TAUBES Now here’s one question for you, you know the Freakonomics guys, right? Did you read their last column on obesity?

INTERVIEWER About bariatric surgery?

TAUBES Yes. In particular, the last two paragraphs, about their recommendation that fat people, in effect, carry around something nauseating. I felt like I was reading something from 150 years ago, where they were using anal suppositories to try to cure obesity. Do you remember those paragraphs?

INTERVIEWER Yes, I do.

TAUBES They’re saying, “let’s get fat people to have willpower, like we do.” Here’s a way they could do it, they could carry some nauseating-smelling thing in a pouch around their neck, and whenever they find themselves going to the refrigerator, they could open it up and smell it.

INTERVIEWER I think they were trying to illustrate the concept of commitment device.

TAUBES I got what they were trying to do, but…

INTERVIEWER You’re saying that trivializes the problem.

TAUBES More than that. I’m saying it misses the point entirely. It’s not about how much they eat. Remember, you can starve fat animals, for instance, and they’ll die with their fat tissue intact. It’s not about how much they’re eating; it’s about the regulation of their fat tissue. And if you don’t understand that, you’re not doing anyone a favor by discussing it publicly. If these guys are going to write about this subject, and they’re so now so influential and noticeable, they should have some understanding of what’s actually going on physiologically. We talked earlier about how I can become flabbergasted — your words was “radicalized” — by the idea that people can write about obesity without stopping to think “what’s the mechanism? Should I know anything about the underlying biology?” And again, I never did until the last five years. It was only when I did the research for the book that I realized that you have to actually pay attention to the underlying biology — the hormonal and enzymatic regulation of fat tissue — or you can’t understand what’s going on. Imagine writing about growth defects, about gigantism or dwarfism, without caring about the hormonal regulation of growth. If the Freakonomics guys are going to write about obesity in the New York Times, then maybe they should read my book (he said, ego-maniacally), so they know what they’re talking about. And since I don’t know them personally, maybe you could…

INTERVIEWER I’ll recommend your book to them. It’s great that you were invited to Berkeley; that shows people trust you. The fact that they invited you means you’re not a heretic, you’re not off the reservation, you’re a respectable person. The fact that you continue to write for the New York Times, that’s very good. Every article you publish from now on will push your book forward, will push your case forward, will say that you are a serious person who is respected by serious people. Just maybe, just maybe, this is one of the cases where the authorities were wrong. We’re all familiar with this happening in the past, and maybe this is just another case. For everybody but the tiny faction of people at the top of the health establishment, I think they’re perfectly fine with the idea that the authorities are wrong. I think that the lack of progress on the obesity epidemic is making more and more people dissatisfied. That’s just a guess. More and more people, outside of the people who are responsible for the current policies.

TAUBES I think that’s true, but there’s this contrary effect that happens. I said this in my lecture. The science I’m trying to get across can be accepted up until the point at which I say the the word carbohydrate, and then people shut down, and they think “Oh, it’s that Atkins stuff again.” Their minds close and they turn around and go back to their lives. Anyway, I look forward to seeing the interview and getting your book and reading it. I enjoyed this. Again, I like nothing better than talking about this stuff.

INTERVIEWER I learned a lot from our conversation. I’m sure my blog readers will enjoy this.

Interview directory. The whole interview.

INTERVIEWER Did you ever hear of Israel Ramirez? He was one of Mark Friedman’s colleagues.

TAUBES That’s the Ramirez you quoted. I forgot that. I didn’t put it together, because I always knew him as I. Ramirez. I saw that, too — here’s my other carp, and then I’ll stop. It doesn’t do any good to have somebody discuss my arguments who hasn’t read the book.

INTERVIEWER I asked him to, so it’s my fault.

TAUBES Then other people see someone refuting me, and they don’t care whether they read the book or not. You know what I mean?

INTERVIEWER Well, I appreciate that it would be irritating.

TAUBES The problem is, you can’t ask Mark, because I know what Mark thinks of the book. He’s read it — he read it in draft and critiqued it for me. He’s in the book, so you can’t ask him, either, even though he would probably say tremendous things about it. You have to find people whose research I don’t discuss. I’ll tell you one guy who would be worth knowing what he thinks: George Wade. He’s at U. Mass Amherst. He did these rat experiments. He’s an expert on animal reproduction and I sent him a draft of the book, and I didn’t ask him to critique it, but I was asking him a fact-checking question and I sent him a copy of the book and he never got back to me. I don’t know if he read it or not. I’d be curious what he thinks, because he was my revelation, Wade. He shifted my paradigm.

INTERVIEWER You said something about that in your Berkeley talk.

TAUBES He was the one who got me to realize that we overeat because we get fat; we don’t get fat because we overeat. That’s the paradigm shift, the literal paradigm shift. He’s describing his ovariectomized rat experiments to me. That’s how he did it.

INTERVIEWER Do you know about someone named Michel Cabanac?

TAUBES Yeah, I read a lot of Cabanac’s stuff. I forget what the details were. I only remember that I was disappointed and decided that he was missing the point.

INTERVIEWER Well, he had a big effect on me, at least. His idea is that I’m sure there’s a set point, but that’s an old idea. The new idea is that the set point depends on what you eat. He had some ideas about that.

TAUBES Well, that’s the thing. There is a settling point, whatever you call it. The weird thing is that insulin regulates the settling point. It obviously goes up and down. It obviously goes up, anyway.

INTERVIEWER He might not disagree with your book. I asked him “Can insulin regulate the settling point?” I thought that was unlikely, but he didn’t; he thought, “Why not?”

TAUBES Insulin levels correlate with weight, with fat. The question is whether insulin goes up because we get fat, or we get fat because insulin levels go up. There’s always two ways of interpreting the observations in this business. So the establishment viewpoint is that insulin goes up because we get fat. I tracked that belief down to see if there was evidence for it, and indeed, there’s not; there’s a sort of misinterpretation of these experiments done by Ethan Sims 40-odd years ago. On the other hand, it’s easy to show that you can manipulate insulin levels by manipulating the carb content of the diet. If you manipulate the carb content of the diet, then the question becomes, does insulin and the weight still track? So the hypothesis is insulin regulates the settling point and the question is how do we test that rigorously to find out of that’s indeed what’s happening.

Interview directory.

A generation of Americans reduced their egg intake because eggs contain cholesterol and cholesterol = bad. Now comes this study from the Journal of Nutrition of the effect of 3 eggs/day:

In this study, 28 overweight/obese male subjects (BMI = 25–37 kg/m2) aged 40–70 y were recruited to evaluate the contribution of dietary cholesterol from eggs in a CRD [calorie-reduced diet]. Subjects were counseled to consume a CRD (10–15% energy from carbohydrate) and they were randomly allocated to the EGG group [intake of 3 eggs per day (640 mg/d additional dietary cholesterol)] or SUB group [equivalent amount of egg substitute (0 dietary cholesterol) per day]. Energy intake decreased in both groups from 10,243 ± 4040 to 7968 ± 2401 kJ (P < 0.05) compared with baseline. All subjects irrespective of their assigned group had reduced body weight and waist circumference (P < 0.0001). Similarly, the plasma TG [triglycerides] concentration was reduced from 1.34 ± 0.66 to 0.83 ± 0.30 mmol/L after 12 wk (P < 0.001) in all subjects. The plasma LDL-C concentration, as well as the LDL-C:HDL-C ratio, did not change during the intervention. In contrast, plasma HDL-C concentration increased in the EGG group from 1.23 ± 0.39 to 1.47 ± 0.38 mmol/L (P < 0.01), whereas HDL-C did not change in the SUB group. Plasma glucose concentrations in fasting subjects did not change.

I want to raise my HDL. I am going to eat more eggs. Perhaps nose-clipped.

From the SLD forums:

Thinking that I was doing a good thing, about twenty-two years ago, I stopped buying salt to keep at home — believing the hype about Americans eating too much salt, etc. I suppose that, in my younger years, it was not too dangerous as I was eating out a lot, and, at times, eating from packaged foods. Also, Pre-SLD, I would get cravings for popcorn (with a little salt added) and give in — so I did get salt at times.

But, for years, I have mainly cooked at home and have eaten foods high in potassium (garlic, onions, et al). Potassium depletes sodium further — and I was even taking potassium pills in order to ease a separate condition. I rarely go out and do not eat packaged foods. I had no idea that sodium was essential (stupid me). I thought that it was like sugar — best to cut it out completely.

On SLD (not that this is SLD’s fault, of course!), I could rein in my cravings for popcorn. And so I was getting no salt. At the end with SLD (and for many, many months, afterwards), I began to have an issue that if I ate anything sweet, I would begin to stutter, feel like I could not breathe, feel faint, dizzy, etc. It was like the sugar bypassed the blood-brain barrier and went directly to my head. Honestly, it was terrifying and I was fairly sure that I was becoming diabetic.

The doctors, noting atypical symptoms and a frightened, teary woman, naturally diagnosed panic attacks. Then low iron. And a million other things which had no effect. Of course they really thought that I was a hysteric (an hysteric?). The irony is that they thought that maybe I was dehydrated so I increased my water intake. The worst possible thing.

And then I began to faint, to black out. And then had two seizures.

A friend of mine who is a chef (my ex, actually) figured it out. I bought some sea salt and the minute I ate it, my body lunged! Like this was exactly what I needed. After three heavily salted meals, everything normalised — even things which I had not noticed as abnormal. My eyesight sharpened, my balance improved, and I felt sane — like I wasn’t drowning anymore. Overnight I felt better than I had in years.

Later neurological consultations confirmed that I probably injured my brain as badly as I did in the car accident I was in as it may have been chronically swollen from the lack of salt. Who knew? I had no idea how important — vital — salt was to the diet.

INTERVIEWER What happened when you met with the [UC Berkeley School of Public Health] epidemiology students?

TAUBES Again, it was a little discouraging, only because these kids really want to do good, they want to make a difference in the world. That’s why they go into the field. They want to have an effect. But as I say at the end of the book, to do science right, your primary motivation has to be to learn the truth, and if you’re infected with this desire to change the world, to save lives, it takes you away from the fundamental motivation, which is to get it right. If you want to save lives, then you want to get the word out as quickly as possible. You don’t want to wait ten or twenty years or more for definitive evidence, for the rigorous tests to be done; you want to give advice and tell people what you’ve learned, even if you only think that you’ve learned it. Doing science right takes a long time. So does good journalism. You can say the difference between my book and Gina Kolata’s book is — not counting whatever difference in intellect we begin with– my book took five years, more than full time, because I wasn’t going to say anything until I was certain that what I was saying was sound. She wrote her book in two years, part-time, while still working full-time as a New York Times reporter.

INTERVIEWER Yeah, they’re very different.

TAUBES Even when I was writing magazine articles, if I was in danger of missing a deadline, which was often the case, I would ask my editors, “Do you want it on time, or do you want it right?”.

INTERVIEWER There was a managing editor at The New Yorker, one of the first, whose motto was “Don’t get it right, get it written.”

TAUBES When I was a young journalist working for Discover, which was owned by Time, Inc., the philosophy was that one of the worst things anybody could do was over-report a story. Just get the facts and get it out. Except science doesn’t work like that. Science, you’ve got to get it right, and that takes time, and you can’t do it on deadline. Along those lines, I did read one of your blog entries about settling points versus set points, and I thought it might be… You know, I Google myself, as all writers do fairly regularly, so first you read all news stories that day, hoping that the Google Alert might have missed something, and then you go to the blogs.

INTERVIEWER So you read my post about the most surprising thing in your book?

TAUBES What was the most surprising thing?

INTERVIEWER That you didn’t agree that set points play a role in homeostasis.

TAUBES It’s funny – the more I think about it, the more Claude Bernard was brilliant. (I’d like to do a book on Claude Bernard, but probably can’t because my French is terrible.) In particular, this idea of the milieu interieur? The fundamental idea of homeostasis is that the body works to maintain the stability of what he called the milieu interieur, which gets translated to “internal environment”. What he meant by that is the conditions right outside the membrane of the cell, every cell in the body. So the body wants to maintain stable this internal environment — the pH, the blood pressure, the ionic potential, everything — of the cell itself. So it wants to make sure that the environment the cell lives in — every cell — remains relatively stable. in that sense, we’re this huge symbiotic organism made up of billions of individual cells, and homeostasis functions to keep the conditions that these cell live in stable. So each cell lives in this little isolated world, and it’s got to see stable conditions, or it’s going to die. The idea of the set point is that there’s some central controller in the brain that maintains homeostasis, but that’s naive. Rather, there’s an unbelievably complicated mechanism composed of individual settling points. Like the fatty acid concentration on the interior, and exterior of the fat cell. If there’s more fatty acids on the outside of the cell membrane than the inside, then fatty acids flow into the cell, and you get slightly fatter. There’s no brain in charge. The brain may respond, and the hypothalamus sends signals back and forth, and effects changes in hormones in response to changes in the environment, but there’s so many different interrelated, interconnected feedback loops involved that to refer to a set point is to grossly oversimplify things this beautiful homeostatic system, and it directs attention away from the body, where all these feedback loops interact, to the brain. Did you ever read any books on chaos theory?

INTERVIEWER No, I haven’t.

TAUBES Well, to understand homeostasis you have to understand this concept of dynamic equilibrium, where there can be hundreds of forces acting simultaneously. And the point is, you’ve got these negative feedback loops all over the body, and they involve the brain, but on some level, the dynamic equilibrium you’re looking at is right at the cellular level. That’s where the forces converge to make us leaner or fatter. And the brain is part of these loops, but to concentrate on the brain misses the big picture.

INTERVIEWER The brain is sensitive to the environment — sure, the set point doesn’t really exist anywhere, and sure it’s a function of about a zillion things, not all of them in the brain, sure. But the reason I like that idea of a setpoint is that it’s easy to imagine something going up and down, rather than a million things going up and down.

TAUBES But the problem is once you oversimplify, there’s a tendency to believe the oversimplification. You should go back and read the papers on settling points. There were a couple, if I remember correctly, written by psychologists from the University of Chicago. You should go back and read those original papers. They’re fascinating, and the point they make, is that you don’t need the brain involved. Like we don’t think of the brain regulating blood pressure. You don’t really think of your brain regulating blood glucose. Those cycles I described in my lecture, you know, the triglyceride fatty acid cycle and the Randall cycle, serve to regulate blood sugar. Then hormones are layered on top of those cycles, and the hormones are determined, in part, by the hypothalamus, so you get the brain involved, and the sensing of the environment, but there are other ways to sense the environment, like temperature sensing of the skin, evaporation. There are other ways that we adjust to the environment without the involvement of the brain. One of the things I left out of the book, for instance, is this theory that hunger is perceived by the liver.

INTERVIEWER Perceived, or controlled?

TAUBES Perceived. Or sensed by the liver. You know, your eyes collect photons, and then they send the signal back through the optic nerve. The perception of the universe is done in the inside of the brain, but the eyes are the sense organ that collect the photons. Your ears detect sound waves, but your perception of what you’re hearing is inside of the brain. This theory says that your liver senses fuel availability and then your brain integrates the signals from the liver and registers them as hunger or the absence of hunger.

INTERVIEWER Hunger is internal. It’s like the recognition. Hunger is not something external to the body.

TAUBES Let me re-phrase it. It senses fuel ability. Then your brain perceives it as hunger and initiates — that would be a better way of putting it. But the sense organ of fuel availability is your liver. I had some discussions with Mark Friedman, a fascinating guy, really smart. He’s at the Monell Institute.

Interview directory.