Cholesterol Reducing Drugs/Sandy

[Guest guest]

Someone mentioned not taking cholesterol drugs right now. I know you

are facing surgery soon. Before you decide whether to begin these or

not, please go to:

http://www.peoplespharmacy.com/index.asp

and do a search for statin drugs. Reports of severe side effects

continue to be posted there and other places on the Internet. Still,

some doctors think they should be put in the water supply...

My own father will not stop taking these despite severe lower body

weakness which was NOT present prior to taking these. There are

reports of an ALS like syndrome, pain and also neuropathy.

Please check this out.

Cathie

[Guest guest]

Research policosanol for cholesterol lowering ability, no liver

damage and works pretty well. There are other supplements, such as

garlic. One does not need statin drugs.

Lynda

At 12:50 AM 8/24/2008, you wrote:

>Someone mentioned not taking cholesterol drugs right now. I know you

>are facing surgery soon. Before you decide whether to begin these or

>not, please go to:

>

><http://www.peoplespharmacy.com/index.asp>http://www.peoplespharmacy.com/index.\

asp

>

>

>and do a search for statin drugs. Reports of severe side effects

>continue to be posted there and other places on the Internet. Still,

>some doctors think they should be put in the water supply...

>

>My own father will not stop taking these despite severe lower body

>weakness which was NOT present prior to taking these. There are

>reports of an ALS like syndrome, pain and also neuropathy.

>

>Please check this out.

>

>Cathie

>

>

[Guest guest]

There are some medical professionals who believe that high

cholesterol levels are NOT DANGEROUS:

http://www.westonaprice.org/moderndiseases/benefits_cholest.html

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.2 Eleven

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 R. s 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 s and his group,

together with Dr. 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, -

Luther-University in Halle, Germany (Universitätsklinik und

Poliklinik für Innere Medizin III, -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.

-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 -Lemli-Opitz syndrome have very low

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 & #945;-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 & #945;-toxin

with human serum (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 & #945;-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 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

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. 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

Ross, a professor of pathology, and 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. s 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 -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. 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, LA, Benditt EP.

Chlamydia pneumoniae strain TWAR and atherosclerosis. European Heart

Journal Suppl K, 66-71, 1993. 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.

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) JL and others. Circulation

99, 1540-1547, 1999. 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, www.second-opinions.co.uk.

>

> Someone mentioned not taking cholesterol drugs right now. I know you

> are facing surgery soon. Before you decide whether to begin these or

> not, please go to:

>

> http://www.peoplespharmacy.com/index.asp

>

> and do a search for statin drugs. Reports of severe side effects

> continue to be posted there and other places on the Internet. Still,

> some doctors think they should be put in the water supply...

>

> My own father will not stop taking these despite severe lower body

> weakness which was NOT present prior to taking these. There are

> reports of an ALS like syndrome, pain and also neuropathy.

>

> Please check this out.

>

> Cathie

>