Researching the Triggers for Obesity and Diabetes
Feb 15, 2013, 9:00 AM, Posted by Gary Taubes
Gary A. Taubes, MSE, MS, is recipient of a Robert Wood Johnson Foundation Investigator Award in Health Policy Research, and co-founder of the Nutrition Science Initiative. He is an award-winning science and health journalist, and author of Why We Get Fat and Good Calories, Bad Calories.
Human Capital Blog: Why did you and Dr. Attia start the Nutrition Science Initiative (NuSI)? What was the problem you saw that needed to be addressed?
Gary Taubes: I spent the better part of a decade, from the late 90s through 2007, doing an extensive journalistic investigation of the research that led us to our established beliefs about the environmental triggers of obesity, type 2 diabetes and their associated chronic diseases, which include heart disease and cancer. During these years it also became clear that the economic burden of these diseases was becoming unsustainable and were driving health care costs in this country. Obesity alone is estimated to cost the health care system $150 billion a year, and add type 2 diabetes and that number might double.
My research led me to two major conclusions. One is that our understanding of what fundamentally causes obesity may be incorrect: that it may not be what researchers refer to as an "energy balance" disorder— that we merely consume more calories than we expend—but rather a hormonal/regulatory defect, just like any other growth disorder. This was the hypothesis embraced by European clinicians prior to the Second World War. What I learned in my research was that this hypothesis vanished with the war and the evaporation of the relevant medical research community. Instead we all came to believe that obesity is simple–caused by eating too much or being too sedentary or some combination of the two—and this is what our national guidelines have communicated to the public and to individuals. While this has happened, the nation has waxed fatter and fatter.
The second conclusion of my work and my books was that the research in nutrition and obesity has simply never been rigorous enough to establish reliable knowledge in this field, one way or the other. There are a lot of good reasons for this, in particular that doing rigorous experimental trials with humans is difficult and exceedingly expensive. But without these experiments, we're just guessing when we say we know why humans get fat. It's quite likely that one reason we've seen an obesity epidemic is because our fundamental understanding of the disorder itself and how to cure and prevent it is incorrect. And if this is true about obesity, it's true about diabetes and heart disease as well.
When I met Dr. Attia in April 2011 we discussed this problem at length and decided one way to solve it would be to try to raise money for the kind of rigorous experiments that would be necessary to resolve these controversies. So the Nutrition Science Initiative (NuSI) was begun as a kind of nights and weekends endeavor with the hope that we could raise a few million dollars through crowdfunding on the Internet.
In November 2011 I was interviewed on an economics podcast—EconTalk with Russ Roberts—and a few days later got an e-mail from John Arnold, a Houston-based philanthropist, expressing interest in supporting the kind of studies that I discussed on the podcast. Last spring, the Laura and John Arnold Foundation (LJAF) agreed to give us seed money to launch NuSI. We’re now in discussions with the Foundation about the funding for several experiments that hold promise of being the most rigorous experiments ever done in humans to elucidate the dietary triggers of obesity and excess adiposity.
Human Capital Blog: So how is NuSI working to address that problem?
Taubes: Our belief in a nutshell is that nutrition research has been fundamentally flawed and that this is the first problem that has to be addressed to make progress with obesity and the obesity epidemic. We believe what's needed is a concerted effort to target the most important questions and to design experiments that will resolve them, and to do these experiments without compromise.
As well as reaching out to researchers who we believe are already doing meaningful research that targets this question of the dietary triggers of obesity, we've put together a consortium of some of the best – and most influential—scientists in the field, and we'll be funding key experiments that they will do.
If these experiments see what we would predict—and this being science, that's not a given by any means—then we think these researchers will begin to change their beliefs about the cause of obesity and will communicate that to their colleagues.
I've had researchers in this field, as well as nutritionists, dietitians and physicians, tell me that no amount of science or studies will change what they believe to be true right now. We believe that if the best scientists in the field begin to change what they believe, then even these folks will follow. And what's necessary to achieve that is the best possible science. So that's what we hope to fund and facilitate.
HCB: Tell us about the kind of research that will be conducted. Is there something in particular you’re looking for or expecting to find?
Taubes: All the studies we'll be funding will address this fundamental issue of what is the dietary or lifestyle trigger of the epidemics of obesity and diabetes. And it's very likely to be the same trigger for both, since these diseases are so closely associated. It's these recent upsurges in obesity and diabetes that tell us that something has changed in the environment from, say, the early 1960s, when only 12 percent of the population was obese, compared to today, when some 34 or 35 percent of the population is.
The accepted explanation is that we merely eat more than we did previously and expend less energy and so the meaningful societal changes have been the proliferation of fast food joints and computers and video games, etc. that lead us to take in too many calories and expend too few. The alternative hypothesis is that the type of food we eat has changed, and in particular we've consumed more sugar and refined grains and that this change in the quality of carbohydrates in particular has led to hormonal/metabolic effects that work directly to store fat in the fat cells.
The first experiments we’ll be funding will specifically address the question of whether fat accumulation is regulated by the balance of calories or by the macronutrient content of the diet—the proportion and type of proteins, fats and carbohydrates we consume.
Now let's look at one experiment that our consortium has designed to address this issue. The idea is to take overweight and obese humans, get them weight stable on a typical American diet – they’re neither gaining nor losing weight, in other words -- and then measure how much energy they expend. The conventional wisdom is that if they eat the same amount of calories as they expend, they'll remain weight stable and the only way to lose fat is to consume fewer calories or expend more.
An alternative hypothesis suggests that the hormone insulin regulates fat accumulation in fat cells and that if insulin levels are lowered, fat will be lost independent of the total calories consumed. The best way to do that is to significantly reduce the carbohydrate content of the diet as we secrete insulin primarily in response to carbohydrates. So this trial will match calories-in to calories-out (at baseline) and the prediction is that the subjects eating the insulin-inhibiting, very-low-carbohydrate diet will lose fat and weight anyway. And as a result, their energy expenditure will go up. And this is why I say the diet will match calories-in to calories-expended at baseline, because if the alternative hypothesis is correct, the energy expended will increase over the course of the experiment, while fat mass goes down.
A study like this will have to meticulously measure energy expenditure in the subjects and has to be carried out in a metabolic ward so that the diets being given to the subjects and eaten by the subjects can be closely monitored. This is what we mean by making these studies rigorously well-controlled. As a result, these experiments are very expensive, but we think that's what's necessary to resolve these controversies.
With luck this will be the first of many experiments that we'll fund along the same lines. This will depend, though, on how successful we are at raising funds. The better we can do, the more such well-controlled experiments we can get done and the sooner we can have results.
HCB: What will NuSI’s findings mean for the future of obesity prevention and policy, or health care in general?
Taubes: One of the quotes I often use when I lecture about this is from Robert Burton in The Anatomy of Melancholy, which was published almost 400 years ago. "It is in vain to speak of cures, or think of remedies," Burton wrote, "until such time as we have considered of the causes . . . cures must be imperfect, lame, and to no purpose, wherein the causes have not first been searched."
We think that's the case with obesity and type 2 diabetes. There's a very good possibility that we've been prematurely speaking of cures and thinking of remedies for 50 years and that what has been disseminated, as a result, over that period is simply wrong. If so, then the first step is to establish what the cause is beyond reasonable doubt and make that happen. if the science goes as we would hope and predict, then the next step will be to do our best to make sure it's widely disseminated and that physicians, nutritionists, journalists, policy-makers, the leaders of health organizations like the American Heart Association and the American Diabetes Association, and others understand the implications and craft new guidelines, recommendations and policies that reflect what has been learned. But that's down the road. Step one is to get the best possible science done and see what it teaches us.
This commentary originally appeared on the RWJF Human Capital Blog. The views and opinions expressed here are those of the authors.