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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The controversial study that started the War on Cholesterol - Watson

The controversial study that started the War on Cholesterol…

      

Alan Watson | June 14, 2012   

Revisiting the Coronary Primary Prevention Trial (CPPT) – 1973 to 1984

Using "relative risk statistics" and changing the study's design, the CPPT researchers declared success and the War on Cholesterol began in earnest

 

Launched in 1973 by the National Institutes of Health, the Coronary Primary Prevention Trial (CPPT) set out to prove that lowering blood cholesterol with a drug and a low cholesterol, low saturated fat diet would reduce the risk of coronary heart disease and extend the lives of the study participants.

(As part of the study, twelve new Lipid Research Clinics were set up by the Heart Institute at large universities throughout the country including Baylor, Stanford, Johns Hopkins and the University of Washington in Seattle.)

The researchers were looking for middle-aged men with total cholesterol levels exceeding those of 95 percent of Americans. (Only men with the highest 0.8 percent total cholesterol qualified.) The CPPT researchers screened 480,000 applicants in order to select 3,806 high risk men between the ages of 35 and 59.

This meant that many of the participants had familial hypercholesterolemia, a rare genetic defect in cholesterol metabolism present in about 1 percent of the population. The trials chance of success was therefore greatly increased by focusing on this particular group of presumably vulnerable men.
In their preliminary report, CPPT researchers announced that they would study two separate outcomes:  (1) Nonfatal heart attacks and (2) fatal heart attacks or deaths from coronary heart disease. The CPPT directors emphasized that they would be satisfied with nothing less than the strongest statistical proof of their findings; they had to be “99 percent certain that the results were not due to chance.”

The researchers also announced their goal of reducing blood cholesterol in the treatment group by 25 percent and reducing the risk of heart disease in the treatment group by at least 50 percent.
Approximately half of the 3,806 men were provided low cholesterol, low saturated fat dietary advice and were treated with cholestyramine, a cholesterol-lowering bile acid resin (Questran).

(Cholestyramine lowers cholesterol by interfering with digestion. Statins such as Lipitor, Mevacor and Zocor were not available yet.)

The control group was provided the same dietary advice and an unpleasant tasting placebo – an indigestible mixture of sand, sugar and food coloring. Both trial groups suffered with moderate to severe gastrointestinal distress. There were eight gastrointestinal cancer deaths in the treatment group (out of 21 cases) and one in the placebo group (out of 11 cases).

(There were more deaths from cancer, intestinal disease, stroke, violence and suicide in the group taking the cholesterol-lowering drug, and overall mortality was essentially the same for both groups.)

Disappointing Results

In 1984, the disappointing results were tabulated. Cholesterol levels in the treatment group had decreased by no more than 7 percent. Cholestyramine and the low cholesterol, low saturated fat diet had failed to lower cholesterol enough to prove that lowering cholesterol would reduce the risk of heart disease and extend the lives in the treatment group.

The difference in nonfatal heart attacks was not statistically significant. In the treatment group, 130 participants (6.8 percent) had a heart attack versus 158 in the placebo group (8.3 percent). After 7 years, the fraction of the treatment group that had benefited was less than 2 percent.

                                       Nonfatal heart attacks               Fatal heart attacks/coronary deaths
1,900 Control Group:         158 or 8.3 percent                               38 or 2.0 percent
1,906 Treatment Group:     130 or 6.8 percent                              30 or 1.6 percent

The difference in fatal heart attacks was not significant either. In the treatment group, 30 participants (1.6 percent) suffered a fatal heart attack compared to 38 in the placebo group (2.0 percent) Again – after 7 years of taking an unpleasant drug (and following a low fat diet), the fraction of the treatment group that benefited was less than 1 percent.

However, by applying relative risk statistics (a percentage of a percentage), the CPPT researchers improved their results. They took the number of people who presumably didn’t have a heart attack because of taking the drug (28) and looked at it as a percentage of the people who did have heart attacks (158) but didn’t take the drug:

The less than 2 percent absolute difference in nonfatal heart attacks rose to a reported 19 percent reduction in risk of a heart attack!

 

In similar statistical fashion, the researchers announced a 24 percent reduction in the risk of dying from a heart attack. The 8 men or 1.6 percent out of 1,900 who presumably did not have a fatal heart attack because they took the drug became the same 24 percent who reduced their risk of mortality compared to those in the control group who did die (38) but did not take the drug.

Additional study design changes

To prop up their victory, the CPPT researchers decided to exclude  “uncertain” nonfatal heart attacks from the treatment group while including  “uncertain” fatal heart attacks in the placebo group. Also, using the original 99 percent standard, the small favorable trend in either group could only be explained by chance (as defined by the researchers themselves at the start of the trial.)
By applying the less stringent 95 percent standard and by combining the two groups into one (nonfatal and fatal heart attacks), the CPPT researchers improved their results – declared victory – while the press responded with unbridled enthusiasm.

In 1984, the press and medical journals portrayed CPPT as the long sought proof that animal fats were the cause of heart disease. It was widely reported that for the first time:

“It had been proven that lowering cholesterol would reduce the mortality from heart disease and lower the risk of having a heart attack.”

 

Much of what we hear today about diet and heart disease can be traced back to this notorious failed study. When other scientists voiced their objections to the trial’s design changes, the CPPT directors simply denied that they had ever embraced the original more stringent standards.

In January 1984, the Journal of the American Medical Association (JAMA) dutifully reported:

“The trial’s implications…could and should be extended to other age groups and women, and to others with more modest elevations of cholesterol levels. The benefits that could be expected from cholestyramine treatment are considerable.”

 

George Mann, M.D., professor in medicine and biochemistry at Vanderbilt University, severely criticized the CPPT directors and the trial’s unsupportable results:

“The managers at the National Institutes of Health have used Madison Avenue hype to sell this failed trial in the way the media people sell an underarm deodorant…”

 

 Giving cholestyramine for over seven years to 1,906 middle age men – many with a genetic predisposition to atherosclerosis – had only saved the lives of eight but the Heart Institute was now recommending that cholesterol-lowering drug treatment be extended to patient groups that had not been part of the trial.

Even without the solid evidence they sought, the medical elite in the American Heart Association and the National Institute of Health decided to push ahead with cholesterol-lowering drugs and the still unproven low cholesterol, low saturated fat diet:

 “Now we have proved that it is worthwhile to lower blood cholesterol; no more trials are necessary. Now is the time for treatment.”

 

 The long War on Cholesterol had begun
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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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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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