The Drama of Nutrition

Intro

When I started this podcast/blog a few years ago, I was basically doing it as a way to kill time. I really liked listening to podcasts, I enjoyed talking to people smarter than me, and I enjoyed editing and producing the audio. I started it in grad school and found it to be terribly satisfying. The blog portion of this endeavor was mainly as a “show notes” page or summary page. Eventually the podcast portion of this site went dormant some years ago, although I keep telling myself I will revive it soon. It’s very common for me to run across someone in person or in a book or something and think. “This is fascinating. I should see if they would not mind being interviewed.” But I rarely actually reach out to people for interviewing anymore because I know I won’t have the time. Others can interpret that as I choose not to make time for doing it which is probably fair, too.

Then I got out of school and started climbing the career ladder and the blogging itself became less and less frequent. Nonetheless I always imagined this would be a place to discuss academic nutrition science, nutrition science in the news, the food industry, food safety, food chemistry, and all that nonsense. However, this post will be a little different. This is going to effectively be about stupid he-said-she-said bullsh*t, high school drama with only a passing relation to actual nutrition science, so if that kind of thing is not your bag then just skip this post.

Background

I became compelled to write this post after seeing a tweet by Nina Teicholz the other day.

This tweet links to a post that paints Teicholz as something of a nutrition policy martyr: someone who just wanted to bring capital-T Truth to the ignorant masses and is crucified for it like some sort of modern day Galileo. I don’t know much background on what exactly happened, but the Consumer Federation of America organized a conference on nutrition policy that included several panels on the topic of nutrition policy. Apparently someone over there had the boneheaded idea of inviting Teicholz to be one of the panelists.1

Who knows what happened after that. Maybe someone decided to do some actual research on her or maybe all the other panelists were insulted to even be on the same panel as Teicholz.2 Now they have two choices, both of which are sub-optimal: keep Teicholz on the panel and undermine your other panelists and possibly your organization’s reputation or uninvite her and give her perhaps the greatest marketing gimmick she has had all year. It would seem CFA chose the latter. She can now claim that the self-proclaimed nutrition elite are attempting to silence discussion and debate, and she has trumpeted this quite loudly at least on Twitter. It plays right into her narrative.

Vigorous Debate

Here we get to the meat and potatoes of this post. I don’t think Teicholz has any real desire for a substantive debate on the science, she just wants to appear that she does because it sounds good to the people who buy her books and the (misinformed) billionaires that fund her fledgling Nutrition Coalition advocacy group.

I know she cares not for any kind of scientific debate because she had agreed to come on my podcast to discuss her book in a more skeptical light then blew it up. She agreed, but then mere hours before we were to meet she told me that she would not do the interview, but that if I scrubbed my posts on her she would “feel more enthusiastic” about meeting.

teichols emails

For some context I had invited her on the podcast multiple times and was ignored each time.3 That is until Marion Nestle linked to my blog and Techolz admonished her for doing so in the comments, along with some contradicting opinions regarding my blog: it was the only serious critique of her work she had seen and even thanked me for my “good work” yet it was apparently sloppy and riddled with errors.4 I again invited her to discuss these alleged errors on my podcast to which she surprisingly agreed!5

So we emailed back and forth to nail down a time that worked for both of us. Then at literally 2:25am, a few hours before we were supposed to get together, she emails me claiming that she was too busy to meet. (She also asked me if I was going to some sort of BBQ dinner which is what that is about.) Then I said what I did above.

I think the message is pretty clear. She will not engage with any skeptics, despite the following statement in her book6:

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

Also around this time I heard more than just a rumor from an acquaintance at NYU that Teicholz was attempting to hire a NYU grad student to research the citations in my critique of her book. The fact that she attempted this speaks volumes. Shouldn’t she posses the studies she herself cited, and shouldn’t she be able to understand and interpret them?

Interestingly this attempt to hire someone to presumably research my critique was immediately after she agreed to come on my podcast: Feb 24, 2015. I am assuming since no rebuttal to my critique has appeared from Teicholz, no grad student took her up on her temporary employment offer. Either that or perhaps someone did but found no errors in my work.

Bottom Line

It’s pretty evident that Teicholz is not interested in debating the merits of “her” ideas. She wants no part in a vigorous scientific discussion. She does not want to engage with anyone skeptical of the ideas she writes about.

Still I am open to the possibility that people can change. If she at any point is interested in having that conversation we should have had over a year ago in Austin I welcome it. Despite the fact that she gave me the shaft that day, Nina can consider this an open invitation to have that great debate.

Epilogue

I read a piece in the New Yorker today by Atul Gawande.7 It was about science deniers. A paragraph caught my eye and made me think of the low-carb movement:

Science’s defenders have identified five hallmark moves of pseudoscientists. They argue that the scientific consensus emerges from a conspiracy to suppress dissenting views. They produce fake experts, who have views contrary to established knowledge but do not actually have a credible scientific track record. They cherry-pick the data and papers that challenge the dominant view as a means of discrediting an entire field. They deploy false analogies and other logical fallacies. And they set impossible expectations of research: when scientists produce one level of certainty, the pseudoscientists insist they achieve another.

If anyone follows the diet wars I think you can see where I am going here. I’m not about to write a treatise on this, but a few bullet points are okay, right?

They argue that the scientific consensus emerges from a conspiracy to suppress dissenting views.

  • This is literally what The Big Fat Surprise and Good Calories, Bad Calories are about. Most all other low-carb nonsense being derived from Good Calories, Bad Calories, anyway.

They produce fake experts, who have views contrary to established knowledge but do not actually have a credible scientific track record.

  • Just look at the parade of clowns that Tom Naughton in Fat Head claims are experts. What other standard-bearers do we have for the current low-carb movement? Jimmy Moore?  Zoe Harcombe? Are you kidding me with these people? Gary Taubes and Nina Teicholz have been so thoroughly discredited it’s amazing they can still pretend to be experts. Oh yeah, money. Volek and Phinney are probably the best they have. Or Kevin Hall. No wait he is a traitor because he might be publishing results not favorable to NuSI.

They cherry-pick the data and papers that challenge the dominant view as a means of discrediting an entire field.

http://carbsanity.blogspot.com/2014/06/nina-teiholz-shaister-part-i-diets-of.html

http://carbsanity.blogspot.com/2014/06/nina-teiholz-shaister-part-ii.html

http://carbsanity.blogspot.com/2014/06/nina-teiholz-shaister-part-iii-well.html

http://carbsanity.blogspot.com/2014/06/nina-teiholz-shaister-part-iv-random.html

http://carbsanity.blogspot.com/2014/06/plagerizing-plagiarism-and-plagiarists.html

http://carbsanity.blogspot.com/2014/05/no-big-surprise.html

http://carbsanity.blogspot.com/2015/02/nina-teicholz-distorts-facts-again.html

http://carbsanity.blogspot.com/2015/02/nina-teicholz-corrects-big-fat-surprise.html

http://carbsanity.blogspot.com/2015/03/nina-teicholz-distorts-fatty-acid.html

Slipp Digby discusses Teicholz’s biases

http://slippdigby.wordpress.com/2014/10/15/nina-teicholz-health-ministers-and-the-swedish-government-low-carb-diet-guidelines/

http://slippdigby.wordpress.com/2015/03/30/eat-like-an-ancient-egyptian/

And others:

http://velvetgloveironfist.blogspot.com/2015/03/nina-teicholzs-big-fat-surprise.html

http://www.huffingtonpost.com/david-katz-md/diet-and-nutrition_b_5266165.html

http://www.huffingtonpost.com/david-katz-md/were-fat-and-sick-and-the-broccoli-did-it_b_6744724.html

http://www.huffingtonpost.com/michael-f-jacobson/distorting-nutrition-facts-to-generate-buzz_b_6776024.html

http://www.foodpolitics.com/2015/02/dietary-guidelines-shouldnt-be-this-controversial/

(I might be leaving a few out…)

They deploy false analogies and other logical fallacies.

  • Like it’s going out of style. The ad hominem, the straw man, tu quoque, petitio principii, special pleading, and the good ol’ anecdotal evidence are also popular.

And they set impossible expectations of research: when scientists produce one level of certainty, the pseudoscientists insist they achieve another.

  • Indeed. Epidemiological studies are used to make the case for low carb diets, yet when they are used in favor of a more plant-based diet then all of a sudden epidemiology is not a real science, and clinical trials are the only acceptable evidence. When clinical trials are marshaled in favor of diets that are not low-carb then there is always a reason to dismiss them: The population is too small, the duration was too short, they didn’t measure the right things, the diets weren’t controlled well enough, some people dropped out, the author of the study spoke at a vegetarian conference, or one study doesn’t prove anything. I am not making any of these up, by the way. They are real excuses.

cloud

1. Not that panels like this have any real effect on policy making. It’s not like the Consumer Federation of America is an arm of the government or anything. It appears to be a private non-profit advocacy group. And speaking as someone who has attended a number of conferences like these it’s just a lot of navel-gazing, and I think an excuse for some people to get away from their jobs for a week and stay in a Hilton on their employer’s dime. Networking for the purposes of advancing one’s career is probably the the only real outcome of conferences like these. But that’s just my opinion, I could be a cynical old coot.

2. I know I would be upset if I had spent my entire career involved with nutrition policy and I get invited to speak on a panel with someone who clearly has no knowledge or education in nutrition or policy (other than cranking out a poorly researched book). I mean, imagine a different panel discussing something like foreign policy and you have a four-star general, a professor of political science, a former ambassador… and Alex Jones. Just being on the panel lends credibility to crackpot ideas.

3. If you click that reddit link to Teicholz’s AMA you’ll find links by /u/melissaf1015 that I actually think is really Teicholz herself trying her hand at astroturfing.

4. Interestingly, every time Teicholz mentions me in a comment section of a site or elsewhere she makes a number of errors about yours truly that are completely made-up, while the actual facts about me are easily found on my About page.

5. Not that it really matters, but I was actually both very excited and very nervous about the prospect. I wanted it to be a really well-done episode, so I spent a great deal of time researching and even bought some fancy new recording equipment. This had all the makings of a great podcast episode.

6. Gary Taubes unsurprisingly makes the exact same statement in Good Calories, Bad Calories.

7. As it happens, Atul Gawande unfortunately kind of, sort of (but not really) endorses Teicholz in a tweet. Shame he wasn’t a bit more discerning before tweeting her out.

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

 

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.

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.

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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

cover

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.

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Adele Hite, Nina Teicholz, and Logical Fallacies

Introduction

Some weeks ago I got a call from a reporter.1 This reporter had just attended an event called “Politics of the Plate: The Evolution of American Food Policy” presented by Real Clear Politics that included Nina Teicholz and Adele Hite. You can view the event below, but the gist of the event was that the US government’s nutrition policy is bad, it has been based on bad science for years, it advocates a low-fat/high-carbohydrate diet, is anti-fat, and has contributed to the rise in obesity and many chronic diseases we see today.

According to this reporter, the event was compelling enough that he or she wanted to write a piece on it and kind of examine the merits of our nutrition recommendations.2 I was told the piece would be published about a week after our conversation, but as of this writing many weeks later it has not come out. Perhaps I was successful in convincing the reporter that Teicholz and Hite did not know what they were talking about. Or maybe the senior editor of the news outlet didn’t feel it was something that needed to be published. I don’t know. But what I’d like to do here is give something of an expanded version of what I told the reporter.

[Link to the video on Real Clear Politics]

False Dichotomies

I’m going to get into the merits of the arguments in a moment, but before I do I would like to spend several paragraphs on one logical fallacy I have encountered often when I engage the work of popular low-carb authors and increasingly when the more zealous low-carb adherents engage with me: the false dichotomy.

One employs the false dichotomy when there is little evidence for their position, but there is another position for which there is even less evidence (or there is good evidence against the other position). If the charlatan can convince their audience that these are the only two positions available then their job becomes much easier. All they need to do is poke some holes in the opposing position, and then the charlatan’s position is accepted by default – the charlatan doesn’t even need to provide positive evidence for their own position. In other words, reduce the spectrum of positions, of which there may be countless, to only two, and make sure the opposing position is a rather weak one.

Okay, that last paragraph was perhaps too abstract. Let’s talk about something more concrete. What I see very, very often among proponents of low-carb diets is that there are essentially only two diets out there to follow: the low-fat/high-carbohydrate diet or the high-fat/low-carbohydrate diet. When low-carbers are asked why one should follow a low-carbohydrate diet, often they begin by telling you that a low-fat diet is bad. Nina Teicholz does this in her recent book The Big Fat Surprise: Why Butter, Meat, and Cheese Belong in a Healthy Diet. You might think that the book is a collection of evidence for butter, meat, and cheese being healthy, but it is not. The bulk of the book is dedicated to pointing out how and why a low-fat diet might not be healthy. Very little ink in the book is actually dedicated to making the case for butter, meat, and cheese.

This is actually a pretty smart move on her part, since not a lot of evidence exists that butter, meat, and cheese are healthy. So instead of trying to show legitimate evidence in favor of her position, she reduces the spectrum of diets in the world to essentially low-fat or low-carb and pokes holes in the low-fat diet, hoping her readers accept her low-carb position by default.3

This logical fallacy is also used by the young-earth creationist community. If you follow that issue at all you will notice that the cornerstone of the creationists’ argument is not “Let me present all the scientific evidence suggesting that our deity created life and the universe…” But rather their argument is “Here are some possible inconsistencies with evolution by natural selection…” Now of course creationists can try to poke all the holes they want in evolution, but doing this does not make the scientific case for why young-earth creationism is true. They still have all their work ahead of them.

FalseDilemma

I feel like I need a picture to break up the wall of text.

 

Teicholz also employs this tactic when trying to create a bizarre crusade against the USDA. For decades official dietary guidelines have consistently recommended a diet that is 1/3rd fat. A diet that includes ~33% calories from fat may not be considered a high-fat diet, but nobody in their right mind would call this a low-fat diet. No one, that is, except for hyper-dogmatic low-carb proponents like Teicholz. You see, since there are only two diets in existence, and the USDA does not recommend a high-fat/low-carbohydrate diet, it must therefore be recommending a low-fat diet.

Although this kind of argumentation is clearly based on flawed reasoning it seems to be quite effective at both convincing the less-skeptical among the audience and at rallying the troops for the ridiculous anti-government crusade du jour. I have criticized false and misleading statements by low-carbohydrate proponents like Teicholz and Taubes on this website, and I have also made evidence-based criticisms other places online such as Reddit. I am always accused of both following and promoting a low-fat diet.4 It never fails. Nevermind that there is no evidence of this promotion because I have never advocated such a diet; if I point out dishonesty by low-carbers then I must follow a low-fat diet. There is no alternative.

For those too busy to read the long-winded explanation above, I will sum it up as I did in an earlier post: Many LCHF proponents reduce the multiplicity of diets that exist in the world to a low-fat or high-fat dyad. This is overly-simplistic and creates a false dichotomy, which only benefits people interested in deception.

Adele Hite Wants to Change the Dietary Guidelines

If you watched the above video, you’ll notice that Adele Hite is not a big fan of the dietary guidelines. She blames the guidelines for the rise in obesity over the last several years as well as a major contributor to chronic diseases such as heart disease, diabetes, and cancer. She has written a manifesto on her website, complete with a letter-writing campaign where you can print a pre-written letter by Hite and send it to the USDA.

In Hite’s blog post she says the letter “is not a call for low-carb, high-fat dietary recommendations,” but it kind of is. She criticizes what she says are plant-based recommendations, and lists a series of “specific recommendations” that she takes issue with because they are apparently anti-fat and too focused on carbohydrates. By the way, I’m pretty sure these “specific recommendations” are straw men (another logical fallacy!), because I can’t find them anywhere in the full 95-page document of the 2010 Dietary Guidelines for Americans. At least not in the specific wording she uses.

As an aside, I doubt very highly that the Dietary Guidelines for Americans have any meaningful influence over our food consumption. I don’t have any evidence to back this up, but neither do I think Hite or Teicholz have any evidence to the contrary. I bet you dollars to donuts that you could do a man-on-the-street style interview and grab 100 random people and ask them questions about the dietary guidelines like

  • According to the Dietary Guideline for Americans, how much folic acid should a woman who wishes to become pregnant consume daily? Answer in micrograms, please.
  • According to the Dietary Guideline for Americans, persons aged 51 years or older should consume no more than how many milligrams of sodium per day?
  • According to the Dietary Guideline for Americans, pregnant or breast-feeding women should consume seafood ranging from ______ oz to ______ oz per week?

…and NONE of them would know the answers. I bet you could even repeat the experiment with actual medical doctors and you wouldn’t do much better. Besides most of the guidelines are so freaking vanilla that I have a hard time understanding why anyone would be against them? Who could possibly be against recommending a variety of vegetables? Who could be against recommending physical activity? Only people with personality disorders that need attention.

In the video Teicholz says that the guidelines are aggressively influential and she makes ridiculous claims like the NSF and the NIH will only fund research that conforms to the guidelines, ALL nutritionists must conform to the guidelines, ALL doctors must use the guidelines to educate their patients, ALL the Health and Human Services programs are required to abide by the guidelines, school lunch programs must conform to the guidelines… methinks there is a teensy bit of exaggeration going on. I could explain why these claims are ridiculous, but this post is long enough as it is.

 

Apparently this plate is the worst thing to happen to public health since the cigarette.

Apparently this plate is the worst thing to happen to public health since cigarettes.

In any case, Hite makes some claims in her manifesto that have actual citations. If you are a follower of the blog you know how much I love citations. Let’s dive in!

The DGA have contributed to the rapid rise of chronic disease in America.

In 1977, dietary recommendations (called Dietary Goals) created by George McGovern’s Senate Select Committee advised that, in order to reduce risk of chronic disease, Americans should decrease their intake of saturated fat and cholesterol from animal products and increase their consumption of grains, cereal products, and vegetable oils. These Goals were institutionalized as the DGA in 1980, and all DGA since then have asserted this same guidance. During this time period, the prevalence of heart failure and stroke has increased dramatically. Rates of new cases of all cancers have risen. Most notably, rates of diabetes have tripled. In addition, although body weight is not itself a measure of health, rates of overweight and obesity have increased dramatically. In all cases, the health divide between black and white Americans has persisted or worsened.

obesity-trends-cdc-2009-chartbook

From the video

 

Right off the bat, before we even check any sources, Hite is shown to be a hypocrite. How? I’ll tell you. Hite discusses supposed increases in chronic disease since the DGA have been introduced, arguing that “the DGA have contributed to the rapid rise of chronic disease in America.” She also makes this same case in the video with the fancy graph she had made at Kinkos. To break this down a bit: Event happened (dietary guidelines); then some other things happened (increased disease, allegedly); therefore the event caused the things.5 In case you can’t tell this is the post hoc ergo propter hoc fallacy. Some might know it better as “correlation does not equal causation.” Its use is often criticized by people who know the difference between spurious correlations and causes. People like Adele Hite.

Now let’s get into the claims and the evidence. Since the DGAs were introduced…

Claim: The prevalence of heart failure and stroke has increased dramatically.

Facts: Hite cites the Morbidity and Mortality: 2007 Chart Book on Cardiovascular, Lung, and Blood Diseases. Don’t know why she doesn’t cite the more up-to-date 2012 chart book, but it’s the one I’m going to use. According to the report, heart failure has pretty much stayed constant since the 1980s, with a slight increase for blacks over the years. She is right about stroke, though, at least partly. Prevalence of stroke rose quite a bit up until 2008 when it started declining. But there’s a lot of data in the chartbook that was not mentioned. Why? Because it doesn’t fit nicely into the story Hite is trying to craft. For example:

  • The death rates for cardiovascular disease have dropped precipitously since 1980. [chart]
  • The death rates for stroke have fallen since 1980. [chart]
  • Age-adjusted death rates for coronary heart disease have plunged. [chart] This remains true even when stratifying by race. [chart] [chart]
  • Hospital case-fatality rates for acute myocardial infarction have plummeted. [chart]
  • Hospital case-fatality rates for heart failure have dropped like crazy. [chart]
  • Hospital case-fatality rates for stroke have sunk dramatically. [chart]
  • Age-adjusted death rates for stroke have cratered. [chart] Again, this remains true when stratifying by race. [chart] [chart]

Now if Hite wants to blame the DGAs for an increase in stroke prevalence (which she has no business doing in the first place, considering the evidence) then she must also say that the above improvements are also due to the DGAs.

Claim: Rates of new cases of all cancers have risen.

Facts: Her evidence for this is a decade-old publication on cancer statistics.6 The way Hite words that claim you might think each subgroup of cancer (lung, brain, colorectal, ovarian, etc.) have all risen, but this is not the case. Incidence of most cancers has dropped, but if you average all the cancer incidence over the past several years they have risen very slightly as a whole. It seems that the substantial increase in lung cancers skews the average upward. Although, if you look at cancer death rates they have all decreased slightly. Technically correct, but potentially misleading.

Claim: Rates of diabetes have tripled.

Facts: According to the cited source, the total number of persons with diabetes has tripled – not the rate.7 Technically incorrect, but I’ll let this one slide.

Claim: Rates of overweight and obesity have increased dramatically.

Facts: Absolutely true.8 Well, at least obesity rates have increased dramatically. Overweight actually has remained pretty stable through the years.

Claim: All available data show Americans have shifted their diets in the direction of the recommendations.

Facts: This is a juicy one that needs unpacking. This is kinda something that has been batted about on all sides of the nutrition spectrum for several years. Hite cites another old statistics report based on self-reported dietary intakes from 1971-2000.9 Here’s the low-down on that and similar reports: Since 1971 (and even earlier, I’m sure) 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.10 Thing is we have increased our CHO intake more than we have increased our fat and protein intake, which means that if you look at the relative changes in macronutrient intake we will have narrowly increased our percentage of calories from carbohydrate, and narrowly decreased our percentage of calories from fat and protein. Then what happens is people like Teicholz, Hite, and anyone else with a moneyed agenda claim that the DGAs forced Americans on a low-fat diet which has caused a rise in obesity, diabetes, and all that which is extraordinarily misleading because TOTAL FAT ACTUALLY INCREASED & TOTAL CALORIES INCREASED. This highly relevant context is left out to hornswoggle an unskeptical audience. Don’t be deceived.

Claim: Current choline intakes are far below adequate levels, and choline deficiency is thought to contribute to liver disease, atherosclerosis and neurological disorders. Eggs and meat, two foods restricted by current DGA recommendations, are important sources of choline. Guidance that limits their consumption thus restricts intake of adequate choline.

Facts: Almost entirely false. The source for this claim is a review article on choline.11 An article funded by the American Egg Board if you were curious. The article kinda says that intakes among women are suboptimal. According to the paper the Nurses Health cohort has intakes of about 411 mg/day which is not quite the recommended 450 mg/day. But the eggs and meat statement is preposterous on two levels. One, the current DGAs don’t restrict eggs or meat. In fact they explicitly recommend an increase in egg consumption and lean meat consumption. Secondly, choline is widely available in plant foods as well. In fact the article mentions soy flour as having one of the highest concentrations of choline, along with quinoa and wheat germ.

Claim: In young children, the reduced fat diet recommend by the DGA has also been linked to lower intakes of a number of important essential nutrients, including calcium, zinc, and iron.

Facts: Again, the DGAs do not recommend a reduced fat diet, unless your idea of “reduced fat” is simply “not extremely high in fat.” Further, the study she cites for this claim actually makes the case that lower fat diets are actually healthy for children! From the conclusion: “Lower fat intakes during puberty are nutritionally adequate for growth and for maintenance of normal levels of nutritional biochemical measures, and are associated with beneficial effects on blood folate and hemoglobin.”

Claim: DGA guidance rejects foods that are part of the cultural heritage of many Americans and indicates that traditional foods long considered to be important to a nourishing diet should be modified, restricted, or eliminated altogether: ghee (clarified butter) for Indian Americans; chorizo and eggs for Latino Americans; greens with fatback for Southern and African Americans; liver pâtés for Jewish and Eastern European Americans.

Facts: Nope. At least not explicitly.

Claim: Recommendations to prevent chronic disease that focus solely on plant-based diets is a blatant misuse of public health authority that has stymied efforts of researchers, academics, healthcare professionals, and insurance companies to pursue other dietary approaches adapted to specific individuals and diverse populations, specifically, the treatment of diabetes with reduced-carbohydrate diets that do not restrict saturated fat. In contradiction of federal law, the DGA have had the effect of limiting the scope of medical nutrition research sponsored by the federal government to protocols in line with DGA guidance.

Facts: Nope. At least Hite provides no evidence for these absurd claims. Plus the DGAs even explicitly say that “plant-based sources and/or animal-based sources can be incorporated into a healthy eating pattern.”

Claim: The science behind the current DGA recommendations is untested and inconsistent. Scientific disagreements over the weakness of the evidence used to create the 1977 Dietary Goals have never been settled. Recent published accounts have raised questions about whether the scientific process has been undermined by politics, bias, institutional inertia, and the influence of interested industries.

Facts: For fuck’s sake. Here Hite cites Gary Taubes’s Good Calories, Bad Calories and Teicholz’s The Big Fat Surprise. How many times must we revisit the lies??

Claim: Two recent meta-analyses concluded there is no strong scientific support for dietary recommendations that restrict saturated fat.

Facts: Actually the only one of the two cited studies is a meta-analysis; the other is a review article.12,13 The meta-analysis has been widely misinterpreted to suggest that saturated fatty acids are harmless, but that’s not the case. As we all know some saturated fatty acids are basically benign, like those found in coconut and other tropical oils. Typically the short and medium chain fatty acids. But the data from that paper show that the longer chain fatty acids definitely increase the risk of heart disease, especially stearic and palmitic acids which are the most abundant in animal fats. http://i.imgur.com/H72g1eP.png The only one that appears to decrease risk is margaric acid, a synthetic fat found in margarine. Even when you pool all the saturated fatty acids the net effect is an increased risk of heart disease, although a modest one. All the polyunsaturates, however, were shown to decrease risk of heart disease: http://i.imgur.com/e7lJ6PL.png http://i.imgur.com/YfC1qMx.png

The review article also gets misinterpreted, willfully it seems. It states that replacing saturated fatty acids in the diet with polyunsaturated fats has been conclusively shown to reduce the risks of CVD. It also says replacing saturated fats with carbohydrate offers no real benefit. However, low-carbers like Hite and Teicholz take that last result and make the leap to “saturated fats are good” or “restricting saturated fat is bad.” It is truly deceitful.

Claim: Federal dietary guidance now goes far beyond nutrition information. It tells Americans how much they should weigh and how to lose weight, even recommending that each American write down everything that is eaten on a daily basis.

My sarcastic response: How dare they?? This is clearly an attack. The horror… The horror…

Claim: This focus on obesity and weight loss has contributed to extensive and unrecognized “collateral damage”: fat-shaming, eating disorders, discrimination, and poor health from restrictive food habits.

My response: The government is responsible for fat-shaming now? The USDA caused eating disorders and discrimination because they recommended incorporating more fruits and vegetables? I can’t imagine that demonizing carbohydrates and vegetable oils would cause any kind of eating disorders, though.

At the end of the letter Hite ends with such vague and nonspecific recommendations that no matter what the committee actually decides you would have real difficulty making the case that Hite’s precepts were not followed. Seriously… have the recommendations apply to all Americans; expand nutrition research; include traditionally nourishing foods; are directed towards health and well being; are clear, concise, and useful… I mean, unless the committee recommends a diet of used tires and uranium and does so in an 800 page report written in pig latin, I imagine Hite will have difficulty proving that the USDA did not do just as she instructed.

Conclusion

There may indeed be a case for modifying the current dietary guidelines, but Hite and Teicholz make a bad case based on logical fallacies and the willful misinterpretation of nutrition science. Let’s hope that the people tasked with actually creating these recommendations rely on evidence instead of nonsense.

 cloud

1. A reporter, by the way, that writes for a legitimate news publication. It wasn’t like Bubba’s Food Blog or anything.

2. I’m keeping the identity of the reporter vague for a couple reasons. First, on the off-chance that he or she still is planning on publishing something I don’t want to scoop them. Secondly, I know from firsthand experience and secondhand knowledge that the more zealous of the low-carb bunch can be rather cruel, and I wouldn’t want the reporter to experience any of that just for speaking to me.

3. She also hopes her readers will assume that a low carbohydrate diet necessarily means a diet high in butter, meat, and cheese, even though the few studies she cites in favor of a low carb diet often use vegetarian sources of protein and plant-based fats in the low-carbohydrate groups.

4. Amusingly, very often I also get accused of being brainwashed by the government and/or being a paid shill for Big Vegetable. I wish I was kidding.

5. In case you want to argue semantics with me and say some crap like ‘she said CONTRIBUTED not caused,’ then I say that’s a distinction without much of a difference. Webster defines contribute as ‘to help to cause something to happen.’

6. Jemal, A. et al. Cancer Statistics, 2005. CA. Cancer J. Clin. 55, 10–30 (2005).

7. CDC – Number of Persons – Diagnosed Diabetes – Data & Trends – Diabetes DDT. at <http://www.cdc.gov/diabetes/statistics/prev/national/figpersons.htm>

8. Products – Health E Stats – Overweight, Obesity, and Extreme Obesity Among Adults 2007-2008. at <http://www.cdc.gov/nchs/data/hestat/obesity_adult_07_08/obesity_adult_07_08.htm>

9. Wright, J., Kennedy-Stephenson, J., Wang, C., McDowell, M. & Johnson, C. Trends in Intake of Energy and Macronutrients — United States, 1971–2000. (National Center for Health Statistics, CDC, 2004). at <http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm>

10. Ford, E. S. & Dietz, W. H. Trends in energy intake among adults in the United States: findings from NHANES. Am. J. Clin. Nutr. 97, 848–853 (2013).

11. Zeisel, S. H. & da Costa, K.-A. Choline: An Essential Nutrient for Public Health. Nutr. Rev. 67, 615–623 (2009).

12. Siri-Tarino, P. W., Sun, Q., Hu, F. B. & Krauss, R. M. Saturated fat, carbohydrate, and cardiovascular disease. Am. J. Clin. Nutr. 91, 502–509 (2010).

13. Chowdhury, R. et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann. Intern. Med. 160, 398–406 (2014).

Good Calories, Bad Calories: A Critical Review; Chapter 12 – Sugar

Introduction

This post is another in a long line of self-abusive posts in which I spend way too much time combing Gary Taubes’s Good Calories, Bad Calories (GCBC), and usually end up disappointed at the publishing industry and feel depressed for the masses of people that actually trusted Taubes’s “research.”

This chapter is not as bad as many of the others, though. It happens to be about sugar, and the fact is that you don’t need to heavily distort scientific publications to indict sugar. Taubes still manages it, however. If you’d like to read other chapter reviews of GCBC by yours truly, visit my Book Reviews page.

As you read this post you might leave with the impression that I advocate sugar consumption. Nothing could be further from the truth: it is clearly an ingredient that Americans (and perhaps any country with a Pepsi presence) consume far too much. It would only benefit your health to reduce your consumption of it. What I do advocate is intellectual honesty which is why I come to sugar’s defense when journalists like Taubes make up or distort evidence against it.

Not the Introduction

On page 200 Taubes states 

The more fructose in the diet, the higher the subsequent triglyceride levels in the blood. For this reason, fructose is referred to as the most lipogenic carbohydrate.*

*Credit for this observation dates to 1916, to Harold Higgins of the Nutrition Laboratory of the Carnegie Institution.

I’m not sure that Taubes can really state this. The Higgins paper he cites does not really measure lipogenesis. It measures respiratory quotient. In the paper Higgins does say that one might say that levulose (fructose) and galactose, judging by the RQ, could preferentially turn into fat.1 However, Higgins actually observed the sugars being burned:

A study of figure 1 shows clearly that levulose [fructose], sucrose, probably lactose and possibly maltose give indications by the respiratory quotients of being metabolized, and in all probability burned by the fourth to the seventh minute after ingestion “on an empty stomach,” which is quite as rapidly as alcohol in the same subject and much quicker than alcohol in four other subjects.

* * *

On page 200, Taubes states

Although sugar also seemed to raise cholesterol levels, particularly LDL, as would be expected for any nutrient that increased triglyceride synthesis in the liver. In 1992, John Bantle reported that LDL cholesterol in diabetic patients was elevated more than 10 percent on a high-fructose diet after a month, which is comparable to what can be achieved by saturated fats.

For this claim he cites two references. One is a study co-authored by Bantle (although he is not the lead author, Joyce Swanson is).2 That study does show that at a couple of points in the study LDL was elevated compared to the controls, as was triglycerides at one point and total cholesterol at one point. (See pic below) However, contrary to Taubes’s claim this study used normal, healthy patients – not diabetics.

Metabolic effects of dietary fructose in healthy subjects

Dietary fructose effects on lipoprotein metabolism and risk for coronary artery disease

The other citation for his claim that fructose elevates LDL is a review article that makes more of a point to state that the evidence on this issue is quite conflicting.3 (see pic above) From the author’s conclusion:

Perhaps the most general conclusion that could be drawn from this review of the effects of dietary fructose on lipoprotein metabolism is how little we actually know.

Does Taubes even read the studies he cites? And shockingly Taubes now admits that sat fat can raise LDL cholesterol levels!

Also from the conclusion:

[I]t would seem unlikely, based on available data, that dietary fructose at quantities obtainable from natural sources provided in a well-balanced diet would result in any deleterious metabolic effects.

* * *

On page 201 Taubes claims:

[F]ructose elevates blood pressure more than an equivalent amount of glucose does, a phenomenon called fructose-induced hypertension.

What you might think after reading this statement is that if you consume fructose this might lead to some degree of hypertension, but unless you’re a rat you would be wrong. Taubes cites two publications for this claim: one by Hodges and Rebello and one by Hwang et al.4,5 Both mention that fructose consumption leads to hypertension in rats. In fact the title of the Hwang paper is “Fructose-Induced Insulin Resistance and Hypertension in Rats.” However, you will find the opposite is true in humans. The other paper makes it clear that fructose has no effect on blood pressure in humans. From the text: “Fructose ingestion produced no significant changes in blood pressure […]” The authors also mention that lactose and galactose also showed no increase in blood pressure. Although to be fair to Taubes the study does mention that both sucrose and glucose increased blood pressure in humans so he’s not way off base here. Nevertheless, he seems to give all the studies he cites a mere cursory glance before writing about their results and very often getting them wrong.

* * *

Page 202, Taubes claims: “The American Journal of Clinical Nutrition dedicated an entire issue to the deleterious effects of dietary fructose.” Not exactly true. The AJCN did do a supplement of one issue that focused on fructose, and it wasn’t focused on the deleterious effects, either. Some of the reports had nothing to do with fructose and health. Just look at some titles like “Manufacturing, composition, and applications of fructose” and “Worldwide production of high-fructose syrup and crystalline fructose.” Other reports indicated neutral to favorable data regarding fructose and health. For example, one report on diabetes concluded6:

In summary, the side effects of fructose supplementation do not seem at this time to be of particular concern when fructose is ingested in modest amounts.

Another report on the public health implication of fructose states7:

On the basis of currently available information, as reviewed in this monograph, fructose is a valuable, traditional source of food energy, and there is no basis for recommending increases or decreases in its use in the general food supply on in special dietary use products.

Another report says that fructose aids in mineral absorption.8 Another says that fructose may increase physical performance.9 These are all from the same supplement that Taubes mentions. I know this because Taubes even cites yet another report on fructose and thermogenesis that concludes the following10:

The greater thermic effect of fructose, its nondependence on insulin for its metabolism, and its greater sweetening potency compared with glucose are factors that may speak in favor of fructose as a valuable carbohydrate for the dietary management of obesity and NIDDM [non insulin-dependent diabetes mellitus].

But of course there was no way in hell Taubes was going to mention this part of the conclusion. Instead he mentions the part that says more research is needed – a sentiment you can find at the end of literally all nutrition studies and likely any scientific study period.

* * *

Page 203:

In 2002, the Institute of Medicine of the National Academies of Science released its two-volume report on Dietary Reference Intakes (subtitled Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids), and spent twenty pages discussing the possible adverse effects of sucrose and high-fructose corn syrup. It then concluded that there was still “insufficient evidence” to set up an upper limit for sugar consumption in the healthy diet.

Despite Taubes’s attempt to make this seem like a huge scandal because of a wildly incompetent Institute of Medicine, this is pretty standard stuff. No tolerable upper limits (UL) were set for any macronutrient. ULs are set for things like vitamin A and iron; micronutrients at which there is a point where they start to become acutely toxic.

Refs

1. Higgins, H. L. The Rapidity with Which Alcohol and Some Sugars May Serve as Nutriment. Am. J. Physiol. 41, 258–265 (1916).

2. Swanson, J. E., Laine, D. C., Thomas, W. & Bantle, J. P. Metabolic effects of dietary fructose in healthy subjects. Am. J. Clin. Nutr. 55, 851–856 (1992).

3. Hollenbeck, C. B. Dietary fructose effects on lipoprotein metabolism and risk for coronary artery disease. Am. J. Clin. Nutr. 58, 800S–809S (1993).

4. Hodges, R. E. & Rebello, T. Carbohydrates and blood pressure. Ann. Intern. Med. 98, 838–841 (1983).

5. Hwang, I. S., Ho, H., Hoffman, B. B. & Reaven, G. M. Fructose-induced insulin resistance and hypertension in rats. Hypertension 10, 512–516 (1987).

6. Gerrits, P. M. & Tsalikian, E. Diabetes and fructose metabolism. Am. J. Clin. Nutr. 58, 796S–799S (1993).

7. Glinsmann, W. H. & Bowman, B. A. The public health significance of dietary fructose. Am. J. Clin. Nutr. 58, 820S–823S (1993).

8. O’Dell, B. L. Fructose and mineral metabolism. Am. J. Clin. Nutr. 58, 771S–778S (1993).

9. Craig, B. W. The influence of fructose feeding on physical performance. Am. J. Clin. Nutr. 58, 815S–819S (1993).

10. Tappy, L. & Jéquier, E. Fructose and dietary thermogenesis. Am. J. Clin. Nutr. 58, 766S–770S (1993).

The Metabolism of Plant Lignans via Human Intestinal Microbiota

Thinkingbact1 GutBacteriaFactory1

Introduction

Hey kiddos! I’m working on a series of posts on gut bacteria and I thought I’d start off with a post about the gut bacterial metabolism of plant lignans and its role in health and disease, primarily because it is something I know a great deal about. Or should I say “it is something about which I know a great deal”? Probably the latter. Proper use of prepositional phrases confounds me sometimes. Wait, this isn’t a blog about grammar; it’s about nutrition! Moving on…

What are lignans?

Lignans are polyphenolic compounds found in many plants that play a role in plant defense. It’s really quite extraordinary what lignans do for the plant. They have quite an array of defensive properties, protecting the plant from harmful pests and pathogens.1 For example, lignans have been shown to have insecticidal properties comparable to that of pyrethrins.2 If you have ever used that to kill aphids in your home garden then you know how powerful that is. They also have other properties that protect plants such as antifungal properties and somewhat paradoxically antimicrobial properties.3,4 I say “paradoxically” because I am about to discuss the fact that some species of bacteria that can live in the gut go nuts for these lignans.

Lignans are not to be confused with their homophone lignins, which are kinda similar in that they are also found in plants and are chemically related. However, lignins are much larger polymers that intercalate with cellulose and hemicellulose within the cell wall to provide structure and support. Interestingly though, since there are lignan structures within the larger lignin molecule, gut bacteria are able to metabolize lignins to some degree and “release” lignans for further metabolism.5,6

lignins

lignin_lignan3

What Foods are Lignans Found In?

Or maybe I should say “In What Foods are Lignans Found?” Damn those prepositional phrases! So they are found in a variety of foods. You can find a fair amount in cereal grains (corn, oats, wheat, rye), cruciferous vegetables, fruits (like apricots, oranges, kiwi, strawberries), and you can even find small amounts in beverages like coffee, tea, beer, and wine.7–31 But by far the largest concentration of lignans can be found in seeds, particularly flaxseeds. Seriously. A handful of flaxseeds contain about ten thousand times more lignans than an equivalent amount of broccoli, and about a hundred thousand times the lignans of, say, an orange.

flax-seeds

So Where do Gut Bacteria Come In?

Or should I say “In Where do Gut –“ ah, forget it. So it turns out that plant lignans can be converted to what are sometimes called mammalian lignans or enterolignans by bacteria found in the gut.8,32–68 There are several steps involved when converting a plant lignan to an enterolignan, however, and as far as we know there is not one bacterium that can catalyze all the reactions. Rather, a consortium of bacteria is needed to complete the conversion to the enterolignans enterodiol and/or enterolactone. These more physiologically active enterolignans then get absorbed via colonic epithelial cells.69

But the thing is that not everyone possesses the bacterial community necessary to complete this transformation. According to research by Possemiers and others maybe about 2/3rds of the population has the appropriate species in their gut to convert lignans to enterodiol and far fewer are able to convert lignans to enterolactone.70

Metabolism of isoflavones, lignans and prenylflavonoids by intestinal bacteria producer phenotyping and relation with intestinal community.

 

diagram w bacteria

Here’s a little diagram I made of common food lignans and the bacteria that convert them. Or at least some of them.

I made a diagram of sesaminol if you’d like to see that, too.

Why Should I Care About Lignans Anyway?

There is quite a bit of evidence that lignans have a variety of beneficial health effects.71–90 Let’s look at all these bennies in slightly more detail.

In Vitro Evidence

  • Lignans inhibit the proliferation of cancer cells.91–107
  • Lignans suppress the flu virus.108
  • Lignans have antimicrobial activity.109
  • Provide therapeutic effects to cardiovascular tissue by promoting vasorelaxation and reducing fibrosis, inflammation, apoptosis, and oxidative stress.110,111
  • Have neuroprotective effects.112,113
  • General antioxidant and anti-inflammatory effects.114
  • Prevents angiogenesis.115

Evidence from Animal Studies

  • A topical cream made with flax lignans aid in wound healing by their antioxidant activity and stimulating collagen synthesis.116
  • Reduced breast tumors.117–121
  • Protects bone tissue.122
  • Can reduce pain and inflammation.123
  • Improves vascular biomarkers.124–126
  • Reduces radiation damage.127
  • Reduced colon cancer biomarkers.128
  • Reduced biomarkers of liver cancer.129

Human Studies

Epidemiological Evidence

  • Lignan intake is negatively associated with esophageal cancer.130
  • Enterolignans are associated with a reduced risk of type 2 diabetes.131
  • Enterolactone levels are negatively associated with asthma.132
  • Lignan intake is negatively associated with bladder cancer, especially urothelial cell carcinoma.133
  • Reduced risk of breast cancer.117,134–144
  • Associated with reduced risk of colon cancer.140,145–148
  • Associated with a decreased risk of prostate cancer.140,148–150
  • Lignans are associated with a reduction in cardiovascular disease risk factors.151–153
  • Inversely associated with obesity and overweight.154

Clinical Trials

  • Flaxseed intake improves lipid profiles and reduces CVD risk factors.155–157
  • Might reduce breast tumor growth.117,158
  • Small reductions in prostate cancer biomarkers.159
  • Lignans attenuate blood glucose levels.160

Not-So-Good Outcomes

There is some evidence that lignans might not be so beneficial, particularly in men. This may be due to the fact that plant lignans and enterolignans are considered to be phytoestrogens with weak estrogenic and antiestrogenic properties.56,161–163

  • Associated with male infertility.164
  • Associated with an increase in prostate cancer.165,166

Conclusion

Despite the bit of evidence that dietary lignans may not be so good for men, I would say that the benefits outweigh the risks, especially if you are one of the lucky people to have the gut bacterial community that makes for efficient lignan conversion.

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