IRA FLATOW, host:
For the rest of the house, we'll take a look at the connection between the diet, weight and disease. My next guest says to forget just about everything you've learned about what you should eat to maintain a healthy weight and ward off chronic diseases like diabetes and heart disease.
He's taken a hard look at what's been long-considered the healthiest diet - the kind we see all the time that we should be on is low-fat diet that's high in carbs - and he says the science just does not support a low-fat diet for weight control and disease prevention, and that fats aren't the problem but carbs are. The best diet, he says, is one that's high in protein and fat and low in carbs. But does the science support his claims? Some critics accuse him of ignoring research that didn't support his physician.
Gary Taubes joins us today to lay out his case that he makes in his book, "Good Calories, Bad Calories: Changing the Conventional Wisdom on Diet, Weight Control, and Disease." And he's a contributing correspondent for Science magazine. He's here in our New York studios. Welcome back to the program, Gary.
Mr. GARY TAUBES (Author, "Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease): Thank you, Ira. It's good to be here.
FLATOW: You're welcome. Ronald Krauss, a senior scientist at Lawrence Berkeley National Lab. He's adjunct professor of nutrition at University of California at Berkeley; senior scientist and director of Atherosclerosis Research at China's hospital - Children's Hospital Oakland Research Institute in Oakland, California. Hope he doesn't have this all in that little plaque on his desk.
(Soundbite of laughter)
FLATOW: He joins us today from his office there. Welcome to the Program, Dr. Krauss.
Dr. RONALD KRAUSS (Senior Scientist, Lawrence Berkeley National Laboratory): Oh, thanks Ira. It's great to be here.
FLATOW: Let's begin, Gary, talking about "Good Calories, Bad Calories: Challenging the Conventional Wisdom," it always seems like the conventional wisdom changes over the years, doesn't it?
Mr. TAUBES: Yeah, the conventional wisdom does change. But what I've been sort of challenging is something we've come to believe for the past 40 years should change and hasn't.
Mr. TAUBES: I started about seven years ago, actually, just reviewing the research supporting some of our public health recommendations - do salt cause high blood pressure, do low-fat diets cause, oh - you know, do high-fat diets cause heart disease. And I just found myself going deeper and deeper, looking for something that was actually based on sound evidence. And another sort of five years of research and hundreds of interviews later, I end up believing that the - really, that what seems to be the most compelling evidence points to the carbohydrates in our diet, not the fats.
FLATOW: Mm-hmm. Would that be what basically what Dr. Atkins said when he was coming out with his diet?
Mr. TAUBES: Yeah. It's basically - I mean, again, people like to say that I advocate the Atkins diet. I do not not advocate it. I just - Atkins read many of the same research studies that I did and came to similar conclusions.
FLATOW: Mm-hmm. Dr. Krauss, is Gary Taubes on to something here?
Dr. KRAUSS: Well, you know, those of us doing nutrition research are aware of the challenges in drawing conclusions from these kinds of studies that we are forced to do that are not necessarily definitive. However, with regards to the issue of fat in the diet and the outcomes that are associated with recommending fat restriction as a primary message, many of us, including those of us who work with American Heart Association and other organizations have been aware for some time, that the simple message of low fat has not been based on the best science and that we are seeing increasing concerns regarding substituting carbohydrates for fat that resonate with a lot of what Gary has put into his book.
FLATOW: So the science - basically, the science of nutrition is really doesn't seem like much of a whole lot of science going on there?
Dr. KRAUSS: Well, let me just say that there's a lot of science at the level of mechanisms and understanding how cells work and how animal models work. When it comes to human studies, particularly when you're looking at outcomes, such as do people gain or lose weight or - significantly, do they wind up getting diabetes or heart disease with a certain type of diet, we're really limited in the resources that would be required for carrying out these studies in a way that would satisfy a rigorous scientific interpretation, such as what Gary is seeking.
And I think that we share the goal of putting more resources into funding these kinds of studies. In the meantime, we are forced to make decisions and often times recommendations based on the best science available. And that is a moving target.
Mr. TAUBES: Although - let me take - let me interrupt for a second and say that one of the problems is that, often, the best science available has been forgotten entirely. One of the points - I'll give you an example of what I'm talking about. We all know that obesity associates with a higher risk of heart disease and with diabetes. That means the fatter you are, the more likely you are to get heart disease and become diabetic. If you're diabetic, you're more likely to be fat. You're more likely to have heart disease.
A big study just came out yesterday…
Mr. TAUBES: …that's been all over the paper, saying that obesity is the biggest risk factor for cancer. So the question is what makes us fat? And for 50 years now, everyone's been insisting that basically human beings are thermodynamic black boxes. We're like machines. You put calories in one side, the calories are expanded all over. And whatever the difference is goes to making us either fatter or thinner. Either the energy in minus energy out is what determines whether we get fat or not.
What's been forgotten is that we're actually biological creatures. And obesity is not a disorder of overeating as the authorities will tell us in virtually everything they write, including this American Cancer - this American Institute of Cancer Research report. It's - obesity is a disorder of excess fat accumulation; and fat is regulated.
And we know how fat is regulated. We've known it for 50 years. Fat tissue is primarily - the amount of fat we accumulate is primarily determined by the hormone insulin. And we secrete insulin in response to carbohydrates. And for a hundred years prior to that, there was this conventional wisdom that carbs make you fat. I mean, we grew up, our parents - ours being 51 years old, and Ira, you're probably in that neighborhood.
Mr. TAUBES: Our parents believe that certain foods make you fat - bread, pasta, potatoes, beer. You know, they use the term beer belly not because they believe that a beer belly is caused by eating butter and red meat but because it's caused by drinking beer.
And in the 1960s, physiologists, biochemists actually figured out the mechanisms of what makes us accumulate excess fat. And indeed, it implicated carbohydrates directly. Actually, you need to eat carbs to get fat. That's the surreal part. And this science was just thrown out.
Mr. TAUBES: Well, in part, because people like Atkins embraced it. And this was a period when low-fat diets were - American Heart Association was beginning to tell us we should all eat low-fat diets. And the NIH was beginning to buy into this. This was when Ron Krauss was in his formative years in the '60s, doing research.
FLATOW: But what turns it around? Why did low fat become vogue?
Mr. TAUBES: The idea was low-fat diets cause heart disease - low-fat diets protect against heart disease. And…
Dr. KRAUSS: Could I…
FLATOW: Because the thought that eating fat puts the fat on.
Mr. TAUBES: Yeah. Well, also, dietary trade-off. You eat a low-fat diet, you're going to eat more carbohydrates. So you couldn't simultaneously say that fat causes heart disease if you're saying carbohydrates cause obesity.
Dr. KRAUSS: If I may say…
Dr. KRAUSS: …I think one of the issues that this highlights is the tendency to oversimplify - and for you to say, Gary - misinterpret the science. And I think the message of low fat is something that, as I mentioned, many of us have come to recognize based on the science was not the right message. On the other hand, I think we have to be careful that we don't oversimplify messages that might be considered more scientifically sound but still carry with it the risk of not considering the complexity, something like body weight regulation.
Insulin is clearly a big part of the story. And I think the data you have assembled and reviewed clearly reminds us of all that's been done to support the carbohydrate-insulin-fat connection. But there's an awful lot of regulation that you've mentioned in fat tissue and in systems that determine obesity involving organs like the brain, the intestine and the liver and muscle, that all involve integrated circuits that are not simply responding to insulin.
And I think we are in a very exciting time, scientifically, where we're beginning to unravel these networks and realize how tightly controlled they are so that intervening with anything, be it low fat or low carb, sets off a whole series of reactions that tend to prevent body loss - body fat loss from occurring, or at least minimize it.
Mr. TAUBES: Ron…
Dr. KRAUSS: So the regulation is really much more complex than just insulin or no insulin.
Mr. TAUBES: No. And my point is simple. We're looking for the cause of weight gain the same way 50 years ago people what to know what causes lung cancer. Obviously, lung cancer was a relatively new disease that had been gone from being very infrequent to common among smokers. The question is what did it. And there are equally as many mechanisms involved in cancer formation. But the answer to the question, what causes lung cancer in modern society, is the cigarettes.
What we have with obesity is an interest, and we have societies that didn't have obese people. And they switched to eating Western diets, suddenly, obesity, diabetes, heart disease, cancers appear. We have more obesity now than ever. We're, you know, the experts are drowning on obese and diabetic patients while they're talking about working out the details. The question is what's changed in the environment?
Dr. KRAUSS: Right.
Mr. TAUBES: What's the environmental factor that's setting off this predisposition? And the obvious, simple answer - and this is still ruled by science, and we have Occam's razor here: Never multiply explanations when you have a simple explanation that hasn't been refuted. The obvious answer is carbohydrates drive insulin. Insulin drives fat accumulation, and we're getting fatter because of the kind of carbohydrates we're consuming.
Dr. KRAUSS: Sure. Well, one can even accept that as a very plausible reading of the data, and I don't even think I want to challenge that. The issue is how does that translated into action that could actually achieve the goals of either preventing or treating obesity. And despite the strong arguments that are based on both historical experiences as well as some of the studies that are out there, I think we are still facing the lack of really clear-cut definitive trials that have addressed low carbohydrate as a tool for either preventing or treating obesity over the long term.
Most diets eventually fail, and we don't understand all the reasons for that, but it does color the enthusiasm that many of us have for recommending a particular diet, particularly an extreme diet that has not undergone that kind of testing.
FLATOW: Mm-hmm. Do you believe in having to eat only fats and…
Mr. TAUBES: Well, no. I believe that - the problem, like I said, it's not and -you know, what happens because Ron's in the business of public health, he starts to think in terms of, you know, what diets work. I'm not talking about what diets work. I'm talking about what causes us to get fat. And that's…
Dr. KRAUSS: Yeah. Well, that's an area that we can, I think, converge on…
Mr. TAUBES: Yeah.
Dr. KRAUSS: …in terms of mechanisms. But many, most people are interested in this topic, not for the science and the basis for what other people have recommended, but what we should now be thinking about recommending for their health.
Mr. TAUBES: Well, and that's - and the point is if carbohydrates make you fat, you know - if cigarettes cause lung cancer and you don't want to get lung cancer, you quit smoking, you know? The patch works kind of well, the, you know, the gum works kind of well, cold turkey works. For most people who quit, fail, but that doesn't, you know, solve the problem that if you don't want to get lung cancer, you better not smoke cigarettes.
Dr. KRAUSS: Yeah, it's worth the trial, that's for sure.
FLATOW: It's - I'm talking with Gary Taubes, author of "Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease". Also talking with Ron Krauss, who is - a lot of titles, but he's a scientist at Children's Hospital Oakland Research Institute in Oakland. 1-800-989-8255. Another really interesting - as soon - a lot to chew over in this book, so to speak…
Mr. TAUBES: Right. Yeah.
FLATOW: …but another really interesting section that - where you two come together and where Gary actually cites Dr. Krauss' research and where he's an expert on is the HDL/LDL paradox here. Gary…
Mr. TAUBES: Right.
FLATOW: …you want to talk to us about how that has been dumb down, so that the professor really reflect what do - what we think that what we've been told over the years?
Mr. TAUBES: I'm going to give the introduction, obviously, and I'm going to let Ron do the heavy lifting.
Mr. TAUBES: What basically - what happened is this whole paradigm started 50 years ago with the idea that total fat - the fat in your diet raises total cholesterol, so we started measuring total cholesterol. And in the 1970s, when the NIH actually gets around to funding studies, they've realized total cholesterol really doesn't tell as much about heart disease risk, but HDL was protective and the cholesterol and LDL is the - what they called a marginal risk factor for heart disease. And that 30-year-old science is what we've embraced ever since.
So you go to the doctor, and if he's not very sophisticated, he measures your total cholesterol, which tells you nothing, and he measures your LDL cholesterol, which tells you a little, and then he puts you on the stat and then he sends you home. Since then, the science has evolved. And Ron did much of that science, and what we now know is that it's not the cholesterol and the LDL that's important, you know, the bad cholesterol. It's the LDL particle itself.
FLATOW: The kind of LDL…
Mr. TAUBES: The size and the density, and that's what I'm going to let Ron tell you.
FLATOW: Well, before he does - just to catch our breath, we're talking about fat and gaining weight and health this hour on TALK OF THE NATION: SCIENCE FRIDAY from NPR News. I'm Ira Flatow, with Gary Taubes, author of "Good Calories, Bad Calories," and Ron Krauss, who's going to finish the story, hopefully.
Dr. KRAUSS: Okay. Well, you know, when you look at patients with heart disease, we've known for a long time that their - cholesterol levels are not all that much higher than people without heart disease. And we've been trying to piece apart the reasons for that and along the way, we discovered that there is LDL, so-called bad cholesterol and HDL, so-called good cholesterol, and that helped to understand some of the reasons that perhaps having a low cholesterol, if it was low HDL, would actually be bad.
But what we discovered - and this is what we're rediscovering, information that's been buried in the literature for a while - is that LDL itself comes in different forms, and just measuring LDL cholesterol doesn't give information about the actual particles that carry cholesterol that are most damaging to the artery. And we know go to specific subtypes of cholesterol and LDL particles that do the most damage.
If you measure those particles, you find that they tend to be elevated in patients who are overweight. We found that they increase in concentration when you feed high carbohydrate diets, particularly sugars and processed starches, and that this may be buried in the standard cholesterol profile. Those measurements really are not particularly carried out, and they've led to a lot of confusion as to how we should be using cholesterol measurements to help define our dietary recommendations. So - some may say in the old days, when I did grow into this field, people were eating a lot of saturated fat and there was an enormous amount of data from animal studies in particular that higher saturated fat is associated with higher levels LDL cholesterol; and we can talk about the corollary evidence that tried to link saturated fat with heart disease risk.
People tried to connect the dots and say that higher saturated fat leads to heart disease because of higher cholesterol and higher LDL in particular. Well, what we found is that high saturated fat raises the smaller LDL particle - I'm sorry, high saturated fat raises the large LDL particles and doesn't affect the small LDL particles. And I think some people - and Gary, I think, has made this statement in his book - feel that the large LDL particles aren't hazardous.
Well, it's not all or none. It's just the matter that the - a major impact we feel comes from pathways that result in the smaller LDL particles, and that's where carbohydrates and unsaturated fat play a role. So, our research kind of started to resonate with other studies pointing to carbohydrate as being the culprit for much of what is associated, not just with these particles but also with the whole constellation called the metabolic syndrome, which is triggered by over weight and is influenced by the carbohydrate intake among other things, so that the cholesterol paradigm based on measuring LDL and the - and worrying about saturated fat, has now shifted. It's starting to shift, although we're still not yet practicing this in terms of our public health recommendations. The…
FLATOW: All right.
Dr. KRAUSS: …the rationale is beginning to shift in the direction of lower carbohydrate.
FLATOW: We're going to get back to this LDL big particle, little particle that you probably never heard about until you read Gary Taubes' book, "Good Calories, Bad Calories." So stay with us, we'll be right back after this short break.
I'm Ira Flatow, this is TALK OF THE NATION: SCIENCE FRIDAY from NPR News.
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FLATOW: You're listening to TALK OF THE NATION: SCIENCE FRIDAY. I'm Ira Flatow.
We're talking this hour about diet, obesity and disease with my guest Gary Taubes, contributing correspondent for Science Magazine and author of "Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease."
Also, Dr. Ronald Krauss, who is senior scientist at Lawrence Berkeley Laboratory, adjunct professor at Cal-Berkeley and a senior scientist at the Children's Hospital Oakland Research Institute in California.
Our number: 1-800-989-8255. If I could just summarize some very important statements that Dr. Krauss was saying. In a lay terminology, he was basically saying that we now have another level of LDL, this low-density lipoprotein that we have our blood tested for when we go to the doctors. And there are two kinds, there's a dense kind and the not-so-dense kind. And the dense kind is the bad one?
Dr. KRAUSS: Right.
FLATOW: And the not-so-dense is not as bad.
Dr. KRAUSS: Right. It's a relative difference. They're both bad, but one is - the dense is worse than the other. And just to conclude this sort of dietary story is that when recommendations are now pushing hard for lowering LDL cholesterol by reducing fat and saturated fat that's based on the assumption that this would improve LDL-related heart disease risks. Our evidence is that it doesn't affect the dense LDL at all. And, in fact, substituting carbohydrate for fat, which is the natural consequence of those recommendations, will actually increase levels of the smaller LDL.
FLATOW: That's like a smoking gun.
Dr. KRAUSS: It's potentially an adverse of - a consequence and an unattended one certainly of trying to lower cholesterol by lowering fat.
Mr. TAUBES: And this is…
Mr. TAUBES: …yeah, I just wanted to say one of the problems that I point out in the book is that because we were so zealous in the 1970s and 1980s in giving this recommendation basically jumping to conclusions that saturated fat was evil - when Ron talks about the problem like we're moving towards shifting the paradigm to small, dense LDL and large, fluffy LDL - part of the problem with that movement is the diet studies, because now the diet studies require that we admit that something that we have believed beyond a shadow of a doubt, have been told as unambiguously true that saturated fat is evil.
Then, we admit that it may not be a player at all, in fact maybe good for you. And you can see Ron even - there's this movement to say, well, let's kind of capture some of the old paradigm. So let's - may we could still say carbs are bad, but saturated fat is still maybe a little bad.
Dr. KRAUSS: Right.
Mr. TAUBES: And, you know, my point of view, the difference being - Ron is in the public health business, and part of the public health business remain incredible and it's also this idea of the precautionary principle, let's be on the safe side.
Mr. TAUBES: I, despite the fact that I'm a journalist, I'm more interested in the science. And one of the biggest mistakes people make in science is they don't let hypothesis go when they've been proven to be wrong.
So instead, they accumulate what, you know, we used to call epicycles in the philosophy of science, trying to keep everything together so nobody has to be wrong. And after a point, you just say this hypothesis has not been refuted, get rid of it, so we can think clearly about what might be true and what we should do about it.
FLATOW: Or we wait for the proponents to die out, which was the other…
Mr. TAUBES: Yeah, and from heart disease.
(Soundbite of laughter)
FLATOW: All right, we go to the phone.
Mr. TAUBES: Knock on wood.
FLATOW: 1-800-989-8255. Let's go to Mike in Corvallis, Oregon. Hi, Mike.
MIKE (Caller): Hi, nice program. I'm a neurologist, so I see a lot of stroke patients. And as I'm listening to your guests, I appreciate their views, but I think it's important that your wide listeners realizes - I don't think that so much carbohydrates are intrinsically bad. But I think it's the fact that simple carbohydrates are so available and so cheap. I'm seeing much more obesity now than I did 10 years ago, and I think it's because people are eating more carbohydrates because they're inexpensive.
FLATOW: Made processed - processed foods, things like that.
MIKE: Exactly. They're everywhere and they're so inexpensive. And the last thing I have is just a question. In the neurology literature, the Mediterranean diet has gotten a lot of positive press, and I wonder if either of your guests have any comment on to the value or less value of the Mediterranean diet. And thanks a lot.
FLATOW: Thanks. Let's talk about processed carbohydrates versus whole grains. Does it matter?
Mr. TAUBES: Yeah, well, the argument…
FLATOW: Is the calorie is still the calorie, like, you know…
Mr. TAUBES: Well, no, no. I think that's the point. Obviously, the processed carbohydrates induce the graded sense upon response. And internalize that if you care about the biology of obesity, it's not about eating more. It's not about being cost-conscious, so you're just eating cheap calories because they're out there. The problem is those cheap calories literally make you fat.
Mr. TAUBES: So the people who eat these foods, you know, they may start accumulating fat. They may eat more of them because they're losing so many calories into the fat. But it's not something that's happening in their brain. It's something because they want to save money.
It's not because they lack willpower or have some kind of psychological defect, you know, I'm thin therefore I know how to eat moderation, and they're fat, maybe poor and they don't. It's about what's literally happening at their fat tissue.
Mr. TAUBES: As for the Mediterranean diet, that's fascinating because if you actually look at what evidence it's based on. You know, this comes out of the studies done in the 1960s, based on diet studies done in the early 1960s and the late 1940s, two studies. And in those diets, the one thing you could say for sure about the Mediterranean diet back in this period when the islanders of Crete and Corfu happened to be excruciatingly healthy was they ate no refined carbs. Their bread was not white bread, they had no white flour in their diet, and they ate virtually no sugar.
So since then, people have sort of used this palette of the Mediterranean diet to paint their preconceptions on. You know, we like olive oil, we're going to say it's about the olive oil. We like fruits and vegetables, we're going to imagine these, you know, Mediterranean islanders eating a lot of fruits and vegetables.
The reality - the one thing we know for sure is they had no refined flour and they had virtually no sugar. And that could be the explanation. The point I keep making in the book is science is about refuting alternative hypothesis. If you have two hypotheses that fit the evidence, don't just pick one because you like it better.
FLATOW: Mm-hmm. Dr. Krauss?
Dr. KRAUSS: Yeah. Let me just kind of brief you on both those points. First, I think Gary did point out that it's the processed and refined starches and sugars that are the most deleterious metabolically, and the corollary is that foods that contain lots of insoluble fiber have a low density of energy, that is they have a lot of bulk but not many carbohydrate calories are those that are rich in fiber. And many vegetables and grains fit in that category.
So those are still on the list, although, again, the total amount of carbohydrate should not be pushed higher than most people kind of achieve with grains alone. What happens is people wind up eating too many other kinds of starches and they don't really know how much fiber is in them, so using that recommendation is very difficult in practice. So I tend to agree with Gary and considering all carbohydrates in the category are potentially being adverse.
But the second issue on the Mediterranean diet brings up another tendency to focus on one thing. I mean, Mediterranean diet is really a whole collection of dietary practices, and it brings out the role of polyunsaturated fatty acids. So we've been talking about saturated fat and the evidence or lack of it for its relationship to heart disease risk. But the real concern is can we benefit heart disease risk by eating other kinds of fats.
And the studies of Mediterranean diet, including some more recent studies carried out in France suggests that so-called polyunsaturated fats such as those found in fish oil in particular as well as vegetable oils and seed oils can have beneficial effects on heart disease risk.
And it may have nothing to do with cholesterol to maybe many other actions, including inflammation which is a cause of pathology including heart disease that we haven't touched on and really wasn't discussed much in Gary's book that connects in many ways diet and fat and disease in ways that we're just beginning to understand. Inflammation goes up when you get fat, and inflammation can be affected by dietary practices. This is a new dimension that Gary's book has not gone to explore…
Mr. TAUBES: But, again, if it's the carbohydrates that make you fat through the influence of insulin, then the inflammation is just something that - is another side effect of eating the carbohydrates.
Dr. KRAUSS: Yeah. I think it can still come back to carbohydrate as being one of the causes, but there may be other dietary practices that might ameliorate inflammation as well. And I think polyunsaturated fats and fish oils should be at least brought to people's attention as having some evidence to support their benefits on heart disease risk.
FLATOW: Let's go to Owen in Kenai, Alaska. Hi, Owen.
OWEN (Caller): Hi. I had a - just a quick question kind of - I work outside all day and, you know, I need quick energy so I eat a lot of carbohydrates and I thrive on it. But, you know, I know you can get protein from vegetables, you know, types of vegetables and you still get carbohydrates from different types of vegetables and grains and whatnot. And I was just, you know, curious, has anybody really looked into genetic disposition to types of carbohydrates and whether or not that will affect how much insulin they produce and whether or not they'll grow large because of that?
FLATOW: Dr. Krauss?
Dr. KRAUSS: Well, we know there are big differences in a population that are almost certainly genetically related in how they respond to diets including carbohydrate. We've actually done some studies, finding specific genes or genetic markers is really a challenge that brings in the whole complexity of human genome because we're wired in very complex ways genetically. But it is absolutely true that there is a huge amount of variability in people's responses that represent wiring. Most of us unfortunately are wired to put on fat in response to carbohydrate (unintelligible) feeding.
FLATOW: What about carbohydrates out of fruits and vegetables? Are they the same - the sugars in there doing the same thing as if you're eating other kinds of sugars?
Mr. TAUBES: Well, 95 percent of the - or 85 percent of the weight of a fruit is water, so you have considerably less carbs per volume. And one of the points that was made 40 years ago was that in order to get enough like, say, the average amount of sugar that we eat in the U.S. every day, you would have to eat about 10, 15 apples a day depending on the size of the apples. And if you ate 10 to 15 apples, you wouldn't have much interest in eating anything else.
(Soundbite of laughter)
Mr. TAUBES: You certainly couldn't eat it as quickly as you could, for instance, drink a quarter of Gatorade. The point is if you ate 10 apples a day, would you - would that have a fattening effect? Nobody no does the studies. They just recommend that we all eat fruits and vegetables.
FLATOW: And lots of servings of them.
Dr. KRAUSS: And lots of servings of them.
FLATOW: But we're not - and you say we haven't studied that, how…
Mr. TAUBES: Again, they don't - when they do clinical trials of diet - and people tend to change a lot of different things, and clinical trials are expensive. I mean I could give you a study that I would like to see done that I think would solve a lot of this problem. Okay.
FLATOW: Okay. Are we listening out there?
Mr. TAUBES: Are you listening out there? This is a cheap study. Here's the two issues. You have basically two competing hypotheses about why we gain weight. One is that it's the calories, and the only way to lose weight is by eating less calories than you expend or expending more than you eat. And the other is that it's about the carbohydrates and the calories are virtually worthless. And what you do in science, you said, what hypothesis? I have my hypothesis, what do they now predict? So let me make a prediction and then I'll test that prediction, see if it's true.
So the calorie hypothesis says if you increase your consumption of calories by 500 calories a day, you'll get fat. The carbohydrate hypothesis says, if you increase your consumption by 500 calories a day but don't eat carbohydrates, you'll get thin. So there's actually now a way to measure the energy expenditure of a typical human.
There's something called doubly-labeled water and you could get a weekly measure within 10 percent of the average expenditure every day and you could say, here's I have five obese subjects who eat, say, to each expend twenty-five-hundred calories a day. So our calories hypothesis says if we feed them 3,000 calories and even if there are no carbs in them, these people are going to get fat, and our carbohydrate hypothesis, these people are going to get thin.
So if you actually take five fat subjects - you don't need a lot - measure their energy expenditure and then give them diets, make them eat the Atkins diet but 500 calories more a day than they've eating before. And one hypothesis say lose weight, the other hypothesis say gain weight. It would take six months to do it, might cost you $50,000 which is peanuts by modern funding standards.
FLATOW: And edible. Well…
Mr. TAUBES: And you could have an answer in six months.
FLATOW: Well, let me remind everybody, this is TALK OF THE NATION: SCIENCE FRIDAY from NPR News, talking with Ronald Krauss and Gary Taubes, author of "Good Calories, Bad Calories." Dr. Krauss, what do you think of that?
Dr. KRAUSS: Well, listen I'm all in favor of testing hypothesis by experiments, but I'm not sure if the experiment Gary proposed is going to give us a definitive answer because really what most people are concerned about is if you can lose weight, that's fine, but can you maintain a weight loss over the long term? And we are just notoriously poor at devising any scientific rationale that would convert to a result that would make people thinner after two or three years of following a diet.
Mr. TAUBES: But that's a nihilistic argument, Ron. Again, the question is, you know, we could say we're notoriously poor in getting people to quit smoking. The question is what makes them fat. If you physicians out there could tell this people, look, carbohydrates make you fat; the reason you get fat when you fall off the diet is because you go back to eating the foods that make you fat, it would help people stay off the foods. Instead, what you told is, look, it's really hard to stay on a diet, but try this one, it works just like every other one. They all work by reducing calories which isn't necessarily the case, you know?
Dr. KRAUSS: Sure. I'm just saying the experiment needs to be a longer one to really make it stick in terms of putting a lot of effort into getting people to change their…
Mr. TAUBES: But we're only interested in testing hypothesis. That's all - you know, it's like let us find out what the truth is.
FLATOW: You've gone the next step already, Dr. Krauss.
Dr. KRAUSS: (Unintelligible) putting funding into a project like that, I think, would require a by the public who expects to get some health benefits (unintelligible).
Mr. TAUBES: Well, not if you're talking $50,000.
(Soundbite of laughter)
Dr. KRAUSS: Well…
Mr. TAUBES: I mean, again, it's, you know…
Dr. KRAUSS: That will be great.
Mr. TAUBES: …we'd get some heavyweight guy in Wall Street to fund that tomorrow.
FLATOW: So to speak.
Mr. TAUBES: You know, play your role in the scientific history, you know, like being the guy who funded the Eclipse Expedition in 1917.
FLATOW: But in all seriousness, Dr. Krauss is right. And you've pointed out how overweight or obese the society is that you would think that they would be looking for some simple answer if it's the carbohydrate problem that would be something you could focus on, Dr. Krauss, could you not?
Dr. KRAUSS: I'm just skeptical. I mean, I'm absolutely enthusiastic about the science. I think there's a lot that Gary has highlighted that I think is moving in the right direction to try to explain how he got that, but I'm really concerned that we don't yet have a real strong clue as to how to convert that information into a therapy that will either prevent obesity or treat it effectively. And I think that we're not going to really be able to justify the research until we can show that it could lead us to those kinds of experiments and those are really expensive, really hard to do.
FLATOW: Well, maybe somebody has got a few extra bucks who wants to do Gary's experiment and we'll report it back here on SCIENCE FRIDAY.
Mr. TAUBES: One can only hope.
FLATOW: We'll see how it works. I want to thank you both for taking time to be with us today. Gary Taubes is contributing correspondent for Science magazine, author of "Good Calories, Bad Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease," a very thoughtfully written book. I recommend it. It will get you thinking about things and learning stuff you never knew before. Ronald Krauss, senior scientist and director of atherosclerosis research at Children's Hospital Oakland Research Institute in California. Thank you, Dr. Krauss.
Dr. KRAUSS: Thank you, Ira. It was a pleasure.
FLATOW: Thanks for taking time to be with us.
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