytes) which recall other macrophages to the affected site thus perpetuating the process.
The proliferation of the Foam Cells and of those of the smooth muscle (smooth muscle cells) determines the narrowing of the vessel lumen, to the point of compromising the blood flow itself, ultimately responsible for important clinical consequences such as: heart attack, stroke etc.

From these evidences, we began to investigate the possible connections between the dietary lipid intake and the development of atherosclerosis. The existence of this connection has been named "Lipid Hypothesis", which argues that dietary lipid intake can alter lipidemia (ie the level of fat in the blood) and in turn initiate or aggravate arterogenesis2.
At the heart of the "Lipid Hypothesis" is cholesterol.
The effects of dietary interventions aimed at improving the blood lipid profile are generally measured on the basis of the positive or negative changes they determine on cholesterolemia. Since cholesterol is the major component at the base of the "atheromatous plaque" there is reason to believe that cardiovascular diseases are closely linked to blood cholesterol levels.

It is important to underline that the total level of circulating cholesterol is not so much the indicative-predictive marker of the risk associated with the evolution of heart disease as are the two lipoprotein transport subfractions in which it is distributed: HDL (commonly referred to as "good cholesterol") and LDL (commonly referred to as "bad cholesterol"). In fact, one of the keys to understanding the clinical picture of cardiovascular risk is the "TOTAL CHOLESTEROL / HDL" ratio; as the value of the quotient resulting from this ratio increases, the cardiovascular risk also increases, vice versa otherwise.