Norman Swan: One of the people who influenced Troy Stapleton was Gary Taubes, a science and medical journalist in the United States who's written several books for the general public, but still questioning some of the most basic beliefs in nutrition, not the least of which is that obesity is the result of too many calories in and too few out. Recently he's made his argument in the British Medical Journal.

It might seem like an idea which defies the laws of thermodynamics, but listen on. Gary Taubes:

Gary Taubes: Going back a century at least there have always been these competing ideas about why we get fat. So one of them is it's a physics issue, not a biology issue. If you take in more calories than you expand you have to get fat and that's the cause.

Norman Swan: And nobody got fat in Belsen.

Gary Taubes: Nobody got fat in Belsen, yes, and you hear those kinds of comments all the time. And it's true, you can starve a human being and you can reduce them pretty dramatically, regardless of their weight. One of the interesting observations is that the same thing happens to lean and obese individuals when you starve them. So the question is, why is it that you have to starve an obese individual to get them to be lean, but you don't have to starve a lean individual to do the same thing? And that's the kind of observation that I would argue that the medical research community, obesity researchers, don't make.

Norman Swan: Just expand on that, because I'm not sure I fully understood what you've just said.

Gary Taubes: So let's say I'm 50 pounds overweight, but I've remained 50 pounds overweight for 10 years. That means I’m matching the energy I take in to the amount of energy I expend. I'm in energy balance, as researchers would say, but I'm only in energy balance when I've got 50 pounds of excess fat, whereas if you're lean, you get to be in energy balance without that 50 pounds of excess fat. So the question is, why do I have to be semi-starved to be lean and you don't?

Norman Swan: Well, aren't you eating more calories at 50 pounds over? You're eating the level of calories…

Gary Taubes: But I'm not gaining or losing weight, so I'm matching my intake to my expenditure. I had to eat more calories than I expended to get fat, but once I've plateaued…there are people like this all over the world, he or she is matching intake to expenditure, so the question is why can she only match intake to expenditure at 50 pounds with 50 pounds of excess fat? But if we starved her back to being lean, as soon as we stop starving her she'll go back to gaining weight. She'll take in more calories than she expends until she gets back up to that same 50 pounds of fat or maybe 10 pounds more.

Norman Swan: And the reason, according to Australian and other research, is that her hormones that control appetite are in overdrive and it's almost impossible to reset them.

Gary Taubes: That's the reason. But, remember, if I starve you, a lean…I'm assuming you're lean, let's assume for the sake of argument you're lean, and we starve you, you're going to have the same metabolic hormonal responses. You too will go into…your appetite will go into overdrive, but it will stop being in overdrive once you get back to being lean instead of emaciated.

Norman Swan: There is a problem lying behind the calorie issue, is what you are arguing.

Gary Taubes: Yes, well, this is one of the many arguments against. But the alternative hypothesis…I spent about 10 years studying this. My background was in rigorous science, I started out in physics, but I moved into nutrition and was stunned at how bad the science was. And I started going back in time to try and find some baseline experimental data that you could believe in.

So in the course of my research I ended up reading the European literature prior to World War II. Science is effectively a European invention, done best in pre-World War II Germany and Austria. And it turned out that these researchers had a different perspective of obesity. And they had come to embrace a different hypothesis of obesity. They said, yes sure, somebody gets fatter, they take in more energy than they expend, that's a given. They're just saying I believe in the laws of thermodynamics.

Norman Swan: So in a sense what they were arguing was calorie intake and energy in and energy out, it was a downstream manifestation of a phenomenon which was inherent in the body in some shape or form.

Gary Taubes: Very well put, better put than I could do it! Yes, some biological factors stimulating the growth of the fat tissue, the generation of new fat cells, the over-accumulation of fat in the existing fat cells, this is a growth phenomenon. And one of the metaphors they used to describe it was a tumour. So just like a tumour grows and takes in all the energy from the environment that it can get to fuel its growth, the growth is being caused by, as we know now, oncogenes and tumour suppressor genes being mutated so that the tumour itself is being driven to grow and multiply. And these changes in energy balance of the tumour, taking in more energy, is a response to the growth. And they were arguing a similar phenomenon. It's not just that our bodies are taking in more energy than they expend, our fat cells are taking in more fat in the form of fatty acids than they are mobilising. I started looking at this as a fat cell problem.

Norman Swan: And so the light went on for many of these researchers with the discovery of insulin, because insulin is one of the key hormones which decides where energy goes, including into fat.

Gary Taubes: And I would say insulin is the key hormone that does this job of orchestrating how we store and burn energy. So insulin was the prime suspect for a fattening hormone. There was a lot of evidence pre-World War II that insulin indeed was what they called lipogenic, which would mean it would just create new fat. You can take diabetics, for instance, uncontrolled diabetics who will die emaciated with a voracious hunger, they will eat constantly and yet they will be emaciated. Then you give them insulin and they just put on fat.

Pre-World War II insulin was used as a treatment for what we would call anorexia today. Feed them a carbohydrate rich diet and they believed they could put fat on patients. Indeed, insulin shock therapy was used for schizophrenics, and the schizophrenics invariably gained weight when they got insulin. So there was a lot of evidence that insulin was what they considered a fattening hormone. But the problem was type II diabetics, the type of diabetes that associates with obesity, was seen to be an argument against this because they believed that all diabetes was due to an absence of insulin, not enough insulin. So if you don't have enough insulin, how could a type of diabetes be very common in obese subjects, if you think that insulin is a fattening hormone?

The people who came closest to solving this would say it seems like insulin should be the problem, the cause of this obesity, except if it is how can we explain type II diabetics? And unfortunately by the time we understood that type II diabetics actually had elevated insulin levels rather than depleted insulin, these researchers and their theory had died away.

Norman Swan: And so obesity is defined as a fat accumulation disorder, going to this upstream notion that it's something before the calories probably go into play, rather than an energy imbalance disorder.

Gary Taubes: Throughout history there was this idea that obesity was caused by gluttony and sloth, and that's because obese individuals tended to have greater appetites than lean individuals and they tended to be more sedentary. That could be an effect as well as a cause of the problem. But after World War II when this European school vanished and obesity research was kind of recreated in the United States with some young doctors and nutritionists who really had no experience in it. They weren't metabolism experts, and they believed that this was a simple problem, that fat people just ate too much. And then it got embraced first as an eating disorder and then this idea that it's an energy balance disorder.

One good practice in science is start with the simplest definition of a problem. So if you define obesity as a disorder of excess fat accumulation, the first question you would ask is what regulates fat accumulation in the human body? Just as if we were looking at any growth disorder, so an adult male who is, say, four foot tall, you wouldn't say, boy, this guy is four feet tall, I bet he never ate enough food or he's been in negative energy balance or he didn't grow enough, you would start looking at various blood tests and genetic tests to establish is this a growth hormone deficiency, is it a growth hormone receptor deficiency, is it an insulin-like growth factor deficiency?

Norman Swan: But apart from a small number of individuals or families around the world, these are not really genetic problems, they are environmental problems. The hormones that control fat are actually quite complicated.

Gary Taubes: That's one of the key observations. Many of the hormones that we study have names like ghrelin and melanocortin and NPYY, are these hormones that are actually perceived as appetite stimulating or satiation hormones…and the idea again is that the reason we get fat is because we eat too much, but we don't exercise enough, and the hormones that are related to this are hormones that are stimulating or inhibiting appetite or energy expenditure, as opposed to just asking the question; what is actually stimulating fat accumulation or mobilising fat. And insulin is far and away the most important hormone there.

So what's interesting is what you point out, is it's an environmental problem. So we know from the obesity epidemics worldwide that obesity rates have been skyrocketing. Type II diabetes rates…I don't know what they are doing in Australia, but in the United States the incidence of type II diabetes has quintupled in the past 40 years, it has gone up five-fold. And there was a similar dramatic increase in diabetes from the 1870s to the 1920s. In some US cities diabetes mortality increased 15-fold.

And back then this coincided with the creation of the soft drink industry, the candy industry, the dried cereal industry, and the dramatic increase in sugar consumption with the Industrial Revolution. So the argument that you end up making, if you start with this idea that obesity is this excess fat accumulation, you ask the question what regulates fat accumulation, and that is, for all intents and purposes, the hormone insulin. And then you just ask what stimulates insulin secretion, and the answer is in the short term it's refined grains and easily digestible starches, what nutritionists would call high glycaemic index carbohydrates. And in the long term it looks like sugar, through its effect in the liver, would be driving insulin resistance and so a long-term elevation in insulin levels.

Norman Swan: So this is the idea that sucrose, table sugar, is 50% fructose. We don't add too much fructose in the Australian diet, but certainly you're getting plenty of fructose through table sugar. Just give the line of causality if your theory is right.

Gary Taubes: Yes, so easily digestible carbohydrates, high glycaemic index carbohydrates in sugars raise insulin levels, and when you raise insulin levels you start storing calories as fat and not burning them. Say, I don't want to gain 20 pounds every decade, so 10 kilograms every decade, because if I do that I'll gain 20 kilograms in 20 years, and between my 20s and my 40s I'll go from being lean to obese. So how many calories do I have to avoid storing so I avoid this gaining of 10 kilograms per decade, a kilogram every year?

Norman Swan: It is tiny.

Gary Taubes: Yes, a tiny amount. 20 calories of my fat tissue that I don't burn I'm going to gain as a kilogram a year. And if you think about it, like, I'm a big guy, so if I eat 3,000 calories a day, let's say I do that over the course of 150 swallows of food, 150 bites. That's 20 calories a bite. So if I burn off 149 of those and the 150th gets into my fat tissue, I'm going to be obese, and there's nothing I'm going to be able to do about it. By elevating insulin you set up this hormonal milieu where you're now storing just a little bit of fat every day that you don't burn. Like a ratchet wrench, it only goes in one direction. So you go 20 calories today, 20 calories tomorrow. You burn off everything else you eat, but your 20 calories shy gets stuck in your fat tissue, you end up obese. And the only way to prevent it is to lower insulin levels, and this has been known since the 1960s. The way to get fat out of your fat tissue is to lower insulin levels, and the way you lower insulin levels is by reducing the carbohydrate content to your diet, or eating higher quality carbohydrates, getting rid of the sugars and eating green vegetables instead of breakfast cereals, for instance.

Norman Swan: And of course this has been the battleground because you get people like Atkins who introduced the Atkins diet, which was very low carbohydrate, high fat, he said it didn't matter what kind of fat you ate, it was your carbohydrates, and people would have almost died at the barricades over this battle.

Gary Taubes: Atkins brought it to the fore. He read the same research I did, and he said, hey, if insulin stimulates fat accumulation, then let's get rid of the carbohydrates. And you replace them with fat because fat does not stimulate insulin secretion. Protein actually does a little bit. So you end up with a high fat diet. And the medical community in the US, this was just intolerable to them. He's pushing a high-fat diet at a period in our history when we were beginning to embrace this idea that a high-fat diet causes heart disease, and particularly a high saturated fat diet. Plus the nutrition community didn't like the idea that this practicing physician, unaffiliated from any academic institution, was saying he understood obesity and they didn't. And he wasn't the first person who said it, and he said he wasn't the first person who said it.

Norman Swan: Why don't you put on weight? Because it can be a very high calorie diet.

Gary Taubes: Think of it that the reason you've amassed fat by this hypothesis, because your insulin levels are elevated, and while you're insulin levels are elevated you are storing calories as fat that you are not burning. When you lower insulin levels your fat tissue mobilises fat, it dumps fatty acids into the bloodstream. And simultaneously lowering insulin tells your organs and your skeletal muscles to burn that fat for fuel. So you simply start taking this internal fuel supply that you've amassed, perhaps for decades, and you start burning it, which is what you were supposed to be doing with it all along. And when you start burning it your energy expenditure goes up.

Norman Swan: So what you're doing in a standard weight loss diet is fighting against your insulin and the insulin wins, whereas what you're arguing is with a low carb diet you're attacking the insulin at source and it kind of all sorts itself out.

Gary Taubes: Yes, precisely, and again, said better than I've said it in the seven years I've been talking about this.

Norman Swan: You're very kind, your cheques in the mail, Gary!

Gary Taubes' books include Why We Get Fat: And What to Do About It. He's also co-founder of the Nutrition Science Initiative.

As I said earlier, next week the endocrine empire fights back.

I'm Norman Swan and this has been the Health Report. See you next time.