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The Good, the Bad, and the Ugly Cholesterol Lies.



Despite what the “experts” might tell you, cholesterol is cholesterol. There is only one type of cholesterol and it is a high molecular weight organic molecule (an alcohol or a sterol) found only in animal foods such as meat, fish, cheese, eggs, and butter. Cholesterol is an essential nutrient that is necessary for maintaining and repairing every cell membrane in your body. It plays an important role in immunity and synthesizing hormones.


The Good, the Bad, and the Ugly Cholesterol Lies.


by Simon Lee, Science Officer, Anew UK.


Cholesterol is a precursor to vital corticosteroids, and to sex hormones like androgen, testosterone, oestrogen and progesterone. It is a precursor to vitamin D, a vital fat-soluble vitamin essential for healthy bones and nervous system, proper growth, mineral metabolism, muscle tone, insulin production, reproduction and immune system function. It is the precursor to bile salts, which are essential for digestion and the assimilation of dietary fats. Recent research has shown that cholesterol acts as an antioxidant thereby helping to reduce oxidative damage in the body.


Cholesterol is required for the proper function of serotonin receptors in the brain. Serotonin is one of the body’s natural “feel-good” neurotransmitters. This explains why low cholesterol levels have been linked to aggressive and violent behavior, depression, and suicidal tendencies.


Breast milk is especially rich in cholesterol and also contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system. Dietary cholesterol also plays an important role in maintaining the health of the intestinal wall, which is why low-cholesterol vegetarian diets can lead to leaky gut syndrome and other intestinal problems.


Your doctor probably forgot to mention all of the above.


The Ugly Lies That Demonised an Essential Nutrient


In 1954 a Russian researcher called David Kritchevsky published a paper describing the effects of feeding cholesterol to vegetarian rabbits. He discovered that cholesterol added to vegetarian rabbit chow caused the formation of atherosclerotic plaques that can block arteries and contribute to heart disease.


At the time, scientists were aware that there had been a dramatic increase in heart disease compared to the beginning of the twentieth century when heart disease caused no more than 10% of all deaths, much less than diseases such as pneumonia and tuberculosis.


By 1950, Coronary Heart Disease (CHD) was the leading cause of death in the United States, causing more than 30% of all deaths.












The Kritchevsky papers lent apparent support to the lipid hypothesis which is the idea that saturated fat and cholesterol from animal-based foodstuffs raise cholesterol levels in the blood, leading to deposition of cholesterol and fatty material as pathogenic plaques in the arteries.

Kritchevsky’s animal findings were assumed to be relevant to the human CHD problem. The lipid hypothesis was assumed to be a valid explanation for the new epidemic of heart disease which, it was assumed, could be avoided by reducing animal products in the diet.


However, in the years that followed, several population studies showed that the animal model, especially one based on vegetarian animals, was not a valid approach to studying heart disease in human omnivores.


One study on the Japanese population showed that the Japanese had almost as much pathogenic plaque as the Americans even though the Japanese diet at the time was much lower in animal products and fat.


A 1957 study of the mostly vegetarian Bantu found that they had as much plaque buildup in the arteries as other races from South Africa who ate more meat.


A 1958 study found that black Jamaicans had a degree of atherosclerosis comparable to that found in the US, although they suffered from lower rates of heart disease.


The 1968 International Atherosclerosis Project, in which over 22,000 autopsies were performed in 14 different countries showed the same degree of atheroma in all parts of the world. The same degree of atheroma was found in populations that consumed large amounts of fatty animal products compared to those that were mostly vegetarian. The same degree of atheroma was found in populations that had a great deal of heart disease and in populations that had very little or none at all.


A 1994 study in the Lancet showed that almost three-quarters of the fat in artery clogs is unsaturated. Indicating that the “artery-clogging” fats are not animal fats but vegetable oils.


All of these studies pointed to the fact that the lipid hypothesis was wrong and could not explain what caused the tendency towards fatal blood clots that caused myocardial infarction (heart attack) in humans.










Atherosclerosis

Since Kritchevsky’s early studies, many other trials had shown that serum cholesterol can be lowered by increasing consumption of polyunsaturates. The physiological explanation for this is that when excess polyunsaturates are incorporated into the cell membranes, resulting in reduced structural integrity or “limpness,” cholesterol is sequestered from the blood into the cell membranes to give them “stiffness.”


The problem was that there was no proof that lowering serum cholesterol levels could lower the risk of CHD.


The Framingham Study, which began in 1948, included 5,209 people from Massachusetts and was instrumental in starting the myth that high total cholesterol is a major risk factor for heart disease.


What the Framingham Study actually found was that there was virtually no difference in Coronary Heart Disease (CHD) “events” for people with cholesterol levels between 205 mg/dL and 294 mg/dL which is the vast majority of the US population. Even for those with extremely high cholesterol levels—up to almost 1200 mg/dL, the difference in CHD events compared to those in the normal range was trivial. The study found that for people in their 50s, 60s and older as cholesterol DROPPED, mortality rate INCREASED.


This did not stop Dr. William Kannel, the Framingham Study Director at the time, from making outrageous claims about the Framingham results. He said:


“Total plasma cholesterol is a powerful predictor of death related to CHD.”


It wasn’t until more than a decade later that the real findings from Framingham were published, in an obscure journal, without fanfare. Dr. Kannels successor, Dr William Castelli admitted:


“In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol. . . we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least and were the most physically active.”


Dr George Mann who was once involved with the Framingham study went on to study the Masai in Africa, whose diet is extremely high in cholesterol and saturated fat, but they have virtually no heart disease. This convinced him that the lipid hypothesis was “the public health diversion of this century. . . the greatest scam in the history of medicine.”


This made him determined to raise public awareness by organizing a conference in Washington DC in November of 1991.


In Mann’s invitation to conference goers, he wrote:


“Hundreds of millions of tax dollars are wasted by the bureaucracy and the self-interested Heart Association. Segments of the food industry play the game for profits. Research on the true causes and prevention is stifled by denying funding to the ‘unbelievers.’ This meeting will review the data and expose the rascals.”


The “rascals” did their best to stop the meeting from taking place. Promised funding was subsequently withdrawn, forcing Mann to pay for the event himself. A press release falsely claiming the conference had been cancelled was issued to speakers and participants. Several speakers did actually cancel after being warned that attendance would jeopardise future funding.


Against all the odds the conference did go ahead and Dr. George Mann used the platform to speak out:


“You will see, that many of our contributors are senior scientists. They are so for a reason that has become painfully conspicuous as we organized this meeting. Scientists who must go before review panels for their research funding know well that to speak out, to disagree with this false dogma of Diet/Heart, is a fatal error. They must comply or go unfunded. I could show a list of scientists who said to me, in effect when I invited them to participate:


‘I believe you are right, that the Diet/Heart hypothesis is wrong, but I cannot join you because that would jeopardize my perks and funding.’ For me, that kind of hypocritical response separates the scientists from the operators—the men from the boys.”


The Manufacturing of the Fake Cholesterol “Consensus”


The Multiple Risk Factor Intervention Trial (MRFIT) studied the relationship between heart disease and serum cholesterol levels in 362,000 men and found that annual deaths from CHD varied from slightly less than 1 per thousand at serum cholesterol levels below 140 mg/dL, to about 2 per thousand for serum cholesterol levels above 300 mg/dL, once again this is a trivial difference.


An unexpected MRFIT finding the media forgot to report was that deaths from all causes (cancer, heart disease, accidents, infectious disease, kidney failure, etc.) were SUBSTANTIALLY HIGHER for men with cholesterol levels below 160 mg/dL.


The NHLBI, who had run the MRFIT trial, went on to sponsor the so-called National Cholesterol Consensus Conference. When an attendee accidentally picked up some papers before the conference had even begun she was surprised to discover that the “consensus” report had already been written.


Dr Edward Ahrens, a respected researcher, raised strong objections about the so-called “consensus,” but he was told that he had misinterpreted his own data and that if he wanted a conference to arrive at different conclusions, he should pay for it himself.


The 1984 Cholesterol Consensus Conference final report was a preordained whitewash, which made no mention of the large body of evidence that conflicted with the lipid hypothesis.


The many objectors to the whitewash were ignored and the final report of the Cholesterol Consensus Conference called for mass cholesterol screening. Acting against good scientific evidence the medical bureaucracy picked a cholesterol level that would place the vast majority of the American adult population “at risk” for heart disease. This ensured that the lucrative screening program would need to be carried out on a massive scale.


The report recommended that all Americans now defined as “at risk” should avoid saturated fat and cholesterol and specifically advised replacing butter with margarine.


The “Consensus” Conference also spawned the nationwide US National Cholesterol Education Program (NCEP), which had the stated goal of “changing physicians’ attitudes.” The general population had bought into the lipid hypothesis and was obediently using margarine and eating low-cholesterol foods, but the medical profession remained sceptical. “Physicians Kits” were sent to all doctors in America, who were indoctrinated about the supposed importance of cholesterol screening, the supposed advantages of cholesterol-lowering drugs, and they were told to recommend margarine rather than butter.


The hospitals, laboratories, pharmaceutical companies, the vegetable oil industry, margarine manufacturers, food processors and, of course, doctors would benefit enormously from the mass screening of cholesterol levels in all adults. A multi-billion dollar industry was created by turning healthy people into patients based on their cholesterol number. It has been a public health disaster.


“I began my practice as a cardiologist in 1921 and I never saw an MI patent until 1928. Back in the MI-free days before 1920, the fats were butter and lard and I think that we would all benefit from the kind of diet that we had at a time when no one had ever heard the word corn oil.”


Dr. Dudley White


Many people with normal cholesterol levels may have heart attacks and studies in the elderly have shown that those with the LOWEST levels of cholesterol are at HIGHEST risk of death from all causes.


A comprehensive review of the literature in 2018 found that “LDL-C Does Not Cause Cardiovascular Disease”. The authors ( Uffe Ravnskov et al.) discovered “obvious falsification of the cholesterol hypothesis … the conclusions of the authors…are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations.”


They went on to say:


“The idea that high cholesterol levels in the blood are the main cause of CVD is impossible because people with low levels become just as atherosclerotic as people with high levels and their risk of suffering from CVD is the same or higher.”


The Good and the Bad


According to the “experts,” there are two main kinds of cholesterol: the “good” cholesterol or High Density Lipoprotein (HDL), and the “bad” cholesterol or Low Density Lipoprotein (LDL).

Because cholesterol is not soluble in water it is transported around the body attached to these lipoprotein particles.


LDL is referred to as “bad” cholesterol because it is often found in the walls of diseased arteries afflicted with atherosclerosis. HDL, is called the “good” cholesterol, because it is thought to help remove cholesterol from the arteries.


An LDL particle is a type of lipoprotein made by the liver. One of its functions is to deliver cholesterol and triglycerides from the liver to other cells in the body.


High Density Lipoprotein (HDL) and Low Density Lipoprotein (LDL) cholesterols are complex particles that contain exactly the same cholesterol. It is only the carriers that are different.


There are two types of LDL particle, namely, large and buoyant, and small and dense. The small and dense LDLs are considered to be much more atherogenic, whereas the large, buoyant LDLs are considered to be less atherogenic. About 80% of total LDL cholesterol level consists of the large, buoyant LDLs, with small, dense LDL making up the remainder.


People with more large, buoyant LDLs are categorised as Pattern A type of cholesterol profile, and these people are said to be at low risk of atherosclerosis. People with more small, dense LDLs are categorised as Pattern B cholesterol profile and are said to be at higher risk of atherosclerosis. Their markers for metabolic disease risks may also be raised.


Interestingly, fats increase large, buoyant LDLs and decrease small, dense LDLs, whereas refined carbohydrates increase small, dense LDLs. Research has found that consumption of refined carbohydrates is more relevant than saturated fat in the causation of coronary heart disease.


This idea that there are “bad” and “good” blood lipids that contribute to heart disease has added further complexity to the lipid hypothesis. It would seem that the only way to prevent the whole scam from being exposed is to keep adding more complexity to the story on a regular basis.


An Inversion of the Truth


What your doctor will not tell you (because they most likely do not know) is that cholesterol carrying lipoproteins are essential for innate immunity to infection and for muscle growth. Blaming heart disease on high cholesterol levels is like blaming firefighters for starting the fires.


Infection and inflammation are associated with marked changes in lipid and lipoprotein metabolism. Besides their role in lipid transport, lipoproteins participate in innate immunity, which is the first line of defence against invading microbes. The changes in lipoproteins during infection/inflammation help protect against the harmful effects of the microbes and their toxins.


These changes result in increased cholesterol delivery to immune cells and decreased reverse cholesterol transport (from the periphery back to the liver).


The lipoproteins are part of the Acute Phase Response (APR) to infection which protects against injury by neutralising invading microbes, minimising the extent of tissue damage, participating in the local immune response, and replenishing and regenerating damaged tissue.


Bacterial infection stimulates increased activity of the enzyme HMG-CoA reductase which is crucial in the mevalonate biosynthetic pathway of cholesterol production. The lucrative cholesterol lowering drugs statins, inhibit this important enzyme, which is crucial in providing innate protection against invading microbes and their toxins.


Ordinarily when bacteria are sensed, the clearance of LDL from the circulation is significantly inhibited. Statins have the opposite effect, causing an increase in cellular LDL receptors, resulting in an increase in cellular LDL uptake, thereby removing protective LDL from the circulation.


Adequate lipoprotein levels are needed to block and neutralise the bacterial toxins that induce fever, hypotension, circulatory collapse, and death due to sepsis.


Lipoproteins can help neutralize the lethal effects of bacterial toxins by accelerating their clearance from the blood, redirecting them away from monocytes and macrophages, decreasing immune cell activation, and reducing the release of cytokines, thus attenuating toxicity and preventing sepsis. What’s bad about that?


Lipoproteins also protect from certain parasitic infections namely trypanosomes, schistosomes, and malaria. What’s bad about that?


Furthermore, infection is often associated with cellular injury, and areas of injury may need extra cholesterol for new membrane synthesis and repair.


The changes that occur to the structure, composition, and function of lipoproteins during infection are the same as those proposed to promote atherogenesis. This is not a coincidence.


Studies have shown that the risk and/or incidence of coronary artery disease (CAD) is higher in people with infections. Several different specific microbes have been detected directly in atherosclerotic lesions of arterial walls. The bacteria that cause chronic dental infections have been detected in atherosclerotic plaques and they possess all of the capabilities needed to cause atherosclerosis.


These same dental bacteria also cause the supposedly incurable and chronic autoimmune/inflammatory diseases such as rheumatoid arthritis as well as Alzheimer’s disease.

LDL delivers essential cholesterol to tissues for repair, and HDL, the good cholesterol, cleans up after the repair is done. The more LDL you have in your blood, the better you are able to build muscle during resistance training. What’s bad about that?


According to Dr. Steve Riechman, a researcher at Texas A&M University:


“LDL is not the evil Darth Vader of health it has been made out to be in recent years.”


Dr. Riechmans team has shown that people with the highest levels of LDL cholesterol gain the most muscle mass after working out.


“We need to change this idea of LDL always being the evil thing—we all need it, and we need it to do its job.”


Dr. Steve Riechman


Conclusions


There is only one type of cholesterol and it is an essential nutrient that is vital for good health. What doctors often refer to as “good” and “bad” cholesterol are actually complex carrier lipoprotein particles. There is nothing “bad” about LDL, in fact it plays an important role in protection against microbes and their toxins as well as in muscle growth. Despite this many doctors have been indoctrinated and are financially induced to lower LDL levels in their patients often using toxic harmful drugs like statins.


References


1) The Oiling of America MARCH 29, 2006 BY SALLY FALLON AND MARY G. ENIG, PHD Copyright © 1999 Mary G. Enig, PhD and Sally Fallon. First Published in Nexus Magazine, December 1998-January 1999 and February 1999-March 1999. (Source)

2) LDL-C Does Not Cause Cardiovascular Disease: a comprehensive review of current literature (2018) Expert Review of Clinical Pharmacology. Uffe Ravnskov et al. (source)

3) Cholesterol: It’s All Good. HEALTH VIEWPOINTS Epoch Times, Margie King. Mar 21 2023 (source)

4) ‘Bad’ Cholesterol May Not Be So Bad. Epoch Times, Marina Zhang (source)

5) Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. Journal of Lipid Research Volume 45, (2004) Weerapan Khovidhunkit et al. (source)


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