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Author Topic: Statins & cholesterol- a mistake?/inflammation theory  (Read 6653 times)
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« on: January 24, 2007, 11:57:53 PM »


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 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 at £9.99.
« Last Edit: January 30, 2007, 11:40:48 AM by Crafty_Dog » Logged
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Posts: 42462

« Reply #1 on: January 24, 2007, 11:58:24 PM »

Cholesterol, Statins, and Heart Attack
By Doug Hornig

Ischemic heart disease (IHD) is a condition whereby the heart muscle receives insufficient oxygen for continued healthy function, due to arterial blockages that prevent oxygenated cells from getting to their destination. The result is what is commonly called a heart attack.

As researchers examined those who died of IHD-related causes, what they often found were arterial cholesterol buildups that had become so large they blocked blood flow in the vessel. Cholesterol became public enemy #1 and reducing the amount in the blood became accepted as the way to avoid IHD.

Now, that is gospel. So much so that pharmaceutical research has been almost entirely devoted to developing drugs that block the body’s production of cholesterol, the most common of which are a class called statins. Statins such as Lipitor®, Zocor®, Crestor®, Vytorin®, the now discredited Baycol®, and others all work in basically the same way. They’re mevalonate inhibitors. Simply put, they attack the weak link in the cholesterol synthesis chain, by inhibiting the enzyme that activates cholesterol production inside the cell.

And they work. They both lower serum cholesterol and are proven to be effective in preventing heart attacks. Thus, statins have become the most prescribed (and profitable) drugs in the country, with tens of millions of Americans regularly taking them. Case closed.

Or is it? As the anti-cholesterol era progressed, a few open-minded researchers began to question whether cholesterol buildup on arterial walls might be a symptom, rather than a root cause. To put it another way, is excess cholesterol a bad thing per se, or is the actual bad thing some underlying condition that causes the cholesterol to stick?

Before answering that question, a brief side trip into physiology is necessary. Many people have the mistaken impression that cholesterol is some evil, alien substance that we’d do much better without. Not so. It is present in every cell of our bodies. Its functions are numerous, and still not fully understood. Suffice it to say that without it, we wouldn’t be alive.

Cholesterol is produced naturally by the body, as well as being absorbed from food. Generally lumped under the term are triglycerides, low-density lipoproteins (LDL—the “bad” cholesterol), and high-density lipoproteins (HDL—the “good” cholesterol).

Despite the labels, all do important things. The problem arises, according to conventional wisdom, when LDL levels become too high, and the elimination function performed by HDL breaks down. The excess LDL is not passed back through the liver, it clogs blood vessels, and it begins to coagulate and clump within them. But why should it? Furthermore, why is it that the majority of heart attack victims have normal cholesterol levels?

Those are key questions. Increasingly, the focus is shifting away from the cholesterol itself and onto chronic inflammation of the arterial walls.

Inflammation is a killer. It can weaken blood vessels until they rupture, causing a heart attack (or stroke), regardless of cholesterol levels. It can also result in the weakened sites latching onto passing cholesterol molecules in the body’s attempt to repair the damage, thereby initiating the process that ends with a cholesterol blockage.

Thirty years ago, at Harvard Medical School, research pioneer Dr. Kilmer McCully was looking for a better marker for heart attack risk by linking high levels of the inflammation-causing amino acid homocysteine to the disease. McCully’s views were out of the mainstream at that time, and it would take until the late ’90s for the profession to catch up, as homocysteine finally came under broad scrutiny.

Inflammation theory got another big boost in 2003, when a massive longitudinal study at Boston's Brigham and Women's Hospital was published in the New England Journal of Medicine. It showed that the presence of a compound called C-reactive protein (CRP), a substance manufactured by the liver in response to the presence of inflammation in the body, was the best predictor of heart attack and stroke risk.

In this context, we can return to a consideration of statins. Suppose that their efficacy in reducing the risk of heart attack is due not to the fact that they inhibit cholesterol production, but to their powerful anti-inflammatory properties. That’s precisely the conclusion reached by Dr. Duane Graveline, a flight surgeon and original NASA scientist/astronaut, who has been studying the subject for years.

Well, what does it matter? one might reasonably ask. If the drugs decrease the risk of heart attack, what’s not to like?

As with all drugs, the answer is that there are trade-offs involved. No one knows the extent of them yet. The inhibition of mevalonate, for example, involves more than just cholesterol suppression, since it’s a precursor of other substances with important biological functions.

What is known is a list of side effects associated with statins. According to Swedish researcher Dr. Ulle Ravnskov, these include fatigue, muscle soreness/weakness, peripheral neuropathy of the legs, short temper, aggressive behavior, and (rare) muscle problems leading to kidney failure. Pregnant women should avoid statins because of the likelihood of birth defects in their newborns.

Perhaps most disturbing is the possibility that statins may interfere with cognition. While reports linking the drugs to such disorders as transient global amnesia and other Alzheimer’s-like symptoms are anecdotal at the moment, there is real cause for concern.

In a landmark 2001 study by Dr. Frank Pfrieger et al, of France’s Centre de Neurochimie, the group discovered a link between brain cholesterol metabolism and nerve cell development, learning and memory. Cholesterol proved to be the heretofore elusive factor responsible for the development of synapses, the contact sites between adjacent neurons in the brain. We can’t think properly without cholesterol.

Now, here’s the rub. Cholesterol circulating in the bloodstream is unavailable to the brain; both LDL and HDL are too large to pass the blood/brain barrier. Cholesterol needed by the brain must be manufactured on-site.

Statins, however, do pass the barrier and enter the brain, where, it is reasonable to assume, they exercise their proven ability to inhibit cholesterol production. A scary possibility.

Dr. Graveline suggests that dosage levels be reconsidered. The relatively high dosages of statins required to lower cholesterol may not be necessary if the drugs’ protective qualities are actually due to their anti-inflammatory action. A smaller, and far less risky, dose may work just fine.

And who knows, future generations may marvel that we spent so much time and money developing ever more sophisticated cholesterol inhibitors when all we really needed was the simplest, least expensive anti-inflammatory of them all, aspirin.
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« Reply #2 on: January 25, 2007, 11:38:35 AM »

Trans Fat Leads To Weight Gain Even On Same Total Calories, Animal Study Shows
Main Category: Obesity / Weight Loss / Fitness News
Article Date: 15 Jun 2006 - 8:00 PST
| email this article | printer friendly | view or write opinions |

The "apple" body shape that increases the risk of diabetes and heart disease may be accelerated by eating trans fat such as partially hydrogenated vegetable oil, according to new animal research at Wake Forest University School of Medicine.

"Diets rich in trans fat cause a redistribution of fat tissue into the abdomen and lead to a higher body weight even when the total dietary calories are controlled," said Lawrence L. Rudel, Ph.D., professor of pathology and biochemistry and head of the Lipid Sciences Research Program.

"What it says is that trans fat is worse than anticipated," Rudel said. "I was surprised."

According to the U.S. Food and Drug Administration (FDA), consumption of saturated fat, trans fat, and dietary cholesterol raises low-density lipoprotein (LDL), or "bad" cholesterol, levels, which increases the risk of coronary artery disease.

Kylie Kavanagh, D.V.M., presented the findings at the 66th annual Scientific Sessions of the American Diabetes Association in Washington, D.C. She said that over six years, male monkeys fed a western-style diet that contains trans fat had a 7.2 percent increase in body weight, compared to a 1.8 percent increase in monkeys that ate monounsaturated fats, such as olive oil.

All that extra weight went to the abdomen, and some other body fat was redistributed to the abdomen. Computed tomography (CT) scans showed that the monkeys on the diet containing trans fats had dramatically more abdominal fat than the monkeys on the monounsaturated fat. "We measured the volume of fat using CT," Kavanagh said. "They deposited 30 percent more fat in their abdomen."

The monkeys all were given the same amount of daily calories, with 35 percent of the calories coming from fat. The amount of calories they got should only have been enough to maintain their weight, not increase it, Rudel said. "We believed they couldn't get obese because we did not give them enough calories to get fat."

One group of monkeys got 8 percent of their calories from trans fat while the other group received those calories as monounsaturated fat. The researchers said that this amount of trans fat is comparable to people who eat a lot of fried food.

"We conclude that in equivalent diets, trans fatty acid consumption increases weight gain," said Kavanagh.

Over the entire course of the study, there was a small but significant difference in weight between the two groups. "In the world of diabetes, everybody knows that just 5 percent weight loss makes enormous difference," Kavanagh said. "This little difference was biologically quite significant."

Rudel said, "The study was specifically funded to look at the role of trans fatty acids in atherosclerosis."

He said that at the time he got a grant from the National Heart, Lung and Blood Institute, there was not much evidence in the literature and no animal models that documented the hazards of trans fats, though there are data showing it was a risk factor for atherosclerosis.

Kavanagh said the six-year length of the study was equivalent to 20 years in people.

According to the FDA, trans fat is found in vegetable shortenings, some margarines, crackers, cookies, snack foods, and other foods made with or fried in partially hydrogenated oils. Unlike other fats, the majority of trans fat is formed when food manufacturers turn liquid oils into solid fats like shortening and hard margarine by adding hydrogen.

Since Jan. 1, the FDA has required the amount of trans fat to be listed in the nutrition facts panel on all foods. But the restaurant industry is exempt.


Other researchers on the American Diabetes Society report include Janice D. Wagner, Ph.D., D.V.M., John Jeffrey Carr, M.D., Kate Jones, B.S., Janet Sawyer, M.S., and Kathryn Kelly., B.S., all from Wake Forest University School of Medicine.

Media Contacts: Robert Conn,, Shannon Koontz,, or Karen Richardson,, at (336) 716-4587.

Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university's School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in family medicine, 20th in geriatrics, 25th in primary care and 41st in research among the nation's medical schools. It ranks 32nd in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.

Contact: Karen Richardson
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« Reply #3 on: January 25, 2007, 11:59:04 AM »

Second post of the morning:

As part of an email group of which I am a member, I asked the doctors who are members of the group to comment on the inflammation theory.  Here is a sidebar response which I received.


I am currently out of town and unable to respond
to the entire group.  I just received the
following email this morning that partially
addresses your question.  My understanding is
that inflammation is a normal bi-product of body
metabolism.  It is naturally held in check by
proper diet and exercise.  Simple sugar is
perhaps the single worst nutrient we ingest that
affects the body's ability to hold inflammation
in check.  The excess inflammation can lead to,
among other things, etching of the lining in the
arteries of the heart and other organs. The
defects caused by the etching allows cholesterol
plaques to form that build up over time leading
to blockage.  Blood tests for inflammation
levels are homocysteine and c-reactive protein.

In general, we are what we eat, but few of us
eat correctly.  A diet of balanced, whole,
unprocessed foods is the way to go.  Everything
I have read says not to be afraid of eggs.  In
fact there was one story of a person who was
incarcerated in some third world county and fed
basically a diet of eggs for several months.
When checked after his release he had a very low
cholesterol level.  Usually, people do not make
cholesterol from the cholesterol they eat in
foods.  Cholesterol is made by our liver from
saturated fat.  Cholesterol is necessary for a
normal life including the manufacture of sex


"Dear Dr. Mirkin: You've said that inflammation can lead to a heart
attack; aren't I causing inflammation when I exercise so hard that
my muscles hurt?

     Anything that damages tissue can cause inflammation,
such as smoking, high cholesterol or hypertension. When a
germ gets into your body, your immunity produces
proteins called antibodies, white blood cells and cytokines that
kill germs. However, as soon as the germ is gone, your
immunity is supposed to shut down. If it doesn't shut down,
these same factors attack and destroy your body tissues;
this is called inflammation. Inflammation increases risk for
heart attacks, strokes, certain cancers, and diabetes and even
worsens diseases such as psoriasis, rheumatoid
arthritis, and asthma.

Many scientists have expressed concern that hard
exercise damages muscles, so it may turn on
inflammation and harm you. However, a study from Verona, Italy
shows that hard exercise does not cause inflammation (Journal of
the Canadian Medical Association, October 25, 2005). It
measured C reactive protein, a blood test that indicates
inflammation, and showed that there was no difference in levels in sedentary
people, those who cycle for fitness, competitive professional
bicycle racers and international-class cross country skiers. So
muscle damage from hard exercise does not increase inflammation.
More on inflammation at
Power User
Posts: 7826

« Reply #4 on: January 26, 2007, 10:50:47 AM »

Interesting read.

Funny aspirin is praised but statins demonized.  Aspirin can be a very dangerous drug.   It can cause gout, allergic reactions, trigger asthma and, of course, life threatening gastrointestinal bleeds.  I remember going to a chiropracter who made me sit through a video describing in detail how MDs are murdering patients with drugs like motrin and aspirin which are responsible for many hospitalizations and deaths.

It just goes to show how one can manipulate science to say whatever they want.

Funny one of the writers discusses the increase in fat intake in diet from 1959 to present in Japan yet cardiovascular death has gone down during the same period.

Well Americans are much heavier now then they were in the 50's and deaths from cardiovascular disease has gone down.
I suppose drugs have nothing to do with it?

If my bad cholesterol is 200 I am taking a statin to get it down.

And to say low cholesterol or saturated fat diets do not work is misleading.  I know peolple who changed their diets to avoid just these substances and their cholesterols have plummetted (even without weight loss).  This doesn't occur with everyone but there is clearly a subset of individuals who respond extremely well to this kind of diet manipulation.   angry
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Posts: 42462

« Reply #5 on: January 30, 2007, 11:41:56 AM »

A doctor friend writes:



I recently ran across the link below to a page with a 45 minute video (bottom of that page) as described below. This video helped me understand why the CRP Test for Inflammation is important…though one that, at this time, most doctors don’t offer. Inflammation may be a bigger culprit in heart and vascular concerns than cholesterol.

It’s pretty technical (and a bit dry), but the point is well made.


Hope this helps, David Gilbertsen


Narrated by Peter Libby, MD, a widely published expert on inflammation in vascular disease, these slides provide an overview of the clinical importance of markers of inflammation — notably, C-reactive protein (CRP). Dr. Libby explains how high-sensitivity CRP (hs-CRP) can be used to identify apparently healthy patients who nevertheless are at increased risk of cardiovascular disease. Drawing on the landmark Women’s Health Study, he shows how hs-CRP adds to the predictive value of traditional risk factors, and how simple hs-CRP assays can be used to target lipid-lowering therapy more appropriately. He also provides an overview of a large study now in progress, JUPITER, that is expected to more clearly delineate the value of statin therapy in patients with average LDL-cholesterol levels but slightly elevated levels of hs-CRP.

Dr. Libby is the Mallinckrodt Professor of Medicine at Harvard Medical School and chief of cardiovascular medicine at Brigham and Women’s Hospital, Boston, where his research focuses on vascular biology, particularly inflammation and atherogenesis. After receiving his MD from the University of California, San Diego, in 1973 he completed a residency in internal medicine and a fellowship in cardiovascular diseases at the Peter Bent Brigham Hospital.

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Posts: 7826

« Reply #6 on: April 18, 2015, 11:41:49 AM »

I have started warning patients of this probable though not yet definite risk.
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