The Great Cholesterol Myth (6 page)

BOOK: The Great Cholesterol Myth
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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.

Well.

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.”
10
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.

Did they?

Not exactly.

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.
12

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.
13

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.
16
)

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.
14
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
most
cholesterol, ate the
most
saturated fat, [and] ate the
most
calories weighed the least and were the most physically active [italics ours].”
15

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.”
17

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