The Nov. 12 presentation is free to the public.
SPRINGFIELD - Award winning journalist and nutrition author Gary Taubes will speak on “Why We Get Fat and What to do About It,” on Nov. 12, at 7 p.m., in Judd Gymnasia, Union West, on the Springfield College campus. Taubes' presentation is free to the public, and is sponsored by the college's Center for Wellness Education and Research, and the class of 2016.
The focus of Taubes' writing is how food, particularly carbohydrates, affect the cells of the body, its production of insulin and how fat is then stored. The approach differs from much research where the focus is on the amount of calories consumed in contrast to exercise to reduce the storage of bodily fat. His focus is on how the processing of food can make someone fat, rather than on behavioral aspects, and on a different approach to research.
"The conventional thinking is we get fat, because we eat too much and exercise too little," Taubes. "The idea based on the laws of physics, and the argument that I have been making in my books, based on copious research, is that the laws of physics have nothing to do with it."
Rather, Taubes called obesity a biological problem, most likely linked to the hormone insulin.
"All of this is based on science, from the 1960s, that has been sort of swiped under the rug, as obesity has tend to be seen as the result of gluttony and sloth. But, if you take the biological perspective, insulin is implicated because it regulates fat accumulations in fat cells, and we secret insulin, primarily in response to carbohydrates that we consume."
A correspondent for Science magazine, Taubes is a graduate of Harvard and Stanford universities, as well as the Columbia University Graduate School of Journalism. In 2012, he co-founded the Nutrition Science Initiative with the aim of "reducing the individual, social, and economic toll of obesity and its related diseases by improving the quality of science in nutrition and obesity research."
"Gary's incredible work has provided the nutrition field with convincing evidence that we need to bring widely-held nutritional guidelines completely into question,” said Richard J. Wood, who holds a doctorate in nutritional science, and heads the college's wellness center. “Gary has not been afraid to question prior research. We are honored that he will take the time to speak to members of the Springfield community and offer new ways to think about health.”
Following his presentation, Taubes will sign copies of his books. With a background in physics and engineering, he was asked, in this edited interview, what led him into nutrition, and some of his controversial findings.
What sparked your own interest in this field?
I spent much of my youth in the 1980s writing about controversial research in hard sciences -- researchers in physics, biology, even mathematics -- who got the wrong answers. In the process, I became obsessed with the issue of how hard it is to do science right, and how easy to screw up. In the early 1990s, some of my friends in the physics community suggested I look at public health research, because they thought it was so poorly done. I did and they were right. I continued investigating controversial science into the late 1990s when, just by chance, my editor at Science asked me to write an article on a new study on diet and hypertension. I thought it would be an easy story, but realized in just a few interviews, that there was an enormous controversy over whether or not salt raised high blood pressure, and what constitutes a healthy diet. Since I love reporting on controversies, I dived in, and the end result was several almost year-long investigations for Science and virtually all my work ever since.
You have been critical of research into what foods are good or bad for the body. What has been wrong about this research?
As I noted in a New York Times editorial last February, human nutrition research is so difficult to do -- in particular, working with human subjects to establish the causes of diseases that have taken years or decades to develop -- that nutritionists and epidemiologists have lowered their standards, as to what they'll accept as compelling evidence. This is a classic symptom in any bad science, but it's rife in nutrition. So they make observations -- nutritional epidemiology -- and assume the associations represent cause and effect, because it's too difficult to actually test them. They do studies on lab rodents and assume they apply to humans, which may be true, but has to be tested; they do human studies of a few weeks to a few months and assume that the results apply to what happens over years to decades. Again, it may be true, but there's no way to tell without testing.
How do you see the research being done through the Nutrition Science Initiative different from other research in the field.
One of the problems I didn't mention is that much of the research done by nutritionists on obesity and related chronic diseases -- diabetes, heart disease, non-alcoholic fatty liver disease, cancer, to name a few -- is based on a series of assumptions that may or may not be true. The primary one is that obesity itself is caused by taking in more calories than we expend -- by eating too much and sedentary behavior. This is an idea that dates back to the early years of the 20th century when nutritionists were enamored with the new science of calorimetry -- measuring energy expenditure -- and it's oddly naive. It's descriptive but not explanatory. It's like saying that if someone gets richer, they did so because they made more money than they spent. Well, of course they did, but it doesn't tell us anything about why they got rich.
When someone gets fatter, they have to take in more calories than they expend, but we don't know why. Is there something wrong with the system that regulates intake and expenditure, or is there something wrong with the system that regulates the amount of fat they store in their fat tissue? Either one could result in the observation of someone getting fatter, and simultaneously being hungrier and relatively sedentary.
So two of our ongoing studies -- one led by researchers at Boston Children's Hospital, and one by researchers at Columbia University, NIH, the Pennington Biomedical Research Institute (Baton Rouge, LA) and the Translational Research Institute (Orlando Fla.) -- are designed to directly test those two competing hypotheses, and determine which of the two are more likely to be correct. This would then speak directly to the cause of obesity, and give us vital information on what is actually necessary to prevent and reverse it.
So, to further the point, how does fat become stored in the body to make someone obese, over time?
One point that's often ignored in discussions of obesity is that fat accumulation, in the human body, is very well regulated by a system of hormones and enzymes that work to store fat while were eating, and immediately after, as we're absorbing the nutrients into our blood stream, and then release it later to be used for fuel. This system is dominated by the hormone insulin, so that when insulin levels are elevated, we store fat and when they drop, we release it from the fat tissue and burn it for fuel. This is all conventional wisdom and can be found in obesity and endocrinology (the study of hormones) text books.
What I've argued in my books, and others certainly have before me, is that obesity is a disorder of excess fat accumulation, so the obvious place to look for the cause is in this system that is supposed to regulate our storage of fat and our use of fat for fuel. It's a pretty simple idea, but because researchers, in the decades following World War II, convinced themselves that obesity was a character disorder (gluttony and sloth), they paid precious little attention to this simple idea. In fact, by the 1960s, most clinicians trying to treat obesity, or come up with treatments, were psychologists and knew little about human biology, endocrinology, metabolism, physiology.
They were trained in the ways of the brain and behavior and that's what they looked to manipulate -- how to get us to eat less and exercise more. What they should have been doing, arguably, is asking the question what dysregulates a person's storage of fat and how can that be reversed.
Can you give an example of some carbohydrates a person would consume, and how their reception by the body leads to fat storage?
As I said above, insulin is the hormone that dominates the regulation of fat storage and metabolism. The amount of insulin circulating in our blood stream is determined in large part by the carbohydrates we consume, or the carbohydrates and fat. The more carbs, the less fat, the higher our insulin levels and, counter-intuitive as it may seem, the more fat we should store. On top of this, sugars (sucrose and high fructose corn syrup) may be particularly problematic, because there's significant evidence that they cause a disorder called insulin resistance, which is the fundamental defect in type 2 diabetes and maybe obesity as well. When you're insulin resistant, you have to secrete more insulin to respond to the carbohydrates you're eating, which means higher levels of insulin during the day and more fat storage. Or at least so this hypothesis goes and it has to be rigorously tested.
If it's right, the problematic carbohydrates are not just sugars, but what are known as high glycemic carbohydrates or highly processed carbs. These are the ones we digest very easily and they hit our blood stream fast; they raise blood sugar fast and prompt a greater insulin response. These are also the carbohydrates -- bread, pasta, potatoes, rice (plus sweets, of course) -- that we're considered uniquely fattening until the 1960s, when nutrition researchers came along and argued that fat was fattening, and these carbs became the base of the food guide pyramid. That this coincided with the latest obesity epidemic is one of the observations that got me started in this research. There's nothing new about any of it, and its been said by diet book doctors back to the 1820s, at least, but that's as much an argument that it should be taken seriously, as that it shouldn't.
Why, in your opinion, at this point in time are so many Americans overweight?
The question is what is it about processed foods that cause obesity. As I point out in my books, obesity and diabetes epidemics have happened world-wide and can be traced back to the 19th century. It's a very common observation: populations start eating western processed foods, they get obese, diabetic and they get heart disease, cancer, and a host of others that are now often known as western diseases, because of this link with western diets and lifestyles. I've been arguing that it's the sugars (again sucrose and high fructose corn syrup), and the highly refined grains in these western processed foods that cause these diseases, and the sugars are the primary culprit. So why are so many Americans overweight? Because of the quality and the quantity of the carbohydrates we consume.
Carbohydrates are essential features in many global cuisines. Are there good/bad carbs in their effect on insulin?
Yes, as discussed in the previous two answers. But one key observation is that populations that eat high carb diets and are relatively absent diabetes, obesity, heart disease and even cancer, are populations that have historically very little sugar -- hence my point that sugar is probably the key in all this.
The Southeast Asians, for instance, eat carb-rich diets and even a significant amount of white rice, but historically they've had exceedingly little sugar. In the 1960s, for instance, the Japanese ate as much sugar as we did in the 1860s, and diabetes in Japan was an exceedingly rare disease. But, diabetes in the U.S. was an exceedingly rare disease in the 1860s. Add sugar to the diet, any diet (whether omnivore, carnivore, or plant-based) historically, and you see the development of all these western diseases.
What is your view on the "China Study," which linked chronic disease to animal protein, and health to plant based foods?
I obviously think Colin Campbell missed the boat on this one (as he thinks I did). Even if you think about cancer, as I point out in my book "Good Calories, Bad Calories," at length, from the 1870s or so through the 1930s, colonial and missionary physicians published their observations in the best medical journals of the day that the isolated populations to which they were administering had a relative absence of cancer. This is the idea that cancer -- like obesity, diabetes, heart disease -- is a disease of western lifestyles and diets. The catch is that some of these populations were almost exclusively carnivores -- the Inuit (in which freakishly low cancer rates were observed through the 1970s), the pastoralists like the Masai in Africa, the native Americans of the Great Plains. So even back in the 1910s and 1920s when physicians discussed this observation that suggested maybe it was red meat that caused cancer, but then others would say, hey, here are all these carnivorous populations that also don't have cancer. So meat can't be the key factor. By focusing only on China, Campbell says, hey maybe it's meat. But he could have chosen another population that ate a lot of meat, and also had low cancer rates, and he'd have come up with a different hypothesis. What I argue is that if you look at all these populations together, the picture implicates sugars and refined grains.
To what extent does it matter whether it is calories or carbs? And is it individual diets that need to change or what is made available to people to buy?
The first thing you have to do to treat any disease successfully is establish the cause of it. If the cause of obesity is the carbohydrates we consume, then just eating less or exercising more doesn't solve the problem and it can arguably make things worse. Every time I see obese children being made to run around a track at a gym recess, I think these poor kids have to deal with their obesity and now their well-meaning teachers (and societies) are torturing them more by forcing them to run around the track, something that happens to come easy to their thin, greyhound-like friends who are not only born to be slender, but born to run as well. If it's calories, then the running and the semi-starvation are required and it's sad, but that's the case. If it's the carbohydrates, but they can eat fat and protein to their hearts desire -- burgers, no bun, in effect -- then we at least know what we have to do help these people and we can argue, or at least I do, that given time they'll lose their cravings for the bun and the fries and be happy eating the foods -- the fats , proteins, green vegetables -- on which they can be slim and healthy and still eat until they're satiated.
What do you hope to stress to students in your talk, particularly those going on in health careers?
On the one hand, i want them to rethink their ideas about obesity, assuming they're still holding the conventional ideas. As for any health careers, I'll get Susan Sontag speak for me. This is how I phrased it in my book "Why We Get Fat":
In 1978, Susan Sontag published an essay called "Illness and Metaphor," in which she discussed cancer and tuberculosis and the "blame the victim" mentality that often accompanied these diseases in different eras. "Theories that diseases are caused by mental states and can be cured by will power," Sontag wrote, "are always an index of how much is not understood about the physical terrain of a disease."
As long as we believe that people get fat because they overeat, because they take in more calories then they expend, we're putting the ultimate blame on a mental state, a weakness of character, and we're leaving human biology out of the equation entirely. Sontag had it right, It's a mistake to think this way about any disease. And it's been disastrous when it comes to the question of why we get fat.