Dr. Masquelier on Cholesterol and OPCs

Statins and sterols fail to address the real dangers of cholesterol. OPCs do.
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Millions of people around the world are using statins or plant-sterols to lower their cholesterol-level. The practice is highly profitable for the manufacturers of cholesterol-lowering pharmaceuticals (statins) and foods (plant-sterols), but is rather pointless when it comes to addressing the real dangers of cholesterol. Besides that, statins produce numerous nasty side-effects, which makes that many users stop taking statins. Such to the dismay of organized medicine. Dr. Jack Masquelier explains why and how OPCs can be of help.

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For decades, we have been told to fear “cholesterol” more than we should fear the devil. The very word “cholesterol” causes people to think of imminent death and decay. Under pressure of all the anti-cholesterol propaganda and official warnings, most of us seem to have forgotten that cholesterol is not a poison but a vital substance that is essential for survival. Without cholesterol we’re dead. This is why the body itself produces lots of cholesterol, so that it is not entirely dependent on food-borne sources. Well then, why lower the level of a substance that plays a vital role in the human body ? Why send cholesterol to damnation by demonizing it as very dangerous ? And, why do people who have perfectly healthy levels of cholesterol still develop plaque and cardiovascular disease ?

Yes ! Cholesterol plays an essential role in the formation of the membranes of the cells. Together with a special form of fat, the phospholipids, cholesterol determines the fluidity and flexibility of the cell’s membrane. The integrity of the membranes of all body-cells throughout the body is based mainly on phospholipids and cholesterol. The cell’s membrane is like a film made up of revolving doors that control what goes in and out of the cell. Cholesterol forms a keu element in that system of revolving doors. A very small amount of the body’s cholesterol is used by the adrenal glands to form certain hormones. Cholesterol-based hormones are progesterone and estrogen (formed in the ovaries) and testosterone (formed in the testes). These glands can also synthesize their own cholesterol.

To understand what could go wrong with cholesterol, you should know that cholesterol is a fatty substance that cannot be transported through the body in its pure “free” form. Like all fatty substances, it needs an “emulsifying” carrier, to make it transportable in the bloodstream. This fat-carrier is a protein that can enclose cholesterol and fats. Together, cholesterol, fats and the protein-carrier make up the lipo-proteins. The lipoproteins that contain fat and cholesterol and phospholipids are called Very Low Density Lipoproteins or VLDLs. On their first rounds through the body, the VLDLs pick-up of fats and cholesterol in the liver and offload the fat in the tissues where it is used for energy or stored.

After the fats have been delivered to fatty tissue, the VLDLs become Low Density Lipoproteins or LDLs. The only substances that LDL still carries around are cholesterol and phospholipids. LDL and its fatty cargo is recognized by the cell membranes, which then attract and “swallow” the entire package of LDL&Cholesterol&Phospholipids. Inside the cell, the LDL-package is “opened” and the cholesterol and phospholipids are offloaded and used. And then, under normal healthy circumstances, any excess of cholesterol is picked up from the cells by High Density Lipoproteins (HDL) to be returned to the liver.

“When everything goes smoothly,” said Dr. Masquelier in an interview I had with him quite some years ago, “LDL comes and deposits its cholesterol while HDL comes and collects excess cholesterol, circulates it and carries it back to the liver. However, when free radicals interfere, the LDL cholesterol in the blood stream is oxidized and under these conditions it forms a deposit although it can no longer play a meaningful role on and in the cells. Meaning that the deposit is no longer part of the LDL-HDL transitional system. The oxidized LDL cholesterol can no longer be used, but the body must get rid of it. So, this oxidized cholesterol is “absorbed” by lymphocytes, or white blood cells. When the HDL cholesterol, which arrives empty, finds nothing, it leaves empty. The purification therefore does not occur. And as the oxidized LDL deposits cholesterol in the lymphocytes, mast cells and white blood cells that are there, these cells become swollen with cholesterol. They are called foam cells which accumulate on the vascular wall and start to form an artherosclerotic lesion. This is how the first artherosclerotic lesions occur. Because the artherosclerotic lesion forms a growth that decreases the diameter of the blood vessel through which the blood normally circulates and blocks it, as is the case for instance in coronary vessels, a heart attack may occur due to lack of oxygenation of the surrounding heart tissue. The same goes for the capillaries in the brain.”

In answer to this question, Masquelier explained that “any substance that prevents what is called lipoprotein oxidation will reduce this danger of plaque formation. We can prevent heart attacks thanks to antioxidative substances and OPCs are the type of substance that may prevent LDL from becoming oxidized. It wasn’t until the 1970s till we knew exactly how it happened. For several years, we could see this mechanism there, but only in the laboratory. We conducted experiments with OPCs on human LDL and we saw that the oxidation rate was certainly decreasing. We learned that by inhibiting the oxidation of LDL, which is the first carrier of cholesterol, we can protect the wall against a build-up of artherosclerotic plaque.

Masquelier: “Yes, you're right. You see, it’s vital that there is cholesterol in all cells, absolutely essential. The problem is not being able to eliminate it when it can no longer be used, when it has been oxidized, so that HDL no longer recognizes it and LDL and HDL no longer work together in unison.”

Plaque formation begins because the vascular wall does not recognize the LDL and cargo after they have been oxidized, deformed, and wrecked by free radicals. Plaque formation, according to Dr. Masquelier, begins when the LDL is wrecked and its cargo turns rancid. Then the vascular wall actively attempts to neutralize what it no longer recognizes as safe and beneficial. In fact, the reaction of the vascular wall is the normal inflammatory response of any tissue that is confronted by what it perceives as an invader. Normal LDL-cholesterol is not an invader. To the contrary, it is welcomed by the cells. But, the wrecked LDL must be kept from re-entering circulation. It must be kept in the parking lot where it ended up after it was hit and damaged by free radicals. It must be neutralized. And this process forms the onset of atherosclerotic plaque and cardiovascular disease. OPCs interfere with this process by protecting LDL- cholesterol against oxidation, so that we can supply all our body-cells with healthy cholesterol.