Cholesterol is an essential building block of every cell in the body, required for all metabolic processes. It is particularly important in the production of nerve tissue, bile and certain hormones. On average, our body produces about half of a gram to one gram of cholesterol per day, depending on how much of it the body needs at the time. By and large, our body is able to produce 400 times more cholesterol per day than what we would obtain from eating 3,5 ounces (100 grams) of butter. The main cholesterol producers are the liver and the small intestine, in that order. Normally, they are able to release cholesterol directly into the blood stream, where it is instantly tied to blood proteins. These proteins, which are called lipoproteins, are in charge of transporting the cholesterol to its numerous destinations. There are three main types of lipoproteins in charge of transporting cholesterol: Low Density Lipoprotein (LDL), Very Low Density Lipoprotein (VLDL), and High Density Lipoprotein (HDL).
In comparison to HDL, which has been privileged with the name ‘good’ cholesterol, LDL and VLDL are relatively large cholesterol molecules; in fact, they are the richest in cholesterol. There is good reason for their large size. Unlike their smaller cousin, which easily passes through blood vessel walls, the LDL and VLDL versions of cholesterol are meant to take a different pathway; they leave the blood stream in the liver.
The blood vessels supplying the liver have a very different structure from the ones supplying other parts of the body. They are known as sinusoids. Their unique, grid-like structure permits the liver cells to receive the entire blood content, including the large cholesterol molecules. The liver cells rebuild the cholesterol and excrete it along with bile into the intestines. Once the cholesterol enters the intestines, it combines with fats, is absorbed by the lymph and enters the blood, in that order. Gallstones in the bile ducts of the liver inhibit the bile flow and partially, or even fully, block the cholesterol’s escape route. Due to back-up pressure on the liver cells, bile production drops. Typically, a healthy liver produces over a quart of bile per day. When the major bile ducts are blocked, barely a cup of bile, or even less, will find its way to the intestines. This prevents much of the VLDL and LDL cholesterol from being excreted with the bile.
Gallstones in the liver bile ducts distort the structural framework of the liver lobules, which damages and congests the sinusoids. Deposits of excessive protein also close the grid holes of these blood vessels (see the discussion of this subject in the previous section). Whereas the ‘good’ cholesterol HDL has small enough molecules to leave the bloodstream through ordinary capillaries, the larger LDL and VLDL molecules are more or less trapped in the blood. The result is that LDL and VLDL concentrations begin to rise in the blood to levels that seem potentially harmful to the body. Yet even this scenario is merely part of the body’s survival attempts. It needs the extra cholesterol to patch up the increasing number of cracks and wounds that are formed as a result of the accumulation of excessive protein in the blood vessel walls. Eventually, though, the life-saving cholesterol begins to occlude the blood vessels and cut off the oxygen supply to the heart.
In addition to this complication, reduced bile flow impairs the digestion of food, particularly fats. Therefore, there is not enough cholesterol made available to the cells of the body and their basic metabolic processes. Since the liver cells no longer receive sufficient amounts of LDL and VLDL molecules, they (the liver cells) assume that the blood is deficient in these types of cholesterol. This stimulates the liver cells to increase the production of cholesterol, further raising the levels of LDL and VLDL cholesterol in the blood.
The ‘bad’ cholesterol is trapped in the circulatory system because its escape routes, the bile ducts and the liver sinusoids, are blocked or damaged. The capillary network and arteries attach as much of the ‘bad’ cholesterol to their walls as they possibly can. Consequently, the arteries become rigid and hard.