How Little We Know: Big Gaps in Psychology and Economics

Seth’s final paper “How Little We Know: Big Gaps in Psychology and Economics” is published in a special issue of the International Journal of Comparative Psychology (Vol 27, Issue 2, 2014). This issue is about behavioral variability and is dedicated to Seth. Abstract of the paper follows:

A rule about variability is reducing expectation of reward increases variation of the form of rewarded actions. This rule helps animals learn what to do at a food source, something that is rarely studied. Almost all instrumental learning experiments start later in the learning-how-to-forage process. They start after the animal has learned where to find food and how to find it. Because of the exclusions (no study of learning where, no study of learning how), we know almost nothing about these two sorts of learning. The study of himan learning by psychologists has a similar gap. Motivation to contact new material (curiousity) is not studied. Walking may increase curiosity, some evidence suggests. In economics, likewise, research is almost all about how people use economically valuable knowledge. The creation and spread of knowledge are rarely studied.

The family is grateful to Aaron Blaisdell Ph.D. who completed final edits to Seth’s final manuscript for publication.

Cause of Death

Hello, this is Seth’s mother Justine. I’d like to offer what little information I have to try to answer some of the questions that were posted about Seth’s death. We’re told that we’ll get a full coroner’s report in about 6 months. In the meantime we were given only “Cause A: Occlusive coronary artery disease” and “Other significant conditions: cardiomegaly.”

Most of you won’t be surprised to learn that Seth had not visited his doctor in Berkeley in many years, and, responding to a recent question, said that he hadn’t been to a doctor during his stay in Beijing either. We are left with 3 sets of paper records. The earliest, dated 2009, reports a Coronary Calcium (Agatston score) screening which he discussed here last October. He obtained a second screening 1-1/2 year later. The first report showed his coronary artery occlusion to be about average for a man his age, with an accompanying risk of heart attack, but no cardiomegaly. The second report, following his conclusion that butter was beneficial for him, and his heavy ingestion of it, showed an improvement in his score: “Most people get about 25% worse each year. My second scan showed regression (= improvement). It was 40% better (less) than expected (a 25% increase).” The report showed the calcification to be unevenly distributed, with most found in his left main coronary artery, and none in all but one of the other arteries. Again, no heart enlargement was reported.

The second medical report set, done in December 2011, was from Beijing and covered an exam that may have been required by his employer, Tsinghua University. This included a physical exam, an x-ray and EKG. All reports were negative, i.e., no abnormal findings and no cardiomegaly.

The third set of reports, from a laboratory in St. Charles, Ill., used data collected in Berkeley. They list toxic and essential elements in his hair. The latest report, dated July 18, 2013, showed one element rated “high.” This was mercury, “found to correlate with a 9% increase in AMI [acute myocardial infarction]” according to the report. His level was assumed to indicate exposure gained from eating fish. Presumably Beijing’s toxic smog contributed directly both to the mercury level of the fish that he ate there, and to the level in his hair.

The only information about his blood pressure was in the Beijing report where it was recorded at 117/87. I could find no information about cholesterol levels, though it has not been a familial problem. Of the remaining Framingham Study risk factors: Seth did not smoke or have diabetes. He was not overweight and was physically active. Seth’s father died of a heart attack at 72.

Of course, I can’t end this posting without sending my deepest thanks for all of the kind notes posted here. They were hurtful to read because of the reminding. They were healing to read because of the solace gained from learning about his friends and that he was able to help many people.

Justine

Interview with Gary Taubes (part 3)

INTERVIEWER You wrote that New York Times piece, and from my take on it, you had a bunch of evidence, and then you got a book contract. Is it fair to say that you found out that what you wrote in the piece was mostly right?

TAUBES It’s a difficult question. I had actually pitched the New York Times piece on fat as an attempt to determine the cause of the obesity epidemic. The proposal was very open ended. I had several ideas. I actually believed, going in to the story, that the answer was going to be that high-fructose corn syrup was responsible for Americans getting fatter over the last 30 years.

INTERVIEWER I’m glad to hear that.

TAUBES The thing about the obesity epidemic is that we can say when it starts, give or take five years: sometime between the mid-1970s and late 1980s. So we have a starting point, and that happens to coincide with the introduction of a type of high-fructose corn syrup known as HFCS-55, which was developed to taste exactly like sugar when it’s put in sodas and juices. In fact, it is effectively identical to sugar, as far as the body is concerned — sugar (sucrose) is 50-50 glucose and fructose and HFCS-55 is 45 percent glucose and 55 percent fructose — although I didn’t know that when I pitched the article. But I thought that high-fructose corn syrup is so cheap. Basically this is an idea that Greg Critser in a book called Fatland picked up on, and subsequently Michael Pollan, too, that high fructose corn syrup allows you to saturate the market with sugar, without any fear that price fluctuations will cause you to go out of business, or lose you a lot of money. If the international price of sugar suddenly spikes, as it did in the 70s, and you’re committed to fulfilling this enormous demand for sugar you’ve created, then you’re in trouble. But if you have a cheap reliable source of sugar, at a price that won’t change from year to year, then you can create an enormous market without fear. This was, more or less, my naive idea of how the economics of HFCS might have caused an entire nation to get fat. Once they had this dependable low-cost sugar substitute, the sugar industry and the soda industry could then expand their production and sell Big Gulps, etc. Then I did the reporting. I talked with industry analysts, and they said that was nonsense; that the primary cost of selling sodas and fruit juices is the bottling and the shipping, and that the cost of the sweeteners is such a tiny portion of the cost of the end product that it wouldn’t have made any difference whether it was sugar or high-fructose corn syrup. So I moved to my next idea, which was based on the fact that the beginning of the obesity epidemic coincided with the institutionalization of the low-fat dogma. As I’m doing that reporting, I stumbled upon what was, at that time, five trials of the Atkins diet, all of which had been finished, but not yet published. At one point, when I was doing the reporting, I actually got worried that some other journalist would beat me to the punch.

INTERVIEWER What was it about the Atkins diet that made these trials so important to your article?

TAUBES: Well, remember, my background, as a journalist and in school, was more or less in physics. In the kind of physics I used to write about, you’ve got some complicated detector that’s looking at particles and atoms smashing together inside it and you’re looking for some byproduct of a collision that you’ve never seen before. A new particle. But the first thing you have to do is make sure you understand your detector. Can you believe what it’s telling you. So you to have to calibrate it. If you want to know how much you weigh, for instance, one thing you might do before you step on the scale is you calibrate that. You make sure that when you’re not on it, the little arrow on the scale is pointing to zero. If it’s registering one or two pounds when you’re not standing on it, then it might be off by five or ten pounds or more when you are. So you want to calibrate your equipment. You want to know that when you set it to zero, it says zero. That’s an idea that’s always resonated with me. Measure what happens at an extreme, make sure you understand that, and then see what happens from there. So here’s the Atkins diet: in theory, you’re removing virtually all of the carbohydrates, but you don’t tell people to eat less. You tell them to eat as much as they want. It’s like you’re setting the diet to zero carbohydrates, and as much fat as possible. According to conventional wisdom, you should certainly not lose weight and you might even gain it. But here were five studies saying that, lo and behold, people really do lose weight when you remove the carbohydrates from the diet, and they lose more weight than they do when you tell them to keep the carbohydrates but eat less calories. What’s more, their cholesterol profiles actually improve, so how can fat or saturated fat be bad for your cholesterol, if these high fat, high saturated fat diets make your cholesterol levels better. To me that had to tell you something about the validity of the low-fat dogma and about the underlying physiology. What do carbohydates do, and what does their removal do. So once I learned about those five studies, I was confident that I had a story that was now worth writing. As for your original question, about whether I found out most of what I originally wrote was right, obviously the book supports the message of the article, but I no longer believe a fair number of things I believed when I wrote that story. For instance, when I wrote the Times article I inherently believed that the key was still calories consumed.

INTERVIEWER You mean things that you believed then, that you don’t believe now?

TAUBES Yes, that I don’t believe now. In that original article, I discussed what David Ludwig has argued — that easily digestible carbohydrates cause these blood sugar and insulin spikes, and that in turn causes blood sugar to plummet, and the result is blood sugar so low a few hours later that this in turn makes you hungry. So you eat more and that’s why you get fat with carb-rich diets. Ludwig works with obese children at Harvard and I believed that his hypothesis was probably true. Then I also talked about Michael Schwartz’s research at the University of Washington. Schwartz believes that insulin’s primary role is to suppress hunger in the brain, but that somehow we become resistant to that effect and so, once again, we eat too much and that’s why we get fat. Both these theories are predicated on the notion that we get fat because we eat too much and that’s what I believed. We consume more calories than we expend and we get fat; something about carbohydrates facilitates that excess consumption. Now I believe the causality is reversed, and that’s what I discuss in the book and in the lecture. Carbohydrates make us accumulate calories in our fat tissue, and that in turn makes us eat too much. It’s all about the regulation of fat metabolism. All those things that Ludwig and Schwartz were talking about might have been true (I mean, they are true, on some level), but they’re not the driving force of why we get fat, or why removing the carbohydrates makes us lean.

INTERVIEWER I see. So that’s a good summing up of what was in your article that you believe, and what you don’t believe anymore.

TAUBES There are other related facts, as well. I never imagined when I wrote that original article that I would come to believe that exercise won’t make you lose weight, even though I’ve been an athlete my entire life and it’s never helped me. So it’s fair to say that when I wrote that New York Times article five years ago, I had an entirely different conception about the causes and cures of obesity and overweight. Carbohydrates were key, but my understanding of the mechanisms was completely different. That’s the kicker with research and reporting: you don’t know what you’ll find until you do it.

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Interview with Gary Taubes (part 2)

INTERVIEWER What do you think about prions?

TAUBES Here’s the problem with prions: the claim is that here’s a radical discovery — an infectious agent that doesn’t have nucleic acid — and it’s based fundamentally on a negative result, which is that when researchers have gone looking for the nucleic acids they failed to find them. Therefore, so the logic goes, they must not be there. The original claim, by Stan Pruisner, another Nobel Prize winner, was premature. He made some claims in his early papers that were definitively wrong. Yet everything he’s done since then supports his initial claim, which suggests he’s was either remarkably lucky to begin with, or he’s only capable of interpreting his results so that they agree with his preconceptions. One of the themes in all of my work is that if you go public on premature data, what happens is that the motivation to do really good science ceases. By “really good science”, what you’re supposed to do, as brutally as you can, is to try to come up with tests that would refute your own hypothesis. The idea is that if your hypothesis survives every rigorous test you can imagine, and all those that everyone else can imagine, then you can start believing itss true. But once you’ve staked a claim based on premature data — once you’ve gone out on a limb without doing any of those rigorous tests — now your motivation becomes to prove that you were right., which you can never do in any case. But the point is that you stop trying to refute your hypothesis, and you start trying to accumulate evidence that supports it and the latter isn’t science. It’s more like what happens in religions.

INTERVIEW That’s what happened with Peter Duesberg. He was a good scientist until he started making claims about HIV.

TAUBES When I wrote this prion article in 1987, the science was so bad that it was a joke. Still, I never said that the prion concept wasn’t correct; I just said there was excruciatingly little evidence to support it, and there were plenty of reasons to believe it was wrong. How do you get strains of an infectious agent without nucleic acids (RNA or DNA) to encode the information in the strains? If you actually look today, even though Prusiner has won the Nobel Prize, if you go to the WHO website or the NIH website and you read up on prions, you’ll see that it’s still considered a hypothesis. There’s still no way to explain how you can get strains without a virus. Prusiner has these ideas, but they’re along the lines of now “a miracle happens”. It’s another long story, but one of the problems (and this is a theme in my book), when you let an untested hypothesis grow and infect the science to the point where people start to believe it’s true, even though it’s never been rigorously tested, the obstacles against ever overturning it get bigger and bigger. It’s like the dietary fat hypothesis: you let it sit around for 40 years, and it evolves to the point that people consider it dogma; it’s virtually impossible to overturn it. The situation with prions isn’t so bad because the public doesn’t care about prions the way that they care about diet, but once the Nobel Prize is awarded, even though it’s still considered a hypothesis, people tend to ignore the studies that suggest it’s wrong. There’s one researcher from Yale who is constantly publishing evidence in major journals that she’s found the nucleic acids, and people just ignore her. They believe the question has already been answered.

INTERVIEWER What’s her name?

TAUBES Laura Manuelidis.

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Interview with Gary Taubes (part 1)

I interviewed Gary Taubes shortly after he gave a talk about the main ideas of his new book — Good Calories, Bad Calories — at UC Berkeley. The interview lasted 2 hours.

INTERVIEWER I just spoke to someone who reduced the carbohydrate in his diet, for various reasons, including your book. He found that his performance on mental problems started improving again. It had stopped improving; it had been constant for a long time, and then it started getting better. So it may be that when you reduce the carbohydrate in your diet, your brain starts working better.

TAUBES Well, there is evidence that your brain works more efficiently on ketones, as does your heart. So if he reduced his carbohydrate consumption sufficiently, he probably increased the level of ketones in his blood. But I’m just speculating here.

INTERVIEWER: The book seems to have had an unusual beginning. You’d been writing about salt, and you learned that a scientist you didn’t trust about salt was also talking about obesity?

TAUBES Well, I’ve spent over 20 years now writing about controversial science. In the mid-1980s, I lived at CERN for ten months, the big physics lab outside Geneva, watching physicists discover non-existent elementary particles. Then I wrote a somewhat infamous story about prions, the supposed causative agents of Mad Cow Disease. I wrote a book about cold fusion: I got obsessed with this question of how it happened, because it was so obviously wrong. After all that, I developed what I believe is a very good feel for who’s a good scientist, and who’s a bad scientist, just by talking to them. There are certain ways that good scientists describe their data, describe the caveats, and describe the conditions by which they may or may not be right. I had also, obviously, with cold fusion, interviewed some of the worst scientists in the world. I used to joke with my friends in the physics community that if you want to cleanse your discipline of the worst scientists in it, every three or four years, you should have someone publish a bogus paper claiming to make some remarkable new discovery — infinite free energy or ESP, or something suitably cosmic like that. Then you have it published in a legitimate journal ; it shows up on the front page of the New York Times, and within two months, every bad scientist in the field will be working on it. Then you just take the ones who publish papers claiming to replicate the effect, and you throw them out of the field. A way of cleaning out the bottom of the barrel.

INTERVIEWER I thought your NY Times article, “What if It’s All Been a Big Fat Lie,” sort of did that. The people who came out against it, they were the bad journalists. Just throw them out!

TAUBES Well, how I got onto that: I was doing this story for Science on salt and blood pressure, looking into the controversy about whether salt consumption plays any role at all in raising blood pressure and causing hypertension. One of the prime players in this salt/blood pressure controversy was obviously one of the worst scientists I’d ever met — one of the five worst”¦you can’t say, in that five, who is the very worst, but they’re all pretty bad. This is a group that includes guys like Stan Pons and Martin Fleischman who claimed to have discovered cold fusion. While I’m on the phone with this guy, interviewing him, he takes credit for getting Americans to eat less fat and fewer eggs. I literally finished the interview, called my editor at Science, and I said “You know, one of the worst scientists I’ve ever interviewed just took credit for getting Americans to eat less fat and fewer eggs, and I don’t know what the story is, but when I’m done with this salt story, I’m going to look into fat, cholesterol, and saturated fat.” I had a great relationship with Science. My editors had faith in me. If I said there was a story there, they’d give me the support I needed to pursue it. A year later, I ended up with that first story in Science, saying that there’s no evidence that reducing the total fat in the diet makes a damned bit of difference in our health. The evidence that saturated fat and monounsaturated fats are players is, at best, marginal. And that led to the N.Y. Times article.

INTERVIEWER What did that scientist say that made you rank him so low?

TAUBES There are all kinds of signs. He told me there was no controversy, when there was obviously a controversy. His side might have been right, but to deny there as a controversy was ludicrous. He talked about the legitimacy of throwing out negative data. You measure salt consumption one way; you don’t see any effect on blood pressure, and so you decide that’s obviously the wrong way to measure it. The implication of everything he told me was that he knew what the answer was before he did his experiments, and then he adjusted his experimental techniques and methodology until he got the answer that he wanted. And he believed this was legitimate science. There are other signs. I’m a stickler about the use of words like “evidence” and “proof”. So if someone tells you there’s no evidence for some controversial belief, you can be fairly confident that they’re a bad scientist. There’s always evidence, or there wouldn’t be a controversy. If somebody says that “we proved that this was true” or “we set out to prove that this was true” that’s another bad sign. The point here, as Popper noted, among others, is that you can never prove anything is true; you can only refute it. So researchers who talk about proving a hypothesis is true rather than testing it make me worried.

INTERVIEWER Yeah, I see what you’re saying. They overstate; they twist things around to make it come out the way they want. They are way too sure of what they”¦

TAUBES Yes, and the really good scientists are the ones, almost by definition, who are most skeptical of evidence that seems to support their beliefs. They’re most aware of how they could have been fooled, how they could have screwed up, or how they might have missed artifacts in their experiment that could have explained what they observed. They’re very careful about what they say. If you ask them to do play devil’s advocate, and tell you how they could have screwed up, then at the very least, they’ll say “Well, if I knew how I could have done it, I would have checked it before I made the claim”. So when I’m talking about discerning the difference between a good scientist and a bad scientist, I’m talking about how they speak about their research, the evidence itself, it’s presence or absence. My friends in journalism would often ask me this question: by what right do I think make decisions about who’s a good scientist and who’s not. I’d say “Well, when you’re an English major, you can be confident that Norman Mailer was a better writer than John Grisham, even though John Grisham makes 10 to 100 times more money”. It’s just a feel for what you do; I don’t know how else to describe it. I know a good scientist when I talk with one. I might be fooled, on occasion, but….

INTERVIEWER It’s not particularly well-correlated with how famous they are, or how many Nobel Prizes they’ve won.

TAUBES My first book was about a Nobel Prize winner who discovered non-existent elementary particles.

INTERVIEWER Who was that?

TAUBES An Italian physicist named Carlo Rubbia.

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