Is cholesterol the cause of heart disease?

I've watched some videos on YouTube and was under a different impression.

Posted Answers


Featured in: Nutrition & LifeThe lipid hypothesis needs to be re-evaluated - it has very serious flaws.
First of all, it is important to understand that that "risk factor" does not mean the same thing as "cause". A risk factor is a characteristic that is associated with a diagnosis. For example, for women, being tall is associated with breast cancer. Does that mean that being tall causes breast cancer? Of course not.

It is also important to understand cholesterol is an essential component of our cell membranes, it acts as an anti-oxidant, it is a precursor for the synthesis of vitamin D as well as bile for digesting fats, and is the only source out of which our steroid hormones, such as cortisol, as well as estrogen, progesterone and testosterone which are key to reproduction, can be made. Therefore it is safe to say that without cholesterol we would not survive. Cholesterol is also the precursor to calcitrol, the steroid hormone that regulates calcium levels in our bodies by helping us absorb calcium from our food, thus playing a key role in the mineralization of our bones and teeth. Cholesterol is also manufactured in the glial cells of the brain to aid with synapses.

Cholesterol is used by our bodies to repair lesions in the arteries. Dr. Mary Enig, fat researcher, suggests that blaming cholesterol for heart disease is something like blaming firefighters for starting fires. Is it really a good idea to reduce our arteries' firefighters? The key to stopping heart disease is to stop the lesions (fires) in the arteries from occurring in the first place, by minimizing glycation by eating less sugar and high fructose corn syrup, and minimizing free radical damage by not consuming refined and therefore rancid vegetable oils AND by reducing systemic stress.

Our bodies consider cholesterol to be so essential to our survival, that every cell in our body can manufacture it as needed. If we eat little or no cholesterol, our bodies manufacture more, and if we eat a lot, our bodies don't manufacture as much. This way our cholesterol levels maintain homeostasis irrespective of our diet, and this is the reason it is so difficult to reduce or raise cholesterol levels much with diet alone.

Dr. Uffe Ravnskov, MD, PhD, who wrote the book The Cholesterol Myths, goes through study after study destroying the idea that high cholesterol levels are the cause of heart disease. In the Framingham heart study done near Boston that spanned 30 years , the researchers concluded that high cholesterol was a risk factor for heart disease, but when one really dissects the data, one must question how they came to that conclusion. For example, when the participants of the study are plotted on a graph it clearly shows that those with cholesterol levels between 182 and 222 did not survive as long as those with higher cholesterol levels of between 222 and 261. The study shows that about half the people with heart disease had low cholesterol, and half the people without heart disease had high cholesterol.

Most studies have found that for women, high cholesterol is not a risk factor for heart disease at all - in fact, the death rate for women is five times higher in those with very low cholesterol. In a Canadian study that followed 5000 healthy middle-aged men for 12 years, they found that high cholesterol was not associated with heart disease at all. And in another study done at the University Hospital in Toronto that looked at cholesterol levels in 120 men that previously had heart attacks, they found that just as many men that had second heart attacks had low cholesterol levels as those that had high. The Maoris of New Zealand die of heart attacks frequently, irrespective of their cholesterol levels. In Russia, it is low cholesterol levels that are associated with increased heart disease. The Japanese are often cited as an example of a population that eat very little cholesterol and have a very low risk of heart disease. But the Japanese that moved to the US and continued to eat the traditional Japanese diet had heart disease twice as often as those that maintained the Japanese traditions but ate the fatty American diet. This suggests that it is something else, like stress perhaps, that is causing the heart disease.

Dr. Malcolm Kendrick noticed that in the MONICA study that has been going on for about 40 years, there is no association between high cholesterol levels and heart disease. See the graph for yourself at the bottom of the article. (Dr. Kendrick wrote another interesting piece about the "disappointing results" of low fat diets in the Women's Health Initiatives heart intervention study, and the lack of association between death rates from CVD and saturated fat consumption based on the MONICA study).

These are but a small sample of the studies that contradict the idea that cholesterol is the villain in heart disease. So why has this idea held on so long? Perhaps pharmaceutical companies and the processed-food industry have a lot to gain by keeping this belief alive. Statin drugs (Lipitor, Mevacor, Zocor etc.) are mega money makers, and they definitely do lower cholesterol, but if high cholesterol does not cause heart disease, why are they necessary?

Furthermore, statin drugs may not lower overall mortality rates, as lower cholesterol levels seem to be associated with higher rates of cancer. Statin drugs work by blocking the synthesis of mevalonate, which is a vital step in the body's
synthesis of cholesterol. By blocking this step, every following step is also blocked, and this is a problem, because the synthesis of Coenzyme Q10 (ubiquinone) and squalene, both precursors to cholesterol, is also blocked. Coenzyme Q10 is very important for heart function, it acts as an antioxidant in conjunction with Vitamin E, and it is important in energy metabolism in the mitochondria of muscles, which is why muscle pain is a common side effect of statin drugs. Coenzyme Q10 is important for healthy brain function as well, and when Coenzyme Q10 levels are low, through statin use or otherwise, memory is affected. Squalene is also an antioxidant and is a potent cancer fighter. If you are on statin drugs, supplementing with Coenzyme Q10 and squalene may be very helpful.

I realize that suggesting that cholesterol levels are not associated with heart disease goes against current dogma. I am not making this suggestion in order to create controversy. After looking at the evidence, I am convinced that we are going down the wrong path. I am not alone in thinking this way - there are more and more scientists and physicians that believe that cholesterol and saturated fat stand wrongly accused. For me, the epidemiological evidence is most convincing. If we ate saturated fat and cholesterol in the form of animal fats, eggs, and full-fat dairy liberally for millennia and were heart-disease free up until the early 1900s, and just as we reduced our consumption of these foods and replaced them with sugar, vegetable oils and processed food, heart disease rates began to climb - to me it seems rather obvious that we are putting the blame on the wrong thing. Feel free not to believe this idea, but please don't simply dismiss it out of hand, either. If you have high cholesterol and you are taking, or thinking about taking cholesterol-lowering drugs, please read The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease so that you can make an informed decision regarding this important issue. Two other very well researched books worth reading, written by scientists but geared to the lay person are Nutrition and Physical Degeneration, by Dr. Weston A. Price, on primitive cultures, their health and their eating habits versus more modern cultures, their health and their eating habits (probably the most important book on nutrition ever written), and Mary Enig's book on lipid chemistry, Know Your Fats: The Complete Primer For Understanding the Nutrition of Fats, Oils and Cholesterol. These books are each very different from the other, but they will open your eyes to the other side of the argument, and only then will you be able to come to an informed conclusion on this issue.

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Ravnskov, Uffe, MD, PhD The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease, New Trends Publishing Inc., Washington D.C., 2000.

Online at Cholesterol And The French Paradox, The Swiss Paradox, The Russian Paradox, The Lithuanian Paradox...Etc... by Malcolm Kendrick (an interesting article about the MONICA study, a long term study of cardiovascular disease, comparing cholesterol levels to CHD deaths in various countries.)

Online at How to bury $400 million by Malcolm Kendrick (an article about the "disappointing" results of the low fat Women's Health Initiative's heart intervention study, and even more interesting, a statistical analysis of deaths from CHD vs. % saturated fat consumption in various countries in Europe, based on MONICA 1998 data)

Online at Cholesterol - Friend or Foe? by Dr. Duane Graveline (an article that explains all the roles cholesterol plays in the body)

Online at The dangers of low blood cholesterol by Barry Groves

Online at Rapid Response - Statins and Cancer: Cause for Concern by Uffe Ravnskov, MD, PhD.

Online at The Oiling of America by Dr. Mary Enig, lipids researcher (an article about how the lipid hypothesis came about)

Online at Cholesterol - A Vital Building Block of Life (a website devoted to cholesterol)

Online at The International Network of Cholesterol Skeptics (a website of researchers, scientists and medical doctors that do not believe in the lipid hypothesis)

Online at Cholesterol, longevity, intelligence and health by Ray Peat

Anderson KM, Castelli WP, Levy D. Cholesterol and Mortality. 30 years of follow-up from the Framingham Study Journal of the American Medical Association 257, 2176-2180, 1987.

Krumholz HM and others. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. Journal of the American Medical Association 272, 1334-1340, 1994.

Forette B, Tortrat D, Wolmark Y. Cholesterol as risk factor for mortality in elderly women. The Lancet 1, 868-870, 1989.

Dagenais GR and others. Total and coronary heart disease mortality in relation to major risk factors - Quebec cardiovascular study. Canadian Journal of Cardiology 6, 59-65, 1990.

Shanoff HM, Little JA, Csima A. Studies of male survivors of myocardial infarction: XII. Relation of serum lipids and lipoproteins to survival over a 10 year period. Canadian Medical Association Journal 103, 927-931, 1970.

Bottiger LE, Carlson LA. Risk factors for death for males and females. Acta Medica Scandinavica 211, 437-442, 1982.

Beaglehole R and others. Cholesterol and mortality in New Zealand Maoris. British Medical Journal 1, 285-287, 1980.

Shestov DB and others. Increased risk of coronary heart disease death in men with low total and low-density-lipoprotein cholesterol in the Russian Lipid Research Clinics prevalence follow-up study. Circulation 88, 846-853, 1993.

Marmot MG, Syme SL. Acculturation and coronary heart disease in Japanese-Americans. American Journal of Epidemiology 104, 225-247, 1976.

Newman, Thomas B. et al. Carcinogenicity of Lipid-Lowering Drugs Journal of the American Medical Association. January 3, 1996-Vol 275, No. 1.

Caso G et al. Effect of coenzyme Q10 on myopathic symptoms in patients treated with statins 2007 May 15; 99(10):1409-12.

Eric J G Sijbrands et al. Mortality over two centuries of in large pedigree with familial hypercholesterolaemia: family tree mortality study BMJ 2001;322:1019-1023 ( 28 April )

Cholesterol Does Not Cause Coronary Heart Disease
Control tactics

Practical Health

Cholesterol Does Not Cause Coronary Heart Disease, Statins Don´t Work by Lowering Lipids. The Role of Inflammation and Stress.

Paul Rosch; MD, FACP, Clinical Professor of Medicine and Psychiatry, New York Medical College, President, The American Institute of Stress, Honorary Vice President, International Stress Management Association, 124 Park Ave.Yonkers, NY 10703, USA.

1. Increased dietary fat intake does not significantly elevate cholesterol or lipid levels.

2. Elevated serum cholesterol and/or other lipids are not the cause of coronary heart disease.

3. Statins can have significant side effects that have been overlooked or deliberately suppressed. In addition to rhabdomyolysis and liver dysfunction, these include: muscle pain, weakness and fatigue and biopsy evidence of myopathy and tendinopathy in the absence of elevated CK, memory loss, global amnesia, difficulty in sleeping and concentration, erectile dysfunction, problems with temperature regulation, difficulty in managing diabetes, and peripheral neuropathy.

4. All statins have been shown to be carcinogenic in experimental animals in dosages that approximate those given to patients. Although the lag time between exposure to a carcinogen and clinical detection is often a decade or more, a disturbing increase in breast cancer has already been reported in the CARE trial as well as certain skin malignancies in the simvastatin trials. Statins could initiate and/or accelerate malignant growth by a) blocking the production of Coenzyme Q10, which has been shown to have anti-cancer effects; b) stimulating the growth of new blood vessels that malignancies require to promote their propagation; c) decreasing the cytotoxicity of natural killer cells; d) blocking the production of squalene, an intermediate cholesterol metabolite with anti-cancer activities in animal studies and currently used as adjunctive therapy in treating cancer; e) reducing the production of DHEA, which has been shown to have anticancer and immune stimulating effects in experimental studies.

5. Cardioprotective effects are seen regardless of baseline cholesterol or LDL levels or the degree to which they are reduced and are achieved far too rapidly to be due to lowering LDL. If statins worked by lowering LDL one would expect to see dose-response relationship, which has not been demonstrated in any statin trials. Cardioprotective effects are seen in the elderly where LDL or other lipids are not a risk factor for coronary heart disease and in the HPS study statin treatment also prevented ischemic stroke although high LDL is not a risk factor for stroke.

6. There is abundant evidence that reducing inflammation, thrombotic factors and endothelial
damage may explain the statin effects. For example, in the CARE, the outcome was related to the degree of inflammation but independent of any lipid response.

7. Most coronary events are not due to progressive blockage of a vessel by gradual accumulation of lipid material but to thrombosis and disruption of an asymptomatic fibrous plaque with minimal protrusion. Human atherosclerotic plaque bears little resemblance to experimental atherosclerosis in animals force-fed high-fat and high cholesterol diets, but has all the hallmarks of an inflammatory response to infection and there is considerable evidence to support such an etiology, particularly for chlamydia pneumoniae. Homocysteine, angiotensin II and a host of inflammatory agents have also been implicated.

8. Therefore, the current therapy goals of lowering LDL to arbitrary levels are not only inappropriate but also dangerous, since this will only lead to larger doses and more side effects.

Stress can contribute to the pathogenesis of coronary heart disease via a number of well documented neuroendocrine activities. With respect to inflammation, it should also be noted that CRP levels correlate best with abdominal obesity, which has been shown to be largely due to increased cortisol activities that increase adipocyte production of inflammatory cytokines. In addition to these chemical/molecular pathways there is an emerging paradigm of communication at a physical/atomic level that may help to explain other stress-related cardiovascular effects as well as the success of novel "energy treatment" effects.

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.

Coronary heart disease, regardless of whether it is caused by smoking, drinking excessive amounts of alcohol, overeating protein foods, stress, or any other factor, usually does not occur unless gallstones have impacted the bile ducts of the liver. Removing gallstones from the liver and gallbladder can not only prevent a heart attack or stroke, but also reverse coronary heart disease and heart muscle damage. The body’s response to stressful situations becomes less damaging, and cholesterol levels begin to normalize as the distorted and damaged liver lobules are regenerated. Cholesterol-lowering drugs don’t do that. They artificially reduce blood cholesterol, which coerces the liver to produce even more cholesterol. But when extra cholesterol is passed into the bile ducts, it remains in its crystalline state (versus soluble state) and, thereby, turns into gallstones. People who regularly use cholesterol-lowering drugs usually develop an excessively large number of gallstones. This sets them up for major side effects, including cancer and heart disease.

Cholesterol is essential for normal functioning of the immune system, particularly for the body’s response to the millions of cancer cells that every person makes in his body each day. For all the health problems associated with cholesterol, this important substance is not something we should try to eliminate from our bodies. Cholesterol does far more good than harm. The harm is generally symptomatic of other problems. I wish to emphasize, once again, that ‘bad’ cholesterol only attaches itself to the walls of arteries to avert immediate heart trouble, not to create it.
This is confirmed by the fact that cholesterol never attaches itself to the walls of veins. When a doctor tests your cholesterol levels, he takes the blood sample from a vein, not from an artery. Although blood flow is much slower in veins than in arteries, cholesterol should obstruct veins much more readily than arteries, but it never does. There simply is no need for that. Why? Because there are no abrasions and tears in the lining of the vein that require patching up. Cholesterol only affixes itself to arteries in order to coat and cover up the abrasions and protect the underlying tissue like a waterproof bandage. Veins do not absorb proteins in their basements membranes like capillaries and arteries do and, therefore, are not prone to this type of injury.

‘Bad’ cholesterol saves lives; it does not take lives. LDL allows the blood to flow through injured blood vessels without causing a life-endangering situation. The theory of high LDL being a principal cause of coronary heart disease is not only unproved and unscientific. It has misled the population to believe that cholesterol is an enemy that has to be fought and destroyed at all costs. Human studies have not shown a cause-and-effect relationship between cholesterol and heart disease. The hundreds of studies so far conducted on such a relationship have only shown that there is a statistical correlation between the two. And there should be, because if there were no ‘bad’ cholesterol molecules attaching themselves to injured arteries we would have millions of more deaths from heart attack than we already have. On the other hand, dozens of conclusive studies have shown that risk of heart disease increases significantly in people whose HDL levels decrease. Elevated LDL cholesterol is not a cause of heart disease; rather, it is a consequence of an unbalanced liver and congested, dehydrated circulatory system.

If your doctor has told you that lowering your cholesterol with medical drugs protects you against heart attacks, you have been grossly misled. The #1 prescribed cholesterol-lowering medicine is Lipitor. I suggest that you read the following warning statement, issued on the official Lipitor web site:

“LIPITOR? (atorvastatin calcium) tablets is a prescription drug used with diet to lower cholesterol. LIPITOR is not for everyone, including those with liver disease or possible liver problems, and women who are nursing, pregnant, or may become pregnant. LIPITOR has not been shown to prevent heart disease or heart attacks.

“If you take LIPITOR, tell your doctor about any unusual muscle pain or weakness. This could be a sign of serious side effects. It is important to tell your doctor about any medications you are currently taking to avoid possible serious drug interactions…”

My question is, “Why risk a person’s health or life by giving him/her a drug that has no effect, whatsoever, in preventing the problem for which it is being prescribed?” The reason why the lowering of cholesterol levels cannot prevent heart disease is because cholesterol does not cause heart disease.

The most important issue is how efficiently a person’s body uses cholesterol and other fats. The body’s ability to digest, process and utilize these fats depends on how clear and unobstructed the bile ducts of the liver are. When bile flow is unrestricted and balanced, both the LDL and HDL levels are balanced as well. Therefore, keeping the bile ducts open is the best prevention of coronary heart disease.

[Excerpt from the new edition of The Amazing Liver and Gallbladder Flush, by Andreas Moritz]

Andreas Moritz is a medical intuitive; a practitioner of Ayurveda, Iridology, Shiatsu and Vibrational Medicine; a writer and an artist. He has authored four books on health and healing: “The Amazing Liver and Gallbladder Flush”, “Timeless Secrets of Health and Rejuvenation,” “Lifting the Veil of Duality,” and “It’s Time to Come Alive" (all books are available through or Andreas also is the artist who created the oil paintings for a new innovative approach to healing through energized art, called Ener-Chi Art.

His latest healing tool for clearing emotional blocks and fear is called “Sacred Santèmony – Divine Chanting for Every Occasion.” Andreas runs a free forum “Ask Andreas Moritz” on the popular health website (5 million readers and increasing). For more information contact Andreas Moritz, visit his Web site or contact him at tel. 1-864-848-6410, Greer, South Carolina, USA, E-mail

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