Cholesterol is absolutely vital for our existence - Attia

the essential nature of cholesterol

 

 

 

 

“Cholesterol is absolutely vital for our existence.       

  Peter Attia, MD

 

Let’s note right off the bat, there’s no such thing as ‘good and bad’ cholesterol. As shown below, cholesterol is a single natural substance – the grandmother steroid – featuring a four-ring structure of carbon atoms.

All steroid hormones (such as Vitamin D) are made from cholesterol, but, as we shall learn, cholesterol is much more than a hormone.

 

Cholesterol is made in a complex 27-step process from the 2-carbon substance called acetyl-CoA. The 4-ring structure is the chemical signature of a steroid. On the bottom left, there’s a hydrocarbon tail (HO), where cholesterol esterifies (or attaches) to other molecules and a hydroxyl group- top right.

 

Classified as a fat-soluble lipid, cholesterol is not a fat, it has no calories, and it’s not a source of energy. Cholesterol is a sterol – a high molecular weight alcohol. Animals, plants, and microorganisms require different sterols.

 

Cholesterol is the animal sterol – found in every cell in animal bodies. It is true that, as a minor component, cholesterol can be found in plant membranes, but the sterols  sitosterol and stigmasterol predominate in plants.

 

According to UK lipid biochemist Michael Gurr:   “Only cholesterol will allow animal cells to function as required. Without cholesterol, our bodies would not function properly and we would die.”

 

Cholesterol waterproofs our trillions of membranes, making it possible for our cells to regulate their internal environments – policing and maintaining “cellular security.” Cholesterol also plays a key role in intra and inter-cellular communications and signaling.

 

Cholesterol ensures that the cell’s lipid bi-layer (two layers of fat in phospholipid form) is neither too rigid nor too flexible. If that’s not enough, cholesterol is the goddess-like precursor to all adrenal, steroid and sex hormones such as estrogen and testosterone. Without cholesterol, we could not stand, move, think, respond to stress – or reproduce!

 

Cholesterol is also a major component of bile, an emulsifier required for dietary fats to be broken down and utilized. As a constituent of bile – on its singular route out of the body – cholesterol coats our slowly transiting feces. Only the liver can order cholesterol out of the body – and much of it is recycled.  Sorry Cheerios!

The liver is the main site of cholesterol synthesis, but every cell can make cholesterol (except nervous tissue).  Our bodies contain up to 100 grams of cholesterol – 90 percent in cell membranes and the rest dissolved in adipose and other tissues. The highest concentration (25 percent) is in the nerve cell connections and in the myelin that protects brain and nervous tissue.

 

In particular, infants need a large amount of cholesterol for proper brain development – and very large amounts of cholesterol are supplied in human milk – not in formula. Cholesterol is needed to properly form the part of the brain that allows the eyes to develop normally. In young and old alike, cholesterol is a primary raw material for many healing processes.

As an example, when an injury occurs on the Teflon-like, slick endothelial layer in an artery – say from high blood sugar – the body’s first responders are cholesterol, blood platelets, specialized white blood cells, and other materials that patch up the injury – similar to a scab forming over a break in the skin.

In the Optimal Diet, eggs are a “free food.”

 

“Cholesterol is absolutely essential for life,” writes Peter Attia, MD, President and co-Founder of the Nutrition Science Initiative:

“The animal body must have cholesterol to function properly and  to manufacture vital hormones and chemicals.”

And, for people whose bodies may not properly synthesize cholesterol, cholesterol in food may be a conditionally essential nutrient.

As you may note, the medical profession has utterly failed to properly describe the essential nature of cholesterol. Future editions of Diet Heart News will continue to expound on the importance of cholesterol and saturated fat in the American diet.
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Read the complete article here.

Will 2015 Dietary Guidelines Advisory Committee address Dr. Rimm’s legitimate concerns? - Watson

Why was a respected Harvard researcher afraid he would get “kicked off the stage”?

Alan Watson | May 10, 2012 

 

On October 31, 2008, during that first meeting of the 2010 Dietary Guidelines Advisory Committee (DGAC), Dr. Eric B. Rimm, Associate Professor of Medicine, Harvard Medical School, questioned what he called the “artificial limit” on dietary fat in the U.S. Dietary Guidelines.

 

From the transcripts:  www.cnpp.usda.gov/DGAs2010-Meeting1.htm

 

Dr. Rimm: “I wanted to make a radical point, one for which I’ll probably get kicked off the stage, but the whole issue of total fat and the 20 to 35 percent of calories from fat is one that has troubled me…”

Dr. Rimm:  “… But the high end, 35 percent of calories from fat, actually was not really based on much science; it’s based on the fact that we don’t have a lot of science beyond 35 percent, and there was a concern that higher fat diets would lead to obesity.”

Dr. Rimm:  I think if you look at the science, there is actually no good human data to suggest that higher fat diets lead to obesity. If anything, higher fat diets, at 35 to 40 percent, lead to lower triglycerides because it’s a lower carbohydrate intake.

Dr. Rimm:  “… I think there is the dogma that low-fat diets are beneficial, and you can go in the grocery store and see a lot of low-fat foods that are essentially just high in carbohydrate, highly processed sugars.”

Dr. Rimm did not get “kicked off the stage,” but the issue never came up again. He was simply ignored. The final report of the 2010 Dietary Guidelines ultimately contained even more stringent reductions in saturated fats – recommending that most Americans reduce saturated fat intake to just 7 percent of calories.

In an interview with Melissa Healy in the Los Angeles Times, June 28, 2010, Dr. Walter C. Willett, Chairman, Department of Nutrition, Harvard School of Public Health, agreed with his Harvard associate:

“The best available evidence demonstrates that percent of calories from fat in a diet has no bearing on weight loss – a point the dietary guidelines committee acknowledges.”

 

“It makes no sense to base the dietary guidelines on an outdated recommendation.”

 

Why did the Committee table Dr. Rimm’s concerns about artificial limits on dietary fat? Why was a respected Harvard researcher afraid he would get “kicked off the stage”? Are Committee members not allowed to question “low fat equals good health”? If so, why has USDA and HHS convened a 2015 Dietary Guidelines Advisory Committee?

New evidence exonerating saturated fats as a cause of heart disease continues to accumulate:

Dr. Ronald Krause – a highly respected American Diet Heart researcher – reviewed 21 studies involving 350,000 subjects to assess the correlation between saturated fat consumption and cardiovascular disease. The conclusion:

Intake of saturated fat was not associated with an increased risk of heart disease or stroke (American Journal of Clinical Nutrition, Jan. 13, 2010).

 

A prospective study from Australia looked at adults over a period of 15 years and found that people who ate the most full-fat dairy products had a 69 percent lower risk of cardiovascular death than those who ate the least (European Journal of Clinical Nutrition, April 7, 2010).
The Japan Collaborative Cohort Study for Evaluation of Cancer Risk found that saturated fat intake was inversely associated with mortality from stroke (American Journal of Clinical Nutrition, Aug. 4, 2010).

Researchers at Louisiana State University found that eating eggs for breakfast resulted in greater weight loss and better energy levels than eating two bagels even though the number of calories was about the same (The FASEB Journal 2007; 21:538.1).

Will the 2015 Dietary Guidelines Advisory Committee address Dr. Rimm’s legitimate concerns?
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Read the complete article here.

Should Women take Statin Drugs – ever? - Watson

http://dietheartnews.com/2012/11/should-women-ever-take-statin-drugs/

Should Women take Statin Drugs – ever?

Alan Watson | November 27, 2012 |

 

A true story…

In 1987, Mevacor, the first statin cholesterol-lowering drug, was introduced in record short time. Within a decade, Zocor, Pravachol, Lescol, Lipitor and Baycol were added. In August 2001, after 31 deaths from a muscle-destroying side effect, Bayer of Germany withdrew Baycol.

While clinical studies have demonstrated a small benefit among people with active, late stage heart disease, the threat of muscle-destroying side effects, liver damage and cancer are on the rise.

As reported in the Felix Letter, in the “supposedly successful” Simvastatin trial (Zocor), where the average life extension in the treatment group after 5 years was 24 days, Dr. Louis Krut is quoted as saying:

“If we were to set a very modest goal to extend their average life by only 1 year, it would require them to take simvastatin for 83 years.”

 

According to Dr. Uffe Ravnskov, statin drugs may stimulate cancer. Because the latency period between exposure and incidence is as long as 20 years, we do not know the extent to which the statin drugs will increase the rate of cancer in coming decades.

In the CARE study (Pravachol), 12 women in the treatment group developed breast cancer compared to just one in the control group (not taking the drug). And blood levels in the patients taking statin drugs were close to those that cause cancer in rodents.

Why take a chance with muscle-destroying side effects, liver failure and cancer? That’s what I asked my now deceased mother-in-law several years ago when she started taking Zocor.

Doris’s total cholesterol was 285. She was a little overweight but, at age 72, she was enjoying life and had no history of chronic illness. She drove a car, went shopping, and was even looking for a boyfriend!

As she lay in ICU one year later with elevated liver enzymes and a serious blood infection, her doctor took her off of Zocor. Once she stabilized, suspecting the drug had caused harm, we asked her doctor to recheck her cholesterol.

Yes – Doris was dying, but why not see if the drug treatment nonetheless had succeeded in lowering her cholesterol. When the doctor reluctantly complied – it took a letter from the family – Doris’s cholesterol was 130 – a drop of 155 mg/dl in less than a year.

After a few more agonizing hospitalizations, Doris was dead – Zocored within a year of starting the drug. Her doctor said she died of leukemia. Women – don’t let this happen to you. There are no circumstances – ever – when a woman should take a drug to lower cholesterol.

Women with higher cholesterol – live longer. Also, you must ask your doctor for a complete lipid evaluation. Just focusing on total cholesterol is a serious medical mistake. The ultimate price you may pay is an agonizingly slow death from cancer, liver failure or leukemia.
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Read the complete article here.

Know All 10 Heart Disease Risk Factors? - Alan Watson

Do You & Your Doctor Know All 10 Heart Disease Risk Factors?

 March 7, 2012 by Alan Watson

If you're new here, you may want to subscribe to my RSS feed. Thanks for visiting!

 

Heart disease is the #1 cause of death. About 50 percent of all people who die suddenly from heart disease have low or normal cholesterol. To protect yourself from heart disease, ask your doctor for a complete lipid evaluation. Fast 10-12 hours before blood is drawn (you can drink water). Because Total Cholesterol (TC) and LDL cholesterol are not the most reliable predictors of heart disease, they are not posted in the following chart.

 

QUICK SUMMARY:

Focus on Fasting Glucose, HDL, Triglycerides (TG) and the all important TG:HDL ratio. Keep in mind that before the advent of cholesterol-lowering statin drugs, the normal range for Total Cholesterol (TC) was: 180 mg/dl to 340 mg/dl. Also, it’s important to note that LDL is actually a family of particles. A discussion about LDL subclasses and LDL subclass testing follows in the summary of this article.

 

1. C-reactive protein (CRP) is produced by the liver in response to inflammation in the body. If monitored early enough, elevated CRP can be an early warning of a heart attack several years in advance. Optimum levels are below 1 mg/l. (You will have to request this test with most doctors.)

2. Fasting Glucose (FG) measures fasting blood sugar. Lowest all-cause mortality is associated with fasting glucose in the range of 80-89 mg/dl. According to the clinical experience of Dr. Robert Atkins, the risk of heart disease increases in linear manner as your Fasting Glucose goes over 100 mg/dl. (Specifically ask for this inexpensive test.)

3. Fibrinogen is a protein that in excess promotes blood clots. Elevated fibrinogen = thicker blood. Thicker blood flows less easily through partially blocked arteries. Consistent elevated fibrinogen (over 350 mg/dl) conveys a 250 percent increased risk of heart disease compared to people with fibrinogen levels below 235. (People who have recently suffered a heart attack will have elevated fibrinogen levels.)

4. Homocysteine is normally rapidly cleared from the bloodstream. Elevated homocysteine is a result of B-vitamin deficiencies, particularly folic acid, B-6 and B-12. Elevated homocysteine is associated with increased risk of heart attack, stroke, and all cause mortality. Levels less than 8 mmol/L are associated with longevity. (Again, you may have to request this test.)

5. Lipoprotein(a) has been called the “heart attack cholesterol.” Lipoprotein(a) is a sticky protein that attaches to LDL and accumulates rapidly at the site of arterial lesions or ruptured plaque. Readings of 30 mg/dl or more indicate serious increased risk of heart disease, especially in the presence of elevated fibrinogen (>350). While the Lp(a) level is largely genetically determined, it can be influenced by nutritional factors, such as high blood sugar and trans fatty acid consumption. (This test may not be as important as the rest and is seldom done routinely.)

6. HDL is made in the liver and acts as a cholesterol mop, scavenging loose cholesterol and transporting it back to the liver for recycling. HDL is associated with protection from heart disease. You want as much HDL as possible. HDL of 60 or more is associated with protection for men—70 or more for women.

7. Triglycerides (TG) should be under 100 mg/dl. Triglycerides are blood fats made in the liver from excess energy – especially carbohydrates. Risk is linear—the higher the number, the greater the risk, especially for women. While doctors may insist that a reading up to 150 is okay, Dr. Atkins’ clinical experience suggested otherwise.

8. TG:HDL ratio is the most reliable predictor of heart disease. Calculate your ratio by dividing TG by HDL. As an example, if TG = 80 and HDL = 80, your ratio is 1:1 representing low risk of heart disease. If your TG = 200 and your HDL = 50, your ratio is 4:1 representing serious risk of heart disease.

9. VLDL – Increasingly, Very Low Density Lipoprotein is measured/calculated. VLDL is sent out from the liver to deliver those liver made fats (Triglycerides) – as opposed to a Chylomicron that delivers dietary fat from the gut. Generally, VLDL is one fifth of your triglyceride level, although this is less accurate if your triglyceride level is greater than 400 mg/dl. (Beyond the scope of this article, LDL is the offspring of VLDL – they are closely-related.)

LDL particle size: Small dense Pattern B/Large fluffy Pattern A

An illustration from the Berkeley Heart Labs showing these particles

LDL – low density lipoprotein – is a family of particles. A lot of people with elevated LDL do not develop coronary artery disease, while individuals with low or modest levels often develop serious disease. This can be explained by the LDL particle number and size. Routine cholesterol testing only reveals the amount of LDL; not the quality of LDL.

We now know (my doctor didn’t) that there are different subclasses of LDL (and HDL). Under an electron microscope, some LDL particles appear large and fluffy; others small and dense. The big, fluffy particles are benign, while the small dense particles are strongly associated with increased risk of heart disease.

In excess, small dense LDL is toxic to the artery lining (the endothelium), and much more likely to enter the vessel wall – become oxidized – and trigger atherosclerosis. It’s becoming consensus medical opinion that only oxidized LDL can enter the macrophages in the lining of the arteries and contribute to plaque buildup.

HOW DO YOU KNOW WHAT LDL YOU HAVE? Certain clinical factors predict the presence of small dense LDL. These markers include HDL below 40 in men; below 50 in women – and Triglycerides (TG) higher than 120 mg/dl. Diabetes or pre-diabetes also predicts small dense LDL (Pattern B).

To determine LDL particle size, ask your doctor for a VAP (Vertical Auto Profile) test, which separates lipoprotein particles using a high speed centrifuge. The VAP test measures the basic information provided by a routine cholesterol test, but also identifies lipoprotein subclasses, LDL and HDL. (Go to http://thevaptest.com for more information.)

There are other tests as well. The NMR LipoProfile analyzes the number and size of lipoprotein particles by measuring their magnetic properties (http://theparticletest.com). Also Berkeley HeartLab’s LDL Segmented Gradient Gel Electrophoresis test measures all seven subclasses of LDL. (http://bhlinc.com).

If you don’t have insurance and can pay for just one test, get your fasting blood sugar checked. Any number over 100 – over 95 according to the late Dr. Atkins – is an early warning of diabetes, metabolic syndrome, and heart disease. If you have insurance or can afford a complete lipid panel, consider additional testing to determine the size and number of LDL particles. “A stitch in time saves nine.”
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Read the complete article here.

Ask Your Doctor for a Complete Lipid Evaluation - Watson

Ask Your Doctor for a Complete Lipid Evaluation Sent Saturday, March 10, 2012

Diet Heart News, volume 2, number 3

Ask Your Doctor for a Complete Lipid Evaluation

Heart disease is the #1 cause of death. About 50 percent of people who die suddenly from heart disease have low or normal cholesterol. To protect yourself from heart disease, ask your doctor for a complete lipid evaluation. Fast 10-12 hours before blood is drawn (you can drink water). Because Total Cholesterol (TC) and LDL cholesterol are not the most reliable predictors of heart disease, they are not posted in the following chart. QUICK SUMMARY: Focus on Fasting Glucose, HDL, Triglycerides (TG) and the all important TG:HDL ratio. Keep in mind that before the advent of cholesterol-lowering statin drugs, the normal range for Total Cholesterol (TC) was: 180 mg/dl to 340 mg/dl. Also, it's important to note that LDL is actually a family of particles. A discussion about LDL subclasses and LDL subclass testing follows in the summary of this article. 1. C-reactive protein (CRP) is produced by the liver in response to inflammation in the body. If monitored early enough, elevated CRP can be an early warning of a heart attack several years in advance. Optimum levels are below 1 mg/l. (You will have to request this test with most doctors.) 2. Fasting Glucose (FG) measures fasting blood sugar. Lowest all-cause mortality is associated with fasting glucose in the range of 80-89 mg/dl. According to the clinical experience of Dr. Robert Atkins, the risk of heart disease increases in linear manner as your Fasting Glucose goes over 100 mg/dl. (Specifically ask for this inexpensive test.) 3. Fibrinogen is a protein that in excess promotes blood clots. Elevated fibrinogen = thicker blood. Thicker blood flows less easily through partially blocked arteries. Consistent elevated fibrinogen (over 350 mg/dl) conveys a 250 percent increased risk of heart disease compared to people with fibrinogen levels below 235. (People who have recently suffered a heart attack will have elevated fibrinogen levels.) 4. Homocysteine is normally rapidly cleared from the bloodstream. Elevated homocysteine is a result of B-vitamin deficiencies, particularly folic acid, B-6 and B-12. Elevated homocysteine is associated with increased risk of heart attack, stroke, and all cause mortality. Levels less than 8 mmol/L are associated with longevity. (Again, you may have to request this test.) 5. Lipoprotein(a) has been called the "heart attack cholesterol." Lipoprotein(a) is a sticky protein that attaches to LDL and accumulates rapidly at the site of arterial lesions or ruptured plaque. Readings of 30 mg/dl or more indicate serious increased risk of heart disease, especially in the presence of elevated fibrinogen (>350). While the Lp(a) level is largely genetically determined, it can be influenced by nutritional factors, such as high blood sugar and trans fatty acid consumption. (This test may not be as important as the rest and is seldom done routinely.) 6. HDL is made in the liver and acts as a cholesterol mop, scavenging loose cholesterol and transporting it back to the liver for recycling. HDL is associated with protection from heart disease. You want as much HDL as possible. HDL of 60 or more is associated with protection for men--70 or more for women. 7. Triglycerides (TG) should be under 100 mg/dl. Triglycerides are blood fats made in the liver from excess energy - especially carbohydrates. Risk is linear--the higher the number, the greater the risk, especially for women. While doctors may insist that a reading up to 150 is okay, Dr. Atkins' clinical experience suggested otherwise. 8. TG:HDL ratio is the most reliable predictor of heart disease. Calculate your ratio by dividing TG by HDL. As an example, if TG = 80 and HDL = 80, your ratio is 1:1 representing low risk of heart disease. If your TG = 200 and your HDL = 50, your ratio is 4:1 representing serious risk of heart disease. 9. VLDL - Increasingly, Very Low Density Lipoprotein is measured/calculated. VLDL is sent out from the liver to deliver those liver made fats (Triglycerides) - as opposed to a Chylomicron that delivers dietary fat from the gut. Generally, VLDL is one fifth of your triglyceride level, although this is less accurate if your triglyceride level is greater than 400 mg/dl. (Beyond the scope of this article, LDL is the offspring of VLDL - they are closely-related.) LDL particle size: Small dense Pattern B/Large fluffy Pattern A LDL - low density lipoprotein - is a family of particles. A lot of people with elevated LDL do not develop coronary artery disease, while individuals with low or modest levels often develop serious disease. This can be explained by the LDL particle number and size. Routine cholesterol testing only reveals the amount of LDL; not the quality of LDL. We now know (my doctor didn't) that there are different subclasses of LDL (and HDL). Under an electron microscope, some LDL particles appear large and fluffy; others small and dense. The big, fluffy particles are benign, while the small dense particles are strongly associated with increased risk of heart disease. In excess, small dense LDL is toxic to the artery lining (the endothelium), and much more likely to enter the vessel wall - become oxidized - and trigger atherosclerosis. It's becoming consensus medical opinion that only oxidized LDL can enter the macrophages in the lining of the arteries and contribute to plaque buildup. How Do You Know What Size LDL You Have? Certain clinical factors predict the presence of small dense LDL. These markers include HDL below 40 in men; below 50 in women - and Triglycerides (TG) higher than 120 mg/dl. Diabetes or pre-diabetes also predicts small dense LDL (Pattern B). To determine LDL particle size, ask your doctor for a VAP (Vertical Auto Profile) test, which separates lipoprotein particles using a high speed centrifuge. The VAP test measures the basic information provided by a routine cholesterol test, but also identifies lipoprotein subclasses, LDL and HDL. (Go to http://thevaptest.com for more information.) There are other tests as well. The NMR LipoProfile analyzes the number and size of lipoprotein particles by measuring their magnetic properties (http://theparticletest.com). Also Berkeley HeartLab's LDL Segmented Gradient Gel Electrophoresis test measures all seven subclasses of LDL. (http://bhlinc.com). If you don't have insurance, request the inexpensive fasting glucose test. Any number over 100 - over 95 according to the late Dr. Atkins - is an early warning of diabetes, metabolic syndrome, and heart disease. If you have insurance or can afford a complete lipid panel, consider additional testing to determine the size and number of LDL particles. Remember, "A stitch in time saves nine." ============================================================= Read the full article here.

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk Sent Wednesday, November 23, 2011

Diet Heart News, volume 1, number 8

The UCLA Study: Elevated LDL Not Associated With Heart Attack Risk Since the early 1950s, mainstream researchers have been seeking the cause of atherosclerosis and heart disease spearheaded early on by University of Minnesota professor and American Heart Association board member Ancel Keys. The result - the 50 year old Diet Heart or Cholesterol Hypothesis: If you eat too much food containing cholesterol and/or saturated fat, the level of cholesterol in your blood will rise. The excess cholesterol will be deposited in artery walls, causing them to thicken and narrow. In time, this will block blood supply to the heart or brain causing a heart attack or stroke. According to this still unproven but enduring hypothesis, high blood cholesterol is caused by an atherogenic diet high in cholesterol and saturated fat - found mainly in animal products such as red meat, whole milk, eggs, butter - and the tropical saturates coconut and palm. In this scenario, high blood cholesterol is the main cause of atherosclerosis and heart disease. The medical and nutrition communities and various government agencies have been behind Diet Heart ever since. If animal fat and high blood cholesterol are the chief villains, then cholesterol-lowering diets and cholesterol-lowering drugs would appear to be wise choices. But 50 years later - after a lengthy test of time - the incidence of heart disease has not gone down as promised, and researchers like science writer Gary Taubes have uncovered a great deal of their evidence that is unsupportable, contradictory, and hopelessly wrong. A look at the recent five year UCLA/AHA Study The UCLA research team used an American Heart Association database that included 541 hospitals across the country. The database provided detailed information on 136,905 patients hospitalized for cardiovascular disease whose lipid levels upon hospital admission were documented. The results after five years: 75 percent of patients hospitalized for a heart attack had LDL cholesterol below 130 mg/dl - in the so called safe range. Even more astounding, 50 percent of patients had LDL below 100 mg/dL - considered optimal. (21 percent of the patients were taking a statin cholesterol-lowering drug.) Now don't you think that the UCLA researchers would have concluded that there was no association between elevated LDL and risk of heart attacks? After all, this was a five year study of heart attacks suffered by 136,905 patients in an American Heart Association database that included records from 541 hospitals. Yes - this should have been the nail in the coffin for the Diet Heart or Cholesterol Hypothesis, but not according to study director Dr. Gregg C. Fanarow, Professor of Cardiovascular Medicine and Science, David Geffen School of Medicine, UCLA, who concluded: "Almost 75 percent of heart attack patients fell within recommended targets for LDL cholesterol, demonstrating that the current guidelines may not be low enough to cut heart attack risk... " May not be low enough! Low cholesterol is already associated with depression and death by accidents, cancer and violence. According to the American Heart Association's journal Circulation, 1992; 86:3, the all cause death rate increases when total cholesterol drops below 180. Isn't there sufficient evidence now to conclude that elevated LDL and total cholesterol are not the cause of heart attacks and that the cholesterol hypothesis should be discarded along with official low fat diets and cholesterol-lowering drugs? Don't hold your breath! UK cardiologist Dr. Malcolm Kendrick: "I have come to realize that there is, literally, no evidence that can dent the cholesterol hypothesis... The effect of this study on the cardiovascular research community was....as you would expect...nothing at all, a deafening silence..." Dr. Fonarow disclosed that he has conducted research for GlaxoSmithKline and Pfizer and serves as a consultant and has received honorarium from the following drug companies: Abbott, AstraZeneca, GlaxoSmithKline, Merck, Pfizer and Schering Plough. Dr. H. Bryan Brewer, a physician-scientist at the National Heart, Lung and Blood Institute, failed to disclose his ties to AstraZeneca. Brewer had previously written a glowing report in a medical journal about Crestorwithout disclosing that he is a paid consultant and had presided over a company-sponsored symposium." He and the others forgot! Earlier in 2004, the doctors in the National Cholesterol Education Program (NCEP) who wrote the current cholesterol guidelines and, in effect, control cardiology, failed to disclose that six of the nine authors had direct financial ties to the makers of statin drugs, including: Pfizer's Lipitor, Bristol-Myers Squibb's Pravachol, Merck's Lovastatin, and AstraZeneca's Crestor. The new more stringent cholesterol-lowering guidelines boosted statinsales from $15 billion in 2004 to over $23 billion in 2005. And now the UCLA study provides more proof that lowering cholesterol with drugs or diet will not reduce cardiovascular disease or the risk of heart attack. But as Winston Churchill said: "Men occasionally stumble over the truth, but most of them pick themselves up and hurry off as if nothing had happened." [especially if there is money to be made]. ================================================================= Read the complete article here.