The Benefits of High Cholesterol

[Guest guest]

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

 

 

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 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 α-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 α-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 α-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.â€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!â€

 

REFERENCES

 

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21. Harris HW, Gosnell JE, Kumwenda ZL. The lipemia of sepsis:

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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.â€

 

Barry Groves, www.second-opinions.co.uk.

 

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 Radcliffe

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.