cholesterol

VLDL Cholesterol: Is It Dangerous?

VLDL cholesterol is a lipoprotein, just like LDL, HDL and chylomicrons, but with specific composition and density; VLDL stands for Very Low Density Lipoprotein, or "very low density lipoprotein", a physical characteristic deriving from the greater amount of triglycerides than that of cholesterol (which instead prevails in% in LDL, see figure below).

VLDL are fat-laden lipoproteins that are synthesized by the liver and act as lipid transporters to peripheral tissues (especially muscle and adipose); in this way, the VLDLs lose density and are transformed first into IDL ( Intermediate Density Lipoproteins - intermediate) and then into LDL, which continue to circulate transporting cholesterol as LAST element of transfer.

VLDL cholesterol calculation

VLDL cholesterol is part of total cholesterol and, as with HDL, its estimate is indirect; VLDL cholesterol is calculated by triglyceride operation in blood / 5, but the estimate appears to be true ONLY within blood Triglyceride values ​​lower than 400mg / dl.

The calculation of VLDL is an essential step in the well-known Friedewald formula necessary for estimating total blood cholesterol:

CholesterolTOT = HDL + LDL + VLDL

At this point, a question arises:

If VLDL cholesterol carries a large amount of triglycerides and is the precursor of bad cholesterol ... can its excess, like that of LDL, also be called dangerous?

In fact, excessive levels of VLDL cholesterol do NOT constitute a metabolic indicator of good health, on the contrary! They are always indicators of food and / or alcohol abuse, until they reach a direct correlation with the formation of both coronary and cerebral atherosclerosis (heart attack or stroke); we also remember that high levels of VLDL, and therefore of triglycerides in the blood, are associated with arterial hypertension (aggravated above all by excess body fat, sodium and alcohol in the diet) which in itself further increases cardio circulatory risk.

The normal value of VLDL cholesterol in the blood (fasting sampling) is between 5 and 30mg / dl; therefore, if it is true that VLDL = triglycerides / 5, based on the total triglyceride value in the blood we could go back to the circulating VLDL cholesterol fraction.

Taking an example: if the item Triglycerides 150mg / dl appears in the analyzes, the VLDLs will be equal to 150/5 = 30mg / dl .

When the Friedewald formula is not enough ... how is cardiovascular risk predicted?

The Friedewald formula is an excellent means of evaluating lipoproteins, therefore of lipid metabolism in general (cholesterol and triglycerides); however, some insights have shown that this system is inaccurate with triglyceride values ​​exceeding 400mg / dl, totally negating the importance of the formula for estimating cardiovascular risk.

Apoproteins of VLDL, LDL and HDL: blood ratio

We know that lipoproteins are composed of lipids and APOLIPOPROTEIN (with specific functions based on the lipoprotein itself), which interact with each other in the course of lipid metabolism; it is a decidedly very complex process and of specialized interest which (in this article) is not worth investigating further; what may be of interest to readers, on the other hand, is how the Apoproteins manage to facilitate cardiovascular risk prediction

There are 13 apoproteins (Apo), of which the most important are the ApoA1 (constituting + 70% of the APO contained in the HDL) and the ApoB100 (present in the VLDL, in the LDL and in the Lipoprotein (A)); the ApoA1 are therefore generally proportional to the HDL quantity, while the ApoB100 correspond to the circulating VLDL and LDL levels. Knowing that, by virtue of their size, each LDL contains only one ApoB, estimating the amount of ApoB it is possible to indirectly derive the amount of LDL ... which apparently would not seem a great achievement, given that LDLs are also directly extrapolated from common laboratory analyzes. However, through the relationship of one and the other value ( LDL / ApoB ), it is possible to understand if the LDL are "normal and functioning" or "small and dense", therefore probably oxidized and potentially depositing in the arteries; in the latter case, the risk of atherogenesis would greatly increase! In fact, the smaller, dense and atherogenic LDLs are richer in ApoB and less in cholesterol than the larger LDLs, which are less dense and less atherogenic.

if the LDL / apoB ratio is in favor of the apoB there will be many small LDLs, if instead it is in favor of the LDL, these lipoproteins will present large dimensions (resulting therefore less atherogenic).

The "small-dense" -LDL are more susceptible to oxidation and have less affinity for the LDL receptor (they remain longer in the circulation).

Moreover, considering that ApoB represents not only the LDL but also the VLDL atherogenic potential lipoproteins, the ApoB / ApoA1 ratio plays a fundamental role as an independent indicator of cardiovascular risk, with a higher predictive power than the "simple" LDL / HDL.

Ultimately, the Apo research can ALWAYS provide (even with very high triglycerides) an indicative prospectus of the LDL / HDL ratio and make the size and density parameter (hence the hazard level) referable to circulating LDLs understandable.

This value is also related to other important elements: it is a metabolic syndrome marker (since it is associated with insulin resistance and inversely related to circulating adiponectin), it is an indicator of visceral obesity and not subcutaneous, it is a predictor of organ damage borne by the vessels and is an indicator of cholesterol-lowering therapeutic efficacy.

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