Cholesterol is a vital building block of every cell in the body, required for all metabolic processes. It’s particularly critical in the production of nerve tissue, bile and certain hormones. Normally, 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 moment. By and large, our body can produce 400 times more cholesterol per day than what we would obtain from eating 3,5 ounces (100 grams) of butter.

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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 3 major types of lipoproteins in charge of transporting cholesterol: Low Density Lipoprotein (LDL), Very Low Density Lipoprotein (VLDL), and High Density Lipoprotein (HDL).

Compared to HDL, which has been privileged with the title’good’ cholesterol, LDL and VLDL are comparatively large cholesterol molecules; in actuality, they’re the richest in cholesterol. There’s good reason for their large size. Unlike their younger cousin, which goes through blood vessel walls, the LDL and VLDL variations of cholesterol are intended to take another pathway; they leave the blood flow in the liver.

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The blood vessels supplying the liver have a very different structure from those supplying different areas of the body. They’re known as sinusoids. Their unique, grid-like structure enables the liver cells to get the whole blood content, for instance, large cholesterol molecules. The liver cells reconstruct the cholesterol and excrete it together with bile to the intestines. Once the cholesterol enters the intestines, it combines with fats, is consumed by the lymph and enters the bloodstream, in that order.

Gallstones in the bile ducts of the liver inhibit the bile flow and partly, or even entirely, block the cholesterol’s escape path. As a result of backup on the liver cells, bile production drops. Typically, a healthy liver produces more than a quart of bile each day. When the significant bile ducts are obstructed, barely a cup of bile, or even less, will find its way into the intestines. This prevents a lot of the VLDL and LDL cholesterol from being excreted with the bile.

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Gallstones in the liver bile ducts distort the structural frame of the liver lobules, which damages and congests the sinusoids. Deposits of excessive protein also near the grid of those blood vessels (see the discussion of the subject in the last section). Whereas the’good’ cholesterol HDL has little enough molecules to leave the blood through regular capillaries, the larger LDL and VLDL molecules are more or less trapped in the blood. The end result is that LDL and VLDL concentrations start to increase in the blood to levels that look potentially detrimental to the body.

Yet even this situation is only part of the body’s survival efforts. It needs the additional cholesterol to patch up the rising number of fractures and which are formed because of the accumulation of excessive protein in the blood vessel walls. Eventually, however, the life-saving cholesterol starts to occlude the blood vessels and then cut off the oxygen supply to the heart. Besides this complication, reduced bile flow impairs the digestion of food, especially fats. Therefore, there’s inadequate cholesterol made available to the tissues of the and their basic metabolic processes.

Since the liver cells no longer get adequate quantities of LDL and VLDL molecules, they (the liver cells) assume that the blood is deficient in these kinds of cholesterol. This stimulates the liver cells to increase the production of cholesterol, further increasing the levels of LDL and VLDL cholesterol in the blood. The’bad’ cholesterol is trapped in the circulatory system since its escape routes, the bile ducts as well as the liver sinusoids, are damaged or blocked. The capillary arteries and network attach as a lot of their’bad’ cholesterol into their own walls as possible. Consequently, the arteries become stiff and hard.

Coronary heart disease

No matter whether it’s due to smoking, drinking excessive amounts of alcohol, protein foods, , or another variable, usually does not happen unless gallstones have affected the bile ducts of the liver. Removing gallstones in the liver and liver can’t just stop a heart attack or stroke, but also reverse coronary heart disease and heart muscle damage. The body’s reaction to becomes less harmful, and cholesterol levels start to normalize as the twisted and damaged liver lobules are regenerated.

Cholesterol-lowering drugs do not do that. They artificially reduce blood , which coerces the liver to make even more cholesterol. But when additional cholesterol is passed to the bile ducts, it stays in its crystalline state (versus soluble condition ) and, thereby, turns into gallstones. People who regularly use cholesterol-lowering drugs generally develop an excessively high number of gallstones. This sets them up for important side effects, including cancer and cardiovascular disease.

Cholesterol is critical for normal functioning of the immune system, especially for the human body’s reaction to the millions of cancer cells that each and every individual makes in his body every day. For all of the health problems related to cholesterol, this important substance isn’t something we should attempt to remove from our bodies. Cholesterol does far more good than harm. The harm is usually symptomatic of other issues.

Bad Cholesterol

I want to emphasize, once more, that ‘bad’ cholesterol only attaches itself to the walls of arteries to stop immediate heart trouble, not to make it. This is supported by the fact that cholesterol attaches itself to the walls of veins. When a doctor examines your cholesterol levels, he takes the blood sample from a vein, not from an artery. Although blood flow is a lot slower in veins than in arteries, cholesterol should block veins far more easily than blood vessels, but it never does. There simply is not any need for that.

Why? Because there are no abrasions and tears in the lining of the vein which need patching up. Cholesterol only affixes itself to arteries to be able to coat and cover up the abrasions and protect the inherent tissue such as a waterproof bandage. Veins don’t consume proteins in their basements membranes such as arteries and tendons do and, therefore, aren’t prone to this sort of . Bad’ cholesterol saves lives; it doesn’t take lives. LDL allows the blood to flow through injured blood vessels without causing a life-endangering circumstance.

The concept of high LDL being a principal cause of coronary heart disease isn’t just unproved and unscientific. It has misled the people to feel that cholesterol is an enemy which needs to be fought and destroyed at any cost. Human studies haven’t shown a cause-and-effect connection between cholesterol and cardiovascular disease. The countless studies so far conducted on such a connection have only proven that there’s a statistical correlation between the two. And there ought to be, because if there weren’t any ‘bad’ cholesterol molecules attaching themselves to hurt arteries we’d have millions of deaths from heart attack than we currently have.

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On the other hand, dozens of conclusive studies have shown that risk of heart disease increases significantly in people whose HDL levels fall. Elevated LDL cholesterol isn’t a cause of heart disease; instead, it’s a result of an unbalanced liver and congested, dehydrated circulatory system. If your doctor has advised you that lowering your cholesterol with medical drugs protects you against heart attacks, you’ve been grossly misled.