Gary Taubes responds
A couple of weeks ago I posted that Gary Taubes had agree to answer questions from readers of this blog. Over a hundred readers sent in questions through the comment section. Many of these questions were actually multiple questions, so Gary ended up with probably 200+ questions to deal with.
I’ve gone through and compiled a list of the most common questions and presented them to Gary. Here are the questions followed by his responses.
The most commonly asked question was how do Asians and others living a seemingly high-carb existence manage to escape the consequences?
The Asian question first. I do address this in the book and I address it again in the afterward of the paperback. There are several variables we have to consider with any diet/health interaction. Not just the fat content and carb content, but the refinement of the carbs, the fructose content (in HFCS and sucrose primarily) and how long they’ve had to adapt to the refined carbs and sugars in the diet. In the case of Japan, for instance, the bulk of the population consumed brown rice rather than white until only recently, say the last 50 years. White rice is labor intensive and if you’re poor, you’re eating the unrefined rice, at least until machine refining became widely available. The more important issue, though, is the fructose. China, Japan, Korea, until very recently consumed exceedingly little sugar (sucrose). In the 1960s, when Keys was doing the Seven Countries Study and blaming the absence of heart disease in the Japanese on low-fat diets, their sugar consumption, on average, was around 40 pounds a year, or what the Americans and British were eating a century earlier. In the China Study, which is often evoked as refutation of the carb/insulin hypothesis, the Chinese ate virtually no sugar. In fact, sugar consumption wasn’t even measured in the study because it was so low. The full report of the study runs to 800 pages and there are only a couple of mentions of sugar. If I remember correctly (I don’t have my files with me at the moment) it was a few pounds per year. The point is that when researchers look at traditional populations eating their traditional diets — whether in rural China, Japan, the Kitava study in the South Pacific, Africa, etc — and find relatively low levels of heart disease, obesity and diabetes compared to urban/westernized societies, they’re inevitably looking at populations that eat relatively little or no refined carbs and sugar compared to populations that eat a lot. Some of these traditional populations ate high-fat diets (the Inuit, plains Indians, pastoralists like the Masai, the Tokelauans); some ate relatively low-fat diets (agriculturalists like the Hunza, the Japanese, etc.), but the common denominator was the relative absence of sugar and/or refined carbs. So the simplest possible hypothesis to explain the health of these populations is that they don’t eat these particularly poor quality carbohydrates, not that they did or did not eat high fat diets. Now the fact that some of these populations do have relatively high carb diets suggests that it’s the sugar that is the fundamental problem. Ultimately we can only guess at causes using this kind of observational evidence. To know anything with certainty we’d need the kind of randomized controlled trials I yearn for in the epilogue of GCBC.
What is your opinion on leptin in the grand scheme of obesity and fat storage?
I mostly ignore leptin in the book because I think leptin is primarily a signaling molecule and so a downstream effect. In other words, leptin is secreted from the fat cells; it doesn’t regulate directly the amount of fat that accumulates. Moreover, if the primary regulator of fat storage is insulin, which it is, and leptin is secreted in proportion to the amount of fat stored, which it is, then insulin has to regulate leptin.
Where leptin may play a primary role is in the liver. A few years ago Jeff Friedman of Rockefeller University published an article in Science showing that leptin down-regulates SCD-1 in the liver (the only place they looked), which worked in turn to increase oxidation of fatty acids. This makes sense homeostatically: if leptin is released in proportion to the fat accumulated then it is a signal of how much fat we have in reserve. So long as the mitochondria in our lean tissue and organs know that we have fat in reserve, they can continue to burn it without fear of systems failure should they run out of fuel completely. Leptin resistance would then work, like insulin resistance, to make us burn less fat and store more, while the rest of the body would have to rely on carbohydrates (blood sugar) for fuel.
In general, though, I’m interested in the cause of obesity and I don’t think discussing leptin adds much. Here’s what I say about this issue in afterward of the paperback edition of GCBC:
“Another variation on the can’t-possibly-be-so-simple argument that I have heard frequently since Good Calories, Bad Calories was published is the molecular biology theme. The last fifteen years, since the discovery of the hormone leptin in 1994, has seen obesity research become a sub-discipline of molecular biology. As a result, a search of the keyword “obesity” in the National Library of Medicine database will now identify over 100,000 relevant articles in the professional journals (nearly 20,000 review articles alone), a large proportion of which focus on the fruits of molecular biology research and the science of genomics.: It’s a burgeoning field with a cast of thousands, including the role of obesity-related gene variations known technically as polymorphisms, of signaling molecules with names like adiponectin, leptin and grhelin, of the receptors for those signaling molecules and the inhibitors for those molecules and inhibitors of the inhibitors, and so on. The obvious question is how can this research be so extraordinarily fruitful, and yet mostly irrelevant to the cause of obesity? It’s hard to imagine it’s not, and so, as I’ve frequently been told, any discussion of the cause of obesity that doesn’t discuss these molecules, receptors, inhibitors, etc. must be considered amateurish and woefully inadequate. The truth must be complicated.
“Again the counter-argument seems itself simple and straightforward: if you’re hit over the head with a hammer, it will cause both pain and inflammation. The mechanisms of pain and inflammation have also yielded up a wealth of knowledge to the tools efforts of the molecular biologists. These physiological phenomena are understood to be mediated via signaling pathways and molecules (in this case, prostaglandins, tumor-necrosis factors, etc.) that emerge in response to the damage done. The more researchers learn about these responses and the molecules involved, the more complex the pathway from hammer to pain and inflammation to healing will appear. But the relevant fact to all those immediately involved is that both the pain and ensuing inflammation were caused by the hammer and perhaps the person who swung it. Everything else is downstream and may be relevant only to the question of which drugs will best deal with the pain and perhaps accelerate the healing process. “
A number of questioners asked why you think it is more difficult to lose weight the second or third time around on a low-carb diet? And why it seems more difficult to lose on low-carb with increasing age?
I’m curious whether this is in fact true. Another possibility is that it’s more difficult to lose weight on low-carb as we get older; that the carbs effectively do chronic damage to our tissue and so the longer we’ve been overweight or obese, the harder it is to lose weight. I can imagine a scenario in which the fat tissue becomes hypersensitive to the insulin we secrete, or the pancreas becomes hypersensitive to the carbs and secretes even more insulin, or the insulin resistance in the lean tissue becomes less tractable, and so the longer we remain fat, the more our fat tissue compensates when we restrict carbs. It’s also possible that repeated low carb dieting somehow exacerbates this process, but I’d want to see definitive studies (and on all this speculation) before I believed it.
Several people asked for a comment on any important studies that you may have left out of GCBC.
The issue isn’t leaving out studies so much as not wanting to get into the he-said, she-said game of quoting particular studies that support my preconceptions. In this business, you can always find studies that support a particular hypothesis, or at least seem to if you selectively interpret the data. So when I had to make a point about the efficacy of a particular treatment — exercise, for instance, or semi-starvation diets — used meta-analyses or Cochrane Collaboration systematic reviews, which are designed to minimize author bias, to make the general points. When I discussed the saturated fat/cholesterol/heart disease hypothesis in the first few chapters, I did indeed mention virtually every study and certainly every meaningful clinical trial, because I knew if I left anything out I would be accused of cherry picking the data (which, of course, I was anyway). I did omit much of the observational epidemiology on the nature of a healthy diet because I find it meaningless and impossible to interpret correctly, in part for the reasons I discussed above about the Asian diet issue.
When I cut the book down from the initial 400,000 word unfinished draft, a lot of what was removed were indeed the counter- and counter-counter arguments. For instance, obesity researchers will argue that obesity causes hyperinsulinemia, not the other way around. That way they can still say that obesity is caused by over-eating and once we get fat, that causes insulin resistance and jacks up insulin levels. I spent, literally, months writing a lengthy section explaining how this view came about and what the evidence actually did and did not demonstrate. Then when I realized the book had to shrink dramatically, and with the benefit of sage advice from my editor, I decided that it was unnecessary to explain why the mainstream researchers would disagree with my take and then spend yet more space explaining why they were wrong to disagree. One thing I did cut from the book that I regret was a section linking gout to fructose and uric acid, and discussing the history of gout and how it’s frequency in populations and socioeconomic groups paralleled the spread of sugar. Nobody had ever made that point before and I wanted to make it, considering that people have been speculating on what aspect of diet or lifestyle causes gout back to Hippocrates. Still, my friends rightly argued that when your book is a few hundred thousand words long, you can’t afford to keep a section about gout, even if a lot of people get gout these days and, of course, they’re more likely to get it if they’re overweight or obese. Along these lines Dan Harrington asked why his gout goes away on the Atkins diet and that’s my answer: no sugar, primarily, means no fructose and so no fructose-induced hyperuricemia. In other words, fructose raises uric acid levels and gout is caused by the elevated uric acid in the blood stream.
It is true that you can find studies in the literature that seem to contradict the hypotheses in GCBC but are not mentioned in the book, When Gina Kolata reviewed my book in the NY Times, she evoked a study by Jules Hirsch and Rudy Leibel, then both at Rockefeller, suggesting that nutrient composition of the diet has no effect on weight. As I explained in a letter to the Times, the study failed to refute the carbohydrate/insulin hypothesis of weight regulation for a variety of reasons — the subjects, for instance, could have gained as much as 15 pounds a year on one particular diet composition but not another, and the study would not have detected it. And the subjects, almost exclusively, were lean middle-aged individuals. What we’re interested in here, though, is why why people predisposed to obesity get fat, and that may not be something you can study in people who have remained lean into their 40s and 50s. Would Leibel and Hirsch have obtained a different result if they had used, say, obese subjects who had first been slimmed down by some kind of diet (Atkins or a starvation diet)? These types of subjects are considered pre-obese, since they’re so highly likely to go back to being obese. And if Leibel and Hirsch had used them, they might have found that they stay relatively lean on a low carb diet and put on weight easily on a high carb diet. Anyway, rather than get into this kind of too-and-fro in the book, I made the decision not to mention these types of ambiguous studies. I would like to think that had there been a single compelling study refuting the hypothesis — or better yet, two, since you’d like to see things replicated in science — I wouldn’t have written a different book.
What you think of a Slow Burn type of exercise and low-carb dieting? Do you still stand by your notion that exercise doesn’t help people lose weight?
I haven’t looked into the science behind slow burn exercise (although I know Mike has) but I now do it regularly (with Fred Hahn in Manhattan at Mike’s recommendation) and it seems to be helping my lower back pain immensely. I can let you know next spring whether it helps my softball game, where my ability to hit with power has been deteriorating sadly with the advancing years. What fascinates me about it is the weird confluence of the desire for self-improvement with what seems to be deep-set sadomasochistic tendencies. It’s torture when you do it, and then you look forward to going back.
As for exercise, I do not believe that it causes long-term fat loss. I think it might be helpful in a weight loss program only because it gives you a kind of positive feedback that dieting per se does not. You can feel good after a work-out, while it’s hard to feel too good after a meal that didn’t include either the calories or the carbohydrates you preferred. On the other hand, since it does make you hungry — work up an appetite — I worry whether for some or even most people the psychological benefits could be counterbalanced by the drive to consume even more calories than you might have expended during the work-out.
Are you familiar with the work of Dr. Jan Kwasniewski, and, if so, what do you think of it?
I am not.
What kind of response have you gotten from the medical/scientific community about GCBC?
In general, I think it’s safe to say that I’ve been ignored. If obesity researchers have read the book, they haven’t bothered to tell me. When GCBC was published we sent out 150 copies to obesity researchers, authors of obesity task force reports, foundations that fund obesity research, everyone at NIH who funds obesity research, etc. etc. I heard back from 3 or 4 thanking me for sending them the book. Two followed up to tell me they had read it. Some later told me outright that they didn’t have the time to read a 500 page book, and particularly so when they already know what I think because of the 2002 NYT Magazine article and don’t particularly agree. That said, I may be making some progress in getting people to pay attention.
Whenever I do hear from someone who is sympathetic, I ask them to try to set up a lecture at their institution. Often I ask them to contact other researchers they might know and get me lecturers at those institutions. Through this kind of networking, I’ve been invited to lecture at some of the more influential obesity research centers and at least some of those people have taken my arguments seriously. A few months ago, I heard from some contacts at the NIH, that I might be invited down to lecture to the nutrition coordinating committee at NIH, which would be a big step forward, but the fact that I haven’t heard anything since then (August) makes me pessimistic.
When I do give these lectures a common response that I get from nutritionists and obesity researchers, and one that I find profoundly disturbing, is that they find what I say interesting but don’t see it as anything they should think about further. In other words, they have their schtick (as my wife, an almost-academic calls it); whatever research they get their funding to pursue, and even though in theory we’re all in this to cure and prevent obesity and chronic diseases, their schtick may have nothing to do with my schtick. If they’re studying, say, genetic strains of obese rats or questionnaires to improve the accuracy of diet assessment in epidemiologic studies, what does that have to do with my argument that obesity is caused by carbohydrates? So they listen politely, ask a few intelligent questions (in an ideal world) and then go back to their research, because that’s how they make a living. They don’t say to themselves, I’m going to read Taubes’s book and, if I find it compelling, switch my research over to studying the efficacy of carbohydrate restriction. And even if they did, they wouldn’t get funding to do so because they’d have no track record in that field.
So, bottom line, at the moment is that I know of a handful, maybe as many as a dozen researchers, who find the arguments in the book compelling and are doing what they can, in their limited spare time, to help get the message out and maybe get us to the place where the hypotheses are taken seriously and are rigorously tested. The rest either don’t care or don’t know GCBC even exists or just think what I say is wrong and so not worth further discussion, either because they read the book or some of it and think its crap or because they think its crap based solely on what they know about me or heard about the book and so don’t have to read it.
What’s next? Another book?
What am I doing next? As suggested by many readers, I am going to write a short, easy-to-read version of the weight section of GCBC. It won’t be a diet book — no recipes — but it will be far more of a self-help book than GCBC. I might also do a weightier (no pun intended) serious investigation into the sugar and corn syrup industries; their history, political influence, lobbying, etc — that would be interwoven with a more intensive look at the potential health effects of sugar and HFCS and fructose particularly. The first book will definitely be done; the second depends on getting the funding to do so. I’d also like to get back to straight science writing for a while, since I do enjoy writing about good science, which is how I started my career, and it would be a pleasant change from the mainstream nutrition and health nonsense.
How about a blog?
As for a blog, I just haven’t got the time at the moment, although I always hope that that will change in the future.
Many wrote that GCBC had changed their lives. Can you think of a book that has changed your life?
Did any books change my life? Yes, All the President’s Men, by Woodward and Bernstein. I read it in my last year of college or my first year of graduate school and it made me decide that I wanted to be an investigative reporter rather than go to business or law school, which was the direction I seemed to be headed.
What do you know about Dr. Simeon’s HCG protocol?
What led you to the idea that saturated fat doesn’t cause heart disease?
It was a progression of steps. Back in the late 90s, I was reporting a story for Science on the salt-hypertension controversy and one of the worst scientists I ever interviewed (and having written a book about cold fusion, Bad Science, I had interviewed quite a few terrible scientists) took credit not just for getting Americans to eat less salt, but getting them to eat less eggs, meat and butter, too. I literally got off the phone with this guy and called my editor at Science and said, “when I’m done writing about salt, I’m going to do a story on dietary fat. I don’t know what the story is, but if this guy was involved in any substantive way, I know there’s a story to be done.” So that’s what I did. I finished the salt story and then spent a year working on the fat story, which was published in Science.
The story made the point that there was virtually no evidence that a low-fat diet prevented heart disease, but let open a window for saturated fat having some deleterious effect. Then a couple of years later, I was reporting the New York Times Magazine story that would become “What If It’s All A Big Fat Lie?”, when I heard about these five clinical trials comparing low-fat, calorie-restricted diets to Atkins diets. Since the Atkins diet is a high-fat, high saturated fat diet and it improved cholesterol profiles in all these trials, that pretty much clinched it. I’ve been arguing since that these diet trials have to be perceived as tests of the hypothesis that saturated fat is a “bad” fat, although the medical establishment still prefers to ignore that fact.
Is there anything new or updated in the paperback version of GCBC or is it the same as the hardback?
It’s the same as the hardback, but there is a 3000 word (or thereabouts) afterward that’s worth reading.
I tried to come up with a selection of questions that represented the majority of questions asked. I know that some went unanswered, but when Gary agreed to do this I promised him that he wouldn’t have to answer an exhaustive list that would require days of time. So, I’m sorry if any specific question went unanswered, and I hope you understand. Thanks to everyone for the terrific response.