Helping Students Find Their Way

At the EFF party, the friend of a friend made a vivid statement about the value of helping high school and college students figure out what job fits them best. When I asked if I could quote him in my blog, he said he preferred this way of putting it:

I believe a large fraction of people around ages 16-22 are ignorant of what kinds of work environments and activities will make them happy and productive later in life. Current classroom-based training structures do not provide exposure to work environments. The cultural and social pressures from media, family and friends can be overwhelming and can often lead to people being very confused, and hence, making poor choices. I’ve seen that people tend to get very limited and highly biased information that leads to making training choices and work choices early in their life that are often not well matched for the person’s individual genius. By mid 20′s and 30′s, getting out of these poor choices is extremely difficult, as financial requirements as one ages grow and available time to retrain diminishes. Expectations of experience grow as one gets older, and the neural ability to quickly learn and master new skills diminishes, especially much later, after 40 or 50 years. All of these factors point toward a critical need to have experienced, outside input into making early choices about career paths, and what types of experiences individuals would benefit from most. Such advice is available, and can be found – but it is not commonly accepted that expert outside opinion is the best source for career and training choices for young people. Kids get it mostly from their parents and friends – neither of which are consistently accurate, trained in normal psychology, or unbiased in their assessments. While many schools have “guidance counselors”, I have seen most of the service offered as severely lacking (like much of public education) when compared with the needs of students, both in quality and quantity. I think there is are enormous unmet needs in many cultures, the US in particular, to provide more assistance to people in their late teens and college years to deeply explore what career options best fit their personality, and provide assessment and testing with definitive recommendations for majors, mentors, internships, and work choices.

Furthermore, when viewed on the societal level, there is an obvious argument that a society will function better when higher percentage of the population finds work/life situations that leave them happier and more productive. This I feel is even more important than providing education looking out on the 10-20 year technology horizon. In a world where most educational materials and social connections will be portable, open source, and available online – the problem will not be as much about getting information, skills, or training, but in individuals being tracked toward education options, career paths, and work environments that work best for them: a problem not easily solved with mass distribution of content or any technology solution.

This view arises partly from his own experience. He majored in Chemistry and Physics, then got a Ph.D. from Stanford in Biomedical Informatics. After working in that area for several years, he discovered that what he really enjoyed was building communities, and moved in that professional direction. Currently he is building an online community to share digital media content.

How Things Begin (a surprising ALS result)

I recently blogged about a surprising association between ALS and loss of a child: Losing a child reduces your chance of getting ALS. I wrote to the lead author of the study, Dr. Fang Fang, to ask how this study come to be. Here is his reply:

Severe emotional stress, as in the case of loss of a child, has previously been associated with health consequences such as psychiatric hospitalizations, cardiovascular morbidity, etc. Our initial hypothesis was that severe emotional stress might also contribute to the development of ALS. We thus used the unique settings in Sweden including the population based registration of in-patient hospitalizations and familial link registration to explore the relationship between loss of a child and the risk of developing ALS. It was surprising for us to see an inverse association between loss of a child and the risk of ALS. After a series of careful checks on data quality, we came to believe this association was not due to systemic errors.

In other words, they did the study because they expected the opposite result.

Interview with Gary Taubes (part 14–the end)

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.

Interview with Gary Taubes (part 13)

INTERVIEWER My book came out of an accidental observation, which is that I lost weight when I drank sugar soft drinks. Lost weight, not gained weight. That happened in Paris, and I came back to Berkeley, and I found out it was the sugar. In other words, if I drink unflavored sugar water, I lost weight. Not so obvious, right? But Israel Ramirez, who I mentioned a few minutes ago — his experiments with rats are what led me to this discovery. Because I don’t think most people would have thought it was possible to lose weight by drinking Coke, or whatever. But it has to be unflavored. Anyway, the effect never wore off. I drank sugar water for three years, and my weight went down and stayed down. There was no sign that it was ever going to wear off. So this seems to me to be a big problem with your theory, which is that I drank something which obviously raised my insulin level, sugar water. I didn’t measure it. I lost weight and not only did I lose weight, but I kept the weight off, and I lost it without being hungry; I was less hungry than usual. I mean, you’re right, you know, set points, settling points, who cares. . .

TAUBES It’s important to think of it as a settling point. Because it’s important to have this concept of dynamic equilibrium. As long as you’re thinking about what’s happening in the brain, which is what set point implies. My question is, what did the sugar water do to your fat tissue? It should have caused you to accumulate fat, or at least hold on to the fat you had, according to what I know of the underlying regulation of fat tissue. The question is, why did it do what it did?

INTERVIEWER I was less surprised than you are, or than most people are, let’s put it that way, because I was led to this observation by a theory. I had a theory which pre-dated all of this. I was kind of surprised my theory was so helpful, because it hadn’t been that helpful before. But, lo and behold, it really turned out to be helpful and it led me to other ways to keep my weight off, and I’m still way down from where I was.

TAUBES What I ask when I talk with these people. What I say is: Look at the regulation of fat tissue. The question is, how can you lose weight, or gain it — how can you gain weight without either increasing insulin secretion, or increasing the relative insulin sensitivity of the fat tissue to the muscle tissue. Basically, the way we work, at least if you believe the biology that I describe, is that as we secrete insulin in response to the carbohydrates we consume and the insulin works, among other things, to facilitate the movement of glucose into the cells of your muscles and other lean tissues. But blood sugar is kind of toxic, so your muscle tissue doesn’t want the insulin pushing all this blood sugar in, and it becomes insulin resistant. Your fat tissue now remains insulin-sensitive, because your body doesn’t like to waste fuel. So if you eat a high-carb diet, your lean tissue takes up some of the glucose for fuel, and the rest gets dumped in your fat tissue, and your fat tissue remains insulin-sensitive for a long time — far longer. Because once your fat tissue becomes insulin resistant, then you just become diabetic; you have no place to put the glucose. You just pee it out. That’s the last resort, because your body doesn’t want to waste fuel.

The thing that Rosalyn Yalow and Solomon Berson reported forty years ago is that organs respond differently to high levels of insulin, and they get insulin resistant at different periods. One of the things I put into a paragraph in the book is that I can imagine a scenario where fat tissue becomes insulin resistant prior to muscle tissue, and the result would be anorexia or bulimia. The person would eat a meal and would have no place to store the calories temporarily. So they would either lose their appetite and not be interested in eating at all (anorexia), or they might just throw it up afterwards. Because they have no place to temporarily store the calories that aren’t being used immediately. Bulimia would be another option. A third option would just be to get on an exercise bicycle and ride for three hours and burn the calories off — be Lance Armstrong, in effect. So what I’m trying to figure out is what did the sugar water do, unflavored? And it’s interesting — the idea that it’s unflavored might disconnect some of the sort of Pavlovian responses that you’ve developed.

INTERVIEWER Yeah, I think that’s what was key. The reason I lost my appetite in Paris was that I was drinking unfamiliar sugar water. I think this is the reason that so many diets work in the beginning: because people eat unfamiliar food. Once the food becomes familiar, the diets don’t work so well.

TAUBES This is the problem with anecdotal evidence. The idea that oil could suppress your appetite I could understand, because, as I said in my lecture, you need alpha glycerol phosphate to fix fatty acids as triglycerides. You get the alpha glycerol phosphate from eating carbohydrates, so if you only ate oil it would be shipped off to the fat tissue as triglycerides, then broken down by lipoprotein lipase into fatty acids, but those fatty acids couldn’t be stored in the fat. So it would raise the fatty acid level in your blood, and your body would switch over to burning fatty acids, and this would effectively suppress hunger. That makes sense. But I can’t see why unflavored sugar water would be any different than say, Coca Cola itself, which is just flavored sugar water, for all intents and purposes.

INTERVIEWER Well, when I talked about it in the beginning, I was using fructose.

TAUBES Well, pure fructose, I can also understand. Friedman and Ramirez did an experiment showing that fructose suppresses hunger apparently because it is metabolized in the liver and they believe that the liver monitors fuel status in the body…

INTERVIEWER This is very interesting: someone who is not dedicated to my being wrong.

TAUBES I’m open-minded.

INTERVIEWER Your book proved that.

TAUBES The experiments that Freedman and I think Ramirez did to demonstrate that the liver must sense hunger, must sense fuel availability, is they did intravenous infusions of fructose, Fructose is metabolized only in the liver. It’s not metabolized in the brain. So they infused fructose into the blood stream of rats and it suppressed eating behavior. That’s one of many experiments they did that suggested that somehow what we sense as hunger is being communicated by the liver. It’s always made sense to me. So if you only use fructose, and you don’t get an insulin response to fructose, it would make sense that it suppresses hunger. In my book, I discuss the hypothesis that whatever prompts an insulin response is what causes us to get hungry. So, the fructose, I can understand. Actually, if you’re now eating real sucrose, that’s where it gets complicated, because with sucrose, you’re going to get an insulin response. Unless the fructose component outweighs the glucose, but then, what is it about the absence of taste? Why would Coke make you fat, and sugar water not?

INTERVIEWER Well, first it was it was that flavorless fructose worked. Then it was flavorless sucrose worked. Then it was flavorless oils work. Then it was flavorless any food worked, in particular flavorless protein.

TAUBES When you talk about flavorless protein, what do you mean? The oils, I understand; the fructose fits with everything I know. The sucrose starts getting tricky. What do you mean by flavorless protein? Give me an example.

INTERVIEWER Oh, for example, eating chicken holding your nose clipped. It’s flavorless in the sense that you don’t smell it.

TAUBES That’s interesting. Remember I told you that Jaques Le Magnen started his career studying olfaction (because he was blind). He was curious why the smell of a particular food can go from being very pleasurable when you’re hungry to being nauseating when you’re full. The example I used in the book was the smell of a cinnamon bun cooking. You can imagine that being unbelievably enticing when you’re hungry, and then nauseating if you’ve already eaten three cinnamon buns. Le Magnen moved from that to asking similar questions about the taste of a food, which he thought was determined by our level of hunger. It’s conceivable that if you don’t taste a food it somehow works to suppress hunger, but I have no idea why.

Interview directory.

Interview with Gary Taubes (part 12)

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.

Obesity and Refrigerator Design

In the last chapter of The Shangri-La Diet, I discussed what environmental changes my theory of weight control suggested. An article in the LA Times about how to reduce obesity by changing the environment contains some ideas that strike me as unwise:

laws regulating portion size

but also a good one, from Brian Wansink.

A 2006 study in the International Journal of Obesity [by Wansink and colleagues] found that when candy was placed in a clear dish, people ate 71% more than when it was in an opaque dish. The same study found that the closer the food, the more likely it would be eaten. . . . “We need to make small changes in our environment. That can be as small as moving fruits and vegetables to the middle shelf in the refrigerator” [said Wansink].

In Japan — where portion sizes are smaller without the need for legislation — most new refrigerators have three compartments separately accessible from the outside. Two are above freezing, one is below. Wansink’s comment suggests not only that such refrigerators are a good idea but also that one of the above-freezing doors should be transparent. Behind the transparent door you’d put fruits and vegetables.

Thanks to Dave Lull.

Does Cholesterol Cause Heart Disease?

The first links between cholesterol and heart disease were correlational, of course. Then statins, which improved cholesterol levels, turned out to reduce heart disease — experimental evidence of a connection. This strengthened the case for causality, but Malcolm Kendrick argued, based on lots of other evidence, that the heart-disease lowering effect of statins was due to other effects of the drugs, not their cholesterol-lowering properties. Now we have this:

Pfizer stopped development of its experimental cholesterol drug torcetrapib in December 2006, when a trial involving 15,000 patients showed that the medicine caused heart attacks and strokes. That trial — somewhat unusual in that it was conducted before Pfizer sought F.D.A. approval — also showed that torcetrapib lowered LDL cholesterol while raising HDL, or good cholesterol.

This supports Kendrick’s argument. It shows that drugs can have two effects: (a) on heart disease and (b) on cholesterol.

Thanks to Dave Lull.

Addendum. Do cholesterol drugs do any good?

Eggs are Good for You

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.

A Cautionary Tale about Salt

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.