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  #1   ^
Old Tue, Jan-23-07, 04:11
Demi's Avatar
Demi Demi is offline
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Default Have we been conned about cholesterol?

The London Evening Standard
London, UK
23 January, 2007

Have we been conned about cholesterol?

Conventional medical wisdom about cholesterol — and the role of statins — is now being challenged by a small, but growing number of health professionals. Among them is Dr Malcolm Kendrick. A GP for 25 years, he has also worked with the European Society of Cardiology, and writes for leading medical magazines.

When it comes to heart disease, we have been sold a pup. A rather large pup.

Actually, it's more of a full-grown blue whale. We've all been conned.

If you've got a raised risk of heart disease, the standard medical advice is to take a cholesterol-lowering statin drug to cut your chances of having a heart attack — because, as we all know, cholesterol is a killer.

Indeed, many of you already believe that you should take statins for the rest of your natural lifespan.

Nearly everybody is in agreement about the need to lower your cholesterol level. The NHS spends nearly £1 billion a year on prescriptions for statins and possibly the same amount administering the cholesterol tests, surgery visits and the rest.

But is it all worth it? According to an article being published in the medical journal The Lancet this week, the answer is probably no.

A leading researcher at Harvard Medical School has found that women don't benefit from taking statins at all, nor do men over 69 who haven't already had a heart attack.

There is a very faint benefit if you are a younger man who also hasn't had a heart attack - out of 50 men who take the drug for five years, one will benefit.

Nor is this the first study to suggest that fighting cholesterol with statins is bunk. Indeed, there are hundreds of doctors and researchers who agree that the cholesterol hypothesis itself is nonsense.

What their work shows, and what your doctor should be saying, is the following:

• A high fat diet, saturated or otherwise, does not affect blood cholesterol levels.

• High cholesterol levels don't cause heart disease.

• Statins do not protect against heart disease by lowering cholesterol - when they do work, they do so in another way.

• The protection provided by statins is so small as to be not worth bothering about for most people (and all women). The reality is that the benefits have been hyped beyond belief.

• Statins have many more unpleasant side effects than has been admitted, while experts in this area should be treated with healthy scepticism because they are almost universally paid large sums by statin manufacturers to sing loudly from their hymn sheet.

So how can I say saturated fat doesn't matter when everyone knows it is a killer? Could all those millions who have been putting skinless chicken and one per cent fat yoghurts into their trolleys really have been wasting their time?

The experts are so busy urging you to consume less fat and more statins that you are never warned about the contradictions and lack of evidence behind the cholesterol con.

In fact, what many major studies show is that as far as protecting your heart goes, cutting back on saturated fats makes no difference and, in fact, is more likely to do harm.

So how did fat and cholesterol get such a bad name? It all began about 100 years ago, when a researcher found feeding rabbits (vegetarians) a high cholesterol carnivore diet blocked their arteries with plaque.

But it took off in the Fifties with the Seven Countries study by Ancel Keys, which showed that the higher the saturated fat intake in a country, the higher the cholesterol levels and the higher the rate of heart disease.

The countries he chose included Italy, Greece, the USA and the Netherlands. But why these particular ones?

Recently I did my own 14 countries study using figures from the World Health Organisation, and found the opposite.

Countries with the highest saturated fat consumption — Austria, France, Finland and Belgium — had the lowest rate of deaths from heart disease, while those with the lowest consumption — Georgia, Ukraine and Croatia — had the highest mortality rate from heart disease.

Added to this, the biggest ever trial on dietary modification put 50 million people on a low saturated fat diet for 14 years.

Sausages, eggs, cheese, bacon and milk were restricted. Fruit and fish, however, were freely available. I'm talking about rationing in Britain during and after World War Two. In that time, deaths from heart disease more than doubled.

Even more damning is what happened in 1988. The Surgeon General's office in the US decided to gather all evidence linking saturated fat to heart disease, silencing any nay-sayers for ever.

Eleven years later, however, the project was killed. The letter announcing this stated that the office "did not anticipate fully the magnitude of the additional expertise and staff resources that would be needed".

After eleven years, they needed additional expertise and staff resources? What had they been doing? If they'd found a scrap of evidence, you would never have heard the last of it.

Major trials since have been no more successful. One involved nearly 30,000 middle-aged men and women in Sweden, followed for six years.

The conclusion? "Saturated fat showed no relationship with cardiovascular disease in men. Among the women, cardiovascular mortality showed a downward trend with increasing saturated fat intake." (In other words, the more saturated fat, the less chance of dying from heart disease).

Even stronger evidence of the benefits of increased fat and cholesterol in the diet comes from Japan. Between 1958 and 1999, the Japanese doubled their protein intake, ate 400 per cent more fat and their cholesterol levels went up by 20 per cent.

Did they drop like flies? No. Their stroke rate, which had been the highest in the world, was seven times lower, while deaths from heart attacks, already low, fell by 50 per cent.

It's a bit of a paradox, isn't it? That's one of the features of the dietary hypothesis - it involves a lot of paradoxes.

The most famous is the French Paradox. They eat more saturated fat than we do in Britain; they smoke more, take less exercise, have the same cholesterol/LDL levels, they also have the same average blood pressure and the same rate of obesity.

And you know what? They have one quarter the rate of heart disease we do.

The official explanation is that the French are protected from heart disease by drinking red wine, eating lightly cooked vegetables and eating garlic.

But there is no evidence that any of these three factors are actually protective. None. By evidence, I mean a randomised, controlled clinical study.

Every time a population is found that doesn't fit the saturated fat/cholestrol hypothesis - the Masai living on blood and milk with no heart disease, the Inuit living on blubber with low heart disease - something is always found to explain it.

One research paper published more than 20 years ago found 246 factors that could protect against heart disease or promote it. By now there must be more than a thousand.

The closer you look the more you find that the cholestrol hypothesis is an amazing beast. It is in a process of constant adaptation in order to encompass all contradictory data without keeling over and expiring.

But you don't need to look at foreign countries to find paradoxes - the biggest one is right here at home. Women are about 300 per cent less likely to suffer heart disease than men, even though on average they have higher cholesterol levels.

For years there was an ad hoc hypothesis to explain this apparent contradiction - women were protected by female sex hormones.

In fact, there has never been a study showing that these hormones protect against heart disease in humans.

But by the Nineties, millions of women were being prescribed HRT to stave off heart disease.

Then came the HERS trial to test the notion. It found HRT increased the risk of heart disease.

So what to do? Put them on statins; bring their cholesterol level down — below 5.0 mmol is the official advice.

But, as The Lancet article emphasises, women do not benefit from statins. The phrase "Statins do not save lives in women" should be hung in every doctor's surgery.

But it's not just hugely wasteful handing out statins to women and men who are never going to benefit; it also exposes them to the risk of totally unnecessary side effects.

These include muscle weakness (myopathy) and mental and neurological problems such as severe irritability and memory loss.

How common are they? Very rare, say experts, but one trial found that 90 per cent of those on statins complained of side effects, half of them serious.

Only last week, a study reported a link between low LDL cholesterol and developing Parkinson's disease.

Statins are designed to lower LDL. In the face of anticholesterol propaganda, it is easy to forget cholesterol is vital for our bodies to function.

Why do you think an egg yolk is full of cholesterol? Because it takes a lot of cholesterol to build a healthy chicken.

It also takes a hell of a lot to build and maintain a healthy human being.

In fact, cholesterol is so vital that almost all cells can manufacture cholesterol; one of the key functions of the liver is to synthesise cholesterol.

It's vital for the proper functioning of the brain and it's the building bock for most sex hormones.

So it should not be such a surprise to learn that lowering cholesterol can increase death rates.

Woman with a cholesterol level of five or even six have a lower risk of dying than those with a level below four.

The Lancet reported that statins didn't benefit anyone over 69, not even men; in fact, there's good evidence that they may hasten your death.

The Framingham study in the US found that people whose cholesterol levels fell were at a 14 per cent increased risk of death from heart disease for every 1mg/dl.

Set up in 1948, the study screened the whole population of Framingham near Boston for factors that might be involved in heart disease and then followed them to see what happened to them.

It is still going today, making it the longest running and most often quoted study in heart-disease research.

A massive long-term study that looked specifically at cholesterol levels and mortality in older people in Honolulu, published in The Lancet, found that having low cholesterol concentration for a long time increases the risk of death.

This may be because cholesterol is needed to fight off infections or there may be other reasons — but many other studies have found exactly the same thing.

Low cholesterol levels greatly increase your risk of dying younger. So the cholesterol hypothesis looks something like this:

There is no evidence that saturated fat is bad - and there are lots of 'paradoxes' where countries with a high cholesterol intake don't have a higher death rate from heart disease.

But there is an even more fundamental problem. The theory claims fat and cholesterol do things in the body that just don't make sense.

To begin with, saturated fat and cholesterol are talked of as if they are strongly connected. A low-fat diet lowers cholesterol; a high-fat diet raises it.

What is never explained is how this works. This isn't surprising because saturated fat doesn't raise cholesterol. There is no biochemical connection between the two substances, which may explain all those negative findings.

It's true that foods containing cholesterol also tend to contain saturated fats because both usually come from animals.

It's also true that neither dissolve in water, so in order to travel along the bloodstream they have to be transported in a type of molecule known as a lipoprotein - such as LDLs (low-density lipoproteins) and HDLs (high-density lipoproteins).

But being travelling companions is as close as fats and cholesterol get. Once in the body, most fat from our diet is transported to the fat cells in a lipoprotein called a chylomicron.

Meanwhile, cholesterol is produced in the liver by way of an incredibly complicated 13-step process; the one that statins interfere with.

No biochemist has been able to explain to me why eating saturated fat should have any impact on this cholesterol production line in the liver.

On the other hand, the liver does make fat - lots of it. All the excess carbohydrate that we eat is turned first into glucose and then into fat in the liver.

And what sort of fat does the liver make? Saturated fat; obviously the body doesn't regard it as harmful at all.

Recently, attention has been shifting from the dangers of saturated fat and LDL "bad" cholesterol to the benefits of HDL "good" cholesterol, and new drugs that are going to boost it.

But the idea that more HDLs are going to fight off heart disease is built on equally shaky foundations.

These lipoproteins seem to be cholesterol "scavengers", sucking up the cholesterol that is released when a cell dies and then passing it on to other lipoproteins, which return it to the liver.

Interestingly, the "bad" LDL lipoproteins are involved in the relay. The idea seems to be that HDLs can also get the cholesterol out of the plaques that are blocking arteries.

However, there is a huge difference between absorbing free-floating cholesterol and sucking it out of an atherosclerotic plaque which is covered by an impermeable cap.

• Extracted from The Great Cholesterol Con by Malcolm Kendrick, published by John Blake on January 29.
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  #2   ^
Old Tue, Jan-23-07, 06:10
64dodger 64dodger is offline
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Great article. Over time I am certain that Statins will be taken off the market because of the dangers associated with them.
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  #3   ^
Old Tue, Jan-23-07, 07:54
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Rheneas Rheneas is offline
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Hooray!! Sense at last. Great article.
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  #4   ^
Old Tue, Jan-23-07, 09:28
obtunded obtunded is offline
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Didn't Anthony Colpo write "The Great Cholesterol Con"? Still a great article, though...
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  #5   ^
Old Tue, Jan-23-07, 09:28
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KvonM KvonM is offline
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So how did fat and cholesterol get such a bad name? It all began about 100 years ago, when a researcher found feeding rabbits (vegetarians) a high cholesterol carnivore diet blocked their arteries with plaque.

what scares me is that nobody stopped to realize that giving an animal a diet that its body wasn't suited for in the first place might possibly have detrimental results. makes me wonder if the research team's conversation went something like this:

researcher 1: hey, let's see what happens when we feed a diet of meat to a giant sloth!
researcher 2: wait... we can't, the sloth's an endangered species. the zoo will get mad at us, and we can't afford to buy a lab sloth for the $500 we got in grant money for animals.
r1: oh... well how about we feed a diet of meat to a herd of sheep? they're not endangered!
r2: we don't have enough space for cages that big.
r1: oh fine... then how about a bunch of rabbits?
r2: BINGO!

articles like this really make me realize that the medical profession can be guilty of sticking its fingers in its ears and yelling "LA LA LA LA LA LA LA I'VE MADE UP MY MIND, DON'T CONFUSE ME WITH THE FACTS!"
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  #6   ^
Old Tue, Jan-23-07, 10:12
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GeorgeMead GeorgeMead is offline
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Great to hear something from Dr. Kendrick! I miss his column in Red Flags. For those who would like to read more by Malcolm:

I thought the title sounded familiar, apparently there is an error there.


The Great Cholesterol Lie: The Truth About What Really Causes Heart Disease and How to Avoid It (Paperback)
by Dr. Malcolm Kendrick

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The Great Cholesterol Con (Paperback)
by Anthony Colpo
(27 customer reviews)
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Availability: In Stock. Ships from and sold by Gift-wrap available.

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  #7   ^
Old Tue, Jan-23-07, 11:34
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Squarecube Squarecube is offline
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At first I felt sorry for the Evening Standard -- I wouldn't want to have made a mistake with Colpo's name -- he can be a little rough. However, maybe this will give Colpo's very worthy book even more attention.

They'll probably correct it soon.
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  #8   ^
Old Tue, Jan-23-07, 13:06
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BoBoGuy BoBoGuy is offline
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Last edited by BoBoGuy : Tue, Jan-23-07 at 13:14.
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  #9   ^
Old Tue, Jan-23-07, 13:07
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rightnow rightnow is offline
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"Wow" is all I can say.

There are some other fields of science that look like this impossibly gigantic conspiracy of evil, moreso than this, but it's starting to look like this is just another.

There is a book -- have patience with the title -- called 'Murder by Injection'. It's the story of the founding of the AMA, and it details the 1986 supreme court judgement and issues against the AMA for behaving pretty much just like the mafia to kill off the field of chiropractic. Near the end of the book it has a listing of, at the time he published it, the board of directors of every major government and chemical company and major media company etc.

It's terrifying. All of these people are related to each other in some way. He points out the ways. Eventually you realize that when Time-Warner which owns every kind of media imaginable, and a few medical-chemical companies, and a few poisonous chemical companies, and the FDA and USDA, all SHARE either the same people or usually, people who are related to each other (or the people literally do a round-robin from one group to the other), that there is just no way you can 'assume' that the AMA, the FDA, the USDA, or many other agencies even that are "government", are in any way "unbiased" -- or in any way "not affected by" the fact that their mega stock in a (statin chem company for instance) would be destroyed if they let it get out that they are not only mostly-useless but usually-harmful.

It's one of those things, you know, nobody wants to be overly cynical, or to think the worst without reason. But the more you look into the medical industry (from child immunizations to any other subject, like this one), the more horrifying it becomes.

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  #10   ^
Old Wed, Jan-24-07, 13:28
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BoBoGuy BoBoGuy is offline
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  #11   ^
Old Wed, Jan-24-07, 19:27
LC FP LC FP is offline
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According to an article being published in the medical journal The Lancet this week, the answer is probably no.

Can't seem to find this article to link it, but I found it in my library. It's actually just a comment, by J Abramson and JM Wright from Harvard Med School and the Univ of British Columbia Dept of Anesthesiology.

They reviewed the 8 big randomized trials of 47,925 patients comparing statin with placebo in "primary prevention populations at increased risk". But they admit their analysis is "imperfect because these trials are not solely primary prevention. 8.5% of patients had occlusive vascular disease at baseline". 6570 patients had had a stroke, or peripheral vascular occlusion, but they hadn't had a cardiac event, so they were considered primary prevention. But they were at much higher 5-year risk for a cardiac event (25-30%) than the true primary prevention group (9%), and that lumping them together made statins seem more beneficial.

They basically said these studies "cheated"; they weren't really primary prevention, because these people in question had the "equivalent" of heart disease. Despite this cheating, there still wasn't statistically significant proof that statins helped any woman, or anyone over age 69.

The main complaint was that the "Cholesterol Treatment Trialists collaboration (CTT) have access to all the data, and they could re-analyze the existing studies to find out just how inneffective statins were for the truly primary prevention patients. But they haven't done it. The CTT is a group that does periodic meta-analysis of all the available trials, and they are aparently shirking their jobs.

The article estimates that if it's shown that statins have no benefit (just risk!) for primary prevention patients, about 3/4 of all statin recipients could stop their drugs.

There is an interesting disclaimer though. A footnote states that Dr. Abramson is "an expert consultant to plaintiff's attorneys on litigation involving the drug industry, including Pfizer for it's marketnig of atorvastatin". I guess this could tarnish the credibility of this piece. In the eyes of some
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Old Thu, Jan-25-07, 10:20
kaypeeoh kaypeeoh is offline
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Originally Posted by BoBoGuy

The louder a person screams, "Conspiracy! Conspiracy!" the more likely the person is so one-sided he can't be trusted. Yes, it is true that some people die of heart disease with normal cholesterol levels, but it is just as true that many more die of heart disease caused by atherosclerosis, the end result of too much cholesterol in the blood.

I agree the problem is may be more complicated than simply too much cholesterol. But where there can be shown a connection between hyperlipemia and heart disease, there are clues as to what a person can do to lower the odds of a heart attack.

Caveman didn't have heart disease because he didn't eat sugar? Maybe. But he also didn't eat 5000 calories a day of any type of food. Maybe the problem is TOO MUCH FOOD. Cholesterol has a function in the body. It moves fatty acids through the bloodstream. Too much cholesterol can mean too much fat in the blood. Just my opinion.
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  #13   ^
Old Thu, Jan-25-07, 10:36
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Nancy LC Nancy LC is offline
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Isn't the real problem though that the body is using the cholesterol to patch up damage to the arteries? If the body doesn't need to do the repair work, it isn't going to care how much cholesterol (within certain limits, of course).

It just seems like medicine has fingered the wrong bogey man. Lame analogy but taking away the sealant from the kit that fixes your flat tire doesn't correct the fact there's still a nail in the tire.
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  #14   ^
Old Thu, Jan-25-07, 10:39
Zuleikaa Zuleikaa is offline
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Originally Posted by Yes, it is true that some people die of heart disease with normal cholesterol levels, but it is just as true that many more die of heart disease caused by atherosclerosis, [B
the end result of too much cholesterol in the blood. [/B]
Proof???? It hasn't been proven that atherosclerosis is caused by high cholesterol levels.

That's what the advocates against statins are saying/pointing out from reanalyzing the setup and data from orignal studies.
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  #15   ^
Old Thu, Jan-25-07, 11:25
kaypeeoh kaypeeoh is offline
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Originally Posted by Zuleikaa
Proof???? It hasn't been proven that atherosclerosis is caused by high cholesterol levels.

Tons of research suggesting the connection. Here's one:

Annual Review of Pathology: Mechanisms of Disease
Vol. 1: 297-329 (Volume publication date February 2006)

First published online as a Review in Advance on October 26, 2005


Göran K. Hansson, ~ Anna-Karin L. Robertson, and ~ Cecilia Söderberg-Nauclér~
Department of Medicine and Center for Molecular Medicine, Karolinska Institute, Stockholm SE-17176, Sweden; email:,,

Atherosclerosis, the cause of myocardial infarction, stroke, and ischemic gangrene, is an inflammatory disease. The atherosclerotic process is initiated when cholesterol-containing low-density lipoproteins accumulate in the intima and activate the endothelium. Leukocyte adhesion molecules and chemokines promote recruitment of monocytes and T cells. Monocytes differentiate into macrophages and upregulate pattern recognition receptors, including scavenger receptors and toll-like receptors. Scavenger receptors mediate lipoprotein internalization, which leads to foam-cell formation. Toll-like receptors transmit activating signals that lead to the release of cytokines, proteases, and vasoactive molecules. T cells in lesions recognize local antigens and mount T helper-1 responses with secretion of pro-inflammatory cytokines that contribute to local inflammation and growth of the plaque. Intensified inflammatory activation may lead to local proteolysis, plaque rupture, and thrombus formation, which causes ischemia and infarction. Inflammatory markers are already used to monitor the disease process and anti-inflammatory therapy may be useful to control disease activity.

ACS: acute coronary syndrome
CAD: coronary artery disease
IFN: interferon
LDL: low-density lipoprotein
MDA: malondialdehyde
MHC: major histocompatibility complex
TGF: transforming growth factor
TLR: toll-like receptor
TNF: tumor necrosis factor
VCAM: vascular cell adhesion molecule
Terms and Definitions
Atheroma: raised atherosclerotic lesion with a lipid core containing both foam cells and extracellular lipid, also a type IV lesion
Fatty streak (type II–III lesions): early lesions containing foam cells
Pattern recognition receptors: broad-specificity receptors that bind ligands with pathogen-associated molecular patterns
Plaque: mature atherosclerotic lesion, synonymous with atheroma
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