Gary Taubes is an investigative science and health journalist. He began writing and reporting on science and medicine for Discover magazine in 1982. As a free-lance journalist, he’s written for The Atlantic Monthly, The New York Times Magazine, Esquire, Science, Nature, the British Medical Journal, and a host of other publications. He is the author of The Case for Keto (2020),The Case Against Sugar (2016), Why We Get Fat and What to Do About It (2011) and Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control and Disease (2007), published as The Diet Delusion in the UK. Taubes is the recipient of a Robert Wood Johnson Foundation Investigator Award in Health Policy Research, and has won numerous other awards for his work, including the International Health Reporting Award from the Pan American Health Organization and the National Association of Science Writers Science in Society Journalism Award. Taubes was also co-founder and president of the non-profit Nutrition Science Initiative (NuSI.org). He has focused his reporting on controversial science and, specifically, the confluence of research in nutrition, obesity, chronic disease and public health policy. Taubes studied applied physics at Harvard as an undergraduate and holds an M.S. degree in engineering from Stanford University (1978) and in journalism from Columbia University (1981). He lives in Oakland, California with his wife and two sons. He has answered couple of questions for The European Scientist.
The European Scientist : Since the late ’70s, the US population has been subjected to an epidemic of obesity: the proportion of obese adults has more than doubled, reaching nearly 36% by 2010 (Ogden and Al., 2012). Could you comment on this trend? Do you think it can still worsen?
Gary Taubes : First, living here in the U.S., it’s very easy to believe. I don’t doubt the phenomenon and the existence of the obesity epidemic. And, yes, I still think it can and likely will get worse.
There are several phenomena involved, the most troubling being one known as “fetal programming.” While obesity experts will rightly say that we can’t explain the extraordinary increases in the prevalence of obesity by a change in our genes – we can certainly explain it by this fetal programming concept and the change in what’s called the “epigenetic expression” of those genes. Fetal programming means that the conditions in the womb of a pregnant mother will influence the way different genes express themselves. It’s not controversial that maternal obesity, diabetes, gestational diabetes, and significant weight gain during pregnancy will all increase the risk of obesity and diabetes in children. This implies that as more and more women suffer from obesity and diabetes and what’s called Metabolic Syndrome during their child-bearing years, they’ll give birth to ever more children pre-disposed to become obese and diabetic as they age. The prevalence of obesity and diabetes will increase with each generation, even if the food environment in which these children come of age stays the same or doesn’t improve significantly.
All of this is compounded by the conventional thinking about obesity and diabetes. The idea is that type 2 diabetes is caused by weight gain and weight gain is caused by eating too much, and hence can be prevented by getting people to eat less and exercise more. And because dietary fat is the densest source of calories, this goes along with the idea that people predisposed to obesity and diabetes — those who have trouble controlling their weight and blood sugar — should eat less fat and more carbohydrates. If this advice is wrong, which I and others have been arguing it is, then as populations and individuals get fatter and more diabetic, they’re given precisely the wrong advice from physicians and dietitians and public health authorities about how to reverse the problem.
Public health authorities ignore critics of their policies because, if we’re right, then they’re doing far more harm than good. Acknowledging they’ve been wrong is as serious a problem for the credibility of these institutions.
TES. : This distressing trend has spread worldwide, with the average adult BMI rising in 200 countries. Children and adolescents are not spared. How can this be explained?
GT. : Everyone agrees that when populations transition from their traditional diets to Western diets and lifestyles, they will experience an obesity and diabetes epidemic.
The conventional wisdom is that when these populations become Westernised, they eat more, and become less active. Maybe they even eat more meat, and those are the mechanisms behind the associated increases in obesity and diabetes. Westernisation is characterised first and foremost by increases in sugar (sucrose and high fructose syrups) consumption and processing of carbohydrates. These are the cause obesity and diabetes, not through the quantity of calories consumed, but the effect of those sugar and carbohydrate calories on insulin signalling and so fat accumulation.
My thinking, simplistic as it sounds, is that if you want to cause an obesity and/or diabetes epidemic in a population, you simply have to add sugar and perhaps, particularly, sugary beverages to whatever it is they’re eating traditionally — whether it’s the mostly carbohydrate diets of Southeast Asian populations or the mostly carnivorous diets of the Inuit or pastoral populations like the Masai in Kenya — and then wait for at most a generation or two to see these disorders manifest themselves.
TES. : Back in 1960, the American Heart Association recommended low fat diets as the best way to reduce the incidence of coronary heart disease. That low-fat ideology has spread widely in the US and Europe, despite what you claim is a lack of compelling evidence supporting such a diet. And it clearly didn’t prevent the obesity epidemic. How do you explain what happened and why
GT. : The simplest way to put this is that a lot of physicians, perhaps well-trained in practicing medicine but not in science, decided the existence of a reasonable (and fashionable) hypothesis was reason enough to believe it was true. As early as 1960, the AHA was telling doctors to tell their patients that eating fat-rich diets not only makes people fat but gives them heart disease — through the effect of the saturated fat on LDL cholesterol.
While these hypotheses were repeatedly tested in randomized clinical trials and typically failed the tests, the physicians who ran these trials and who had also come to believe that these hypotheses were true, could always find enough evidence to blame the tests/trials for the failure, rather than the hypotheses themselves. The sociology involved would be fascinating, if the whole thing wasn’t so depressing and, ultimately, tragic.
TES. : Your main thesis is that the obesity epidemic is related to the effect of diet on insulin signaling, building on the thinking from the mid-19th century of the famous French physiologist Claude Bernard. Can you explain this concept to us?
GT. : Since the 1930s, obesity researchers have, simply speaking, blamed eating too much, and their research since then has tried to explain why people with obesity might eat more than they require and lean people don’t. They discuss this in terms of energy balance. Folks with obesity were in positive energy balance as they got fatter, taking in more calories than they expend. Lean people are in perfect energy balance and match their intake to expenditure.
In the medical literature prior to the 1960s, there used to be two hypotheses of obesity, and the researchers didn’t know which was true. One was the energy balance idea, and the other was that obesity is caused by a disruption in the neuro-endocrine regulation of fat metabolism and fat storage. People who got too fat had a constitutional predisposition to do so, and this manifested itself in the nervous system (neuro) and hormonal (endocrine) regulation of the fat tissue.
Thus, scientists were concerned not with how much people eat and exercise because the fat cells themselves can’t monitor this. They only respond to their immediate environment, the signals from the nervous system (neuro) and from hormones (the endocrine system), and it’s this internal milieu — using Bernard’s terminology — of the fat cells that determines how much fat they take up and retain. And because the hormone insulin exerts the dominant effect on fat storage, then it’s a reasonable hypothesis that dysregulation in insulin signaling is involved.
Post-1960s thanks to improving technology, researchers identified high levels of insulin and a concept called insulin resistance as common to both obesity and type 2 diabetes. In the early 2000s, this became known as Metabolic Syndrome and it more or less explained both the obesity epidemics around the world and the link between obesity, type 2 diabetes and heart disease. But by then, the conventional wisdom was that we get fat because we eat too much and we get heart disease because we eat too much saturated fat, and this far more parsimonious hypothesis could not displace this thinking for all the reasons we’ve discussed.
TES. : You’re famous for advocating the “low-carb, high-fat” diet, which has emerged as a real paradigm shift, being totally opposed to the prevailing ideology. Can you delve into this controversy? Are your ideas making progress in public opinion?
GT. : The gist of the thinking behind these low-carb/high-fat diets is pretty simple: carbohydrates are the problem and we have to avoid them. Yes, this is controversial. And yet from roughly 1825 through the 1960s, this was the conventional wisdom. My mother’s generation grew up believing that carbohydrates were fattening — this is “what every woman knows” as a 1963 article in the British Journal of Nutrition put it — and in the 1960s, the research linking insulin to fat accumulation should have been seen as confirming this belief. Not until the very early 2000s did physicians begin clinical trials with these LCHF diets and the trials confirmed that you can tell people to avoid carbohydrates but otherwise eat as much as they want and they will lose weight, and significant weight, so long as they adhere to the advice. And they’ll lose weight without being hungry, which is key.
By this time public health organizations and health associations worldwide were advocating carbohydrate-rich diets and avoiding fat and particularly saturated fat. This idea could not be reconciled with the idea that carbohydrate-rich foods could be fattening for many of us, that they could cause heart disease (the refined grains and sugars, specifically) and that many of us are best served by avoiding these foods. Unfortunately, public health organizations and health associations, and expert advisors are particularly resistant to acknowledging their mistakes.
That take, of course, is dependent on my belief that the evidence is compelling for what I’m arguing. Clearly, not everyone agrees.
TES. : There are now plenty of studies confirming that the intake of saturated fats is not associated with all-cause mortality, cardiovascular disease, chronic heart disease, ischemic stroke, or type 2 diabetes (de Souza et al., 2015). On the contrary, many studies seem to link sugar intake and type 2 diabetes (Chatterjee et al., 2017). Why is it that this information doesn’t seem to matter to the public and influence food behavior?
GT. : Again, assuming I’m right, all the reasons we’ve been discussing; cognitive dissonance, institutional inertia, financial conflicts (most food companies are in the business of selling carb-rich foods and/or beverages), the institutional resistance to acknowledging errors that might have done far more harm than good, and, finally, the nature of the evidence available in nutrition research. Since the 1960s, the field has relied on epidemiologic surveys to establish what healthy and unhealthy people eat. The way these epidemiologic studies are interpreted is fatally flawed.
These epidemiologic studies establish associations between food consumption and health. While the epidemiologists and the world of authorities who rely on this kind of evidence will acknowledge that associations don’t imply causality, they use them to do so nonetheless. Nutrition researchers have decided that gathering this association data from surveys is the best that can be done. Which it might be. But these studies are conventional wisdom confirmation machines.
You need randomized controlled trials. These trials, are expensive and impractical to run for more than a year or two. But if you look at those, as I did and others who think as I do, you find that people who avoid carbohydrates and particularly refined grains and sugars get healthier.
That the two kinds of studies — epidemiologic surveys over the course of several decades and randomized controlled trials that last for a year two — result in two distinctly different perspectives on the nature of a healthy diet is a serious problem. In an ideal world, the public health community would do the kind of studies necessary to resolve it, but there’s no evidence that they’re actually interested in doing so. However, it seems that they would prefer to double down on what they’ve been insisting is true all along, despite having to do so in the midst of this pandemic of obesity and diabetes. It should be seen as at least some evidence that conventional thinking is wrong, but that’s not how it’s perceived.
TES. : More and more, public health policies are developing Front-of-Package (FOP) food labeling systems to help consumers choose their food (traffic light labeling in the UK, Nutriscore in France, Battery score in Italy, etc.). What’s your take on these solutions? Do you think they can tackle the issue of obesity?
GT. : Short answer here, finally: No, they will not help. This is more of the same doubling down on the conventional wisdom. Rather than considering the possibility that our conception of the nature of a healthy diet is wrong authorities are trying even harder to disseminate it. I hope they’re right, but I would bet against it.
TES. : Europeans are currently embroiled in a controversy over Nutriscore. Opponents accuse the algorithm of being biased a priori by labeling healthy foods such as olive oil, cheese, or meat with a bad mark. What would be your advice to consumers and EU policymakers?
GT. : Take a step back. Rethink. They have to stop blaming the public in the midst of an obesity and diabetes pandemic and consider the possibility that the nutritionists, themselves, and the obesity researchers are the ones who got it wrong. It happens in science all the time. Maybe it really did happen here. And then pay more attention to the clinical trials than the epidemiologic surveys.
TES. : Your latest book, “The Case for Keto,” was published just before COVID. During this period, it has become quite apparent that people with obesity and chronic metabolic diseases have been more affected. Some have concluded that obesity is the real killer behind COVID. Do you share this point of view?
GT. : I’m biased to believe this is true, but I haven’t studied the literature enough in this case to have confidence that I’m right.
TES. : What advice do you have for our readers?
GT. : If you’re lean and healthy now, then you can probably follow the conventional thinking on healthy eating and you’ll be fine. (With that, though, you might still avoid sugar and sugary beverages so that you stay relatively fine. Beer is up to you.) If you have trouble controlling your weight, your blood pressure and/or your blood sugar, and the conventional wisdom has not worked for you, then try something different.
In particular, you should try more or less rigidly abstaining from carbohydrate-rich foods. At the risk of sounding like I’m plugging my own work, which I am, I wrote The Case for Keto so that people could understand why anyone would eat such a seemingly restrictive diet and why it, or something very much like it, might be necessary to achieve and maintain good health. I also wrote the book so that if people wanted to try following a low-carb, high-fat way of eating, then they should know how to do it right. Then I recommend trying it for a few months to see if, as the clinical trials, suggest, you get leaner and healthier. If so, you might consider listening to your body and not the experts.
Image par Mohamed Hassan de Pixabay
Portrait of Gary Taubes Par AncestryFoundation — AHS12 Gary Taubes Calories vs Carbohydrates: Clearing up Confusion over Competing Obesity Paradigms at 0:31, CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=103356235
This post is also available in: FR (FR)
Leave a Reply