Gary Taubes responds to George Bray

The May 2008 issue of Obesity Reviews, the journal of the International Association for the Study of Obesity, contained a review written by George Bray, M.D. of Gary Taubes’ book Good Calories, Bad Calories (GCBC). Gary Taubes has written a rebuttal that will appear in this same journal. Before we get to Gary’s response, I would like to spend a little time on Bray’s review, which I found interesting and troubling on a number of fronts.

Most reviews of books in academic journals are of academic books and are, at most, a page and a half, maybe two pages, long. The Bray review of GCBC was 13 pages long, including two plus pages of citations. And this for what is basically a popular book written for a general audience, not an academic tome. In all the reading I do of the medical literature, I’ve never seen a book review come even close to this in terms of length and comprehensiveness. Obviously Taubes’ work struck a chord.

George Bray, M.D. is probably the most renowned figure in the field of obesity research today. He is the Boyd Professor at the Pennington Biomedical Research Center (and former executive director) in Baton Rouge, LA; he holds numerous other professorships at various academic institutions; he has held leadership positions in virtually every academic obesity organization in existence; he has authored or co-authored more than 500 scientific papers; he has written at least a dozen books and authored chapters in many more; and he figures prominently in the recent history of how the academic ideas of the causes and cures of obesity are what they are today. It speaks volumes that someone of Dr. Bray’s academic stature would be tapped to write a review (a review, in fact, that is longer than most scientific papers) of a popular book. GCBC has gotten the attention of the academic community.

I don’t think there is anyone out there who would be less likely to pooh pooh the idea that there is an obesity epidemic today than George Bray, yet he starts out his review with a couple of quotes from two centuries ago juxtaposed with a sentence from GCBC (see below) in an attempt right at the get go to belittle Gary’s arguments.

I believe no age did ever afford more instances of corpulency than our own. (Short, T. 1727)

If the increase of wealth and the refinement of modern times have tended to banish plague and pestilence from our cities, they have probably introduced to us the whole train of nervous disorders, and increased the frequency of corpulence. (Wadd, W. 1810)

Some factor of diet and/or lifestyle must be driving weight upward, because human biology and our underlying genetic code cannot change in such a short time. (Taubes, G. 2007)

Early on in the review after describing how GCBC is laid out, Dr. Bray writes the following:

As I read through Good Calories, Bad Calories, I found a number of errors of omission or commission that are important when relating diet to disease. There is no mention in the Diet-Heart section of low-density lipoprotein-cholesterol (‘bad cholesterol’) or of high-density lipoprotein-cholesterol (‘good cholesterol’).

I find this comment curious for a couple of reasons. First, anyone who has read GCBC knows that LDL- and HDL-cholesterol are covered in depth. Second, this review is published in an academic journal read by pretty much only academics (as compared to, say, the New England Journal of Medicine, which is also academic but has a much higher general and medical readership), so why the need to identify LDL-cholesterol as ‘bad cholesterol’ and HDL-cholesterol as ‘good cholesterol’? Surely the readers of this journal – academic obesity researchers – would know what LDL- and HDL-cholesterol are. Even JAMA and the New England Journal of Medicine wouldn’t identify these molecules this way. I suspect the intent was for this review to have wide circulation in the popular press and, consequently, was made more understandable for the lay reader.

Bray goes on to clarify his own position as to the cause of obesity:

Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result. An energy deficit produces weight loss and tips the balance in the opposite direction.

Again, I find the notion of Dr. Bray’s laying out his own view of the cause of obesity to be curious. Isn’t this supposed to be a review of GCBC? I would think that it would be more important to lay out the position of the author of the book being reviewed. Which Bray does by mischaracterizing Taubes’ position. Taubes’ ideas, according to Bray’s interpretation of them, run counter to the laws of thermodynamics, which interpretation is the refuge for all those who can’t or won’t understand what Gary is trying to say.

Bray is saying that obesity is a matter of creating a positive energy balance, i.e., consuming more calories than are being burned off. He implies that obesity is simply a matter of overeating and under exercising. If you consume more calories than you burn over time, you get fat. Gary’s perspective is that fundamentally obesity is a disorder of fat accumulation. And that this disorder drives people to overeat. Obesity, the disease, drives people to overeat and be lethargic. Bray believes that people overeat and are lethargic and, consequently, bring on the disease of obesity.

I’ve met George Bray, I’ve read many of his publications, and I’ve heard him lecture numerous times. And I can tell you that George Bray believes that obesity is a disease. And he believes that it should be regarded as a disease and treated with drugs. In an interview in 2005, he said

Obesity is multifactoral, develops over time, and manifest differently among individuals. I define it as a relapsing, chronic neurochemical disease. No specific dietary regimen can change that. We must accept the fact that we cannot cure obesity with diets.

Since we don’t fully understand the causes of obesity, we should take the patient’s responsibility out of it. Rather than focusing on the gluttony, sloth, and moral issues, it is far better to address the neurochemical imbalance and why it occurs. [In other words, let’s give them drugs.]

But in this review we have Dr. Bray telling us that obesity is “the result of a prolonged small positive energy surplus.” He has definitely taken on the mantle of George you’re-fat-because-you-overeat Bray. It does make one wonder.

Enough of my preamble. You can decide for yourself.

Here is the link for the full-text version of George Bray’s review: bray-review-of-gcbc

Take a look about two thirds of the way down the right-hand column of the third page. Bray takes off on a riff about thermodynamics while completely missing the point Gary makes in GCBC. Unfortunately, the academics who read this, most of whom know little or nothing about thermodynamics, will swallow it hook, line and sinker and think they’ve been enlightened.

And here is Gary’s response: taubes-response-to-bray-ob-reviews


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75 thoughts on “Gary Taubes responds to George Bray

  1. “Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result.”

    You’re right. That comment alone makes me wonder about the rest of this article (which I plan to print and read, along with Taubes’ response).

    Taubes clearly outlines that different macro-nutrients work on different pathways into the body and have different effects… which makes sense.

    So, I’m looking forward to see how/if he addresses this.

    Personally, I only care about his stature in the way that you listed: that it sounds like they are bringing out the big guns. Everything else is an argument from authority! Evidence, evidence! (Which is why I’d love to see what Taubes wants done… hard evidence for what he’s proposing… no matter how rational it sounds in the book, and no matter how much personal success people have had on the diet).

    But, I digress and undress and slip off to bed to read these responses. :)

  2. Dr Eades,

    Dr Bray writes: “The cholesterol receptor, the discovery of which earned Brown and Goldstein the Nobel Prize, is not mentioned, nor are the statin drugs that arose from this discovery. The statin class of drugs has been very important in reducing the deaths from heart disease.”

    Not a citation, among two pages of citations, to back up this passage. Taubes is condemned because he denies the wond’rous power divine of statins! Or rather, doesn’t even bother to mention them.

    Unstatinatingly yours,
    Michael Richards

    I’m quite sure that Bray is a statinator of the deepest dye.

  3. Taubes’s rebuttal is succinct, to the point, and devastating. And that zinger at the end is perfect.

    Pompous dogmatists like Bray often become intellectually lazy, as they are used to bullying their way around academia, either through force of personality or through their hold on the funding purse strings. So they make specious, easily-rebutted statements such as the one about LDL and HDL. Clearly he must have known those subjects were addressed, unless he never actually read the book, just asked one of his assistants to summarize the basic tenets. I would suggest that latter is likely, and any assistants he would trust would obviously share the same bias and be seduced by the same dogmatic position.

    It is shocking that someone of such little scientific integrity should have so much power and influence over the debate about such an important topic. I have to agree with Gary when he says that Bray is not really interested in reviewing Taubes’s book, he is desperately trying to defend his (Bray’s) career. What a sad man.

  4. Yikes, I’m posting twice in a row, and it’s much later than I said I was going to stay up, but other things have intervened and I’ve ended up skimming the articles and a thought popped into my head.

    There was/is a comedy show in Canada, back when I had TV that was called… Kenny vs Spenny or something. I caught one episode and it was about carrying extra weight. In the episode they “put on” 80 pounds of extra weight and walked around with it. I thought about it seriously. I’m 5’11” and 190 pounds or so, and not very muscular. I tried to picture myself at the same height, but 270 pounds. I pictured myself at the gym lifting 80 pounds of weight, or walking around with two 40 pound dumbells.

    Wow! It really puts it into perspective. Seriously. Go to the gym and imaging strapping 50-200 pounds of weight on your body (mostly on your midsection) and then doing your daily tasks. I think I’m ravenous now (just starting on low-carb), I can’t imagine it with that kind of energy expenditure (weights) and with the carb-insulin response system!

    One of Gary Taubes’ concepts (as I recall) is homeostasis and that increased energy expenditure equals greater appetite (I know I always feel hungry after aerobic exercise). Well, if you are carrying around extra weight, aren’t you expending more energy and thus requiring more input energy? Thus homeostasis? Do most studies/books/diets take this into consideration?

    Maybe that sounds elementary, but I don’t recall it being stated directly?

    Thanks ya’ll!

    The situation you describe has been addressed in the literature. It’s one of the reasons it is easy to lose weight early on during a diet and more difficult later. As dieters lose weight they reduce their energy expenditure, making it more of a chore to create the deficit needed to continue to lose.

  5. Interesting. Gary’s last thought was my first one – I knew I’d seen the name George Bray before, and a quick check of my copy of GCBC (Actually ‘The Diet Delusion’ in these parts) confirmed my suspicions: There are 15 page citations for him in the index. How can anyone who is that much referred to in a book be an impartial “reviewer” of it? There ought to be a convention against that. I mean, if he wants to write a rebuttal, or a challenge, fine … but a review?

    By the way, apropos of your comments about publishers’ prerogative to choose book titles: Why oh why oh why did they have to rename GCBC for other markets? That just drives me crazy because it’s self-defeating. I bet it cost him sales when people who saw CGBC reviewed or quoted on the internet or in international magazines went to their bookshop and asked for it by name, only to be told that no such title was in stock. I nearly missed it myself even though I was looking right at it (I had the “butter on toast” image in my mind’s eye). Dumb, dumb, dumb. A book should be an international product.

    I didn’t realize GCBC was titled differently elsewhere. And I agree with you that Bray was a poor choice as an impartial reviewer since he was dealt with so much in the book. He ends up defending himself instead of reviewing the book.

  6. It sounds like the Bray’s mind was made up about obesity’s origin, and no book, no study, nothing would change that. It’s too bad. But I’d guess that a majority of the US believes people are fat because they’re lazy and gluttonous…and are just looking for a way to justify their belief instead of forming their belief from the facts. One would hope someone with a medical degree would take a more scientific approach to their perspectives.

  7. Hmm…it appears that Dr. Brays review of Taubes book is rather lacking in objectivity. I’m personally convinced that calories absolutely do count. But I think Taubes hypothesis that carbohydrates are what drives excess eating (and reduces physical activity) via subsequent insulin production is indeed correct. I’d love to see Taubes come out with a “Lite” version of GCBC with less science jargon, making it more accessible to a lay audience.

  8. It’s interesting how the ‘experts’ are so resistant to the hypothesis that fatty acids can be positively PULLED into fat tissue, reducing circulating fuel, and thereby creating normal physiological hunger, and thereby inducing eating.

    Taubes makes the point in GCBC clearly and brilliantly — and may in fact be one of the most important hypotheses in the book — but Bray doesn’t even touch the issue, as if it short-circuits in his brain. He doesn’t refute it or present evidence against it, just ignores it. I’ve found most MDs and nutrition gurus the same way. Never address the issue. Maybe the hypothesis is wrong, maybe not. But they somehow don’t want to discuss it. Dissonance, I guess.

    Many will quickly acknowledge that certain drugs can induce weight gain, but don’t readily explain why. (“Makes you hungry?” How? Um . . . in the brain or something. Lotta hand-waving.) Could it be that some drugs could conceivably affect fat tissue, driving fat fat accumulation (a la Taubes) which drives hunger? Or influences someother hormonal system that affects fac accumulation? There may be a revealing connection there, but I’ve not seen obesity researchers address it.

    Bray also misses Taubes’s point about nutrient composition affecting hunger. Why are you not hungry on a 1800 kcal low-carb diet, and starving on 1800 calories of starch and sugar? Why did Ancel Keys’s’ 1700 kcal regimen create raging, unrelenting hunger in his emaciated subjects? Would 1700 kcal of beef per day do the same?

    Anyway, I must admit to some satisfaction thinking of Bray squirming at Taubes’s response.

    It’s sad to see that academia doesn’t really reward free-thinkers. It should be the province of mavericks and apple-cart-upsetters with imagination, and the stones to test their own ideas. Seems to be mostly sheep, though.

  9. Wow, talk about the sublime & the ridiculous. Did you get a load of Bray’s comments to Taubes’ epilogue conclusions in table one? Hilarious, yet sad.

    I can’t say I’m surprised at Bray’s “review”. I’m glad Gary Taubes showed class and restraint in his response.

  10. GCBC made a great (and original, I think) argument against Bray’s ‘energy surplus’ theory of obesity: over twenty years we’ll each eat something like 25 million calories. How in the heck are we supposed to consciously balance out exactly 25 million calories?! There should be wild swings in EVERYbody, up and down, if it were up to us to maintain the energy balance. We’d be spending every day workin’ on the ol’ energy balance.

    No, there must be something else going on. I enjoyed his ‘reversal of causality’ section.

    The root of the energy theory could be the gross simplification of foods- which are bundles of all sorts of organic chemicals- into mere ‘calories’. Imagine prescribing medicines and drugs that way. “Here, take 20 calories of anything on in that cabinet and call me in the morning”.

  11. When I read this:

    “Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result. An energy deficit produces weight loss and tips the balance in the opposite direction.”

    I suddenly remember one of the quotes in the book “Mistakes were made (but not by me)” attributed to a British politician:

    <>(pp. 17)

    The whole ‘review’ sounds just like that. “I’ll bother with reviewing this but I’m still right…” You would think that when someone with Bray’s scientific stature would really push the field forward. What is so frustrating is that when one of us (scientists that don’t have a long trajectory in the field even come up with ideas similar to Taubes’) suggests something different, based on solid science, we are laughed at and, of course, not funded. My students look at me in a very weird way when I say (within the context of nutrition), ‘take what an expert says with a big pinch of salt… it was because of the ‘experts’ that we ended up with the current dietary guidelines.’

    This passage from Tabues’ reply:


    I wish his book would’ve come out five years ago. Back then, the lab where I was doing my postdoc was actively engaged in dissecting the effects of catecholamines in fat cells using a mouse model. The first thing I noticed is that the commercial and standard ‘high-fat’ diet (~58%) that was given to ‘obesity-prone’ mice (also known as ‘B6’) was also a bit high in carbohydrates (~25%). Moreover, the fat composition of the diet was also high in soybean oil. I don’t think that back then one could’ve found soybean oil that didn’t contain transfats (it makes it cheaper). Of course I was the ‘newbie’ and when I asked why the macronutrient composition was like that, I was told that ‘everyone in the field uses the same commercial and standard high fat diets’. Yes, I was new to their lab but not new to nutritional biochemistry… that, unfortunately, was not that important.

    Soon after I started to work with mouse fat cells, I found an article from a Spanish group in which the rats they were using (which were suppose to get obese due to the high fat content in their diet), didn’t become as obese as the authors were expecting. When I checked the source of the fat, it was coconut oil and not soybean oil. I traced the source of the coconut oil (the researchers specified the company, etc.) and ask for the process by which their coconut oil was obtained. They sent me all the information and the analysis of their oils and there was no transfats there. So, there I had a comparable high-fat diet but without transfats. That alone begged the question about composition of the diet. When I suggested a rather simple experiment just comparing high-fat diets with and without transfats I was kind of laughed at… here goes the newbie, which is also an Atkins fat (which I’ve never been). One thing I’ve learned is that when you go up against beliefs, rather than true scientific argument, there’s no win situation, especially if you’re the ‘newbie’. Funny, now this feels as a little vindication, even if five years have passed. I’m sure there are so many out there that feel the same way. It will be interesting to see what other ‘experts’ have to add after Taubes’ reply is published.

  12. I find Bray’s most alarming comment to have been: “Since we don’t fully understand the causes of obesity, we should take the patient’s responsibility out of it.”

    This seems to be the way of much of medicine these days. “It’s not your fault. You needn’t take any responsibility for your condition. Here’s a prescription. Good luck. Next patient?”

    My interpretation of modern genetics and epigenetics studies is the exact opposite: never before have we seen such a wealth of evidence and opportunity to direct or redirect gene expression in our favor regardless of prior unfortunate choices or having been dealt a “bad hand.” And no one has explained this vis a vis weight-loss better than Taubes. Well, maybe Eades…

  13. Just a thought, maybe your publisher can answer: Is Dr. Bray coming out with his own ‘popular’ (i.e. directed at general audiences) book in the near future? That would explain his unusually extensive ‘review’ of a non-academic book, as well as why that ‘review’ is a thinly veiled platform for his own positions on the matter.

    I don’t think he is coming out with a popular book. He is the stand-in for all of the academic obesity researcher that Gary savaged for sorry research in his book.

  14. Indeed our friend, Dr Bray, has a book out, Handbook of Obesity: Clinical Applications.

    Here’s a telling excerpt from the press release available at

    “Pharmacological alternatives are thoroughly explored with individual chapters on sibutramine and orlistat (both FDA approved) and pramlintide (currently approved in Europe”

    … you know the drill


    I know the drill well.

  15. When I began checking in to read a few low-carb blogs a couple of years ago, I was simply looking for some motivation to stick to this manner of eating. While the blogs I read still serve that purpose, the more in-depth ones, such as yours, have made me think a lot more about issues of trust in scientists and doctors. I’ve learned not to take reports of studies found in popular media at face value, I’ve learned that I will need to educate myself as best a lay person can about my health and not just blindly swallow whatever my doctor tells me to do, and I’ve learned that scientists are just as likely to be victims of their own prejudices, assimilated commonplaces, and self-interest as anyone else. The popular icon of the scientist as an objective, honest inquirer into the truths of the physical world who follows the evidence and revises his/her theories accordingly is mostly a myth. So am I now surprised that big-time scientist Dr. Bray is unable to respect the monumental accumalation of evidence that Taubes presents? Am I surprised that he shoots it down because it does not conform to what he already “knows” is true? No.
    Another blog I read regularly for different reasons is that of Dinesh D’Souza. One of his recurring themes is the refutation of atheism and how attached atheists are to the Great God Science to support their tenets. In a recent post (“The Dogma of Materialism,” 7/18/2008; he offers these quotes that I think are pertinent to the underlying problem that Bray has with Taubes’ work. He quotes Richard Dawkins as saying: “Even if the evidence did not favor it [evolution], it would still be the best theory available.” Doesn’t this sound like all the doctors who argue that low-fat eating is healthful, that cholesterol causes heart disease, despite all the evidence that does not favor it? D’Souza goes on to quote The biologist Richard Lewontin: “We take the side of science in spite of the patent absurdity of some of its constructs, in spite of its failure to fulfill many of its extravagant proises [sic] of health and life, in spite of the tolerance of the scientific community for unsubstantiated just-so stories, because we have a prior commitment–a commitment to materialism. It is not that the methods of science somehow compel us to accept a material explanation for the phenomenal world, but, on the contrary, that we are forced by our a priori commitment to material causes to create an apparatus of investigation and a set of concepts that produce material explanations, no matter how counter-intuitive, no matter how mystifying to the uninitiated. Moreover, the materialism is absolute, for we cannot allow a Divine Foot in the door.” The following excerpts from this quote reminded me of all the Dr. Brays out there telling us to limit our saturated fat consumption and take our statins: “The patent absurdity of some of its constructs,” “its extravagant promises of health and life,” “the tolerance of the scientific community for unsubstantiated just-so stories, because we have made a prior commitment….” D’souza commended Lewontin for admitting that scientists make prior dogmatic commitments, but most of them can’t see that their beliefs contaminate their interpretation of data. It’s awfully hard to admit you have been totally wrong about something, especially when your pronouncements have endangered people’s lives, especially when all your colleagues will turn on you and ridicule you, so most scientists will go to incredible lengths to avoid these unpleasant consequences. Mistakes may be made, but never by someone so eminent as Dr. George Bray!

  16. uge case of cog. dissonance and of course it’s the biggest compliment to Herr Taubes that “Bray got into the Fray” as it were.

    Taubes response sticks it up him good and proper..wonderful and far better than warfare anyday !

    Rock Not Pop

  17. “The situation you describe has been addressed in the literature. It’s one of the reasons it is easy to lose weight early on during a diet and more difficult later. As dieters lose weight they reduce their energy expenditure, making it more of a chore to create the deficit needed to continue to lose.”

    So why do low-carb books tell people to add carbs (calories) back into their diets, instead of cutting them forever? This seems very unwise – to add carbs (calories) to your diet as you get near your target weight, when your metabolism has slowed down. It would make more sense, IMO, to simply drop carbs to a certain level and keep them there. And then if you want to be lean like a fitness model or professional body-builder, you may have to drop the carbs and/or calories even lower if you want to acheive that goal. But most low-carb books don’t even talk that much about calories. Also, I think it would make more sense to limit protein and carbs as Jan Kwasniewski does, than to cut back on fat as you have suggested.

    Dietary Fat has nothing to do with the obesity epidemic. Excess carbs and protein seem more like the problem. When you don’t overeat carbs OR protein, it becomes very hard to stay fat. All the people on Jan Kwasniewski’s diet are thin, according to newspaper articles and videos I’ve seen online. He limits protein to adequate levels (1g/kg – more for highly athletic people). Carbs are limited to under 1g/kg. The rest of the diet is pure fat.

  18. In reading George Brae’s “review,” one can clearly hear him say: “Mistakes were made (but not by me.”

    The message that Dr. Brae needs to take to heart was quoted in the book by that title:

    “We are all capable of believing things which we know to be untrue, and then, when we are finally proved wrong, imprudently twisting the facts so as to show that we were right. Intellectually, it is possible to carry on this process for an indefinite time: the only check on it is that sooner or later a false belief bumps up against solid reality usually on a battlefield.”
    — George Orwell (1946)

    Dr. Brae’s review demonstrates nothing except that George Orwell is shown to be correct in this assessment of human nature.

  19. Gabe is right. Most of the animal studies use things like corn oil, soybean oil, safflower oil, and other garbage. The results won’t be the same if you test coconut oil, beef suet, butter, ghee, and other natural fats. It’s not just the potential trans fatty acids in unsaturated vegetable oil, but most of them are very high in PUFAs. Coconut oil is extremely low in PUFAs, like 1-2% of fat content. Centrifuged coconut oil has no PUFAs at all, according to gas chromatography tests. That oil would be highly immune to rancidity and lipid peroxidation.

    It’s dishonest of scientists to say that a “high-fat” diet causes some disease if the fat they are using is sky-high in PUFAs and/or trans fats. They should test fats that are very low in PUFAs, like coconut oil, macadamia oil, cocoa butter, foie gras, butter, ghee, beef fat, kidney suet, palm kernel oil, leaf lard, lamb fat, and so forth. That way, we would know whether “fat” was the problem or toxic vegetable fats they were using.

    Colin Campbell commits the same type of dishonesty by saying that casein and animal protein cause cancer. The problem is that he fed animals a diet of corn oil, table sugar, corn starch, AND casein. So maybe the casein was only bad in the context of those other foods and if you re-did the experiment with coconut oil, butter, and suet, there would be no cancer. Maybe if you did the study with a low-carb diet, there would be no cancer. The scientific method is not being followed. You MUST isolate all of your independent variables.


  20. I have to admit I (partially) agree with Bray. When reading GCBC I couldn’t help but also find fault in the lack of mention the role fat and calories have in obesity. I do not mean in terms of some simplistic “energy in energy out” function that Dr Bray would subscribe… but rather the profound modifying effect calories (total energy) and dietary fat have on insulin resistance. This is the reason we on low carb diets cannot have glucose tolerance tests until we eat a normal diet for a few days – physiologic insulin resistance from fat will cause us to test false positive for diabetes. Dietary fat plays a crucial role in determining glucose tolerance, thus how much insulin we make to process our carbohydrate. This explains “fat induced obesity” – adding fat to carb chow makes the carbs very obesigenic because fat causes insulin resistance.
    Total calories are much the same – even if we eat a mixed meal of fat and carb, if energy is sufficiently low, there will be no not chronic hyperinsulinemia or fattening. This explains the sumo, who eat low fat diets but tremendous calories, but the natives do not have obesity because their total energy is very low.

    Personally I thought it was a very important point Taubes should have at least mentioned – obesity is about insulin, but insulin is NOT as simple as carbohydrate and that is a major point every obese person must understand if they are to successfully reduce weight and keep it off. Insulin is also profoundly affected by a host of conditions like dietary fat, calories, sleep, exercise, just to name a few major ones.

    Still, when you compare Taubes minor error to Bray’s fundamental willful ignorance (an inability to recognize the crucial role of insulin/hormone balance in controlling feeding behavior and propensity to exercise) … Taubes analysis is pristine perfection by this standard. At least an obese person can BEGIN to make progress reading GCBC… if he or she were to go by Bray’s advice, they’d be idle waiting for the next wonder drug to fix the break in the regulating system.
    Taubes empowers obese people with the foundations of knowledge – for many of us with obesity, the flawed regulation system Bray talks of is entirely controlled by insulin balance. While rarely as simple as reducing carbs (for true obesity anyway) reducing carbs is at least the beginning of figuring out a long term solution. As Bray mentions there are many types of obesity and not all respond to diet… but I have a sneaking suspicion these types of obesity are not making up the dramatic increase in type 2 diabetic children and severe obese individuals in the midwest.

    I’ve been maintaining a weight loss of 160 lbs for 4 years now; my BMI is 20; I would love to discuss this matter with Dr Bray in person. I’m a real human example of the crucial role insulin plays in disregulating the regulating system… I’ve managed to restore integrity to the system by taking necessary steps to balance insulin (in order: very low carbs, moderate calories, small serves of food and utilizing forced exercise/activity to reduce insulin and blood sugar after dietary indiscretions).
    As a result of these changes, I have obtained the ability to regulate my food intake long term (just like a thin person), and I have also newly obtained the ability to want to exercise, especially if I eat more food. My regulating system, once dysfunctional and driven toward fat growth, now works like a normal thin person. I credit this change entirely to controlling insulin.
    It’s almost as if he has never even interacted with a real human who has obesity. Incredible, for someone who fancies himself an expert.

    Hi ItsTheWooo–

    Thanks for the long and detailed comment. I pretty much agree with you down the line, but I do have to take exception to the following statement:

    This is the reason we on low carb diets cannot have glucose tolerance tests until we eat a normal diet for a few days – physiologic insulin resistance from fat will cause us to test false positive for diabetes.

    It’s not really the “physiologic insulin resistance from fat” that causes the problem you describe; it is simply a temporary deficiency of enzymes. Virtually all physiological functions in the body are controlled by the enzymes that catalyze the various reactions required. Our DNA codes for all of these enzymes, all of which are proteins. Our DNA codes for many enzymes that we may never use because we don’t need them given our lifestyle, but the coding and ability to make them are still present. We send signals to the DNA that we need them when we need them, and our RNA/DNA system cranks them out. Such is the case with the enzymes we use to metabolize carbohydrates, which are different than those used to metabolize fats. If we are on a long-term low-carb diet, we don’t need the enzymes to metabolize a lot of carb, so we don’t make them. We do need the enzymes to metabolize fat, so we have plenty of those. If we take in a large load of carbohydrate, we don’t have the enzymes we need to dispose of the carbs quickly, so they remain in the blood as sugar a little longer, giving a glucose tolerance test reading that looks like that of one with glucose intolerance or outright diabetes. If we eat carbs for a few days before, we crank out the enzymes, which are then in place when we take the glucose tolerance test, and we get a normal reading. It has nothing to do with the fat causing insulin resistance; it’s simply a matter of lack of enzymes.

    It is this same lack of necessary enzymes that causes those going on low-carb diets to be fatigued for a few days right at the start. The enzymes are there for the normal high-carb diet, but not for the higher-fat, low-carb diet. Those starting a low-carb diet can’t metabolize the fuels from the new diet as quickly or as efficiently as they could the old diet because they haven’t produced the enzymes yet.



  21. On a slightly different note, what does this line mean:
    No conflict of interest was declared.

    Does it mean there is no conflict of interest or that there is a conflict of interest, but the author chose not to declare it.


    It’s a weasel way that the journals can hide behind if one of the researchers is found later to have a conflict of interest. It supposedly means that there is no conflict of interest, but the journal is relying on the author of the paper to be truthful in declaring no conflict of interest.

    I find it interesting that one who has been taken to task for shoddy research in a book can declare that he has no conflict of interest in reviewing that book.

  22. Dr., can you please inform me as to why some people’s faces sweat when they eat certain foods. I’ve noticed this in others and myself. Some seem to react badly to carb-rich foods, while others react to protein based foods like beef. Funny thing is, one day i eat a certain food and it may cause me facial sweating, and the next time i eat the same food, i don’t sweat. Is this very common and is there an underlying cause? Perhaps it is nothing to “sweat” about if a person is non-diabetic.

    As far as I know – and I’m no expert on this – the sweating is caused by a response to a particular spice or condiment in the food. For example, many people tend to sweat profusely when they eat certain types of peppers. The same thing can happen with other condiments as well.

  23. I thought it was interesting that in response to

    ‘Authors comment 1
    Dietary fat, whether saturated or not, ….’

    Bray’s comment does not mention saturated fat specifically. He says
    ‘Dietary fat produces obesity…’

    So maybe he has no easy summary of why saturated fat is a bad thing (because he knows it isnt a bad thing?)


    ps (as previous poster) why is it called ‘the diet delusion’ in the UK edition? to me it sounds like a Fat Acceptance ‘why no one should ever diet book’; surely limiting its appeal. ‘GCBC’ seems a more accurate title.

  24. ITW: low-carb diets don’t cause insulin resistance. That’s a myth. The Eskimos were tested on their native diets, with oral glucose tolerance tests, and found to be normal. The reason may have been that they ate a lot of protein and they got a fair amount of carbs from the organ meats and other things they ate. If you eat a zero-carb diet, extremely high in fat, you might become insulin resistant. That’s what happened to Stefansson and his partner in the Bellevue study eating meat exclusively for over a year. They were eating about 80% fat and 20% protein with negligible carbs. Most low-carb dieters don’t achieve that.

  25. _Bray’s comment does not mention saturated fat specifically. He says
    ‘Dietary fat produces obesity…’_

    He means that dietary fat produces obesity when it’s high in PUFAs or trans fat, a lot of carbs are also being eaten (esp refined). I’ve heard many places about farmers trying to fatten their cows or pigs with coconut oil and they became lean and hungry. They usually fatten animals with corn and soybeans. Both contain highly unsaturated oils and a lot of carbs. So, the ideal combination for fattening seems to be carbs and PUFAs and maybe trans fattya cids.

    I didn’t get why Taubes said in his rebuttal that animals in experiments are often fattened by feeding them hydrogenated oils. Most of the experiments I’ve seen gave animals soybean oil, corn oil, safflower oil, and other worthless junk, not hydrogenated oils. What do fat people eat? Doughnuts, french fries, cookies, cakes, pies, chips, crackers, fried fish, fried chicken. All of those are full of PUFAs and trans fats, with very little saturated fat (25% or less).

    Bray and colleagues need to start testing multiple types of fat, instead of blaming fat for the problems caused by PUFA vegetable oils and/or hydrogenated oils. If they want to blame the problems on “saturated fat”, they should use an oil that’s at least 60% saturated and at most 3-4% poly-unsaturated. Examples: butter, ghee, cocoa butter, beef suet, coconut oil, etc. It is simply correlation to blame saturated fat when you are not isolating SFAs from the PUFAs, trans fatty acids, and rancid unsaturated fats in general.

  26. Regarding titles, it’s really too bad the author has very little say in what his or her book will be titled.

    I think that “Protein Power” and “Good Calories, Bad Calories” are both exceedingly informative and serious books, but I always hesitate to recommend them because of the titles. I’ve been trying to get my husband interested in LC eating for years, but he simply won’t read either of these books because he can’t get past the titles. Ya gotta admit, they both sound like fad diet books that provide no informed scientific information.

    A sad but a true fact of publishing life.

  27. I was wondering if you would indulge me in just one more off-topic question.

    Does your surname rhyme with “Wheaties” or “Weeds”?

    I’ve always thought of you as “Dr. Wheaties,” though “Dr. Meaties” might be closer to the mark!

    Thanks for yet another great blog article!

    Hey, that’s a question I can answer definitively. It’s Eades as in Weeds. Based on all the mispronunciations I’ve heard, I’ve got to say that it’s the most difficult to pronounce five letter name in existence.

  28. “If we take in a large load of carbohydrate, we don’t have the enzymes we need to dispose of the carbs quickly, so they remain in the blood as sugar a little longer, giving a glucose tolerance test reading that looks like that of one with glucose intolerance or outright diabetes. If we eat carbs for a few days before, we crank out the enzymes, which are then in place when we take the glucose tolerance test, and we get a normal reading. It has nothing to do with the fat causing insulin resistance; it’s simply a matter of lack of enzymes.

    It is this same lack of necessary enzymes that causes those going on low-carb diets to be fatigued for a few days right at the start. The enzymes are there for the normal high-carb diet, but not for the higher-fat, low-carb diet. Those starting a low-carb diet can’t metabolize the fuels from the new diet as quickly or as efficiently as they could the old diet because they haven’t produced the enzymes yet. ”

    Clearly I need to do some more reading; I’m now finding a blank space in my brain regarding the carb-disposal enzymes and the timeframe necessary to “register” as glucose-tolerant, for lack of a better term. Can you refer me to a specific publication, such as the PPLP perhaps, where this is explicitly described? Many thanks.

    I looked in PP and found a small section on it (pg 144-145 in the paperback), but it doesn’t give you much more than I already wrote in the comment.

  29. By the way, vis a vis:
    ” There are 15 page citations for him in the index. How can anyone who is that much referred to in a book be an impartial “reviewer” of it? There ought to be a convention against that. I mean, if he wants to write a rebuttal, or a challenge, fine … but a review? ”

    Indeed. Not just a convention, an outright fact-checking prohibition should be called for. As this excerpt illuminates, from another site (and if it’s even partially true, it’s damning) :

    George Bray is a leading obesity researcher and is the former director of a CORE facility. He is also Director Emeritus of AOA. Bray has been described by author Ellen Ruppel Shell as a “tireless proselytizer for obesity drugs.” A July 2005 Seattle Times article noted:

    “A consultant for numerous drug companies for more than three decades, Bray holds patents for such things as low-fat potato chips, a cream to reduce fat thighs, and treatment for metabolic disorders.”

    Bray was a leading investigator of Roche’s Xenical, along with Xavier Pi-Sunyer. The financial disclosure of one study on the drug’s effects stated that Bray:

    “…has received research grant support for the study of Orlistat from Hoffman-La Roche. He has also received research grants from Johnson & Johnson, Regeneron, Proctor and Gamble, and Novartis and has been a member of advisory boards and speaker bureaus for Johnson & Johnson and Takeda Pharmaceuticals.”

    These are companies that benefit from the notion that obesity is a disease, rather than an issue of personal responsibility—as do the companies that produced the weight-loss thigh cream he researched. Bray has come under fire for testifying on behalf of fen-phen makers at FDA advisory panel hearings and for being paid for court testimony on behalf of a company whose ephedra product his center researched. ”

    Thanks to Turtle2003 for digging it out and discussing it here:

    Yes, indeed, there is reaction “out there” to the so-called review and the rebuttal. I wonder, though, what the reaction is in the scientific community (present company excepted, of course) rather than we, the outraged, in the lay community.

  30. I have my own research study. I read Good Calories, Bad Calories. It scared the #@**ing carbs out of me. I cut out sugar, starch and bread. The weight dropped off steadily over a few weeks and I went from 195 to 165 which I have maintained almost effortlessly for almost a year. My wife also tried it with similar results. My parents now eat similar with the same results.

    Our study sample size is small but I know it works. I have a body to protect and a life to live. Good Calories, Bad Calories (and Protein Power, too) probably saved my life and the lives of those I love. Following dietary advice from people like Bray and other low-fat advocates is sending people to an early grave.

    Thank you Gary Taubes and Mike and Mary Dan Eades! You are my heroes!


    Hey Guy–

    Thanks for the kind words, but you and fam are the ones who did the hard work. keep it up.



  31. I just wish Taubes had actually said something of value instead of his hand waving. It was as bad as Brays commentary.

  32. If you keep the books meticulously, you will find that calories in will match calories out (nothing so far has ever invalidated the basic laws of thermodynamics – not for want of trying). Trouble is, almost no one does. But if you measure calories in accurately, and measure the change in energy stores (fat, but of course also glycogen and protein), you can by simple arithmetic calculate the amount of calories out – within the limited precision of the measurements, of course.

    But that’s about it. Assuming that the calorie expenditure is independent of the calorie input, or its actual composition of nutrients, has never predicted correctly the change in energy stores with changes in diet. It still doesn’t, and only by trying the same thing a bit harder will it ever succeed 😉


  33. That double labeled water thing–is it really that good a way to measure energy consumption?
    Looks like these people sell it

    Quoted from the above link;

    “Further experiments by Lifson, Gordon and McClintock showed that total daily CO2 production could be measured from the differential elimination of water labeled with stable isotopes of hydrogen and oxygen. After the administration of doubly labeled water (2H218O), the labeled hydrogen (2H2) would be eliminated as water (2H2O), corresponding to water output, whereas the oxygen isotope would be eliminated as water (H218O) and as expired carbon dioxide (C18O2). By measuring the difference between the elimination rates of labeled oxygen and hydrogen, the carbon dioxide production rate can be calculated. The carbon dioxide production rate is converted into energy expenditure by knowing the respiratory quotient (RQ) of the food ingested during the observation period.”

    If you don’t know what people are eating when they go home, and can’t trust their food diaries, how can you know the RQ of the foods that they are eating? And two men, of equal weight, eating exactly the same diet, will probably convert and store different amounts of the carbohydrate portion of that diet as fat–and also burn different amounts of that newly produced fat. I know that women generally burn a greater percentage of fat than men, and thus have a lower RQ, and probably not coincidentally live longer than men.

    Anything that prompts Taubes to go into more detail, I have trouble getting too upset about.

    The doubly-labeled water is not something you do at home to measure energy expenditure; it is a technique used in research labs.

    The RQ is a measurement that tells what your body is burning – fat or carbohydrate. Typically if you are on a low-carb diet you will primarily be burning fat and your RQ will be lower than if you are burning carbs.

  34. Dr. Eades —

    I’ve gone back and forth from 130 to 160 pounds for the past 15 years of my life (female, 5 foot 4 inches). I have gone on Weight Watchers several times and I lose weight but it’s a big pain with all the counting and hunger I experience. Because it’s unsustainable over the long term, I always gain back. After several months of trying to follow a “low carb” diet, I’ve been unsuccessful at losing a pound. I’ve never read your books and recently realized by reading on your site that I wasn’t doing it correctly. I wasn’t counting carbs and would eat a piece of bread here, a piece of bread there, fruit here, fruit there… I estimate that I was eating between 50-75 g. carbs per day, enough to maintain my weight. This past week as relatives visited, I made a ton of bad, carby goodies and gained 4 pounds. I decided “enough is enough!” After extensive reading on your site, and months of relative inaction on the issue, I finally understood the issue scientifically. I’ve been a believer in the low carb way for months now, but didn’t have an adequate scientific understanding of the subject. I knew it worked for many people, and I believed in the evolutionary argument, but I didn’t know the exact physiological mechanisms of how this works nor how much to limit my carb intake.

    I have been a carb lover since birth. It’s amazing I’m not larger than I am. Potatoes, bread, chips, fruits, you name it (I’ve never been into processed sugar snacks or soft drinks of any kind, though.) It started from babyhood. My mother had me young (she was only 20 herself), fed me no green veggies (because she didn’t like them), and I had a diet of mostly yellow veggies (corn, squash, etc.) with added sugar to make it taste good…. the pediatrician wanted to know why I was orange and weighed 16 lbs. at only four months… ha!

    So I truly started a low carb diet. I have kept carbs to below 30 g. per day for the past four days. At first it was tough. I had a headache and was tired. I long to crunch into an apple. I did not realize how many carbs I was truly eating. However, I’ve lost 5 pounds in only 4 days. At a starting weight of 163, that’s almost unbelievable to me. I’ve never had weight drop so fast. The week is not even out. Of course, I am sure it will slow down but it’s still amazing. I am not hungry and spontaneously reduced calories to around 1200 per day.

    I can’t thank you enough for putting such detailed information on the internet. I hope you and your wife and everyone else trying to spread the truth about an evolutionarily appropriate diet make a boatload of money off of your books. If you do, you will have deserved it.

    I’m glad to hear that you’ve done so well. You’re weight loss will slow down a little after the first week, but you should continue to feel energetic and non-hungry as long as you stick to it. Just be careful that you don’t let a little carb here and there creep back in or the hunger will come back and the weight loss will slow.

    Keep me posted.

  35. Dr Eades – I did not realize enzyme deficiency was the reason for the false positive diabetes test. I had just assumed it must have been dietary fat. Thank you for your explanation.

    Bruce Kleisner – Dietary fat will always impair how easily cells can take up glucose. This is a basic fact of physiology. The more dietary fat calories an individual eats, the less glucose they can tolerate. This is where the myth that fat causes obesity comes from – in studies it is repeatedly shown adding more fat to carbs will cause higher insulin levels and the associated sequelae. Unfortuanately no one seems to know (or want to admit) that the primary problem is the carbs… fat just passively acts to make the carbs that much more obesigenic by reducing the rate at which cells can take up sugar energy.

    Also, fat induced insulin resistance is physiologically normal, it is not the same as pathological insulin resistance. Fat induced insulin resistance lasts only as long you are eating the dietary fat… and it is worth mentioning that this is in no way harmful because fat requires extremely small amounts of insulin to maintain homeostasis and the cells are getting adequate energy. That is why diabetics on low carb high fat diets must use more insulin per gram of carb than they otherwise would have to on a low fat diet. This seems bad, until we calculate the total insulin use – and it turns out to be much, much lower than it would be on a low fat high carb diet. At the end of the day, total insulin level is what counts. Insulin resistance is not at all a problem, as long as the cells are getting energy and insulin levels are not excessive… in a low carb high fat diet both of these conditions are met.

    If you measured the glucose tolerance of someone existing on a fat based diet, who was properly inducted into a diet with enough carbs, it would certainly be much, much better than a carb eater all other things being equal (calories, weight, age etc). However, as long as the diet contains ample fats and calories, glucose tolerance logically must be reduced because the energy making cells of the body are metabolizing fats and therefore are not able to handle all of the sugar. Compensatory hyperinsulinemia and fat storing protects the body from what would otherwise become (toxic/damaging) hyperglycemia.

  36. If I understand Dr. Eades’ reply to ItsTheWoo correctly it is the physiologic adaption to fat as the primary source of fuel combined with a down regulation of the physiologic processes responsible for the regulation of sugar from carbohydrates used as a primary source of fuel that is the issue and not a form of insulin resistance caused by the consumption of fat. The problem seems to be that the mechanism(s) of insulin resistance are poorly understood. Because of this the term is probably being applied too broadly and at times inappropriately.

    It appears that the physiologic adaptation to fat when as a primary source of fuel at the expense of the efficient regulation of sugars derived from carbohydrates led some investigators to assume that consuming carbohydrates enhances BG regulation and that eating fat causes insulin resistance.

    I think you’re correct.

  37. “A sad but a true fact of publishing life.”

    Do you know if GCBC was the title Taubes wanted to use? If not, what title did he want? I think it’s pretty stupid that publishers are able to choose the title and art-work, rather than let the author get the decision. Having a different titles in different English speaking countries is very confusing for readers. I was surprised you didn’t know Gary’s book was titled the Diet Delusion in England. If Gary doesn’t know what his book’s titled in another country, that would be even more ridiculous. I’m sure Michael Crichton, Stephen King, and John Grisham don’t get told the title of their books by the publisher. Why should non-fiction authors?

    I know that Gary agonized over the title of the book. He and I (and I’m sure he and a dozen other people) kicked around numerous titles that just didn’t seem right. As I recall, his publisher came up with GCBC.

  38. First, thanks so much for bringing this review and response to a wider audience. I appreciate the effort you make to keep your readership abreast of current issues. I never would have known about this if not for your blog.

    Second, the entire conflict of interest issue appears to me to be a red herring. If someone writes a favorable review, she probably has previously had a favorable outlook towards low-carb diets. If she writes an unfavorable review, she probably previously had an unfavorable outlook towards low-carb diets.

    Gary Taubes was reported to have received a $700,000 advance for GCBC after the publication of his 2002 New York Times Magazine article, “What if It’s All Been a Big Fat Lie?” As we all remember, low-carb diet was a huge social phenomenon at the time, peaking in 2003-4 and then crashing. (I know, because my wife subscribes to Prevention magazine. I’ve been eating low-carb for 20 years and was accustomed to Prevention’s monthly bashing of low-carb. Finally, at the peak of Atkinsmania, Prevention couldn’t stand to see so much money being left on the table and it started pushing its own low-carb diet books, tapes, etc. That’s when I knew it was the beginning of the end of low-carb as fad.) Taubes had a monetary interest in substantiating in book form the claims he made in his NYT Magazine article.

    I don’t begrudge Taubes his advance. I wouldn’t be surprised if some heads rolled at Knopf, since the book came out three years after the bubble had burst.

    But at the end of the day, ad hominem arguments don’t count. If anything, that is the larger point of Taubes’s book. Let us make our judgments by rationally considering the internal coherence of Bray’s review and the evidence he offers. Attacking an argument by attacking the person who makes the argument is not an effective way to increase knowledge. Let’s critically evaluate the logic of the review, not the man who wrote it.

    My first thought when I started Bray’s review was that he was misstating Taubes’s position regarding the first law of thermodynamics. Sure enough, Gary understood his own book at least as well as I did, and explains that Bray got it wrong. I agree completely with Gary’s rebuttal.

    I find it salutary that Bray acknowledges the deleterious effects of fructose, both in sucrose and HCFS.

    One of the key points that I understood Bray to be making was that Taubes must show that “insulin is both necessary and sufficient to produce obesity . . ” Bray claims that insulin has been shown to be necessary for obesity but it is not sufficient. His argument appears to be that when insulin is injected into anorexics, they gain 20 pounds over 3 months, but that does not make them obese. And people with insulinoma, “who secrete insulin continuously,” gain weight with insulin injections, but do not become obese [260].

    His argument appears to be:

    1. Taubes says insulin is sufficient for obesity.
    2. Some people get insulin injections and do not become obese.
    3. Therefore, insulin is not sufficient for obesity.
    4. Therefore, Taubes is wrong.

    I haven’t read the research, but I will accept that 2 and 3 are correct. I disagree with 1 and 4. Even Gary Taubes does not believe that every person in the US on a high-carb diet is obese. The “science” of human nutrition is probabilistic. It is inductive, not deductive. The demand that any participant in debate propose necessary and sufficient conditions is raising the bar too high for anyone.

    Bray is making a straw man argument which can be turned against him as follows:

    1. Bray says high-fat diets are sufficient for obesity [258].
    2. Dr. Michael Eades, Dr. Mary Eades, and I eat high-fat diets and are not obese.
    3. Therefore, high-fat diets are not sufficient for obesity.
    4. Therefore, Bray is wrong.

    The above argument is a ridiculously weak. And the logic that Bray mobilizes against Taubes is similarly weak. The fact that insulin brought about weight-gain in anorexics and insulinoma tells us that insulin appears to be responsible for weight-gain in large numbers of people. Yes, there must be some other factor in addition to insulin that explains why one person injected with insulin becomes obese and another merely gains weight. But to use this fact to hammer away at Taubes demonstrates to me the desperation of Taubes’s opponents.

  39. Sorry for another post I just wanted to expand on my comment about fat and glucose intolerance…

    It may be that coconut oil may be a bit of a special case, because it is high in MCTs which stimulate the thyroid, which help actually raise carbohydrate tolerance (when metabolic rate goes up, the cells use more energy, which translates into an enhanced capacity to tolerate glucose, all other things equal). Fats higher in MCTs may raise glucose tolerance because they raise metabolic rate which can help balance glucose load (i.e. you can eat more carbs while eating these fats in lieu of others). Of course I’m just speaking hypothetically… but those fats which do not cause health problems in the context of a calorie-adequate higher carb diet appear to be the exception, not the rule, and therefore must be explained. The most likely explanation seems to be that some fats are capable of raising the total energy needs of the body, which allows cells to still accept glucose in spite of a high energy level from fats.
    It is a property of fat to create energy in cells, and whenever cells create energy, they stop being able to accept glucose as easily. The amount of energy our cells make is very tightly controlled. This is accomplished through resisting insulin in the presence of adequate cellular energy. This redirects otherwise toxic sugar and fats (in the blood) to fat tissue where it is stable. High levels of fatty acids and glucose are very, very toxic otherwise.

    Regarding experiments where farmers fed animals coconut oil and the animals became lean and hungry… I do wonder if these farmers were replacing other fats and/or carbs with the coconut oil…I would be very interested to read more about this!

  40. On the calories in, calories out, I’d note that with some food patterns you get a lot more futile cycling, where the body shuffles in place, so to speak, resulting in calories being burned, but not much happening. I’d call that calories in, expended in place 😉

    True. But calories expended – even in place – are calories out. :-)

  41. In one of Jimmy Moore’s podcasts, Gary Taubes talks about where the title of the book came from. I believe it was his publisher that came up with it. He didn’t like it at all at first. He’s still not crazy about it, but I think he has warmed up to it a bit.

    He said the title he wanted was “The Alternative Hypothesis.”

  42. Who runs really fast? Whippet. Cheetah. Polar Bear. Who flies really fast? Hawk, Kestrel. Why? So they can catch the things they eat. Has anyone ever needed to be slender to catch a blade of grass? Has anyone ever had to hunt a potato or an ear of corn at a high rate of speed?

    I wish people like Bray could embrace the notion that form follows function. Abdominal leanness governs how fast you can run down prey (prey=fat and protein and only so much carb as is left in prey’s tummy). You simply can’t sprint without a tuck up (unless you have a horse to carry you).

    Predators of the world would all be fat (and unable to remain predators) if a low carb diet did anything other than maintain a svelte physique.

    Since there’s safety in numbers there’s less need for a herd animal to be thin and in fact being ponderous may place a herd animal at an advantage because the lionness will prey on the weakest. So baby wildebeests and their equivalent need to drink up and get big fast and have excess so they can produce horns before the lion tigers and bears show up. And while they’re babies they better be slim enough to keep up with momma or they’re in trouble.

    And if this wasn’t all ringing true enough, we invented corn to feed to our modern day wildebeests to fatten them even faster and make them even bigger and we keep them in pens so even if they had the urge to roam they couldn’t and they get bigger and bigger.

    And then there’s the whole childhood and puberty thing. Has anyone noticed, young creatures of all types who are too big to carry are generally slender and light? ITS BECAUSE THEY MUST BE! OTHERWISE HOW WOULD THEY KEEP UP WITH GROWNUPSWHO’s LEGS ARE TWICE AS LONG? Generally they are also hyper-very playful. Why? Because they can be! Its fun because its easy.

    And why does the biggest hormonal metabolic shapeshifter not happen until we’re almost to adult size (puberty)? Because only adults can afford to slow down and pack on the extra weight needed for childbearing or fighting over mates. This huge metabolic event adds fat and slows us down but we can afford to be slowed down because we’re big enough to defend ourselves. Adults don’t play much because we’re generally not lean enough to feel its fun.

    Just the fact that everyone piles on mass during adolescence oughta be a wakeup call that hormones play a role in fat accumulation. Why would this be only the purview of estrogen and testosterone?

    Finally, given the law of the jungle (run fast enough to catch dinner or go hungry, loom large enough to be scary or get eaten) its is surprising to me so many people don’t see a need for us to eat like predators when we live like predators (specifically male lions). By that I mean most of us sit around most of the day, sleep a fair amount, eat the best we can get and don’t even have to go hunting (in the case of the lion the lioness does it for him, in the case of most people they go to the Piggly Wiggly). We don’t live like migratory animals that walk or fly or stampede with the seasons and cover many miles or like hibernators that have to store up for a long winter’s nap. Most modern people have territories (our homes, cars, offices, desks) and exericise is optional. Pretty much all I need to power is my brain and basic life support and hygiene and I get paid.

    Why do I need a carb to do that?

    Most of us in the US aren’t farmers anymore. We aren’t laborers laying railroad tracks or digging ditches. We aren’t even gatherers picking the harvest or ranging even further and picking wild berries.

    We don’t need to walk for miles behind a plow. So why do we need carbs and expect them to do anything other than fatten us like they fatten the beasts?

    Bray needs to get a grip!

    If I was an attorney I’d love to round up every teenage girl who ever spent the summer at boot camp disguised as Fat Camp and pursue a class action law suit against the forces that promote exercise and low fat diets as the panacea to a high carb diet and puberty. I personally was a normal weight teen who spent countless hours beating the heck out of my hips trying to land a double axel at the ice rink for months on end between ages 12-14 and have the scar tissue to prove it. Its only now at age 40 I find at my weight and height and muscular development it was not possible without violating the laws of physics to jump high enough to spin fast enough to land that jump.

    We need to quit tormenting ourselves and the teens of the world with exercises that can do far more harm than good in the name of weight loss and health. If people want to be lean we need to give them practical tools to manage their moods, temptations, and above all hunger!

  43. Dear Dr Eades,

    From various postings, I gather you are in touch with Gary Taubes, and also more or less in tune with him, give or take some details.

    Having read (the UK edition of ) GCBC several times (some parts 3 or 4 times), one question I am left with, which you may care to comment on, either from your own knowledge, or what you know of GT’s views:

    (oversimplifying here for brevity), one of GT’s themes is that hunger is caused when FFAs are not available to be mobilized out of the adipose cells (which could be because insulin is effectively locking them in; could also be for other reasons).

    Now taking the case of a fairly overweight/obese person who has established themselves on a quite low-carb diet, such that they should have started burning fat from their adipose cells.

    Now, given that they clearly have a _lot_ of fuel packed away in those fat cells of theirs, if they have managed to get their insulin down to a reasonable level, I am not clear now what
    ever makes them hungry!

    (I guess blood glucose must come into the equation here, but I am not quite sure how it fits in, in this situation).

    I can only surmise that one factor is that (I think as stated in GCBC), insulin levels (other things being equal) are in proportion to the amount of body fat. If so, then even though
    the person is low-carbing, their insulin levels are still likely to be higher than ideal, and
    so to some exent the FFAs are still locked away, and not available for fuel.

    Sorry if this seems like a naive and oversimplistic question, but I am really quite puzzled about this. I know that (as a still overweight low-carber myself), we _do_ certainly still get hungry!
    (but not in between meals, on the whole).

    With thanks and kind regards,

    Hi Mike–

    I think Gary is referring more to the long-term anti-hunger effects of low-insulin than the short-term effects. Plus there other hunger modulating substances (leptin, for example) involved. Then there is the issue of ketosis. It appears that, for most people, being in ketosis limits hunger as well. If one is eating a low-carb diet that is basically a lower-carb diet (as opposed to a real under 30-50 g per day low-carb diet), one may not be in ketosis and one may still have a higher than desirable insulin response. There are many, many factors involved, but I do think the ability to release fat from the fat cells is probably the greatest de-stimulator of the feeding response.

    Hope this helps.



  44. I find it very odd that in his book Gary Taubes does not even mention Dean Ornish, who has demonstrated in JAMA, for one, that heart disease can be reversed in individuals who eat a diet very high in carbohydrates (a low-fat diet). Gary recently said in the New York Times that the central question is which diet is healthier – a diet high in carbohydrates or a diet high in fat/protein. Why are Dean Ornish’s results not considered convincing?

    He probably doesn’t mention him because GCBC is basically a history of how nutritional science went off the rails. By the late 50s early 60s the science of nutrition had concluded that the low-carbohydrate diet was the best, most scientifically valid means of losing weight and improving health. Then came Ancel Keys and others of his ilk who took the science in the direction of the low-fat diet. We, as a population, have paid the price in terms of the consequent diabetes and obesity epidemics. Ornish was a minor player in this process and didn’t come on the scene until after most of the damage was done. Plus, in my opinion, Ornish hasn’t proven much of anything. See here for a post on the subject.

  45. p.s. Is the George Blackburn of your “award” fame, the same George Blackburn who features in a few places in GCBC? Curious if so, because back then, he seemed to be in favour of low-carbs, and comes over as one of the “good guys” in the history.

    It is the same, and he was featured in GCBC. It’s all proof that a leopard can indeed change his spots.

  46. Dr or anyone ‘ello….. is there any consensus please about what reduction in cals will take the body into starvation mode and thus impinge on metabolism please ?

    My email is supachramp at yahoo dot com

    Any pointers would be great please ?

    Thankee and

  47. When would statins be appropriate? MY NMR Lipoprofile just came back and says my LD-LP(Particle Number)is 1795, and small LDL-P is 1795. MY HDL-C is 40, and my triglycerides are 37. LDL-C is 93. Doc says with these numbers statin needs to be taken and problem is genetic vs. diet. Perhaps for some of us genetics rule; Would you agree?

    Nope, I wouldn’t agree. Maybe the genetics, yes, but the statins, no. Unless you’re a male under 656 with a proven history of heart disease, then taking statins will not increase your overall chances of dying. Which is really what it’s all about.

  48. Of course, Bray is correct in saying that, in order to store more calories than we lose, we have to store more calories than we lose. Since every calorie we store must first be consumed, and since we generally lose calories by expending them (mostly not be excreting fats and oils), we will gain weight if we consume more calories than we expend. If an obese person is expending more calories than a lean person, but not losing weight, then the obese person has to be consuming enough calories to replace those expended. That’s basic, and shouldn’t need discussion.

    The real discussion is about what factors influence how many calories we consume and expend. Which factors influence hunger and metabolism? Bray seems to highlight a combination of refined carbohydrates and fats (croissants? energy bars?) as being particularly likely to lead to eating more than we expend.

    His review seems to be motivated by the idea that Taubes says that one can lose weight without cutting calories or increasing exercise. Is that what Taubes says? Or does Taubes’ statement that “calories don’t make sense” mean something else? That it can be very difficult to properly count up how many calories we consume and how many we expend?

    Bray does state that “There are many kinds of obesity, and only some depend on diet composition. Genetic factors play a role as do the contributions of other environmental agents.” He points out that Taubes has misunderstood some facts on the progression of the science of obesity.

    Bray does concur “low-fat diets are as efficacious as other weight-reducing diets for achieving sustained weight loss,” and also “but not more so”.

    Taubes does point out some very interesting things. But he also fails to understand other interesting things. Whatever else you think of Bray, you have to admit he has been in the trenches for years, studying obesity, and studying how to study obesity. Finding scientific truths is like searching for an unknown island on an uncharted sea while blindfolded. The path is never going to be straight. Figuring out confusing this takes a lot of arguing things out and picking apart those arguments meticulously, looking for the holes, finding mostly blind alleys, and then looking for more holes.

    While it is true that Bray has been in the trenches for years, it is also true that his paycheck for laboring in these trenches has come primarily from the pharmaceutical industry. Dr. Bray is at the forefront of recommending drugs for just about everything. He thinks obesity can’t be treated with diet, but he thinks it is perfectly okay to treat the condition for life with a drug regimen. I find it difficult to trust the judgment of one with such a mind set.

  49. Of course we are fat because we consume excess calories – take Jimmy Moore for example – he put on 30 lbs. because he eats huge amounts of food – have you ever checked out his menus?

    Ultimately, calories count, even if you don’t count ’em. And this is nothing personal against Jimmy Moore! Just one more example of the failure of indiscriminate low carbing.

    It’s difficult to gain weight on an indiscriminate low-carb diet. The problem comes if the diet isn’t truly low-carb. I posted on this here.

  50. I thought, big deal, an establishment guy gave a skewed review. But, reading a little slower than all you guys, it turns out that George Bray is one of the main characters in Chapter 23, as one of the two people who waved their hands and ‘disappeared’ carbs from the national obesity equation in the early 70’s.

    When he says “Let me make my position very clear…”- yeah, yeah, I know, it’s in the book. Right after a quick summary of the then-current research and practice that said he was misguided.

    Chapters 13, 23, 12, and then 10 seem to be the good ones. I’m going to recommend them to some friends (the whole book is too much if you’re not already on board).

  51. Family Nutritionist – I’m evidence bray is wrong. I’ve lost all of my excess weight and have kepti t off for years (5+ on the low carb, 4+ maintaining a healthy BMI). How many obese people has Bray’s advice helped? Probably 0, except maybe a few who feel so hopeless and are so misinformed they are comforted by the “wait until we find a drug” line. On the other hand, Dr Eades, Taubes, Atkins etc has helped thousands of obese people, including myself, take control of their health and lose the weight for good. Bray is flat out wrong when he says carbs do not contribute to obesity, to the detriment of all people with obesity who might hear his message.

    The real ironic thing is I believe that pharmaceutical intervention is more efficacious if not mandatory not for weight loss but weight maintenance of a reduced weight. Perhaps not for people who’ve lost 20, 30 pounds but for people like myself who are maintaining a loss of 160 pounds I can say my body does not work normally after. My leptin level is extremely low (which I have had verified by doctors) even though my calorie intake and body fat is normal. This makes weight maintenance more diffiuclt than it should be, and causes numerous secondary problems (low T3 and low TSH, total infertility, immune system deficits, slow growing hair/nails, osteopenia and eventual osteoporosis, a return of glucose tolerance problems in spite of maintenance of a very low carb / moderate cal diet).

    My theory is that chronic high insulin, especially earlier in life, damages fat tissue by making fat cells grow, like a tumor of fat cells. This is the cause of morbid obesity, and explains why it is intractable for all except the most dedicated to weight maintenance. You cannot become normal weight again without being in a state that is metabolically like starvation because the fat cells no longer function properly with a normal fat mass (because there are so many of them, your absolute fat mass requirement increases for your body to maintain a state of non-starvation).

    If Dr Bray wants to get a drug approved for treating fatties, that drug should be leptin replacement during and after weight loss. … and this is ONLY required if you’ve already been damaged by insulin to the point that you were severely obese. Weight maintenance is the only place where pharmaceuticals can help, and that is only because of the damage done by insulin is not entirely reversible.

    Looking for a drug to fix the break in the regulating system, though, is freaking pointless because garden variety obesity is purely an issue of a diet too high in carbohydrates. The system works when you feed it properly.

    I guess research looking for that next “wonder drug that makes us thin” is a LOT more sexy and gets the dollars more than research for a drug that makes maintenance easier (but requires still eating a restricted diet for life).

  52. I am slightly off topic here, but I am getting quite irked by efforts to discount Taubes brilliant analysis by saying that he is “only a journalist,” and that more credence should be given to those “in the trenches.” First of all, Bray is not in the trenches, he is on the research sidelines. The Eades and other practicing physicians are in the trenches, or were. Their commitment is based on real world results with real people, not the results of drug tests in the lab.

    Still, one doesn’t get a good view of the war from the front lines. Most researchers don’t have time to look much past the the end of their own subject. That is why we need people who will look at the big picture. Taubes has the expertise to evaluate scientific findings. He took the time to examine the research. More important, he personally looked up every reference and verified it. He took all this unwieldy data and wrestled it into cogent, accurate prose. All the conclusions in the body of the work were statements by either the researchers themselves or by their professional peers. He presents the evidence with integrity, and gives us sufficient information to dispute the conclusions.

    He gives us the case as he sees it and gives us the critical tools to agree or disagree. He holds his conclusions until the last chapter and states them clearly. He makes no sweeping generalizations or dietary mantras (“Eat food. Not too much…”).

    That IS journalism, as it should be done, as it is most useful to us as a society. He has done us a great service and I hope he is well rewarded for his efforts.

    (Is Michael Pollen a journalist? No. Merely a paper blogger. No offense to you, Dr. Eades.)

    I agree with all your points about Gary. Nothing beats a good journalist to get to the bottom of an issue, which Gary certainly did as to the status of nutritional ‘science’ today.

  53. Hi Dr Mike:

    Sometimes I do okay with the assault on the low carb way of life. Sometimes, when I have been out in our society, and seen the faces of my fellow Americans, the obesity, the illness, I don’t do very well with it. I need to tell somebody about a front page article, dated August 1, 2008, in the St Pete Times, of St Petersburg, FL. A researcher named Jeffrey Krischer, a University of South Florida diabetes researcher who already had earned the school’s largest research grant, has won even more money for USF. He was awarded a $128 million, seven year grant from NIH to coordinate worldwide studies on prevention and treatment of Type 1 diabetes. That’s on top of the $169 million, 10 year NIH grant to study why diabetes rates are rising in young children. The other grants this man has brought to the school total $389 million. I’ll tell you at absolutely no charge why kids are getting diabetes. Unforgivable amounts of trans fat, high fructose corn syrup and other carbohydrates, mainly simple carbohydrates, are in their diet. They get very little meat, almost no fish or shellfish, few eggs, their vegetable regimen is corn and potatoes, their fruit is nothing, or an occasional apple or banana. they get little to no exercise. Their environments contain a lot of pollutants, and they may be on drugs for attention span or athsma that adversely affect their bodies. Conscientious parents give their kids a vitamin but what good can that do against all these other assaults to the developing body? Little children suffering from diabetes is heartbreaking. How can people ignore the truth? thanks for listening.

    robyn cardy

    ps I read the comments to this post. my husband and i have it easy. we get lots of exercise, weightlift and run (he runs lots less than I do, I like it he doesn’t) and if we stick to lean meat and low carb veggies, we stay very lean, and my husband stay incredibly muscled up. the guy is so heavily muscled he looks like he takes performance enhancing stuff and he has never touched it. he simply has a low carb diet. I guess I sometimes underestimate how hard low carb can be for some folks. thank you again for all you and MDE do.

  54. ItsTheWoo,

    Leptin won’t help (they’ve tried it) because if your insulin is chronically high, so is your leptin. And leptin resistance goes hand in hand with insulin resistance. So giving leptin to fat people is like giving insulin to hyperinsulinemic people. They unfortunately already have too much leptin but their brain won’t listen to its signals.

    I should know. I was one of those people.

    Fortunately, bringing excess leptin down and making brain more sensitive to leptin takes just the same measures as bringing high insulin down and making the tissues more sensitive to insulin: eating foods that don’t require much insulin. I.e. low carb foods. I’ve reduced my insulin levels almost by 500% in just 5,5 months. No drug can do that. You can imagine the weight loss that followed …

    And talking about drugs, maybe pharmaceuticals can help with weight maintenance. But why use pharmaceuticals when you can use Protein Power or other similar plans to achieve the same goal and even surpass it?

  55. Xenia – Oh I know leptin won’t do anything for weight LOSS… weight maintenance is another story. The weight reduced obese are leptin deficient, and this is a major cause of weight maintenance failure and a return of cravings/hunger that leads to diet failure.

    When you give leptin to weight reduced people they can maintain weight much more easily.

    An article about a study in june which demonstrates leptin allows people to maintain weight after a diet

    I speak not only hypothetically but from personal experience. I have lost over 100% of my body weight. This has left me with a leptin level that is almost non-existent and I have all symptoms of leptin deficiency (other than obesity, of course). I am pariticpating in a study for hypothalamic amenorrhea which involves leptin replacement. Since starting a very low dose leptin all of my symptoms (including infertility) are much, much better! I feel like a normal weight person, it is very easy to eat normal calories, my glucose tolerance is better (less hypoglycemia) and I have so much more energy. I have had menses again when I haven’t had them in four years (after all the weight loss).

    Don’t get me wrong – a low carb diet (like protein power) is essential to STOP obesity, and to reduce weight… but this obesity thing is a lot more complex and permanent than insulin stuffing food in fat cells. I believe that insulin damages the fat tissue, possibly because insulin makes too many fat cells grow in morbid obesity (sort of like a tumor). Google “insulin adipocyte hyperplasia”.
    Because of how insulin changes the fat tissue permanently, dieting alone will not allow you to maintain a low fat mass normally (i.e. without metabolic consequences). Your depleted fat tissue will behave as if starving because the glut of depleted fat cells does not make leptin normally (even if your absolute fat mass is within a healthy range, your number of fat CELLs are not in normal range so you have a whole lot of small fat cells that act as if starving).

    This is not something I”m making up… I actually had blood tests and it was all verified. My leptin level was extremely low.

    Low carb will bring your insulin down and stop the disease process.
    However, once developed, obesity is intractable because insulin changes the body and fat tissue in such a way that a high weight becomes “normal” weight. Leptin supplementation is a major, major part in allowing the previously obese to achieve a normal weight without starvation symptoms.

    • to maintain a weight loss where leptin is low,would liposuction be a good choice?

      i,ve often thought that because obesity causes a growth in the number of fat cells(appears to be permanent)then one of the best therapies should be to reduce the total number of fat cells.

      reduce through a low carb diet along with permanent fat cell removal through lipsuction.this should return the system to normal.

      any thoughts?

  56. What are we to do (as physicians) to at the very least open the eyes of our colleagues to the flawed minimally-based ‘theories’ (ie Bray) of obesity, weight gain/loss and nutritional health? Merely by asking these questions among my colleagues and with my patients (and friends for that matter!) has caused a flurry of consternation… If this is what it takes to stimulate a re-evaluation based on sound scientific method then count me in….

    Hey Doc–

    Glad to have you join the fray. I’m sure it will prove to be an interesting ride for you.



  57. Ouch, guys. It’s “renowned.” Don’t you folks have copy editors?

    We do now. Thanks. At least is wasn’t ‘reknowned.’



  58. “I would suspect that Dr Bray does not want to bite the hand that feeds him.”

    Exactly. I’m sure that a defense of his own career is the least of Dr. Bray’s conflicts of interest. Just one more pseudoscientist in the pocket of larger interests.

  59. The discussion about leptin (above) begs the NEXT question:

    Assuming the ‘insulin connection’ is dealt with, what can an obese (Or FORMERLY obese) person do to NATURALLY increase his/her leptin sensitivity?

    I would expect that time at the new lower weight would help, but I don’t know for sure. I don’t think the issue has been studied. And I would make sure to keep my triglycerides low so that the leptin I did have could easily get into my brain.

  60. This has been a very interesting discussion. I’ve had to read more and think more to try to understand. It seems that Taubes and many of you are pointing out that Bray is missing the point that, in some cases, the body preferentially stores available energy as fat rather than keeping it readily available for daily activity. So, even though the obese individual expends more energy than his thinner counterpart, the body is focussing on feeding the fat cells, not emptying them to cover the excess energy requirements. The individual feels low on energy and hungry enough to keep eating, even though he doesn’t appear to need additional calories or nutrition. This is the context, I think, of the assertion that overeating and sedentary habits can be a consequence of weight gain rather than the cause. Have the studies been done to test this hypothesis from end to end, with no missing links? It seems it would be very subtle and complicated to prove or disprove.

    I read “Dr. Neal Barnard’s Program for Reversing [type II] Diabetes”, in which he focusses on the role of fat stored in muscle cells in causing insulin resistance in individuals who have a tendancy to store fat in their muscle cells (who also tend to have relatives with type II diabetes). This can lead to the whole metabolic syndrome spiral. He has clinical trial results that show his good carbs, VERY low-fat vegan diet with exercise is effective for weight loss, improved insulin sensitivity and improved cholesterol.

    In the other corner is Dr. Richard Bernstein, whose “[type I or II] Diabetes Solution” involves “a low carbohydrate diet and exercise”. There are studies that support his approach for weight loss, blood sugar control, and improved blood lipids.

    So there is more than one way to skin a cat. When Bray says “Weight loss is related to adherence to the diet, not to its macronutrient composition.” he is rolls several valid ideas into that one statement, but misses issues that statement does not address. Like — what influences adherence to the diet, do some diets just make weight loss more difficult, and why can’t everyone lose weight on a Michael Phelps diet?

  61. “what influences adherence to the diet, do some diets just make weight loss more difficult, and why can’t everyone lose weight on a Michael Phelps diet?”

    I gave up on dieting because I was so hungry and so tired all the time. I couldn’t adhere to a lowfat or calorie restricted diet very long. When I started eating fewer carbs the constant hunger went away, my appetite was cut in half.

  62. Hi , Dr Eades.

    You’d think that Dr. Bray being a doctor (who probably is a statinator) would realize that statins have 11 other very strong effects besides mere cholesterol lowering.

    You’d think he could figure out that non – statin cholesterol lowering trials have been complete failures for reducing CAD deaths. And that dietary cholesterol lowering clinical intervention trials also have been failures. You’d think he’d take note of the JUPITER and ENHANCE trials. You’d also think he would know (as Dr. Uffe Ravnskov points out ) there is no dose response with statins.

    You’d think he’d realize any ( slight ) reduction in CAD deaths amoung patients WITH CAD from the use statin drugs is enitrely due to these 11 effects , epsecially in light of the above mentioned evidence.

    It really amazes me just how many doctors can’t seem to grasp that just because statin drugs (which lower cholesterol, but also do a myriad of other things ) lower CAD death rates amoung patients WITH CAD a little bit, doesn’t mean cholesterol lowering is the mechanism. They can’t seem to seperate mere cholesterol reduction from the use of statin drugs. Cholesterol lowering trials using non statin drugs (which have no pleotropic effects) and their lack of benefit should make this blatantly obvious to them , you would think.

    For example The Lipid Research Clinics Coronary Primary Prevention Trial found that out of 3,086 pateints those taking cholestyramine had 30 CAD deaths vs 38 in the controls. Total mortality was 68 in the treatment group vs 71 in the controls. Another non – supportive result amoung many for the cholesterol theory proponents.

    If anything statin drugs strongly challange the lipid hypothesis.

    Take Care,