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Book Notes: 'The Case Against Sugar' by Gary Taube

In the last few weeks, I read The Case Against Sugar by Gary Taubes.

I found it to be compelling (more on that in a moment) and I want to be impacted by them. I want the daily decisions that I make to be subtly influenced by this author and these books.

Related but in a different vein, Nat Ellison has his collection of book notes. Derek Sivers has his. Patrick Collison has a list of books he recommends. I’ve got my own list of recommended books, but I’ve wanted to dive a bit deeper on some of them. So, like Nat Ellison and others, I’m grab-bagging quotes (helpfully brought over from highlights on my Kindle) and some thoughts interspersed between.

I’ve not settled (yet) on a format I like, but as in most things, this is an iterative process. These notes may be useful to others (at least to help them decide if the book is worth reading) but primarily this is a helpful process to me.

After reading The Case Against Sugar, I read (and did a write-up of) Why We Get Fat: And What To Do About It

Notes on formatting

I’ve included broad quotes from the book; headings, non-quoted text, bold/italicized text, etc all my addition to help with the skimming, unless I indicate otherwise.

The Case Against Sugar

The dominant views of obesity and weight have problems

Starting this out with a strong shot across the bow, Taubes argues that the “modern” understanding about why we get fat falls into two dominant approaches, and both are catastrophically wrong.

Since the 1930s, to summarize briefly, nutritionists have embraced two ideas that ultimately shaped our judgments about what constitutes a healthy diet. These would be the pillars on which the foundation of nutritional wisdom about the impact of foods — including sugar — on obesity, diabetes, heart disease, and other chronic diseases would be based. They were both products of the state of the science of the era; they were both misconceived, and they would both do enormous damage to our understanding of the diet-disease relationship and, as a result, the public health.

The first idea was that the fat in our diets causes the chronic diseases that tend to kill us prematurely in modern Western societies.

At its simplest, this focus on dietary fat — specifically from butter, eggs, dairy, and fatty meats — emerged from a concept that is now known as a nutrition transition: As populations become more affluent and more urban, more “Westernized” in their eating habits and lifestyle, they experience an increased prevalence of these chronic diseases. Almost invariably, the dietary changes include more fat consumed (and more meat) and fewer carbohydrates…

The second pillar of modern nutritional wisdom is far more fundamental and ultimately has had far more influence on how the science has developed, and it still dominates thinking on the sugar issue. As such, it has also done far more damage. To the sugar industry, it has been the gift that keeps on giving, the ultimate defense against all arguments and evidence that sugar is uniquely toxic. This is the idea that we get obese or overweight because we take in more calories than we expend or excrete.

By this thinking, researchers and public-health authorities think of obesity as a disorder of “energy balance,” a concept that has become so ingrained in conventional thinking, so widespread, that arguments to the contrary have typically been treated as quackery, if not a willful disavowal of the laws of physics.

According to this logic of energy balance, of calories-in/calories-out, the only meaningful way in which the foods we consume have an impact on our body weight and body fat is through their energy content — calories. This is the only variable that matters. We grow fatter because we eat too much — we consume more calories than we expend — and this simple truth was, and still is, considered all that’s necessary to explain obesity and its prevalence in populations.

This thinking renders effectively irrelevant the radically different impact that different macronutrients—the protein, fat, and carbohydrate content of foods—have on metabolism and on the hormones and enzymes that regulate what our bodies do with these foods: whether they’re burned for fuel, used to rebuild tissues and organs, or stored as fat.

By this energy-balance logic, the close association between obesity, diabetes, and heart disease implies no profound revelations to be gleaned about underlying hormonal or metabolic disturbances, but rather that obesity is driven, and diabetes and heart disease are exacerbated, by some combination of gluttony and sloth.

It implies that all these diseases can be prevented, or that our likelihood of contracting them is minimized if individuals - or populations - are willing to eat in moderation and perhaps exercise more, as lean individuals are assumed to do naturally. Despite copious reasons to question this logic and, as we’ll see, an entire European school of clinical research that came to consider it nonsensical, medical and nutrition authorities have tended to treat it as gospel.


Breakfast Cereal companies have been sketchy for a while

Next time you walk down the cereal isle of an American supermarket, think of this section:

[He] then began the trend of rationalizing how a company positioned as a producer of health foods could justify selling a cereal coated in sugar. Echoing the logic of Jim Rex, Post executives would argue that pre-sweetened cereal actually contained less sugar than what children would add on their own.

By adding sugar, Post was merely “trading off sugar carbohydrates for grain carbohydrates and sugar and starch are metabolized in exactly the same way.” Biochemists had already demonstrated that this was untrue, but it was not widely known.

Either way, Post argued that “the nutritional value of the product” remained unchanged, with sugar calories replacing those from cereal grains. Sugar Crisp (now called Golden Crisp) sold spectacularly well, forcing the rest of the industry to play catch-up.

Nabisco quickly released Ranger Joe nationwide, now renamed Wheat and Rice Honeys. Kellogg’s, in 1950, released Sugar Corn Pops, even though most of the company stock was still held by the W. K. Kellogg Foundation, “a charitable organization established to promote children’s health and education.”

Kellogg’s set out to produce a sugar-coated version of its iconic cornflakes as if “it was their salvation,” releasing Sugar Frosted Flakes in 1952 and Sugar Smacks, a direct competitor to Post’s Sugar Crisp, a year later.

Kellogg’s failed to produce a sugar-coated oat cereal and turned to chocolate instead. The company logic, again guided by nutritionists, was that “all this sweetness is not the best for children, [and] that bittersweet chocolate was good and healthy and it wouldn’t be harmful to them.” The result was Cocoa Krispies.

When the first, bittersweet-flavored version didn’t sell, the company added even more sugar. “The new cereal,” as one Kellogg’s salesman put it, “was a dietary flop, and a sales bonanza.”

General Mills executives worried about the “possible dietary effects” of sugar-coated cereals, and its in-house nutritionist delayed the company’s entry into the pre-sweetened market for years, but eventually they were overruled.

The marketing team at General Mills argued that if the company didn’t compete, it wouldn’t survive. In 1953, General Mills released Sugar Smiles, a mixture of Wheaties and sugar-frosted Kix; by 1956, they had released three more sugar-coated cereals—Sugar Jets, Trix, and Cocoa Puffs.

Is ‘the sugar industry’ really a thing?

Vilifying sugar can seem a bit tinfoil-hat-esque

By the mid-1930s, when the U.S. Congress passed the Sugar Act, which would stay in force, with amendments, for forty years, the domestic sugar industry was distributed so widely — beet sugar in the Northern, Central, and Western states; cane in the South; refiners on the coasts; and the candy, soda, and paint industries (sugar is an essential ingredient in paint) — that President Franklin Roosevelt was calling the sugar lobby, according to The New York Times, “the most powerful pressure group that had descended on the national capital during his lifetime.”

The Sugar Act effectively guaranteed that producing and refining sugar in the United States would always be a profitable business. It established the price of raw sugar (typically higher, if not significantly so, than world prices), put limits on domestic production, and set quotas on imports.

The Sugar Act also allowed for subsidies to be paid to producers either for the sugar they didn’t produce or the sugar they couldn’t sell - “benefit payments to domestic producers,” in the words of the Times. As a result, consumers were invariably paying more for sugar than would have been the case without the quotas and price supports. And yet that didn’t stop us from buying sugar.


The sugar industry built a research arm to support its goals; the research arm would shape research and legislation. Some of the key players in this enterprise would use the same tactics promoting the idea that cigarettes are safe. (Or, rather, “we cannot be sure that they’re dangerous”)

The Sugar Research Foundation, befitting its name, would not indulge in any of the questionable activities that led to the demise of [it’s predecessor,] the Sugar Institute. Rather, it would focus on the single major challenge that the entire industry had in common - “the defense of sugar as a food and the expansion of post-war markets for sugar.”

The dilemma for such an organization is one that would become common to all such industry-funded research programs and, most notably, those of the tobacco industry: how to defend and promote the use of a product - sugar, in this case - while simultaneously funding research that is ostensibly meant to secure all known facts about the product and its effect on human health. Because this research could elucidate the problematic aspects of sugar, the two goals could turn out to be mutually exclusive.

Executives of the sugar industry might hope this would never happen, but there was no guarantee. If results of the research in any way challenged “the defense of sugar,” the organization would have to find a way to spin its research and its program of education to make it appear as though it didn’t.

By 1951, the Sugar Research Foundation, by then renamed the Sugar Association Inc. (SAI), had distributed three million dollars in research grants throughout the highest levels of academia — from Princeton and Harvard on the East Coast to the California Institute of Technology on the West.

At a time when academic researchers were encouraged to work closely with industry, the SRF/SAI grants went to some of the most prominent researchers in nutrition, carbohydrate chemistry, and metabolism. The program was exceptional, and the grants themselves would regularly be written up in Science and other influential scientific journals.

The first award went to the Massachusetts Institute of Technology (MIT): $125,000 to fund five years of research on carbohydrate metabolism. The MIT researchers would look for new industrial uses for sugar, while training a generation of young scientists in carbohydrate chemistry.

MIT announced the grant along with the news that Robert Hockett, an assistant professor of chemistry, would take a leave of absence from the university to become scientific director of the SRF/SAI. The president of MIT would later say that he hoped this collaboration with the sugar industry would be a model for how industry and universities worked together in the future, and to a great extent it was.

Robert Hockette later served as scientific director for the Council for Tobacco Research, per this next section:

In the early 1970s, Hockett served as scientific director for the Council for Tobacco Research.

In that role, he dealt with the dilemma of funding research while simultaneously promoting consumption of the product by threatening at least one investigator with a cessation of his funding if he didn’t spin the interpretation of the evidence to make it less obvious that cigarette smoke was carcinogenic.


In 1951, the American Sugar Refining Company launched an intensive advertising campaign…stressing how important it was for children, in particular, to benefit from the energy contained in pure sugar.

Three years later, the Sugar Association took over the effort, working through its public-relations arm, Sugar Information, Inc., which would now be dedicated to communicating the proposition that sugar was an indispensable food in any diet. The Sugar Association budgeted $1.8 million for a three-year advertising blitz—an “educational campaign”—and hired the legendary Leo Burnett advertising agency in Chicago to craft it.

[…]

Burnett’s agency was famous, among other things, for the Jolly Green Giant, Tony the Tiger, the Pillsbury Doughboy, and the Marlboro Man. In 1998, Time magazine listed Burnett, the “Sultan of Sell,” as among the hundred most influential people of the twentieth century.


While physicians at Harvard, Cornell, and Stanford medical schools were now publishing in the medical journals anti-obesity diets that advocated avoiding sugar and sweets entirely, as did the occasional medical textbook, the sugar industry, reported The Times, was dead set on convincing the public that its product was anything but fattening. Sugar Information, Inc., with the help of Leo Burnett, would do so by taking advantage of two assumptions of the nutritionists themselves.

The first, as we discussed, was that obesity was caused by the excess consumption of all calories. If so, there was nothing unique about sugar. It was “neither a ‘reducing food’ nor a ‘fattening food,’ ” as the sugar-industry advertisements were now proclaiming.

Assumption number two was based on the idea that hunger is a response either to low blood sugar or to the diminished utilization of glucose for fuel by the central nervous system. (The latter was an idea of Jean Mayer, working in Fred Stare’s department at Harvard, and funded, at least in part, by the Sugar Association.)

Both assumptions would be repeatedly refuted in experiments and would remain at best controversial for another twenty years, but nutritionists had a tendency, as they still do, to hold on to their hypotheses once adopted, regardless of the evidence that might accumulate against them. These ideas continued to suggest that foods that had the ability to raise blood sugar quickly or to be metabolized quickly - as sugar did and was - would be particularly effective at staving off hunger and thus overeating.


An article expressing a negative view of sugar almost appeared in Readers Digest. Almost.

Mayer had published an article in June 1976 in The New York Times Magazine - “The Bitter Truth About Sugar” - linking sugar not just to cavities and tooth decay but to obesity and type 2 diabetes, what Mayer called the “fat-and-forty type” of diabetes because of its association with obesity and aging.

For children, Mayer suggested, sugar is quite possibly as addictive as tobacco. “The limited bill against sucrose which can be documented is sufficient to justify a drastic decrease in our consumption”, Mayer had written.

At the Scottsdale meeting, four months after the Times had published Mayer’s article, Tatem described how the Sugar Association had come to learn that Reader’s Digest was planning to run an excerpt of it.

Tatem and his colleagues had then managed to kill the excerpt, he said, first with an hour-and-a-half call to a Reader’s Digest editor, followed by a three-page telegram to the managing editor himself.

Mayer’s article, according to the telegram, which was distributed to board members at the meeting, was a “scientific farce and a journalistic disgrace,” and the Sugar Association could say this because “not one shred of substantiated, admissible scientific evidence exists linking sugar to the death-dealing diseases.”

This was the story that the sugar industry believed, and this was the story the Sugar Association was now widely selling to the American public. “We have moved to the defensive - the defense of our primary product,” Tatem said. “In confronting our critics we try never to lose sight of the fact that no confirmed scientific evidence links sugar to the death-dealing diseases. This crucial point is the lifeblood of the Association.”


Sugar and the FDA, getting cyclamates and saccharin banned

The ‘threat’ mentioned below was non-caloric sweeteners displacing sugar in food.

Publicly, the sugar industry would address the threat by looking for ways to diversify their products—continuing to fund research on the use of sugar in paints, detergents, water purification, and cigarettes, among other items—but none of these held the promise of replacing the sugar sales that were in danger of being lost to artificial sweeteners.

Privately, the industry would try to generate the evidence that the FDA needed to put the competition out of business. Although industry executives were remarkably open about this strategy, at least once it was showing signs of success.

In 1969, after the Sugar Association created the International Sugar Research Foundation, John Hickson, the Foundation’s vice president, described the sugar industry’s position as

find new arguments to use as leverage to force the FDA to fulfill its regulatory functions or expect to see major fractions of its markets taken over.

To The New York Times, Hickson phrased this position in slightly more colloquial terms:

If anyone can undersell you nine cents out of 10,

he said, speaking of cyclamates and saccharin,

you’d better find some brickbat you can throw at him.

That brickbat, to be precise, was a 1958 amendment to the Pure Food and Drugs Act that had been passed by Congress twenty years earlier.

The original act had mandated that the FDA approve any new ingredient in processed foods as safe before it could be used, specifying that the only criterion for approval was safety. If a product had a safety risk, no amount of benefit from its use would work in its favor. There would be none of the trade-offs that Roosevelt had perceived or Philip Handler would later describe.

A New York congressman named James Delaney chaired the congressional committee responsible for the 1958 amendment, and Delaney had recently lost a close relative to cancer. Hence, the amendment came with what would come to be called the “Delaney clause,” specifying that “no additive shall be deemed to be safe if it is found to induce cancer when ingested by man or animal.”

The 1958 amendment had also allowed the FDA to exempt some seven hundred existing substances from the approval process on the grounds that they were “generally recognized as safe,” a designation that depended on the opinions of experts with the appropriate qualifications.

These substances, which included both cyclamates and saccharin, had what would come to be known as GRAS (generally recognized as safe) status: the industry could freely use and sell them as food additives, but if new evidence came along to raise questions about their safety, the FDA would have to reassess these as well.

Between 1963 and 1969, the Sugar Association spent more than two-thirds of a million dollars (over four million today) on research designed to force the FDA to remove cyclamates from the GRAS list and have them banned.

Much of the funding went to then obscure research organizations such as the Wisconsin Alumni Research Foundation (WARF) and the Worcester Foundation for Experimental Biology. The researchers at these foundations would look at the effects of saccharin or cyclamates on ingestion and excretion, metabolism, blood transport, drug interactions, the stunting of growth, cell or chromosomal damage that might lead to cancer, on sex hormones, birth defects, behavior, and even gastric distress.

The aim was to find something that could prompt the FDA to reassess the GRAS status of these artificial sweeteners. If nothing else, the research reports from these institutions would keep cyclamates and saccharin in the news as a potential health hazard and increase consumer anxiety about their safety.

In May 1965, the FDA published its first review of the medical literature on cyclamates and concluded that there was little to fear.

Five months later, the Sugar Association announced that WARF had published a one-page letter in the prestigious journal Nature suggesting that cyclamates could stunt the growth of rats—at least when the rats consumed these noncaloric sweeteners in quantities equivalent to hundreds of twelve-ounce cans of diet soda daily. This was the only study the WARF researchers would publish on cyclamates, but the two researchers involved (apparently the president and head of the biological department at WARF) continued their research through the early 1970s, first on cyclamates and then on saccharin.

They reported directly to the Sugar Association and paid multiple visits to the FDA to discuss their unpublished results and why they believed that cyclamates should be banned from public use of any kind, suggesting to the FDA investigators that cyclamates were capable of causing everything from birth defects to “mental disturbance.”


If all the “modern” science is suspect, has there ever been a correct understanding of nutrition, sugar, etc?

Yes. Pre-WWII nutrition research in Europe was good, and informs most of the author’s views on diet and nutrition. The research saw the obesity as a hormonal regulatory disorder; it’s ignored/lost today. Why?

[This body of literature existed…] Then it virtually vanished. As the German and Austrian medical-research communities evaporated with the rise of Hitler and the devastation of the Second World War, the notion of obesity as a hormonal regulatory disorder effectively evaporated with it.

The primary German textbook on endocrinology and internal medicine in the 1950s still included a discussion of this thinking, but that textbook never saw an English translation, which is significant, since the lingua franca of medical science had now shifted from German prewar to English afterward.

The German-language journals from the prewar era, and with them the best scientific thinking of the era in all the disciplines relevant to both obesity and diabetes—including metabolism, endocrinology, nutrition, and genetics—would no longer be read, nor would they be referenced.

In the United States, which would now dominate medical research for decades, physicians treating obese patients in their clinics and researchers studying it in the laboratory embraced the ideas of Louis Newburgh as documented facts. “The work of Newburgh showed clearly,” they would say in seminars, or “Newburgh answered that” would be the response to any suggestions that obesity was caused by anything other than a perverted appetite.


There’s research on diet. There’s also value in correlation and the change in health in populations over time. The book spends non-trivial time on the topic.

The logic that sugar was likely to be causally involved was based on a series of propositions:

First, that the prevalence of heart disease was increasing in Western nations (whether as dramatically as some believed or not) and increased with affluence; it was higher in developed nations than undeveloped.

Second, that the same was true of the prevalence of diabetes, obesity, and hypertension (high blood pressure).

Third, that these disorders are intimately related: the obese are likely to be diabetic and hypertensive and have heart attacks; those who have heart attacks are likely to be hypertensive and obese and/or diabetic; diabetics are very likely to be obese and hypertensive and very likely to die of heart attacks.

So, whatever the causal factor was, it was likely to be something that accompanied affluence and was an integral part of Western diets or lifestyles, and something that could cause all these diseases, not just heart disease alone.


The “eating fat makes you fat” movement

Through the 1960s and 1970s, researchers launched ever more elaborate and expensive trials in which the subjects were randomized to diets of differing amounts or types of fat and then followed for a year or several years to see the effect: Did they have more or less heart disease or cancer?

Did they live longer or tend to die prematurely?

Those trials would consistently fail to confirm that eating less fat or replacing saturated fat with polyunsaturated fat could prolong lives. No such equivalent effort would be pursued in testing sugar.


The sugar industry spent lots of money on shiny things for the premier research institutions of the day

The point man for the Sugar Association’s Food and Nutrition Committee was Fred Stare, founder and longtime chairman of the department of nutrition at the Harvard School of Public Health.

The sugar industry had been supporting Stare and his department since the early 1940s, and the International Sugar Research Foundation estimated that its grants to Stare (to study the relationship between blood sugar, appetite, and obesity) had resulted in the publication of thirty research articles and reviews between 1952 and 1956 alone.

In 1960, when Stare’s nutrition department broke ground on a new five-million-dollar building, it was paid for largely by private donations, including the “lead gift,” as Stare described it, of $1.026 million from the General Foods Corporation, the maker of Kool-Aid and the Tang breakfast drink.

By the late 1960s, Stare had become, in academia, the most public defender of sugar — it was not even “remotely true,” he would write, “that modern sugar consumption contributes to poor health” — while his department received funding from the sugar industry, the National Confectioners Association, Coca-Cola, PepsiCo, and the National Soft Drink Association. (Tobacco - industry documents reveal that Stare’s department, at his request, also received money from the Tobacco Research Council, specifically to fund projects that might exonerate cigarettes as a cause of heart disease.)

Stare freely acknowledged that he did not use sugar in his coffee or cereal; he was saving the calories, he said, for a martini at night. But he also argued that it was unsound “and may be hazardous” to recommend that anyone, including children, avoid sugar, on the grounds that if they did they would be likely to replace it with saturated fat, “and that, I hope, everyone will agree, is not desirable.”


In November 1976, Stare’s copious conflicts of interest were finally exposed in an article by Michael Jacobson, founder of the Center for Science in the Public Interest, and two colleagues, entitled “Professors on the Take.”

“In the three years after Stare told a Congressional hearing on the nutritional value of cereals that ‘breakfast cereals are good foods,’ ” Jacobson and his colleagues wrote, “the Harvard School of Public Health received about $200,000 from Kellogg, Nabisco, and their related corporate foundations.” (“A lot of the public, and unfortunately some of my colleagues, think I’m a monster,” Stare would later acknowledge, “a paid tool of the food industry.”)

By 1976, however, Stare was no longer necessary for the public-relations campaign, and the Sugar Association could turn to an FDA document that took up where “Sugar in the Diet of Man” left off.


In 1986, the FDA returned to the question of whether sugar should be generally recognized as safe. Three FDA administrators, led by Walter Glinsmann (who would later become a consultant for the Corn Refiners Association), now took up the job that the SCOGS committee had left off in 1976. After reviewing the evidence once again, these FDA administrators determined that “no conclusive evidence demonstrates a hazard to the general public when sugars are consumed at the levels that are now current.”

The FDA assessment then became the official government position on sugar, its logic and conclusions echoed in a series of official reports on diet and health that came after — particularly the 1988 Surgeon General’s Report on Nutrition and Health and the 1989 National Academy of Sciences report Diet and Health, which are the two seminal documents on the subject in the last half-century, and even reviews by the Institute of Medicine as late as 2005.

All of these official documents focused on fat as the root of dietary evils: The “disproportionate consumption of food high in fats,” according to the Surgeon General’s report, played a prominent role in five of the ten most common causes of death and thus could be held chiefly responsible for two-thirds of the 2.1 million deaths in the United States that year. All repeated the FDA’s conclusion that the evidence linking sugar to chronic disease was inconclusive, and then effectively equated “inconclusive,” as the Sugar Association did, with “nonexistent.” (As of March 2016, the Sugar Association Web site was still misquoting the FDA report to make that point.)


In 1986, the average American consumed forty-two pounds of sugar a year. Today, the number is closer to 120 pounds.

In their 1986 report, Glinsmann and his colleagues estimated the levels at which sugar was currently consumed to be forty-two pounds of sugar per person per year, or the equivalent every day of the amount of sugar in eighteen ounces — a can and a half — of Coke or Pepsi.

This was only slightly more than half of what the USDA was estimating at the time — seventy-five pounds per capita — and significantly less than half (44 percent) of what the USDA estimated we were consuming by the early twenty-first century, ninety pounds per capita.

Even the most ardent critics of sugar would probably be content if Americans consumed only forty-two pounds of added sugar and high-fructose corn syrup each year on average, but the evidence suggests we consume significantly more.


Nutrition science convinced that high-fat diets were bad

What happened after that tells us a lot about the particular pitfalls of nutrition science and public-health policy and how they interact.

Instead of the billion-dollar test of the dietary-fat hypothesis, the NIH invested a quarter-billion dollars in two trials that tested variations on the same theme, or links in a hypothetical chain of reasoning.

The first trial would test the supposition that men with high cholesterol levels who were told to eat a low-fat diet (and also took blood-pressure medication and received counseling to quit smoking, if either of these was necessary) would live longer than men who weren’t.

The results of this study were published in 1982 and failed to confirm the hypothesis.

The men on the low-fat diet suffered more deaths than the men who were left to their own devices. (The investigators refused to believe that a low-fat diet could be harmful, and certainly not the smoking cessation, so they concluded, questionably, that the blood-pressure medication had unforeseen side effects and caused more deaths than it prevented.)

The second trial tested the hypothesis that a cholesterol-lowering medication given to men with very high levels of cholesterol would lengthen their lives, compared with men who took no such medication. The results of this study, published in 1984, indicated that the medication helped, albeit just barely.

The authorities at the National Institutes of Health then took what amounts to a leap of faith. (“It’s an imperfect world,” as one of the NIH administrators later phrased it. “The data that would be definitive are ungettable, so you do your best with what is available.”)

Concerned, as they were, that hundreds of thousands of Americans were dying of heart disease yearly, they assumed that if a drug that lowered cholesterol would extend the lives of men with very high cholesterol, then a diet that also lowered cholesterol would do the same for all the rest of us.

Equally important, they assumed that the benefit of communicating this leap of faith on a nationwide scale was worth the risks.

In 1984, attended by considerable controversy, they initiated a massive public-relations campaign to induce every American over the age of two to eat a low-fat diet.

We’ve been living with the consequences ever since. Had scientific progress stopped there, we wouldn’t know whether the leap of faith was justified. But we do.

The NIH eventually spent between half a billion and a billion dollars, depending on the estimate, testing the hypothesis that a low-fat diet would prevent chronic disease in women and bestow on them a longer life.

The authorities involved had little doubt that it would, and were responding to political pressure to include women in medical trials; women had been underrepresented until then. The trial, known as the Women’s Health Initiative, was launched in the early 1990s, and the results were reported in 2006.

Once again, it failed to confirm the hypothesis. The roughly twenty thousand women in the trial who had been counseled to consume low-fat diets (and to eat more fruits, vegetables, and whole grains, and less red meat) saw no health benefits compared with the women who had been given no dietary instructions whatsoever.

Once again, the researchers involved and the public-health authorities chose not to perceive this negative result as reason to question their belief that fat causes heart disease and that low-fat diets will prevent it. Rather, they chose to assume that the trial—the largest such randomized trial ever done—simply failed to get the right answer, or would have gotten the answer they expected (“statistically significant,” in the scientific jargon) had the study lasted longer or included more subjects, or had the women in the trial done a better job of adhering to a low-fat diet.

These authorities had now spent decades (nearly half a century, in the case of the American Heart Association) telling us that dietary fat was killing us. Thus they found it easier to accept, or at least easier to communicate, the notion that the study had failed (or almost but not quite succeeded) than that their preconceptions about diet and the dietary advice they had been giving, based largely on that initial leap of faith, had been incorrect.


Metabolic Syndrome (mechanism by which we actually get fat)

The medical research community came to recognize that insulin resistance and a condition now known as “metabolic syndrome” is a major, if not the major, risk factor for heart disease and diabetes.

Before we get either heart disease or diabetes, we first manifest metabolic syndrome. The CDC now estimates that some seventy-five million adult Americans have metabolic syndrome.


Metabolic syndrome ties together a host of disorders that the medical community typically thought of as unrelated, or at least having separate and distinct causes:

  • getting fatter (obesity)
  • high blood pressure (hypertension)
  • high triglycerides
  • low HDL cholesterol (dyslipidemia)
  • heart disease (atherosclerosis)
  • high blood sugar (diabetes)
  • inflammation (pick your disease)

as products of insulin resistance and high circulating insulin levels (hyperinsulinemia). It’s a kind of homeostatic disruption in which regulatory systems throughout the body are misbehaving with slow, chronic, pathological consequences everywhere.


As Reaven described it, the condition of being resistant to insulin — the key defect in metabolic syndrome — is the underlying cause of type 2 diabetes.

Not everyone with insulin resistance becomes diabetic, however; some continue to secrete sufficient insulin to overcome their bodies’ resistance to the hormone. And this hyperinsulinemia in turn has deleterious effects throughout the human body, including causing heart disease by raising triglyceride levels and blood pressure, lowering levels of HDL cholesterol, and further exacerbating the insulin resistance.

It’s a vicious cycle in which secreting too much insulin can cause insulin resistance, and insulin resistance will cause the body to secrete still more insulin. Diabetes and heart disease are likely to follow. Getting ever fatter may be a cause, but it could be a result as well.


For the past fifty years, as the Tokelau case illustrates, nutritionists and heart-disease researchers have assumed that eating too much salt is the cause of hypertension, which can be defined as chronically and pathologically high levels of blood pressure.

That hypertension is one of the five criteria that a physician will use in diagnosing metabolic syndrome would make it seem obvious that it’s likely caused by the same trigger - dietary or otherwise - as the other conditions.

In other words, if your blood pressure is elevated, that’s a sign that you’re insulin-resistant and have metabolic syndrome; it also means you’re likely to be overweight, or at least getting fatter, and your triglycerides are elevated, you’re glucose-intolerant, and your HDL cholesterol is low.

They all go hand in hand and are probably caused by the same thing.

By Occam’s Razor and Burkitt’s logic, if sugar causes insulin resistance and elevates triglycerides and makes us fat, then it very likely causes hypertension, too — if not directly, then at least indirectly, through its effect on insulin resistance and weight.


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