Gary Taubes on why we get fat and the future of nutritional advice. Interview (part 2).

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Here is the other part of our interview with Gary Taubes, an internationally recognized journalist and science writer, the author of Nobel Dreams (1987), Bad Science: The Short Life and Weird Times of Cold Fusion (1993), Good Calories, Bad Calories (2007) and Why We Get Fat (2011). Before continuing you may first want to check out part one of this Q&A.

This time Gary discusses the science behind the carbohydrate hypothesis and speaks about the health benefits of high-fat diets, he also comments on the toxic-environment hypothesis and the future of nutritional advice.

You are an advocate of the carbohydrate hypothesis  of obesity and chronic illness, the so-called the insulin theory. According to this concept it is the consumption of carbohydrates, especially refined ones, that leads to weight gain and sickness. Why are dietary carbohydrates, not fats, uniquely fattening? What is some of the most compelling scientific evidence behind this theory? Why does this paradigm offer a better explanation for the current obesity and chronic disease epidemic than the fat-cholesterol hypothesis?

The carbohydrate hypothesis is simple. What is a given is this well established scientific fact, present in the textbooks and absolutely non-controversial, that hormone insulin regulates fat accumulation, i.e. the amount of fat we carry in our fat tissue. Another given, also found in the textbooks, is that insulin levels in our blood stream are more or less determined by the carbohydrates in our diet. So the carbohydrate hypothesis merely puts those two non-controversial facts together: if insulin levels are determined by carbohydrates, and fat accumulation is determined by insulin, then, fundamentally, it’s the carbohydrates in our diet that drive fat accumulation and, so, are making us fat.

Among the compelling evidence to support this view is the fact that we have observations of populations that never ate western diets, didn’t eat sugar and refined carbohydrates, which are most insulin-stimulating nutrients, and these populations tend to be lean. However, when they add sugar, flour and refined carbs to their diets, they start getting obese and diabetic and they get heart disease. As an association, it’s a compelling one.

Then there are experimental trials that show that when people go on carbohydrate restricted diets they tend to lose weight relatively effortlessly, independent of the calories they consume. They are allowed to eat as much as they want. Then there’s evidence showing that if you give a type 2 diabetic insulin therapy, for instance, or give them drugs that stimulate insulin secretion from the pancreas, they get fatter. And if you give them drugs that lower insulin secretion, they get leaner. This can also be shown in animals.

So there’s a whole line of evidence and it would be very easy to test rigorously, if the medical and nutrition community thought it was worth testing, which is the challenge that we have.

Many observers argue that not only is the diet-heart hypothesis scientifically wrong , but it has also contributed to the growing problem of obesity, diabetes, heart disease and other chronic ailments of the West. In other words, the current low-fat paradigm may have created many of the problems it was initially supposed to fix or prevent. Would you agree with this opinion?

Yes, I agree. The very first article I wrote on this subject back in 1999, titled “The Soft Science of Dietary Fat” in the journal Science, looked at how this belief that a low-fat paradigm is good for health evolved, and how it was locked in as conventional wisdom between 1977-1984. This prompted the food industry to start generating all these low-fat foods and we began to believe that we should eat them. But if you remove the fat, you tend to eat more carbohydrates. So what happened was that the kinds of carbohydrates that in the 1960s were believed to be uniquely fattening became, by the 1980s, “heart-healthy diet foods”. In effect, the base of the famous food guide pyramid that the USDA began publishing in the US were all the foods that my mother’s generation believed were inherently fattening e.g. bread, rice, pasta, potatoes etc. They are all low in fat but high in easily digestible carbohydrates. Meanwhile, sugar consumption also started going up, in part because of a theory circulating at the time – considered corroboration of the low-fat doctrine — that if a food didn’t have fat in it, it couldn’t make you fat. So sugar, being fat-free, got a free pass.

Very quickly low-fat foods, which were high in sugar and easily digestible carbohydrates, became portrayed as “heart-healthy” and industry started producing them by the thousands. And what you can see is that these changes in our national diet happen in coincidence with the obesity epidemic. It is at this time that we started eating marginally less fat and more carbohydrates, much of which was sugar or high fructose corn syrup (HFCS), which are effectively the same thing. So there is observational evidence that supports the idea that as you increase the consumption of carbohydrates and particularly of sugars, you increase the adiposity of the population with it.

If you look at the experimental evidence, not only does it refute the diet-heart hypothesis, but it also suggests that the diets that we have all been told will kill us (high in meat, eggs bacon, butter, cream etc.) are actually the healthiest diets out there. These trials suggest that if you go on a high-fat, carbohydrate-restricted diet you’ll not only lose weight by eliminating foods that are making you fat, but you’ll also improve your heart disease risk factors. And by this I mean the risk factors as scientists understand them in 2012, not necessarily the old risk factor concepts from the 1970s — total cholesterol, LDL cholesterol and other effectively meaningless variables.

The conventional wisdom of obesity and chronic diseases has in recent years been backed up by the toxic-environment hypothesis. It says that people become obese and ill not only because they overeat, but also because our environment (the food we eat, the air we breathe, the water we drink etc.) is becoming increasingly toxic. For instance, the critics of meat-based diets often claim that eating meat, which is filled with chemicals and antibiotics, can cause many health problems, most significantly cancer. What is your take on the toxic-environment hypothesis?

I do think that the environment is toxic, but I am not sold on the idea that it’s all those chemicals, hormones in the meat etc. that are driving the obesity and chronic disease epidemic. Why not? Well, a whole body of observational evidence existed prior to the 1960s suggesting that the major chronic diseases that beset us – the whole cluster of westerns illnesses including obesity, diabetes, heart disease, cancer, gout, hypertension etc. – appeared in populations at pretty high levels as soon as they started eating sugar and flour. They could be relatively isolated populations, but they would still have high levels of heart disease, diabetes and obesity, once they started eating sugar and flour. And although these are observations, associations, the evidence suggests that the diseases we’d like to blame on toxic chemicals and hormones in our meat became common long in populations long before the toxic chemicals and the hormones did.

In the 1970s and 1980s leading cancer epidemiologists were castigating the environmental movement for hijacking, in effect, data that linked cancer to some aspects of the environment. While researchers would emphasize some aspect of food or lifestyle, the environmental movement chose to implicate chemicals and succeeded in making us sensitive to the environmental chemicals issue, even though these could only explain a tiny proportion of cancer rates. So the toxic-environment hypothesis could be true, the proposed toxicity could have an effect, but before I would believe it, I would want to see a population that didn’t eat sugar and refined grains, but still had the same level of these environmental pollutants, hormones in the meat etc. That kind of a population might tell us what diseases can be attributed to those environmental factors rather than just sugar and refined grains and their effect on insulin signaling.

You have recently published an extensive article in “The New York Times” titled “Is Sugar Toxic” discussing the impact of sugar on our metabolism and health. Why is it such an important issue to investigate?

We have historical data showing that when populations began consuming relatively large portions of sugar and refined grains they would get all the major chronic diseases that we suffer from today. What’s interesting is that there are populations that eat very high-carbohydrate diets and have obesity and diabetes (e.g. South Pacific islanders, Caribbean islanders), and there are populations that eat these high-carb diets and have very low levels of obesity and diabetes, for instance Southeast Asians.

In the light of these observations we need to ask the question – what’s the difference between these two scenarios? One possibility is that I’m completely wrong in postulating that it’s the carbohydrate content of diet that matters. The other possibility is that it’s the sugar content that makes the fundamental difference. Accordingly, the populations that ate high sugar diets had obesity and diabetes, while those that ate low sugar diet didn’t have these diseases. So the South Asians, who traditionally had very low sugar diets, had low rates of obesity and diabetes despite eating relatively carb-rich diets. This is one reason why the sugar question is so important. It says that one epicycle to the carbohydrate hypothesis is that sugar is necessary to trigger the fundamental insulin resistance. That then leads to elevated levels of insulin and all the other hormonal, metabolic problems we’re discussing here. In addition, there is all this research from the 1960s onwards that’s been building lately showing that sugar, by which I mean the combination of fructose and glucose (so both sucrose and HFCS), can be uniquely capable of causing insulin resistance in laboratory research.

Thus the difference between the two scenarios described above is the idea that sugar is the fundamental problem, and if we didn’t eat sugar, if we never ate sugar, if our parents didn’t eat sugar, we could eat all the other carbohydrates with impunity. But once we start eating significant amount of sugar, and what “significant” means is open to debate, then all the other carbohydrate in the diet become problematic.

In Good Calories Bad Calories you documented and discussed an massive amount of scientific evidence showing how the dominating low-fat paradigm is wrong and why adopting the carbohydrate hypothesis may be a much more effective strategy to conquer obesity and chronic illnesses. What was the rationale behind your decision to write your new book Why We Get Fat? What objectives do you want to achieve with the new book? How would you recommend Why We Get Fat to Polish readers? (Polish edition of Why We Get Fat is about to be published)

Good Calories, Bad Calories is a huge, 500-page tome. I wrote it because I wanted to convince the authorities, the experts and the researchers of the power of this argument. I didn’t ever want to say “trust me on this”. My tendency is to err in giving more evidence rather than less, so the book goes into a great deal of detail following the various trails of the arguments – both historically and scientifically. After I wrote GCBC, I realized that nobody had time to read a 500-page book arguing that everything you know about nutrition is wrong, particularly the experts themselves.

And then I started getting emails from people, letters from readers saying “Look, this book changed my life. It’s the most important book I’ve ever read. Now would you write one that my husband could read? Or my son could read? Or my doctor could read?” I get letters from doctors saying “Would you write one that my patients could read? One that isn’t 500 pages, one that gets the point across, but does it much more simply and is easier to read”, something we would call in the US an airplane read, in that it can be read easily on a plane flight from, say, one coast to the other.

This is why I decided to write Why We Get Fat. It’s more argumentative and less historical, it makes the argument as though I’m a prosecuting attorney making the case to judge and jury in a criminal case. It’s relatively short; it’s less dense, less scientific in its details than GCBC, so I hope much more readable. And I think it’s been proven that with WWGF I’ve started to have much greater effect on how people perceive this problem.

It is sometimes the case that a thinker aspires to become an advisor to “The Prince.” Is your ambition to influence health authorities and thus shape the policy-making, or do you see your work as a purely intellectual mission aimed at winning the struggle for “the truth”?

I would say that it’s a little of both. Once you come to the realization (or delusion, if I’m wrong) that the entire public health, medical, research community worldwide has simply missed the point, that they’re misunderstanding, mistreating, mis-preventing the most important chronic disease of our era, (in the US, for instance, obesity and diabetes are overwhelming our health care system), it’s hard to just walk away and not want to do something about it. The truth is important and getting it out there is important, but once you believe you have the truth on a very important issue, it seems inherent that you have to act on it. So I am acting on it.

I don’t know if I would describe myself as becoming ‘an advisor to the Prince’, but I certainly want to influence health authorities and shape policy-making, so we can get this problem solved and, hopefully, 20, 30, 40 years from now stop arguing about it. I believe obesity and diabetes are simple problems to solve if the medical community understands what the cause is. This is what I am now committed to achieving. I just hope I’m right.

As a best-selling science author over the last several years you have been busy giving lectures and presentations to students, health professionals and public officials at major research centers and universities across the USA. You have also appeared in the mainstream media discussing health and diet issues with doctors and dieticians. How is your work received by the US medical community and public authorities?

The ideas are spreading and I am definitely making progress in the United States and around the world. Now I have a team working with me to help get these ideas across. Every day I hear from people reading the books; I hear from physicians and researchers, from professors and department heads at universities down to graduate students and undergraduates, who have read the books and found them compelling.

Nonetheless, that’s still a very tiny percent of the people we have to reach. For instance, quite recently the „New York Times” had a story by one of their health reporters, Tara Parker-Pope, on dietary fat and obesity and on why she cannot lose weight. But it’s all the same conventional wisdom about energy balance. And I’ve written for the „New York Times”, I’ve done my most influential articles for this magazine, and I can’t even convince its editors or this author, Tara Parker-Pope,that there exists an alternative hypothesis of obesity that should be taken seriously. Obviously, a lot of work has to be done and it could take 10 years; it could take 50.

We’re accumulating supporters every day, and that’s the numerator, but the denominator is still enormous. I have a colleague, Peter Attia, who likes to quote Malcolm Gladwell to the extent that says we have to get 10 to 20 percent of physicians to buy into our views, and then the conventional wisdom will start to shift. We’ll start shifting the paradigm on a huge public health level. I would argue we have a hundred or a thousand times more supporters than we had four years ago, when GCBC first came out, but that’s probably still less than 1%. So we have a long way to go.

It is becoming increasingly evident that the entire low-fat/high-carb, calories-in-calories-out paradigm is a colossu s with feet of clay. On the one hand, many conventional views on a “healthy diet” have recently come under growing criticism from the research community. On the other hand, more and more ordinary people become disillusioned with the low-fat health advice and turn to various types of low-carb lifestyles and theories, the paleo hypothesis being an example. What do you think is the future of the low-fat paradigm? Is it going to go away, is it going to be replaced by another dominant theory, or is it likely to be downgraded and become one of many competing dietary hypotheses available out there? Do you expect the medical establishment and all the health bureaucracy that have built up around the diet-heart hypothesis to resist any form of revision, or maybe they will choose to make minor corrections here and there, so the structure can be kept standing?

In the epilogue of GCBC I more or less answered this question and I still believe what I wrote then. I think the end result will be a compromise. The authorities will accept the idea that some carbohydrates are particularly bad because of their effect on insulin and maybe others bad because of they contain gluten and some fats are bad because they’re saturated and they’ll stick with the saturated fat story because they’ve been backing it all along. So they won’t get the science completely right, but it will be more right than it is now. And you can already see this shift happening. The question is how far will it go and how far can we push it by funding the right kinds of studies and putting pressure on the medical establishment to do good science and on the public health authorities to recognize good science when they see it.

What is it that you are working on at the moment? Are you going to continue researching diet and health, or do you consider you mission complete as far as these topics are concerned? What is coming next by Gary Taubes?

I have a grant to write a book on the history, politics and health effects of sugar and high fructose corn syrup. I hope to finish it in the next year, but that may be optimistic. I’m also starting a non-profit organization with some very smart, talented collaborators with the goal of educating the public on the ideas in my books and raising money for the kind of research we think needs to be done. We’re hoping to have the non-profit – the Nutrition Science Initiative, or NuSI – up and running by the end of March and then we’ll see what kind of influence we can have in getting the medical research establishment and the public health authorities to understand what’s really happening in obesity, diabetes and the chronic diseases that associate with them.

Gary, thank you for your time.

Interview by Mateusz Rolik and Tomasz Gabiś

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