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What is Cholesterol?
Cholesterol is a HEALTH creating molecule with many beneficial aspects that contribute to a healthy body. Cholesterol is an anti-inflammatory molecule that is often misunderstood. The cause of heart dis-ease is various forms of inflammation and infection. Cholesterol in the arteries of the heart is the body’s attempt to fight inflammation. Neither HDL or LDL are cholesterol, and they are both good. Researchers have shown there is no relationship between high cholesterol and atherosclerosis.
The following articles and links to the websites below contain a great deal of information that will help us to understand what cholesterol really is and how it affects the body and our health.
THE WONDERFUL MOLECULE OF CHOLESTEROL
There is an extraordinary amount of misinformation, disinformation and lack of information about cholesterol. To start with here are some interesting facts about this beautiful and vitally important molecule.
*Cholesterol is the precursor to our sex hormones. This is why one of the side effects of cholesterol lowering drugs such as statins is loss of libido.
*Cholesterol is the precursor to the steroid hormones that regulate blood pressure, blood sugar, and mineral balance.
*The myelin sheath that serves as insulation around the nerves in the brain and body is made of cholesterol. Another side effect of statin drugs is loss of memory.
*The body makes bile acids from cholesterol which is an important part of digestion.
* Cholesterol is in the membrane of every cell in the body including the muscle cells. That is why another common side effect of statins is muscle pain and ache.
*Now get this- People with high cholesterol live longer and have less cancer.
*Cholesterol is not the cause of heart disease!!!!!!!!!!!!!!!!!!!!! How about that for a shocker?
This has been born out in the medical literature but has been ignored by those selling the cholesterol as a nasty molecule hypothesis. Dr Uffe Ravnskov has done an enormous amount of research on cholesterol and has clearly showed these facts are straight from medical research. His wonderful website https://www.ravnskov.nu/cholesterol.htm gives a great deal of information clarifying the true nature of cholesterol.
Another person that has done great service making sense of the misinformation is Dr. Chris Kresser. One of his websites https://www.cholesterol-and-health.com/ is very easy to understand even though he goes into a bit of biochemistry. For a lay person or a doctor it is equally informative. His other website https://chriskresser.com/ has a great deal of practical information on how to help a person establish and maintain optimal levels. In both sites he invites other top professionals to contribute.
In this day where advertising has bombarded us with information it is a challenge to know where to get objective and easy to understand direction. These are a great way to start informing ourselves so we can make our own decisions and take back control of our own health.
Blood cholesterol has nothing to do with atherosclerosis.
An excerpt from my previous book The Cholesterol Myths (out of print).
A link to the next section is available at the end.
One of the most surprising facts about cholesterol is that there is no relationship between the blood cholesterol level and the degree of atherosclerosis in the vessels. If a high cholesterol really did promote atherosclerosis, then people with a high cholesterol should evidently be more atherosclerotic than people with a low. But it isn´t so.
The pathologist Dr. Kurt Landé and the biochemist Dr. Warren Sperry at the Department of Forensic Medicine of New York University were the first to study that question. The year was 1936. To their surprise, they found absolutely no correlation between the amount of cholesterol in the blood and the degree of atherosclerosis in the arteries of a large number of individuals who had died violently. In age group after age group their diagrams looked like the starry sky.
Drs. Landé and Sperry are never mentioned by the proponents of the diet-heart idea, or they misquote them and claim that they found a connection, or they ignore their results by arguing that cholesterol values in the dead are not identical with those in living people.
That problem was solved by Dr. J. C. Paterson from London, Canada and his team . For many years they followed about 800 war veterans. Over the years, Dr. Paterson and his coworkers regularly analyzed blood samples from these veterans. Because they restricted their study to veterans who had died between the ages of sixty and seventy, the scientists were informed about the cholesterol level over a large part of the time when atherosclerosis normally develops.
Dr. Paterson and his colleagues did not find any connection either between the degree of atherosclerosis and the blood cholesterol level; those who had had a low cholesterol were just as atherosclerotic when they died as those who had had a high cholesterol.
Similar studies have been performed in India, Poland, Guatemala, and in the USA, all with the same result: no correlation between the level of cholesterol in the blood stream and the amount of atherosclerosis in the vessels.
The question about blood cholesterol and atherosclerosis has been studied by coronary angiography also. It seems as if every specialist in coronary angiography in America has performed his own study, funded with federal tax money awarded by the National Heart, Lung and Blood Institute. In paper after paper published in various medical journals, using almost identical words, these medical specialists emphasize the importance of the blood cholesterol level for the development of atherosclerosis.
But the reports offer no individual figures, only correlation coefficients, and these are never above a minimal 0.36, usually even smaller. And they never mention any of the previous studies that found no association between degree of atherosclerosis and level of blood cholesterol.
Studies based on coronary angiography are fundamentally flawed if their findings are meant to be applied to the general population. Coronary angiographies are performed, mainly, on young and middle-aged patients with symptoms of heart disease, which means that a relatively large number of patients with familial hypercholesterolemia must have been included. Again, there is an obvious risk for the kind of bias that I described above. The fact that this objection is justified was demonstrated in a Swedish study performed by Dr. Kim Cramér and his group in Gothenburg, Sweden. As in most other angiographic studies the patients with the highest cholesterol values had on average the most arteriosclerotic coronary vessels.
But if those who were treated with cholesterol-lowering drugs were excluded, and almost certainly this group must have included all patients with familial hypercholesterolemia, the correlation between blood cholesterol and degree of atherosclerosis disappeared.
Your cholesterol tells very little about your future health
Cholesterol is a peculiar molecule. It is often called a lipid or a fat. However, the chemical term for a molecule such as cholesterol is alcohol, although it doesn’t behave like alcohol. Its numerous carbon and hydrogen atoms are put together in an intricate three dimensional network, impossible to dissolve in water. All living creatures use this indissolvability cleverly, incorporating cholesterol into their cell walls to make cells waterproof. This means that cells of living creatures can regulate their internal environment undisturbed by changes in their surroundings, a mechanism vital for proper function. The fact that cells are waterproof is especially critical for the normal functioning of nerves and nerve cells. Thus, the highest concentration of cholesterol in the body is found in the brain and other parts of the nervous system.
Because cholesterol is insoluble in water and thus also in blood, it is transported in our blood inside spheric particles composed of fats (lipids) and proteins, the so-called lipoproteins. Lipoproteins are easily dissolved in water because their outside is composed mainly of water-soluble proteins. The inside of the lipoproteins is composed of lipids, and here are room for water-insoluble molecules such as cholesterol. Like submarines, lipoproteins carry cholesterol from one place in the body to another.
The submarines, or lipoproteins, have various names according to their density. The best known are HDL (High Density Lipoprotein), and LDL (Low Density Lipoprotein). The main task of HDL is to carry cholesterol from the peripheral tissues, including the artery walls, to the liver. Here it is excreted with the bile, or used for other purposes, for instance as a starting point for the manufacture of important hormones. The LDL submarines mainly transport cholesterol in the opposite direction. They carry it from the liver, where most of our body’s cholesterol is produced, to the peripheral tissues, including the vascular walls. When cells need cholesterol, they call for the LDL submarines, which then deliver cholesterol into the interior of the cells. Most of the cholesterol in the blood, between 60 and 80 per cent, is transported by LDL and is called “bad” cholesterol, for reasons that I shall explain soon. Only 15-20 percent is transported by HDL and called “good” cholesterol. A small part of the circulating cholesterol is transported by other lipoproteins.
You may ask why a natural substance in our blood, with important biologic functions, is called ”bad” when it is transported from the liver to the peripheral tissues by LDL, but ”good” when it is transported the other way by HDL. The reason is that a number of follow-up studies have shown that a lower-than-normal level of HDL-cholesterol and a higher than-normal level of LDL-cholesterol are associated with a greater risk of having a heart attack, and conversely, that a higher-than-normal level of HDL-cholesterol and a lower-than normal LDL-cholesterol are associated with a smaller risk. Or, said in another way, a low HDL/LDL ratio is a risk factor for coronary heart disease.
However, a risk factor is not necessarily the same as the cause. Something may provoke a heart attack and at the same time lower the HDL/LDL ratio. Many factors are known to influence this ratio.
What is good and what is bad?
People who reduce their body weight also reduce their cholesterol. In a review of 70 studies Dr. Anne Dattilo and Dr. P.M. Kris-Etherton concluded that, on average, weight reduction lowers cholesterol by about 10 per cent, depending on the degree of the reduction. Interestingly, it is only cholesterol transported by LDL that goes down; the small part transported by HDL goes up. In other words, weight reduction increases the ratio between HDL- and LDL-cholesterol (1). An increase of the HDL/LDL ratio is called ”favorable” by the diet-heart supporters; cholesterol is changed from ”bad” to ”good”. But is it the ratio or the weight reduction that is favorable? When we become fat, other harmful things occur to us. One is that our cells become less sensitive to insulin, so that some of us develop diabetes. And people with diabetes are much more likely to have a heart attack than people without diabetes, because atherosclerosis and other vascular damage occur very early in diabetics, even in those without lipid abnormalities. In other words, overweight may increase the risk of a heart attack by mechanisms other than an unfavorable lipid pattern, while at the same time overweight lowers the HDL/LDL ratio.
Also smoking increases cholesterol a little. Again, it is LDL-cholesterol that increases, while HDL-cholesterol goes down, resulting in an ”unfavorable” HDL/LDL ratio (2). What is certainly unfavorable is the chronic exposure to the fumes from burning paper and tobacco leaves. Instead of considering the low HDL/LDL ratio as bad it could simply be smoking itself that is bad. Smoking may provoke a heart attack and, at the same time, lower the HDL/LDL ratio.
Exercise decreases the bad LDL-cholesterol and increases the ”good” HDL-cholesterol (3). In well-trained individuals the ”good” HDL is increased considerably. In a comparison between distance runners and sedentary individuals, Dr. Paul D. Thompson and his colleagues found that the athletes on average had a 41 per cent higher HDL-cholesterol level(4). Most population studies have shown that physical exercise is associated with a lower risk of coronary heart disease, and a sedentary life with a higher risk. It also seems plausible that a well-trained heart is better guarded against obstruction of the coronary vessels than a heart always working at low speed. A sedentary life may predispose people to a heart attack and, at the same time, lower the HDL/LDL ratio.
A low ratio is also associated with high blood pressure (5). Most probably, the hypertensive effect is created by the sympathetic nerve system, which is often overstimulated in hypertensive patients. Hypertension (or too much adrenalin) may provoke a heart attack, for instance by inducing spasm of the coronary arteries or by stimulating the arterial muscle cells to proliferate, and, at the same time, lower the HDL/LDL ratio.
Univariate and multivariate
As you see, it is not easy to know what is bad. Is it bad to be fat, to smoke, to be inactive, to have high blood pressure, or to be stressed? Or is it bad to have a lot of bad cholesterol? Or both? Is it good to be slim, to stop smoking, to exercise, to have normal blood pressure, to be emotionally calm? Or is it good to have much ”good” cholesterol? Or both? Thus, the risk of having a heart attack is greater than normal for people with high LDL-cholesterol, but so is the risk for fat, sedentary, smoking, hypertensive and mentally stressed individuals. And since such individuals usually have elevated levels of LDL-cholesterol, it is, of course impossible to know whether the increased risk is due to the previously mentioned risk factors (or to risk factors we do not yet know) or to the high LDL-cholesterol. A calculation of the risk of high LDL-cholesterol that ignores other risk factors is called a univariate analysis and is, of course, meaningless.
To prove that high LDL-cholesterol is an independent risk factor, we should ask if fat, sedentary, smoking, hypertensive and mentally stressed individuals with a high LDL-cholesterol level are at greater risk for coronary disease than fat, sedentary, smoking, hypertensive and mentally stressed individuals with low or normal LDL cholesterol.
Using complicated statistical formulas, it is possible to do such comparisons in a population of individuals with varying degrees of the risk factors and varying levels of LDL-cholesterol, a so-called multivariate analysis. If a multivariate analysis of the prognostic value of LDL cholesterol also takes body weight into consideration, it is said to be ”adjusted for body weight”. A major problem with such calculations is that the data generated by these and other complicated statistical methods are almost impossible for most readers, including most physicians, to comprehend. For many years researchers in this area have not presented primary data, simple means, or simple correlations. Instead, their papers have been salted with meaningless ratios, relative risks, p-values, not to mention obscure concepts such as the standardized logistic regression coefficient, or the pooled hazard rate ratio. Instead of being an aid to science, statistics are used to impress the reader and cover the fact that the scientific findings are trivial and without practical importance.