By Jonny Bowden & Stephen Sinatra | Mother Earth Living
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 Rise of the Cholesterol Theory
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.
Related Article: Insulin, Not Cholesterol, Is the True Culprit in Heart Disease
Consensus? Not Exactly
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!”
Cholesterol’s Crucial Role in Our Bodies
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.
“Good” and “Bad” Cholesterol: A Completely Outdated Concept
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.