The Big Fat Surprise: A Critical Review; Part 1

The-Big-Fat-Surprise

[go to The Big Fat Surprise: A Critical Review; Part 2]

Introduction to Part 1

Nina Teicholz’s The Big Fat Surprise (BFS) is a book that claims to reveal “the unthinkable: that everything we thought we knew about dietary fats is wrong.” This is a trope that is often exploited to sell diet/nutrition books, and it works surprisingly well.

What makes this particular book interesting is not so much that it is bad (which it is) or that it is extravagantly biased (which it also is). No, what really fascinates me about this book is that the author excessively and shamelessly lifts other people’s material. Most notably Teicholz lifts from another popular low-carb book called Good Calories, Bad Calories (GCBC) by Gary Taubes.

If I had written a book and I had “borrowed” other people’s work, here’s what I would do: I would cross my fingers and pray that no one ever notices. I would never bring it up, and diffuse it as quickly as I could if someone else brought it up. Not Teicholz. She gets in there and picks fights, accusing others of plagiarizing her work if they write a piece that is also critical of low-fat diets.

 

Despite all this finger-wagging Teicholz does try to bring something new to the table. She makes an effort to speak to some people involved that Taubes did not. Although given the excessive misrepresentation of not only her work but those of others I am deeply skeptical that Teicholz fairly represented her conversations with some of these individuals.

Teicholz also attempts to appeal to the soccer mom demographic by writing a chapter about how women and children are not adequately studied when it comes to low-fat diets. However, any study she might cite in favor of her low-carb narrative (Shai, for example) has similar male:female ratios, and most don’t include children. There are good reasons for this, of course, but I won’t discuss them here.

At any rate, to wrap up this introduction, the results of fact-checking the first five chapters of BFS are below. I posses all of the texts that are discussed. I will be happy to provide them if you like. Let me know.

Chapter 1: The Fat Paradox: Good Health on a High-Fat Diet

On page 11-12 Teicholz discusses the Masai tribe of Africa and how they consume quite a bit of milk daily yet have very low cholesterol (much like Taubes does in ch. 2 of GCBC). She also mentions that they are not fat and they don’t have high blood pressure. I don’t know why she throws the blood pressure and leanness in there since no one claims that milk causes high blood pressure, nor that these African tribes that walk about 30 miles per day and burn 300-500 kcals/hour would be fat because they drink milk. The real crime here is one of omission.

In support of her argument that diets heavy in saturated fat won’t lead to high cholesterol because the Masai do it, she cites an article published in the NEJM titled “Some Unique Biologic Characteristics of the Masai of East Africa.”1 The entire point of that article was to claim that the reason that the Masai have such low cholesterol levels despite a diet heavy in saturated fats was because they have a unique feedback mechanism that suppresses endogenous cholesterol synthesis that most of us don’t have. Yet there of course is no mention of this in the text (or GCBC) because to suggest that their low cholesterol was due to genetics would hurt her meat-is-good-for-you narrative.

Continuing with the Masai on page 12, Teicholz discusses George Mann and his findings:

If our current belief about animal fat is correct, then all the meat and dairy these tribesmen were eating would have caused an epidemic of heart disease in Kenya. However, Mann found exactly the opposite—he could identify almost no heart disease at all.

As evidence for this she cites a paper titled “Atherosclerosis in the Masai” that does indicate very little evidence of infarctions, but does state the following:

We find the Masai vessels do show extensive atherosclerosis; they show coronary intimal thickening which is equal to that seen in elderly Americans.

Mann goes on to say that the reason why there are so few occlusions despite the extensive atheroslcerosis is that the Masai’s blood vessels enlarge as they age.2

Now that we have uncovered some very important points that were concealed by Teicholz, we are still confronted with an odd reality. The Masai consume a ton of milk and likely a fair amount of meat and yet they do not have elevated cholesterol levels due to a unique biological mechanism. Despite the low cholesterol they still get atheroslcerosis. Enough that men in their prime have the blood vessels of elderly Americans. Yet despite even this they manage to escape heart attacks because their vessels are larger than average. Wow. I don’t know what to make of the Masai, except that they are indeed a unique people. In this case I think we can treat the Masai as outliers and not assume that we can live like they do and remain free of heart disease.

* * *

On page 14 Teicholz discusses a text by Hrdlicka3,4 published near the turn of the (last) century and states:

The Native Americans he visited were eating a diet of predominantly meat, mainly from buffalo, yet, as Hrdlicka observed, they seemed to be spectacularly healthy and lived to a ripe old age.

However, if you go look at the text you will find that the diet of Native Americans is based around, y’know, the most abundant crops in the Americas: corn and wheat. There are several pages devoted to describing the diet, so I don’t want to quote all of it, but perhaps this will give you an idea of what Hrdlicka really found. Page 19:

The principal article of diet among the Indians throughout the Southwest and Mexico is maize, which is eaten in the form of bread of various kinds, or as mush, or boiled entire. It is also parched on charcoal and eaten thus, or is ground into a fine meal, which, sweetened, constitutes the nourishing pinole of some of the tribes. Wheat is used in similar ways but less extensively. Next in importance to corn and wheat in the Indian diet are meat and fat and beans. Meat is scarce.

For a more nuanced view of the issue see this post and scroll down to “Hrdlička and the diet of Southwestern Native Americas.”

* * *

Page 15, Teicholz attempts to make the case that Africans living in British colonies nearly 100 years ago ate a ton of meat and had basically no cancer. As evidence for both of these claims she cites what amounts as a Letter to the Editor in the BMJ by George Prentice.5

The British Medical Journal routinely carried reports from colonial physicians who, though experienced in diagnosing cancer at home, could find very little of it in the African colonies overseas. So few cases could be identified that “some seem to assume that it does not exist,” wrote George Prentice, a physician who worked in Southern Central Africa, in 1923.

If you bother to look at the publication by Prentice you will notice that right after he says that some seem to assume that cancer does not exist, he immediately states why this is both a false and dangerous belief that has led to a patient of his dying of cancer because he himself believed that Africans did not get cancer when he was a younger doctor. He didn’t remove a breast tumor when he could have and should have and that his patient died because of this. Prentice also says in addition to breast cancer he sees other cancers all the time:

I have also seen epithelioma of the face. In this case the eyelids and the whole of one eye were completely destroyed, and the bone of the eye socket was attacked; the case was inoperable. I have seen a tumour, fungating and evidently malignant, that had practically split the bones of the face, causing the eyes to bulge laterally and giving a strange chameleon look to the patient. It was inoperable. I have seen cancer of the left ovary that proved fatal. I believe I have seen cases of malignant disease of the liver, but as there was no autopsy the diagnosis was not confirmed. I have removed many large tumours of the testicle which, if not cancerous, are of a nature unknown to me. Keloids and fatty tumours are very common.

In case you could not tell, Teicholz takes Prentice’s words completely out of context to make it appear he was communicating the opposite of what he was actually communicating.

I’m sure she’s also hoping that the reader won’t realize that – true or not – all she has been discussing so far in the book are very tenuous and unscientific correlations, and that by the time the readers get to the part where she bashes these types of associations that they won’t realize she’s being wildly inconsistent and even hypocritical in how she deals with studies and observations.

* * *

Page 16:

It is true that American beef from a cow raised on grain does have a different fatty-acid profile from an ox hunted in the wild. In 1968, the English biochemist Michael Crawford was the first to look at this question in detail. […] His paper seemed to confirm that modern-day people should not consider their domesticated meat to be anywhere near as healthy as hunted meat from the wild. And for the past forty-five years, Crawford’s paper has been widely cited, forming the general view of the subject. What Crawford buries in his data, however, is that the saturated fat content of the wild and domesticated animal meats hardly differed at all.

Yep. Crawford “buries” it by making it Figure 1 in his paper.6 I know when I want to bury data in a paper I visualize it and put it at the head of the results.

fatty acid ratios

By the way, this “widely cited” paper has been cited only 183 times since it’s publication in 1968. Truly a landmark paper, this one.

Chapter 2: Why We Think Saturated Fat Is Unhealthy

Cribbing Taubes Alert

In GCBC on page 14 Taubes discusses a century-old document that was published by a German journal that is both very difficult to find and written in German.

The evidence initially cited in support of the hypothesis came almost exclusively from animal research-particularly in rabbits. In 1913, the Russian pathologist Nikolaj Anitschkow reported that he could induce atherosclerotic-type lesions in rabbits by feeding them olive oil and cholesterol.

Do you think Taubes both A) possesses that obscure text AND B) is fluent in German? It’s possible, although my money would be on Taubes simply reading what others had written about the study and simply paraphrasing.

BFS page 22:

Early evidence suggestively linking cholesterol to heart disease also came from animals. In 1913, the Russian pathologist Nikolaj Anitschkow reported that he could induce atherosclerotic-type lesions in rabbits by feeding them huge amounts of cholesterol.

What are the odds that Teicholz also speaks German and has the German text that was published over 100 years ago? Again, possible, but given the similarity of how she and Taubes discuss the paper my guess is that she simply paraphrased Taubes without attribution.

* * *

Here’s something interesting… On page 16 of GCBC Taubes says the following:

In 1937, two Columbia University biochemists, David Rittenberg and Rudolph Schoenheimer, demonstrated that the cholesterol we eat has very little effect on the amount of cholesterol in our blood.

As evidence he cites Rittenberg and Schoenheimer’s 1937 paper titled “Deuterium as an indicator in the study of intermediary metabolism XI. Further studies on the biological uptake of deuterium into organic substances, with special reference to fat and cholesterol formation.”7

On page 23 of BFS Teicholz writes the following:

The notion that cholesterol in the diet would translate directly into higher cholesterol in the blood just seemed intuitively reasonable, and was introduced by two biochemists from Columbia University in 1937.

She also cites the same exact paper. You see the problem, right? Both Taubes and Teicholz claim opposite things yet cite the same paper as evidence. So who is correct? Actually neither of them are correct because the cited text doesn’t address the issue. The paper discusses experiments on animals such as rodents and chicks, not humans as is implied by both Taubes and Teicholz. Furthermore, the only thing these experiments demonstrate is that these animals are capable of synthesizing cholesterol, and has essentially nothing to do with dietary cholesterol influencing or not influencing serum cholesterol.

* * *

Continuing with the dietary cholesterol controversy, on page 23 immediately after the above statement Teicholz claims:

It was Ancel Keys himself who first discredited this notion. Although in 1952 he stated that there was “overwhelming evidence” for the theory […]

She then accuses him of being a hypocritical flip-flopper for arrogantly walking the statement back three years later by saying that tremendous amounts of cholesterol have only a trivial effect on serum cholesterol and that “this point requires no further consideration.”

Damn, this guy sounds like an arrogant prick considering he wholly endorsed the theory a few years before, right?!

…Except if you look at the 1952 paper where Teicholz pulls that quote Keys says the EXACT OPPOSITE of what Teicholz claims.8 In the paper Keys argues that the animal experiments that have shown that feeding high cholesterol to, say, rabbits have no relevance to humans, going on to say

No animal species close to man in metabolic habitus has been shown to be susceptible to the induction of atherosclerosis by cholesterol feeding.

AND

From the animal experiments alone the most reasonable conclusion would be that the cholesterol content of human diets is unimportant in human atherosclerosis.

AND

Direct evidence on man in this connection is unimpressive.

Besides, even if he did hold an erroneous belief beforehand, why would you want to knock a guy for simply following the evidence? This is science: you are supposed to always be self-correcting.

* * *

Page 23-24:

In 1992, one of the most comprehensive analyses of this subject concluded that the vast majority of people will react to even a great deal of cholesterol in the diet by ratcheting down the amount of cholesterol the body itself produces. […] Responding to this evidence, health authorities in Britain and most other European nations in recent years have rescinded their advisories to cap dietary cholesterol.

Emphasis mine. The reason for bolding “in recent years” is because the evidence cited for this sentence is a paper published in 1987!!9 And of course the evidence they were apparently responding to was a meta-analysis published in 1992.10 There’s a chronology problem here. A meta-analysis, by the way, whose first sentence of the summary states:

Serum cholesterol concentration is clearly increased by added dietary cholesterol but the magnitude of predicted change is modulated by baseline dietary cholesterol.

Again, emphasis mine.

* * *

On page 25 you will see this structure:

fatty acid

This structure is incorrect on many levels. For one it is not even a fatty acid. It’s actually not anything because it is not a legitimate chemical structure, but it’s closest to pentane which no one would want to consume. In order for it to be a fatty acid it would at least need a carboxyl group at one end. However, that would make the structure into valeric acid which is not commonly found in foods (especially the butter, meat, and cheese Teicholz promotes) and not commonly consumed unless you’re eating valerian root.

I pointed this out on my Amazon review of the book and I got pilloried because apparently I was supposed to simply know that the Fisher projection was not really supposed to be a fatty acid, but was supposed to be a simple, generic structure to illustrate how hydrogens are arranged around carbon atoms. However, if Teicholz didn’t want to put a proper carboxyl group because she was afraid it might confuse her audience she could have at least put an “R” or ellipses or something to indicate that part of the fatty acid is being left out in order to concentrate on the hydrogens. Even so, if it is indeed just a generic structure used to illustrate how hydrogens are arranged then why are the end hydrogens arranged incorrectly, and why are there two missing hydrogens? This structure is absolutely wrong no matter how you slice it.

* * *

The lies about Ancel Keys continue on page 27 when Teicholz discusses a paper of his called “Atherosclerosis: A Problem in Newer Public Health” and says this paper received “enormous attention” and was the genesis of America’s alleged fear of fat.

There is no evidence at all that Keys’s 1953 paper received “enormous attention.” In fact, the evidence that exists would suggest the opposite. There was no mention of the paper in the lay press. That is until relatively recently when Gary Taubes began lying about it. What about academia? According to Google Scholar this highly influential paper has only been cited 247 times since its publication, which spans 61 years as of this writing. An average of four citations per year. It was cited merely 99 times from the time it was published to 1973, a full twenty years after its publication. For comparison, on page 159-160 Teicholz mentions a study whose results she claims were “ignored.” That study was published in 1992 and has received 682 citations.

* * *

Page 31:

Keys found further ammunition for his hypothesis from a compelling observation made during World War II, which is that deaths from heart disease dropped dramatically across Europe during wartime and rebounded soon afterward. These events led Keys to presume that the food shortages— particularly of meat, eggs, and dairy—were very likely the cause. There were, however, other explanations: for instance, sugar and flour were also scarce during the war; people breathed fewer car-exhaust fumes due to gasoline shortages and got more exercise by cycling or walking to get around. Other scientists noted these alternative explanations for the decline in heart disease, but Keys dismissed them outright.

The paper that noted the alternative explanations was published in 1957, yet Keys was apparently dismissing them in 1956.11,12

* * *

On page 34, Teicholz discusses a paper by Yerushalmy and Hilleboe that criticized a graph in Keys’s “Atherosclerosis: A Problem in Newer Public Health” paper mentioned above.13

Yerushalmy’s objection was that Keys seemed to have selected only certain countries that fit his hypothesis. There were other factors that could equally well explain the trends in heart disease in all these countries, he asserted.

If you actually read Keys’s paper you will note that Keys mentioned that he left out some less-developed countries because they had very poor vital health statistics.14 Some more developed European countries he claims he would have included if the Nazi’s had not very recently invaded, occupied, and rationed food which would confound his simple cross-sectional analysis. It wasn’t that he was a diabolical scientist bent on lying to the public about the cause of heart disease. Or if he was he had a damn fine excuse for not using those countries.

It’s funny because on pages 34-36 Teicholz criticizes Keys for not including more European countries like France and Switzerland (which incidentally would have fallen right in line with Keys’s graph). Then a few pages later on 37-38 Teicholz discusses Keys’s Seven Countries Study and criticizes him for including countries that Nazi Germany had invaded and occupied several years before.

At any rate, Yerushalmy and Hilleboe did indeed point out some other factors in their paper, most prominently they pointed out that both animal fat and animal protein were far better correlated with heart disease than total fat. Many different types of heart disease, in fact. This held true whether or not it was calculated as total amounts or as a percentage of total calories. Moreover, vegetable protein and vegetable fat were negatively correlated with heart disease.

Of course there was no way that Teicholz was ever going to mention this.

* * *

Page 40:

I looked more closely into the dietary data on Greece, because it became the exemplar for the Mediterranean diet (see Chapter 7), and I found one of the most stunning and troubling errors. In that country. Keys had sampled the diets on Crete and Corfu more than once, in different seasons, in order to capture variations in the food eaten. Yet in an astonishing oversight, one of the three surveys on Crete fell during the forty-eight-day fasting period of Lent.

Astonishing oversight? One of the most stunning and troubling errors? Despite what appears to be insincere hand-wringing over this gravest of all scientific errors, I don’t really see the problem here. The question that needs to be asked here is: Does collecting dietary information during a period where some Christians adhere to a quasi-fasting ritual invalidate the dietary data? I suppose it would if a sufficient number of participants were strictly adhering to the fast. Was this the case? According to the 211-page write-up of the study programs and objectives this was not the case15:

The seasonal comparisons in Crete and Corfu were of interest because the survey in Crete in February and part of the survey in Corfu in March-April were in the 40-day fasting period of Lent of the Greek Orthodox church, but strict adherence did not seem to be common in the populations of the present study.

How would the scientists come to the conclusion that there was no strict adherence? They could simply compare the dietary data collected during the spring with the dietary data collected during other times of the year. What if the participants were all lying on their dietary surveys? The researchers also collected the actual foods eaten by participants, lyophilized them, and sent them out for chemical analysis. Apparently there were no significant differences with that data either.

Even if the alleged “error” of collecting data in the spring was so insurmountable it had to be thrown out, it would not invalidate the other two dietary collections in Crete and it would certainly not be nearly enough to nullify the entire study. It seems pretty clear to me that while writing this book Teicholz is actively searching for any hint of impropriety. She discovered a mention of Lent, decided to ignore the rest, and enthusiastically proclaimed that she had unearthed some alarming facts about the study.

Additionally she tries to make the case on pages 41 and 42 that Keys tried to sheepishly bury the flawed methodology of his crappy study. If this is true he did an exceedingly poor job of it, considering in addition to all of the analyses published from the data. Keys published:

  • A 211-page paper describing the study objectives and methods15
  • A 300+ page monograph describing the particular details of data collection in each country16
  • A 300+ page book describing in great detail the study and its results17

In addition there were other entire books published on the study.18,19 Keys is not being obfuscatory.

Chapter 3: The Low-Fat Diet Is Introduced to America

Cribbing Taubes Alert

On page 49 Teicholz discusses an AHA nutrition committee report:

Committee members went so far as to rap diet-heart supporters like Keys on the knuckles for taking “uncompromising stands based on evidence that does not stand up under critical examination.” The evidence, they concluded, did not permit such a “rigid stand.”

On page 20 of GCBC, Taubes makes a similar statement regarding the same report and uses the same quotes.20 I would argue that both get it wrong. The report seems to have somewhere between a neutral and a favorable view of Keys, as evidenced by the following quotes:

  • “Mayer et al. found that high-fat animal or vegetable diets increased and low-fat diets decreased serum cholesterol of normal subjects, confirming earlier data of Keys.”
  • “Keys, in particular, has placed emphasis on the proportion of total dietary calories contributed by the common food fats […] Certainly there is an abundance of data, both clinical and experimental, that tends to relate excess fat intake to atherosclerosis.”

* * *

Cribbing Taubes Alert

On page 49 Teicholz continues discussing the views of the AHA:

The AHA committee swung around in favor of their ideas, and the resulting report in 1961 argued that “the best scientific 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.

On page 21 of GCBC Taubes says essentially the same thing and uses the same quote from the same paper.21

Continuing on the report, page 50:

Keys himself thought that the 1961 AHA report he had helped write suffered from “some undue pussy-footing” because it had prescribed the diet only for high-risk people rather than the entire American population […]

On page 21 of GCBC Taubes says almost the exact same thing, including the undue pussy-footing quote. However, Taubes cites the quote correctly as being from Time magazine’s article titled Fat in the Fire, whereas Teicholz cites it incorrectly as The Fat of the Land.22,23

* * *

Cribbing Taubes Alert

There is getting to be too many of these alerts. On page 4 of GCBC Taubes states:

“People should know the facts,” Keys told Time. “Then if they want to eat themselves to death, let them.”

BFS page 50:

“People should know the facts,” he said. “Then, if they want to eat themselves to death, let them.”

This quote is found in Time magazine’s The Fat of the Land article.23 Continuing…

GCBC page 21:

The Time cover story, more than four pages long, contained only a single paragraph noting that Keys’s hypothesis was “still questioned by some researchers with conflicting ideas of what causes coronary disease.”

BFS page 51:

In the Time article, there is only a brief mention of the reality that Keys’s ideas were “still questioned” by “some researchers” with conflicting ideas about what causes coronary disease.

* * *

On page 54 Teicholz educates the reader on case-control studies:

These studies are understood to suffer from “recall bias,” whereby patients may inaccurately remember past consumption.

Immediately after this disclaimer Teicholz goes on to produce several case-control studies that fit her narrative. By doing so, this is what I hear as a reader: “Case-control studies suck. Don’t try to use them as evidence. But here are a few whose results I like and you should know about them.”

* * *

Cribbing Taubes Alert

GCBC page 26:

[JAMA] reported that the mostly Italian population of Roseto, Pennsylvania, ate copious animal fat – eating prosciutto with an inch-thick rim of fat, and cooking with lard instead of olive oil – and yet had a “strikingly low” number of deaths from heart disease, Keys said it warranted “few conclusions and certainly cannot be accepted as evidence that calories and fats in the diet are not important.”

BFS page 55:

[T]he mostly Italian population living there had a “strikingly low” number of deaths from heart disease […] the local diet included copious amounts of animal fats, including prosciutto with fat an inch thick around the rim, and most meals cooked in lard. […] Keys concluded that the Roseto data “certainly cannot be accepted as evidence that calories and fats in the diet are not important.”

There is so much information in both those publications, yet surprisingly the same exact quotes are independently plucked by Teicholz.24,25

* * *

Page 56:

F. W. Lowenstein, a medical officer for the World Health Organization in Geneva, collected every study he could find on men who were virtually free of heart disease, and concluded that their fat consumption varied wildly.

I suppose that’s true according to the study.26 Fat intake varied from 21 g/day to 355 g/day in the case of the Somalis. Although, if you remove the Somalis as something of an outlier (they also consume 6,247 kcals/day according to the paper), then fat intake in all the other populations drops to 100 grams of fat per day or less.

* * *

Cribbing Taubes Alert

Teicholz uses Taubes’s Karl Popper quote.

GCBC page 24-25:

[The scientific method requires] that scientists not just test their hypotheses, but try to prove them false. “The method of science is the method of bold conjectures and ingenious and severe attempts to refute them,” said Karl Popper.

BFS page 56-57:

A scientist must always try to disprove his or her own hypothesis. Or, as one of the great science philosophers of the twentieth century, Karl Popper, described, “The method of science is the method of bold conjectures and ingenious and severe attempts to refute them.”

* * *

Page 57:

[…] Keys was not on the lookout for his own biases. He considered the burden of proof to be on those opposing him. He made no attempts to refute his own ideas, as Popper advised. He promoted the “idol of his mind” without hesitation.

OMG. What?! How?? Can I get some evidence for that?

* * *

 

Page 65 Teicholz then pivots to Framingham and mentions how they found cholesterol to be a big predictor of death. BUT…

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.

Is she talking about the paper that states in the conclusion “This study and the Coronary Drug Project results on nicotinic acid therapy show a direct association of cholesterol levels with mortality, which becomes stronger with lengthy follow-up”?28 Is that the one she’s talking about? Because that’s the one she cited. The paper also states that the association holds strong even after adjusting for individual differences in blood pressure, smoking, relative weight, and diabetes.

* * *

Page 67:

Not until 1992, in fact, did a Framingham study leader publicly acknowledge the study’s findings on fat. “In Framingham, Mass, the more saturated fat one ate . . . the lower the person’s serum cholesterol. . . and [they] weighed the least” wrote William P. Castelli […]

What the reader doesn’t know is that 1) this quote is taken from an editorial that extols the virtues not of meat and cheese, but of the unsaturated fat in nuts, 2) there is literally a half page of text between the ellipses, 3) the italics are not part of the original quote, and most importantly 4) Teicholz cuts off the quote immediately before the author mentions that he is talking about the people that were the most physically active.29 But I’m sure their physical activity has no effect on their weight or cholesterol levels, right?

* * *

Cribbing Taubes Alert

On page 159 of GCBC Taubes quotes from a 1967 JAMA editorial30:

JAMA published an editorial in response to Kuo’s article, suggesting that the “almost embarrassingly high number of researchers [who had] boarded the ‘cholesterol bandwagon'” had done a disservice to the field. “This fervent embrace of cholesterol to the exclusion of other biochemical alterations resulted in a narrow scope of study,” the editorial said.

On page 71 of BFS Teicholz uses the same exact quote:

An “almost embarrassingly high number of researchers boarded the ‘cholesterol bandwagon,'” lamented the editors of the Journal of the American Medical Association in 1967, referring to the narrow, “fervent embrace of cholesterol” to the “exclusion” of other biochemical processes that might cause heart disease.

Chapter 4: The Flawed Science of Saturated versus Polyunsaturated Fat

Cribbing Taubes Alert

Much like elsewhere in BFS, Teicholz appears to take an incredible amount of what might be called “inspiration” from GCBC. Much like in GCBC, Teicholz discusses the Anti-Coronary Club trial, plucks the same quotes, and discusses the same media reactions.

GCBC, page 36:

The first and most highly publicized was the Anti-Coronary Club Trial, launched in the late 1950s by New York City Health Department Director Norman Jolliffe.

BFS, page 73:

An early and celebrated trial was called the Anti-Coronary Club, launched by Norman Jolliffe, director of the New York City Health Department, in 1957.

 

GCBC, page 36:

The eleven hundred middle-aged members of Jolliffe’s Anti-Coronary Club were prescribed what he called the “prudent diet,” which included at least one ounce of polyunsaturated vegetable oil every day. The participants could eat poultry or fish anytime, but were limited to four meals a week containing beef, lamb, or pork.

BFS, page 73:

He signed up eleven hundred men to his Anti-Coronary Club and instructed them to reduce their consumption of red meat, such as beef, lamb, or pork, to no more than four times a week (which would be considered a lot by today’s standards!) while consuming as much fish and poultry as they liked.

GCBC, page 36:

[T]wenty-six members of the club had died during the trial, compared with only six of the men whose diet had not been prudent.

BFS, page 74:

[T]wenty-six members of the diet club had died during the trial, compared to only six men from the controls.

 

Okay, maybe both Taubes and Teicholz did independent research and came across the same study and both found it was compelling enough to include in their books. And maybe they both independently included the same info from the study as well. It’s certainly possible. But would they mention the same NYT article?

GCBC, page 36:

“Diet Linked to Cut in Heart Attacks,” reported the New York Times in May 1962.

BFS, page 74:

“Diet Linked to Cut in Heart Attacks,” reported the New York Times in 1962 […]

Would they independently use the same quote from the multiple trial publications?

GCBC, page 36:

Eight members of the club died from heart attacks, but none of the controls. This appeared “somewhat unusual,” Christakis and his colleagues acknowledged.

BFS, page 74:

[I]nvestigators began to find “somewhat unusual” results: […] Eight members of the club had died of heart attacks, but not one of the controls.

They also both misrepresent the study:

GCBC, page 36:

They discussed the improvements in heart-disease risk factors (cholesterol, weight, and blood pressure decreased) and the significant reduction in debilitating illness “from new coronary heart disease,” but omitted further discussion of mortality.

BFS, page 74:

In the discussion section of the final report, the authors […] emphasized the improved risk factors among the men in the diet club but ignored what those risk factors had blatantly failed to predict: their higher death rate.

Notice how both Taubes and Teicholz minimize the main results of the study, namely that the prudent diet did exactly what researchers imagined it would do: reduce not only risk factors for heart disease, but also actual coronary events.31–33 Further, they both misrepresent the study by claiming those devious scientists omitted discussion of death rate when nothing could be further from the truth. Both cited publications discuss death rate and mortality among participants very clearly. In fact, the slight difference in death from causes other than heart disease was not even significant. From the 1966 publication31 (emphasis mine):

The rates for these deaths in the 50-59 age group were 689 per 100,000 person-years in the experimental group, and 666 per 100,000 in the control group. The difference between these two rates is slight and not statistically significant.

* * *

Cribbing Taubes Alert

In GCBC, Taubes immediately segues from discussing the Anti-Coronary Club trial to discussing the Dayton’s LA Veterans trial.34–36 Strangely enough Teicholz does the exact same thing.

GCBC, page 37:

In July 1969, Seymour Dayton, a professor of medicine at the University of California, Los Angeles, reported the results of the largest diet-heart trial to that date. Dayton gave half of nearly 850 veterans residing at a local Veterans Administration hospital a diet in which corn, soybean, safflower, and cottonseed oils replaced the saturated fats in butter, milk, ice cream, and cheeses. The other half, the controls, were served a placebo diet in which the fat quantity and type hadn’t been changed. The first group saw their cholesterol drop 13 percent lower than the controls […]

BFS, page 75:

It was conducted by UCLA professor of medicine Seymour Dayton on nearly 850 elderly men living in a local Veterans Administration (VA) home in the 1960s. For six years, Dayton fed half the men a diet in which corn, soybean, safflower, and cottonseed oils replaced the saturated fats in butter, milk, ice cream, and cheese. The other half of the men acted as controls and ate regular foods. The first group saw their cholesterol levels drop almost 13 percent more than did the controls.

Is it just me or do those paragraphs sound very similar?

GCBC, page 37:

“Was it not possible,” Dayton asked, “that a diet high in unsaturated fat…might have noxious effects when consumed over a period of many years? Such diets are, after all, rarities […]”

BFS, page 75:

“Was it not possible,” he asked, “that a diet high in unsaturated fat. . . might have noxious effects when consumed over a period of many years? Such diets are, after all, rarities.”

Both Taubes and Teicholz introduce the author and gives a brief background of the trial, then relate the conditions and methods of the study, then they cherry-pick from the results. They both then interpret the results for you. ONLY AFTER ALL THAT do Teicholz and Taubes reproduce a couple sentences from the journal article questioning whether a diet of unsaturated fat might have “noxious effects” presumably because of the study results. What they likely want the reader to think is that after the results of the study are in and the numbers have been crunched and the data has been analyzed Dr. Seymour Dayton is sitting at his desk and ruminating on what could have produced these results. As if he is asking a rhetorical question or providing a hypothesis for a future dietary trial.

In reality Dayton actually asks that question in the beginning of the paper to kind of whet the reader’s appetite. He then goes on to answer that very question in the text with an answer that would not be favorable to Teicholz’s (or Taubes’s) argument. Do you want to know if the experimental diet has noxious effects? Well there’s a section in the results portion of the study titled “Does the Experimental Diet Have Noxious Effects?” where Dr. Dayton states34:

As indicated in table 29 and discussed in some detail above, the excess mortality in nonatherosclerotic categories was not sufficiently impressive to justify the conclusion that harmful effects had been demonstrated.

AND

One may also wonder whether the experimental diet may have exerted its effect on mortality data primarily by accelerating nonatherosclerotic deaths (see table 28), decreasing the atherosclerotic mortality by inducing early death due to other cause. Such a mode of action would be associated with higher numbers of deaths in the experimental group compared with the controls, whereas the reverse was true in this trial (fig. 13).

AND

The other observation which raised some question of a possible toxic effect was the low arachidonic acid concentrations in atheromata of long-term, high-adherence subjects on the experimental diet (tables 37 to 40). For reasons already cited, this may be more appropriately viewed as evidence of a salutary rather than a toxic effect.

Teicholz both 1) Uses the exact same quote Taubes does in GCBC, phrases it the exact same way, and removes the same exact words from within the quote; and 2) Takes the quote out of context just like Taubes does in order to imply something antithetical to what Dayton actually meant.

Moreover, both Taubes and Teicholz either minimize or outright ignore results of the study that they do not like (ironically, a trait they accuse the big, bad nutrition researchers of doing). Remember the control group was high in saturated animal fat, and the experimental group was high in unsaturated fats from plants.

The number of men sustaining events in major categories, in the control and experimental groups, respectively, was: definite silent myocardial infarction, 4 and 9; definite overt myocardial infarction, 40 and 27; sudden death due to coronary heart disease, 27 and 18; definite cerebral infarction, 22 and 13. The difference in the primary end point of the study-sudden death or myocardial infarction was not statistically significant. However, when these data were pooled with those for cerebral infarction and other secondary end points, the totals were 96 in the control group and 66 in the experimental group; P = 0.01. Fatal atherosclerotic events numbered 70 in the control group and 48 in the experimental group; P < 0.05. Life-table analysis in general confirmed these conclusions. For all primary and secondary end points combined, eight year incidence rates were 47.7% and 31.3% for the control and experimental groups, respectively; P value for the difference between the two incidence curves was 0.02.

If you don’t want to read the above block quote, I’ll summarize it for you: in all but one endpoint that was measured the experimental diet of unsaturated fats had less overt myocardial infarction, sudden death, cerebral infarction, fatal atherosclerotic events, etc. And not by a tiny margin – a significant margin.

* * *

Page 75:

[V]egetable oils had been introduced into the food supply only in the 1920s, yet suddenly the oils were being recommended as a cure-all. In fact, the upward curve of vegetable oil consumption happened to coincide perfectly with the rising tide of heart disease in the first half of the twentieth century […]

Not true. At least not true by the study she cites.37 The study by Blasbalg et al simply shows the trends of fatty acid consumption from various sources. Specifically, it shows from which foods Americans have been getting their linoleic acid and alpha linolenic acid. It has absolutely zero analysis of heart disease or any other disease for that matter. Nor does she cite a separate paper that shows trends in heart disease to compare the paper on fatty acid consumption.

Just for kicks, let’s do Teicholz’s work for her. Let’s start with the Blasbalg paper. It appears that in the 20th century butter and lard dropped precipitously at about mid-century. Shortly afterward poultry and shortening consumption rose. Soybean oil also rose concurrently with shortening probably because it was a prominent ingredient. Canola oil consumption also increased in the 90s.

oils1

oils2

What about heart disease? According to a paper by Cooper et al CVD rose until about mid-century, but then begins a steady decline into the millennium.38

F1.large

You have to ask yourself: does the vegetable oil correlate perfectly with CVD?

Cribbing Taubes Alert.

In GCBC, after discussing the LA Veterans trial, Taubes moves immediately to discuss the Helsinki Mental Hospital Study. Strangely enough Teicholz does the exact same thing! What are the odds that they would both independently discuss the same trials in the very same order!

GCBC, page 37:

Ordinary milk was replaced with an emulsion of soybean oil in skim milk, and butter and ordinary margarine were replaced with a margarine made of polyunsaturated fats. These changes alone supposedly increased the ratio of polyunsaturated to saturated fats sixfold.

BFS, pages 76-77:

Ordinary milk was replaced with an emulsion of soybean oil in skim milk, and butter was replaced by a special margarine high in polyunsaturated fats. The vegetable oil content of the special diet was six times higher than in a normal diet.

* * *

Page 86:

[R]emarkably, when Jerry Stamler reissued his 1963 book. Your Heart Has Nine Lives, it was published as a “professional” red leather edition by the Corn Products Company and distributed free of charge to thousands of doctors. Inside, Stamler thanks both that company and the Wesson Fund for Medical Research for “significant” research support.

The very same point was also made by Taubes in GCBC, but that’s not my point here. What I’d like to say about this is that there is roughly half a page in the book that lists people and organizations that have lent financial support to the research in the book. Taubes and Teicholz, however, only list the vegetable oil manufacturers. However, neither list the National Dairy Council which is also named among the research supporters. The reason for leaving out organizations like the NDC should be pretty obvious by now. But let me spell it out for you just in case you’re confused: Both Teicholz and Taubes are attempting to craft a narrative where Big Vegetable Oil and greedy nutrition researchers are in cahoots with each other (and also the government) to dupe the American consumer into eating less butter and cheese. If Teicholz or Taubes were to mention that the National Dairy Council funded the same research, well, then that conspiracy narrative would be weakened.

* * *

On pages 94-95, Teicholz makes the case that low cholesterol is associated with cancer in some studies, and strongly implies that low cholesterol might cause cancer:

By 1981, nearly a dozen sizable studies on humans had found a link between lowering cholesterol and cancer, principally for colon cancer.

This is kind of nit-picky, but notice how Teicholz uses the words “lowering cholesterol” and not “low cholesterol.” This implies that the act of lowering cholesterol leads to cancer and not that the condition of low cholesterol is somehow linked to cancer. To the average Joe Schmo this may seem like I’m being petty and unreasonably contrarian, but if you ever take an epidemiology class you will know that how you phrase things matters a great deal.

Anyway, let’s take a look at the studies Teicholz cites…

Cribbing Taubes Alert

The first thing to notice is that ALL of the studies she cites in favor of the link between low cholesterol and cancer are also cited by Gary Taubes in GCBC when he makes the same argument. Hmmm…

  • Pearce and Dayton 197136: Cited by Taubes, and as previously mentioned it is a bad study to cite in favor of this association.
  • Nydegger and Butler 197039: Cited by Taubes. Does show a link between cancer and low lipoprotein levels. However, the authors point out this is likely due to some cholesterol-lowering effect of cancer and not the other way around, since people with chronically low cholesterol levels do not show an increased incidence of cancer.
  • Oliver et al 197840: Cited by Taubes. The high-cholesterol group had a lower cancer rate than the two low-cholesterol groups, but it was not significant. From the paper: “These figures are surprisingly close to the rates observed in trial subjects in Groups I and III. Thus the data for all cancer do not give rise to special concern.”
  • Beaglehole et al. 198041: Cited by Taubes. Shows a significant inverse relationship.
  • Kark et al. 198042: Cited by Taubes. Also shows an inverse relationship between low cholesterol and cancer, but the authors suggest that the cancer is not likely a result of low cholesterol. From the paper: Were high cholesterol levels associated with improved survival, one would expect that those prevalent cases surviving until 1974 as well as live incident cases (surviving until 1974) would also have high cholesterols. The reverse was true.
  • Garcia-Palmieri et al. 198143: Cited by Taubes. Shows a significant inverse relationship.
  • Stemmermann et al. 198144: Cited by Taubes. Shows a significant inverse relationship with colon cancer, but also shows a positive relationship with CHD but that, of course, is never mentioned.
  • Miller et al. 198145: Cited by Taubes. Shows a significant inverse relationship, but makes it clear that suggesting low cholesterol might cause cancer is almost certainly wrong: “Although we found colon cancer patients to have significantly lower serum cholesterol levels than controls, the observed differences may partially reflect the metabolic influence of advancing disease, since there were no significant differences in serum cholesterol levels between controls and cases with early tumors. Our data suggest that low serum cholesterol levels in colon cancer patients do not necessarily precede tumor formation but may be a consequence thereof.”
  • Kozarevic et al. 198146: Cited by Taubes. Shows a non-significant relationship. Also mentions the following that is never discussed: “Serum cholesterol, as expected, was positively related to the incidence of coronary heart disease death.”
  • Rose et al. 197447: Cited by Taubes. Shows a significant inverse relationship with colon cancer. Again, the authors suggest that low-cholesterol might be a result of colon cancer. And again, this is not mentioned.
  • Williams et al. 198148: Cited by Taubes. Shows a significant inverse relationship with colon cancer, but also mentions that it is possible that cancer of the colon can affect cholesterol absorption and excretion leading to low serum levels. I’m shocked this was not mentioned. Shocked.

* * *

Page 94:

[E]ver since corn oil had been shown to double the rate of tumor growth in rats in 1968, there had been a baseline level of concern about vegetable oils and cancer.

There has? I don’t think so. But anyway, the study Teicholz cites is waaayy off the mark.49 For some brief detail some rats were fed either a low-fat diet, a diet high in coconut oil, or a diet high in corn oil. Then they were injected with a carcinogen known to cause breast cancer. Turns that the rates of uptake and clearance of the carcinogen was equal on all three diets.

* * *

Page 94:

Other studies from this time led to the supposition that corn oil might cause cirrhosis of the liver.

As evidence she cites a very obscure study on rats that were fed a diet explicitly designed to induce cirrhosis where some were also supplemented with corn oil. The researchers found that the corn oil did not exert a protective effect.50 Not preventing cancer DOES NOT EQUAL CANCER-PROMOTION. This is possibly the most twisted and misleading claim Teicholz has made so far in the chapter.

* * *

Page 94:

NIH investigators found that Japanese people with cholesterol levels below 180 mg/dL suffered strokes at rates two to three times higher than those with higher cholesterol.

The cited text does state that the people with the lowest cholesterol did have the highest incidence of stroke51, but I want to note a few things. First, this is not a study, but a letter to the editor. Second, these were not NIH investigators nor do I think it had anything to do with the NIH considering the NIH is never mentioned and the studies discussed in the letter were conducted by Japanese researchers on Japanese participants in Japan. Why would American taxpayer money fund this effort? Please correct me if I am wrong.

* * *

Page 94-95:

The NHLBI became so concerned about the cancer findings that it hosted three workshops in 1981, 1982, and 1983. The evidence on the topic was reviewed and rereviewed by an extremely prominent group of scientists […] One suggestion was that low cholesterol might be an early symptom of cancer, rather than a cause. It was a plausible bit of logic. In the end, however, although the assembled researchers could find no convincing explanation for the cancer findings, they concluded that they did “not present a public health challenge” and did not “contradict” the more urgent, “commonsense” public health message for everyone to lower their cholesterol.

A couple of minor things, but I could not find the word “commonsense” that was quoted above in either of the Feinleib papers that were cited.52,53 Moreover, as I recall the public health message for everyone to lower their cholesterol never even existed. The message was/is for those with high cholesterol to lower their cholesterol. There’s a difference.

The scientists involved included nearly all of the above authors of the scary observational studies that indicated a link between low serum cholesterol and cancer.52 Furthermore, the consensus of the panelists was unanimous in that there was not nearly enough evidence to suggest that lowering cholesterol is a risky behavior.

If Teicholz was not an extraordinarily biased journalist, and she wanted to write BFS with a modicum of honesty she could have easily included some more recent studies that show no association with cholesterol-lowering and an increased risk of cancer.54–58 Some even indicate a protective effect of low serum cholesterol on cancer. But when has the truth ever been able to move books?

* * *

Page 95:

When I mentioned all this to Stamler, he didn’t remember any part of this cancer-cholesterol debate. In this way, he is a microcosm of a larger phenomenon that allowed the diet-heart hypothesis to move forward: inconvenient results were consistantly ignored; here again, “selection bias” was at work.

WOW… Pot. Kettle. Black!

* * *

Cribbing Taubes Alert

GCBC, page 38:

The principal investigator on the trial was Ivan Frantz, Jr., who worked in Keys’s department at the University of Minnesota. Frantz retired in 1988 and published the results a year later in a journal called Arteriosclerosis, which is unlikely to be read by anyone outside the field of cardiology. […] When I asked Frantz in late 2003 why the study went unpublished for sixteen years, he said, “We were just disappointed in the way it came out.”

BFS, page 96:

Frantz, who worked in Keys’s university department, did not publish the study for sixteen years, until after he retired, and then he placed his results in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, which is unlikely to be read by anyone outside the field of cardiology. When asked why he did not publish the results earlier, Frantz replied that he didn’t think he’d done anything wrong in the study. “We were just disappointed in the way it came out,” he said.

At least Teicholz cites Taubes as the source of the Frantz quote.

* * *

On page 97, Teicholz discusses the Western Electric study:

But the results, after twenty years of study, actually showed that diet affected blood cholesterol only a tiny bit and that the “amount of saturated fatty acids in the diet was not significantly associated with risk of death from CHD [coronary heart disease],” as the authors wrote.

Strangely enough, on page 29 of GCBC Taubes discusses the very same study and quotes the very same line. Whooda thunk? Well, by now everyone shoulda thunk.

Anyway, it is true that Western Electric found only non-significant relationships between saturated fat and CHD mortality.59 But yet again, evidence that runs contrary to the overall thesis is left out. From the paragraph immediately before the saturated fat quote (emphasis mine):

When the risk of death from CHD was analyzed in terms of the component dietary variables, it was inversely related to intake of polyunsaturated fatty acids and positively related to intake of dietary cholesterol.

Those evil vegetable oils that are toxic and cause all kinds of disease evidently protect from CHD death. And all that cholesterol from the butter, meat, and cheese that Teicholz wants people to eat is evidently increasing it. What was that Teicholz was saying about “selection bias”?

* * *

Page 98, Teicholz discusses a study in which participants were from either Hiroshima or Nagasaki and tries really hard to convince you to not to pay attention to the results by saying:

The possible radiation exposure of these men to the atomic bombs dropped on their cities at the end of World War II was not factored into the analysis.

If the only participants are from areas with essentially the same amount of radiation then the results are controlled for. If one cohort had been from Osaka and the other from Nagasaki AND their diet or lifestyle was different then she would have a point, but that is clearly not the case. Not to mention the lead author on the publication in question is a STATISTICIAN working in Japan’s ATOMIC BOMB CASUALTY COMMISSION. Ladies and gentlemen, this is what you call a hail mary.

* * *

On page 99, Teicholz discusses the results of a large cohort study she refers to as the Ni-Hon-San. The results indicate that a diet high in saturated fat increases risk of pretty much “all manifestations of CHD” and that you might do well to eat less of it. Of course Teicholz will have none of this so she again scours the publications to find a molehill to portray as a mountain:

So I dug up the paper on NiHonSan’s diet methodology, published two years earlier. It seems that the team in the San Francisco Bay Area had completely fallen down on the job. Not only did they get diet information from only 267 men, compared to the 2,275 interviewed in Japan and a whopping 7,963 in Honolulu, but they had done these interviews only one time and in only one way (a twenty-four-hour recall questionnaire), whereas the other two teams had assessed diet on two different occasions, several years apart, and in four different ways; this was clearly not the “same method” that the authors claimed. Yet these issues were never mentioned […]

These issues are “never mentioned” except where they are explicitly mentioned… in a published article… by the most widely-read nutrition journal… that is completely free and does not require any kind of subscription to access… which is where Teicholz found them.

A few things:

  • Teicholz seems to think that because CA completed less diet records that somehow invalidates the results.
  • California did more than just the 24-hour recall, according to the methods paper.60 They also did a 7-day food record and a food acculturation questionnaire.
  • Teicholz assumes incompetence by the CA researchers, when in fact it was funding issues. It is described in detail in the book Honolulu Heart Program.61 Books are often compiled from large cohort studies like these (e.g. The Seven Countries Study and The China-Cornell-Oxford Project). Investigative journalism, anyone?

* * *

Page 100:

[T]he Japanese have recently been eating far more meat, eggs, and dairy than they used to since the end of World War II, rates of heart disease have dropped to levels seen by Keys in the 1950s. This means that although the story of diet and disease in Japan is complex, we can pretty well say that based on this trend alone, a diet low in saturated fat was not the factor that spared the Japanese from heart disease in the postwar years.

That’s a bold claim for which Teicholz cites a review article not on heart disease, but on stroke – a particular subset of heart disease.62 Additionally, the article never even mentions meat or even fat consumption. It does mention cholesterol as a risk factor, though. Perhaps Teicholz should have read the conclusion:

The atherogenic effect of hypercholesterolemia is well established and is based on evidence from numerous epidemiological, pathological, and biological studies. Furthermore, the proportion of atherothrombotic cerebral infarctions may have recently increased in Japan, because this subtype currently accounts for approximately one third of cerebral infarctions in the Japan Standard Stroke Registry Study (JSSRS). We should formulate a confirmed strategy for lipid management to prevent cerebral infarction.

Teicholz cites no evidence for the increased meat consumption, but no matter. I know how to Google. It seems that meat consumption has increased in Japan over the years, although it still pales in comparison to US consumption which is probably why Japanese heart disease remains comparatively low.

meat_consumption_per_capita_graph-1024x682

Source here and here.

* * *

Page 101:

Seymour Dayton was concerned about the extremely low levels of arachidonic acid, an essential fatty acid present mainly in animal foods, among his prudent dieters.

A few things: 1) Arachidonic acid is one of those evil polyunsaturates, 2) Arachidonic acid is not an EFA, and 3) Here’s what Dayton said about AA on the exact page from the exact paper Teicholz cites34 (emphasis mine)

The other observation which raised some question of a possible toxic effect was the low arachidonic acid concentrations in atheromata of long-term, high-adherence subjects on the experimental diet (tables 37 to 40). For reasons already cited, this may be more appropriately viewed as evidence of a salutary rather than a toxic effect.

* * *

Page 101-102:

In the United States, Pete Ahrens, who was still the prudent diet’s most prominent critic, continued to publish his central point of caution: the diet-heart hypothesis “is still a hypothesis … I sincerely believe we should not. . . make broadscale recommendations on diets and drugs to the general public now.”

A few things:

  1. Ahrens is not referring to the diet-heart hypothesis in this text, he is referring to the lipid hypothesis. There is a difference. Teicholz actually clips the words “lipid hypothesis” from one of the quotes: “The Lipid Hypothesis is still a hypothesis.” In fact, he never even mentions the diet-heart hypothesis in the text.
  2. Ahrens does write those words, but all three phrases are out of order. As a journalist, are you allowed to do that? Take bits of text and arrange them however, as long as you put ellipses in there? If they were to go in order of appearance it would be “[…] make broadscale recommendations on diet and drugs to the general public now […] I sincerely believe we should not […] is still a hypothesis […]” By the way there is about one and a half paragraphs between the last two quotes.
  3. This is another example of quote-mining by Teicholz, because Ahrens actually says some not-so-bad things about the Lipid hypothesis in the text and cholesterol-lowering in general. Two can play the quote-mining game. For instance:

[When asked whether we should abandon the Lipid Hypothesis] My reply to the last question is “no”: I submit that the Lipid Hypothesis has never really been put to an adequate test, and that therefore we cannot conclude that the premise is false.

AND

[I]t seems entirely logical, indeed essential, for internists to screen routinely for hyperlipidemia […] If hyperlipidemia persists, a full year’s evaluation should be made of a low-cholesterol, low-saturated, high polyunsaturated-fat diet, with moderation in alcohol intake.

AND

The Lipid Hypothesis is still a hypothesis. I have tried to show that it is a viable one, and how in the future we may better put it to test.

* * *

Cribbing Taubes Alert

On page 22 of GCBC Taubes states the following:

The resulting literature very quickly grew to what one Columbia University pathologist in 1977 described as “unmanageable proportions.”

On page 102 of BFS Teicholz writes:

By the late 1970s, however, the number of scientific studies had grown to such “unmanageable proportions,” as one Columbia University pathologist put it, that it was overwhelming.

This quote is from Dietary Goals for the United States—Supplemental Views publication which is an 881-page text, at least in PDF format. What are the odds that Teicholz independently arrived at “unmanageable proportions” in that enormous publication? Do you think this is original research?

* * *

Page 102:

The ambiguities inherent to nutrition studies opened the door for their interpretation to be influenced by bias— which hardened into a kind of faith. There were simply “believers” and “nonbelievers,” according to cholesterol expert Daniel Steinberg.

Interestingly enough, this person that Teicholz calls a “cholesterol expert” would almost certainly disagree with the entire thesis of BFS, since he appears to accept that high cholesterol plays a role in heart disease, and that serum cholesterol can be controlled to some degree via the diet. This is made pretty clear if you read the publication Teicholz cites for this.63 In fact, Ahrens himself (whom Teicholz describes above as the biggest critic of the diet-heart hypothesis – although she confuses it with the lipid hypothesis) was, according to Steinberg, one of the first to conduct “the definitive demonstration that saturated fats tend to raise while polyunsaturated fats tend to lower blood cholesterol in humans […]” Steinberg’s entire review series on the pathogenesis of atherosclerosis is both quite interesting and readable. I highly suggest reading them if you are interested in the topic. They are open access papers, but if you didn’t want to go to the trouble of finding them here is a link to the series.

Chapter 5: The Low-Fat Diet Goes to Washington

 

Cribbing Taubes Alert

BFS, page 112:

[W]hen Senator McGovern announced his Senate committee’s report, called Dietary Goals, at a press conference in 1977, he expressed a gloomy outlook about where the American diet was heading. “Our diets have changed radically within the past fifty years,” he explained, “with great and often harmful effects on our health.”

The problem here is that Teicholz cites the source of this quote as “Select Committee on Nutrition and Human Needs of the United States Senate, Dietary Goals for the United States (Washington, DC: US Government Printing Office, 1977); 1.” However, this quote does not appear on page 1. It appears on page XIII. Normally I would chalk this up to a simple citation error.64 The reason I mention it is because Taubes uses the same exact quote on page 10 of GCBC, and also mistakenly cites the source of the quote as being on page 1. I would argue (as I have done previously many times) that this is good evidence that Teicholz is simply lifting sentences from others and simply citing what they cite – likely without ever even seeing the source material.

* * *

Cribbing Taubes Alert

Page 112:

The New York Times health columnist Jane Brody perfectly encapsulated this idea when she wrote, “Within this century, the diet of the average American has undergone a radical shift away from plant-based foods such as grains, beans and peas, nuts, potatoes, and other vegetables and fruits and toward foods derived from animals—meat, fish, poultry, eggs and dairy products.”

This Brody quote appears word-for-word on page 10 of GCBC. It’s from a book Brody published 30 years ago. Isn’t it astonishing that both Taubes and Teicholz can do completely independent research, find the exact same publications, and use the same quotes from those publications?

* * *

Page 122:

Ahrens chose a nine-member task force representing the full range of scientific views on the diet-heart hypothesis. The panel deliberated for several months over each link in the chain of the diet-heart hypothesis, from eating saturated fat, to total cholesterol, to heart disease. The results, however, were not exactly welcome news to diet-heart supporters […] The final report from the Ahrens task force in 1979 made it clear that the majority of its members remained highly skeptical of the idea that reducing fat or saturated fat could deter coronary disease.

Actually, the task force didn’t make that clear at all.65 I actually blogged about this not too long ago because Taubes cites the same obscure paper and comes to a similar but still erroneous conclusion.

The paper gives a score of 0-100 to associations between a given dietary issue and atherosclerosis, where 0 is the weakest evidence for the association and 100 is the most rock-solid evidence. The final score is an aggregation of scores by several experts in the field based on epidemiological evidence, animal studies, human interventions, autopsies, biological plausibility, etc. Cholesterol alone received a score of 62. Saturated fat alone received a 58. Cholesterol and fat together received a 73. For comparison the association between alcohol and liver disease received an 88, and the association between carbohydrate and atherosclerosis got an 11. Carbohydrate and diabetes got a 13.

I don’t want to tell you how you should interpret that data, but it seems pretty clear to me that the evidence that cholesterol and fat play a role in atherosclerosis is quite strong: well above the halfway point and approaching the level of alcohol and liver disease. Teicholz, however, tells her readers that the committee was “highly skeptical” for reasons that should be pretty clear by now.

 

* * *

Cribbing Taubes Alert

On pages 56-59 of GCBC Taubes discusses lipid trial and a consensus conference. On page 127-134 Teicholz discusses the same trial and conference in a strikingly similar way.

GCBC page 56:

The second trial was the $150 million Lipid Research Clinics (LRC) Coronary Primary Prevention Trial. The trial was led by Basil Rifkind of the NHLBI and Daniel Steinberg, a specialist on cholesterol disorders at the University of California, San Diego. The LRC investigators had screened nearly half a million middle-aged men and found thirty-eight hundred who had no overt signs of heart disease but cholesterol levels sufficiently high-more than 265 mg/dl-that they could be considered imminently likely to suffer a heart attack.

BFS page 127:

The other trial was the $150 million Lipid Research Clinic Coronary Primary Prevention Trial (LRC) […] LRC was led by Basil Rifkind, chief of NHLBl’s Lipid Metabolism Branch, together with Daniel Steinberg, a cholesterol specialist at the University of California, San Diego. They screened nearly half a million middle-aged men and found 3,800 with levels of cholesterol high enough (265 mg/dL or above) to be considered likely to have a heart attack soon […]

GCBC page 57:

To call these results “conclusive,” as the University of Chicago biostatistician Paul Meier remarked, would constitute “a substantial misuse of the term.”

BFS page 130:

The biostatistician Paul Meier commented that to call the results “conclusive” would constitute “a substantial misuse of the term.”

GCBC page 57:

As Rifkind told Time magazine, “It is now indisputable that lowering cholesterol with diet and drugs can actually cut the risk of developing heart disease and having a heart attack.”

BFS page 130:

[…] Rifkind told Time magazine, “It is now indisputable that lowering cholesterol with diet and drugs can actually cut the risk of developing heart disease and having a heart attack.”

sorry it's true gcbc

sorry it's true bfs

Conclusion

 Some have called this review mere quibbling or nit-picking, and that the true thesis of BFS still stands. I would strenuously argue the opposite. If I was nit-picking I would have also brought up one or more instances where Teicholz misquotes someone, but the actual quote is not substantively different. I imagine those are innocent mistakes. Nor do I think that Teicholz’s main arguments still hold up. The arguments in this book are scientific claims that are purportedly supported by scientific evidence. If it turns out, however, that the evidence was never really there in the first place then you can no longer make the claim.

The issues I bring up in this review are too substantial and too numerous to be ignored. If you were to remove all of the instances where Teicholz deeply distorts a study or publication, and you were to remove all conclusions that she draws from the distortions you would be left with nothing but a pamphlet.

 cloud

Refs

1. Biss, K., Ho, K.-J., Mikkelson, B., Lewis, L. & Taylor, C. B. Some Unique Biologic Characteristics of the Masai of East Africa. N. Engl. J. Med. 284, 694–699 (1971).

2. Mann, G. V., Spoerry, A., Gray, M. & Jarashow, D. Atherosclerosis in the Masai. Am. J. Epidemiol. 95, 26–37 (1972).

3. How the hell does one even pronounce that, by the way??

4. Hrdlicka, A. Physiological and medical observations among the Indians of southwestern United States and northern Mexico. (Washington, Govt. Print. Off., 1908). at <http://archive.org/details/physiologicalmed00hrdl>

5. Prentice, G. Cancer Among Negroes. Br. Med. J. 2, 1181 (1923).

6. Crawford, M. A. Fatty-acid ratios in free-living and domestic animals: Possible Implications for Atheroma. The Lancet 291, 1329–1333 (1968).

7. Rittenberg, D. & Schoenheimer, R. Deuterium as an indicator in the study of intermediary metabolism XI. Further studies on the biological uptake of deuterium into organic substances, with special reference to fat and cholesterol formation. J. Biol. Chem. 121, 235–253 (1937).

8. Keys, A. Human Atherosclerosis and the Diet. Circulation 5, 115–118 (1952).

9. Truswell, A. S. Evolution of dietary recommendations, goals, and guidelines. Am. J. Clin. Nutr. 45, 1060–1072 (1987).

10. Hopkins, P. N. Effects of dietary cholesterol on serum cholesterol: a meta-analysis and review. Am. J. Clin. Nutr. 55, 1060–1070 (1992).

11. Mann, G. V. The epidemiology of coronary heart disease. Am. J. Med. 23, 463–480 (1957).

12. Keys, A. The diet and the development of coronary heart disease. J. Chronic Dis. 4, 364–380 (1956).

13. Yerushalmy, J. & Hilleboe, H. E. Fat in the diet and mortality from heart disease; a methodologic note. N. Y. State J. Med. 57, 2343–2354 (1957).

14. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y. 20, 118–139 (1953).

15. Keys, A. Coronary heart disease in seven countries. I. The study program and objectives. Circulation 41, I1–8 (1970).

16. Keys, A. Epidemiological Studies Related to Coronary Heart Disease: Characteristics of Men Aged 40–59 in Seven Countries. Acta Med. Scand. 180, (1966).

17. Keys, A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. (Harvard University Press, 1980).

18. Kromhout, D., Menotti, A. & Blackburn, H. W. The Seven Countries Study: A Scientific Adventure in Cardiovascular Disease Epidemiology. (Brouwer, 1994).

19. Toshima, H., Koga, Y. & Blackburn, H. Lessons for Science from the Seven Countries Study: A 35-Year Collaborative Experience in Cardiovascular Disease Epidemiology. (Springer Japan, 2011).

20. Page, I. H., Stare, F. J., Corcoran, A. C., Pollack, H. & Wilkinson, C. F., Jr. Atherosclerosis and the fat content of the diet. Circulation 16, 163–178 (1957).

21. Page, I. H. et al. Dietary Fat and Its Relation to Heart Attacks and Strokes. Circulation 23, 133–136 (1961).

22. Medicine: Fat in the Fire. Time (1960). at <http://content.time.com/time/magazine/article/0,9171,895155,00.html>

23. The Fat of the Land. Time 77, 48 (1961).

24. STOUT, C., MARROW, J., BRANDT, E. N., Jr & WOLF, S. UNUSUALLY LOW INCIDENCE OF DEATH FROM MYOCARDIAL INFARCTION. STUDY OF AN ITALIAN AMERICAN COMMUNITY IN PENNSYLVANIA. JAMA 188, 845–849 (1964).

25. Keys, A. Arteriosclerotic heart disease in Roseto, Pennsylvania. JAMA 195, 93–95 (1966).

26. Lowenstein, F. W. Epidemiologic Investigations in Relation to Diet in Groups Who Show Little Atherosclerosis and Are Almost Free of Coronary Ischemic Heart Disease. Am. J. Clin. Nutr. 15, 175–186 (1964).

27. Ahrens, E. H., Jr, HIRSCH, J., OETTE, K., FARQUHAR, J. W. & STEIN, Y. Carbohydrate-induced and fat-induced lipemia. Trans. Assoc. Am. Physicians 74, 134–146 (1961).

28. Anderson, K. M., Castelli, W. P. & Levy, D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA 257, 2176–2180 (1987).

29. Castelli WP. Concerning the possibility of a nut… Arch. Intern. Med. 152, 1371–1372 (1992).

30. Coronary heart disease and carbohydrate metabolism. JAMA 201, 1040–1041 (1967).

31. Christakis G, Rinzler SH, Archer M & Kraus A. Effect of the anti-coronary club program on coronary heart disease risk-factor status. JAMA 198, 597–604 (1966).

32. Christakis, G., Rinzler, S. H., Archer, M. & Maslansky, E. Summary of the research activities of the anti-coronary club. Public Health Rep. 81, 64–70 (1966).

33. Jolliffe, N., Rinzler, S. H. & Archer, M. The Anti-Coronary Club; Including a Discussion of the Effects of a Prudent Diet on the Serum Cholesterol Level of Middle-Aged Men. Am. J. Clin. Nutr. 7, 451–462 (1959).

34. Dayton, S., Pearce, M. L., Hashimoto, S., Dixon, W. J. & Tomiyasu, U. A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis. Circulation 40, II–1 (1969).

35. Dayton, S. & Pearce, M. DIET AND ATHEROSCLEROSIS. The Lancet 295, 473–474 (1970).

36. Pearce, M. L. & Dayton, S. Incidence of cancer in men on a diet high in polyunsaturated fat. Lancet 1, 464–467 (1971).

37. Blasbalg, T. L., Hibbeln, J. R., Ramsden, C. E., Majchrzak, S. F. & Rawlings, R. R. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am. J. Clin. Nutr. 93, 950–962 (2011).

38. Cooper, R. et al. Trends and Disparities in Coronary Heart Disease, Stroke, and Other Cardiovascular Diseases in the United States Findings of the National Conference on Cardiovascular Disease Prevention. Circulation 102, 3137–3147 (2000).

39. Nydegger, U. E. & Butler, R. E. Serum Lipoprotein Levels in Patients with Cancer. Cancer Res. 32, 1756–1760 (1972).

40. A co-operative trial in the primary prevention of ischaemic heart disease using clofibrate. Report from the Committee of Principal Investigators. Br. Heart J. 40, 1069–1118 (1978).

41. Beaglehole, R., Foulkes, M. A., Prior, I. A. & Eyles, E. F. Cholesterol and mortality in New Zealand Maoris. Br. Med. J. 280, 285–287 (1980).

42. Kark, J. D., Smith, A. H. & Hames, C. G. The relationship of serum cholesterol to the incidence of cancer in Evans County, Georgia. J. Chronic Dis. 33, 311–322 (1980).

43. Garcia-Palmieri, M. R., Sorlie, P. D., Costas, R. & Havlik, R. J. An apparent inverse relationship between serum cholesterol and cancer mortality in Puerto Rico. Am. J. Epidemiol. 114, 29–40 (1981).

44. Stemmermann, G. N., Nomura, A. M., Heilbrun, L. K., Pollack, E. S. & Kagan, A. Serum cholesterol and colon cancer incidence in Hawaiian Japanese men. J. Natl. Cancer Inst. 67, 1179–1182 (1981).

45. Miller, S. R., Tartter, P. I., Papatestas, A. E., Slater, G. & Aufses, A. H., Jr. Serum cholesterol and human colon cancer. J. Natl. Cancer Inst. 67, 297–300 (1981).

46. Kozarevic, D. et al. Serum cholesterol and mortality: the Yugoslavia Cardiovascular Disease Study. Am. J. Epidemiol. 114, 21–28 (1981).

47. Rose, G. et al. Colon cancer and blood-cholesterol. Lancet 1, 181–183 (1974).

48. Williams, R. R. Cancer Incidence by Levels of Cholesterol. JAMA 245, 247 (1981).

49. Gammal, E. B., Carroll, K. K. & Plunkett, E. R. Effects of Dietary Fat on the Uptake and Clearance of 7,12-Dimethylbenz(α)anthracene by Rat Mammary Tissue. Cancer Res. 28, 384–385 (1968).

50. Patek, A. J., Kendall, F. E., De Fritsch, N. M. & Hirsch, R. L. Cirrhosis-enhancing effect of corn oil. Protection by choline. Arch. Pathol. 82, 596–601 (1966).

51. Ueshima, H., Iida, M. & Komachi, Y. Is it desirable to reduce total serum cholesterol level as low as possible? Prev. Med. 8, 104–105 (1979).

52. Feinleib, M. Summary of a workshop on cholesterol and noncardiovascular disease mortality. Prev. Med. 11, 360–367 (1982).

53. Feinleib, M. On a possible inverse relationship between serum cholesterol and cancer mortality. Am. J. Epidemiol. 114, 5–10 (1981).

54. Jacobs, E. J., Newton, C. C., Thun, M. J. & Gapstur, S. M. Long-term Use of Cholesterol-Lowering Drugs and Cancer Incidence in a Large United States Cohort. Cancer Res. 71, 1763–1771 (2011).

55. Murai, T. et al. Low Cholesterol Triggers Membrane Microdomain-dependent CD44 Shedding and Suppresses Tumor Cell Migration. J. Biol. Chem. 286, 1999–2007 (2011).

56. Hu, J. et al. Dietary cholesterol intake and cancer. Ann. Oncol. 23, 491–500 (2012).

57. Bardou, M., Barkun, A. & Martel, M. Effect of statin therapy on colorectal cancer. Gut 59, 1572–1585 (2010).

58. Law, M. R., Thompson, S. G. & Wald, N. J. Assessing possible hazards of reducing serum cholesterol. Br. Med. J. 308, 373–379 (1994).

59. Shekelle, R. B. et al. Diet, Serum Cholesterol, and Death from Coronary Heart Disease. N. Engl. J. Med. 304, 65–70 (1981).

60. Tillotson, J. L. et al. Epidemiology of coronary heart disease and stroke in Japanese men living in Japan, Hawaii, and California: methodology for comparison of diet. Am. J. Clin. Nutr. 26, 177–184 (1973).

61. Kagan, A. Honolulu Heart Program. (CRC Press, 1996).

62. Tanaka, T. & Okamura, T. Blood Cholesterol Level and Risk of Stroke in Community-based or Worksite Cohort Studies: A Review of Japanese Cohort Studies in the Past 20 years. Keio J. Med. 61, 79–88 (2012).

63. Steinberg, D. Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy: part II: the early evidence linking hypercholesterolemia to coronary disease in humans. J. Lipid Res. 46, 179–190 (2005).

64. Let’s face it. They are bound to happen. There are surely citation errors in this blog post.

65. Ahrens, E. H. The evidence relating six dietary factors to the Nation’s health. Introduction. Am. J. Clin. Nutr. 32, 2627–2631 (1979).

66. Broad, W. J. NIH deals gingerly with diet-disease link. Science 204, 1175–1178 (1979).

Advertisements

86 thoughts on “The Big Fat Surprise: A Critical Review; Part 1

  1. Very well thought out and written.
    Proves that words indeed can have an effect.

    But actions do speak louder than words, and results even louder.

    I have placed many patients on lower carb higher natural fat diets with tremendous success. The physiology works.

    You may not pick all you want but lowfat diets do not work as well in controlling obesity, hunger, lipoproteins, etc, etc.

    So while I believe you are on the wrong side of the physiological debate, I do give you kudos for your research and preparation.

    Now you just need to work out proper conclusions.

    • Fair enough. You and others probably get the impression that I am against low-carb diets. This is not the case. I am simply against lying and misrepresentation. If someone wants to eat a low-carb, high-fat diet that’s fine with me. But books such as this give people reading them the impression that eating a plate full of meat and butter is actually healthier than a banana or a baked potato or a piece of bread. This is simply not the case.

      I think one can write a very evidence-based diet/nutrition book about the benefits of low-carb diets. But this is not one of those books.

      Anyway… Thank you for the kind words.

      • Seth

        Everyone has a bias.
        While you may not be anti-low carb, professionally from my experience in my practice, the substitution of natural fats for processed carbs has produced terrific results in he majority.

        My issue is not with carbs in general but more with processed carbs.

        I also do not believe that there is a one size fits all diet for everyone.

        But in the metabolically challenged, which have increased exponentially since the govt advocated low fat high carb diets, lower processed carb diets work.

      • This reply is aimed at drhorvitz, but I can’t reply to his/her comment.
        “But in the metabolically challenged, which have increased exponentially since the govt advocated low fat high carb diets, lower processed carb diets work.”
        You’ve made the error that many others make, in assuming that the American population paid any attention to anything that their government had to say about diet. Please see:-

        http://racingweight.com/blog/dont-blame-the-dentist-for-your-cavities/

        http://nutsci.org/2014/06/13/no-dietary-guidelines-are-not-making-us-sick/

        The American population were bamboozled by marketing. Please see:-

        http://vimeo.com/67977038

      • In my 20 years in practice dealing with obesity, diabetes, heart disease, etc, the patients who suffer from these issues overwhelming follow a standard American diet loaded with carbs and trying to keep fats down.
        When these same patients switch to a low processed carb diet, they improve their health in most all markers checked.

        These are not my opinions based only reading the literature or studies. These are my opinions based on the patients I take care of, evaluate and follow closely.

        Now the metabolically challenged are a different animal than let’s say athletes who have a different metabolism based on their exercise regimen.
        Also industrialized processed carbs are different from natural carbs.
        So we agree on more that you might think, and I am not looking for an argument, I am just stating the results I see every day in my practice.
        Now if someone comes in on a Vegan diet, looks great, feels great and all their biomarkers are good, I tell them to keep doing what they are doing.
        There is much more to this debate but let’s not nitpick just to nitpick.

      • “When these same patients switch to a low processed carb diet, they improve their health in most all markers checked.” “Also industrialized processed carbs are different from natural carbs.”
        I completely agree with you.

        Your first comment to Seth said:-
        “I have placed many patients on lower carb higher natural fat diets with tremendous success. The physiology works.
        You may not pick all you want but lowfat diets do not work as well in controlling obesity, hunger, lipoproteins, etc, etc.”
        Those sentences gave the distinct impression that you prescribe low-carb, high-fat diets to your patients. If you’d written:-
        “I have placed many patients on high natural carb diets with tremendous success. The physiology works.
        You may not pick all you want but high processed carb diets do not work as well in controlling obesity, hunger, lipoproteins, etc, etc.”,
        I wouldn’t have argued with you!

      • Indeed. Well, now Mister Kinbrum, I’ve been on a low fat diet, numerous times in my life and I was always starved. Ravenous. Foaming at the mouth. I even lost 42lb on one. I cracked each time. I’m on a low carb diet now, am also down 42lb and have no hunger at all. No sign of cracking. From your photo, I think you should try it!

    • As a cardiologist who lost 65 pounds eating meat, eggs, beans and green veggies, and who lost 10 inches on his waist, and watched his HDL (the good stuff) rise to an amazing 120 while eating bacon and eggs, I am a firm believer that irrespective of the issues with Ms. Teicholtz’s work, some facts remain.

      We should not worry about cholesterol in our diet, and to continue to encourage the US population to fatten themselves with whole grains and fruits is neither healthy or good public policy.

      http://www.health.harvard.edu/blog/panel-suggests-stop-warning-about-cholesterol-in-food-201502127713

  2. Probably the good doctor too would rather see patients choose low-carb for the right reasons & have realistic expectations instead of listening to pseudoscientific claims.

    As for low-fat high carb diets having created the obesity problem: I’ve yet to see any shred of evidence for this. The Western diet , which is essentially the diet most closely connected to the problem, is not a) particularly low-fat nor b) has it ever been recommended by any authority (junk food, sodas and candy = carbs in Western populations). The mistake made in the past was too much focus on the quantity of fat instead of quality AS PART of a healthy diet. However, it’s evident that people today simply never followed the core of the recommendations –> hence more and more obese.

    • Our guidelines are obeseogenic. As somebody who feeds a family and has always tried to observe Canada’s food rules, I could not understand why as I progressed through middle age I began to get wider and develop high blood pressure. When I examine those guidelines again through the Tiecholz lens, I see they advocate almost 300 grams of carbs daily for a 51 year old woman. I am managing quite fine on 60, losing weight, eating well and, best of all, reducing blood pressure. There is a problem in North America with diet and obesity. People who follow the guidelines advocated by nutritionists, educated through biased and false research, eat too many carbs and are always hungry as a result (Hallberg). The guidelines don’t work. They make us metabolically challenged. Look again at your statement about people in this culture. If most people are becoming sick and overweight, starting in childhood, maybe there is something wrong with the advice being handed out by the so-called nutrition experts. Time for “experts” with integrity to re-examine the issue without resorting to blaming people who tried to follow the standard guidelines without success. When those same people try a different and alternative approach that actually works, you might want to examine those facts with some detachment instead of shooting the messenger.

      • Kathy,

        I completely agree with you, I am currently a student dietitian, and I simply disagree with what I am being learned. Most people are conformed with the ideology that is taught but for me it doesn’t make sense, this is me being a student dietitian for a year, have year to go so I have no made my conclusion yet, but as of now I’m a little concerned about my schooling.

  3. I hope Seth’s writing reaches a wide audience. If this is nit-picking, well, isn’t that how scientists work? His criticisms build up to a powerful refutation of Teicholz’s work.

  4. Fantastic work Seth. I find it sad that there are so many books out there trying to tell a story that misinterpret the science in order to support said story. It takes so much time for us scientists to fact check every little thing that I fear the layman will never be able to (or just won’t bother to) distinguish the good from the bad.

  5. Seth said: “It’s funny because on pages 34-36 Teicholz criticizes Keys for not including more European countries like France and Switzerland (which incidentally would have fallen right in line with Keys’s graph).” Well, if Denise hasn’t put the wrong graph (or I misunderstood which one you are referring to) in her analysis, Switzerland had (20) had more or less half the “arteriosclerotic and degenerative heart disease” mortality incidence than Australia with about the same average fat ingestion as per cent of calories, France half that of Italy with higher fat ingestion. I wouldn’t call it falling in line.

    Nina wrote: “He made no attempts to refute his own ideas, as Popper advised. He promoted the “idol of his mind” without hesitation.” and Seth said: “OMG. What?! How?? Can I get some evidence for that?” Did he published anywhere the impact of sugar on cardiovascular and all-cause mortality? Nina says that was Alessandro Menotti et alter in 1999 (I don’t have access to it) who did the nearer thing to an analysis of this kind for “sugar products and pastries” excluding “chocolate, ice cream and soft drinks”. If I remember it correctly Dr. Lustig has written something along the same line about sugar not been analyzed independently as first potential causal factor in the Seven Countries study.

    Not that I am interested at all in anything but overall mortality.

    • If you look at the original Y&H paper and scroll to the end you will see the raw data they used. (Data, by the way, that is actually a few years off from the data Keys used in his paper so it’s not an exact comparison, but that’s not terribly important.)

      Let’s look at France. France consumes a diet of 29% fat according to this data. If you look at heart disease in the ages of 45-49 and 55-59 you get 79.9 and 282.1 deaths per 100,000, respectively. Or about 0.8/1,000 and 2.8/1,000. Where do you think those data points would go on this graph? I’m just eyeballing here, but I think it would be close to this.

      What about Switzerland? Switzerland’s fat intake is 33% fat. What about death from heart disease? Again, in the ages of 45-49 and 55-59 you get 110.0 and 331.3 per 100,000 respectively. Or 1.1/1,000 and 3.3/1,000. Are you following me? Can you eyeball where that might go on the same graph? I’ll wait…
      It would probably look something like this. I’m just eye-balling this on MS Paint so it’s not exactly scientific, but it would be very close. I recommend you get your information directly from the source instead of food blogs.

      As for the other part of your comment, there was no reference for that quote or the paragraph where it came from. I was trying to point out that it was simply hyper-biased nonsense without evidence. There is of course no way Teicholz can know what Keys was thinking.

      • Well, the figure included by Denise that I have linked is a veracious replica of Figure 3 from the paper by Yerushalmy and Hilleboe that you have provided (thanks!) and she thoroughly commented upon. Actually I am not certain that you have read either Denise’s critique or Y&M’s paper since your comment on Table I from Y&H is about B-26 (“arteriosclerotic and degenerative heart disease”) AND B-27 (“other diseases of the heart”) mortality while Figure 3 is about B-26 alone, nearer what Keys used (B-26 minus 421 “chronic endocarditis not specified as rheumatic”). Of course as Y&M discussed it is much more informative taking into account both complete B-26 and B-27 at the same time (it seems Keys’ original paper didn’t do it —I don’t have access to it either) but even better if we focus on all-cause mortality as seen on Table IV from Y&H’s paper and commented upon by Denise: no reason here to fear fat.

        About Keys don’t analyzing sugar as an independent factor I have no access to the paper copy of Nina’s book and I haven’t figured out how to look for page numbers but I have finally located Dr. Lustig’s The Fructose Epidemic cite: “However, Keys neglected to perform the converse analysis demonstrating that the effect of saturated fat on cardiovascular disease (CVD) was independent of sucrose. In other words, sucrose and saturated fat co-migrated; it is impossible to tease out the relative contributions of sucrose vs. saturated fat on CVD from this study.” It seems that Alessandro Menotti et alter actually did the nearest thing to address it.

      • Perhaps I am confused as to what you’re getting at. I took the numbers from the Appendix of the Y&H paper. The mortality numbers there appear to combine B-26 and B-27.

        At any rate, I read Minger’s post a couple years ago. I seem to recall that she agreed that people have been unfairly using the 1953 Keys paper and the Y&H paper as some kind of “proof” that Keys was a dishonest scientist and therefore everyone is free to eat a bunch of beef and lard and no heart disease will come to you. I have blogged about this in the past. There you will also find a copy of the 1953 Keys paper if you wish to peruse it. To be clear, I’m not saying people should fear fat. What I am against is the misrepresentation of science.

        As for the Menotti paper, here it is if you’d like to read it: http://ge.tt/9wztP6r1/v/0 I doubt you’ll find anything scandalous there. As far as I know, no one is arguing that pastries are good for your health.

      • Andrés, if you’re still reading the comments here — I’ve seen that Lustig quote a few places, and he’s incorrect. Keys did look at sugar in his Seven Countries analyses and found that its association diminished once saturated fat was adjusted for (whereas the association with saturated fat remained strong even when adjusting for sugar). In that sense, at least from a mathematic perspective, saturated fat was confounding the relationship between sugar and heart disease, rather than sugar confounding the relationship between fat and heart disease. Hence why Keys didn’t pursue the sugar relationship any further.

        This was the quote from Keys’s Seven Countries book:

        “Partial correlation analysis showed that, with dietary saturated fat held constant, the correlation between dietary sucrose and the incidence of coronary heart disease is not significant (r= 0.13). On the other hand, with sucrose held constant in the partial correlation analysis, the correlation of the coronary incidence rate with the mean percentage of calories from saturated fat is 0.62.”

  6. In my opinion, death rates due to heart disease are not the best measure, as they depend not only on lifestyle, but also on other variables like, for example, the quality of the country’s health system (better treatments available, and to more citizens, may result in lower death rate due to CVD, with the same prevalence of heart disease). I think it would be better to graph prevalence of CVD instead of deaths, if we want to establish an association between diet and development of heart disease. Of course, I am all for hard endpoints instead of surrogate markers, but we cannot ignore this fact.

  7. I am probably to stupid to debate the nuances of each so called study that purports to show x y or z. I would probably rather cut my wrists than write up a detailed review like this as well.

    The issue I have with the critique in this article are perhaps encapsulated in the following quote “…the experimental diet of unsaturated fats had less overt myocardial infarction, sudden death, cerebral infarction, fatal atherosclerotic events, etc. And not by a tiny margin – a significant margin.”

    Exactly what does this tell us if anything at all? Does the presence of saturated fat come with normal carb or high carb intake or was the saturated fat taken with a low or no carb diet. It’s not clear but to my mind given what is supposedly known, saturated fat together with normal to high carb is very likely to show elevated myocardial infarction etc when compared to a plant based unsaturated fat diet. So if that is the case why exactly would a normal to high carb diet with lots of saturated fat be evidence that a low to no carb saturated fat diet is bad for health?

    I have recently noticed the many times that proponents of the anti saturated fat type or those seeking to dismiss studies supporting saturated fat will use the argument as stated above, without qualifying at all what in fact the diet which damns saturated fat is made up of. To my mind this type of intellectual dishonesty is as bad as the author being castigated here.

    I have grown extremely wary of those who profess superior intellectual knowledge/rigor, yet seemingly fall into the same trap they seek to dismiss others with. I am also inherently suspicious of listening to a critique which when read leaves one wondering exactly what the critiquing author actually does believe.

    I am probably one of the few who can be considered disappointed with this article but then I suppose that is down to my inability to understand the intellectual side of this critique.

    • Jay, I am not arguing for a specific diet, whether high-CHO, low-CHO, vegan, high-fat, high-protein, macrobiotic…whatever. My point with the above quote is that Teicholz (and others) use the Dayon/Pearce studies as evidence that vegetable oils are detrimental to health. However, if you actually read the studies you will find that the authors don’t claim that vegetable oils are associated with poor health. In fact, the evidence they provide would suggest the opposite.

      My argument is not that everyone should throw away the butter and pick up the peanut oil, but rather that Teicholz and Taubes are in effect lying to their audience about the content of the publications. Make sense?

      • Seth,

        There is no doubt you have done a huge amount of analysis and much digging to come to your conclusions. I think where you are losing some of us is using emotive language i.e. “lying” which may be correct but seems to punctuate your findings/conclusions on a confrontational ending.

        Debate and refutation are all good for people to make decisions on issues, especially from people more qualified than ourselves. This is why I try to listen to as many views as possible. However I tend to stay clear of and avoid views which are always seem to rely on what I will refer to as the “bigger dick” syndrome.

        For instance on the vegan side I find Dr MacDougall to be a particularly repulsive individual, whose message no matter how persuasive for some is just plain repugnant in the way it is forced onto others who have not taken sides. This is in my view the danger in analysing and critiquing other’s work, that one starts to display personality onto otherwise objective (maybe subjective) work and in so doing you lose not only your prospective audience but also your message.

        My 5 pennies worth is that you are taking some really good work and clouding it with emotive speak, but then again that’s purely my view.

      • Admiring the time and energy you put into this review. It certainly helps me a lot through the transition to a vegetarian. Truth about nutrition for the public is puzzling enough, and maybe that is why books to promote healthy benefits of fat sell. But you are absolutely right, if these books make their claim on studies and research. It is a sin to deliberately make misinterpretation.

      • Jay – Seth is using the English language. You think it is emotive because it contradicts your beliefs. Would you rather he said she was economical with the truth?

        to lie: noun. 1. a false statement made with deliberate intent to deceive; an intentional untruth; a falsehood.

      • Frankly Joe you seem to be one of those insufferable people who believe they have some superior knowledge of intent, objectivity and what others are thinking. Thanks for the English lesson. Perhaps next you can read my mind too!

        Listen to Seth’s first podcast with his sister and tell me he is not letting emotion and his subjective views of others run away with his clearly great intellect – which is my actual point. Frankly I stopped listening after a 20 mins because rather than me disagreeing with Seth, I got tired of Seth calling others stupid and less intelligent than himself.

        It is not for you Joe to troll others who happen to disagree with some of what Seth says or how he explains what he believes. Rather than pointing out my or someone else’s inherent bias, perhaps you should introspect a little and check up on your own immature manner and subjective bias, and the manner in which you engage with other’s about whom you know very little.

        But alas I suspect you are too egotistical to see that perhaps others can speak English, even if it is not their first language, and have an alternative view of the world, all of which may actually be superior to yours rather than inferior as you seem to think.

      • While I appreciate your insults, I don’t think you’re being honest. I just listened back to the podcast you mentioned. I didn’t recall ever saying anyone was stupid or less intelligent than myself, and I did not hear myself saying it either. However, I will happily recant if I am shown to be wrong. Saying other people are less intelligent than I am is not only uncharacteristic of me, but I certainly don’t believe it, either.

  8. How long did it take me to find this with Google…
    Three seconds…

    But there’s not a photo post on this.

    Google Dayton Pearce Veterans and 31 and up pops a table with a summary of the results including exactly what Nina and Gary quote.
    They are not making it up. It’s just that you’re a bit of an incompetent..

    • You are correct. There were at least 2 papers published from this trial. I must have been looking at the wrong paper when I wrote that. It has been removed.

    • Apologize? To who? For what? I wrote: “I can’t for the life of me find where Taubes got those numbers. If someone can find where he gets those numbers please let me know.” You let me know. I corrected. Get off your high horse.

  9. No, I won’t. You are a shit, Seth. You’ve behaved like a shit. You’ve done down two of the greatest literature research writers of modern medicine. Had I done that, I would profoundly apologise. But, maybe I’m not a shit.

    • Pathetic. Well done – you spotted a mistake – and he acknowledged it and changed his theory. That is how science works. Now go disprove the other 499 holes he found in this book.

  10. I think it was useful of Gearóid Ó Laoi to point out Seth’s mistake, and it was right for Seth to acknowledge his mistake. No more is needed. And I would suppress comments that include profanity and insults.

  11. He, the shit of whom I speak, in order to subconsiously bolster his feeling of inferiority has got his teeth, the nit-picking ones, stuck into two of the great leaders of modern nutritional science who by dint of sheer deep research have pulled the strings of knowledge together from numerous disciplines, thereby overcoming one of the great stumbling blocks of modern science, compartmentalisation. Minor errors in no way detract from the fundamentally correct message, which in my case has me down 19% of my longterm body weight, without hunger. Taubes and Teicholz are giants. Seth is a minnow. If he got on their shoulders he might make a flounder..
    As for insults etc., I’ve called him no more than he deserves and probably a lot less. Someone who couldn’t find what I found in three seconds on Google, should shut up.
    Go on, Seth, apologise. You’ll feel better after it.
    As for profanity.
    I’ll tell you what’s profane. The thousands of obese Americans dying of diabetes because of incorrect advice.

    • You are deluded. If Americans have been eating a low-fat diet for the past few decades then I’m Santa Claus.

      Like I said – you found a mistake which was corrected. Now go dispove the other 499 holes he found. As for profanity – you will notice that Seth managed to get through a massive article without insulting either Taubes or Teicholz once – and you’ve managed to insult him several times in just one short comment.

  12. Pingback: Science of Nutrition Podcast | Weight Loss - xcuz.me
  13. Pingback: Science of Nutrition Podcast
  14. Seth,
    Interesting blog, but I found your remarks about Teicholz quoting William Castelli most confusing:

    “What the reader doesn’t know is that 1) this quote is taken from an editorial that extols the virtues not of meat and cheese, but of the unsaturated fat in nuts, 2) there is literally a half page of text between the ellipses, 3) the italics are not part of the original quote, and most importantly 4) Teicholz cuts off the quote immediately before the author mentions that he is talking about the people that were the most physically active.”

    I googled “Castelli WP. Concerning the possibility of a nut” and got to the following JAMANET link:

    http://archinte.jamanetwork.com/article.aspx?articleid=616375

    where in both the abstract and the photographically reproduced full text Castelli says:

    “Most of what we know about the effects of diet factors, particularly the saturation of fat and cholesterol, on serum lipid parameters derives from metabolic ward—type studies.2,3 Alas, such findings, within a cohort studied over time have been disappointing, indeed the findings have been contradictory. For example, 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. The opposite of what one saw in the 26 metabolic ward studies, the opposite of what the equations provided by Hegsted et al2 and Keys et al3”

    Sure, most of the editorial is about the Seventh Day Adventists, but here Castelli is speaking strictly about Framingham.

    Later in the editorial, Castelli more or less repeats something similar while talking about the Adventists along with the mention that in Framingham “the people in who ate the most cholesterol and saturated fat weighed the least and were the most physically active.” But he does not try to demonstrate that these two characteristics explained the impact on coronary disease in fact, he says (and this now relating to the Seventh Day Adventists):

    “However in the Cox model, neither weight nor exercise explained the impact on coronary disease.”

    So there is no reason to assume that they would in Framingham either, at least not from what was offered in the editorial.

    So you could possibly accuse Teicholz of cherry picking her quotes, but I don’t think it is fair to say that she butchered the quote she did use or that she distorted it to completely mislead.

    Am I missing something?

    • LexTrey,

      I don’t think you’re confused. What Teicholz does in this instance is not terribly egregious. I have attached the full text article above in the references section if you’re interested in reading it.

      I probably did a poor job of articulating my complaints as well. First off, I’m pretty sure the whole article is a sardonic take on how the results of cohort studies are misinterpreted. But even if we are to take Castelli seriously here, my main point is that Teicholz leaves out important context in order to make bits of the article fit her narrative. For example (like you mentioned) the 26 metabolic ward studies, the Adventist results described in the paper that indicate beef and cheese are associated with CVD risk while nuts and whole wheat conferred a decreased risk, the part that included the exercise, and removing about half the article to string her sentence together.

  15. Adventist studies.. blah blah. These people are deeply religious and law-abiding. This is a huge factor in CAD. Meat eaters who are similarly behaved get a similar effect. This cheese and beef “association”, whatever it is you are talking about is at the level of Tarot cards, or even worse.
    Did you apologise to the lady?

  16. Pingback: Science of Nutrition Podcast | Health Republic Blog
  17. Pingback: Science of Nutrition Podcast | Sports Quebec
  18. Pingback: Le gras saturé: mauvais coupable concernant les maladies cardiaques? Partie 3 de 3. | Le Minarchiste
  19. You’ve done a great job critiquing this book. I had to wade through page after page of favourable reviews of this book on Google to find somebody to dispute Taicolz’s claims. Thanks for making the effort. It makes me believe that authors have a strong motivation to present a book telling readers what they want to hear, i.e saturated fat is good for you and that the motive for the author to make money is a serious impediment to the task of being ethical, truthful and accurate with the facts.

    Here is a point of confusing for me as a reader of your paper however. Regarding the following section;
    “Yep. Crawford “buries” it by making it Figure 1 in his paper.6 I know when I want to bury data in a paper I visualize it and put it at the head of the results.”

    I can’t see how Crawford’s table contradicts Taicolz’sc statement. Am I misinterpreting the table?

    • Thanks for the kind words. The table doesn’t exactly contradict Teicholz’s claims about the results. What I was pointing out was that Teicholz claims Crawford buried the results or tried to hide them in some way, which helps to promote Teicholz’s story that there was some sort of effort by scientists to hide data about saturated fat for some reason. I guess because scientists like to mislead the population in the most inefficient way possible. Or maybe they were all hypnotized by the Great Sorcerer Ancel Keys. Whatever the conspiracy… Craford clearly didn’t hide or bury the results about saturated fat because he made a nice graph with the results and started talking about it at the very beginning of the paper.

  20. Pingback: Le gras saturé coupable des maladies cardiaques ? (III) | Contrepoints
  21. https://www.dropbox.com/sh/x98jt3x4v9dux6o/AADdPxkpGQIetaNBOv725Tdya?dl=0

    Here is a link to many studies on Low Carb High Fat Diets for Dr. Horovitz. Forget about anecdotes, and look at studies, thanks.

    I have had excellent success with patients on a low fat, low animal protein, moderate to high plant protein, and lowish carbs, high veggies. That’s my anecdote, but based on the evidence below:

    https://www.dropbox.com/s/7c1bffygzb60zyo/Reference%20List%20for%20Vegan%20Diet%20and%20Health.rtf?dl=0

    Best to all!

    • Dr Mehta:
      Thanks for the links.
      However what you call anecdotes, I call many years of experience.
      Day in day out I treat patients with all different types of maladies and metabolisms. The Paleo diet is by far the healthiest diet in my practice for which I have seen the best results equaling healthiest weight, metabolic parameters, feeling of being fit, and overall feeling of control and understanding of their body.

      I work in the biggest laboratory in my practice. It is called the “real world” and it can not be duplicated by any double blinded placebo controlled study.

      Paleo is a natural diet that avoids grains and processed foods and for some they also avoid dairy and legumes. A vegetarian lowfat diet can be Paleo. So can a steak and eggs three meals a day. It really depends upon each individual.

      I check each patients wellness and biomarkers prior to giving guidance on diet. If they are a Vegan but in excellent health, I recommend they continue. Same goes if they eat meat, meat and more meat!

      It really all comes down to what works best for each individual.

      • If we left all advances to RCT’s, especially in today’s cronied politicized who has the most money world, the Earth would still be flat and would be sponsored by Monsanto and Coca Cola.

        At a certain point in time, after many years of experience, our brains see patterns that work. A RCT is not always necessary. A RCT can never control all the variables that occur in a day.

        RCT’s are helpful, but they are far far from the answer to everything.

  22. Seth,
    In her article to the New York Times “American’s Nutritional Guidelines are based on weak Science” statistically speaking what you think is Teicholz biggest reasoning flaw?

  23. Thanks for your review of The big fat surprise. I became interested in learning more about it when Nina Teicholz was interviewed by Anna Maria Tremonti on CBC Radio, a journalist I generally admire (if you’re interested, listen to it here). I was surprised that she gave Teicholz a very uncritical reception, quite unusual for her, and, on following days, made comments that she had bought the piece, hook, line and sinker.

    So, a few comments on your conclusions.

    I have always been sceptical of expose pieces (I consider books described as “The Untold Story” or “The Forgotten Story” as being by and for people with very short attention spans).

    I am a historian ,not a scientist, but the respect for original sources is a common principle in both fields. My first brow-raising moment in your review come in the Hrdlicka mis-representation. Even before reading your commentary on her treatment, I thought 1) by 1898-1905 bison were virtually extinct in the North American great plains, so where were they getting the buffalo meat ?and 2) the American southwest is not prime bison country, their native extent being (generally) bounded on the west by the Rocky Mountains. So I was not surprised to learn that she had conflated two sources relating to different locations and time periods (the Lakota reference would have referred to the 1870s and earlier). Not a good start.

    The citation system that so annoys you is quite common in consumer, as opposed to academic, histories. It does not generally have the nefarious purpose ascribed to it by you, it is simply a way to remove all those pesky superscript numbers from littering up the text while retaining some semblance of academic credentials. But it certainly is annoying, though slightly less so than the practice in some histories of grouping citations under one footnote at the end of a paragraph, without providing any information about what bits in the paragraph are supported by each cited work. Laziness equals bad scholarship.

    The mis-use of ellipses is staggering. Properly used, they remove elaborations in a sentence in order to bring together the main point of the sentence. It is arguable in some cases that the elaboration in a paragraph could be handled the same way, but the risk is greater. But no, no one, journalist or other, have licence to reform phrases into a thought the original author never composed.

    I suspect that some of the mis-representations of statistics, like the NHANES study, is fundamentally due to ignorance about interpreting statistical data. For example, I hate people generalizing from averages, without providing information about, for example, skewness in the data. Teicholz obviously did not see that a percentage decline in fats did not necessarily imply an absolute decline in the face of the charted increase in intake. I noted that graph line immediately, so was not surprised that absolute fat consumption had increased. That’s the generous view, of course. Not reading the stats correctly supported her conclusion – had it not would she have mis-read the stats the same way?

    It seems pretty obvious from examples that Teicholz 1) copied citations (at least) from other references, not the source, when she copied in previous errors 2) that she read, at most, abstracts or summaries of technical articles, which are generally easier to get at on the internet than the body of the work. These are undergraduate errors that frequently trip up plagiarizers. She, and others, seem not to have grasped how easy it is the track phrases by electronic searching now.

    It is a pity that someone has to go through all the fact-checking after publication to counter such a disreputable book, because the marketplace does care to do it before-hand. But thank you for making the effort. I referred your site to Anna Maria Tremonti.

  24. Pingback: Distorting Nutrition Facts to Generate Buzz | Pinoria News
  25. Pingback: Distorting Nutrition Facts to Generate Buzz | UltraDrift
  26. Pingback: Distorting Nutrition Facts to Generate Buzz | Oh Alright!
  27. Pingback: Distorting Nutrition Facts to Generate BuzzMy Weight Loss Blog | My Weight Loss Blog
  28. Pingback: Distorting Nutrition Facts to Generate Buzz - HCM Healthy LifeStyle
  29. Pingback: Distorting Nutrition Facts to Generate Buzz | tiernkey
  30. Thank you Seth, for a great analysis. I find the intentional distortion of scientific research to reach a non-scientific conclusion abhorrent, whether the goal is financial gain, fame, or the promotion of political or religious views. It doesn’t matter whether the topic is health, diet, evolution, climate change, etc. –many are very eager to lap up a conclusion that they want to believe without considering the integrity of the supporting arguments. The venomous backlash against those who criticize Teicholz’s pseudo-scientific expose because they want to protect their own faith in the healthfulness of a high-animal-fat diet is just one example of an over willingness of too many people to choose an appealing idea over real science.

  31. Hi Seth~ thanks for doing this. As a PhD, RD nutrition researcher, I have never supported low-fat diets (due to my long standing interest in the benefits of extra virgin olive oil). I picked up this book to read on a business trip expecting to like it. I have no problem with journalist wading into nutrition science and have great respect for the work of Mark Bittman, Michael Moss, and some others. I was truly appalled by “The big, fat surprise”. While she claims to have read “original papers” she clearly had absolutely no understanding of the published data. I started taking notes of errors on p 106 and ended with close to 6 single lined pages of handwritten notes. I kept thinking – why didn’t her editor employ ever someone with an undergraduate degree in nutrition? I can certainly understand an interpretation error or 2 from a journalist writing on nutrition. Her errors were truly stunning. Due to my interest in olive oil, I was curious how she would treat it (admitting this was well into my read and wondering how she was able to get this work published). The study she uses to dismiss the health benefits of olive oil studied chocolate, soy, and black and green tea; not only was olive oil not used in the study, they were looking a compounds not found in olive oil. Even a google search would introduce one to the large literature on olive oil. Conversely, she does not mention one study showing the potential negative effects of red meat on health. I do appreciate your work in carefully presenting the multiple errors in this work. I must say that the publication of this work will make me less likely to buy any science book published by Simon and Schuster as they apparently do not hire editors who are capable of reviewing a layperson’s work that involves science. best, Mary

  32. Great job poking holes where they need to be poked. While I know her intentions are likely good – when you are writing a book about nutrition, you need to be scientific and know all the ins and outs of your research articles and sources. Anyone who has ever defended a thesis or dissertation will tell you that — and they will agree that they actually /need/ someone else to poke holes to make a more perfect analysis. Bravo with this article!! I’d hate for you to review my early writings…Ahem.

  33. Pingback: The-Big-Fat-Surprise - A Critical Review - Healthy Lifestyle Ideas
  34. Pingback: Distorting Nutrition Facts to Generate Buzz | Michael F. Jacobson
  35. Pingback: Distorting Nutrition Facts to Generate Buzz | Pictures.Dot.News – Global Magazine – World, Breaking News, Current Affairs
  36. Pingback: A big fat surprise for dietary dogma? Fat chance | Enlightened Eater
  37. Pingback: Eating Salmon Inhibits Prostate Cancer | News in Nutrition
  38. Pingback: Reseñas de libros: The Diet Fix, The Big Fat Surprise y The World Turned Upside Down | Metodo Quema Grasa
  39. Pingback: Science of Nutrition Podcast | health center
  40. Pingback: Matt Ridley Spins Conspiracy Theories and More in a Classic Denial of Science | Enjeux énergies et environnement
  41. Pingback: This week in Food, Health, and Fitness - Sheila Kealey
  42. Pingback: Never a dull moment: the BMJ’s attack on the Dietary Guidelines Advisory Committee report | Dana Hender
  43. Pingback: Fats vs Carbs: Clarifying Conspiracies, Controversies, and Confusion - Sheila Kealey
  44. I really appreciate the work you put into this website, and particularly you’re detailed critique of Teicholz.

    At the request of someone else that I read and give an assessment of BFS I started reading and researching her claims (thank God for SciHub!) and I was appalled at what I was finding. I have spot checked you own critiques of Teicholz, and every single one of them checked out and was on the money.

    The page-by-page approach is understandable, but I found it productive to do some topic-by-topic research, e.g. checking out everything about the Maasai, and finding other literature on the subject (like “Daily energy expenditure and cardiovascular risk in Masai, rural and urban Bantu Tanzanians”, Mbalilaki et al, Br J Sports Med 2010;44:2 121-126, doi:10.1136/bjsm.2007.044966).

    I found the original work by Mann was quite tendentious, clearly trying to underplay the extreme level of Maasai physical activity, and flatly rejecting any possibility of a genetic role. In his 1972 study he mentions giving the Maasai pedometers, but reports no activity data. And in his 1964 study he asserts bizarrely: “More than most primitive people the Masai find subsistence easy, labor light.” So he is claiming they have an “easy, light” labor regimen in comparison to other, unspecified, primitive people with absolutely no justification or explanation. Teicholz renders this as ‘But he also acknowledged that subsistence was “easy” and labor “light”‘ (dropping the qualification entirely) and uses this to entirely ignore the crucial role of high levels of physical exercise for the rest of the book.

    It is clear from Mbalilaki (among many other sources, readily available to Teicholz) that the Maasai have extremely high levels of physical activity, burning some 45 kcal/kg/day ABOVE basal metabolic requirements, and are extremely thin (BMI 18.5, Day 1976 data) because given their activity level they are consuming a severely calorically restricted diet! If a 6 foot American wants to drop their weight to 136 lb, and burn 2800 kCal every single day in exercise, probably they too could live like the Maasai.

    BTW, the Day 1976 study of urban Maasai did contain the conclusion that “We feel that our results argue against the view that the low serum cholesterol of the Maasai who lives on a high cholesterol diet is genetically controlled” but if you look at their actual data, they show the urban Maasai have significantly lower levels of cholesterol compared to Europeans included in the study (202.9 mg/dL vs 232.5) though higher than the rural Maasai (160) leaving open the possibility of a partial genetic role.

    Also I was literally shocked by the misrepresentation that Teicholz applies to cardiac health in the U.S.

    On pages 4 and 5 where she cites stats on increased fruit, vegetable, and grain consumption, and decreased fat intake since 1960, and that obesity has climbed from “roughly one in seven … [to] one in three” and diabetes rates “rise drastically from less than 1 percent of the adult population to more than 11 percent”. But then she says “while heart disease remains the leading cause of death for men and women”. That too is true BUT for this no mention of the net change. Why is that? She does not mention that heart disease death rates plummeted by more than two-thirds during that period! Can’t let the reader know there is good news, eh?

    In fact the only place in the entire book that she acknowledges what is the most dramatic achievement on public health in the last 50 years is on page 327 saying “And although deaths from heart disease have gone down since the 1960s, no doubt due to improved medical treatment, its not clear that the actual occurrence of heart disease has declined much in that time.” Note that again she does not mention any figures, hiding the dramatic nature of the decline, so the reader is unaware of how stunning the drop really has been.

    It is true that cardiovascular disease incidence is harder to track over long period of time than mortality (which is obvious, and final) since there are many changes in diagnostic criteria and technology, but an hour of Googling in those seven years of exhausting research would have turned a lot of evidence that incidence rates are declining not just death rates.

    For example here is a stunning set of statistics:
    “In an analysis of 3,832 autopsies performed on USA military personnel (98% male, mean age 26 years) who died during combat or due to unintentional injuries between October 2001 and August 2011, the prevalence of CHD was 8.5% (21). This represents a marked decline in the prevalence of autopsy-documented CHD compared with the rates seen during the Korean War in the 1950s (77%) and the Vietnam War in the 1960s (45%) ”
    See:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4958723/

    8.5% in 2001-2011 versus 77% in the 1950s. Think about that. Wow! And this is hard data.

    Also we can look at an easy to diagnose sub-set of cardiovascular disease, stroke, we find that:
    “A systematic review of worldwide stroke incidence studies from the 1970s through 2008 found that the age-adjusted
    stroke incidence rates in high-income countries declined 42% overall with declines in each subsequent decade of the study.” and that stroke recurrence rates have fallen by 50%.
    See:
    http://www.ncbi.nlm.nih.gov/pubmed/24309587

    And yes, there are studies showing that rate of infarcts (not just death) have plummeted:
    http://heart.bmj.com/content/early/2015/06/09/heartjnl-2015-307868
    http://www.ncbi.nlm.nih.gov/pubmed/25261010

    “Although the overall rate of myocardial infarction declined over time (APC, -3.3; 95%
    CI: -2.8, -3.8), the magnitude of the decline varied widely. Incident hospitalized
    myocardial infarction rate fell 2.7%/y (95% CI: -2.1, -3.3), compared with decreases of
    1.5%/y (95% CI: -0.5, -2.6) in recurrent hospitalized myocardial infarction, 14.1%/y
    (95% CI: -11.9, -16.2) in pre-hospital fatal incident myocardial infarction, and 12.3%/y
    (95% CI: -9.2, -15.2) in pre-hospital fatal recurrent myocardial infarction (all P for
    diverging trends<0.05)."

    Given Teicholz's deliberate suppression of the real facts of CHD, and the proof on this blog that nearly every page of the Big Fat Book is filled with deception, which she works hard at, it is not just sloppiness, I cannot agree with the poster here that asserts against all evidence that "her intentions are likely good".

    Teicholz is a hard core liar-for-profit, the health of her readers be damned. We should not sugar coat that.

  45. BTW the molecular diagram in the book has been changed in recent printings so that valences are correct and it has a carboxyl group (there is no mention of revision in the front matter though).

  46. Pingback: BMJ, Nina Teicholz sponsrade "granskning" och dess utvärdering - Träna Styrka

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s