Good Calories, Bad Calories: A Critical Review; Chapter 23 – The Fattening Carbohydrate Disappears

 

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Introduction

This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

In this particular chapter Taubes attempts to make the case that the notion that low-carb diets were optimal for nearly everyone was pretty much settled science, until a cabal of highly influential obesity researchers decide to deliberately and systematically bury the “truth.”

Tabues on page 424

[A] generation of obesity authorities were determined to dismiss the practical significance of carbohydrate-restricted diets, they dismissed the potential theoretical significance at the same time. Obesity researchers today say they still have no hypothesis of weight regulation that can explain obesity and leanness, let alone account for a century of paradoxical observations.

Let’s explore some of his evidence for this consipracy.

 

The Fat Mafia

One thing I have discovered while fact-checking this book is that often Taubes will cite some text as evidence for a claim; sometimes it actually substantiates the claim and sometimes it does not. But even when it does support a claim it’s often useful to read the entire document for context. Frequently, all or part of the rest of the cited text is actually contrary to much of what Taubes says. Of course, rarely is this contrary evidence mentioned. You can call it the suppression of evidence or cherry picking. I’ve even heard the term “Occam’s Broom” (sweeping inconvenient data under the carpet). Here is one such example. The opening paragraph of chapter 23 discusses a portion of what Taubes seems to believe is a cataclysmic event in the history of nutrition: The McGovern Committee on Nutrition and Human Needs.

The tenor of the hearing was inquisitorial, and a pithy condemnation of Atkins and his diet by the Harvard nutritionist Fred Stare was read into the record by Senator Charles Percy of Illinois (Stare did not attend). “The Atkins diet is nonsense,” Stare declared. “Any book that recommends unlimited amounts of meat, butter and eggs, as this does, in my opinion is dangerous. The author who makes the suggestion is guilty of malpractice.”

This is a completely legitimate quote, at least according to the transcripts. But the quote is not what I want to explore; it’s everything surrounding it. In particular Dr. Atkins himself testifies on behalf of his 1972 diet book titled Dr. Atkins’ Diet Revolution: The High Calorie Way to Stay Thin Forever. I haven’t read it, to be honest, but apparently in the book he argues that counting calories is a hoax.1 However, under oath he walks that back.2 Below is a smattering of what he says:

[When confronted with a statement mentioning that a majority of human beings remain lean on diets extremely high in carbohydrate and correspondingly low in fat in Asia and Africa] Is this not explained by the low total caloric intake of these cultures?

[Talking about his own diet] The control of pathologic hunger patterns as well as the increased satiety value of this diet do, in general, lead to a significant decrease in caloric consumption. This, indeed, represents the principal advantage the diet provides […]

[When asked if calorie reduction for weight loss is a hoax] No, clearly not. I would never deny that a person who had the stomach for it could lose weight by cutting calories. That would be sheer nonsense.

Again, I haven’t read Dr. Atkins’s infamous treatise, but whatever he wrote he appears to be “clarifying” his position to some degree to indicate that low-CHO diets are really a means of achieving the caloric deficit that would lead to weight loss.

If anyone is wondering why I bring this up it’s because Dr. Atkins is considered The Godfather of the low-cab diet by many, including Taubes. Indeed Taubes’s theories on nutrition are clearly derived from Atkins and his books. And if you have read GCBC or any of Taubes’s other writings on nutrition you will be aware that one of Taubes’s central (and controversial) theories is that calories are unconnected to weight loss or gain; the real culprit is the carbohydrate. However, any mention otherwise, especially from The Godfather himself, is scrubbed.

* * *

The next page is another example of Occam’s Broom. I’m going to quote a bit more text here than usual because there’s some unpacking to do, but starting on page 405:

Three years later, in July 1976, McGoverrn’s committee returned to the subject of diet and disease in the hearings that would lead, a half year later still, to the publication of Dietary Goals for the United States. The first witness was Assistant Secretary of Health Theodore Cooper, who repeatedly emphasized the need for further research to establish reliable knowledge about the diet-disease connection. McGovern and his fellow congressmen, however, wanted to tell the American public something more definitive, so McGovern asked Cooper if he could, at least, agree with the proposition that “overconsumption may be as serious a problem of nutrition as underconsumption.”

“Particularly overconsumption of the wrong things,” Cooper replied. “Very often in the poor we see people who are plump who might be called obese, and people would then conclude that they do not have a deficiency because they look rotund, healthy in one sense of the word. But it is true that the consumption of high carbohydrate sources with the induction of obesity constitutes a very serious public health problem in the underprivileged and economically disadvantaged. I would agree with that.”

This response seems clear enough: the overconsumption of “high carbohydrate sources”-a phrase used to describe carbohydrate-dense starches and refined carbohydrates rather than leafy green vegetables and fruits-was associated with obesity in the poor, and perhaps even the cause. McGovern then asked Cooper to provide a “general rule of thumb” about eating habits that would help prevent disease and lengthen our lives, and Cooper reluctantly agreed to do so.

“What kinds of foods in general should we be consuming less of and what should we be eating more of?” McGovern asked.

“I think what we need to consider doing is to reduce our total fat intake,” Cooper replied. “Fat adds a caloric substance-almost twice as much-nine calories per gram-as compared to sugar. I think in order to have an effective reduction in weight and realignment of our composition we have to focus on reducing fat intake.”

With that answer, Cooper had contradicted himself, and the conventional wisdom on diet and health in America had shifted. The problem was no longer overconsumption of high-carbohydrate sources, but the overconsumption of fatty foods. And if Cooper realized that reducing our total fat intake meant increasing our consumption of carbohydrates, he neglected to say so.

Can’t you feel the smugness dripping off the page with that last sentence? I imagine Taubes made this face after typing the period:

smug face

Okay, let’s unpack this a little. When reading the above passage you may get the impression that Dr. Cooper looks like a jackass because he immediately contradicted himself, while the rest of the committee is blithely unaware of the incongruity. But nothing gets past Taubes, right? He is here to shed a light on these ignoramuses that made us all fat and sick. First off, let’s go back and look at the references section.

chapter 23 refs

So when McGovern asked Cooper about overconsumption in the testimony transcript it’s found on pages 9 and 10. When McGovern asks Dr. Cooper about the rule of thumb it’s found on pages 19 and 20. So there’s a FULL 10 PAGES OF COOPER’S TESIMONY that is concealed, in which Cooper discusses a number of public health and nutrition concerns including malnutrition, prenatal nutrition, lipids and atherosclerosis, the importance of exercise, etc. Moreover, Cooper’s response to the rule-of-thumb question is slightly more verbose that what Taubes elects to quote. And by “slightly” I mean “considerably.”

Here’s a bit more of Cooper’s response to McGovern’s rule-of-thumb question:

Well my first advice would be to eat less. As a general rule, I think the American public eats too much. With very few exceptions, and there are people obviously who would suffer from a weight reduction, most of us would not be terribly affected if we could reduce our total caloric intake.

[…]

I personally believe there is some benefit to reducing our preoccupation with sweet things.

[…]

I would recommend an appropriate amount of protein intake which we could give some recommendations to by group and target populations. A healthy intake of fresh fruits and vegetables with substantial fiber content.

[…]

It is very attractive for me to say stop eating commercially prepared foods.

Taubes suppresses all of this, of course, because it’s Taubes’s goal to make Cooper and the rest of the government look like clueless hacks. So instead he provides the most uncharitable characterization of Cooper’s testimony.

For that last sentence… Taubes uses a tried and true tactic oft-used by the more disingenuous low-carbers: intentionally conflating total and relative amounts. For example, it has often been said that once Big Brother began recommending “low-fat” diets the obsequious populace complied: eating less fat, more carbohydrates, and getting fat as a result. However, since 1971 Americans have been steadily eating more daily calories. In terms of macronutrients we have been eating more of everything. More CHOs, more protein, more fat, but we increased our CHO intake slightly more than we have increased our fat and protein intake. So it might appear that we have decreased our fat intake and increased our CHO intake if you look at only the % change in macronutrient intake, when in reality TOTAL FAT ACTUALLY INCREASED & TOTAL CALORIES INCREASED. Make sense?

So back to that last sentence: “And if Cooper realized that reducing our total fat intake meant increasing our consumption of carbohydrates, he neglected to say so.” Reducing total fat does not mean increasing total carbohydrates. One could reduce or elevate total fat consumption completely independent of whether or not one increased or decreased total CHOs. Or total protein for that matter. However, if one adjusted their proportion of calories from fat, that may affect their proportion of calories from carbohydrate. Or it might not affect it at all, depending on how one’s protein intake is adjusted. It’s the difference between relative amounts and actual amounts. And if you were to ask me the former is rarely more relevant than the latter.

So to summarize, Cooper neglected to mention that reducing total fat intake would necessarily lead to an increase in carbohydrate consumption because he has a few brain cells to rub together.

* * *

On pages 407-408 Taubes discusses an obesity symposium held on the other side of the pond way back in the Summer of ’69. A text was published on the proceedings of this symposium.3 If you read through the text you will find it a relatively sober look at obesity that discusses its etiology and treatment. Some time is clearly spent in the text examining the multi-factorial causes of obesity: genetic, environmental, psychological, metabolic, and social & lifestyle factors. But Taubes doesn’t want to mention any of this to his readers; it’s too messy and confusing and doesn’t exactly fit with the narrative he is trying to craft. So instead he tries to find a sentence or two that would make his audience believe that all those smart Englishmen got together and concluded the carbohydrate was the scourge of the obesity epidemic.

At the London conference, Howard reviewed the literature on carbohydrate restriction dating back to Banting and concluded that this was the only effective method to induce and maintain weight loss. “A common feature of all who have written on the subject,” he said, is “that the patient’s hunger is satisfied whilst on a diet high in carbohydrate of the same caloric value, patients complain of hunger.”

Again, legitimate quote, but removed from a broader context because the broader context is unkind to Taubes. Elsewhere in Dr. Alan Howard’s presentation he effectively disproves Taubes’s entire thesis. There’s even a nice graph that Taubes would not want you to see.

Howard 103

And on page 103 Howard states

In conclusion, therefore, one can state that there is no evidence that over a long period, fat, carbohydrate and protein calories are substantially different, and the loss in body weight still depends on the total number of calories consumed.

I could quote endlessly from the proceedings that contrast starkly with how Taubes presents the symposium specifically and his arguments generally, but in the interest of readability I will refrain. I am not going to say that sugars and other carbohydrates can’t play a role in the development of obesity, but it’s certainly not nearly as one-dimensional as Taubes makes it out to be.

* * *

On pages 412-413, Taubes discusses a paper by Edgar Gordon, MD that influenced Atkins:

Gordon’s diet, as described in JAMA, began with a forty-eight hour fast-“not to produce a spectacular loss of weight, but rather to break a metabolic pattern of augmented lipogenesis”-and then allowed protein and fat as desired but limited carbohydrates to minimal fruits, green vegetables, and a half-slice of bread every day. “The total caloric value is quite high in terms of reducing diets,” wrote Gordon. Atkins later said his attention was caught by Gordon’s observation that his subjects lost weight without ever complaining of hunger.

This is a minor point so skip over it if you wish, but I’d like to note some things about the diet. First, it does not allow protein and fat as desired. It’s actually very specific in the amounts you are allowed (100 grams of protein, 80 grams of fat, and 50 grams of CHO totaling 1,320 calories daily), and it’s somewhat specific in the types of fat (emphasis is placed on polyunsaturated, while saturated fat is very limited – butter is a contraindicated food in this diet).4 I’m not sure where Taubes gets this “protein and fat as desired” claim, but it’s possible he misinterpreted a sentence in the paper. For instance, Gordon is a big proponent of having several meals (or “feedings”) per day as opposed to one or two larger meals. He explicitly stated that the prescribed diet be divided into at least six meals per day or more if desired. Maybe Taubes got confused and thought more meals = unlimited fat and protein.

A couple other things worth noting about the diet is that patients were also prescribed triiodothyronine (a lipolytic hormone) 3X daily in addition to diuretics: either injections of mercurials or daily administration of ammonium chloride.

* * *

As I mentioned in the intro, essentially this chapter attempts to make the case that the nutrition “elite” are terrified of the idea of low-carbohydrate diets so they systematically attempt to invalidate the idea by subtly impugning low-carb diets in obscure medical texts. If you think that idea is absurd then you’re not alone. Taubes however, seems to think it’s perfectly reasonable.

One example of this is page 420 where Taubes writes:

He [George Bray] dismissed as irrelevant the work of those investigators who did actively study the dietary treatment of obesity, like Charlotte Young, who gave the presentation on dietary therapy at the NIH conference on obesity that Bray organized and chaired in 1973. Young specialized in the study of body composition, and she had been studying diets and obesity at Cornell since 1950. In the official NIH report on the conference, Obesity in Perspective, Bray treated her discussion of carbohydrate-restricted diets as naïve and of no consequence. In the book he coedited the year after the conference, Treatment and Management of Obesity, Young’s observations on carbohydrate- restricted diets are described as still requiring further “confirmation before they can be fully accepted …. The question of the value of a low carbohydrate diet and its effectiveness in weight loss is still unresolved.” In The Obese Patient, published three years after the NIH conference, Bray wrote of Young’s studies, “The data are suggestive and require careful replication with larger groups of individuals.”

The first cited text is page 43 of Obesity in Perspective.5 The whole book is a summary of the conference and what each presenter discussed. Below is the paragraph where Young is mentioned.

In her presentation, DR. YOUNG noted that conventional nutritional treatment of the obesities has not been an outstanding success, although we know of people for whom it has been of great value. The use of behavioral modification, a technique introduced by DR. STUART, seems to be a move in the right direction since, in at least some cases, it is behavior which needs to be modified. Some questions which need probing are whether the obesities are primarily behavioral and consequences of habits or whether they are symptoms of some more fundamental psychologic or psysiologic abnormality. Dr. Young also asked whether there were alterations in the efficiency with which energy was utilized by obese and lean subjects. She also questioned the role of the changes in the number of fat cells in juvenile and adult onset forms of obesity. Finally, in reviewing nutritional approaches to treatment, she raised questions about the mechanisms by which the hypothalamus senses the abnormalities present in the obese state.

I’m gonna leave it up to you to decide if in his summary of Young’s presentation he editorialized it in such a way as to indicate her ideas were “naïve and of no consequence.” Actually, I’m not gonna leave it up to you. I’m just gonna tell you that it didn’t. Taubes just made that up. In no way did anything in that paragraph characterize Young as naïve and of no consequence. It’s not even Bray’s opinion: it’s just a summary of what Young presented herself.

In Treatment and Management of Obesity the full context of the quote is thus: The author of this chapter of the text – which was actually written by Grant Gwinup and not George Bray as Taubes implies – discusses some studies on the topic of diet and exercise and their effects on obesity.6 In one paragraph he mentions some studies where people were put on diets that varied greatly in proportions of carbohydrates, protein, and fat, yet weight loss was consistent despite the fraction of macronutrients. Then he follows with this paragraph:

Recent studies by Young et al. has suggested, on the other hand, that a very low carbohydrate diet may indeed increase the rate at which body fat is catabolized. Their studies, on a small number of college students, require confirmation before they can be fully accepted. However, they suggest that a carbohydrate content of less than 50 g/day in the diet is sufficient to cause increased rates of weight loss compared to 60-104 g of carbohydrate in a diet with the same total number of calories. Thus, the question of the value of a low carbohydrate diet and its effectiveness in weight loss is still unresolved.

Does that sound at all dismissive of Young or her studies? Or is it the exact same thing you will find in any good piece of scientific writing that discusses a given topic (i.e. some studies demonstrate X, while these others suggest Y)? Hint: It’s the latter.

And as for that quote in The Obese Patient I can’t find it.7 I found three times in the book where Young is cited and none have anything to do with that quote. Perhaps it’s in there, but if it is I cannot find it. If you’re interested in the context where Bray does cite Young… Regarding changes in body composition over a lifetime on page 22 he writes “The data from several cross sectional studies of men and women have been summarized by Forbes and Reina (1970) (see also Behnke, 1963; Krzywicki and Chinn, 1967; Young et al., 1963; Norris, Lundy and Shock, 1963; Flynn et al., 1968).” And on page 179 in discussing how smaller, more frequent meals affects cholesterol levels where Bray writes “This reduction of cholesterol with frequent ingestion of small meals has been confirmed in several other studies (Gwinup et al., 1963; Jagannathan et al., 1964; Irwin and Feeley, 1967; Young et al., 1972). Glucose tolerance curves are also improved when eating three or more meals as compared with one or two large meals (Fabry et al., 1964; Gwinup et al., 1963l Young et al., 1972).”

Bray is so devastatingly cruel to Young, right? How could Bray live with himself after saying such harsh things?

* * *

The Carb Cosa Nostra is at again! Time for good research to sleep with the fishes. An example of this is found on page 421:

When M. R. C. Greenwood discussed the effect of insulin on the enzyme lipoprotein lipase, LPL, the “gatekeeper” for fat accumulation in cells, at the Fourth International Congress on Obesity, Hirsch ignored the implications in his review of dietary therapy, even though Greenwood had received her doctoral degree with Hirsch.

Let’s unpack this because there is quite a bit of bullshit in that single sentence. First off, Taubes cites the same source for Greenwood’s LPL presentation and Hirsch’s presentation that allegedly “ignored” Greenwood: The Proceedings of the 4th International Congress on Obesity.8 I think it’s worth pointing out a few things:

  1. Hirsch was Greenwood’s thesis advisor. Hirsch was also the chair of the Fourth International Congress on Obesity. I think it’s reasonable to assume that Hirsch played a role in Greenwood’s presence at the conference, so he’s not trying to silence her.
  2. Taubes stating that Greenwood “discussed the effect of insulin on the enzyme lipoprotein lipase” is generous. She does discuss LPL, but insulin in mentioned literally one time and not in context of LPL – at least not directly.
  3. In regards to both of the presentations, they were given at the same conference. Hirsch appeared to have given two very brief presentations on diet and obesity; both very generalized, like an overview. Did Taubes expect that Hirsch was in the audience for Greenwood’s presentation, fully absorbed everything Greenwood had to say about normal and abnormal growth and maintenance of adipose tissue vis-à-vis LPL and insulin (which was mentioned only once), amend his original presentation that he had prepared on a basic overview of diet, and get into the weeds of the cellular mechanisms of fat cell regulation? I mean, really? Is this how Taubes operates at conferences? Does he incorporate details of all the previous presentations at the same conference, even if it is outside the scope of his talk? If he doesn’t do this does some asshole accuse him of ignoring research?

* * *

Another instance of the above is found on page 420-421 where Taubes states:

Donald Novin, director of the Brain Research Institute at UCLA, discussed what he called the “carbohydrate hypothesis of ingestive behavior” at Bray’s Second International Congress on Obesity. Novin suggested that the “widespread popularity of the low carbohydrate diets” could be explained by the effect of carbohydrates on insulin, and then of insulin on fat deposition and thus hunger. Bray, who had worked closely with Novin at UCLA, gave the summary talk at the conference on obesity therapies and omitted mention of Novin’s hypothesis.

And the same bullet-points apply.

  1. Bray chaired the goddamned 2nd International Congress on Obesity and edited its proceedings. I’m sure he wasn’t trying to bury Novin’s research, but if he was he was doing a real bad job at it.
  2. I’m not sure Novin’s presentation has much overlap with Bray’s. If you read Novin’s presentation you will discover that he discusses how glucose infusion suppresses feeding in rabbits, but if you perform a vagotomy on the rabbits the infused glucose will stimulate feeding to some extent.9 (At the time Novin doesn’t even know why this is stating “We have no explanations, only speculation.”) While Bray’s presentation is about the risk-benefit ratio of certain dietary treatments of obesity.
  3. Taubes shits on Bray for not performing the completely absurd and irrational practice of revising and incorporating a pre-prepared talk on risk-benefit analysis with some preliminary and inconclusive research on rabbits that was given earlier in the day. Presumably Bray should have also revised and incorporated the results of all 25 talks that preceded his own, lest someone like Taubes accuse him of “omitting” important research and attempting to stifle scientific progress some thirty years later.

Conclusion

If you didn’t read the wall of text above I will attempt to summarize. Throughout this chapter Taubes attempts to craft the narrative that the TruthTM of the efficacy of low carb diets were systematically buried or conspicuously ignored by unscrupulous diet researchers (which inevitably led to the rise of Coke and Pepsi and the obesity epidemic). However, the evidence presented for this cover-up is either very weak or completely made up. The only cover-up presented in this chapter is Taubes’s use of Occam’s Broom: where inconvenient facts are swept under the carpet.

cloud

Refs

1. It seems pretty clear in his newspaper ad, though, which looks pretty scammy if you ask me.‘Only 10 years out of medical school I was already a fat man. 40 pounds overweight, with 3 chins! Yet I have no willpower – even the idea of hunger scares me. I knew I could not follow a low-calorie diet for even a single day.’ He read about FMH, and by using his own body as a laboratory, discovered that he could command it to make this miracle hormone whenever he wished.” FMH by the way stands for Fat Metabolizing Hormone according to the ad, and as far as I know it’s completely made up.

2. United States. Nutrition and diseases–1973 [-1974] Hearings, Ninety-third Congress, first[-second] session. (U.S. Govt. Print. Off., 1973).

3. Obesity: Medical and Scientific Aspects : Proceedings of the 1st Symposium of the Obesity Association of Great Britain Held in London, October 1968. (E. & S. Livingstone Limited, 1969).

4. Gordon ES, Goldberg M & Chosy GJ. A new concept in the treatment of obesity: A 48-hour total fast followed by six meals a day and later by stepwise increases in food and calorie intake has permitted patients to lose weight that they show no tendency to regain for periods of up to 6 months. it also promoted spontaneous evolution of good dietary habits. JAMA 186, 50–60 (1963).

5. Bray, G. Obesity in Perspective. Vol 2. (DHEW, 1973).

6. in Treatment and Management of Obesity (eds. Bray, G. A. & Bethune, J. E.) 93–102 (Harper and Row, 1974).

7. Bray, G. A. The obese patient. (W. B. Saunders, 1976).

8. Hirsch, J. & VanItallie, T. B. Recent Advances in Obesity Research, Volume IV: International Congress Proceedings: 4th. (CRC Press, 1985).

9. Recent Advances in Obesity Research: International Congress Proceedings: 2nd. (Hemming Information Services, 1978).

Good Calories, Bad Calories: A Critical Review; Chapter 24 – The Carbohydrate Hypothesis III: Hunger and Satiety

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Introduction

This is another post in my ongoing series of posts on Gary Taubes’s Good Calories, Bad Calories (GCBC). One of the main challenges I have encountered while reviewing this chapter is that Taubes devotes several pages to discussing the work of Jacques Le Magnen and attempting to associate Le Magnen’s research with Taubes’s own theories. My undergraduate advisor actually spent some time in France and worked directly with Le Magnen, so of course all his students were educated on Le Magnen’s work. However, Taubes cites a number of texts by Le Magnen that I was either unable to find or are written entirely in French. For that reason I cannot comment on the specifics of the texts, and unless I find some of the specific texts Taubes cites these pages are outside the scope of this chapter review.

Not the Introduction

On pages 425-426 Taubes describes a diet that was designed by JB Sidbury and RP Schwartz to help obese children lose weight, stating “The diet that Sidbury eventually used in his clinic and claimed to be uniquely effective contained only 15 percent carbohydrates-‘the remaining being apportioned approximately equally between protein and fat […]’” Taubes makes great hay of Sidbury’s diet and how it reduced insulin levels and therefore fat mass, stating also “insulin will ‘facilitate lipogenesis’ and inhibit the release of fat in the adipose tissue, this in turn created what Sidbury called the ‘milieu for positive fat balance’ in the cells of the adipose tissue” and “’decreased insulin levels would then permit normal fatty acid mobilization’” and “he [Sidbury] described an approach to obesity therapy that differed from Robert Atkins’s only in the details of the application.”

Leaving aside that Sidbury and Schwartz never claimed their diet was “uniquely” effective, they do claim that their dietary treatment was effective to some degree, which is really no surprise if you read the details of their diet.1 From page 67 of Childhood Obesity:

Prior to our interest in the subject, we routinely had the dietitian give the mother a 1000 calorie diet for an obese child, whether 4 or 14 years old. The results could have been predicted with a little reflection. Indeed an adult should be given a 700 or 800 calorie diet if weight loss at a reasonable rate is the goal. We then arbitrarily designed a 300 calorie diet to be used for children 3 to 8 years, 500 calories from 8 years to puberty, and 700 calories over puberty. This schedule has been effective; hence we have continued it.

This is all to be expected, except that it essentially contradicts items 5 & 6 of Taubes’s “inescapable” conclusions found on page 454. For those that haven’t read GCBC, Taubes attempts to make the case that overeating, exercise, or caloric intake of one’s diet is of no real consequence with regard to weight loss or gain. The only factor that really matters, according to Taubes, is insulin which can be manipulated by dietary carbohydrates.

Of course if Taubes is correct then Sidbury and Schwartz could have prescribed diets of 6000 kcals or more and weight loss would have been just as effective so long as the diet was ketogenic.

* * *

Starting on page 436 Taubes attempts to make the case that carbohydrates cause infertility! So if you’re trying to get pregnant and you’re sitting down to a nice meal of meat and potatoes, put your fork down, discard your potatoes, and help yourself to some more meat.

He starts off by setting up the straw man of Conventional WisdomTM, or in this case Common Belief.

[T]he critical variable in fertility is not body fat, as is commonly believed, but the immediate availability of metabolic fuels.

I’m not even sure why he brings this part up. I guess to add to the list of all the Conventional WisdomTM he has “debunked.” At any rate, as evidence for what is commonly believed he cites a paper by Frisch and MacArthur titled “Menstrual Cycles: Fatness as a Determinant of Minimum Weight for Height Necessary for Their Maintenance or Onset” that concludes the following “The data suggest that a minimum level of stored, easily mobilized energy is necessary for ovulation and menstrual cycles in the human female.”2 The authors also mention that “If a minimum of stored fat is necessary for normal menstrual function, one would expect that women who live on marginal diets would have irregular cycles, and be less fertile, as has been observed, and that poorly nourished lactating women would not resume menstrual cycles as early after parturition as well-nourished women, as also has been observed.” Notice anything funny here? And he contrasts this with two papers by Schneider and Wade that conclude the exact same thing, only they used animals for their studies instead of people.3,4

Whatever. Not a big deal, but strap in because this next one is a whopper. Continuing on pg 436-437 Taubes tries to make the argument that insulin is responsible for infertility, citing some research by Wade and Schneider.

[I]nfusing insulin into animals will shut down their reproductive cycles. In hamsters, insulin infusion “totally blocks” estrous cycles, unless the animals are allowed to increase their normal food intake substantially to compensate.

However, if you actually read the research you will find that it wasn’t the insulin they were studying, but hypoglycemia.4 Insulin was simply a way of artificially inducing hypoglycemia in the hamsters. The authors even mention this:

[I]nsulin was used as a tool to demonstrate the effects of fuel partitioning on reproductive function. Treatments with high doses of insulin that produced hypoglycemia inhibited reproductive function. The results do not support a role for insulin per se, independent of effects on fuel availability.

Emphasis mine. Unless something was really wrong with you, you likely are not going to experience hypoglycemia if you consume a diet that includes at least some carbohydrates. Indeed, those deciding to consume low-carbohydrate diets would be at greater risk of hypoglycemia.5

* * *

If you’re still not convinced that meat = magic then Taubes has a tobacco tale for you on page 437; and a tall tale it is.

Consider nicotine, for instance, which may be the most successful weight-loss drug in history, despite its otherwise narcotic properties.

I wanna stop right here. This is a bold claim. The most successful weight loss drug IN HISTORY? If that’s true then the majority of smokers that I know should be thin. As a matter of fact they should be downright anorexic considering their frequency. Actually, the reverse is true if my experience is any indication. Of course using anecdotal arguments like this is not at all scientific, but c’mon has Taubes never heard of ephedrine? Sibutramine? Dinitrophenol? Amphetamines for god’s sake? Even cocaine?

Absurd historical claim nothwithstanding, he attempts to make the claim that if and when people gain weight after they stop smoking is because smoking is hormonally similar to eating a low-carb diet.

There seems to be nothing smokers can do to avoid this weight gain. The common belief is that ex-smokers gain weight because they eat more once they quit.

[…]

[A]s Judith Rodin, now president of Rockefeller University, reported in I987, smokers who quit and then gain weight apparently consume no more calories than those who quit and do not gain weight. (They do eat “significantly more carbohydrates,” however, Rodin reported, and particularly more sugar.) Smokers also tend to be less active and exercise less than nonsmokers, so differences in physical activity also fail to explain the weight gain associated with quitting.

There’s the ol’ Common BeliefTM again. I guess he figures he wore out Conventional Wisdom so he’ll go with another phrase that means the same thing. Nevertheless, reading this passage Taubes would have you believe that people lose weight after they quit smoking and weight gain in these instances is completely divorced from the amount of calories they eat. As evidence he cites a paper by Judith Rodin, but perhaps more importantly he does NOT mention contradicting evidence from other papers that he cited on the very same page! Por ejemplo, when discussing other aspects of nicotine he cites a review paper titled “Smoking Cessation and Weight Gain” published in 2004, which states

Mechanisms of weight gain [following smoking cessation] include increased energy intake, decreased resting metabolic rate, decreased physical activity and increased lipoprotein lipase activity (14–16,20–23). Nicotine significantly decreased body weight and food intake via a decrease in meal size and a longer inter-meal interval […]6

Another review titled “Weight Gain Following Smoking Cessation” that Taubes cites on this very page relates the following:

Nicotine has commonly been called an anorectic, an agent that suppresses eating. Consistent with this view, the vast majority of prospective studies have found a sharp increase in eating during the first few weeks of smoking cessation (e.g., Hatsukami, Hughes, Pickens, & Svikis, 1984; Perkins, Epstein, & Pastor, 1990; Spring, Wurtman, Gleason, Wurtman, & Kessler, 1991). The magnitude of this increase (approximately 250-300 kcals/day) is strikingly similar across studies, despite important differences in food measurement methodology (e.g., observation of food intake in in-patients, subject self-report by means of food diaries) and subject populations (female subjects, male subjects, or both).7

But Taubes dismisses all of this evidence by glossing over it and highlighting the single Rodin publication, which looks at current smokers and those that recently quit.8 If you actually read the text of the study you’ll find that the quitters on average did not gain significantly more weight than the smokers. Moreover, almost half actually lost weight after quitting. It is also worth noting that the measurement of caloric intake was self-reported, and self-reporting energy intake has been shown to be notoriously unreliable. But I’m sure this singular study with self-reported intake and non-significant results trumps all the other evidence to the contrary.

* * *

On page 446 Taubes says the following:

Avoiding carbohydrates will lower insulin levels even in the obese […]

Now this is a pretty anodyne and uncontroversial statement. I doubt you’ll find any nutrition professional worth their salt that would disagree with the above statement. What is interesting about this is not the statement, but the source Taubes cites for this. It absolutely backs up that claim, but it is devastating to his other claims. Namely, #6 and #9 of his “inescapable” conclusions found in the epilogue.*

The cited study take obese individuals and feeds them isocaloric high and low carb diets as well as hypocaloric high and low carb diets.9 All participants on the isocaloric diets10 maintained their weight whether fed high or low carb diets. All participants fed the hypocaloric diets lost weight regardless of the relative amount of CHO was in the diet. This is actually a pretty damn good experiment to test Taubes’s main hypothesis of calories vs carbs, and the good old calorie wins.

high low carb insulin

* * *

Not a major point but on page 446 Taubes says

It also makes us question the admonitions that carbohydrate restriction cannot “generally be used safely,” as Theodore Van Itallie wrote in 1979, because it has “potential side effects,” including “weakness, apathy, fatigue, nausea, vomiting, dehydration, postural hypotension, and occasional exacerbation of preexisting gout.”

It’s basically a misquotation on two accounts. Van Itallie actually states that low calorie diets “can generally be used safely.”11 Secondly, he states that low calorie diets that are ALSO low in carbohydrates have potential side effects. He is not speaking of carbohydrate restriction in general terms as Taubes implies.

* * *

Page 447, Taubes contends that, although cholesterol levels may rise on a low-CHO diet, it is by no means permanent.

The existing evidence suggests that this effect will vanish with successful weight loss, regardless of the saturated-fat content of the diet. Nonetheless, it’s often cited as another reason to avoid carbohydrate-restricted diets and to withdraw a patient immediately from the diet should such a thing be observed, under the mistaken impression that this is a chronic effect of a relatively fat-rich diet.

Maybe this is another minor point, but the “often cited” part of his claim is in reality a single newspaper article about a guy that sues the Atkins estate for his high cholesterol.12 The article seems to imply that the case is kind absurd and that a judge would almost certainly throw out the suit.

 

 

*For those that don’t have the book…
“6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.”
“9. By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity. The fewer carbohydrates we consume, the leaner we will be.”

cloudReferences

1. in Childhood Obesity (ed. Collip, P. J.) (Distributed by Medical and Technical Publishing Co, 1975).

2. Frisch, R. E. & McArthur, J. W. Menstrual cycles: fatness as a determinant of minimum weight for height necessary for their maintenance or onset. Science 185, 949–951 (1974).

3. Schneider, J. E. & Wade, G. N. Availability of metabolic fuels controls estrous cyclicity of Syrian hamsters. Science 244, 1326–1328 (1989).

4. Wade, G. N. & Schneider, J. E. Metabolic fuels and reproduction in female mammals. Neurosci. Biobehav. Rev. 16, 235–272 (1992).

5. Colle, E. & Ulstrom, R. A. Ketotic hypoglycemia. J. Pediatr. 64, 632–651 (1964).

6. Filozof, C., Fernández Pinilla, M. C. & Fernández-Cruz, A. Smoking cessation and weight gain. Obes. Rev. 5, 95–103 (2004).

7. Perkins, K. A. Weight gain following smoking cessation. J. Consult. Clin. Psychol. 61, 768–777 (1993).

8. Rodin, J. Weight change following smoking cessation: The role of food intake and exercise. Addict. Behav. 12, 303–317 (1987).

9. Grey, N. & Kipnis, D. M. Effect of Diet Composition on the Hyperinsulinemia of Obesity. N. Engl. J. Med. 285, 827–831 (1971).

10. (except for one that did not consume all of the prescribed diet).

11. Bray, G. A. Obesity in America: a conference. (U.S. Dept. of Health, Education, and Welfare, Public Health Service, National Institutes of Health, 1979).

12. Burros, M. Dieter Sues Atkins Estate and Company. New York Times 1 (2004).

Good Calories, Bad Calories: A Critical Review; Chapter 8 – The Science of the Carbohydrate Hypothesis

coverIntroduction

This is another post in my ongoing series of posts on Gary Taubes’s Good Calories, Bad Calories (GCBC). Several of the publications that Taubes cites for various claims are amazingly obscure. I’m working on getting a couple of them right now, so perhaps this post will be updated in the future when I receive and look through them. In the meantime this post is the fact-checking I have done of chapter eight so far.

Surprisingly it doesn’t contain that much “science of the carbohydrate hypothesis.” It’s really more of an introduction to the similarly-named chapters toward the end of the book. He spends some time with Tokelau (which I will get to soon), discusses what homeostasis is, and then reworks one of his earlier articles about salt toward the end of the chapter.

Not the Introduction

God, I love the beach. I bet it's paradise over there.

Ian Prior in Tokelau, 1971

For the first several pages of chapter eight Taubes discusses a rather interesting cohort study involving the people of the Tokelau Islands in the south pacific. Briefly, Ian Prior, an epidemiologist from New Zealand, decided to study the residents of Tokelau while the New Zealand government wanted to organize a large voluntary migration effort of the peoples from the islands to NZ. Some opted to stay on the Tokelau Islands rather than migrate, which provided Prior an excellent opportunity to study the two populations and compare their lifestyles, diet, and health. As you might guess, the islanders that “immigrated” to NZ ended up having more health problems than those that stayed behind.

Why? What happened? According to the University of Minnesota synopsis of the study, it is due to “the tendency for migrants at all ages to be heavier than non-migrants. Migrants had more diabetes and smoked more, drank more alcohol, and exercised less.1 These factors make the poorer health among the migrants pretty easy to explain. Taubes, however, doesn’t want you to think that any of this has to do with the study results so he straight-up lies to you on page 138:

A number of factors combined to make this higher disease incidence among the migrants difficult to explain. For one thing, the Tokelauans who emigrated smoked fewer cigarettes than those who remained on the atolls, so tobacco was unlikely to explain this pattern of disease.

He goes on to state that the migrants were far more physically active and had a much more “rigorous” lifestyle than the non-migrants because they worked in sewing factories and had to walk to shops. I’m not even kidding. Again, this directly contradicts the actual study results.

So how does Taubes explain the health discrepancy? Why, it’s exclusively due to saturated fat intake, of course! Yes, as it turns out the native diet of the Tokelauans ate a diet largely composed of fish, coconuts, and fruit. According to Taubes it was the coconut oil in the Tokelauan diet that was apparently uniquely protective because coconut oil has saturated fats. Moreover, Taubes also mentions that the migrants to NZ started eating bread and potatoes which contributed to their health problems. And, of course, he has to drag Keys into this saying “If Keys’s hypothesis was correct, the migrants should have manifested less evidence of heart disease, not more.”

Actually, no. The non-migrants should have manifested less heart disease. Taubes is conflating the fatty acids in coconuts with all saturated fatty acids. The fatty acids in coconuts are quite a bit different from that fatty acids found in the foods that Taubes promotes throughout the book (beef tallow, bacon, cheese, etc.) It has been demonstrated to the satisfaction of most people that coconut oil does not have a huge impact on serum cholesterol levels and by extension heart disease. Matter of fact, the first person to demonstrate this was none other than Ancel “Beelzebub” Keys himself!2,3

Aside from alcohol consumption, diet was not even mentioned in the study synopsis as being a potential factor in the health decline. Nevertheless, Taubes credits the saturated coconut oil for the good health of the non-migrants, and blames the bread and potatoes on the poor health of the migrants. What Taubes glosses over are other dietary components introduced to the migrants which include salt, eggs, dairy, and red meats.4

* * *

One of the main goals of GCBC is to upend everything we all thought we knew about nutrition: Saturated fats from animals are actually good for you! Carbohydrates from fruits, vegetables, or grains are actually the enemy! Calories don’t matter! You can gorge yourself of whatever you like, and as long as it doesn’t include carbohydrates you’re in the clear! Dietary fiber is meaningless! I suspect Taubes does this not because these things are true or even that he believes these things are true, but rather because it sells more books. It’s a shame people have to get wildly inaccurate information about how to take charge of their own health for the financial gain of one individual, but that seems to be the case.

Another one of these bits of “conventional wisdom” that he upends is the idea that salt has anything to do with high blood pressure. Page 146:

[P]ublic-health authorities for the past thirty years have insisted that salt is the dietary cause of hypertension and the increase in blood pressure that accompanies aging. […] That’s the hypothesis. But in fact it has always been remarkably difficult to generate any reasonably unambiguous evidence that it’s correct.

He goes on to state that even if by some miracle salt really does somehow influence blood pressure, it has such a negligible effect that cutting salt intake “makes little difference” to our overall health. As evidence he cites a 2004 Cochrane Review by He and MacGregor. Old versions of Cochrane reviews are difficult to find. It seems they usually replace the old ones every time the data gets updated. In this case I was only able to find the 2013 version of the same title by He and MacGregor.5 Let me quote from the end of the review (emphasis mine):

Our meta-analysis of randomised trials of longer-term modest reductions in salt intake demonstrates a significant effect on blood pressure in individuals with both elevated and normal blood pressure. The blood pressure fell, on average, by 5/3 mmHg in hypertensives and 2/1 mmHg in normotensives. These falls in blood pressure would have an immediate and significant impact on population blood pressure and would, therefore, be predicted to reduce stroke deaths by approximately 14% and ischaemic heart disease (IHD) deaths by 9% in individuals with elevated blood pressure, and in individuals with normal blood pressure reduce stroke and IHD deaths by approximately 6% and 4% respectively. It is important to note that these reductions in stroke and IHD deaths were estimated from a previous meta-analysis of prospective observational studies. A recent meta-analysis of 1 million adults in 61 prospective studies demonstrates that the relationship between blood pressure and cardiovascular risk is much stronger than previously estimated. Therefore, the reductions in stroke and IHD with the modest reductions in salt intake might be even greater. Since raised blood pressure is also a major risk factor for heart failure, a reduction in salt intake would likely reduce the incidence of heart failure.

I’ll leave it up to you if you think if a modest reduction in salt intake in fact “makes little difference.”6

* * *

Taubes tries to make the case that CHOs are the real culprit leading to insulin resistance which leads to hypertension and ultimately atheroslcerosis. Page 150 of the hardback Taubes states:

Finally, by the mid-1990s, diabetes textbooks, such as Joslin’s Diabetes Mellitus, contemplated the likelihood that chronically elevated levels of insulin were “the major pathogenetic defect initiating the hypertensive process” in patients with Type 2 diabetes. But such speculations rarely extended to the potential implications for the nondiabetic public.

Taubes is quoting out of context here. The actual quote states7:

Should hyperinsulinemia be the major pathogenetic defect in initiating the hypertensive process in patients with NIDDM, it is unlikely that it sustains the hypertension indefinitely. With increasing insulin resistance, the pancreas must secrete higher levels of insulin. Eventually, its reserve capacity is exhausted and plasma insulin levels fall. Other mechanisms must then sustain the hypertension.

Interestingly, immediately before the cherry-picked quote from Taubes is a statement that contradicts Taubes’s argument:

[H]ypertension and insulin resistance may be different clinical manifestations of a common underlying cellular defect by which the level of cytosolic free calcium is increased and the level of intracellular free magnesium is decreased.

As a matter of fact the entire paper makes the argument that the cause of hypertension is clearly multifactorial.

* * *

Page 150:

Though this carbohydrate-induced water retention and the hypertensive effect of insulin were occasionally discussed in nutrition and dietetics textbooks-Modem Nutrition in Health and Disease, for example, which was published in 1951 and was in its fifth edition by the 1970s-they would appear solely in the technical context of water and electrolyte balance (sodium is an electrolyte), whereas the discussion of hypertension prevention would focus exclusively on the salt hypothesis.

Nope. Not even close. Modern Nutrition in Health and Disease describes a variety of factors associated with hypertension. And when it comes to prevention does not “focus exclusively on the salt hypothesis.” Example from the 1999 edition that I have:

In hypertensives whose blood pressures have been controlled with medications, weight loss or NaCl restriction more than doubles the likelihood of maintaining normal blood pressure after withdrawal of drug therapy. The following lifestyle modifications have been recommended as adjunctive or definitive therapy for hypertension: weight reduction if overweight; aerobic exercise; limited NaCl and alcohol intake; maintenance of adequate dietary potassium, calcium, and magnesium intake; smoking cessation and reduced dietary saturated fat and cholesterol intake for overall cardiovascular health.

It’s a shame Taubes never reads what he cites.

cloud

Refs

Good Calories, Bad Calories: A Critical Review; Chapter 9 – Triglycerides and the Complications of Cholesterol

cover

Introduction

This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

Not the Introduction

Page 158 Taubes discusses a paper1 by Pete Ahrens

By 1957, Ahrens was also warning about the dangers of oversimplifying the diet-heart science: maybe fat and cholesterol caused heart disease, or maybe it was the carbohydrates and triglycerides. “We know of no solid evidence on this point,” wrote Ahrens, “and until the question is further explored we question the wisdom of prescribing low-fat diets for the general population.”

However, that quote is taken out of context. Taubes makes you think Ahrens is saying that there is “no solid evidence” regarding whether or not carbohydrates caused heart disease, but Ahrens is really referring to the ambiguity (at the time) of whether HDL or LDL causes heart disease. Actual quote:

[W]e are tempted to ask whether the lower density lipoproteins are less “atherogenic” than the higher-density lipoproteins rich in cholesterol and phospholipids. We know of no solid evidence on this point […]

I don’t think it’s a big deal, but it is misleading. What is even more misleading, though, is the information that is in the Ahrens paper that was purposefully ignored by Taubes because it runs contrary to his argument.

In this chapter (among other chapters) Taubes tries to make the case that cholesterol is not very relevant in discussions of atherosclerosis. The real culprit, according to Taubes, is triglycerides which are raised by those evil carbohydrates. Triglycerides are the only biomarker that matters. But while the Ahrens paper cited by Taubes does indicate that high CHOs can lead to elevated triglycerides it also makes clear a few other things, like vegetarian diets and very low fat diets are best for reducing lipids (triglycerides and cholesterol) and that plant-based fat is preferable to animal fats in the same regard.

Don’t believe me? Here are a few quotes from the paper:

  • “Experience to date has shown that two regimens are effective in lowering serum lipid levels of our outpatients. The first is total vegetarianism, in which all dairy products are omitted except for skim milk, washed cottage cheese, skim milk cheeses, and egg whites.”
  • “The second regimen consists of a very low fat diet (less than 25 Gm. per day) supplemented by an ounce or more of corn oil at least three times daily.”
  • “Serum lipids can be altered by dietary means, and experimental data lead to the presumptive conclusion that unsaturated fats in the diet cause depressions in levels of cholesterol and phospholipids.”
  • “[P]atients with existent or threatening arteriosclerosis may be justifiably advised to eat higher proportions of unsaturated fats.”

There is even a nice graph in the paper that Taubes would probably prefer you not see.

ahrens

I don’t think it needs any editorializing, but in case you can’t tell ALL of the lipid measurements – triglycerides, phospholipids, free cholesterol, and total cholesterol – are higher when fed animal fats at ALL points compared to plant fats.

* * *

On page 159 Taubes discusses a publication by Kuo2 that Taubes uses to support his carbohydrate-leads-to-hypertriglyceridemia-and-therefore-CHD argument. The study in question does show that his study patients with high levels of serum triglycerides were able to lower them when on a low-CHO diet. However, what is made clear in the study is that this is only true for patients with an abnormal condition of carbohydrate sensitivity, and that a diet with moderate carbs does not lead to hypertriglyceridemia in normal patients. In fact, Kuo mentions that one would need to eat an absurd amount of CHOs to induce elevated triglycerides. From the paper (emphasis mine):

A moderately high dietary sugar and other carbohydrate intake, amounting to 35% to 40% of total daily calories, did not appear to exert a significant effect on the blood lipid levels of young normolipemic subjects with negative family history of coronary disease and abnormality in carbohydrate metabolism. It was necessary to raise the carbohydrate intake to 85% to 90% of total calories to induce hyperglyceridemia in patients who were not abnormally sensitive to carbohydrates.

In the same paragraph in which he mentions the Kuo paper, Taubes claims the CHO-triglyceride-CHD hypothesis was confirmed by two other big studies at the time (Goldstein et al. and Carlson and Bottiger).3,4 Except they don’t even mention the pièce de résistance of Taubes’s argument: the carbohydrates. They simply discuss the association between CHD and triglycerides, which has never been disputed as far as I know. No mention of carbs at all in these papers.

* * *

On page 160 Taubes claims that the US government – and, by extension, researchers – ignored triglycerides as a risk factor for CHD in favor of studying cholesterol because everyone had a huge hard-on for Keys, apparently:

The National Institutes of Health, which was effectively the only source of funding for this research in the United States, had already committed its resources to three enormous studies-the Framingham Heart Study, Keys’s Seven Countries Study, and the pilot programs of the National Diet-Heart Study. These studies would measure only cholesterol and so test only Keys’s hypothesis. No consideration was given to any alternative hypothesis.

I’m sure you’ll be shocked to discover that Taubes is not exactly being honest here. Two out of the three studies that he said measured only cholesterol in fact measured both cholesterol and triglycerides (among other things).5-7 In fact, one of the Framingham papers mentions that triglycerides are a risk factor, albeit not as predictive as cholesterol is (emphasis mine):

The data presented suggest that in men the moderately elevated cholesterol values commonly encountered in the general population, regardless of the metabolic aberration responsible or how it is transported or partitioned among the lipoproteins, are associated with increased risk of coronary heart disease. Elevated endogenous triglyceride values appear significant in coronary atherogenesis only when accompanied by high cholesterol values.

* * *

On pg 160 of hardback Taubes states:

By 1961, Keys and his collaborators in the Seven Countries Study had measured cholesterol in over ten thousand men. By 1963, they had completed the exams on another eighteen hundred men. Even had it been technically possible to include triglycerides in the measurements, or to return to the original locales and retest for triglycerides, the cost would have been astronomical. The result, as we’ve seen, was considered a resounding victory for Keys’s fat-cholesterol hypothesis.

His citation for this is page I-7 in the study program and objectives which is a table of causes of death and a table of death rates from US vital statistics.8 There is no reference for cholesterol or triglycerides or exams or cost or really anything that Taubes claims here.

* * *

On page 161 Taubes discusses a series of papers published in the NEJM that report on various disorders of lipoprotein metabolism….. aaaaaaand makes some claims about them that are not backed up by the evidence in the actual papers (emphasis mine):

Four of the five lipoprotein disorders described in this series were characterized by abnormally elevated levels of triglycerides in the very low density lipoproteins. For this reason, Fredrickson, Levy, and Lees also warned against the dangers of advocating low-fat diets for all patients, because these diets increased carbohydrate consumption and so would elevate triglycerides[…]

As evidence for the claim Taubes cites page 219 of Fredrickson et al. 1967.9 That paper neither advocates for or warns against low-fat diets. In fact it’s never mentioned, but here are a few things that are mentioned in the section on dietary management of this disorder:

  • “[A] patient with a marginal Type II pattern who has neither of the other components of the triad diagnostic for the familial syndrome and who has a high intake of foods rich in cholesterol and saturated fats warrants dietary advice, for the expectation is good that he will respond.”
  • “The 2 components in dietary treatment of the Type II abnormality are limited intake of cholesterol and the substitution of polyunsaturated for saturated fats. Cholesterol and saturated (usually from animal) fats occur together in foods, and many therapists today are more concerned with their elimination […]”
  • “Substitution of skim-milk over whole-milk products, severe restriction or even elimination of egg yolks and reduction in meat intake for a daily intake of about 100 mg of cholesterol and 20 to 30 g of fat is one of the most effective dietary regimens.”
  • “Most Type II patients (provided they have normal glucose tolerance) can tolerate carbohydrate intakes of approximately 4 or 5 gm. Per kilogram of body weight per day without significant rise in their glyceride concentrations.”

That particular paper he cited dealt with only Type II of the five types of abnormal lipoprotein metabolism. Just FYI. He cites others though. Continuing with Taubes on that same paragraph:

By far the most common of the five lipoprotein disorders was the one designated Type IV, characterized by elevated VLDL triglycerides-“sometimes considered synonymous with ‘carbohydrate-induced hyperlipemia,'” they wrote-and it had to be treated with a low-carbohydrate diet.

Wrong on so many levels. Let’s take a look at the quote first. Taubes excises what follows that quote because the authors go on to say that while some might classify Type IV as “carbohydrate-induced,” it is really not true. Here’s the entire quote on page 273 of the same Fredrickson series, bolding mine:

The Type IV pattern (hereafter called simply “Type IV”) is a valuable indicator of metabolic imbalance; it does not describe a specific disease. It is sometimes considered synonymous with “carbohydrate-induced hyperlipemia.” This is probably too narrow a concept since most patients who have this pattern on a regular diet do not lose it entirely when their diet is changed so that 10 per cent of their calories come from carbohydrate, and an occasional patient does not have an abnormal increase in plasma glycerides when fed 80 per cent of his calories as carbohydrate.

That deals with the blatant quote-mining. What about the claim that the treatment had to be a low-carb diet? The authors also clearly state that carbohydrates should not be assumed to be the cause of the hyperlipemia, at least regarding Type IV, and that weight loss should be considered the primary treatment of such a disorder.

How does Taubes get away with this?

* * *

From page 168 in the hardback:

When they finally were tested in two clinical trials in the 1990s—the Lyon Diet Heart Trial and an Italian study known as GISSI-Prevenzione—both supported the contention that the diet prevented heart attacks, but neither provided evidence that it did so by either raising HDL or lowering LDL, which was how it was now alleged to work

The GISSI study does not measure diet.10 The diets remain the same throughout. The variable of interest in the study is one omega-3 gel capsule with the primary endpoints being death, non-fatal myocardial infarction, and stroke (i.e. not cholesterol). Conclusion: Dietary supplementation with n-3 PUFA led to a clinically important and statistically significant benefit. This study does not prove his claim.

Regarding the Lyon Diet Heart trial, Taubes’s inclusion of HDL and LDL makes his claim technically correct. However, the results of the Lyon Diet Heart trial are actually pretty devastating to Taubes’s overall thesis. What Taubes leaves out is that total cholesterol was very predictive of a second myocardial infarction. From the study: “[E]ach increase of 1 mmol/L of total cholesterol increased the risk of recurrence by 20% to 30%.”11 Not to mention the experimental diet contained – among other things – less saturated fat.

* * *

On pages 168-169:

Consider a porterhouse steak with a quarter-inch layer of fat. After broiling, this steak will reduce to almost equal parts fat and protein. Fifty-one percent of the fat is monounsaturated, of which 90 percent is oleic acid. Saturated fat constitutes 45 percent of the total fat, but a third of that is stearic acid, which will increase HDL cholesterol while having no effect on LDL. (Stearic acid is metabolized in the body to oleic acid, according to Grundy’s research.) The remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL. In sum, perhaps as much as 70 percent of the fat content of a porterhouse steak will improve the relative levels of LDL and HDL cholesterol, compared with what they would be if carbohydrates such as bread, potatoes, or pasta were consumed. The remaining 30 percent will raise LDL cholesterol but will also raise HDL cholesterol and will have an insignificant effect, if any, on the ratio of total cholesterol to HDL. All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly. The same is true for lard and bacon.

For this paragraph of claims Taubes cites two studies, one by Katan and one by Grundy.12,13 He also cites the USDA National Nutrient Database for the fatty acid profile of his hypothetical steak.

If you actually look at the National Nutrient Database for a porterhouse steak you will note that Taubes is correct when he breaks down the fatty acid composition. However, you’ll notice that he focuses on the stearic acid (18:0) which is only one-third of the SFAs, the other two-thirds that he neglects to mention is palmitic acid (16:0) which according to the Katan study he cites raises LDL cholesterol monumentally compared to stearic acid.
Nutrient data for 23002, Beef, short loin, porterhouse steak, trimmed to 0.12 fat, cooked, broiled

fatty acids and cholesterol

As for the claim that the “remaining 4 percent of the fat is polyunsaturated, which lowers LDL cholesterol but has no meaningful effect on HDL,” this is blatantly untrue, even by the studies Taubes himself cites.

fatty acids and cholesterol2

Again, does Taubes even bother to read the studies he cites?

“All of this suggests that eating a porterhouse steak in lieu of bread or potatoes would actually reduce heart-disease risk, although virtually no nutritional authority will say so publicly.”

I’m not sure he can make that claim. Based on his own references, carbs seem to decrease both HDL and LDL. That would suggest a more-or-less neutral effect on the HDL/LDL ratio and therefore a neutral effect on CVD.
fatty acids and cholesterol3

By the way, does Taubes now accept that cholesterol plays a role in heart disease? It seems that the reason red meat is beneficial for you, according to Taubes, is that is helps lower LDL and raise HDL. The same notion he was arguing against the entire chapter! Moreover, it seems that the source of the cholesterol-mitigating properties is the unsaturated fats that are found more abundantly in vegetable oils. Here’s Taubes again:

The observation that monounsaturated fats both lower LDL cholesterol and raise HDL also came with an ironic twist: the principal fat in red meat, eggs, and bacon is not saturated fat, but the very same monounsaturated fat as in olive oil.

So why not just go for the olive oil? Oh yeah, because vegetable fats cause cancer or some such nonsense. But not meat, of course; it’s perfect.

Refs

 

1. Ahrens, E. H., Jr et al. Dietary control of serum lipids in relation to atherosclerosis. JAMA 164, 1905–1911 (1957).

2. Kuo PT. Hyperglyceridemia in coronary artery disease and its management. JAMA 201, 87–94 (1967).

3. Goldstein, J. L., Hazzard, W. R., Schrott, H. G., Bierman, E. L. & Motulsky, A. G. Hyperlipidemia in Coronary Heart Disease I. Lipid Levels in 500 Survivors of Myocardial Infarction. J. Clin. Invest. 52, 1533–1543 (1973).

4. Carlson, L. & Böttiger, L. E. Ischaemic heart-disease in relation to fasting values of plasma triglycerides and cholesterol. Stockholm prospective study. The Lancet 299, 865–868 (1972).

5. Chapter XIII: Serum Triglyceride Changes. Circulation 37, I–224–I–226 (1968).

6. Kannel, W. B., Castelli, W. P., Gordon, T. & McNamara, P. M. Serum Cholesterol, Lipoproteins, and the Risk of Coronary Heart Disease: The Framingham Study. Ann. Intern. Med. 74, 1–12 (1971).

7. In fact, Taubes’s citation for Framingham here is actually a newspaper article that doesn’t even mention Framingham. I am assuming it is an innocent citation error.

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

9. Fredrickson, D. S., Levy, R. I. & Lees, R. S. Fat Transport in Lipoproteins — An Integrated Approach to Mechanisms and Disorders. N. Engl. J. Med. 276, 34–44 (1967).

10. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. The Lancet 354, 447–455 (1999).

11. De Lorgeril, M. et al. Mediterranean Diet, Traditional Risk Factors, and the Rate of Cardiovascular Complications After Myocardial Infarction: Final Report of the Lyon Diet Heart Study. Circulation 99, 779–785 (1999).

12. Katan, M. B., Zock, P. L. & Mensink, R. P. Dietary oils, serum lipoproteins, and coronary heart disease. Am. J. Clin. Nutr. 61, 1368S–1373S (1995).

13. Grundy, S. M. Influence of stearic acid on cholesterol metabolism relative to other long-chain fatty acids. Am. J. Clin. Nutr. 60, 986S–990S (1994).
 

Good Calories, Bad Calories: A Critical Review; Chapter 1 – The Eisenhower Paradox

cover

Introduction

This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

Not the Introduction

Early in the chapter Taubes claims that most mainstream nutrition authorities were saying that the American diet changed during the 20th century, from a plant-based diet to a diet heavy in meat. On pages 10 and 11 he attempts to refute this notion by saying that the USDA statistics from which this notion is drawn is very flawed, citing a personal interview with David Call and a paper on food disappearance data.1 Specifically he says

  • “The USDA statistics, however, were based on guesses, not reliable evidence.”

  • “The resulting numbers for per-capita consumption are acknowledged to be, at best, rough estimates.”

  • “The reports remained sporadic and limited to specific food groups until 1940 […] Until then, the data were particularly sketchy…”

However, the very next paragraph he makes the argument that the US has always been a meat-eating country, and as evidence he cites data from the USDA! “By one USDA estimate, the typical American was eating 178 pounds of meat annually in the 1830s, forty to sixty pounds more than was reportedly being eaten a century later.” Either the food stats are reliable before 1940 or the are not. Pick a side and be consistent.

He’s really all over the map in this section because he then claims that in fact we did eat less meat in the early 20th century due to a few reasons: the cattle industry could not keep up with population growth, meat rationing during WW1, and Upton Sinclair’s The Jungle. He then makes the argument that Americans started eating more fruits and vegetables and decreased consumption of animal products. Following this change, incidents of heart disease skyrocketed to become an epidemic – an epidemic that earlier in the chapter he claims was completely bogus.

* * *

On pages 14 and 15 Taubes talks a bit about cholesterol and says

Despite myriad attempts, researchers were unable to establish that patients with atherosclerosis had significantly more cholesterol in their bloodstream than those who didn’t. “Some works claim a significant elevation in blood cholesterol level for a majority of patients with atherosclerosis,” the medical physicist John Gofman wrote in Science in 1950, “whereas others debate this finding vigorously. Certainly a tremendous number of people who suffer from the consequences of atherosclerosis show blood cholesterols in the accepted normal range.”

It’s interesting to note that immediately after that sentence in the cited text Gofman also wrote2

There does exist a group of disease states (including diabetes mellitus, nephrotic nephritis, severe hypothyroidism, and essential familial hypercholesteremia) in which the blood cholesterol level may be appreciably elevated. Such patients do show, in general, earlier and more severe atherosclerosis than the population at large.

In fact, most of the text makes the case that there are particular cholesterol particles to blame for atherogenesis, specifically those with a density of 10-20 Svedberg units that are currently known as LDL. However, since this paper was published in 1950 they are referred to as the Sf 10-20 class of cholesterol molecules. Gofman also noted – prior to even anything that Keys published on the subject – that dietary lipids affect these Sf 10-20 molecules, stating:

Our preliminary study of a group of 20 patients whose diet we have restricted in cholesterol and fats has demonstrated that the concentration of the Sf 10-20 class of molecules is definitely reduced or even brought down to a level below resolution ultracentrifugally in 17 of the cases studied within two weeks to one month.

I can’t understand why Taubes didn’t mention that, can you?

* * *

Taubes knocks me for a loop on page 15 when he states:

The condition of having very high cholesterol—say, above 300 mg/dl—is known as hypercholesterolemia. If the cholesterol hypothesis is right, then most hypercholesterolemics should get atherosclerosis and die of heart attacks. But that doesn’t seem to be the case.

Actually that seems to be exactly the case… even by the study Taubes cites.

Coronary Artery Disease in 116 Kindred with Familial Type II Hyperlipoproteinemia

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That study even seems to be in agreement with the other studies on familial hypercholesterolemia at the time3:

Our results are qualitatively similar to analyses on a smaller scale which have established an enhanced risk of premature CAD in affected members of families with familial hypercholesterolemia.

But since certain thyroid and kidney disorders might also cause hypercholesterolemia I suppose Taubes can just ignore all that evidence linking cholesterol to heart disease.

* * *

Pg. 15

Autopsy examinations had also failed to demonstrate that people with high cholesterol had arteries that were any more clogged than those with low cholesterol. In 1936, Warren Sperry, co-inventor of the measurement technique for cholesterol, and Kurt Landé, a pathologist with the New York City Medical Examiner, noted that the severity of atherosclerosis could be accurately evaluated only after death, and so they autopsied more than a hundred very recently deceased New Yorkers, all of whom had died violently, measuring the cholesterol in their blood. There was no reason to believe, Sperry and Landé noted, that the cholesterol levels in these individuals would have been affected by their cause of death (as might have been the case had they died of a chronic illness). And their conclusion was unambiguous: “The incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum per se.”

I was unable to find the cited Landé and Sperry paper. It is so old and obscure that not only was I unable to find it, the databases I used (PubMed, WorldCat, Academic Search Complete) could not find a record of it even existing. But let’s do something we probably should not do and take Taubes at his word here. It is still interesting to note that this is an example of an observational study, specifically a cross-sectional study. Later in the book Taubes will make the case that observational studies are worthless. In fact, you will see throughout the book that Taubes will cite observational studies, usually without caveat, if it fits his meat-is-good narrative. However, if he doesn’t like the conclusion of a study (observational or otherwise) you will find that he impugns the methodology, the authors, or even the entire field of science of which it is a part. Get your popcorn ready.

* * *

Like the above point, this is not a real significant issue, but it shows that Taubes is not above quote mining to try and paint someone in a negative light. On page 16:

Henry Blackburn, his longtime collaborator at Minnesota, described him as “frank to the point of bluntness, and critical to the point of sharpness.” David Kritchevsky, who studied cholesterol metabolism at the Wistar Institute in Philadelphia and was a competitor, described Keys as “pretty ruthless” and not a likely winner of any “Mr. Congeniality” awards.

I imagine the point of these quotes is to paint Keys as kind of an asshole, just in case any reader might find themselves sympathizing with Keys when Taubes takes massive, diarrhea-like shits all over Keys’s research and Keys personally. I cannot verify the Kritchevsky quote above because it was from a personal interview, but adding a bit of context to the Blackburn quote can change the tone entirely4:

Ancel Keys has a quick and brilliant mind, a prodigious energy, and great perseverance. He can also be frank to the point of bluntness, and critical to the point of sharpness. But by the boldness of his concepts, the vigor of his pursuits, and the rigor of his methods, as well as by his personal example, he led several generations of investigators in making powerful contributions to the public health.

The entire article is actually quite praiseworthy.

* * *

Pg. 15:

This was a common finding by heart surgeons, too, and explains in part why heart surgeons and cardiologists were comparatively skeptical of the cholesterol hypothesis. In 1964, for instance, the famous Houston heart surgeon Michael DeBakey reported similarly negative findings from the records on seventeen hundred of his own patients. And even if high cholesterol was associated with an increased incidence of heart disease, this begged the question of why so many people, as Gofman had noted in Science, suffer coronary heart disease despite having low cholesterol, and why a tremendous number of people with high cholesterol never get heart disease or die of it.

I’m not sure why Taubes names DeBakey as the primary source here, since he was actually the fourth author in the study that was cited, but no matter… It’s interesting to find that if you check the 1964 paper that is cited, it’s a type of observational study called a case series that examines 1,700 surgical patients treated for some sort of atherosclerosis.5 Turns out 1,416 out of the 1,700 (or 83%) have what the Mayo Clinic would describe as “high” cholesterol levels (over 200 mg/dL).

Does Taubes even read the studies he cites? Or does he read them and deliberately misrepresent them?

A second paper he cites in support of that paragraph is not even a study, but a statement by the president of the American Heart Association6 (wait… they’re supposed to be the bad guys, right?). He says many things in that statement, but what is most relevant to this paragraph is he says that

In a nation of over a quarter of a billion people we are a remarkably heterogeneous lot, and in truth there are no two of us alike. Those with low cholesterols as a group seem to have less coronary disease than those with high cholesterols, but this is too often extrapolated to apply directly to one individual.

He goes on to expound that, sure, cholesterol levels are important, but sometimes people get heart disease and don’t have high cholesterol levels so we should individualize our advice. I don’t think it really helps or hurts Taubes’s argument, but evidently he cited it anyway. Probably to pad his references.

* * *

If Taubes’s irrational contempt for Keys was not obvious before, it should be crystal clear after this passage on page 16:

When Keys launched his crusade against heart disease in the late 1940s, most physicians who believed that heart disease was caused by diet implicated dietary cholesterol as the culprit. We ate too much cholesterol-laden food—meat and eggs, mostly—and that, it was said, elevated our blood cholesterol. Keys was the first to discredit this belief publicly, which had required, in any case, ignoring a certain amount of the evidence.

Before Keys came along all of the “evidence” that dietary cholesterol substantially affects serum cholesterol was from animal studies. Studies that, just two pages earlier, Taubes argues have no bearing on human physiology. So Keys decides to conduct some cholesterol research on actual humans, and concludes that dietary cholesterol actually doesn’t have a substantial effect on serum cholesterol.7 If this were anyone else other than Keys Taubes would likely praise them for not following the conventional wisdom of the day and conducting proper scientific research, but instead Keys is accused of “ignoring” evidence. I think that’s fair.

In the same paragraph as above Taubes discusses a cholesterol study:

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.

Although the statement “the cholesterol we eat has very little effect on the amount of cholesterol in our blood” is true for most people, as we have just discovered, the Rittenberg/Schoenheimer study that Taubes mentions has almost nothing to do with that statement.8 Firstly, the study was conducted on mice, and extrapolating results on people from cholesterol studies on animals are certainly dubious as Taubes himself admits. Moreover, the study itself involves feeding mice water labeled with deuterium then measuring deuterium in their cholesterol and fatty acids in the mice’s tissues to see how much deuterium had been incorporated into those molecules. As far as I can tell it has nothing to do with feeding them cholesterol and seeing if that impacts their blood cholesterol levels. But correct me if I am wrong.

Pg. 16 continued:

As a result, Keys insisted that dietary cholesterol had little relevance to heart disease. In this case, most researchers agreed.

Most researchers agreed… 16 years later.9

* * *

On page 17 Taubes writes:

By 1952, Keys was arguing that Americans should reduce their fat consumption by a third, though simultaneously acknowledging that his hypothesis was based more on speculation than on data: “Direct evidence on the effect of the diet on human arteriosclerosis is very little,” he wrote, “and likely to remain so for some time.”

This is another minor point, but it should be pointed out that THAT IS WHAT A HYPOTHESIS IS. It’s a guess based on little or no evidence, and all scientists have them. Just for context, here’s the quote from Keys that Taubes plucked with a bit more… umm… context10:

[W]e may remark that direct evidence on the effect of the diet on human atherosclerosis is very little and is likely to remain unsatisfactory for a long time. But such evidence as there is, plus valid inferences from indirect evidence, suggests that a substantial measure of control of the development of atherosclerosis in man may be achieved by control of the intake of calories and of all kinds of fats, with no special attention to the cholesterol intake. This means: (1) avoidance of obesity, with restriction of the body weight to about that considered standard for height at age 25; (2) avoidance of periodic gorging and even temporary large calorie excesses; (3) restriction of all fats to the point where the total extractable fats in the diet are not over about 25 to 30 per cent of the total calories; (4) disregard of cholesterol intake except, possibly, for a restriction to an intake less than 1 Gm. per week.

Taubes gets the quotation a smidge wrong, but it still keeps the spirit of the original. The bigger picture here is that Keys is recommending (in an academic journal, by the way) to avoid becoming obese, avoid gorging on food, a diet that’s about 30% fat, and to not worry too much about cholesterol intake. Pretty uncontroversial stuff, if you ask me. Yet Taubes portrays Keys here and elsewhere as some kind of radical crusader, religious zealot, idiot, and kind of an asshole.

* * *

On page 18 Taubes discusses a 1957 paper by Jacob Yerushalmy and Herman Hilleboe, which is something of a response to Ancel Keys’s 1953 paper Atherosclerosis: A Newer Problem in Public Health.11 If you’re not familiar with the Keys paper I will give you a brief synopsis. Keys published some data that suggested a remarkable relationship between fat in the diet and heart disease. Included in the paper was a striking (if oversimplified) figure looking at several countries and their population’s typical fat intake juxtaposed with deaths from heart disease.

YH4

Taubes says:

Many researchers wouldn’t buy it. Jacob Yerushalmy, who ran the biostatistics department at the University of California, Berkeley, and Herman Hilleboe, the New York State commissioner of health, co-authored a critique of Keys’s hypothesis, noting that Keys had chosen only six countries for his comparison though data were available for twenty-two countries. When all twenty-two were included in the analysis, the apparent link between fat and heart disease vanished. Keys had noted associations between heart-disease death rates and fat intake, Yerushalmy and Hilleboe pointed out, but they were just that. Associations do not imply cause and effect or represent (as Stephen Jay Gould later put it) any “magic method for the unambiguous identification of cause.”

I have actually written about this in a previous blog post, but I will revisit this again. Aside from the fact that Keys never claimed a cause-and-effect relationship (much less an unambiguous one) and always identified it as an association, Taubes completely misrepresents the results of the study. It’s true that after Yerushalmy and Hilleboe added more data into the graph the relationship becomes a bit more muddied, but it certainly does not vanish as Taubes claims. There is still a noticeable relationship.12 See for yourself.

YH1

What’s even more interesting is that Y&H actually conclude that consumption of animal fat and/or animal protein is much more strongly associated with heart disease than total fat. Moreover, vegetable fat and/or vegetable protein is actually negatively correlated with heart disease. The resolution is not very sharp, but here are the results. I’ll leave it to you to wonder why Taubes ignores this highly pertinent information.

YH3

YH-2

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See Taubes response #1

* * *

On pages 19-20 Taubes claims that Keys “insisted” that fat elevated cholesterol. I am not sure what Keys was doing that made him so insisting, other than writing a few academic articles concluding that there was an association between dietary fat and serum cholesterol (which there was), while also making sure to point out that there are many details about this association that have yet to be discovered (which there also were). Taubes then goes on to mention some studies that examined those details:

In 1952, however, Laurance Kinsell, director of the Institute for Metabolic Research at the Highland–Alameda County Hospital in Oakland, California, demonstrated that vegetable oil will decrease the amount of cholesterol circulating in our blood, and animal fats will raise it. That same year, J. J. Groen of the Netherlands reported that cholesterol levels were independent of the total amount of fat consumed: cholesterol levels in his experimental subjects were lowest on a vegetarian diet with a high fat content, he noted, and highest on an animal-fat diet that had less total fat. Keys eventually accepted that animal fats tend to raise cholesterol and vegetable fats to lower it, only after he managed to replicate Groen’s finding with his schizophrenic patients in Minnesota.

In other words, Keys did what any good scientist should do: he followed the evidence. Yet the syntax of the last sentence would have you imagine that Keys was some sort of stubborn asshole that refused to accept the truth until the evidence overwhelmed him.

* * *

This may be another nitpicky issue, but the following quote is misleading. Page 20:

This kind of nutritional wisdom is now taught in high school, along with the erroneous idea that all animal fats are “bad” saturated fats, and all “good” unsaturated fats are found in vegetables and maybe fish. As Ahrens suggested in 1957, this accepted wisdom was probably the greatest “handicap to clear thinking” in the understanding of the relationship between diet and heart disease.

First of all, I was never taught that kind of “nutritional wisdom” in high school. Come to think of it I was never taught any nutritional wisdom in high school, but that’s neither here nor there. My issue with this is that in the text that Taubes cites as the source of that quote, Ahrens does not say that the animal fat = bad / vegetable fat = good binarism is the greatest handicap to clear thinking. What he does say is that the good-bad dyad was a greater handicap than the confusion about why experimental diets were designed to be eucaloric.13

* * *

Tabues uses a 1957 review article titled “Atherosclerosis and the Fat Content of the Diet” as a source for three claims in this chapter. One is simply a block quote on page 8. The other two claims are very tenuous, especially the following found on page 20:

In 1957, the American Heart Association opposed Ancel Keys on the diet-heart issue.

The article does mention Keys a few times, as well as a number of other researchers involved with dietary research involving atherosclerosis, but it is very neutral on Keys. In fact, you might even say the author mildly endorses Keys at a couple of points: “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.” And “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.”14

After reading the article I certainly didn’t get the idea that the AHA opposed Keys. Even if they did they never explicitly stated this.

* * *

On page 21 Taubes pulls some numbers from thin air:

As Time reported, Keys believed that the ideal heart-healthy diet would increase the percentage of carbohydrates from less than 50 percent of calories to almost 70 percent, and reduce fat consumption from 40 percent to 15 percent.

The Time article actually does report that Keys suggested American reduce their fat intake from 40 to 15 percent. However, there is no mention in the entire article about Keys recommending an increase in carbohydrates.15

Go to Good Calories, Bad Calories: A Critical Review; Chapter 2 – The Inadequacy of Lesser Evidence

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Refs

1. Call, D. L. & Sánchez, A. M. Trends in fat disappearance in the United States, 1909-65. J. Nutr. 93, Suppl:1–28 (1967).

2. Gofman, J. W. et al. The Role of Lipids and Lipoproteins in Atherosclerosis. Science 111, 166–186 (1950).

3. Stone, N. J., Levy, R. I., Fredrickson, D. S. & Verter, J. Coronary artery disease in 116 kindred with familial type II hyperlipoproteinemia. Circulation 49, 476–488 (1974).

4. Blackburn, H. Ancel Keys. at http://www.mbbnet.umn.edu/firsts/blackburn_h.html

5. Garrett H, Horning EC, Creech BG & De Bakey M. Serum cholesterol values in patients treated surgically for atherosclerosis. JAMA 189, 655–659 (1964).

6. James, T. N. Presidential address. AHA 53rd scientific sessions, Miami Beach, Florida, November 1980. Sure cures, quick fixes and easy answers. A cautionary tale about coronary disease. Circulation 63, 1199A–1202A (1981).

7. Keys, A., Anderson, J. T., Mickelsen, O., Adelson, S. F. & Fidanza, F. Diet and Serum Cholesterol in Man: Lack of Effect of Dietary Cholesterol. J. Nutr. 59, 39–56 (1956).

8. 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).

9. Quintão, E., Grundy, S. M. & Ahrens, E. H. Effects of dietary cholesterol on the regulation of total body cholesterol in man. J. Lipid Res. 12, 233–247 (1971).

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

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

12. 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).

13. Ahrens, E. H., Jr. Seminar on atherosclerosis: nutritional factors and serum lipid levels. Am. J. Med. 23, 928–952 (1957).

14. 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).

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

Good Calories, Bad Calories: A Critical Review; Chapter 3 – Creation of Consensus

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Introduction

This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

Not the Introduction

Near the beginning of chapter three Taubes makes some serious unfounded claims. From page 44:

This alliance between the AHA and the makers of vegetable oils and margarines dissolved in the early 1970s, with reports suggesting that polyunsaturated fats can cause cancer in laboratory animals. This was problematic to Keys’s hypothesis […]

Polyunsaturated fats cause cancer?!?!?! That’s a bold claim for which Taubes cites two supporting texts. One is a New York Times article from 1973 titled “Heart Association Strengthens its Advice: Cut Down on Fats,” and it barely has anything to do with Taubes’s claim.1 It mostly deals with atherosclerosis (not cancer), and hardly discusses polyunsaturated fats. The closest thing you will find that even comes close to supporting the claim that “polyunsaturated fats can cause cancer in laboratory animals” is near the end of the article. There is a section titled Challenges and Answers that states the following:

Despite this evidence, doubts and doubters remain. Some of the challenges to the heart disease-fatty diet thesis, and the answers from the heart association, follow: […] Polyunsaturates are dangerous. Dr. Mueller says that there is no evidence that consumption of polyunsaturates is harmful at the recommended levels or even considerably above these levels. While such consumption is known to increase the body’s need for vitamin E, most vegetable oils contain enough vitamin E to satisfy the need.

Hmmm… Is that strong evidence for his claim? Nope. What about the other citation? It not a study involving laboratory animals, but rather a trial of elderly veterans.2 Turns out the data from that trial show a few more people dying from cancer on a diet high in polyunsaturated fat. But the results from the study were something of an outlier. The authors even mention this:

The experience of other investigators using similar diets has not been the same. […] Many of the cancer deaths in the experimental group were among those who did not adhere closely to the diet. This reduces the possibility that the feeding of polyunsaturated oils was responsible for the excess carcinoma mortality observed in the experimental group. […] In both groups, the numbers of cancer deaths among the various adherence strata are compatible with random distribution (table v). A high incidence among high adherers would be expected if some constituent of the experimental diet were contributing to cancer fatality.

Again you must ask yourself “Is this evidence strong enough to justify the claim that polyunsaturated fats cause cancer in laboratory animals?” It’s up to you to decide. I might even ask myself a few more questions like “Is this an innocent citation error? Certainly a book of this depth and magnitude is bound to have a few simple human errors. If it is an honest mistake, why do all the mistakes happen to be in favor of a low-carb, high-fat diet?”

Taubes also uses this study later in the chapter so we’ll revisit this soon. See Taubes response #2 and #3.

 * * *

In chapter three Taubes devotes much ink to slandering discussing the 1977 publication of Dietary Goals for the United States by a committee led by George McGovern. Now I have no problem criticizing the government. In fact, I think that one of the great things about living in the US is the right to just trash the hell out of the government and politicians either in private or in the public eye. I encourage everyone to exercise that right if they see fit; however, criticisms have a little more bite to them when they are actually legitimate. Much of the cited evidence against the Dietary Goals comes from what were ostensibly personal interviews with a few people involved with its drafting. Of course, no one is privy to this information so we can only go on what is publicly available.

On page 46-47 Taubes claims:

Dietary Goals was couched as a plan for the nation, but these goals obviously pertained to individual diets as well. Goal number one was to raise the consumption of carbohydrates until they constituted 55–60 percent of the calories consumed. Goal number two was to decrease fat consumption from approximately 40 percent, then the national average, to 30 percent of all calories, of which no more than a third should come from saturated fats. The report acknowledged that no evidence existed to suggest that reducing the total fat content of the diet would lower blood-cholesterol levels, but it justified its recommendation on the basis that, the lower the percentage of dense fat calories in the diet, the less likely people would be to gain weight, and because other health associations—most notably the American Heart Association—were recommending 30 percent fat in diets. To achieve this low-fat goal, according to the Dietary Goals, Americans would have to eat considerably less meat and dairy products.

When Taubes says “The report acknowledged that no evidence existed to suggest that reducing the total fat content of the diet would lower blood-cholesterol levels…” he is using a straw man that I’m fairly certain is not even discussed in Dietary Goals. By this point total fat was not the issue, but type of fat was and Dietary Goals discusses the evidence that a diet low in saturated fat and high in unsaturated fat will decrease blood-cholesterol levels. Also, I saw no recommendations for eating “considerably less meat and dairy products,” but please correct me if I am wrong.

Taubes’s arguments against Dietary Goals are not even internally consistent at times. For instance on page 45 Taubes writes “McGovern’s staff were virtually unaware of the existence of any scientific controversy” and “They believed that the relevant nutritional and social issues were simple and obvious.” Yet on page 47 Taubes writes “Though the Dietary Goals admitted the existence of a scientific controversy, it also insisted that Americans had nothing to lose by following the advice.” So did the authors know about a controversy or not? I suppose you could imagine a scenario where the authors knew nothing of a controversy yet wrote about one in an official government document anyway, but it seems specious to me.

Let’s go further into Taubes’s Dietary Goals bloodbath shall we? On page 46…

Having held one set of hearings before publishing the Dietary Goals, McGovern responded to the ensuing uproar with eight follow-up hearings. Among those testifying was Robert Levy, director of the National Heart, Lung, and Blood Institute, who said that no one knew whether lowering cholesterol would prevent heart attacks, which was why the NHLBI was spending several hundred million dollars to study the question.

Would Gary Taubes, a New York Times columnist and alumnus of the Ivy Leagues, possibly take someone out of context to misrepresent their position in order to fit his own low-carb narrative? Surely not. But just to be sure let us add a bit more context to Dr. Levy’s statements.3

We have no doubt from the vast amount of epidemiological data available that elevated cholesterol is associated with an increased risk of heart attack, especially some specific types of high cholesterol. We have no doubt that [blood] cholesterol can be lowered by diet and/or medication in most patients. Where the doubt exists is the question of whether lowering [blood] cholesterol will result in a reduced incidence of heart attack; that is still presumptive. It is unproven, but there is a tremendous amount of circumstantial evidence. Not only is there circumstantial epidemiologic data, but there is very exciting animal data. Here is one of many studies that have been done over the last decade with nonhuman primates. It shows that not only can we prevent atherosclerosis from progressing by making dietary changes, but that regression actually occurs. Atherosclerosis will lessen if we lower [blood] cholesterol levels in animals through diet. The problem is we can’t do these kinds of studies in man; it is not ethical. There is no doubt that [blood] cholesterol can be lowered by diet in free-living populations. It can be lowered by 10 to 15 percent.

You have to ask yourself whether Taubes’s characterization of Levy’s testimony is really an accurate representation of Levy’s actual testimony. As a reader are you at all angry that a science journalist like Taubes misrepresents people over and over again? I am genuinely curious. Let me know in the comments section.

 * * *

Taubes makes stuff up again on page 49:

The ASCN committee concluded that saturated-fat consumption was probably related to the formation of atherosclerotic plaques, but the evidence that disease could be prevented by dietary modification was still unconvincing.*

*It also affirmed the suspicion that polyunsaturated fats might be dangerous, and so further diminished the role of margarines and corn oils in dietary recommendations.

As evidence Taubes cites a paper titled The Evidence Relating Six Dietary Factors to the Nation’s Health by Dr. Ahrens.4 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. Taubes, however, tells his readers that the committee found the evidence “unconvincing” for reasons that should be pretty clear by now.

He also tells his readers that the ASCN committee affirmed that polyunsaturated fats might be dangerous, which apparently diminishes the role of margarine and corn oil. However, the committee claims nothing of the sort; there is no implied subtext either. In fact, there is literally no mention of polyunsaturated fats, corn oil, or margarine.

He does cite a separate paper that, as far as I can tell, has nothing to do with the ASCN committee paper other than being published by the same journal.5 There is still no mention of corn oil or margarine or any kind of affirmation that polyunsaturated fats might be dangerous. In fact, the text claims that polyunsaturated fats are generally beneficial, but that the long term effects of specific concerns such as lipid peroxidation of polyunsaturates have yet to be studied.

* * *

On page 54 Taubes strongly implies (like he has done before) that polyunsaturated fats and low levels of cholesterol leads to cancer and death:

The other disconcerting aspect of these studies is that they suggested (with the notable exception of three Chicago studies reported by Jeremiah Stamler and colleagues) low cholesterol levels were associated with a higher risk of cancer. This link had originally been seen in Seymour Dayton’s VA Hospital trial in Los Angeles, and Dayton and others had suggested that polyunsaturated fats used to lower cholesterol might be the culprits.

Dayton actually suggests the opposite in that very study. Pearce and Dayton actually do conduct a trial with elderly veterans where two groups are fed more-or-less the same diet, except one diet has more polyunsaturated fats in it. The results do indicate that in fact the group eating the diet with more polyunsaturates does have a few more cancer deaths in the group. But, as Taubes would say, there were caveats. I’ll let the authors explain:

The experience of other investigators using similar diets has not been the same. […] Many of the cancer deaths in the experimental group were among those who did not adhere closely to the diet. This reduces the possibility that the feeding of polyunsaturated oils was responsible for the excess carcinoma mortality observed in the experimental group. […] In both groups, the numbers of cancer deaths among the various adherence strata are compatible with random distribution (table v). A high incidence among high adherers would be expected if some constituent of the experimental diet were contributing to cancer fatality.

Indeed, other investigators’ experiences was not the same. A survey of five similar dietary trials published that same year suggested there was no link between low serum cholesterol and cancer.6 There are a handful of studies you can find that will support the link between cancer and low cholesterol, though. You can find them. But perhaps those results are due to the cholesterol-lowering effects of cancer, not the other way around.7

In fact, the authors of the MRFIT study (of which Taubes displays the results in the next chapter) explicitly mention this.8 In case you’re interested:

The increased total mortality at the lowest cholesterol levels has been noted before. It is primarily due to an increased risk of cancer death in those with the lowest cholesterol concentrations and is probably explained by a cholesterol-lowering effect of cancer. The most recent evidence for this explanation is an analysis of the MRFIT screening cohort which showed that the association between low serum cholesterol and cancer incidence does not persist beyond 5 years of follow-up, whereas that between high serum cholesterol and CHD incidence remains after 5 years.

In any case, regardless of whether or not it was evident to Taubes at the time GCBC was published, the results are in: a recent meta-analysis of 27 large-scale human trials confirmed no association between low cholesterol levels and cancer.9 Of course Taubes would probably demand a large, randomized clinical trial where healthy people are randomly assigned to get cancer and then have their cholesterol levels measured before accepting it. Hell, even then he would probably find a way to dismiss it. Dismissing good evidence that contradicts him is one of Taubes’s greatest skills.

* * *

On pages 53-54 Taubes discusses several studies that have found negative correlations between carbohydrate intake and heart disease.10,11 In other words, studies that have found that carbohydrates may be slightly protective against heart disease. Uh, oh! It’s time for Taubes to do some serious spinning. But remember what I said above? This is his specialty. He has a PhD in spinning science. You might even call him a Spin Doctor! Get it? Okay, here’s what he says:

When one is reading this report, it’s hard to avoid the suspicion that once the government began advocating fat reduction in the American diet it changed the way many investigators in this science perceived their obligations. Those who believed that dietary fat caused heart disease had always preferentially interpreted their data in the light of that hypothesis. Now they no longer felt obliged to test any hypothesis, let alone Keys’s. Rather, they seemed to consider their obligation to be that of “reconciling [their] study findings with current programs of prevention,” which meant the now official government recommendations. Moreover, these studies were expensive, and one way to justify the expense was to generate evidence that supported the official advice to avoid fat. If the evidence didn’t support the recommendations, then the task was to interpret it so that it did.

Now scientists can’t even be trusted!! Why? They’re greedy whores, of course; willing to do and say anything to keep those sweet, sugary NSF grants rolling in. Researchers have to maintain their lavish lifestyle, and if that means lying to the public and a few people get diabetes and die because of it, well, so be it. Health scientists didn’t get into the field of research because of a love of science or truth or the public good – they did it for the cold, hard cash.

Not only is that sentiment one of the most cynical things I have ever read, it is completely absurd and without merit. (I wonder if there are issues of psychological projection here; like when a cheating spouse unreasonably accuses their partner of cheating.) And lest you think Taubes took that quote from some secret literature of the Scientist Guild that shares tips and tricks on how to bilk the government out of research funding and promote chronic diseases for shits and giggles, here is a little more context:

Although the findings reported here – particularly those related to starch intake – may eventually be found to have practical implications, it would be premature to propose dietary alterations before the findings are examined more carefully. We consider the inverse relation of CHD incidence to the total daily caloric intake as a prescription for greater physical activity rather than for greater caloric intake.

[…]

The apparently protective effect of starch consumption against CHD seems to imply that the proportion of calories coming from starch should be increased. In isocaloric diets, increased intake of starch is a logical way to balance decreased intake of fat. Thus, from a practical point of view there is no difficulty in reconciling our study findings with current programs for prevention of CHD.

Doesn’t really sound so evil, does it? And by the way, there was never any official government “advice to avoid fat.” Never. The Dietary Goals for the United States that Taubes keeps hammering away at recommended a diet consisting of one-third fat. ONE-THIRD. This is not in any way a low-fat diet or advice to avoid fat. What it is is Taubes’s favorite straw man. For the record Dietary Goals recommended Americans cut their sugar intake by nearly 50%, yet no praise was given for that decision. I wonder why.

* * *

On page 57 Taubes discusses a study, the results of which he doesn’t like because they show that lowering cholesterol reduced nonfatal heart attacks, fatal heart attacks, and overall death. Watch the master of spin work his magic:

Nonetheless, these results were taken as sufficient by Rifkind, Steinberg, and their colleagues so they could state unconditionally that Keys had been right and that lowering cholesterol would save lives. Rifkind and his collaborators also concluded that the cholesterol-lowering benefits of a drug applied to diet as well. Although the trial included only middle-aged men with cholesterol levels higher than those of 95 percent of the population, Rifkind and his colleagues concluded that those benefits “could and should be extended to other age groups and women and…other more modest elevations of cholesterol levels.”

Isn’t he good? By the way, the cited source for that Rifkind quote is a National Heart, Lung, and Blood Institute consensus conference, and those words do not appear in it.12

Go to Good Calories, Bad Calories: A Critical Review; Chapter 4 – The Greater Good

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Refs

1. Brody, J. Heart Association Strengthens Its Advice: Cut Down on Fats. N. Y. Times 54 (1973).

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

3. United States. Dietary goals for the United States. (U.S. Govt. Print. Off., 1977). at <http://catalog.hathitrust.org/Record/011389409&gt;

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

5. Glueck, C. J. Appraisal of dietary fat as a causative factor in atherogenesis. Am. J. Clin. Nutr. 32, 2637–2643 (1979).

6. Ederer, F., Leren, P., Turpeinen, O. & Frantz, I. Cancer among men on cholesterol-lowering diets: Experience from five clinical trials. The Lancet 298, 203–206 (1971).

7. Rose, G. & Shipley, M. J. Plasma lipids and mortality: a source of error. The Lancet 315, 523–526 (1980).

8. Martin, M. J., Browner, W. S., Hulley, S. B., Kuller, L. H. & Wentworth, D. Serum cholesterol, blood pressure, and mortality: implications from a cohort of 361,662 men. The Lancet 328, 933–936 (1986).

9. Cholesterol Treatment Trialists’ (CTT) Collaboration. Lack of Effect of Lowering LDL Cholesterol on Cancer: Meta-Analysis of Individual Data from 175,000 People in 27 Randomised Trials of Statin Therapy. PLoS ONE 7, e29849 (2012).

10. Yano, K., Rhoads, G. G., Kagan, A. & Tillotson, J. Dietary intake and the risk of coronary heart disease in Japanese men living in Hawaii. Am. J. Clin. Nutr. 31, 1270–1279 (1978).

11. Gordon, T. et al. Diet and its relation to coronary heart disease and death in three populations. Circulation 63, 500–515 (1981).

12. Consensus Conference. Lowering blood cholesterol to prevent heart disease. JAMA 253, 2080–2086 (1985).

Good Calories, Bad Calories: A Critical Review; Chapter 4 – The Greater Good

cover

Introduction

This is something of an ongoing review, chapter by chapter, of Gary Taubes’s extraordinarily dense book Good Calories, Bad Calories, which I usually shorten to GCBC. You might even consider this more of a fact-checking than a review, but whatever. I’m not going to get into a semantic argument. I wrote my first review of this book back in 2012, but after writing it I felt very unsatisfied. GCBC is such a dense book filled with so many unsubstantiated claims that I felt the book demanded a more thorough review. Other bloggers, like James Krieger at Weightology, seem to feel the same way and have tried to provide such a review only to eventually give up once they realize the gravity of the task. I may also give up at some point. I actually have given up a number of times only to feel compelled to hit at least one more chapter.

If you would like to read other parts of this ongoing review go to the table of contents on my Book Reviews page. FYI: All page numbers in this review refer to the hardback version of the book.

Not the Introduction

On pages 60-62 Taubes discusses a publication by the National Academy of Sciences titled Diet and Health: Implications for Reducing Chronic Disease Risk.

I’m not sure that Taubes actually reads it because he gets a few things wrong about it. First (and this is a minor point) he says the publication is thirteen hundred pages long, when in fact it is not even eight hundred pages long. At least that’s the version I have.

Second — and this is probably a more important point — he says about the publication:

It was no longer about the validity of the underlying science, which was no less ambiguous than ever, but about whether Americans should be eating low-fat diets or very low-fat diets.

Actually, Diet and Health recommends a diet of 30% of total calories from fat.1 I don’t see how this could be seen as a low-fat diet, much less a very low-fat diet. Clearly Taubes wants the committee to have recommended something like a very low-fat diet, but they did no such thing so he just lies and says they did anyway. (See: straw man)

Taubes then says:

One striking fact about this evolution is that the low-fat diets now being recommended for the entire nation had only been tested twice… The results of those trials had been contradictory.

Clearly Taubes didn’t bother to actually read Diet and Health. If he did he would have noticed the literally TWENTY-SEVEN PAGES of references regarding dietary fat alone! In fact, the bulk of the publication was devoted to explaining the evidence behind the recommendations. I don’t really blame Taubes for not reading it, though; it was quite long and it didn’t really fit nicely into the narrative he was attempting to craft. As a matter of fact one of the cited trials, titled Low-fat Diet in Myocardial Infarction in The Lancet, had a group consuming about half the percentage of calories from fat than what the National Academy of Sciences was recommending in Diet and Health so the results aren’t really comparable. Nevertheless, the low-fat group actually had beneficial effects to weight and serum lipids compared to the control group.2

* * *

Taubes does some really excellent minimizing on pages 63 and 64 when he discusses some data from the MRFIT trial:

For every one thousand middle-aged men who had high cholesterol—between, say, 240 and 250 mg/dl—eight could expect to die of heart disease over any six-year period. For every thousand men with cholesterol between 210 and 220, roughly six could expect to die of heart disease. These numbers suggest that reducing cholesterol from, say, 250 to 220 would reduce the risk of dying from a heart attack in any six-year period from .8 percent (eight in a thousand) to .6 percent (six in a thousand). If we were to stick rigorously to a cholesterol-lowering diet for thirty years—say, from age forty to seventy, at which point high cholesterol is no longer associated with an increased risk of heart disease—we would reduce our risk of dying of a heart attack by 1 percent.

By the way, I find it humorous that in the previous chapter Taubes was talking about what a disaster the MRFIT trial was, but here he’s discussing it as if it were the capital-T truth.

I think his data is actually wrong, too. He publishes a graph on the same page taken from a MRFIT article, and I think he’s simply guesstimating. The actual data from the trial says that a serum cholesterol value of 220 mg/dl would correspond to a CHD death rate of 5.81/1,000 and a cholesterol value of 250 mg/dl would have a death rate of 9.1/1,000.3,4 I suppose it’s a minor point, but I am going to use the real data in a second.

His choice of how to present the results is a great study of how to deceive with statistics. It also reminds of a scene in Pulp Fiction. You’ve probably seen it, but if you haven’t I’m not going to explain the context because I don’t really need to to make my point.

                                     VINCENT
                         What do you think about what happened 
                         to Antwan?

                                     MIA
                         He fell out of a window.

                                     VINCENT
                         That's one way to say it. Another 
                         way is, he was thrown out. Another 
                         was is, he was thrown out by 
                         Marsellus. And even another way is, 
                         he was thrown out of a window by 
                         Marsellus because of you.

So Taubes says “These numbers suggest that reducing cholesterol from, say, 250 to 220 would reduce the risk of dying from a heart attack in any six-year period from .8 percent (eight in a thousand) to .6 percent (six in a thousand).” That’s certainly one way to say it. Another way is that it reduces your risk of dying from a heart attack by 36%. Another way is it reduces your relative risk of CHD death from 2.88 to 1.84 (with 1.0 being optimal). And even another way to say it is that this data suggests that 205,954 lives in the US could be spared by lowering serum cholesterol from 250 to 220, assuming 20% of the population has cholesterol in excess of 250 mg/dl.

* * *

Page 65-66

Between 1987 and 1994, independent research groups from Harvard Medical School, the University of California, San Francisco, and McGill University in Montreal addressed the question of how much longer we might expect to live if no more than 30 percent of our calories came from fat, and no more than 10 percent from saturated fat, as recommended by the various government agencies. All three assumed that cholesterol levels would drop accordingly, and that this low-fat diet would have no adverse effects, which was still speculation rather than fact.

The Harvard study, led by William Taylor, concluded that men with a high risk of heart disease—such as smokers with high blood pressure—might gain one extra year of life by shunning saturated fat. Healthy nonsmokers, however, might expect to gain only three days to three months. “Although there are undoubtedly persons who would choose to participate in a lifelong regimen of dietary change to achieve results of this magnitude, we suspect that some might not,” the Harvard investigators noted.

The UCSF study, led by Warren Browner, was initiated and funded by the Surgeon General’s Office. This study concluded that cutting fat consumption in America would delay forty-two thousand deaths each year, but the average life expectancy would increase by only three to four months. To be precise, a man who might otherwise die at sixty-five could expect to live an extra month if he avoided saturated fat for his entire adult life. If he lived to be ninety, he could expect an extra four months.* The McGill study, published in 1994, concluded that reducing saturated fat in the diet to 8 percent of all calories would result in an average increase in life expectancy of four days to two months.

Browner reported his results to the Surgeon General’s Office, and only then submitted his article to JAMA. J. Michael McGinnis, the deputy assistant secretary for health, then wrote to JAMA trying to prevent publication of Browner’s article, or at least to convince the editors to run an accompanying editorial that would explain why Browner’s analysis should not be considered relevant to the benefits of eating less fat. “They would have liked it to come out the other way,” explained Marion Nestle, who had edited the Surgeon General’s Report on Diet and Health and had recruited Browner to do the analysis. This put Browner in the awkward position of protecting his work from his own funding agents. As he wrote McGinnis at the time, “I am sensitive to the needs of your office to put forward a consistent statement about what Americans should do, and to your dismay when a project that you have sponsored raises some questions about current policy. I am also concerned that the impacts of recommendations that apply to 240 million Americans are clearly understood. This manuscript estimates the effects of one such recommendation—altering dietary fat intake to 30 percent of calories—based on the assumptions that underlie that recommendation. Shooting the messenger—or creating a smoke screen—does not change those estimates.” JAMA published Browner’s article—“What If Americans Ate Less Fat?”—without an accompanying editorial.

*Browner’s analysis also assumed that restricting dietary fat would reduce cancer deaths, which was speculative then and is even more speculative now.

Although the analysis is perhaps more pessimistic about the benefits of reducing saturated fat, it is also a bit more nuanced than Taubes makes it seem.5 The figures of 42,000 saved lives are in there as is the extra four months of life, but there’s also the following:

The analysis indicates that if those assumptions are valid, restricting dietary fat to a maximum of 30% of total energy intake could reduce CHD mortality rates by between 5% and 20%. Mortality due to cancers of the breast, colon, and prostate might be reduced by an even greater proportion. Similar reductions would also occur in the incidence of these diseases.

AND

From the public health point of view, an increase of 3 months in life expectancy multiplied by 240 million Americans results in about 60 million years of additional life […]

Browner also points out that since the 3-4 month estimate is a statistical average, the real effects of lowering saturated fat would probably translate to several extra years in some individuals and possibly no increased lifespan in others.

But that is not the interesting part… The interesting part is where Taubes states that J. Michael McGinnis tried to shut down the publication of the article. This is based on a letter (presumably) that Browner wrote to McGinnis back then. I have contacted both Dr. Browner and Dr. McGinnis to see if they can confirm this. As of this writing I have received no response from Dr. Browner, but I did receive one from Dr. McGinnis that was very interesting. McGinnis claims he was never contacted by Taubes for his side of the story and that what Taubes wrote “certainly doesn’t ring either familiar or true.” In McGinnis’s own words:

Neither Marion nor I worked in the Surgeon General’s office—rather in a parallel office in HHS—but if the paper was done when she worked with me, it would have been nearly 30 years ago. I really have no recollections on any of what is reported in the passage—including the commissioning of the paper. I do recall the general reported finding on the limited impact on heart disease deaths of the lipid intake reduction indicated, although not the individuals or center (or centers) making the reports. Given the fact that the finding of small effects of isolated dimensions was not unusual (recall MRFIT), it would not have been particularly surprising. It is certainly possible that I would have been of a mind that a narrowcast analysis could be misleading if interpreted as reflecting on the impact of broader associated dietary changes. But unless I was a reviewer commenting on methodologic limits, it would be very unlike me—I cannot recall a single instance—to separately suggest that an article not be published. Indeed, to the contrary, I am squarely in the camp that there is great merit in publicly “calling the question” on these issues to prompt further analytic advances.

Dr. McGinnis also said that he will happily recant if someone were to produce the letter in question. I also contacted Dr. Marion Nestle and she claims that, while she can’t remember the specifics, what Taubes wrote about her remarks are generally true.

* * *

On page 72 Taubes discusses the famous Nurses Health Study and states

In 1992, Willett published the results from eight years of observation of the Nurses cohort. Fifteen hundred nurses had developed breast cancer, and, once again, those who ate less fat seemed to have more breast cancer. In 1999, the Harvard researchers published fourteen years of observations. By then almost three thousand nurses had contracted breast cancer, and the data still suggested that eating fatty foods (even those with copious saturated fat) might protect against cancer.

Walter Willett and Meir Stampfer are two of several authors of these obervational studies.6,7 (Interestingly, Taubes says in a blog post that Willett and Stampfer are not real scientists, they don’t do “real” science, and epidemiology is not to be trusted.) The cited studies do not provide evidence for his claim that copious amounts of saturated fats might protect against cancer. The best thing he can say is that consumption of SATURATED fat doesn’t appear to increase one’s risk of BREAST cancer. Of course the same could also be said of MONOUNSATURATED, POLYUNSATURATED, and even TRANS fats, at least according to these studies.

* * *

On page 73 Taubes gets on the polyunsaturated-fats-cause-cancer bandwagon again stating:

This laboratory evidence that dietary fat caused breast cancer began to evaporate as soon as Diet, Nutrition, and Cancer was published, and researchers could get funding to study it. By 1984, David Kritchevsky, one of the authors of Diet, Nutrition, and Cancer, had published an article in Cancer Research reporting on experiments that had been explicitly designed to separate out the effects of fat and calories on cancer, at least in rats. As Kritchevsky reported, low-fat, high-calorie diets led to more tumors than high-fat, low-calorie diets, and tumor production was shut down entirely in underfed rats, regardless of how fatty their diet was.

However, the results from the study itself are different:8

The data from 3 separate studies altering caloric and fat intake support the conclusions that a high-fat diet influences initiation as well as promotion of DMBA-induced mammary tumorigenesis, that high caloric intake increases tumor yield, and that restriction of caloric intake (even concomitant with the provision of twice as much dietary fat) inhibits tumor formation during the promotion period.

At least he got part of the study correct. By the way, I wonder how Taubes squares this circle in his mind when he later advocates eating all the calories you want — as long as it’s all meat, of course.

* * *

Pg 74

Nonetheless, the pervasive belief that eating fat causes breast cancer has persisted, partly because it once seemed undeniable. Purveyors of health advice just can’t seem to let go of the notion. […] By 2006, with the next release of cancer-prevention guidelines by the American Cancer Society, the ACS was acknowledging that “there is little evidence that the total amount of fat consumed increases cancer risk.” But we were still advised to eat less fat and particularly meats (“major contributors of total fat, saturated fat and cholesterol in the American diet”), because “diets high in fat tend to be high in calories and may contribute to obesity, which in turn is associated with increased risks of cancers.” (Saturated fats, in particular, the ACS added, “may have an effect on increasing cancer risk,” a statement that seemed to be based solely on the belief that if saturated fat causes heart disease it probably causes cancer as well.)

Of course, Taubes ignores the reference in the text that immediately follows “may have an effect on increasing cancer risk” and instead tells his readers that the statement is based on some unfounded belief. In case you’re wondering the reference is a review article that pours over several relevant studies on fat and cancer.9 What Taubes also omits is that the main reasons the ACS recommends avoiding red and processed meats have little to do with fat content.10 I’ll let the ACS explain:

Many epidemiologic studies have examined the association between cancer and the consumption of red meats (defined as beef, pork, or lamb) and processed meats (cold cuts, bacon, hot dogs, etc.). Current evidence supports an increased risk of cancers of the colon and/or rectum and prostate. More limited evidence exists for other sites. Studies that have examined red meat and processed meat separately suggest that risks associated with processed meat may be slightly greater than red meat, but the consumption of both should be limited.

Meat contains several constituents that could increase the risk of cancer. Mutagens and carcinogens (heterocyclic amines and polycyclic aromatic hydrocarbons) are produced by cooking meat at high temperatures and/or by charcoal grilling. The iron content (heme) in red meat may generate free radicals in the colon that damage DNA. Substances used to process meat (nitrates/nitrites and salt) contribute to the formation of nitrosamines that can damage DNA. It is also possible that the fat content in meat contributes to risk. For example, foods that are high in fat increase the concentration of secondary bile acids and other compounds in the stool that could be carcinogens or promoters of carcinogenesis.

These cancer properties of red and processed meats have been well-documented over the years. There is a mountain of evidence for them. But of course Taubes has never been one to let evidence ruin a good story about how people that disagree with him are pinheaded schmucks.

* * *

Pg 75, Taubes lies about the results when discussing a study by the Women’s Health Initiative claiming that

The women on the diet also consumed fewer calories—averaging 120 calories a day less than the controls over the eight years of the study.*

*They did not, however, lose any weight because of this, which is paradoxical, and an issue we will discuss later.

Actually, everyone on the diet lost a significant amount of weight.11

See Taubes response #4

* * *

On page 84 Taubes discusses the results of a Cochrane review*:

The review concluded that the diets, whether low-fat or cholesterol-lowering, had no effect on longevity and not even a “significant effect on cardiovascular events.”

The first part of that claim is actually true. The second lies about the results of the systematic review. It actually reduced cardiovascular events by 16%. The same authors published the Cochrane results in BMJ and they concluded then12:

The findings on cardiovascular events are broadly in keeping with benefits that might be expected from modest lowering of cholesterol concentration and certainly provide support, at an individual level, for the central role of dietary fat intake in the causation of cardiovascular disease.

The results also indicated a reduction in mortality by 9%, but that figure was within the 95% CI. In any case, if you’re curious about the updated results they are basically unchanged.13 From the 2012 Cochrane review:

Dietary change to reduce saturated fat and partly replace it with unsaturated fats appears to reduce the incidence of cardiovascular events, but replacing the saturated fat with carbohydrate (creating a low fat diet) was not clearly protective of cardiovascular events (despite small improvements in weight, body mass index, total and LDL cholesterol).The protective effect was seen almost exclusively in those who continue to modify their diet over at least two years, and in studies of men (not those of women). Dietary advice to those at high risk of cardiovascular disease (particularly where lipid lowering medication may not be available), and probably also to lower risk population groups, should continue to include dietary fat modification, possibly as part of a Mediterranean dietary pattern, and it should be stressed that this is a permanent pattern of eating.

*Something Taubes holds in high regard, unless of course a result might contradict his thesis (as is the case with a Cochrane review of salt and hypertension) in which case they are meaningless. But more on that later.

See Taubes response #5

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1. National Academy Press. Diet and Health: Implications for Reducing Chronic Disease Risk. (1989). at <http://www.nap.edu/openbook.php?record_id=1222&gt;

2. A Research Committee. Low-fat Diet in Myocardial Infarction: A Controlled Trial. The Lancet 286, 501–504 (1965).

3. Martin, M. J., Browner, W. S., Hulley, S. B., Kuller, L. H. & Wentworth, D. Serum cholesterol, blood pressure, and mortality: implications from a cohort of 361,662 men. The Lancet 328, 933–936 (1986).

4. Stamler J, Wentworth D & Neaton JD. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded?: Findings in 356 222 primary screenees of the multiple risk factor intervention trial (MRFIT). JAMA 256, 2823–2828 (1986).

5. Holmes, M. D. et al. Association of dietary intake of fat and fatty acids with risk of breast cancer. JAMA 281, 914–920 (1999).

6. Browner WS, Westenhouse J & Tice JA. What if americans ate less fat?: A quantitative estimate of the effect on mortality. JAMA 265, 3285–3291 (1991).

7. Willett, W. C. et al. Dietary fat and fiber in relation to risk of breast cancer. An 8-year follow-up. JAMA 268, 2037–2044 (1992).

8. Kritchevsky, D., Weber, M. M. & Klurfeld, D. M. Dietary Fat versus Caloric Content in Initiation and Promotion of 7,12-Dimethylbenz(a)anthracene-induced Mammary Tumorigenesis in Rats. Cancer Res. 44, 3174–3177 (1984).

9. Kolonel, L. N. Fat, meat, and prostate cancer. Epidemiol. Rev. 23, 72–81 (2001).

10. Kushi, L. H. et al. American Cancer Society Guidelines on Nutrition and Physical Activity for cancer prevention: reducing the risk of cancer with healthy food choices and physical activity. CA. Cancer J. Clin. 56, 254–281; quiz 313–314 (2006).

11. Howard, B. V. et al. Low-fat dietary pattern and weight change over 7 years: the Women’s Health Initiative Dietary Modification Trial. JAMA 295, 39–49 (2006).

12. Hooper, L. et al. Reduced or modified dietary fat for preventing cardiovascular disease. Cochrane Database Syst. Rev. Online CD002137 (2001). doi:10.1002/14651858.CD002137

13. Hooper, L. et al. in Cochrane Database Syst. Rev. (The Cochrane Collaboration) (John Wiley & Sons, Ltd, 2012). at <http://doi.wiley.com/10.1002/14651858.CD002137.pub3&gt;