The International Network of Cholesterol Skeptics. This. is a contribution from a member of THINCS, The International Network of Cholesterol Skeptics Home. Nov. 2. 8, 2. 00. WHY THE CHOLESTEROL- HEART DISEASE THEORY IS WRONG Find. Cholesterol. is a much maligned substance, the . If it is, it. must have killed billions of people. Far more than the plague, every war. But. if it does cause heart disease, how does it do it? First. little problem - dietary intake of cholesterol has no impact on the level of. If we look at two major long- term studies. Framingham and Tecumseh, it is clear that those who ate the most cholesterol. Table: Cholesterol intake - The Framingham Heart Study. Blood Cholesterol. The Framingham Heart Study is a long-term, ongoing cardiovascular cohort study on residents of the town of Framingham, Massachusetts. The study began in 1948 with. Heart attacks bring patients into the emergency room in crisis. When blood flow through the coronary arteries is blocked by plaques or blood clots, part of the heart. Average. Cholesterol. Intake. Below. Average. Intake. Above. Average. Intake mg/daymmol/l. Men. 70. 4. . The man, who, more than any other, is responsible for the. To quote Ancel Keys. And we've known that all along. Does. this come as a surprise? Which just blows up a fairly. Updating a 12-Year Experience With Arrest and Reversal Therapy for Coronary Heart Disease (An Overdue Requiem for Palliative Cardiology) by Caldwell B. Wolf receives the American Heart Association's Paul Dudley White Award; Joanne Murabito Named Co-PI, Framingham Heart Study. Title: Dyslipidemia update by Dr Sarma Author: Dr Sarma Last modified by: Dr. Sarma Created Date: 9/23/2003 2:44:29 PM Document presentation format. Dilated cardiomyopathy is a progressive disease of heart muscle that is characterized by ventricular chamber enlargement and contractile dysfunction. Low back pain became one of the biggest problems for public health systems in the Western world during the second half of the 20th century. The lifetime prevalence of. Q and A: Dangers Of Prescription Blood Thinners: And Safer Alternatives Q: Dear Dr. Foster, My best friend's mother has broken out in scabs all over her body.Table . Fat intake and blood lipids - The Tecumseh Study. Blood Cholesterol in Thirds. Daily. Intake: Lower. Middle. Upper. Fat. Saturated (g) 5. 2 5. Polyunsat/Sat. ratio 0. Cholesterol. (mg) 5. Basically, it divides people. The absolute. values are not important. Having. done this we can examine the level of saturated fat consumed by these three. Let us quote William Castelli. Framingham study for many years. However. a special prize to the man, or woman, who can find a long- term study showing. Or, indeed, has any. CHD. Quick. time to move those goalposts again. But. how could they be? For, in the next episode I shall make it clear that there. The. two substances are completely unrelated chemically, and only ever meet when. And. then I will show why a high blood cholesterol level cannot cause heart. Ladies and gentlemen, roll up, roll up and gasp in amazement as the. Some. studies have shown that a high saturated fat intake raises cholesterol. The longest, most prestigious. CHD, the Framingham study, clearly. But. my belief is not an act of personal faith with no foundation on fact. For. the science of fat metabolism confirms that there cannot be any. And I am wondering how best to explain this without getting too. The. first point to make is that you do not have a cholesterol level in your. Cholesterol is insoluble in blood, and therefore has to be carried. There are many. different types of lipoprotein, ranging from the monster chlyomicron to the. High Density Lipoprotein (HDL). Lipoproteins. do not just carry cholesterol. They also carry all sorts of other fats. These fats are all attached. Triglyceride. = three fats attached to a backbone glycerol molecule. Thus. when you eat cholesterol and saturated fat, they are both absorbed into the. Then. within the intestinal wall both are rammed into a chylomicron before being. Most. chylomicrons go directly to the liver where they are absorbed, broken down. Very Low. Density Lipoprotein VLDL. These VLDLs then go out into the general. As they do so, they get smaller. VLDL to Intermediate Density Lipoproteins (IDLs), then Low. Density Lipoproteins (LDLs). The. LDL is either absorbed back into the liver, to be reused to create more. VLDLs, or they are absorbed into other tissues where the contents are used. So. at what point does saturated fat get turned into cholesterol? Answer. it doesn. Cholesterol. when it is made in the liver, starts out as a substance called Acteyl- co A. It has several nitrogen atoms. So why. would eating saturated fat increase cholesterol production in the. But. of course, the substance we are interested in nowadays is LDL. Which is not. the same thing as cholesterol at all. So why do we called a raised LDL level. In. fact, the nomenclature in this whole area is just designed to make things. For example, a raised VLDL level is known. Perhaps if researchers. Time. for a little review. Suddenly. the whole concept of saturated fat intake raising cholesterol levels. But, if the substance in the. CHD is actually LDL, maybe we just need to move the. Does. a high saturated fat intake increase LDL levels? Just. to review some of the facts. So. if you eat more saturated fat (or any other kind of fat), the liver will. VLDL. NOT because there is more cholesterol around, but. Therefore. presumably, after all the VLDLs have shrunk in size, there will be more LDLs. Which means that a high fat consumption could lead to a higher level. LDL, via VLDL metabolism - although we have to abandon the whole. But. even if you move the discussion onto LDLs rather than cholesterol, there is. After a meal VLDL levels go. LDL level remains absolutely constant. So. the amount of VLDL in the blood is totally unrelated to the level of LDL in. Despite the fact that you . What. this proves, beyond any doubt, is that the metabolic system tightly controls. LDL in the blood. So. although fat intake can increase VLDL production, it has no effect on the. LDL. Which means that, not only does saturated fat have no effect. LDL levels. If you eat too much. If you eat too much sugar. Why should fat or. You. will not read this type of information anywhere, but here. However, every. single fact I have used has been demonstrated many, many times. These are. facts beyond dispute. Fact. one: The liver does not use fats, saturated or otherwise to make cholesterol. Fact two: The liver does not make LDL, it makes VLDLFact three: VLDL is converted into LDL through triglyceride loss. Fact four: VLDL levels and LDL levels are totally unrelated - totally. Which means that: Saturated fat intake has no impact on LDL levels. A Raised LDL Level Has No Impact On Heart Disease Having. LDL levels. I now intend to make it. LDL level has no impact on heart disease (CHD). As. most of you probably know, current thinking in CHD is that when the level of. Low Density Lipoprotein (LDL) is raised, LDLs travel through the artery wall. Cholesterol is found in plaques because LDL contains lots of. As. these plaques get bigger they narrow the artery so much that blood flow is. Finally a plaque may burst. This blocks the artery. A myocardial infarction results, which may or may not kill you. I. agree with this basic mechanism underlying CHD, but there are about eight. LDL is the cause. Which. means that we have a disease process on our hands that can occur when the. LDL is level is high, average or low. The first ever example in medical. Yes. LDL is so terrible that any level at all can kill you. The only good LDL is. LDL - or words to that effect. This concept, that a normal level of. So how does LDL get through in the first place? And even if it could, you run into problem. Plaque distribution Plaques. To. use an analogy, if you lie in the sun for too long, all of your body will. But we are expected to. LDL, it will. only leak through in a few discreet areas. Again, quite frankly. I think. Aha, you are thinking. LDL. through. And this could hardly be more obvious. So, the. underlying process that starts a plaque is damage to the endothelium. Of. course it is; there is no other possible explanation. But. to admit this, is to admit that LDL has nothing whatsoever to do with. LDL doesn. Faced. I would say insurmountable problem, what has the. LDL brotherhood chosen to do? Discard the diet- heart/cholesterol/LDL. Or keep trying to find ways to. LDL in plaque formation. No. surprise to find that no- one was remotely willing to discard the hypothesis. Otherwise the entire diet- heart/cholesterol/LDL. So. where are we now? How exactly does LDL cause CHD? Because. it is oxidised. You. may faintly detect the sound of me beating my head against a wall in the. Manchester UK. Because. LDL is oxidised! You have probably heard of anti- oxidants, and. CHD. But how are they thought to provide. Mainly because oxidised LDL can be absorbed by the. LDL on endothelial cells (called. Lox- 1 receptors, if you are interested). So. the thinking goes, once oxidised, the LDL binds to the Lox- I receptor it is. At which point, white blood cells, designed to get rid of all. LDL molecules. But. LDL. allegedly, so they just get bigger and bigger until they explode, releasing. LDL, cholesterol and. Once you have enough exploding white. And that is why oxidised LDL is such a bad thing, and why. There. are so many problems with this proposed mechanism of action that it is. Perhaps the best place to start is. If. there are receptors for oxidised LDL on endothelial cells, then oxidised LDL. But. we do see discreet plaques, and therefore? Therefore the hypothesis is wrong. The. other problem is just as serious, although a little more difficult to. If. plaques are created by oxidised LDL, then the . If this is true, then the. LDL is completely irrelevant, it is only the amount of oxidised LDL. Therefore, if you believe in this hypothesis, then the. You can claim a raised. LDL causes CHD - in which case how can people with a low level get CHD? Or. you can claim that excess oxidised LDL causes CHD. In which case CHD has. LDL levels. Ironically. LDL hypothesis - which was supposed to protect the LDL. LDL hypothesis. But by throwing up so. And. by the way, in the Heart Protection Study (HPS), which lasted five years. On the other hand, there was no evidence of any. Please spare me the claim that they. Once. again, as with almost every part of the diet- heart/cholesterol hypothesis. There is no way that LDL, oxidised. Framingham. first: There is a direct association between falling. CVD death rate increase per 1 mg/d. L per year. drop in cholesterol levels). Anderson. KM JAMA 1. In. Framingham therefore, as LDL/cholesterol levels fell, CHD rates went up. Thus, the earlier that patients start to have lower. Then. Russia: The. Shestov, of the Institute of. Experimental Medicine, Russian Academy of Medical Sciences, St. Prevalence of age- adjusted hypercholesterolaemia of >. Considerable increases in total serum cholesterol. Japan. How. much more evidence would you like? Perhaps another study from the USA? Sixty- three percent had at least 7. Of the 5. 06 men who had. Thirty- two percent. However, in this study. Kummerow noted, 5.
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