Cholesterol is a waxy lipid (a waxy alcohol really) derived from food and from liver synthesis. Cholesterol is the substance from which all steroid hormones are obtained. Both cholesterol and fat are classified as lipids because they do not dissolve in water. However, cholesterol differs from fat because it does not contain fatty acids and cannot be oxidized in the body for energy. Fat represents the body’s major energy reserve. Though cholesterol has the reputation of an unwanted, even dangerous substance, all cells of the body require cholesterol because it is an essential constituent of all cell membranes. Cholesterol forms sex hormones and hormones of the adrenal cortex, which regulate water and electrolyte balance, as well as the metabolism of carbohydrate, fat and protein. In addition the skin converts cholesterol to vitamin D, while the liver converts cholesterol to bile salts, to digest and absorb fat. Bile salts are the primary way in which cholesterol leaves the body.
Cholesterol is not an essential nutrient because the body makes most of the cholesterol it needs. Liver synthesis produces approximately 50% of the cholesterol manufactured in the body. Cholesterol is constructed from a much smaller material, acetic acid, used as an activated form (acetyl coenzyme A). Insulin increases glucose utilization by tissues and stimulates cholesterol synthesis in the liver after a high carbohydrate meal.
Cholesterol Transport
Because cholesterol does not mix with water, specific carriers are required to transport cholesterol in blood, which is mainly composed of water. The liver exports cholesterol to tissues by a carrier known as LDL (Low Density Lipoprotein), which accounts for 60 to 70% of the cholesterol in serum, the clear liquid remaining after blood has clotted. LDL is considered the undesirable form of cholesterolor iause elevated levels have been linked to clogged arteries. LDL originates from VLDL (Very-Low-Density Lipoprotein), a carrier of fat synthesized by the liver. Peripheral tissues such as muscle absorb LDL at specific sites on cell surfaces. HDL (High Density Lipoprotein), the so-called “good cholesterol,” plays a unique role in cholesterol metabolism. HDL acquires cholesterol from peripheral tissues and thus acts as a scavenger. HDL can exchange cholesterol with other lipid carriers, and it also transports cholesterol to the liver for disposal.
I would like to introduce you to a particularly important secondary risk factor, lipoprotein (a). The genuine function of lipoprotein (a) is very useful; it fulfills a variety of repair functions, for example, during wound healing. However, if the artery wall is destabilized by a long- term vitamin deficiency, lipoprotein (a) turns into a risk factor ten times more dangerous than cholesterol. Let’s have a closer look at how lipoprotein (a) molecules differ from other fat molecules.?
Cholesterol and triglycerides do not swim in the blood like fat swims in the soup. Thousands of cholesterol molecules are packed together with other fat molecules in tiny round globules called lipoproteins. Millions of these fat-transporting vehicles circulate in our body at any given time. The best known among these lipoproteins are high-density lipoproteins (HDL, or ?good cholesterol?) and low-density lipoproteins (LDL, or ?bad cholesterol?).?
LDL-cholesterol. Most of the cholesterol molecules in the blood are transported in millions of LDL particles. By carrying cholesterol and other fat molecules to our body cells, LDL is a very useful transport vehicle to supply nutrients to these cells.?
LDL has been named the ?bad cholesterol? because, until recently, researchers believed that it is LDL that is primarily responsible for the fatty deposits in the artery walls. This understanding is now out of date.?
Lipoprotein (a) is an LDL particle with an additional adhesive protein surrounding it. This biological adhesive tape is named apoprotein (a), or brief, apo (a). The letter (a) could in fact stand for ?adhesive.? The adhesive apo (a) makes the lipoprotein (a) fat globule one of the stickiest particles in our body.
LDL has been named the ?bad cholesterol? because, until recently, researchers believed that it is LDL that is primarily responsible for the fatty deposits in the artery walls. This understanding is now out of date.?
Lipoprotein (a) is an LDL particle with an additional adhesive protein surrounding it. This biological adhesive tape is named apoprotein (a), or brief, apo (a). The letter (a) could in fact stand for ?adhesive.? The adhesive apo (a) makes the lipoprotein (a) fat globule one of the stickiest particles in our body.
What Does Medicine Today Know About Lipoprotein (a)?
– Lipoprotein (a), not LDL, is the most important fat particle responsible for the deposition of cholesterol and other fats in the artery walls.?
– Because of its sticky properties, lipoprotein (a) is one of the most effective repair molecules in the artery wall and, with ongoing vitamin deficiency, becomes one of the most dangerous risk factors for atherosclerosis and cardiovascular disease.
– A reevaluation of the Framingham Heart Study, the largest cardiovascular risk factor study ever conducted, showed that lipoprotein (a) is a ten-fold greater risk factor for heart disease than cholesterol or LDL-cholesterol.
THEREFORE, folks, have your physician order a Lp(a) — Lipoprotein (a) test the next time your have your annual physical exam, and especially if you have a history of heart or artery problems. This will tell you whether or not you are having some plaque building process going on in your arteries. The Lp (a) values should be < 10mg/dl as optimum, with 10 to 20 mg/dl borderline and > 20 mg/dl is considered high and potentially dangerous.
– Lipoprotein (a), not LDL, is the most important fat particle responsible for the deposition of cholesterol and other fats in the artery walls.?
– Because of its sticky properties, lipoprotein (a) is one of the most effective repair molecules in the artery wall and, with ongoing vitamin deficiency, becomes one of the most dangerous risk factors for atherosclerosis and cardiovascular disease.
? A reevaluation of the Framingham Heart Study, the largest cardiovascular risk factor study ever conducted, showed that lipoprotein (a) is a ten-fold greater risk factor for heart disease than cholesterol or LDL-cholesterol.
In a Vitamin-Deficient Body, Lipoprotein (a) Becomes the Most Important Secondary Risk Factor for:
? Coronary Heart Disease and Heart Attacks
? Cerebrovascular Disease and Strokes
? Re-stenosis (Clogging) after Coronary Angioplasty
? Clogging of Bypass Grafts after Coronary Bypass Surgery
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Together with his colleagues at Hamburg University, Mathias Rath, M.D. conducted the most comprehensive studies on lipoprotein (a) in the artery wall. These studies showed that the atherosclerotic lesions in human arteries are largely composed of lipoprotein (a) rather than LDL molecules. Moreover, the size of the atherosclerotic lesions paralleled the amount of lipoprotein (a) particles deposited in the arteries. In the meantime, these findings have been confirmed in a series of further clinical studies.?
Lipoprotein (a) blood levels vary greatly between one individual and another. What do we know about the factors influencing the lipoprotein (a) levels in your blood? Lipoprotein (a) levels are primarily determined by inheritance. Special diets do not influence lipoprotein (a) blood levels. Moreover, none of the presently available lipid-lowering prescription drugs lower lipoprotein (a) blood concentrations. The only substances that have thus far been shown to lower lipoprotein (a) levels are vitamins. Professor Carlson could show that two to four grams of vitamin B3 (nicotinic acid) a day could lower lipoprotein (a) levels up to 36%. Because high levels of nicotinic acid can cause skin rash, you are well advised to increase the daily intake of nicotinic acid slowly. Our own research showed that vitamin C alone or in combination with lower dosages of nicotinic acid may also have a decreasing effect on the production of lipoproteins and thereby on lowering lipoprotein blood levels. Together with the ?Teflon? agents lysine and proline, these two vitamins can considerably decrease the cardiovascular risk associated with lipoprotein (a) levels.?
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Therapeutic Approaches to Reduce the Risk from?Lipoprotein (a):
1.- Lowering of Lipoprotein (a) Blood Levels?
– Vitamin B3 (Nicotinate)
– Vitamin C?
2. – Decreasing Stickiness of Lipoprotein(a)
– Lysine
– Proline
SEE: VITAMIN C
Lipoprotein (a) is a particularly interesting molecule because of its inverse relationship to vitamin C. The following discovery triggered my interest in vitamin research: lipoprotein (a) molecules are primarily found in humans and a few animal species unable to produce vitamin C. In contrast, animals able to produce optimum amounts of vitamin C do not need lipoprotein (a) in any significant amount. Lipoprotein (a) molecules apparently compensates for many properties of vitamin C such as wound healing and blood vessel repair. In 1990 I published the details of this important discovery in the Proceedings of the National Academy of Sciences and invited Linus Pauling as co-author for this publication.
The Cholesterol – Heart Disease Fallacy
While reading this section you may have asked yourself the question: ?But what about cholesterol? Are those reports about cholesterol only media hype?? Unfortunately, this is the case. Here are some of the sobering facts:
The leading medical speculation about the origin of cardiovascular disease is as follows: high levels of cholesterol and risk factors in the blood circulation would damage the blood vessel walls and lead to atherosclerotic deposits. According to this hypothesis, lowering of cholesterol is the primary measure to prevent cardiovascular disease. Tens of millions of people worldwide are currently swallowing cholesterol-lowering drugs in the expectation of helping fight cardiovascular diseases. The marketing propaganda behind these cholesterol-lowering drugs is worthy of a close look:
In the 70’s the World Health Organization (WHO) conducted an international study to answer the question whether cholesterol-lowering drugs can decrease the risk for heart attacks. Thousands of study participants received the cholesterol-lowering drug Clofibrate. This study could not be completed because those people who took the cholesterol-lowering drug experienced too many side effects. Thus, in the interest of the health and lives of the study participants, this cholesterol-lowering drug study had to be called off.
In the early 80’s a large-scale study in over 3,800 American men made headline news. In this study it was tested whether the cholesterol-lowering drug Cholestyramine can lower the risk for heart attacks. One study group took up to 24 grams (24,000 milligrams) of Cholestyramine every day over several years. The control group of this study took the same amount of placeboes (ineffective control substance). The result of this study was that in the cholesterol-lowering drug group the same number of people died as in the control group. Particularly frequent among those patients taking this cholesterol-lowering drug were accidents and suicides. Irrespective of these facts, those interested in marketing the drug decided to sell this study as a success. The fact that in the drug group there were slightly fewer incidences of heart attacks was marketed as a confirmation of the cholesterol-heart attack-hypothesis. Hardly anyone bothered with the actual death figures of this study.
In the late 80’s a new group of cholesterol-lowering drugs was introduced which was shown to decrease the production of cholesterol in the body. Soon thereafter it was determined that these drugs not only lower the production of cholesterol in the body, but also the manufacturing of other essential substances in the body, for example, ubiquinone (Coenzyme Q-10). Professor Karl Folkers, from the University of Texas in Austin, rang the alarm bells in the Proceedings of the National Academy of Science. Professor Folkers reported that patients with existing heart failure taking these new cholesterol-lowering drugs could experience life-threatening deterioration of their heart functions.?
A giant blow for the cholesterol-lowering drug industry came on January 6, 1996. On this day the Journal of the American Medical Association published an article entitled ?Carcinogenicity of Cholesterol-lowering Drugs.? Dr. Newman and Dr. Hulley from San Francisco University Medical School showed that most of the cholesterol-lowering drugs on the market are known to cause cancer in test animals at levels currently prescribed to hundreds of thousands of people. The results from this article were so alarming that the authors raised the legitimate question: ?How could it be that the regulatory agency, the U.S. Food and Drug Administration, (FDA), allowed these drugs to be sold to millions of people?? The answer is: ?The pharmaceutical companies manufacturing these drugs down played the importance of these side effects and thereby removed any obstacles for their approval.?
The publication of my popular science book in 1993 explained for the first time that animals don’t get heart attacks because they produce enough vitamin C – not because they have low cholesterol levels. Heart attacks are the primary result of vitamin deficiencies – not of elevated cholesterol. It was immediately clear that cholesterol-lowering drugs, beta-blockers, calcium antagonists and many other pharmaceuticals would eventually be replaced by essential nutrients in eliminating cardiovascular diseases. The time this would take would be dependent on one factor only: How fast can the information about the connection between scurvy and cardiovascular disease be spread. The manufacturers of cardiovascular drugs knew that they will loose an annual drug market of over $100 billion dollars. This multi-billion dollar drug market will collapse once millions of people learn that vitamins and other essential nutrients are the answer to the cardiovascular epidemic.?
This is the background why the pharmaceutical industry is spending hundreds of millions of dollars advertising drugs that are known to cause cancer.
Why Bears Are Not Extinct?
If anyone among my readers still thinks that cholesterol may cause heart attacks, I would like to share the following facts: Bears and millions of other hibernating animals have average cholesterol levels of over 400 milligrams per decilite0066f cholesterol w00062C indeed, the culprit causing heart attacks and strokes, bears and millions of other hibernating animals would have long been extinct from heart attacks. The reason why bears are still among us is simple: they produce high amounts of vitamin C in their bodies, stabilize their artery walls and don’t bother about cholesterol.?
The fact that bears are not extinct proves:?
1. Elevated cholesterol blood levels are not the primary cause of atherosclerosis, heart attacks and strokes.
2. Achieving and maintaining stability of the artery walls through optimum vitamin supply is more important than lowering cholesterol and other risk factors in the blood stream.
3. Cholesterol and other repair factors in the blood stream can only become risk factors if the artery walls are weakened by chronic vitamin deficiency. ??
CHOLESTEROL MYTHS
Did you know ….
. . . that cholesterol is not a deadly poison, but a substance vital to the cells of all mammals?
. . . that your body produces three to four times more cholesterol than you eat?
. . . that this production increases when you eat only small amounts of cholesterol and decreases when you eat large amounts?
. . . that the only effective way to lower cholesterol is with drugs?
. . . that many of the cholesterol-lowering drugs are dangerous to your health and may shorten your life?
. . . that the optimum level of cholesterol in our blood is probably 180 – 300.
Dr. Ravnskov exposes the faulty premises and questionable science behind the diet-heart idea. Before you adopt a low fat diet or take expensive cholesterol-lowering drugs, read his excellent analysis in The Cholesterol Myths.
COMMENTARY ON CHOLESTEROL
From: The Lipid Hypothesis of Arthrogenesis
by William E Stehbens, M.D.
Cholesterol could one day be recognized as the most important steroid in human biology. Cholesterol is no more noxious than oxygen, calcium or hemosiderin. To refer to good cholesterol (HDL) and bad cholesterol (LDL) is unscientific. Use of such terminology to lead the public into accepting a contentious and unproven hypothesis is reprehensible. Promulgation of such concepts in the public arena when there is intense public interest in food and health has led to confusion and an undeserved phobia of cholesterol and in the long-term leads medicine into disrepute.
CHD is most prevalent in the more prosperous, better-fed and long-living communities. Yet, within those communities it is most prevalent in the lowest socio-economic group. The western diet had led to an increase in height and weight and a much reduced infant mortality. Rising affluence is associated with increased longevity and greater resistance to infectious diseases. Caution is needed before instituting alterations to the human diet and it is inadvisable to institute changes on the basis of a controversial and unproven hypothesis. There is evidence that even moderate dietary induced hypocholesterolemia in young children is potentially hazardous to brain and body development and may endanger the cholesterol degradative mechanism. What the serum cholesterol level should be for optimal physiological function at any age is unknown.
It must be concluded that in inherited metabolic disorders in man and several lower species, the grossly elevated blood cholesterol or LDL levels may induce metabolic storage phenomena in the blood vessels, cardiac valves and extravascular tissues but in normo-lipidemic subjects there is no scientific evidence that cholesterol or LDL is noxious at all blood levels nor that they cause atherosclerosis. In effect there should be no cholesterol controversy.
In 1982 Kannel and Gordon in Lancet declared that cholesterol was not a strong risk factor in the way hypertension was for stroke; and for CHD no such strong risk factor existed with cholesterol.
Cholesterol and Lipid in the Advanced Atherosclerotic Plaque
The presence of lipid and cholesterol crystals is a common feature in old, degenerate, necrotic lesions, tumors, fibromyomata and old cerebral infarcts. Their presence is no more indicative of cause than calcification, fibrosis or the presence of smooth muscle cells. However it must be emphasized that the lipid hypothesis is basically an explanation for the influx of lipid into the vessel wall in the mistaken belief that the presence of lipid and cholesterol is the hallmark of atherosclerosis. The assumption has always been that once lipid is present the full gamut of changes of atherogenesis and the complications follow in its wake. Yet LDL and cholesterol are needed by the cells of the blood vessel wall and are therefore continuously percolating through the walls.
No explanation based on the lipid hypothesis has ever been provided for the intimal tears, ulceration, tortuosity, ectasia and aneurysms nor for the lipid accumulation that occurs in the vesiculogranular debris (matrix vesicles). Nor has an adequate explanation been provided for (1) the absence of a minimal change in some veins and arteries, (ii) the disparate severity in various vascular beds or adjacent segments even in the same vessel, (iii) the surgical induction of accelerated atherosclerosis in venous bypass grafts and veins of arteriovenous shunts for renal dialysis or (iv) the experimental production of atherosclerosis in herbivores with low blood cholesterol levels under conditions analogous to those in man. No continuously circulating humoral agent can be responsible for such changes and spontaneous development of atherosclerosis in herbivores, omnivores and carnivorous lower animal species argues against the lipid hypothesis.
It is also widely accepted now that the initial lesion of atherosclerosis is fibromusculoelastic intimal thickening, the lipid being a later secondary manifestation. This early lesion seen in the fetus and neonate is more likely to provide clues to the etiology than the end-stage disease which originally inspired the lipid hypothesis. Yet atherosclerosis is initiated and progresses at a stage of life when serum cholesterol levels are lower than levels which have been alleged to cause regression of disease and are said to be capable of preventing CHD.