Various publications, more or less professional, give information about cholesterol, as well as about the dangers of a high representation of so-called ‘bad cholesterol’ in the blood. They also provide suggestions for trying to reduce it in favour of what is commonly called ‘good cholesterol’. This topic will be discussed in more detail here. Cholesterol is a particular molecule belonging to the lipid class, which can bind to proteins, called apolipoproteins, to form so-called lipoproteins. Lipoproteins can be classified according to their density into four different categories:

1. HDL (High Density Lipoprotein): these are the high-density lipoproteins;
2. LDL (Low Density Lipoprotein): these are the low-density lipoproteins;
3. VLDL (Very Low Density Lipoprotein): these are the absolute lowest density lipoproteins;
4. IDL (Intermediate Density Lipoprotein): these are the lipoproteins with a density between that of LDL and VLDL.

HDL can be classified by maturation level into HDL3 and HDL2, while VLDL can be more or less enriched in apolipoproteins. Depending on this, they can also differ in degree of maturation. LDL is the ‘bad cholesterol’ and a high representation of it in the blood positively correlates with the formation of atheromas, i.e. plaques that can occlude blood vessels and lead to a variety of health problems, including stroke and myocardial infarction (heart attack). HDL, on the other hand, is the ‘good cholesterol’. The more favourable the ratio of HDL to LDL is in favour of the former, the less likely one is to suffer from the aforementioned diseases. Lipoproteins are the result of various exchanges of cholesterol, triglycerides, apolipoproteins and fatty acids between the liver, intestines and peripheral tissues, and their density depends on the way they interact with each other, i.e., again, the way they exchange these components. More precisely, the liver and intestines produce a particular apolipoprotein called apo A-I, which, when released into the blood stream, binds to unesterified cholesterol received from surrounding tissues. Another apolipoprotein, called apo C-II, is then donated by a VLDL that has been depleted of much of the cholesterol it contains, and another apolipoprotein, called apo E, by an IDL. The combination of apo A-I, unesterified cholesterol, apo C-II and apo E constitutes HDL3, which, of the two high-density lipoproteins, is the least mature. It reaches the maturity level of HDL2 as a result of three processes: the first is the transfer of apo C-II and some apo E to a nascent VLDL; the second is a reaction known as esterification, which involves the cholesterol it contains. Esterification is a reaction in which typically an acid and an alcohol react. The alcohol is here the cholesterol, while the acid is a fatty acid donated by lecithin. The enzyme that catalyses this reaction here is LCAT (lecithin-cholesterol-acyl-transferase). The third process is the transfer of the cholesterol, already esterified, in exchange for triglycerides, to a VLDL that has already been depleted of a significant quantity of the latter (we are therefore dealing here not with a nascent VLDL, but with an already mature lipoprotein). In the case of VLDL, on the other hand, the immature nascent molecule is again synthesised by the liver and intestine. By binding to apo C-II and apo E received from HDL3, VLDL reaches a higher degree of maturity. When VLDL releases triglycerides to adipose and muscle tissues (via the interaction between apo C-II and lipo-protein lipase), the core is considerably shrunken, so an exchange of components at the envelope level also takes place: while retaining apo E, it releases apo C-II to HDL3, as seen above. It also gives up other triglycerides in exchange for esterified cholesterol to an HDL in the context of that reaction, also discussed above, which leads, inter alia, to the maturation of HDL. The VLDL then becomes an IDL. IDL at this stage consists of half esterified cholesterol and half triglycerides. Receiving cholesterol from HDL2, releasing triglycerides to the liver, and apo E to HDL3, the IDL becomes an LDL.