Diet-Heart Hypothesis

By 1960, it had more than 300 chapters and brought in more than $30 million annually. With continued support from P&G and other food giants, the AHA would soon become the premiere heart disease group in the United States, as well as the largest not for profit group of any kind in the country. 

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By 1960, the AHA was investing hundreds of millions of dollars in research.The group had become the authoritative source of information about heart disease for the public, government agencies, and professionals alike, including the media."-Nina Teicholz - The Big Fat Surprise - Page 48

From 1954 to 1961, Roseto had nearly no heart attacks for the otherwise high-risk group of men 55 to 64, and men over 65 had a death rate of 1% while the national average was 2%. Widowers outnumbered widows, as well.[1]

These statistics were at odds with a number of other factors observed in the community. They smoked unfiltered stogies, drank wine "with seeming abandon" in lieu of milk and soft drinks, skipped the Mediterranean diet in favor of meatballs and sausages fried in lard with hard and soft cheeses. The men worked in the slate quarries where they contracted illnesses from gases and dust.[5] Roseto also had no crime, and very few applications for public assistance.[5]

The Framingham Study

George Mann, who came to the field in the early 1960s, achieved a remarkable degree of success before he mired himself in controversy by studying the Masai. He was, in fact, an associate director for one of the most famous heart disease investigations ever undertaken: the Framingham Heart Study. Framingham is a small town near Boston, Massachusetts, that has been a virtual petri dish for the study of heart disease since 1948. Now on its third generation of research subjects, it began with some five thousand middle-aged men and women who took part in a survey of every factor researchers could think of that might play a role in the development of heart disease. Participants subjected themselves to comprehensive physicals, interviews, and follow-up tests every two years. It was the first large-scale attempt to find out whether risk factors such as cigarette smoking, high blood pressure, and genes might reliably predict death from heart disease.

In 1961, after six years of study, the Framingham investigators announced their first big discovery: that high total cholesterol was a reliable predictor for heart disease. This is considered one of the most significant findings in the history of heart disease research because before then, even though experts had come to assume serum cholesterol was bad, the evidence was only circumstantial.

The news had broad implications. For one, it solved a problem that had plagued heart disease research from the start, namely, that investigators needed something they could measure to assess heart attack risk before death. It may seem callous to say, but when trying to detect the cause of disease, death is the ideal end point to study. Researchers prefer to follow subjects, looking at what they eat, whether they smoke, and other factors, until they die. Death is the “event,” or “hard end point,” in the language of research; it is the indisputable data at the end of an experiment. (Heart attacks are also considered “hard” end points, but even these are subject to diagnostic uncertainty, as we’ve seen.) Looking back from the undeniable fact of death, researchers can then ask, “Was it how much bacon they ate, or the cigarettes, or something else?”

Waiting for subjects to die, however, means that researchers are burdened with following a population over many years. Finding an “intermediary” or “soft” end point to measure before death has therefore been the subject of a great science hunt. If an indicator could reliably predict heart disease, researchers could run shorter experiments and measure those intermediary factors instead. The identification by Framingham of total cholesterol as a soft end point was therefore seen as a breakthrough for the field: scientists could now presumably conclude that any food that raised total cholesterol would also increase the risk of a heart attack. In all likelihood, doctors could use this factor in helping patients to identify their coronary risk as well.

The Framingham finding about cholesterol was thus highly important. And above all, it seemed to erase any lingering doubts that researchers might have had about the diet-heart hypothesis. William Kannel, the medical director of Framingham, was quoted in a local newspaper as saying, “That blood cholesterol is somehow intimately related to coronary atherosclerosis is no longer subject to reasonable doubt.”

However, thirty years later, in the Framingham follow-up study—when investigators had more data because a greater number of people had died—it turned out that the predictive power of total cholesterol was not nearly as strong as study leaders had originally thought. For men and women with cholesterol between 205 and 264 milligrams per deciliter (mg/dL), no relationship between these numbers and heart disease risk could be found. In fact, half of the people who had heart attacks had cholesterol levels below the “normal” level of 220 mg/dL. And for men aged forty-eight to fifty-seven, those with cholesterol in the midrange (183–222 mg/dL) had a greater risk of heart attack death than those with higher cholesterol (222–261 mg/dL). Total cholesterol turned out not to be a reliable predictor for heart disease after all.

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The Framingham data also failed to show that lowering one’s cholesterol over time was even remotely helpful. In the thirty-year follow-up report, the authors state, “For each 1% mg/dL drop of cholesterol there was an 11% increase in coronary and total mortality [italics added].” This is a shocking finding, the very opposite of the official line on cholesterol lowering. Yet this particular Framingham finding is never discussed in scientific reviews, even though many large trials have found similar results.

Other important findings from Framingham have also been ignored, including—notably—those on dietary risk factors, which were examined in the part of the study that Mann conducted. Together with a dietician, Mann spent two years collecting food-consumption data from one thousand subjects, and when he calculated the results in 1960, it was very clear that saturated fat was not related to heart disease. Concerning the incidence of coronary heart disease and diet, the authors concluded, simply, “No relationship found.”

“That went over like a wet blanket with my superiors at NIH,” Mann told me, “because it was contrary to what they wanted us to find.” The NIH also generally favored the diet-heart hypothesis from the early 1960s on, and “they wouldn’t allow us to publish that data,” he says. Mann’s results lay in an NIH basement for nearly a decade. (To withhold scientific information “is a form of cheating,” Mann lamented.) And even when the findings eventually came out in 1968, they were so deeply buried that a researcher has to dig through twenty-eight volumes to find the news that variations in serum cholesterol levels could not be traced back to the amount or type of fat eaten.

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- Nina Teicholz - page 64

Time magazine memorably captured this thinking again in 1961 when it kicked off the apalling mistake of what became the low-fat diet movement with an influential cover story on the University of Minnesota nutritionist Ancel Keys. Just as Newburgh was central to disseminating the notion that the only meaningful difference between the fat and the lean is in their ability to control their appetite, Keys managed to convince medical authorities worldwide that we get heart disease because we eat too much fat or at least too much saturated fat. Time’s story on Keys and the evils of fat—both dietary and body fat—quoted the textbook Harrison’s Principles of Internal Medicine referring to “the most common form of malnutrition” as “caloric excess or obesity,” as though the two were one and the same. The Time article then observed that obesity in Puritan New England was seen as sinful, implying that perhaps it should still be, and quoted Keys saying, “Maybe if the idea got around again that obesity is immoral, the fat man would start to think.” The ridiculous implication, of course, was that if we did think about it (or if that self-indulgent, menopausal housewife did, rather than nibbling bonbons while she played bridge with her lady friends), we’d stop eating too much or at least stop eating immoderately; we’d control our portion sizes and our cravings and be lean. Our problem would be solved. Whether they know it or not, every doctor, every dietitian and physical trainer and friendly neighbor and sibling, every figure of authority who has ever counseled that we eat less and exercise more to lose weight, that we count our calories and so try to consume fewer than we expend, is wedded to this idea that the lean and the eventually-to-become-obese are physiologically identical; only their behavior sets them apart. This belief system has dominated our thinking on obesity since the 1950s, and we have to leave it behind. There are so many things wrong with this idea, things that were already known to be wrong in 1961 and even 1931, that it’s hard to enumerate all of them. One of the most obvious problems with this thinking is that the logic is circular. Some very good obesity researchers pointed this out repeatedly in the mid-twentieth century, but these physicians-and-nutritionists-turned-moralists didn’t seem to care. If we get fatter, more massive, we are clearly taking in more energy than we expend, and yes, the excess is stored as fat (although technically as fat and some muscle or lean tissue to support it and move it around as necessary). So we must be overeating during this fattening process. But that tells us nothing about the cause. Here’s the circular logic: Why do we get fat? Because we’re overeating. How do we know we’re overeating? Because we’re getting fatter. And why are we getting fatter? Because we’re overeating. Logicians know this kind of round-and-round logic as tautology. It’s saying the same thing in two different ways but offering no explanation for either. If we’re getting fatter, it means our body mass is increasing, our energy stores are increasing, and so we are indeed taking in more energy—calories—than we expend. Okay, we’re overeating. But by the same token, if we’re getting taller we’re taking in more calories than we expend. But nobody would say we get taller because we overeat. If we’re getting richer, we’re making more money than we’re spending. But nobody would say we get rich because we overearn. That’s clearly absurd, even if overearning is what’s happening as we get rich, which it is—by definition. So why is this kind of circular explanation considered acceptable for obesity? It only appears to be an explanation. There is no causal information.

Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 664-668). Knopf. Kindle Edition. 

CURRENT available knowledge is sufficient to warrant a general statement regarding the relation of diet to the possible prevention of atherosclerosis (Appendix I).

A heart attack, also called coronary thrombosis or myocardial infarction, or just plain "coronary," is almost always caused by atherosclerosis (arteriosclerosis or hardening of the arteries). Stroke, or apoplexy, is often caused by the same condition. The problem of preventing or retarding these diseases is, then, one of preventing or retarding atherosclerosis.

How Does Atherosclerosis Develop?—  Athero-Atherosclerosis is a complex disease of the arteries. It is known that a number of factors influence or are related to its development. Among these factors are a high content in the blood of a type of fat called cholesterol, elevation of blood pressure above normal, presence of diabetes, obesity, and a habit of excessive cigarette smoking. Age, sex, and heredity are also important.

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"The AHA committee swung around in favor of Keys,Stamler's ideas, and the resulting report in 1961 argued that "the best available evidence available at the present time" suggested that Americans could reduce their risk of heart attacks and strokes by cutting the saturated fat and cholesterol in their diets.
The report also recommended the "reasonable substitution" of saturated fat with polyunsaturated fats such as corn or soybean oil. This so-called "prudent diet" was still relatively high in fat overall. In fact, the AHA would not stress the reduction of total fat until 1970, when Jerry Stamler steered the group in this direction. For the first decade, however, the group's focus was primarily on reducing the consumption of the saturated fats found in meat, cheese, whole milk, and other dairy products. The 1961 AHA report was the first official statement by a national group anywhere in the world recommending that a diet low in saturated fats be employed to prevent heart disease."

-Nina Teicholz - Big Fat Surprise - page 50

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"Less than four years later, the evidence hadn’t changed, but now a sixman ad-hoc committee, including Keys and Jeremiah Stamler, issued a new AHA report that reflected a change of heart. Released to the press in December 1960, the report was slightly over two pages long and had no references.*6 Whereas the 1957 report had concluded that the evidence was insufficient to authorize telling an entire nation to eat less fat, the new report argued the opposite—“the best scientific evidence of the time” strongly suggested that Americans would reduce their risk of heart disease by reducing the fat in their diets, and replacing saturated fats with polyunsaturated fats. This was the AHA’s first official support of Keys’s hypothesis, and it elevated high cholesterol to the leading heart-disease risk. Keys considered the report merely an “acceptable compromise,” one with “some undue pussy-footing” because it didn’t insist all Americans should eat less fat, only those at high risk of contracting heart disease (overweight middle-aged men, for instance, who smoke and have high cholesterol)."

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-Gary Taubes - Good Calories Bad Calories - Chapter 1