I wanted to write this post on cholesterol because I see a lot of patients telling me they have high cholesterol. Before blaming the patient and treat him with statins, I think it is good to review what is happening at the cellular level. We will see that the cause of hypercholesterolemia does not necessarily come from a bad diet. And even if that were the case, it is important to understand what and how statins can help, and what the consequences are for the metabolism. But perhaps other micro-nutritional alternatives exist…
Cholesterol is a lipid molecule of the sterol family. 2/3 of cholesterol is endogenous, i.e. it is produced by our own liver and intestinal cells. This endogenous production is possible thanks to an enzyme (HMGCoA reductase) which we will discuss later. Only 1/3 comes from our diet. It is particularly found in organ meats, butter, egg yolks and cheeses.
For information, we need 1 g per day of cholesterol, 300 mg of which must be provided by food. Indeed, cholesterol serves to:
- Compose the membrane of our cells, thus giving them a beautiful fluidity which will allow optimal exchanges and therefore a good metabolism
- Form steroid hormones (cortisol, aldosterone and sex hormones)
- Form bile acids for proper digestion
- Form the active form of vitamin D, calcitriol
Cholesterol from food (plus a small part produced by the cells) is either eliminated in the stool thanks to an intestinal bacterium (hence the importance of a good microbiota!), or absorbed by the intestine then the bloodstream to be transported to the liver.
It is in this organ that everything happens. Indeed, this is where the cholesterol is found:
- Which comes from the intestine (food)
- Which is produced by liver cells
- Excess cholesterol that could not enter the cells to be used
All of this cholesterol amalgamates with triglycerides (lipids), fat-soluble vitamins (such as vitamins K, A, D and E) and an apoprotein (protein that allows the transport of this amalgam). This complex, called a VLDL, leaves the liver via the bloodstream. The VLDLs will unload their content in the cells that need it thanks to proteins present on the membranes. Gradually, the VLDL will be discharged mainly in triglycerides. At the end of their journey, the VLDLs will mostly contain cholesterol and they will be called LDLs.
The LDLs will then target the cells that need cholesterol, and in the same way, they will unload cholesterol via membrane proteins in the target cells.
Once discharged, the residual LDL will reach the liver. The receptors that allow these LDLs to enter the liver depend on T3 (active thyroid hormone). Therefore, hypothyroidism can cause high LDL levels.
The liver will try to eliminate the contents of these LDLs via the bile and then through the stool. Again, bile salts of poor quality or secreted in too small quantities promotes hypercholesterolemia.
HDLs, another kind of cholesterol carriers, are produced by the liver or intestinal cells. Their role is to capture excess cholesterol from cells and other transporters to bring it back to the liver for elimination.
If the excess cholesterol really comes from an excess intake, here is what happens: When the LDL is too loaded with triglycerides and cholesterol, the receiver does not recognize the LDL which is then not able to penetrate into the cell and therefore remains in the blood. There, it risks oxidizing if you do not have a good antioxidant status and coming to deposit in your arteries.
So to summarize:
- The term "good" and "bad" cholesterol is not justified, the only "bad" in history is oxidative stress which oxidizes cholesterol and these transporters
- The origin of hypercholesterolemia can be an excess of intake but do not forget that this may be due to hypothyroidism or a problem of bile salts
- Since 2/3 of cholesterol is produced endogenously, reducing food intake is not enough. On the other hand, optimizing the recycling of cholesterol, the regulation of its synthesis and its use by the cells would be much more interesting.
Statins act at the level of HMGCoA reductase: by inhibiting it, they slow down the synthesis of cholesterol (of mevalovate exactly, precursor of cholesterol) by cells and promote the expression of membrane receptors for LDL. Unfortunately not that… They also inhibit by this same mechanism:
- The production of Coenzyme A, an essential unit for the functioning of our mitochondria (see blog on mitochondria)
- The production of certain proteins, including selenoproteins, which are essential for the functioning of enzymes that protect against oxidative stress
Thanks to micronutrition, it is possible to act on:
- Inhibition of HMGCoA reductase
- Improving the clearance of LDLs, the number of their receptors and the limitation of their oxidation
- Inhibition of the hyperglycemic protein PCSK 9
- Food correction
- Improved HDL formation
- Improving the quality and quantity of bile and its excretion