Cholesterol Myths – Cholesterol is Harmless
NOW LET’S TALK ABOUT YOU FOR A MOMENT.
Unless you’re just an information junkie, there’s a good chance that you’re reading this website because you have something at stake here. Let us guess: You’re concerned about your cholesterol.
Maybe you’re a woman whose doctor has read you the riot act because your cholesterol is approaching 300 mg/dL, and your doc has convinced you that you’ll drop dead of a heart attack if you don’t go on medication right away.
Maybe you’re a middle-aged man who has already had a heart attack, and your doctor is adamant about putting you on a cholesterol-lowering drug.
Or maybe you’re a fit guy in your sixties whose cholesterol is 240 mg/dL and whose doctor is “worried” about that number.
However, only one of the three hypothetical cases listed above has any business being on a cholesterol-lowering drug. Can you guess which one? Don’t worry: By the time you finish this category, you’ll not only know the answer, you’ll also know a heck of a lot more about cholesterol than most doctors in America. And, no, we don’t make that statement lightly.
Cholesterol is a waxy substance—technically a sterol—that is an important constituent of cell membranes. The vast majority of cholesterol in the body is made in the liver, while the rest is absorbed from the diet.
Cholesterol is the basic raw material that your body uses to make vitamin D; sex hormones such as estrogen, progesterone, and testosterone; and the bile acids needed for digestion. Cholesterol travels in particles called lipoproteins, the most common of which are high-density lipoproteins (HDL) and low-density lipoproteins (LDL).
Below we address the long-held, conventional views on cholesterol basics that we believe to be outdated.
WHAT IS HDL?
HDL is considered “good” cholesterol because it helps remove so-called “bad” cholesterol, LDL. When measured, HDL levels should be as high as possible, preferably 60 milligrams per deciliter of blood (mg/dL) and above. Maintaining a healthy weight, physical activity, and a diet that includes healthy fats like olive oil are believed to keep HDL levels high.
HDL is much more tightly controlled by genetics than LDL. A 2011 study from the National Institutes of Health, AIM-HIGH, found that raising HDL did nothing to protect against heart attacks, strokes, or death. And all HDL is not the same. HDL-2 particles are large and buoyant and the most protective. HDL-3 particles, on the other hand, are small and dense and may be inflammatory. HDL-2 is anti-inflammatory and anti-atherogenic (atherosclerosis being the condition in which an artery wall thickens from the accumulation of fatty materials, called plaque, induced by inflammation, inhibiting blood flow from the heart). HDL-3, on the other hand, is poorly understood. You want to have higher levels of HDL-2 than HDL-3.
The “New School” generally agrees that higher levels of HDL are desirable, but research is concentrating on the function of HDL subtypes rather than the total amount. Daniel Rader, M.D., director of preventive cardiology at the University of Pennsylvania, wrote in the New England Journal of Medicine, “Recent scientific findings have directed increasing interest toward the concept that measures of the function of HDL, rather than simply its level in the blood, might be more important to assessing cardiovascular risk and evaluating new HDL-targeting therapies.”
WHAT IS LDL?
LDL is “bad” cholesterol because it can build up in the arteries, impeding blood flow. Its levels should be kept low. Current standards are 100 to 129 mg/dL, with lower than 100 being the target for those at risk for heart disease, and lower than 70 being the target for people at very high risk. Too much saturated fat in the diet, inactivity, and being overweight are considered to raise LDL levels.
All LDL is not the same. LDL-A is a buoyant, fluffy molecule that does no harm whatsoever as long as it is not damaged by oxidation (a process caused by free radicals that enables cholesterol to form plaque). LDL-B is a small, hard, dense, molecule that promotes atherosclerosis. A pattern of high LDL-A is the most beneficial. Blood tests today can also measure the number of LDL-A and LDL-B particles.
The most important cholesterol particle of all, which conventional tests do not focus on, is Lp(a). Lp(a) is a very small, highly inflammatory particle that is thrombogenic (blood clotting). Dr. Sinatra calls it “the alpha wolf” of cholesterol particles. In a healthy body, low Lp(a) levels aren’t much of a problem. Lp(a) circulates and carries out repair and restoration work on damaged blood vessels. However, the more repairs you need on your arteries, the more Lp(a) is utilized. Lp(a) concentrates at the site of damage, binds with a couple of amino acids within the wall of a damaged blood vessel, dumps its LDL cargo, and starts to promote the deposition of oxidized LDL into the wall, leading to more inflammation and ultimately to plaque.
Also, Lp(a) promotes the formation of blood clots on top of the newly formed plaque, which narrows the blood vessels further.
HOW CHOLESTEROL IS MEASURED
A standard blood test will tell you your total cholesterol level and your HDL and LDL levels.
Measure cholesterol with the newer particle tests, which tell you how much of your LDL is type A and how much of your LDL is type B. Measure the number of actual particles, and the amount of the potentially dangerous Lp(a). That is the only information that matters.
Eat less 300 mg of cholesterol a day and eat less than 10 percent of calories as saturated fat.
According to the Framingham Heart Study, people who consumed the most cholesterol in their diets did not have any higher blood cholesterol levels than those who consumed the least amount. The effect of dietary cholesterol on blood (serum) cholesterol is very variable and individual, and for most people—though not all—the effect of dietary cholesterol on serum cholesterol is insignificant.
In any case, because cholesterol is not as an important risk factor for heart disease as once believed, it doesn’t matter very much. Saturated fat raises cholesterol, but it raises overall HDL cholesterol and the good part of LDL cholesterol (LDL-A) far more than it raises the bad part of LDL cholesterol (LDL-B). There is no evidence that supports a direct relationship between saturated fat and heart disease.
RELATIONSHIP TO HEART DISEASE
High levels of cholesterol are an important risk factor for heart disease because cholesterol builds up in the arteries, inhibiting blood flow from the heart.
Cholesterol is a relatively minor player in heart disease and a poor predictor of heart attacks. More than half of all people who are hospitalized with heart attacks have perfectly normal cholesterol levels.
When the National Cholesterol Education Program lowered the “optimal” cholesterol levels in 2004, eight out of nine people on the panel had financial ties to the pharmaceutical industry.
Besides the fact that you’re concerned about your cholesterol, there are two other things we can assume. One, you don’t tend to blindly follow recommendations without doing your own research. (If you did, you’d simply be following your doctor’s orders and have no interest in reading this website.)
The second thing we’re pretty sure about you is that you’re smarter than the average reader.
To understand the cholesterol myth—and to fully appreciate how the health advice that follows from the myth is obsolete—you’ll need to know a lot more about cholesterol than the average person knows. But reading—and understanding—the full story of cholesterol, including the myths, misconceptions, outright lies, and misguided medical practices, doesn’t make for easy reading. It’ll take quite a bit more intelligence, motivation, and perseverance than, say, reading the latest romance paperback.
The cholesterol story touches on not only medicine and research but also politics, economics, psychology, and sociology. It’s got a cast of characters ranging from the obnoxious and egotistical to the well-meaning and misguided.
It has heroes and villains, mavericks and traditionalists, all engaged in a battle that, sadly, has little to do with saving lives (though it may have started out that way). It involves staggering amounts of money, the politics of publication, the sociology of belief (why bad ideas continue to survive past their expiration dates), and the revolving door that exists between government advisory committees and the industries they’re supposed to police. (Example: When the National Cholesterol Education Program lowered the “optimal” cholesterol levels in 2004, eight out of nine people on the panel had financial ties to the pharmaceutical industry, most of them to the manufacturers of cholesterol-lowering drugs who would subsequently reap immediate benefits from these same recommendations.)
By now it should be pretty clear that neither of us buys into the myth that cholesterol is the proper target for the prevention of heart disease. But how did the myth get started in the first place? How, exactly, did cholesterol and saturated fat come to be branded as the twin demons of heart disease?
To answer that question, we need to go back to 1953, when a young, ambitious biologist named Ancel Keys proposed the then-radical theory that heart disease was caused by too much fat in the diet.
THE BIRTH OF THE DIET–HEART HYPOTHESIS
It’s hard to imagine that this theory was radical given how widespread its acceptance is today, but at the time the prevailing wisdom was that diet had little to do with heart disease. But 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. The amount of cholesterol they normally get in their diets is pretty close to zero. Other animals, such as rats and baboons, do not react in the same way as rabbits to a high-cholesterol diet, and they metabolize cholesterol very differently. Even Keys himself understood that cholesterol in the diet was of no importance. In 1997, he stated, “There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit.”
Yet the admonition to eat “no more than 300 mg of cholesterol” a day remains the advice of every major health organization to this day, despite the fact that even the scientist most responsible for popularizing the diet–heart hypothesis thought it was ridiculous.
Inconvenient facts to the contrary, excess cholesterol in the blood, not the diet, seemed to Keys to be a likely culprit in the development of heart disease.
Since fat in the diet and cholesterol in the blood were believed to be linked, this led Keys to investigate fat in the diet and its connection to heart disease. He looked at data on fat consumption and heart disease from various countries and published the results of his famous study, the 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. When Keys published the results of his study, he actually had available to him reliable food consumption data from twenty-two 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 dietary fat and heart disease.
The fact that Keys had chosen to include only seven countries and ignored the other fifteen didn’t exactly go unnoticed. Many researchers criticized Keys for conveniently omitting data that didn’t support his theory. Researchers analyzing the data from all twenty-two countries found that the correlation between fat, cholesterol, and heart disease literally vanished.
One of the researchers who questioned Keys was a British doctor named John Yudkin from the University of London. He found that there were countries where the intake of fat was virtually the same, but the rates of cardiovascular disease were vastly different. For example, Finland was one of the countries used by Keys to make his case, because 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, but they had about one-third the rate of heart disease. The paradox was even more pronounced in the Netherlands and Switzerland, which also 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.
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.
Yudkin did a far more extensive analysis of dietary factors than Keys did. He 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’s 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 back to Keys. By all accounts, Keys was a very smart and well-liked man who just happened to be dead wrong on the cholesterol and fat issue. But he was hardly without ambition and ego. Known for being blunt and biting, he presented his theory on fat, cholesterol, and heart disease to a distinguished audience in 1954, when the World Health Organization (WHO) held its first expert committee on the pathogenesis of atherosclerosis. One of his longtime collaborators, Henry Blackburn, recalled that Keys was stunned to find that his ideas were not accepted on the spot. One participant asked him to cite the principle piece of evidence for his diet–heart theory, and he was caught, to put it mildly, off guard. “Ancel fell into a trap, he made a mistake,” Blackburn said. “He cited a piece of evidence, and they were able to destroy it. He got up from being knocked to the ground and went out saying, ‘I’ll show those guys,’ and designed the Seven Countries Study.”
The Seven Countries Study is actually 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, and, lo and behold, he found a straight-line relationship between heart disease, cholesterol levels, and saturated fat intake—exactly what he had hoped to find.
The seven countries were 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. He easily could have chosen a different group of countries and proven a completely different hypothesis.
In fact, British physician Malcolm Kendrick, M.D., did exactly that. 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.
Anticipating a challenge to his “proof” by defenders of the cholesterol hypothesis, Kendrick pointed out that he was merely doing exactly what Keys did—hand-selecting data that would prove his theory. “What do you mean I can’t choose my own countries?” he asked sarcastically. “That’s not fair. Keys did!”
Cherry-picking the countries that proved this theory was only one of the many problems with the Seven Countries Study. There were 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 seventeen 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.
At the time, Keys’s theories about fat and cholesterol weren’t exactly widely known outside scientific circles, and the whole theoretical fight between the advocates of the “sugar” hypothesis and the advocates of the “fat” hypothesis was all so much ivory-tower name-calling, well out of the earshot of the general public. But all that was about to change.
And the man who was indirectly responsible for that change was, interestingly, not a scientist at all but a politician named George McGovern.
The Politics of Science
McGovern, chairman of the Senate Select Committee on Nutrition and Human Needs, practically changed the national policy on nutrition in this country. And they were directly responsible for transforming the idea that dietary fat causes heart disease from a not-so-solid hypothesis into solidified dogma.
McGovern’s committee instituted a wonderful series of landmark federal food assistance programs, but its work on malnutrition started to wind down around the mid-1970s. McGovern’s committee staffers, notably its general counsel, Marshall Matz, and staff director, Alan Stone, both lawyers, decided to go for broke and take on the reverse side of the malnutrition coin: overnutrition. “It was a casual endeavor,” Matz said. “We really were totally naive, a bunch of kids who just thought, ‘Hell, we should say something on this subject before we go out of business.’ ”
The committee listened to two days of expert testimony in 1976 and then assigned a young writer named Nick Mottern to write the whole thing up. The only problem was that Mottern didn’t know anything about nutrition and health and had no science writing background to boot. So he did what any smart young writer would do: He went to the experts for guidance.
WHAT YOU NEED TO KNOW
• The theory that fat and cholesterol cause heart disease became widely accepted despite much evidence to the contrary. This evidence deserves to be reexamined. The case needs to be reopened.
• Many doctors did not agree with the cholesterol myth and questioned the science upon which it was based.
• The studies upon which the cholesterol myth was based were later found to be problematic.
• The adoption of the cholesterol myth by mainstream organizations and the government had a strong political component to it.
Except in this case, Mottern didn’t actually go to the “experts”; he went to one particular expert, Mark Hegsted, a Harvard nutritionist, and relied almost exclusively on Hegsted’s interpretation of the testimony, as well as on Hegsted’s own personal recommendations.
Hegsted was a fervent believer in the emerging theory that low-fat diets would prevent heart disease and that fat and cholesterol were the spawn of Satan.
So Mottern wrote up the committee’s recommendations with Hegsted as the final authority—no more than 30 percent of calories from fat, no more than 10 percent of calories from saturated fat—and in 1977 the committee disbanded. But right around that time, a newly appointed assistant secretary at the U.S. Department of Agriculture (USDA) named Carol Tucker Foreman decided that the USDA ought todo something with these recommendations. Like make them official policy! The only problem was that she needed some good scientific cover.
Fair enough. Foreman wasn’t a scientist herself, but she sure had access to some good ones. So she went to the president of the National Academy of Sciences (NAS), Philip Handler, a distinguished expert in human metabolism.
Want to know what he told her?
The anti-fat dietary goals written by Mottern were utter and complete nonsense.
So Foreman did what other good officials would do when they don’t like the advice they’re getting. She went to someone else.
Can you guess whom she went to?
Hegsted. The champion of the low-fat, low-cholesterol eating plan who had practically written the guidelines in the first place.
Not surprisingly, Hegsted had an entirely different opinion from Handler. With cover from Hegsted, the USDA was able to release Using the Dietary Guidelines for Americans, a low-fat, low-cholesterol manifesto that echoed exactly the same anti-fat, anti-cholesterol sentiments written in the original Mottern–Hegsted document put out by the McGovern committee.
What happened next makes the backstabbing antics of the television show Survivor look like child’s play.
The National Academy of Sciences Food and Nutrition Board, not happy with the USDA report, issued its own set of guidelines titled Toward Healthful Diets. Here’s the Reader’s Digest condensed version of what it said: “Don’t worry about fat.”
This pretty much directly contradicted the report of the USDA, which had recommended very specific fat intakes: less than 30 percent of total calories from fat and less than 10 percent from saturated fat.
The USDA didn’t take this slap in the face sitting down and leaked reports to the press saying that the chairman of the NAS Food and Nutrition Board and one of the board’s members had financial ties to the food industry, as if this were enough to explain why the board as a whole didn’t endorse the USDA recommendations to avoid fat. The beef and dairy industries went nuts and lobbied with all their might against the recommendations, calling them unjustified by science. But the die had been cast. In the current political climate, the “fat cat” cattle ranchers reminded folks of the tobacco industry, which had responded in much the same way when cigarettes first came under attack. Meanwhile, the grain lobbyists, as you can imagine, were in heaven.
The media had a field day, and they were not kind to the NAS. Mainstream apologist Jane Brody, who has written about food and nutrition for the New York Times for decades, accused the NAS board members of being “all in the pockets of the industries being hurt.” And because everyone on both sides of the argument had enormous amounts of money at stake, the debate between the beef industry and the grain industry was hardly a model of scientific objectivity. It was far more about image and public relations: The fat cat ranchers were portrayed as peddling unhealthy, “high-fat,” “artery-clogging” foods, while the grain farmers were seen as the “good guys,” on the side of science, health, granola, and the well-being of the American people. High-carb, low-fat cereals became the new health food, while high-fat meats were seen as poison, peddled by greedy cattle ranchers indifferent to the health of America. Basically, the anti-fat movement didn’t evolve out of science at all, but instead was a grassroots movement fueled by a distrust of the “establishment”—Big Food, Big Medicine, and Big Ranchers. It was also fueled by the countercultural bias against excessive consumption, represented in this case by big, fatty steaks and bacon and eggs.
We all know who won that public relations battle.
Think it’s a coincidence that the obesity and diabetes epidemics went into overdrive around the same time that we started pushing low-fat, high-carb diets as an alternative to those containing more fat and protein? We don’t.
The Snackwell Phenomenon
Low-fat had become the new mantra of the times, something we like to call the “Snackwell Phenomenon.” Food companies rushed to create low-fat versions of every food imaginable, all marketed as “heart-healthy,” with no cholesterol. (No one seemed to notice that manufacturers replaced the missing fat with tons of sugar and processed carbs, both of which are far more dangerous to our hearts than fat ever was.)
Butter was demonized and replaced with margarine, one of the most supremely stupid nutritional swap-outs in recent memory. Only much later did we discover that the supposedly healthier margarine was laden with trans fats, a really bad kind of fat created by using a kind of turkey baster to inject hydrogen atoms into a liquid (unsaturated) fat, making it more solid and giving it a longer shelf life. (Any time you read “partially hydrogenated oil” or “hydrogenated oil” in a list of ingredients, that means the food in question contains trans fats.) Unlike saturated fats from whole foods such as butter, trans fats (at least the manmade kind) actually do increase the risk for heart disease and strokes!
About 80 percent of trans fats in the American diet come from factory-produced partially hydrogenated vegetable oil.11 Yet vegetable oils were (and are!) aggressively promoted as the healthy alternative to saturated fats, even though most of these oils are highly processed, pro-inflammatory, and easily damaged when reheated over and over again, which is standard procedure in many restaurants.
Think it’s a coincidence that the obesity and diabetes epidemics went into overdrive around the same time that we started pushing low-fat, high-carb diets as an alternative to those containing more fat and protein? We don’t.
But by now, fat—and, by extension, cholesterol—had become the new bogeyman of the American diet, defended only by people who clearly had a horse in the race (e.g., the dairy and meat industries), and low-fat had become the new religion of the masses. Now it was left for the science to catch up. The National Institutes of Health (NIH) funded half a dozen studies that were published between 1980 and 1984, hoping it would find persuasive evidence that low-fat diets prolonged lives.
Let’s Go to the Videotape
The first four of these trials compared heart disease rates and diets in four locations: Honolulu, Puerto Rico, Chicago, and, most famously, Framingham, Massachusetts. Not one of these trials showed the slightest evidence that men who ate low-fat diets lived any longer, or had fewer heart attacks, than those who ate high-fat diets.
The fifth trial was the MRFIT study, a research project that cost $115 million and involved twenty-eight medical centers and 250 researchers. In the MRFIT study, 360,000 men, aged thirty-five to fifty-seven, from eighteen different U.S. cities were screened between 1973 and 1977, and eventually about 13,000 middle-aged, healthy men who were considered especially prone to heart disease were selected to participate. These 13,000 men were randomly assigned to one of two groups. The control group received no special instructions about diet or lifestyle and just continued on with whatever general medical care they received from their doctors. The intervention group, however, was urged to avoid eating fat, to quit smoking, to exercise, and to lower their blood pressure.
After seven years of follow-up, the intervention group had slightly lower blood pressure and cholesterol than the control group, but there was no difference in either cardiovascular mortality or all-cause mortality (scientific lingo for “total number of deaths no matter what the reason”). The intervention group had 17.9 deaths per one thousand men from cardio-vascular disease, and the control group had 19.3 deaths per one thousand men, a variation that did not amount to what researchers call statistical significance, meaning it was likely due to chance.
In addition, the data on overall mortality—death from any cause—was troubling. There were actually more deaths in the intervention group—from any cause—than there were in the control group! Remember, the real reason we want to avoid heart disease is so we can live longer; avoiding heart disease isn’t much of a victory if it means you die early from some other disease!
The researchers themselves described the results as “disappointing.” The only real reduction in overall mortality was seen with the people who stopped smoking, regardless of the group they were in.
Leaping to the Wrong Conclusion
The sixth of the NIH-funded trials, the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which was initiated in 1973, is worth mentioning because of an interesting leap of faith made by the investigators based on virtually no evidence. But this leap of faith became the cornerstone of anti-fat policy for decades to come. Here’s what happened.
Researchers from the National Heart, Lung, and Blood Institute measured cholesterol in almost one-third of a million middle-aged men and chose only those with the highest cholesterol levels for the study (about 4,000 men). They gave half of them a new cholesterol–lowering drug (cholestyramine), while the other half got a placebo. The medicine did indeed lower cholesterol levels in the men who had abnormally high levels to begin with, and it modestly reduced heart disease rates in the process. (The probability of suffering a heart attack during the seven to eight years of the study went from 8.6 percent in the placebo group to 7 percent in the group treated with cholestyramine, while the probability of dying from a heart attack dropped from 2 to 1.6 percent, not exactly jaw-dropping numbers.)
WHAT THE FRAMINGHAM HEART STUDY FOUND
One study mentioned most often by the 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 sixteen 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.
It gets better (or worse, depending on your position). When researchers went back and looked at the Framingham data thirty years after the project started, they found that once men passed the age of forty-seven, it didn’t make a whit of difference whether their cholesterol was low or high. Those with high cholesterol at age forty-eight lived just as long as, or longer than, those who have had low cholesterol. So if cholesterol is important only for the relatively few who have had a heart attack before the age of forty-eight, why are the rest of us worried about high-fat food and cholesterol levels?
The question is hardly academic. In 1992, forty-four years after the Framingham project began, study director William Castelli, M.D., wrote the following in an editorial in the Archives of Internal Medicine:
“In Framingham, Mass., 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 mostcholesterol, ate the most saturated fat, [and] ate the most calories weighed the least and were the most physically active [italics ours].”
Okay, cholesterol goes down, heart disease drops by a thimble, and the researchers conclude that lowering cholesterol lowers the risk of heart disease. But remember, this was a drug trial, not a diet trial. The researchers made a huge leap of faith by assuming that if lowering cholesterol is “good” (i.e., it reduces the risk of heart disease), it shouldn’t much matter how you lower it. Lowering it through diet should get you the same “good” result (if you can call the miniscule drop in heart disease that may or may not be related to the drop in cholesterol a “good” result). Their leap of faith was that we should recommend low-fat diets because they will achieve the same result as the drug—cholesterol will go down and everyone will live happily ever after.
But drugs often have many effects in addition to their main purpose. (Remember, Viagra was originally designed as a blood pressure medication!) The drug used in the LRC-CPPT might also have had some good effects, such as lowering inflammation, for example. Assuming that lowering cholesterol with a low-fat diet was identical to lowering it with a multifaceted medication that could in fact have had unintended benefits was a complete leap of faith and led to the wholesale recommendation of a low-fat diet for the prevention of heart disease.
That same year, the NIH held what’s called a “consensus conference” to basically justify the LRC-CPPT and the dietary recommendations that came out of it, yet it was anything but a consensus. Several experts pointed to significant defects in the studies and even called into question their accuracy. But you’d never know it from the final report, which made it seem like everyone had unquestioningly hitched their collective stars to the low-fat bandwagon.
Well, not exactly everyone.
CONSENSUS? NOT EXACTLY
George Mann, M.D., associate professor of biochemistry at Vanderbilt University College of Medicine and a participating researcher in the Framingham Heart Study, was one of the 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 NIH managers “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 United States are too high and should be lowered. Of course, this is exactly what was said.”
But the dissenting voices met with radio silence. With pompous certainty, the committee made clear in its final report that low-fat diets would afford significant protection against coronary heart disease for men, women, and children over two years old. “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.
As Dr. Phil might ask, “And how’s that workin’ for you?”
One study that attempted to answer this hypothetical question was the Women’s Health Initiative, the same program that has suggested that hormone therapy after menopause has more risks than benefits. This $415-million NIH study involved close to 49,000 people, aged fifty to seventy-nine, who were followed 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.
“These studies are revolutionary,” said Jules Hirsch, M.D., physician-in-chief emeritus at the Rockefeller University in New York City and an expert on how diets influence weight and health. The studies “should put a stop to this era of thinking that we have all the information we need to change the whole national diet and make everybody healthy.”
Of course, none of these questionable findings stopped the cholesterol-lowering, fat-avoiding juggernaut that went into full swing in the late 1970s and 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, M.D., author of The Cure for Heart Disease, wryly put it, “They were taking the bull by the horn—but it was the wrong bull.”
When we first met about this project, Steve brought to the meeting a series of papers by one of the most respected researchers in the world, Michel de Lorgeril, M.D., a French cardiologist and researcher at the prestigious National Centre for Scientific Research, the largest public organization for scientific research in France.
De Lorgeril has authored dozens of papers in peer-reviewed journals, and he was the lead researcher for the Lyon Diet Heart Study. The following quotation comes from his only book written in English, and it’s a perfect way to end this post:
“We can summarize . . . in one sentence: Cholesterol is harmless [italics ours]!”