Long-standing dietary advice has told us to reduce cholesterol intake, but a closer look suggests that advice may be misguided. Learn more about the history of this information, studies surrounding cholesterol’s effects on heart health and how to protect your heart’s health.
For decades we've been misinformed about the effects of cholesterol on heart health. Learn how to properly protect your heart's health and more.
In 1953, a young, ambitious biologist named Ancel Keys proposed the then-radical theory that heart disease was caused by consuming too much fat in the diet. It’s hard to imagine that this theory was radical given how widespread its acceptance is today, but at the time the prevailing belief was that diet had little to do with heart disease. However, Keys felt he was on to something. Previous research by Russian scientists had shown that when you fed rabbits large amounts of cholesterol and then dissected them later on, their arteries were filled with cholesterol-containing plaque and looked suspiciously like the arteries of people who died of heart disease. Never mind the inconvenient fact that rabbits are herbivores and the amount of cholesterol they normally get in their diets is pretty close to zero. And that other animals, such as rats and baboons, do not react in the same way as rabbits to a high-cholesterol diet; they metabolize cholesterol very differently.
The recommendation to eat “no more than 300 mg of cholesterol” a day remains the standard dietary advice of every major health organization to this day. Because fat in the diet and cholesterol in the blood were believed to be linked, Keys began to investigate dietary fat and its connection to heart disease. He looked at data on fat consumption and heart disease from various countries and published the results in his famous Seven Countries Study, which supposedly demonstrated a clear link between the amount of dietary fat consumed and the incidence of heart disease. Those countries eating the most fat also had the highest rates of heart disease. Sounds like an open-and-shut case against dietary fat, doesn’t it?
Except it was anything but. Keys actually had available to him reliable food consumption data from 22 countries, but he used only seven. By hand-selecting the seven countries that supported his preconceived hypothesis, Keys was able to make a convincing case that there was a direct connection between fat consumption and heart disease. The fact that Keys chose to include only seven countries and ignored the other 15 didn’t go unnoticed. Many researchers criticized Keys for conveniently omitting data that didn’t support his theory. When analyzing the data from all 22 countries, researchers found that the correlation between fat, cholesterol and heart disease vanished.
The Seven Countries Study is the cornerstone of current cholesterol and fat recommendations and official government policy, so it’s worth looking at in some detail. Keys examined saturated fat consumption in seven countries: Italy, Greece, the former Yugoslavia, the Netherlands, Finland, the United States and Japan. It hardly went unnoticed that Keys chose only the countries that fit his hypothesis. In fact, British physician Malcolm Kendrick used the same data available to Keys and quickly discovered that if you simply chose different countries, you could easily prove that the more saturated fat and cholesterol people consumed, the lower their risk of heart disease.
Another researcher who questioned Keys was a British doctor named John Yudkin from the University of London. He found that, in some countries, the intake of fat was virtually the same, but the rates of cardiovascular disease were vastly different. For example, Finland had a high per capita fat intake and a high rate of heart disease. But Yudkin found that the people of West Germany ate the exact same amount of fat as the people of Finland, yet they had about one-third the rate of heart disease. In addition, the Netherlands and Switzerland had only one-third the rate of heart disease seen in Finland, even though the Dutch and Swedes consumed even more fat than the Finns.
Cherry-picking the countries that proved the theory was only one of the many problems with the Seven Countries Study. There were also tremendous variations in heart mortality within these countries, even though saturated fat consumption was identical. In Finland, for example, the intake of saturated fat was almost identical in two population groups from Turku and North Karelia. But heart mortality was three times higher in North Karelia. Similarly, saturated fat intake was also equal on two Greek islands, Crete and Corfu. But heart mortality was a whopping 17 times higher on Corfu than it was on Crete.
How did Keys explain these facts, which were clearly present in his data? Simple. He ignored them. Keys was a member of the nutrition advisory committee of the American Heart Association, so despite the flaws in his study, he managed to get his theories officially incorporated into the 1961 American Heart Association dietary guidelines, where they have influenced government policy on heart disease, fat consumption and cholesterol for decades.
George Mann, associate professor of biochemistry at Vanderbilt University School of Medicine and a participating researcher in the Framingham Heart Study, was another of Keys’ doubters. The diet-heart idea is the “greatest scam” in the history of medicine, he said. “[Researchers] have held repeated press conferences bragging about this cataclysmic breakthrough, which the study directors claim shows that lowering cholesterol lowers the frequency of coronary disease. They have manipulated the data to reach the wrong conclusions.”
Mann also declared that National Institutes of Health (NIH) “used Madison Avenue hype to sell this failed trial in the way that media people sell an underarm deodorant!” Michael Oliver, a highly respected British cardiologist, concurred. “The panel of jurists...was selected to include experts who would, predictably, say that...all levels of blood cholesterol in the U.S. are too high and should be lowered.” But the dissenting voices were met with radio silence.
In the late 1970s, the Senate Select Committee on Nutrition and Human Needs made its final report: Low-fat diets would afford significant protection against coronary heart disease for men, women and children older than 2. “The evidence justifies...the reduction of calories from fat...to 30 percent, calories from saturated fat to 10 percent or less, and dietary cholesterol to no more than 250 to 300 mg daily,” it declared.
So how did that advice work out? One study that attempted to answer this question was the Women’s Health Initiative, a $415 million NIH study that involved close to 49,000 women, ages 50 to 79, who were examined for eight years in an attempt to answer the question, “Does a low-fat diet reduce the risk of getting heart disease or cancer?”
They got their answer. “The largest study ever to ask whether a low-fat diet reduces the risk of getting cancer or heart disease has found that the diet has no effect,” The New York Times reported in 2006. Of course, these questionable findings didn’t stop the cholesterol-lowering, fat-avoiding juggernaut that continues, albeit bruised and battered, to this day. And we have to give the misguided researchers kudos for their motives—by reducing cholesterol levels, they sincerely believed they would be reducing heart disease. As Dwight Lundell, a doctor and author of The Cure for Heart Disease, wryly puts it, “They were taking the bull by the horn—but it was the wrong bull.”
One of the most respected researchers in the world, Michel de Lorgeril, a French cardiologist at the prestigious National Center for Scientific Research, the largest public organization for scientific research in France, has authored dozens of papers in peer-reviewed journals, and he was the lead researcher for the Lyon Diet Heart Study, a 1999 study on the cardiovascular effects of eating a Mediterranean-style diet. The following quotation comes from his only book written in English: “We can summarize...in one sentence: Cholesterol is harmless!”
Despite cholesterol’s negative reputation, our bodies can’t function without it. It’s found in every single cell and is so essential that the lion’s share of the cholesterol in our bodies is actually made by the liver, which produces this fatty, waxy substance precisely because it is so essential to the health of our cells. The cholesterol we eat has a minimal effect on our blood levels of cholesterol: If you eat less cholesterol, your liver will simply take up the slack and make more. If you eat more of it, the liver makes less.
Cholesterol is the basic raw material that our bodies make into vitamin D; sex hormones such as estrogen, progesterone and testosterone; and the bile acids needed for digestion. The emphasis on lowering cholesterol as much as possible is not only misguided but also dangerous. Studies show that those at the lowest end of the cholesterol spectrum have a significantly increased risk of death from myriad conditions and situations unrelated to heart disease, including, but not limited to, cancer, suicide and accidents. Accidents and suicides? Really? Yes.
Here’s the connection: We need cholesterol to make brain cells. A low cholesterol level (around 160 mg/dL) has been linked with depression, aggression and cerebral hemorrhages. The membranes of our cells contain a lot of cholesterol because it helps maintain their integrity and facilitates cellular communication. Essentially, we need cholesterol for memory. Lower cholesterol too much and it can promote a kind of global amnesia; with too little cholesterol in the cell membranes, nerve transmission can be affected. It’s no surprise that Duane Graveline—a former flight surgeon and astronaut who received international recognition for his research on zero gravity deconditioning—gave his book about the memory loss he experienced after taking statin (cholesterol-lowering) drugs the ominous title, Lipitor: Thief of Memory.
Cholesterol is also one of the important weapons our bodies use to fight infections. It helps neutralize toxins produced by bacteria that swarm into the bloodstream from the gut when the immune system is weakened. When you have an infection, the total blood level of cholesterol goes up, but HDL (which we’ll define in a moment) falls because it’s being used up in the fight. Cholesterol’s ability to fight toxins may be one reason why it’s found at the site of arterial injuries caused by inflammation. But blaming cholesterol for those injuries is a little like blaming firemen for the fire.
Now here’s an interesting fact of which you might not have been aware: It’s actually impossible to measure cholesterol directly in the bloodstream. Being a fatty substance, cholesterol is not soluble in water or blood.
So how does it get in the bloodstream? Simple. Our livers coat it with a “protein wrapper” and bundle it with a few other substances (such as triglycerides); packaging it in this protective shell allows it to enter the circulatory system, much like stones would float in the ocean if they were contained in a buoyant, waterproof container. In our case, the protein wrapper acts like a passport, allowing cholesterol to travel throughout the bloodstream. It’s these packages, known as lipoproteins, that we actually measure when we measure our cholesterol levels. We know these cholesterol-protein combinations as HDL (high-density lipoprotein) and LDL (low-density lipoprotein). Both contain cholesterol and triglycerides, but the percentages are different, and the two types of lipoproteins have different functions in the body. LDL, known as “bad” cholesterol, carries cholesterol to the cells that need it, while HDL, known as “good” cholesterol, picks up the excess and carries it back to the liver.
But this idea of “good” and “bad” cholesterol is a wholly outdated concept. We now know that there are many subtypes of both HDL and LDL, and they do very different things. LDL, the imprecisely named “bad” cholesterol, has several subtypes, and not all of them are bad at all—quite the contrary.
The most important subtypes of LDL are subtype A and subtype B. When most of your LDL is of the “A” type, you’re said to have a “pattern A” cholesterol profile. When most of your LDL is of the “B” type, you’re said to have a “pattern B” cholesterol profile. Subtype A is a big, fluffy molecule that looks like a cotton ball and does just about as much damage, which is to say none. Subtype B, however, is small, hard and dense, like a BB gun pellet. It’s the real bad actor in the system because it’s the one that becomes oxidized, sticks to arterial walls and starts a cascade of damage. Subtype B particles (what we might call the “bad” bad cholesterol) are atherogenic, meaning they contribute significantly to heart disease. As we’ve already noted, big, fluffy LDL particles (the “good” bad cholesterol) are benign. Knowing you have a “high” LDL level is a useless piece of information unless you know how much of that LDL is the small, dense kind (harmful) and how much is the big, fluffy kind (not harmful in the least). A high LDL number with the bulk of it composed of the big, harmless, cotton ball-type molecules (the pattern A distribution) is far preferable to a lower LDL number mostly composed of the BB gun pellet-type
molecules (the pattern B distribution).
Unfortunately, most doctors are behind the times on this one. They look at that total LDL number—not the size and type—and if that number is even slightly higher than the lab says it should be, out comes the prescription pad. Pharmaceutical companies love when advisory committees—often heavily stacked with doctors who have financial ties to pharmaceutical companies—recommend that we maintain lower and lower LDL levels because that means a bigger market for cholesterol-lowering drugs.
Sadly, most doctors do not perform the easily available tests—often covered by insurance—that determine LDL makeup.
Meanwhile, HDL, the so-called “good” cholesterol, isn’t necessarily all good. A study published in the December 2008 issue of The FASEB Journal, produced by the Federation of American Societies for Experimental Biology, challenged the conventional wisdom that simply having high levels of good cholesterol (HDL) and low levels of bad cholesterol (LDL) is necessary for good health. The researchers showed that even good cholesterol has varying degrees of quality and that some HDL cholesterol is actually bad news in terms of overall health.
“For many years, HDL has been viewed as good cholesterol and has generated a false perception that the more HDL in the blood, the better,” says lead researcher Angelo Scanu of the University of Chicago. “It is now apparent that subjects with high HDL levels are not necessarily protected from heart problems and should ask their doctors to find out whether their HDL is good or bad.” Scanu’s study found that the HDL of people with chronic diseases such as rheumatoid arthritis and diabetes is quite different than the HDL of healthy individuals, even when their blood levels of HDL are similar. Normal, “good” HDL cholesterol reduces inflammation; dysfunctional, “bad” HDL does not. “This is yet one more line of research that explains why some people can have perfect cholesterol levels, but still develop cardiovascular disease,” says Gerald Weissmann, editor-in-chief of The FASEB Journal. “Just as the discovery of good and bad cholesterol rewrote the book on cholesterol management, the realization that some of the ‘good cholesterol’ is actually bad will do the same.”
The point is that there is, indeed, “bad” cholesterol—even “ultra-bad” cholesterol—but simply using a shotgun pharmaceutical approach to lowering all cholesterol doesn’t accomplish anything and has significant unwanted side effects.
Let’s go back for a moment to the British doctor John Yudkin, who examined Keys’ Seven Countries Study. Yudkin looked at fat as a percentage of calories. He looked at different types of fats. He even looked at the roles of carbohydrates and protein. And instead of confirming Keys’ hypothesis, Yudkin’s much more comprehensive data showed that the single dietary factor that had the strongest association with coronary heart disease was—wait for it—sugar.
So how did fat get demonized while sugar got a get-out-of-jail-free card? Well, there’s no political lobby for “fat,” but there’s a powerful one for sugar. In 2003, the World Health Organization (WHO) published a conservative report called “Diet, Nutrition and the Prevention of Chronic Diseases.” In it, the WHO made the unexceptional statement that it would be a good idea for people to derive no more than 10 percent of their daily calories from “added sugars,” meaning sugar beyond what we might naturally obtain from fruits and vegetables.
The report suggested that people could lower their risk of obesity, diabetes and heart disease simply by curbing some of the sugar they were consuming. Who could possibly object?
Well, the U.S. sugar industry, for one. “Hoping to block the report...The Sugar Association threatened to lobby Congress to cut off the $406 million the United States gives annually to the WHO,” reported Juliet Eilperin in The Washington Post. Two senators wrote a letter to then Health and Human Services Secretary Tommy G. Thompson, urging him to squelch the report. Not long afterward, the U.S. Department of Health and Human Services submitted comments on the report, stating that “evidence that soft drinks are associated with obesity is not compelling.”
The way sugar damages the heart can be directly related to insulin resistance. Ordinary table sugar, technically known as sucrose, is composed of equal parts glucose and fructose, two simple sugars that are anything but metabolically equal. Glucose can be used by any cell in the body. Fructose, on the other hand, is metabolic poison.
Before you point the finger of blame exclusively at high-fructose corn syrup (HFCS), an additive that’s made it into virtually every processed food on the market, know that sugar and high-fructose corn syrup are essentially the same thing. Fructose is the damaging part of sugar, and whether you get that fructose from regular sugar or from HFCS doesn’t make a whit of difference. It’s the fructose in each of them that’s causing the damage, and here’s why.
Fructose and glucose are metabolized in the body in completely different ways. Glucose goes into the bloodstream and then into the cells, but fructose goes right to the liver. Research has shown that fructose is seven times more likely to form artery-damaging advanced glycation end products. Fructose is metabolized by the body like fat, and it turns into fat (triglycerides) almost immediately. Fructose is the major cause of fat accumulation in the liver, a condition called fatty liver. And there is a direct link between fatty liver and insulin resistance.
Fructose found in whole foods such as fruits, however, is a different story. There’s not all that much fructose in, for example, an apple, and the apple comes with a hefty dose of fiber, which slows the rate of carbohydrate absorption and reduces insulin response. But fructose extracted from fruit, concentrated into a syrup, and then inserted into practically every food we buy at the supermarket—from bread and hamburger buns to pretzels and cereals—well, that’s a whole different animal.
Since the introduction of high-fructose corn syrup to food manufacturing in the 1970s, our fructose consumption has skyrocketed. Today, 25 percent of adolescents consume 15 percent of their calories from fructose alone. As endocrinologist Robert Lustig points out in a brilliant lecture, “Sugar: The Bitter Truth” (available on YouTube), the percentage of calories from fat in the American diet has gone down at the same time that fructose consumption has skyrocketed, along with heart disease, diabetes, obesity and hypertension. Coincidence? Lustig doesn’t think so, and neither do we.
Metabolic syndrome is a collection of symptoms—high triglycerides, abdominal fat, hypertension and insulin resistance—that seriously increases the risk for heart disease. Rodents consuming large amounts of fructose rapidly develop it. In humans, a high-fructose diet raises triglycerides almost instantly; the rest of the symptoms associated with metabolic syndrome take longer to develop in humans than they do in rats, but develop they do.
All told, the case against fructose consumption as a key factor in the development of heart disease seems to be far more cogent than the case against fat. It’s also worth pointing out that every single bad thing fructose does to increase our risk for heart disease—and it does a lot—has virtually nothing to do with elevated cholesterol. The fact is that sugar is far more damaging to the heart than either fat or cholesterol, but that has never stopped the diet establishment from continuing to stick to its story that fat and cholesterol are what we ought to be worried about.
As the old journalistic maxim goes, “Never let the facts get in the way of a good story.”
Unfortunately, this story is long past its expiration date. Sticking to it in the face of all evidence continues to make many people very sick indeed.
One study mentioned often by defenders of the cholesterol theory is the Framingham Heart Study. This long-running research study started back in 1948 and monitored heart disease in more than 5,000 residents of Framingham, Massachusetts. After following up for 16 years, the researchers claimed to find a direct correlation between heart disease and cholesterol levels.
But God is in the details. As it turned out, the group of Framingham residents who developed heart disease and the group of Framingham residents who didn’t had similar ranges of cholesterol levels. In fact, the average cholesterol level of the heart disease group was only 11 percent higher than that of the group without heart disease. Cardiovascular disease struck people with cholesterol levels as low as 150 mg/dL. Low cholesterol, according to this study, was hardly a guarantee of a healthy heart.
When researchers went back and looked at the Framingham data 30 years after the project started, they found that once men passed the age of 47, it didn’t make a whit of difference whether their cholesterol was low or high. Those with high cholesterol at age 48 lived just as long as, or longer than, those who had low cholesterol. So if cholesterol is important only for the relatively few who have had a heart attack before the age of 48, why are the rest of us worried about high-fat food and cholesterol levels?
The question is hardly academic. In 1992, 44 years after the Framingham study began, study director William Castelli wrote the following in an editorial in the Archives of Internal Medicine: “In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person’s serum cholesterol...we found that people who ate the most cholesterol, ate the most saturated fat, [and] ate the most calories weighed the least and were the most physically active.”
Eliminate these foods
• Sugar and soda
• Processed carbs (such as white bread, white pasta, crackers and white rice)
• Trans fats and excess vegetable oils
• Processed meats (such as bacon, ham,
hot dogs, bratwurst and most sausages)
Eat more of these foods
• Wild salmon
• Berries and cherries
• Grass-fed meat
• Dark chocolate
• Garlic and turmeric
• Pomegranate juice, green tea and red wine
• Extra virgin olive oil
Make these lifestyle changes to reduce stress
• Meditate or practice deep breathing
• Express your emotions
• Cultivate intimacy and pleasure
• And most of all…enjoy your life!
If your doctor is concerned about your cholesterol levels, doctors Jonny Bowden and Stephen Sinatra recommend you ask about the following tests, which are more important than the standard test for cholesterol:
LDL particle size: Measures whether your LDL particles are mostly type A, the large, fluffy, benign kind; or mostly type B, the small, dense kind that cause inflammation (one common test is the NMR LipoProfile; others include the Lipoprint, Berkely, VAP and LPP)
Hs-CRP: Measures CRP, a marker for inflammation directly associated with cardiovascular health; an optimal level is less than 0.8 mg/dL
Fibrinogen: Measures the levels of a protein that determines blood’s ability to clot properly; normal levels are between 200 and 400 mg/dL
Serum ferritin (iron): Tests for iron overload, which can contribute to heart disease; optimal levels are less than 80 mg/L for women and less than 90 mg/L for men
Lp(a): Elevated Lp(a) levels are a very serious risk factor for heart attacks
Homocysteine: Elevated levels of homocysteine strongly predict first and recurring cardiovascular incidents; optimal levels are between 7 and 9 umol/L
Interleukin-6: Elevated interleukin-6 levels are a precursor to elevated CRP levels; optimal levels are between 0.0 and 12.0 pg/mL
Coronary calcium scan: Measures coronary calcification; a score above 400 is considered extensive and a risk factor for coronary procedures and events
This article is excerpted from the book The Great Cholesterol Myth by Jonny Bowden and Stephen Sinatra. This book is full of more information about cholesterol, the background of how it became demonized in American dietary guidelines, research on the dangers of statin drugs and much more. A must-read for anyone concerned with their cholesterol levels or heart health, this book is available for purchase in our store.
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