Debunking The Cholesterol – Heart Disease Myth
By Paul D. Tortland, D.O.
The Cholesterol “Problem”
Most everything we’ve been taught about cholesterol and heart disease is wrong.
The second most commonly prescribed drug in America in 2010 was Zocor® (simvastatin). More than 94 million prescriptions were filled. Second only to the pain killer, Vicodin®, Zocor is used to treat high cholesterol. It’s a member of the class of medications known as statins. Two other statins, Lipitor® and Crestor®, ranked in the top 10.
Statins are prescribed to treat high cholesterol and reduce the risk of heart attack and stroke. There’s only one problem. They don’t work!
A 2010 study published in the Archives of Internal Medicine analyzed 11 randomized controlled trials covering 65,229 subjects. The authors concluded that statins do not reduce death rates in people who don’t have established heart disease. And they have no benefit for most people who take them.
In fact, there has not been even one single legitimate study demonstrating any benefit from statins in people who haven’t already had heart attacks; little benefit for men who had suffered heart attacks; and no benefit for women – ever. Statins also supposedly reduce cholesterol, but there’s no proof of that, either.
Of course, that hasn’t stopped the pressure to take statins.
Even more significantly, it has never been shown that reducing cholesterol is actually beneficial. Nonetheless, it’s been ingrained in modern medicine, not to mention in the public’s mind, that cholesterol is a great evil, and that we all need to go on low-fat diets and eat statins to cut cholesterol.
Twenty to thirty years ago, in an attempt to reign-in heart disease, leading medical societies, in concert with the federal government, began pushing low-fat and fat-free food. The thinking went like this: Cardiovascular disease is caused by cholesterol deposits. Cholesterol comes from dietary fat. Therefore, reducing the dietary fat will reduce heart disease.
Surprise – it didn’t work either! In fact, since the push for low-fat diets began (coupled with the admonition to eat a diet “high in whole grains”), people have been getting fatter, and heart disease continues to skyrocket, in spite of lowered cholesterol levels.
The problem is that the association of cholesterol with cardiovascular disease is just that – an association, not a causation. Reducing cholesterol intake to stop heart disease is like saying, “In high crime areas there are more calls to the police. Therefore, to reduce crime, stop calling the police.”
Sounds ridiculous, right? So is the push to lower dietary cholesterol.
What Is Cholesterol?
Cholesterol is a steroid of fat that is produced in the liver or intestines, or ingested. It’s required to build and maintain cell walls. It helps keep the cell wall fluid or pliable over the range of physiological temperatures.
Cholesterol is the direct precursor for key hormones, including estrogen, progesterone, testosterone, cortisol, vitamin D (yes, vitamin D is a hormone, not a vitamin!), and the blood pressure modulator aldosterone.
Bile, which is stored in the gall bladder and secreted to help digest fats and aid in the absorption of the fat-soluble vitamins A, D, and K, is made from cholesterol.
Healthy nerves and brain development depend on cholesterol. Many nerves are encased in myelin, a waxy substance that enhances nerve transmission (like the insulation around an electrical wire). Myelin is rich in cholesterol.
In other words, cholesterol is essential for all animal life. If you don’t get enough, your body will make it anyway, in some cases stealing it from other important areas (such as hormone production).
Sources of Cholesterol
By far, the most abundant source of cholesterol is animal fat. All foods containing animal fat contain cholesterol to some extent. Major dietary sources of cholesterol include beef, poultry, pork, fish, shrimp, cheese, and egg yolks. Human breast milk also is cholesterol-rich.
Cholesterol is not found in significant amounts in plant sources. In fact, plant products such as flax seeds and peanuts contain cholesterol-like compounds called phytosterols that may actually block cholesterol absorption in the intestines.
Contrary to popular belief, HDL (high density lipoprotein) and LDL (low densitylipoprotein) are not respectively “good” and “bad” cholesterol. In fact, they’re not cholesterol at all! They are proteins, specifically, lipoproteins.
Since cholesterol is insoluble in blood (fat & water mix poorly), it is carried in the blood by HDL and LDL. It’s a simple and elegant system. LDL carries cholesterol from the liver to where the body needs it for repair and maintenance purposes. HDL carries the unused or old cholesterol back to the liver for recycling or excretion.
Cholesterol Doesn’t Cause Heart Disease
Shocking, but true. According to Christie Ballantyne, MD, a cardiologist at Baylor College of Medicine, “The majority of people who end up having heart attacks or stroke don’t have high cholesterol.”
The landmark Framingham Heart Study was launched in 1948 to identify the common factors that contribute to coronary artery disease (CAD) by following CAD over a long time period in a large group of people who had not yet developed overt symptoms of CAD or suffered a heart attack or stroke. Almost the entire town of Framingham, MA was followed for 50 years.
The results showed that, with one exception, there was no discernible association between reported diet intake and serum cholesterol. (The one exception was a weak negative association between caloric intake and serum cholesterol level in men. As caloric intake went down, serum cholesterol went up.) Regarding CAD and cholesterol, no relationship was found.
In fact, according to Malcolm Kendrick, MD, commenting on the study, “There is a direct association between falling cholesterol levels during the first 14 years and mortality during the following 18 years.” In other words, death rates went up as cholesterol levels went down!
Sadly, this didn’t stop researchers from misrepresenting the data. After all, if certain data don’t fit your hypothesis (or agenda), just ignore the data! As Dr. William B. Kannel, director of the Framingham Study, has stated, although there is no discernible relationship between reported diet intake and serum cholesterol levels in the study, “it is incorrect to interpret this finding to mean that diet has no connection with blood cholesterol.” Oh really?
In his attempt to demonize the fast food industry, Morgan Spurlock, producer of the documentary film “Super Size Me,” ate at McDonald’s for a month. He gained 25 pounds, his body fat percentage increased from 11% to 18%, his liver was showing signs of damage, and his total cholesterol increased from 168 to 225. However, Spurlock ate over 5,000 calories and a gallon of soda a day!
In response, comedian Tom Naughton wrote and produced the movie “Fat Head.” He, too, ate at McDonald’s for a month. However, he limited his total daily carbs to less than 100 grams, and kept his total daily calories to around 2200. He nonetheless ate the cheeseburgers and fried chicken – not the salads – essentially feasting on protein and saturated fat. At the end of 28 days he had lost 12 pounds. His total cholesterol remained essentially unchanged (231 to 222), and his body fat decreased from 31.2% to 28.2%.
The Historical Record
Dietary history further argues against the cholesterol-causes-heart-disease hypothesis.
Prior to 1970, the inhabitants of the isolated Polynesian atoll of Tokelau subsisted on coconuts and fish. More than 70 percent of their calories came from coconut, and more than 50 percent from fat (90% of which was saturated fat). There was virtually no cultivation of crops on the islands. There was no heart disease nor any of the other degenerative or inflammatory diseases.
By the mid 1960s, the New Zealand government (which had assumed administration of the islands) became concerned about potential overpopulation on the atolls. It initiated a voluntary migration program to move half the population to the mainland.
In the decades that followed, fish and coconuts practically vanished from the migrants’ diets, replaced virtually overnight by bread, potatoes, and meat. Fat and saturated fat consumption also dropped, replaced by carbohydrates, “…the difference being due to the big increase in sucrose consumption” (according to the Tokelau Island Migration Study). There was an almost immediate increase in weight and blood pressure, and a decrease in cholesterol levels. There developed an “exceptionally high level incidence [of] diabetes, gout, osteoarthritis, as well as hypertension.” In fact, as Gary Taubes notes in his best-selling book, Good Calories, Bad Calories, “The migrant experience had led to an increased incidence over the entire spectrum of chronic diseases.”
This is hardly a unique exposé. The historical and scientific record is replete with evidence as far back as the 1700s that, prior to industrialization and the availability of cheap commercially refined flour and sugar, people ate vastly more meat and fat, and far less carbohydrate.
In 1793, according to historian Harvey Levenstein, Americans ate eight times as much meat as bread. As Taubes writes, “By one USDA estimate, the typical American was eating 178 pounds of meat annually in the 1830s, 40-60 pounds more than was reportedly being eaten a century later.”
In 1937, Columbia University biochemists David Rittenberg and Rudolf Schoenheimer showed that dietary cholesterol had little effect on blood cholesterol. Warren Sperry, co-inventor of the blood test for cholesterol, came to the unambiguous conclusion: “The incidence and severity of [CAD] are not directly affected by the level of cholesterol in the blood per se.”
Inflammation is the Real Culprit
The problem is not the cholesterol level by itself but rather what happens to cholesterol in the body.
Cholesterol is susceptible to a process called oxidation. Technically, oxidation is the loss of at least one electron. (A freshly cut apple turning brown is an example of oxidation.) When cholesterol becomes oxidized, it becomes stickier. By itself, this stickiness is not necessarily a problem. The real problem is what causes the oxidation in the first place.
Inflammation increases the presence of free radicals; unstable molecules that steal electrons from other molecules, such as – you guessed it – cholesterol, thus causing oxidation and damage. Inflammation also damages the walls of the arteries, allowing otherwise harmless cholesterol molecules to worm into arterial walls causing plaque formation and vessel narrowing.
Think of the arterial wall as a tennis net. The net prevents a tennis ball and larger items from passing through. But if the net tears, bigger items slip through. So it is with arteries. Healthy walls prevent cholesterol from getting in. But inflammation damages the walls, allowing the oxidized – and sticky – cholesterol to pass through.
Furthermore, there are two types of LDL – large buoyant, and small dense. The large buoyant LDLs are basically harmless. It’s the small dense ones that wreak havoc. They’re smaller than the holes in the ‘tennis net’ and pass through the arterial walls more easily. Inflammation increases the amount of the small dense LDL.
So what causes the inflammation? Dietarily, quite simply, it’s carbohydrates, especially refined, high starch, and high sugar carbs. Carbs cause a spike in insulin, the hormone secreted by the pancreas to lower blood sugar. At normal levels, insulin is both essential and harmless. But persistent high levels cause a multitude of health problems, mostly related to the insulin-induced inflammation.
Misguided Medicine, or Conspiracy?
If the evidence is so overwhelming against cholesterol causing heart disease, why the push to lower cholesterol? Several factors seem to be involved.
Large credit goes to American scientist Ancel Keys. Keys hypothesized that a diet high in animal fats led to heart disease. To prove this, in the 1950s, he collected data both on deaths from CAD and on fat consumption from 22 countries. Despite the fact that 22 countries provided statistics, Keys cherry-picked the data from the 7 countries that supported his theory. Later known as the “Seven Countries Study,” the results appeared to show that serum cholesterol was strongly related to CAD mortality.
As a result, in 1956 the American Heart Association began telling people that a diet rich in butter, lard, eggs and beef would lead to coronary heart disease. The U.S. government piled on, recommending adoption of a low-fat diet to prevent heart disease. Sadly, this idea still prevails despite the fact that there is not a shred of scientific evidence to prove it. (And yes, the Food Pyramid is upside down!)
Secondly, the Food and Drug Administration currently is on the payroll of the drug industry. Pharmaceutical companies are allowed to pay fees to the FDA for speedy approval of their drugs. Thus a large amount of FDA funding comes directly from Big Pharma.
Currently, 70 percent of all new drug research is funded by the pharmaceutical industry and 30 percent is government funded. Control of funding means control over data outcome. Moreover, study conclusions are often written by physicians hired by drug companies and published in medical journals that accept millions in drug advertising funds.
As noted at the beginning, 3 of the top 10 prescription drugs sold in 2010 were for cholesterol. Follow the money.
So What to Do?
There are two keys points: First, dietary cholesterol by itself does not cause heart disease; Second, eating fat does not make you fat. Sugar is the culprit.
Begin by limiting your daily carb intake to 100 grams or less. If you happen to have a higher carb day, balance it by going ultra-low carb the next day. Choose carbs that are complex, high-fiber, and unrefined. Eat whole fruit; avoid fruit juice. Avoid ALL high fructose corn syrup.
Increase daily protein intake to at least 0.5 gram per pound of lean body weight, spread out among breakfast, lunch and dinner. Consume fats from good saturated or monosaturated sources, such as eggs, lean meats, olives, nuts, cheese, butter, plain yogurt, and olive oil. Avoid unsaturated and trans fats, including corn oil and margarine.
Increase Omega-3 fish oil intake to 6000 mg/day or higher. This is a great natural anti-inflammatory and also is the best way to reduce your triglycerides.
Add anti-oxidants to keep oxidation from damaging cholesterol and fish oil. These include: Coenzyme Q10; Vitamins A, C & E; Alpha Lipoic Acid. Raise HDL via exercise, niacin (use sustained-release to avoid flushing), and vitamin D.
As Hippocrates said, “Let food be your medicine, and medicine be your food.”