Re: High cholesterol may protect---book excerpt from Uffe Ravnskov

listener_at_nospam.net
Date: 07/14/04 

Date: Wed, 14 Jul 2004 16:35:44 -0400

For ZEE: Great News!
For the reat of the world: Fribble.

(Sorry for not trimming the crosspost.)

L.

On 14 Jul 2004 13:22:35 -0700, zwalanga@yahoo.com (Zee) wrote:

>Your thoughts, gentlemen? Zee
>
>
>
>>From Uffe Ravnskov MD PhD:
>
>An article published in QJM 2003:
>High cholesterol may protect against infections and atherosclerosis
>http://qjmed.oupjournals.org/cgi/content/full/96/12/927?ijkey=172mwKXqzgmtE&keytype=ref
>
>
>And a book excerpt on the same subject.
>http://www.westonaprice.org/know_your_fats/benefits_cholest.htm#ravnskovome
>
>The benefits of high cholesterol
>
>By Uffe Ravnskov, MD, PhD
>
>People with high cholesterol live the longest. This statement seems so
>incredible that it takes a long time to clear one´s brainwashed mind
>to fully understand its importance. Yet the fact that people with high
>cholesterol live the longest emerges clearly from many scientific
>papers. Consider the finding of Dr. Harlan Krumholz of the Department
>of Cardiovascular Medicine at Yale University, who reported in 1994
>that old people with low cholesterol died twice as often from a heart
>attack as did old people with a high cholesterol.1 Supporters of the
>cholesterol campaign consistently ignore his observation, or consider
>it as a rare exception, produced by chance among a huge number of
>studies finding the opposite.
>
>But it is not an exception; there are now a large number of findings
>that contradict the lipid hypothesis. To be more specific, most
>studies of old people have shown that high cholesterol is not a risk
>factor for coronary heart disease. This was the result of my search in
>the Medline database for studies addressing that question.2Eleven
>studies of old people came up with that result, and a further seven
>studies found that high cholesterol did not predict all-cause
>mortality either.
>
>Now consider that more than 90 % of all cardiovascular disease is seen
>in people above age 60 also and that almost all studies have found
>that high cholesterol is not a risk factor for women.2 This means that
>high cholesterol is only a risk factor for less than 5 % of those who
>die from a heart attack.
>
>But there is more comfort for those who have high cholesterol; six of
>the studies found that total mortality was inversely associated with
>either total or LDL-cholesterol, or both. This means that it is
>actually much better to have high than to have low cholesterol if you
>want to live to be very old.
>
>High Cholesterol Protects Against Infection
>Many studies have found that low cholesterol is in certain respects
>worse than high cholesterol. For instance, in 19 large studies of more
>than 68,000 deaths, reviewed by Professor David R. Jacobs and his
>co-workers from the Division of Epidemiology at the University of
>Minnesota, low cholesterol predicted an increased risk of dying from
>gastrointestinal and respiratory diseases.3
>
>Most gastrointestinal and respiratory diseases have an infectious
>origin. Therefore, a relevant question is whether it is the infection
>that lowers cholesterol or the low cholesterol that predisposes to
>infection? To answer this question Professor Jacobs and his group,
>together with Dr. Carlos Iribarren, followed more than 100,000 healthy
>individuals in the San Francisco area for fifteen years. At the end of
>the study those who had low cholesterol at the start of the study had
>more often been admitted to the hospital because of an infectious
>disease.4,5 This finding cannot be explained away with the argument
>that the infection had caused cholesterol to go down, because how
>could low cholesterol, recorded when these people were without any
>evidence of infection, be caused by a disease they had not yet
>encountered? Isn´t it more likely that low cholesterol in some way
>made them more vulnerable to infection, or that high cholesterol
>protected those who did not become infected? Much evidence exists to
>support that interpretation.
>
>Low Cholesterol and HIV/AIDS
>Young, unmarried men with a previous sexually transmitted disease or
>liver disease run a much greater risk of becoming infected with HIV
>virus than other people. The Minnesota researchers, now led by Dr. Ami
>Claxton, followed such individuals for 7-8 years. After having
>excluded those who became HIV-positive during the first four years,
>they ended up with a group of 2446 men. At the end of the study, 140
>of these people tested positive for HIV; those who had low cholesterol
>at the beginning of the study were twice as likely to test postitive
>for HIV compared with those with the highest cholesterol.6
>
>Similar results come from a study of the MRFIT screenees, including
>more than 300,000 young and middle-aged men, which found that 16 years
>after the first cholesterol analysis the number of men whose
>cholesterol was lower than 160 and who had died from AIDS was four
>times higher than the number of men who had died from AIDS with a
>cholesterol above 240.7
>
>Cholesterol and Chronic Heart Failure
>Heart disease may lead to a weakening of the heart muscle. A weak
>heart means that less blood and therefore less oxygen is delivered to
>the arteries. To compensate for the decreased power, the heart beat
>goes up, but in severe heart failure this is not sufficient. Patients
>with severe heart failure become short of breath because too little
>oxygen is delivered to the tissues, the pressure in their veins
>increases because the heart cannot deliver the blood away from the
>heart with sufficient power, and they become edematous, meaning that
>fluid accumulates in the legs and in serious cases also in the lungs
>and other parts of the body. This condition is called congestive or
>chronic heart failure.
>
>There are many indications that bacteria or other microorganisms play
>an important role in chronic heart failure. For instance, patients
>with severe chronic heart failure have high levels of endotoxin and
>various types of cytokines in their blood. Endotoxin, also named
>lipopolysaccharide, is the most toxic substance produced by
>Gram-negative bacteria such as Escherichia coli, Klebsiella,
>Salmonella, Serratia and Pseudomonas. Cytokines are hormones secreted
>by white blood cells in their battle with microorganisms; high levels
>of cytokines in the blood indicate that inflammatory processes are
>going on somewhere in the body.
>
>The role of infections in chronic heart failure has been studied by
>Dr. Mathias Rauchhaus and his team at the Medical Department,
>Martin-Luther-University in Halle, Germany (Universitätsklinik und
>Poliklinik für Innere Medizin III, Martin-Luther-Universität, Halle).
>They found that the strongest predictor of death for patients with
>chronic heart failure was the concentration of cytokines in the blood,
>in particular in patients with heart failure due to coronary heart
>disease.8 To explain their finding they suggested that bacteria from
>the gut may more easily penetrate into the tissues when the pressure
>in the abdominal veins is increased because of heart failure. In
>accordance with this theory, they found more endotoxin in the blood of
>patients with congestive heart failure and edema than in patients with
>non-congestive heart failure without edema, and endotoxin
>concentrations decreased significantly when the heart's function was
>improved by medical treatment.9
>
>A simple way to test the functional state of the immune system is to
>inject antigens from microorganisms that most people have been exposed
>to, under the skin. If the immune system is normal, an induration
>(hard spot) will appear about 48 hours later at the place of the
>injection. If the induration is very small, with a diameter of less
>than a few millimeters, this indicates the presence of "anergy," a
>reduction in or failure of response to recognize antigens. In
>accordance, anergy has been found associated with an increased risk of
>infection and mortality in healthy elderly individuals, in surgical
>patients and in heart transplant patients.10
>
>Dr. Donna Vredevoe and her group from the School of Nursery and the
>School of Medicine, University of California at Los Angeles tested
>more than 200 patients with severe heart failure with five different
>antigens and followed them for twelve months. The cause of heart
>failure was coronary heart disease in half of them and other types of
>heart disease (such as congenital or infectious valvular heart
>disease, various cardiomyopathies and endocarditis) in the rest.
>Almost half of all the patients were anergic, and those who were
>anergic and had coronary heart disease had a much higher mortality
>than the rest.10
>
>Now to the salient point: to their surprise the researchers found that
>mortality was higher, not only in the patients with anergy, but also
>in the patients with the lowest lipid values, including total
>cholesterol, LDL-cholesterol and HDL-cholesterol as well as
>triglycerides.
>
>The latter finding was confirmed by Dr. Rauchhaus, this time in
>co-operation with researchers at several German and British university
>hospitals. They found that the risk of dying for patients with chronic
>heart failure was strongly and inversely associated with total
>cholesterol, LDL-cholesterol and also triglycerides; those with high
>lipid values lived much longer than those with low values.11,12
>
>Other researchers have made similar observations. The largest study
>has been performed by Professor Gregg C. Fonorow and his team at the
>UCLA Department of Medicine and Cardiomyopathy Center in Los
>Angeles.13 The study, led by Dr. Tamara Horwich, included more than a
>thousand patients with severe heart failure. After five years 62
>percent of the patients with cholesterol below 129 mg/l had died, but
>only half as many of the patients with cholesterol above 223 mg/l.
>
>When proponents of the cholesterol hypothesis are confronted with
>findings showing a bad outcome associated with low cholesterol—and
>there are many such observations—they usually argue that severely ill
>patients are often malnourished, and malnourishment is therefore said
>to cause low cholesterol. However, the mortality of the patients in
>this study was independent of their degree of nourishment; low
>cholesterol predicted early mortality whether the patients were
>malnourished or not.
>
>Smith-Lemli-Opitz Syndrome
>As discussed in The Cholesterol Myths (see sidebar), much evidence
>supports the theory that people born with very high cholesterol,
>so-called familial hypercholesterolemia, are protected against
>infection. But if inborn high cholesterol protects against infections,
>inborn low cholesterol should have the opposite effect. Indeed, this
>seems to be true.
>
>Children with the Smith-Lemli-Opitz syndrome produce very little
>cholesterol because the enzyme that is necessary for the last step in
>the body's synthesis of cholesterol does not function properly. Most
>children with this syndrome are either stillborn or they die early
>because of serious malformations of the central nervous system. Those
>who survive are imbecile, they have extremely low cholesterol and
>suffer from frequent and severe infections. However, if their diet is
>supplemented with pure cholesterol or extra eggs, their cholesterol
>goes up and their bouts of infection become less serious and less
>frequent.14
>
>Laboratory Evidence
>Laboratory studies are crucial for learning more about the mechanisms
>by which the lipids exert their protective function. One of the first
>to study this phenomenon was Dr Sucharit Bhakdi from the Institute of
>Medical Microbiology, University of Giessen (Institut für Medizinsche
>Mikrobiologie, Justus-Liebig-Universität Gießen), Germany along with
>his team of researchers from various institutions in Germany and
>Denmark.15
>
>Staphylococcus aureus a-toxin is the most toxic substance produced by
>strains of the disease-promoting bacteria called staphylococci. It is
>able to destroy a wide variety of human cells, including red blood
>cells. For instance, if minute amounts of the toxin are added to a
>test tube with red blood cells dissolved in 0.9 percent saline, the
>blood is hemolyzed, that is the membranes of the red blood cells burst
>and hemoglobin from the interior of the red blood cells leaks out into
>the solvent. Dr. Bhakdi and his team mixed purified a-toxin with human
>serum (not just the blood cells alone, but the cells and the fluid in
>which the blood cells reside) and saw that 90 percent of its
>hemolyzing effect disappeared. By various complicated methods they
>identified the protective substance as LDL, the carrier of the
>so-called bad cholesterol. In accordance, no hemolysis occurred when
>they mixed a-toxin with purified human LDL, whereas HDL or other
>plasma constituents were ineffective in this respect.
>
>Dr. Willy Flegel and his co-workers at the Department of Transfusion
>Medicine, University of Ulm, and the Institute of Immunology and
>Genetics at the German Cancer Research Center in Heidelberg, Germany
>(DRK-Blutspendezentrale und Abteilung für Transfusionsmedizin,
>Universität Ulm, und Deutsches Krebsforschungszentrum, Heidelberg)
>studied endotoxin in another way.16 As mentioned, one of the effects
>of endotoxin is that white blood cells are stimulated to produce
>cytokines. The German researchers found that the cytokine-stimulating
>effect of endotoxin on the white blood cells disappeared almost
>completely if the endotoxin was mixed with human serum for 24 hours
>before they added the white blood cells to the test tubes. In a
>subsequent study17 they found that purified LDL from patients with
>familial hypercholesterolemia had the same inhibitory effect as the
>serum.
>
>LDL may not only bind and inactivate dangerous bacterial toxins; it
>seems to have a direct beneficial influence on the immune system also,
>possibly explaining the observed relationship between low cholesterol
>and various chronic diseases. This was the starting point for a study
>by Professor Matthew Muldoon and his team at the University of
>Pittsburgh, Pennsylvania. They studied healthy young and middle-aged
>men and found that the total number of white blood cells and the
>number of various types of white blood cells were significantly lower
>in the men with LDL-cholesterol below 160 mg/dl (mean 88.3 mg/l),than
>in men with LDL-cholesterol above 160 mg/l (mean 185.5 mg/l).18 The
>researchers cautiously concluded that there were immune system
>differences between men with low and high cholesterol, but that it was
>too early to state whether these differences had any importance for
>human health. Now, seven years later with many of the results
>discussed here, we are allowed to state that the immune-supporting
>properties of LDL-cholesterol do indeed play an important role in
>human health.
>
>
>Animal Experiments
>The immune systems in various mammals including human beings have many
>similarities. Therefore, it is interesting to see what experiments
>with rats and mice can tell us. Professor Kenneth Feingold at the
>Department of Medicine, University of California, San Francisco, and
>his group have published several interesting results from such
>research. In one of them they lowered LDL-cholesterol in rats by
>giving them either a drug that prevents the liver from secreting
>lipoproteins, or a drug that increases their disappearance. In both
>models, injection of endotoxin was followed by a much higher mortality
>in the low-cholesterol rats compared with normal rats. The high
>mortality was not due to the drugs because, if the drug-treated
>animals were injected with lipoproteins just before the injection of
>endotoxin, their mortality was reduced to normal.19
>
>Dr. Mihai Netea and his team from the Departments of Internal and
>Nuclear Medicine at the University Hospital in Nijmegen, The
>Netherlands, injected purified endotoxin into normal mice, and into
>mice with familial hypercholesterolemia that had LDL-cholesterol four
>times higher than normal. Whereas all normal mice died, they had to
>inject eight times as much endotoxin to kill the mice with familial
>hypercholesterolemia. In another experiment they injected live
>bacteria and found that twice as many mice with familial
>hypercholesterolemia survived compared with normal mice.20
>
>Other Protecting Lipids
>As seen from the above, many of the roles played by LDL-cholesterol
>are shared by HDL. This should not be too surprising considering that
>high HDL-cholesterol is associated with cardiovascular health and
>longevity. But there is more.
>
>Triglycerides, molecules consisting of three fatty acids linked to
>glycerol, are insoluble in water and are therefore carried through the
>blood inside lipoproteins, just as cholesterol. All lipoproteins carry
>triglycerides, but most of them are carried by a lipoprotein named
>VLDL (very low-density lipoprotein) and by chylomicrons, a mixture of
>emulsified triglycerides appearing in large amounts after a fat-rich
>meal, particularly in the blood that flows from the gut to the liver.
>
>For many years it has been known that sepsis, a life-threatening
>condition caused by bacterial growth in the blood, is associated with
>a high level of triglycerides. The serious symptoms of sepsis are due
>to endotoxin, most often produced by gut bacteria. In a number of
>studies, Professor Hobart W. Harris at the Surgical Research
>Laboratory at San Francisco General Hospital and his team found that
>solutions rich in triglycerides but with practically no cholesterol
>were able to protect experimental animals from the toxic effects of
>endotoxin and they concluded that the high level of triglycerides seen
>in sepsis is a normal immune response to infection.21 Usually the
>bacteria responsible for sepsis come from the gut. It is therefore
>fortunate that the blood draining the gut is especially rich in
>triglycerides.
>
>Exceptions
>So far, animal experiments have confirmed the hypothesis that high
>cholesterol protects against infection, at least against infections
>caused by bacteria. In a similar experiment using injections of
>Candida albicans, a common fungus, Dr. Netea and his team found that
>mice with familial hypercholesterolemia died more easily than normal
>mice.22 Serious infections caused by Candida albicans are rare in
>normal human beings; however, they are mainly seen in patients treated
>with immunosuppressive drugs, but the finding shows that we need more
>knowledge in this area. However, the many findings mentioned above
>indicate that the protective effects of the blood lipids against
>infections in human beings seem to be greater than any possible
>adverse effects.
>
>Cholesterol as a Risk Factor
>Most studies of young and middle-aged men have found high cholesterol
>to be a risk factor for coronary heart disease, seemingly a
>contradiction to the idea that high cholesterol is protective. Why is
>high cholesterol a risk factor in young and middle-aged men? A likely
>explanation is that men of that age are often in the midst of their
>professional career. High cholesterol may therefore reflect mental
>stress, a well-known cause of high cholesterol and also a risk factor
>for heart disease. Again, high cholesterol is not necessarily the
>direct cause but may only be a marker. High cholesterol in young and
>middle-aged men could, for instance, reflect the body's need for more
>cholesterol because cholesterol is the building material of many
>stress hormones. Any possible protective effect of high cholesterol
>may therefore be counteracted by the negative influence of a stressful
>life on the vascular system.
>
>Response to Injury
>In 1976 one of the most promising theories about the cause of
>atherosclerosis was the Response-to-Injury Hypothesis, presented by
>Russell Ross, a professor of pathology, and John Glomset, a professor
>of biochemistry and medicine at the Medical School, University of
>Washington in Seattle.23,24 They suggested that atherosclerosis is the
>consequence of an inflammatory process, where the first step is a
>localized injury to the thin layer of cells lining the inside of the
>arteries, the intima. The injury causes inflammation and the raised
>plaques that form are simply healing lesions.
>
>Their idea is not new. In 1911, two American pathologists from the
>Pathological Laboratories, University of Pittsburgh, Pennsylvania,
>Oskar Klotz and M.F. Manning, published a summary of their studies of
>the human arteries and concluded that "there is every indication that
>the production of tissue in the intima is the result of a direct
>irritation of that tissue by the presence of infection or toxins or
>the stimulation by the products of a primary degeneration in that
>layer."25 Other researchers have presented similar theories.26
>
>Researchers have proposed many potential causes of vascular injury,
>including mechanical stress, exposure to tobacco fumes, high
>LDL-cholesterol, oxidized cholesterol, homocysteine, the metabolic
>consequences of diabetes, iron overload, copper deficiency,
>deficiencies of vitamins A and D, consumption of trans fatty acids,
>microorganisms and many more. With one exception, there is evidence to
>support roles for all of these factors, but the degree to which each
>of them participates remains uncertain. The exception is of course
>LDL-cholesterol. Much research allows us to exclude high
>LDL-cholesterol from the list. Whether we look directly with the naked
>eye at the inside of the arteries at autopsy, or we do it indirectly
>in living people using x-rays, ultrasound or electron beams, no
>association worth mentioning has ever been found between the amount of
>lipid in the blood and the degree of atherosclerosis in the arteries.
>Also, whether cholesterol goes up or down, by itself or due to medical
>intervention, the changes of cholesterol have never been followed by
>parallel changes in the atherosclerotic plaques; there is no
>dose-response. Proponents of the cholesterol campaign often claim that
>the trials indeed have found dose-response, but here they refer to
>calculations between the mean changes of the different trials with the
>outcome of the whole treatment group. However, true dose-response
>demands that the individual changes of the putative causal factor are
>followed by parallel, individual changes of the disease outcome, and
>this has never occurred in the trials where researchers have
>calculated true dose-response.
>
>A detailed discussion of the many factors accused of harming the
>arterial endothelium is beyond the scope of this article. However, the
>protective role of the blood lipids against infections obviously
>demands a closer look at the alleged role of one of the alleged
>causes, the microorganisms.
>
>
>Is Atherosclerosis an Infectious Disease?
>For many years scientists have suspected that viruses and bacteria, in
>particular cytomegalovirus and Chlamydia pneumonia (also named TWAR
>bacteria) participate in the development of atherosclerosis. Research
>within this area has exploded during the last decade and by January
>2004, at least 200 reviews of the issue have been published in medical
>journals. Due to the widespread preoccupation with cholesterol and
>other lipids, there has been little general interest in the subject,
>however, and few doctors know much about it. Here I shall mention some
>of the most interesting findings.26
>
>Electron microscopy, immunofluorescence microscopy and other advanced
>techniques have allowed us to detect microorganisms and their DNA in
>the atherosclerotic lesions in a large proportion of patients.
>Bacterial toxins and cytokines, hormones secreted by the white blood
>cells during infections, are seen more often in the blood from
>patients with recent heart disease and stroke, in particular during
>and after an acute cardiovascular event, and some of them are strong
>predictors of cardiovascular disease. The same is valid for bacterial
>and viral antibodies, and a protein secreted by the liver during
>infections, named C-reactive protein (CRP), is a much stronger risk
>factor for coronary heart disease than cholesterol.
>
>Clinical evidence also supports this theory. During the weeks
>preceding an acute cardiovascular attack many patients have had a
>bacterial or viral infection. For instance, Dr. Armin J. Grau from the
>Department of Neurology at the University of Heidelberg and his team
>asked 166 patients with acute stroke, 166 patients hospitalized for
>other neurological diseases and 166 healthy individuals matched
>individually for age and sex about recent infectious disease. Within
>the first week before the stroke, 37 of the stroke patients, but only
>14 of the control individuals had had an infectious disease. In half
>of the patients the infection was of bacterial origin, in the other
>half of viral origin.27
>
>Similar observations have been made by many others, for patients with
>acute myocardial infarction (heart attack). For instance, Dr. Kimmo J.
>Mattila at the Department of Medicine, Helsinki University Hospital,
>Finland, found that 11 of 40 male patients with an acute heart attack
>before age 50 had an influenza-like infection with fever within 36
>hours prior to admittance to hospital, but only 4 out of 41 patients
>with chronic coronary disease (such as recurrent angina or pervious
>myocardial infarction) and 4 out of 40 control individuals without
>chronic disease randomly selected from the general population.28
>
>Attempts have been made to prevent cardiovascular disease by treatment
>with antibiotics. In five trials treatment of patients with coronary
>heart disease using azithromyzin or roxithromyzin, antibiotics that
>are effective against Chlamydia pneumonia,yielded successful results;
>a total of 104 cardiovascular events occurred among the 412
>non-treated patients, but only 61 events among the 410 patients in the
>treatment groups.28a-e In one further trial a significant decreased
>progression of atherosclerosis in the carotid arteries occurred with
>antibiotic treatment.28f However, in four other trials,30a-d one of
>which included more than 7000 patients,28d antibiotic treatment had no
>significant effect.
>
>The reason for these inconsistent results may be that the treatment
>was too short (in one of the trials treatment lasted only five days).
>Also, Chlamydia pneumonia, the TWAR bacteria, can only propagate
>inside human cells and when located in white blood cells they are
>resistant to antibiotics.31 Treatment may also have been ineffective
>because the antibiotics used have no effect on viruses. In this
>connection it is interesting to mention a controlled trial performed
>by Dr. Enrique Gurfinkel and his team from Fundación Favaloro in
>Buenos Aires, Argentina.32 They vaccinated half of 301 patients with
>coronary heart disease against influenza, a viral disease. After six
>months 8 percent of the control patients had died, but only 2 percent
>of the vaccinated patients. It is worth mentioning that this effect
>was much better than that achieved by any statin trial, and in a much
>shorter time.
>
>
>Does High Cholesterol Protect Against Cardiovascular Disease?
>Apparently, microorganisms play a role in cardiovascular disease. They
>may be one of the factors that start the process by injuring the
>arterial endothelium. A secondary role may be inferred from the
>association between acute cardiovascular disease and infection. The
>infectious agent may preferably become located in parts of the
>arterial walls that have been previously damaged by other agents,
>initiating local coagulation and the creation of a thrombus (clot) and
>in this way cause obstruction of the blood flow. But if so, high
>cholesterol may protect against cardiovascular disease instead of
>being the cause!
>
>In any case, the diet-heart idea, with its demonizing of high
>cholesterol, is obviously in conflict with the idea that high
>cholesterol protects against infections. Both ideas cannot be true.
>Let me summarize the many facts that conflict with the idea that high
>cholesterol is bad.
>
>If high cholesterol were the most important cause of atherosclerosis,
>people with high cholesterol should be more atherosclerotic than
>people with low cholesterol. But as you know by now this is very far
>from the truth.
>
>If high cholesterol were the most important cause of atherosclerosis,
>lowering of cholesterol should influence the atherosclerotic process
>in proportion to the degree of its lowering.
>
>But as you know by now, this does not happen.
>
>If high cholesterol were the most important cause of cardiovascular
>disease, it should be a risk factor in all populations, in both sexes,
>at all ages, in all disease categories, and for both heart disease and
>stroke. But as you know by now, this is not the case
>
>I have only two arguments for the idea that high cholesterol is good
>for the blood vessels, but in contrast to the arguments claiming the
>opposite they are very strong. The first one stems from the statin
>trials. If high cholesterol were the most important cause of
>cardiovascular disease, the greatest effect of statin treatment should
>have been seen in patients with the highest cholesterol, and in
>patients whose cholesterol was lowered the most. Lack of dose-response
>cannot be attributed to the knowledge that the statins have other
>effects on plaque stabilization, as this would not have masked the
>effect of cholesterol-lowering considering the pronounced lowering
>that was achieved. On the contrary, if a drug that effectively lowers
>the concentration of a molecule assumed to be harmful to the
>cardiovascular system and at the same time exerts several beneficial
>effects on the same system, a pronounced dose-response should be seen.
>
>On the other hand, if high cholesterol has a protective function, as
>suggested, its lowering would counterbalance the beneficial effects of
>the statins and thus work against a dose-response, which would be more
>in accord with the results from the various trials.
>
>I have already mentioned my second argument, but it can't be said too
>often: High cholesterol is associated with longevity in old people. It
>is difficult to explain away the fact that during the period of life
>in which most cardiovascular disease occurs and from which most people
>die (and most of us die from cardiovascular disease), high cholesterol
>occurs most often in people with the lowest mortality. How is it
>possible that high cholesterol is harmful to the artery walls and
>causes fatal coronary heart disease, the commonest cause of death, if
>those whose cholesterol is the highest, live longer than those whose
>cholesterol is low?
>
>To the public and the scientific community I say, "Wake up!"
>
>
>REFERENCES
>
>1. 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, 1335-1340, 1990.
>
>2. Ravnskov U. High cholesterol may protect against infections and
>atherosclerosis. Quarterly Journal of Medicine 96, 927-934, 2003.
>
>3. Jacobs D and others. Report of the conference on low blood
>cholesterol: Mortality associations. Circulation 86, 1046–1060, 1992.
>
>4. Iribarren C and others. Serum total cholesterol and risk of
>hospitalization, and death from respiratory disease. International
>Journal of Epidemiology 26, 1191–1202, 1997.
>
>5. Iribarren C and others. Cohort study of serum total cholesterol and
>in-hospital incidence of infectious diseases. Epidemiology and
>Infection 121, 335–347, 1998.
>
>6. Claxton AJ and others. Association between serum total cholesterol
>and HIV infection in a high-risk cohort of young men. Journal of
>acquired immune deficiency syndromes and human retrovirology 17,
>51–57, 1998.
>
>7. Neaton JD, Wentworth DN. Low serum cholesterol and risk of death
>from AIDS. AIDS 11, 929–930, 1997.
>
>8. Rauchhaus M and others. Plasma cytokine parameters and mortality in
>patients with chronic heart failure. Circulation 102, 3060-3067, 2000.
>
>9. Niebauer J and others. Endotoxin and immune activation in chronic
>heart failure. Lancet 353, 1838-1842, 1999.
>
>10. Vredevoe DL and others. Skin test anergy in advanced heart failure
>secondary to either ischemic or idiopathic dilated cardiomyopathy.
>American Journal of Cardiology 82, 323-328, 1998.
>
>11. Rauchhaus M, Coats AJ, Anker SD. The endotoxin-lipoprotein
>hypothesis. Lancet 356, 930–933, 2000.
>
>12. Rauchhaus M and others. The relationship between cholesterol and
>survival in patients with chronic heart failure. Journal of the
>American College of Cardiology 42, 1933-1940, 2003.
>
>13. Horwich TB and others. Low serum total cholesterol is associated
>with marked increase in mortality in advanced heart failure. Journal
>of Cardiac Failure 8, 216-224, 2002.
>
>14. Elias ER and others. Clinical effects of cholesterol
>supplementation in six patients with the Smith-Lemli-Opitz syndrome
>(SLOS). American Journal of Medical Genetics 68, 305–310, 1997.
>
>15. Bhakdi S and others. Binding and partial inactivation of
>Staphylococcus aureus a-toxin by human plasma low density lipoprotein.
>Journal of Biological Chemistry 258, 5899-5904, 1983.
>
>16. Flegel WA and others. Inhibition of endotoxin-induced activation
>of human monocytes by human lipoproteins. Infection and Immunity 57,
>2237-2245, 1989.
>
>17. Weinstock CW and others. Low density lipoproteins inhibit
>endotoxin activation of monocytes. Arteriosclerosis and Thrombosis 12,
>341-347, 1992.
>
>18. Muldoon MF and others. Immune system differences in men with hypo-
>or hypercholesterolemia. Clinical Immunology and Immunopathology 84,
>145-149, 1997.
>
>19. Feingold KR and others. Role for circulating lipoproteins in
>protection from endotoxin toxicity. Infection and Immunity 63,
>2041-2046, 1995.
>
>20. Netea MG and others. Low-density lipoprotein receptor-deficient
>mice are protected against lethal endotoxemia and severe gram-negative
>infections. Journal of Clinical Investigation 97, 1366-1372, 1996.
>
>21. Harris HW, Gosnell JE, Kumwenda ZL. The lipemia of sepsis:
>triglyceride-rich lipoproteins as agents of innate immunity. Journal
>of Endotoxin Research 6, 421-430, 2001.
>
>22. Netea MG and others. Hyperlipoproteinemia enhances susceptibility
>to acute disseminated Candida albicans infection in
>low-density-lipoprotein-receptor-deficient mice. Infection and
>Immunity 65, 2663-2667, 1997.
>
>23. Ross R, Glomset JA. The pathogenesis of atherosclerosis. New
>England Journal of Medicine 295, 369-377, 1976.
>
>24. Ross R. The pathogenesis of atherosclerosis and update. New
>England Journal of Medicine 314, 488-500, 1986.
>
>25. Klotz O, Manning MF. Fatty streaks in the intima of arteries.
>Journal of Pathology and Bacteriology. 16, 211-220, 1911.
>
>26. At least 200 reviews about the role of infections in
>atherosclerosis and cardiovascular disease have been published; here
>are a few of them: a) Grayston JT, Kuo CC, Campbell LA, Benditt EP.
>Chlamydia pneumoniae strain TWAR and atherosclerosis. European Heart
>Journal Suppl K, 66-71, 1993. b) Melnick JL, Adam E, Debakey ME.
>Cytomegalovirus and atherosclerosis. European Heart Journal Suppl K,
>30-38, 1993. c) Nicholson AC, Hajjar DP. Herpesviruses in
>atherosclerosis and thrombosis. Etiologic agents or ubiquitous
>bystanders? Arteriosclerosis Thrombosis and Vascular Biology 18,
>339-348, 1998. d) Ismail A, Khosravi H, Olson H. The role of infection
>in atherosclerosis and coronary artery disease. A new therapeutic
>target. Heart Disease 1, 233-240, 1999. e) Kuvin JT, Kimmelstiel MD.
>Infectious causes of atherosclerosis. f.) Kalayoglu MV, Libby P, Byrne
>GI. Chlamydia pneumonia as an emerging risk factor in cardiovascular
>disease. Journal of the American Medical Association 288, 2724-2731,
>2002.
>
>27. Grau AJ and others. Recent bacterial and viral infection is a risk
>factor for cerebrovascular ischemia. Neurology 50, 196-203, 1998.
>
>28. Mattila KJ. Viral and bacterial infections in patients with acute
>myocardial infarction. Journal of Internal Medicine 225, 293-296,
>1989.
>
>29. The successful trials: a) Gurfinkel E. Lancet 350, 404-407, 1997.
>b) Gupta S and others. Circulation 96, 404-407, 1997. c) Muhlestein JB
>and others. Circulation 102, 1755-1760, 2000. d) Stone AFM and others.
>Circulation 106, 1219-1223, 2002. e) Wiesli P and others. Circulation
>105, 2646-2652, 2002. f) Sander D and others. Circulation 106,
>2428-2433, 2002.
>
>30. The unsuccessful trials: a) Anderson JL and others. Circulation
>99, 1540-1547, 1999. b) Leowattana W and others. Journal of the
>Medical Association of Thailand 84 (Suppl 3), S669-S675, 2001. c)
>Cercek B and others. Lancet 361, 809-813, 2003. d) O'Connor CM and
>others. Journal of the American Medical Association. 290, 1459-1466,
>2003.
>
>31. Gieffers J and others. Chlamydia pneumoniae infection in
>circulating human monocytes is refractory to antibiotic treatment.
>Circulation 104, 351-356, 2001
>
>32. Gurfinkel EP and others. Circulation 105, 2143-2147, 2002.
>
>About the author
>
>Dr. Ravnskov is the author of The Cholesterol Myths and chairman of
>The International Network of Cholesterol Skeptics (thincs.org).
>
>
>
>--------------------------------------------------------------------------------
>
>Risk Factor
>There is one risk factor that is known to be certain to cause death.
>It is such a strong risk factor that it has a 100 percent mortality
>rate. Thus I can guarantee that if we stop this risk factor, which
>would take no great research and cost nothing in monetary terms,
>within a century human deaths would be completely eliminated. This
>risk factor is called "Life."
>
>
>Barry Groves, second-opinions.com
>
>
>--------------------------------------------------------------------------------
>
>Familial Hypercholesterolemia -
>Not as Risky as You May Think
>Many doctors believe that most patients with familial
>hypercholesterolemia (FH) die from CHD at a young age. Obviously, they
>do not know the surprising finding of the Scientific Steering
>Committee at the Department of Public Health and Primary Care at
>Ratcliffe Infirmary in Oxford, England. For several years, these
>researchers followed more than 500 FH patients between the ages of 20
>and 74 and compared patient mortality during this period with that of
>the general population.
>
>During a three- to four-year period, six of 214 FH patients below age
>40 died from CHD. This may not seem particularly frightening but as it
>is rare to die from CHD before the age of 40, the risk for these FH
>patients was almost 100 times that of the general population.
>
>During a four- to five-year period, eight of 237 FH patients between
>ages 40 and 59 died, which was five times more than the general
>population. But during a similar period of time, only one of 75 FH
>patients between the ages of 60 and 74 died from CHD, when the
>expected number was two.
>
>If these results are typical for FH, you could say that between ages
>20 and 59, about 3 percent of the patients die from CHD, and between
>ages 60 and 74, less than 2 percent die, in both cases during a period
>of 3-4 years. The authors stressed that the patients had been referred
>because of a personal or family history of premature vascular disease
>and therefore were at a particularly high risk for CHD. Most patients
>with FH in the general population are unrecognized and untreated. Had
>the patients studied been representative for all FH patients, their
>prognosis would probably have been even better.
>
>This view was recently confirmed by Dr. Eric Sijbrands and his
>coworkers from various medical departments in Amsterdam and Leiden,
>Netherlands. Out of a large group they found three individuals with
>very high cholesterol. A genetic analysis confirmed the diagnosis of
>FH and by tracing their family members backward in time, they came up
>with a total of 412 individuals. The coronary and total mortality of
>these members were compared with the mortality of the general Dutch
>population.
>
>The striking finding was that those who lived during the 19th and
>early 20th century had normal mortality and lived a normal life span.
>In fact, those living in the 19th century had a lower mortality than
>the general population. After 1915 the mortality rose to a maximum
>between 1935 and 1964, but even at the peak, mortality was less than
>twice as high as in the general population.
>
>Again, very high cholesterol levels alone do not lead to a heart
>attack. In fact, high cholesterol may even be protective against other
>diseases. This was the conclusion of Dr. Sijbrands and his colleagues.
>As support they cited the fact that genetically modified mice with
>high cholesterol are protected against severe bacterial infections.
>
>"Doctor, don't be afraid because of my high cholesterol." These were
>the words of a 36-year-old lawyer who visited me for the first time
>for a health examination. And indeed, his cholesterol was high, over
>400 mg/dl.
>
>"My father's cholesterol was even higher," he added. "But he lived
>happily until he died at age 79 from cancer. And his brother, who also
>had FH, died at age 83. None of them ever complained of any heart
>problems." My "patient" is now 53, his brother is 56 and his cousin
>61. All of them have extremely high cholesterol values, but none of
>them has any heart troubles, and none of them has ever taken
>cholesterol-lowering drugs.
>
>So, if you happen to have FH, don't be too anxious. Your chances of
>surviving are pretty good, even surviving to old age.
>
>Scientific Steering Committee on behalf of the Simon Broome Register
>Group. Risk of fatal coronary heart disease in familial
>hypercholesterolaemia. British Medical Journal 303, 893-896, 1991;
>Sijbrands EJG and others. Mortality over two centuries in large
>pedigree with familial hypercholesterolaemia: family tree mortality
>study. British Medical Journal 322, 1019-1023, 2001.
>
>>From The Cholesterol Myths by Uffe Ravnvskov, MD, PhD, NewTrends
>Publishing, pp 64-65.
>
>
>
>
>
>
>--------------------------------------------------------------------------------
>
>This article appeared in Wise Traditions in Food, Farming and the
>Healing Arts,
>the quarterly magazine of the Weston A. Price Foundation, SPRING 2004.

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