Celiac Experts Make Less Than Zero Sense

In the 1960s, Edmund Wilson reviewed Vladimir Nabokov’s translation of Eugene Onegin. Wilson barely knew Russian and his review was a travesty. Everything was wrong. Nabokov wondered if it had been written that way to make sense when reflected in a mirror.

I thought of this when I read recent remarks by “celiac experts” in the New York Times. The article, about gluten sensitivity, includes an example of a woman who tried a gluten-free diet:

Kristen Golden Testa could be one of the gluten-sensitive. Although she does not have celiac, she adopted a gluten-free diet last year. She says she has lost weight and her allergies have gone away. “It’s just so marked,” said Ms. Golden Testa, who is health program director in California for the Children’s Partnership, a national nonprofit advocacy group. She did not consult a doctor before making the change, and she also does not know [= is unsure] whether avoiding gluten has helped at all. “This is my speculation,” she said. She also gave up sugar at the same time and made an effort to eat more vegetables and nuts.

Fine. The article goes on to quote several “celiac experts” (all medical doctors) who say deeply bizarre things.

“[A gluten-free diet] is not a healthier diet for those who don’t need it,” Dr. Guandalini [medical director of the University of Chicago’s Celiac Disease Center] said. These people “are following a fad, essentially.” He added, “And that’s my biased opinion.”

Where Testa provides a concrete example of health improvement and refrains from making too much of it, Dr. Guandalini does the opposite (provides no examples, makes extreme claims).

Later, the article says this:

Celiac experts urge people to not do what Ms. Golden Testa did — self-diagnose. Should they actually have celiac, tests to diagnose it become unreliable if one is not eating gluten. They also recommend visiting a doctor before starting on a gluten-free diet.

As someone put it in an email to me, “Don’t follow the example of the person who improved her health without expensive, invasive, inconclusive testing. If you think gluten may be a problem in your diet, you should keep eating it and pay someone to test your blood for unreliable markers and scope your gut for evidence of damage. It’s a much better idea than tracking your symptoms and trying a month without gluten, a month back on, then another month without to see if your health improves.”

Are the celiac experts trying to send a message to Edmund Wilson, who died many years ago?

Posit Science: More Questions

Posit Science is a San Francisco company, started by Michael Merzenich (UCSF) and others, that sells access to brain-training exercises aimed at older adults. Their training program, they say, will make you “remember more”, “focus better”, and “think faster”. A friend recently sent me a 2011 paper (“Improvement in memory with plasticity-based adaptive cognitive training: results of the 3-month follow-up” by Elizabeth Zelinski and others, published in the Journal of the American Geriatrics Society) that describes a study about Posit Science training. The study asked if the improvements due to training are detectable three months after training stops. The training takes long enough (1 hour/day in the study) that you wouldn’t want to do it forever. The study appears to have been entirely funded by Posit Science.

I found the paper puzzling in several ways. I sent the corresponding author and the head of Posit Science a list of questions:

1. Isn’t it correct that after three months there was no longer reliable improvement due to training according to the main measure that was chosen by you (the investigators) in advance? If so, shouldn’t that have been the main conclusion (e.g., in the abstract and final paragraph)?

2. The training is barely described. The entire description is this: “a brain plasticity-based computer program designed to improve the speed and accuracy of auditory information processing and to engage neuromodulatory systems.” To learn more, readers are referred to a paper that is not easily available — in particular, I could not find it on the Posit Science website. Because the training is so briefly described, I was unable to judge how much the outcome tests differ from the training tasks. This made it impossible for me to judge how much the training generalizes to other tasks — which is the whole point. Why wasn’t the training better described?

3. What was the “ET [experimental treatment] processing speed exercise”? It sounds like a reaction-time task. People will get faster at any reaction-time task if given extensive practice on that task. How is such improvement relevant to daily life? If it is irrelevant, why is it given considerable attention (one of the paper’s four graphs)?

4. According to Table 2, the CSRQ (Cognitive Self-Report Questionnaire) questions showed no significant improvement in trainees’ perceptions of their own daily cognitive functioning, although the p value was close to 0.05. Given the large sample size (~500), this failure to find significant improvement suggests the self-report improvements were small or zero. Why wasn’t this discussed? Is the amount of improvement suggested by Posit Science’s marketing consistent with these results?

5. Is it possible that the improvement subjects experienced was due to the acquisition of strategies for dealing with rapidly presented auditory material, and especially for focusing on the literal words (rather than on their meaning, as may be the usual approach taken in daily life)? If so, is it possible that the skills being improved have little value in daily life, explaining the lack of effect on the CSRQ?

6. In the Methods section, you write “In the a priori data analysis plan for the IMPACT Study, it was hypothesized that the tests constituting the secondary outcome measure would be more sensitive than the RBANS given their larger raw score ranges and sensitivity to cognitive aging effects.” Do the initial post-training tests (measurements of the training effect soon after training ended) support this hypothesis? Why aren’t the initial post-training results described so that readers can see for themselves if this hypothesis is plausible? If you thought the “secondary outcome measure would be more sensitive than the RBANS” why wasn’t the secondary outcome measure the primary measure?

7. The primary outcome measure was some of the RBANS (Repeatable Battery for the Assessment of Neuropsychological Status). Did subjects take the whole RBANS or only part of it? If they took the whole RBANS, what were the results with the rest of the RBANS (the subtests not included in the primary outcome measure)?

8. The data analysis refers to a “secondary composite measure”. Why that particular composite and not any of the many other possible composite measures? Were other secondary composite measures considered? If so, were p values corrected for this?

9. If Test A resembles training more closely than Test B, Test A should show more effect of training (at any retention interval) than Test B. In this case Test A = the RBANS auditory subtests and Test B = the secondary composite measure. In contrast to this prediction, you found that Test B showed a clearer training effect (in terms of p value) than Test A. Why wasn’t this anomaly discussed (beyond what was said in the Methods section)?

10. Were any tests given the subjects not described in this report? If there were other tests, why were their results not described?

11. The secondary composite measure is composed of several memory tests and called “Overall Memory”. The Posit Science website says their training will not only help you “remember more” but also “think faster” and “focus better”. Why weren’t tests of thinking speed (different from the training tasks) and focus included in the assessment?

12. Do the results support the idea that the training causes trainees to “focus better”?

13. The Posit Science homepage suggests that their training increases “intelligence”. Was intelligence measured in this study? If not, why not?

14. Do the results support the idea that the training causes trainees to become more intelligent?

15. The only test of thinking speed included in the assessment appears to be a reaction-time task that was part of the training. Are you saying that getting faster on one reaction-time task after lots of practice with that task shows that your training causes trainees to “think faster”?

Update: Henry Mahncke, the head of Posit Science, said that he would be happy to answer these questions by phone. I replied that I was sure many people were curious about the answers and written answers would be much easier to share.

Further update: Mahncke replied that he would prefer a phone call and that some of the questions seemed to him hard to answer in writing. He said nothing about the sharing problem. I repeated my belief that many people are interested in the answers and that a phone call would be hard to share. I offered to rewrite any questions that seemed hard to answer in writing.

Earlier questions for Posit Science.

 

Assorted Links

More Trouble in Mouse Animal-Model Land

Mice — inbred to reduce genetic variation — are used as laboratory models of humans in hundreds of situations. Researchers assume there are big similarities between humans and one particular genetically-narrow species of mouse. A new study, however, found that the correlation between human genomic changes after various sorts of damage (“trauma”, burn, endotoxins in the blood, and so on) and mouse genomic changes was close to zero.

According to a New York Times article about the study, the lack of correlation “helps explain why every one of nearly 150 drugs tested at huge expense in patients with sepsis [severe blood-borne infection] has failed. The drug tests all were based on studies in mice.”

This supports what I’ve said about the conflict between job and science. If your only goal is to find a better treatment for sepsis, after ten straight failures you’d start to question what you are doing. Is there a better way? you’d wonder. After twenty straight failures, you’d give up on mouse research and starting looking for a better way. However, if your goal is to do fundable research with mice — to keep your job — failures to generalize to humans are not a problem, at least in the short run. Failure to generalize actually helps you: It means more mouse research is needed.

If I’m right about this, it explains why researchers in this area have racked up an astonishing record of about 150 failures in a row. (The worst college football team of all time only lost 80 consecutive games.) Terrible for anyone with sepsis, but good for the careers of researchers who study sepsis in mice. “Back to the drawing board,” they tell funding agencies. Who are likewise poorly motivated to react to a long string of failures. They know how to fund mouse experiments. Funding other sorts of research would be harder.

In the comments on the Times article, some readers had trouble understanding that 10 failures in a role should have suggested something was wrong. One reader said, “If one had definitive, repeatable, proof that the [mouse model] approach wouldn’t work…..well, that’s one thing.” Not grasping that 150 failures in a row is repeatable in spades..

When this ground-breaking paper was submitted to Science and Nature, the two most prestigious journals, it was rejected. According to one of the authors, the reviewers usually said, ”It has to be wrong. I don’t know why it is wrong, but it has to be wrong.” 150 consecutive failed drug studies suggest it is right.

As I said four years ago about similar problems,

When an animal model fails, self-experimentation looks better. With self-experimentation you hope to generalize from one human to other humans, rather from one genetically-narrow group of mice to humans.

Thanks to Rajiv Mehta.

The Yakult Women of Seoul

Their name in Korean means Yakult women: street peddlers who sell several probiotic drinks, including Yakult. I encountered them in a Seoul suburb (Bundang) on the way to the subway. During one 15-minute walk, I saw three of them. Other street peddlers in Bundang were often men (selling cookware or socks, for example) but the probiotic sellers were always women. I haven’t seen street peddlers selling probiotic drinks anywhere else. In Japan, Yakult and other probiotic drinks are sold door-to-door but apparently not on the street.

I asked a Korean friend how she (and Koreans in general) got the idea that probiotic drinks are good for health (which I am sure is true). She said she knew it before she went to school and believed she picked it up from TV ads. Apparently these ads are more successful in Korea than elsewhere. General Foods recently paid $9 million to settle a legal case based on Yoplait Yo-Plus ads in America that made similar claims. The lawyers who sued General Foods claimed that healthy people don’t benefit from Yoplait Yo-Plus.

I can think of several reasons that Yakult women exist in Korea but (apparently) nowhere else. Maybe the fact that Koreans eat a lot of kimchi makes them more likely to believe that a probiotic is healthy. Maybe Koreans care more about health than other people. Maybe Koreans are unusually sophisticated about health. Bundang’s density (it is full of tall apartment buildings) is surely one reason, because Yakult women weren’t the only street peddlers. American suburbs, where I almost never see street peddlers, are much less dense. Another certain reason is that Bundang is a wealthy suburb. A third certain reason is that Yakult and similar drinks help you digest lactose. Lactose intolerance is much more common in Asia than elsewhere.

It would be interesting to compare the rate of digestive problems in South Korea versus other countries, especially the United States. I think they are likely to be much less common in South Korea.

Assorted Links

Thanks to Vic Sarjoo.

Web Browsers, Black Swans and Scientific Progress

A month ago, I changed web browsers from Firefox to Chrome (which recently became the most popular browser). Firefox crashed too often (about once per day). Chrome crashes much less often (once per week?) presumably because it confines trouble caused by a bad tab to that tab. ”Separate processes for each tab is EXACTLY what makes Chrome superior” to Firefox, says a user. This localization was part of Chrome’s original design (2008).

After a few weeks, I saw that crash rate was the only difference between the two browsers that mattered. After a crash, it takes a few minutes to recover. With both browsers, the “waiting time” distribution — the distribution of the time between when I try to reach a page (e.g., click on a link) and when I see it — is very long-tailed (very high kurtosis). Almost all pages load quickly (< 2 seconds). A few load slowly (2-10 seconds). A tiny fraction (0.1%?) cause a crash (minutes). The Firefox and Chrome waiting-time distributions are essentially the same except that the Chrome distribution has a thinner tail. As Nassim Taleb says about situations that produce Black Swans, very rare events (in this case, the very long waiting times caused by crashes) matter more (in this case, contribute more to total annoyance) than all other events combined.

Curious about Chrome/Firefox differences, I read a recent review (“Chrome 24 versus Firefox 18 — head to head”). Both browsers were updated shortly before the review. The comparison began like this:

Which browser got the biggest upgrade? Who’s the fastest? The safest? The easiest to use? We took a look at Chrome 24 and Firefox 18 to try and find out.

Not quite. The review compared the press releases about the upgrades. It said nothing about crash rate.

Was the review superficial because the reviewer wasn’t paid enough? If so, Walt Mossberg, the best-paid tech reviewer in the world, might do a good review. The latest browser review by Mossberg I could find (2011) says this about “speed”:

I found the new Firefox to be snappy. . . . The new browser didn’t noticeably slow down for me, even when many tabs were opened. But, in my comparative speed tests, which involve opening groups of tabs simultaneously, or opening single, popular sites, like Facebook, Firefox was often beaten by Chrome and Safari, and even, in some cases, by the new version 9 of IE . . . These tests, which I conducted on a Hewlett-Packard desktop PC running Windows 7, generally showed very slight differences among the browsers.

No mention of crash rate, the main determinant of how long things take. Mossberg ignores it — the one difference between Chrome and Firefox that really matters. He’s not the only one. As far as I can tell, all tech reviewers have failed to measure browser crash rate. For example, this review of the latest Firefox. ”I’m still a big Firefox fan,” says the reviewer.

Browser reviews are a small example of a big rule: People with jobs handle long-tailed distributions poorly. In the case of browser reviews, the people with jobs are the reviewers; the long-tailed distribution is the distribution of waiting times/annoyance. Reviewers handle this distribution badly in the sense that they ignore tail differences, which matter enormously.

Another browser-related example of the rule is the failure of the Mozilla Foundation (people with jobs) to solve Firefox’s crashing problem. My version of Firefox (18.0.1) crashed daily. Year after year, upgrade after upgrade, people at Mozilla failed to add localization. Their design is “crashy”. They fail to fix it. Users notice, change browsers. Firefox may become irrelevant for this one reason. This isn’t Clayton Christensen’s “innovator’s dilemma”, where industry-leading companies become complacent and lose their lead. People at Mozilla have had no reason to be complacent.

Examples of the rule are all around us. Some are easy to see:

1. Taleb’s (negative) Black Swans. Tail events in long-tailed distributions often have huge consequences (making them Black Swans) because their possibility has been ignored or their probability underestimated. The system is not designed to handle them. All of Taleb’s Black Swans involve man-made systems. The financial system, hedge funds, New Orleans’s levees, and so on. These systems were built by people with jobs and react poorly to rare events (e.g., Long Term Capital Management). Taleb’s anti-fragility is what others have called hormesis. Hormesis protects against bad rare events. It increases your tolerance, the dose (e.g., the amount of poison) needed to kill you. As Taleb and others have said, many complex systems (e.g., cells) have hormesis. All of these systems were fashioned by nature, none by people with jobs. No word means anti-fragile, as Taleb has said, because there exist no products or services with such a property. (Almost all adjectives and nouns were originally created to describe products and services, I believe. They helped people trade.) No one wanted to say buy this, it’s anti-fragile. Designers didn’t (and still don’t) know how to add hormesis. They may even be unaware the possibility exists. Products are designed by people with jobs. Taleb doesn’t have a job. Grasping the possibility of anti-fragility — which includes recognizing that tail events are underestimated — does not threaten his job or make it more difficult. If a designer tells her boss about hormesis her boss might ask her to include it.

2. The Boeing 787 (Dreamliner) has had battery problems. The danger inherent in use of a lithium battery has a long-tailed distribution: Almost all uses are safe, a very tiny fraction are dangerous. In spite of enormous amounts of money at stake, Boeing engineers (people with jobs) failed to devise adequate battery testing and management. The FAA (people with jobs) also missed the problem.

3. The designers of the Fukushima nuclear power plant (people with jobs) were perfectly aware of the possibility of a tsunami. They responded badly (did little or nothing) when their assumptions about tsunami likelihood were criticized. The power of the rule is suggested by the fact that this happened in Japan, where most things are well-made.

4. Drug companies (people with jobs) routinely hide or ignore rare side effects, judging by the steady stream of examples that come to light. An example is the tendency of SSRIs to produce violence, including suicide. The whole drug regulatory system (people with jobs) seems to do a poor job with rare side effects.

Why is the rule true? Because jobs require steady output. Tech reviewers want to write a steady stream of reviews. The Mozilla Foundation wants a steady stream of updates. Companies that build nuclear power plants want to build them at a steady rate. Boeing wants to introduce new planes at a steady rate. Harvard professors (criticized by Taleb) want to publish regularly. At Berkeley, when professors come up for promotion, they are judged by how many papers they’ve written. Long-tailed distributions interfere with steady output. To seriously deal with them you have to measure the tails. That’s hard. Adding hormesis (Nature’s protection against tail events) to your product is even harder. Testing a new feature to learn its effect on tail events is hard.

This makes it enormously tempting to ignore tail events. Pretend they don’t exist, or that your tests actually deal with them. At Standard & Poor’s, which rated all sorts of financial instruments, people in charge grasped that they were doing a bad job modelling long-tailed distributions and introduced new testing software that did a better job. S & P employees rebelled: We’ll lose business. Too many products failed the new tests. So S & P bosses watered down the test: “If the transaction failed E3.0, then use E3Low [which assumes less variance].” Which test (E3.0 or E3Low) was more realistic? The employees didn’t care. They just wanted more business.

It’s easy to rationalize ignoring tail events. Everyone ignores them. Next tsunami, I’ll be dead. The real reason they are ignored is that if your audience is other people with jobs (e.g., a regulatory agency, reviewers for a scholarly journal, doctors), it will be easy to get away with ignoring them or making unrealistic assumptions about them. Tail events from long-tailed distributions make a regulator’s job much harder. They make a doctor’s job much harder. If doctors stopped ignoring the long tails, they would have to tell patients That drug I just prescribed — I don’t know how safe it is. The hot potato (unrealistic risk assumptions) is handed from one person to another within a job-to-job system (e.g., drug companies market new drugs to the FDA and to doctors) but eventually the hot potato (or ticking time bomb) must be handed outside the job-to-job system to an ordinary Person X (e.g., a doctor prescribes a drug to a patient). It is just one of many things that Person X buys. He doesn’t have the time or expertise to figure out if what he was told about risk (the probability of very bad very rare events) is accurate. Eventually, however, inaccurate assumptions about tail events may be exposed when people without jobs related to the risk (e.g., parents whose son killed himself after taking Prozac, everyone in Japan, airplane passengers who will die in a plane crash) are harmed. Such people, unlike people with related jobs, are perfectly free to complain and willful ignorance may come to light. In other words, doctors cannot easily complain about poor treatment of rare side effects (and don’t), but patients and their parents can (and do).

There are positive Black Swans too. In some situations, the distribution of benefit has a very long-tailed distribution. Almost all events in Category X produce little or no benefit, a tiny fraction produce great benefit. One example is scientific observations. Almost all of them have little or no benefit, a very tiny fraction are called discoveries (moderate benefit), and a very very tiny fraction are called great discoveries (great benefit). Another example is meeting people. Almost everyone you meet — little or no benefit. A tiny fraction of people you meet — great benefit. A third example is reading something. In my life, almost everything I’ve read has had little or no benefit. A very tiny fraction of what I’ve read has had great benefits.

I came to believe that people with jobs handle long-tailed distributions badly because I noticed that jobs and science are a poor mix. My self-experimentation was science, but it was absurdly successful compared to my professional science (animal learning research). I figured out several reasons for this but in a sense they all came down to one reason: my self-experimentation was a hobby, my professional science was a job. My self-experimentation gave me total freedom, infinite time, and commitment to finding the truth and nothing else. My job, like any job, did not. And, as I said, I saw that scientific progress per observation had a power-law-like distribution: Almost all observations produce almost no progress, a tiny fraction produce great progress.

It is easy enough for scientists to recognize the shape of the distribution of progress per observation but, if you don’t actually study the distribution, you’re not going to have much of an understanding. Professional scientists ignore it. Thinking about it would not help them get grants and churn out papers. (Grants are given by people with jobs, who also ignore the distribution.) Because they don’t think about it, they have no idea how to change the “slope” of the power-law distribution (such distributions are linear on log-log coordinates). In other words, they have no idea how to make rare events more likely. Because it is almost impossible to notice the absence of very rare events (the great discoveries that don’t get made), no one notices. I seem to be the only one who points out that year after year, the Nobel Prize in Physiology/Medicine indicates lack of progress on major diseases. When I was a young scientist, I wanted to learn how to make discoveries. I was surprised to find that everything written on the topic — which seemed pretty important — was awful. Now I know why. Everything on the topic was written by a person with a job.

With long-tailed distributions of benefit, there is nothing like hormesis. If any organism has evolved something to improve long-tailed distributions of benefit, I don’t know what it is. Our scientific system handles the long-tailed distribution of progress poorly in two ways:

1. The people inside it, such as professional scientists, do a poor job of increasing the rate of progress, i.e., making the tails thicker. I think you can make the tails thicker via subject-matter knowledge (Pasteur’s “chance favors the prepared mind”), methodological knowledge (better measurements, better experiments, better data analysis), and novelty. Professional scientists understand the value of the first two factors, but they ignore the third. They like to do the same thing over and over because it is safer. Great for their careers, terrible for the rest of us.

2. When an unlikely observation comes along, the system is not set up to develop it. An example is Galvani’s discovery of galvanism, which led to batteries, which led to widespread electricity. This one discovery, from one observation, arguably produced more progress than all scientific observations in the last 100 years. Galvani’s job (surgery research) left him unable to go further with his discovery. (“Galvani had certain commitments. His main one was to present at least one research paper every year at the Academy.”) His research job left him unable to develop one of the greatest discoveries of all time. In contrast, Darwin (no job) was able to develop the observations that led to his theory of evolution. It took him 18 years to write one book, longer than any job would have allowed. He wouldn’t have gotten tenure at Berkeley.

After a discovery has been made, the shape of the benefit distribution changes. It becomes more Gaussian, less long-tailed. As our understanding increases, science becomes engineering, which becomes design, which becomes manufacturing. Engineering and design and making things fit well with having a job. Take my chair. Every time I use it, I get a modest benefit, always about the same size. Every time I use my pencil, I get a modest benefit, always about the same size. No long-tailed distribution.

Modern science works well as a way of developing discoveries, not making them. An older system was better for encouraging discovery. Professors mainly taught. Their output was classes taught. They did a little research on the side. If they found something, fine, they had enough expertise to publish it, but nothing depended on their rate of publication. Mendel was expert enough to write up his discoveries but his job in no way required him to do so. Just as Taleb recommends most of your investments should be low-risk, with a small fraction high-risk, this is a “job portfolio” where most of the job is low benefit with high certainty and a small fraction of the job is high benefit with low certainty. In the debate over climate change (is the case that humans are dangerously warming the planet as strong as we’re told?) it is striking that everyone with any power on the mainstream side of the debate (scientists, journalists, professional activists) has a job involving the subject. Everyone on the other side with any power (Stephen McIntyre, Bishop Hill, etc.) does not. People without jobs are much more free to speak the truth as they see it.

We need personal science (using science to help yourself) to better handle long-tailed distributions, but not just for that reason. Jobs disable people in other ways, too. Personal science matters, I’ve come to believe, for three reasons.

1. Personal scientists can make discoveries that professional scientists cannot. The Shangri-La Diet is one example. Tara Grant’s discovery of the effect of changing the time of day she took Vitamin D is another. For all the reasons I’ve said.

2. Personal scientists can develop discoveries that professional scientists cannot. Will there be a clinical trial of the Shangri-La Diet (by a professional weight-control researcher) in my lifetime? Who knows. It is so different from what they now believe. (When I applied to the UC Berkeley Animal Care and Use Committee for permission to do animal tests of SLD, I was turned down. It couldn’t possibly be true, said the committee.) Long before that, the rest of us can try it for ourselves and tell others what happened.

3. By collecting data, personal scientists can help tailor any discovery, even a well-developed one, to their own situation. For example, they can make sure a drug or a diet works. (That’s how my personal science started — testing an acne medicine.) They can test home remedies. By tracking their health with sensitive tests, they can make sure a prescribed drug has no bad side effects. Individualizing treatments takes time, which gets in the way of steady output. You have all the time in the world to gather data that will help you be healthy. Your doctor doesn’t. People who have less contact with you than your doctor, such as drug companies, insurance companies, medical school professors and regulatory agencies, are even less interested in your special case.

If You Ever Visit Seoul, You Might Want To Skip Bean Table Restaurant

A restaurant near Seoul named Bean Table got a surprisingly bad review:

Then came a massive chicken salad dish, given the number of people we had we over ordered. The patrons we brought were split 50/50 on enjoyment for the chicken. We had so much leftovers and were wasting so much food, I asked the waiter to wrap the leftovers. . . . Asking the waiter to wrap this chicken came with a resounding “no”, so again to the kitchen to talk to a manager. Actually ended up talking to a chef, a young man who speaks good English, who also declined our request. We had a six year old and a three year old with us and that was the only food they were eating minus the pungent sauce.

Our driver then proceeded to get angry and went to talk to the chef, Sungmo Lee, and surprisingly Mr. Lee and our driver had a conversation that the whole restaurant could hear despite repeated requests by our driver to discuss outside. As that incident occurred being concerned for my family who flew on average 7,000 miles and were picked up for a total driving commute of two hours to come eat at this restaurant I went to calm both parties down. Things progressed from worse to horrible. I identified myself as a food critic, and Mr. Lee proceeded to take that as a threat and stated, “You don’t know who I am.” . . . . My father, a man in his 70′s, tried to speak reason to him only to be found that we were asked to leave.

At the end of the day, police were called, we weren’t allowed to pay the bill till police arrived even after we stated we wished to leave and skip the remaining courses. Police came and scolded Mr. Lee, telling him that if a customer pays for food then containers should be allowed for the customers to take food home. Keep in mind we are talking about cooked chicken, not fish, or tartar, etc. (Mr. Lee’s argument was that there were no take out containers in the restaurant and remained adamant about the no take out policy when we asked the driver to buy some containers). After the police came they asked us to leave while they dealt with Mr. Lee only to find an employee chasing out bus to pay the bill. No discounts, full price and another time suck of 20-30 minutes and the rest of the meal was safely kept in their fridge due to their “no takeout” policy. . . .

Before all of this nonsense came down my whole Korean family all thought that the restaurant was over rated and there was no single outstanding dish.

Until the Internet, stuff like this was never reported.

 

Who Is Listened To? Science and Science Journalism

This book review of Spillover by David Quammen is quite unfavorable about Laurie Garrett, the Pulitzer-Prize-winning science journalist. Several years ago, at the UC Berkeley journalism school, I heard her talk. During the question period, I made a comment something like this: “It seems to me there is kind of a conspiracy between the science journalist and the scientist. Both of them want the science to be more important than it really is. The scientist wants publicity. The science journalist wants their story on the front page. The effect is that things get exaggerated, this or that finding is claimed to be more important than it really is.” Garrett didn’t agree. She did not give a reason. This was interesting, since I thought my point was obviously true.

The book review, by Edward Hooper, author of The River, a book about the origin of AIDS, makes a more subtle point. It is about how he has been ignored.

When I wrote The River, I did my level best to interview each of the major living protagonists involved in the origins-of-AIDS debate. This amounted to well over 600 interviews, mostly of two hours or more, and about 500 of which were done face-to-face rather than down the phone. Although the authors of the three aforementioned books (Pepin, Timberg and Halperin, Nattrass) all devote time and several pages to The River, and to claims that I definitely got it wrong, not one of them bothered to contact me at any point – either to challenge my findings, or to ask me questions. However, I have been contacted by someone through my website (a lawyer and social scientist) who asked me several questions, to all of which I responded. Later, this man read the first two of these three pro-bushmeat books and contacted the authors of each by email, to ask them one or two simple questions about their dismissal of the OPV hypothesis [= the AIDS virus came from an oral polio vaccine]. His letters to Pepin, Timberg and Halperin (which he later forwarded to me) were courteous and non-confrontational, and in two instances he sent three separate letters, but apparently not one of the authors could be bothered to reply to any of these approaches.

In other words, there is a kind of moat. Inside the moat, are the respected people — the “real” scientists. Outside the moat are the crazy people, whom it is a good idea to ignore. Even if they have written a book on the topic. Hooper and those who agreed with him were outside the moat.

Hooper quotes Quammen:

“Hooper’s book was massive”, Quammen writes, “overwhelmingly detailed, seemingly reasonable, exhausting to plod through, but mesmerizing in its claims…”

I look forward to the day that the Shangri-La Diet is called “seemingly reasonable”. Quammen and Garrett (whose Coming Plague has yet to come) write about science for a living. I have a theory about their behavior. To acknowledge misaligned incentives (scientists, like journalists, care about other things than truth ) and power relationships (some scientists are in a position to censor other scientists and points of view they dislike) would make their jobs considerably harder. They are afraid of what would happen to them — would they be kicked out, placed on the other side of the moat? — if they took “crazy” views seriously. It is also time-consuming to take “crazy” views seriously (“massive . . . exhausting”). So they ignore them.

Shangri-La Success in Detail

An Indianapolis man named Hugh, who goes by Nufftin on the Shangri-La Diet forums, has been blogging about his weight loss (including graphs) at increments of 10 pounds lost (he writes a post when he’s lost 10 pounds, 20 pounds, etc.). So far he’s lost more than 50 pounds and is close to his goal weight, which is near his weight in college.

I decided to read all the entries and note what I learned. He started more than a year ago.

November 2011. He’s been gaining weight for a long time. He is about 5 feet 6 inches tall and weighs more than 200 pounds, giving him a BMI in the 30s. He does not explain why he decided to try it. He has nice clothes that no longer fit.

April 2012 (10 pounds down). It took a long time to lose the first 10 pounds because he started just before Thanksgiving and Christmas, big eating holidays, and he gave up. He started again January 1 and gave up again. Then he started again in February. Daily weight spikes can be as much as 4 pounds (he weighs 4 pounds more on Tuesday than he did on Monday), but that only happened once (New Year’s Party?). After he becomes consistent with the diet (in February), the graph of his daily weights is enormously convincing that the diet works.

May 2012 (20 pounds down). Here’s exactly how he does the diet: “a shot glass full of extra-light tasting olive oil in the morning, with no eating for an hour each side; two heaping tablespoons of table sugar dissolved in as much water as it will take to dissolve it in the evening.” (You can see why I would write a rather short book about such a diet.) He also does 15 minutes of exercise most days but I won’t describe it in detail since it doesn’t seem to matter — he stops exercising but keeps losing weight. Some old clothes now fit again. Only two people have commented on his weight loss. Maybe everyone notices but intentional weight loss is so rare it could be he’s dying. (Which is what one of my Berkeley colleagues thought about my weight loss. He actually said, “Are you dying?”) No one wants to hear that.

July 2012 (30 pounds down). The diet does require some effort. “I lost concentration for a couple of nights and, BOOM. To be fair, it was due to two great dinner parties (feta cheese hamburgers and The Descendants at one, Cuban sandwiches at the other).” These two “losses of concentration” did not have long-term effects. After 5-6 days — how long it took an unusually large amount of food to pass through his body and his salt balance to return to normal? — after those parties, his weight returned to its usual downward line.

September 2012 (40 pounds down). One of his shirts is now too big for him. He gained 6 pounds during a two-week trip. The gained weight comes off quickly (in about a week) but this time there is a noticeable long-term effect: Weight loss resumes at the same rate as before but the function is shifted by two weeks. He stops his 15 minutes of exercise and nothing happens to his rate of weight loss.

January 2013 (50 pounds down). It has taken 15 months to lose 50 pounds. There was one serious plateau, from December 2012 to January 2013, where he did not lose weight. Almost all of his pants are too big. He can take off his shirt at the pool.