Nassim Taleb recently criticized the Nobel Prize in Economics:
According to Taleb, there are a number of mistaken ideas about forecasting and measuring risk, which all contribute to events like the 2008 global crisis. The Nobel prize, he says, has given them a stamp of approval, allowing them to propagate.
It isn’t just economics. As I’ve said before, the Nobel Prize in medicine was not given for the discovery that smoking causes lung cancer. It was not given for the discovery that lack of folate causes birth defects. Both enormously useful. It has been given for several discoveries, such as the connection between teleomeres and aging, with (so far) little or no practical value.
This is no mystery. The Nobel Prize must be prestigious, therefore must honor high-prestige research. Veblen argued long ago that in academia high prestige correlates with low practical value. Just today I told a friend Veblen’s idea that professors use jargon for the same reason men wear ties — to show off how useless they are. The economics research (“Harry Markowitz, William Sharpe, Robert Merton, Myron Scholes, Robert Engle, Franco Modigliani and Merton Miller”) that Taleb is criticizing was high prestige. The so-far-useless biology that has received a Nobel Prize was high prestige; the highly-useful epidemiology that didn’t receive the prize was low prestige.
Thanks to Dave Lull.
There’s a difference between work that provides insight into processes of no practical relevance (perhaps the biological research that you cite) and total nonsense (the work taleb cites)
Epidemiology has produced so little of value that it’s a shame that the smoking result wasn’t honoured. It would have meant honouring Third Reich men, though. So be it, say I.
“Epidemiology has produced so little of value” — compared to what?
Vic, yeah, there’s a difference. But are Nobel Prizes in Economics (“total nonsense”) actually more harmful than the Nobel Prizes in Biology (“no practical relevance”)? I don’t know. The Nobel Prizes in Biology, with their emphasis on studies of mechanism, have in certain ways validated the drug-company assumption that the way to solve health problems is to give people a powerful drug. I think that’s been very damaging compared to an alternative research strategy that studied lifestyle changes.
Warren and Marshall got the Nobel for discovering that bacteria cause ulcers…leading to a cure and not just endless treatment of symptoms…that was a good one, no?
Money is numbers on paper and in computers. The national deficit exists because the money printers (the Federal Reserve Banking system) are private entities that lend the money they printed to the USA (which is also a corporation). Just look up “debt based money creation”.
The whole system exists to deceive people. Did the winners tell that? No, because then the system would stop to work. Anyways, it’s just days until it hits the wall, so I’m relaxed and joyfully excited
The financial economists that Taleb criticizes did the most practical work of the econ Nobelists; it translated directly into new financial strategies and companies, which many would say is exactly the problem. So your criticism contradicts Taleb’s.
Fair point Seth, I agree
CTB, I suspect ulcers are a sign of a poorly-functioning immune system, perhaps compounded with poor nutrition. Almost everyone who has the bug that Marshall and Warren say “causes” ulcers doesn’t have ulcers. So, no, that wasn’t a good one. It is another example of using drugs to treat a problem caused by lifestyle.
I agree with you that ulcers probably have multiple factors contributing to their severity. And having a well-functioning immunesystem and good nutrition, whatever that is, is an ideal to strive for. But the reality is that if I’m acutely ill with an ulcer attack and I have those bugs, I’d go for the antibiotics in a heartbeat and be very glad that those guys made the connection. Especially if it lets me get back to work so I can pay the mortgage and put food on the table.
CTB, yes, antibiotics have helped people with ulcers just as you describe. But it’s plausible the Nobel-Prize-winning work by Marshall and Warren has discouraged research into lifestyle causes of ulcers. A poorly-functioning immune system does more than cause ulcers. It probably increases heart disease, for example. You could say that Marshall and Warren did duct-tape science — science that failed to study fundamental causes.
By shining a light on the bacteria, Marshall and Warren put an end to duct-tape treatment of ulcer symptoms (with everything from acid-controllers to stomach resection surgery). They also stimulated a wave of research to figure out how this bacteria evades the immune system and causes stomach pathology.
Check out this review from 2006:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1592695/?tool=pubmed
It has over 250 references describing the known factors by which this bacteria escapes detection and is able to colonize half the world’s population. It’s freaking complicated. But I doubt most of this work would have been done without M & W’s discovery. That’s why they got and deserved the prize, (not to mention that they really bucked the system along the way, bless ‘em).
Lifestyle research is tricky since the human population is so genetically diverse, and multiple genetic factors play a part in immune response. But let’s say there is just one immune factor which is primarily responsible for keeping the bacteria in check…and that eating butter promotes optimal levels of this factor. It might also turn out that 30% of the population carries a mutation in which butter promotes still another factor which actually makes the bacteria more virulent…but no one knows about this second factor yet. So you do your study (butter and ulcers) and get a result. And another group does a similar study and gets different result because the genetic makeup of their group relative to the second factor is different. It’s just not known yet.
We’re still in the dark ages, in a way. Meanwhile, the best we can do is keep on doing the experiments and generating the molecular data, waiting for someone to make the next connection.
“We’re still in the dark ages . . . the best we can do is keep . . . generating the molecular data,” you write. I disagree. I don’t think more molecular data will show us what lifestyle factors make a big difference. Why does half the world have h. pylori in their stomachs but only a tiny fraction have ulcers? I am sure that the tiny fraction with ulcers will have a higher than average risk of many other problems. If we figure out the lifestyle causes of ulcers, we may be able to not only lower risk of ulcers; I think the associated elevated risks (e.g., heart disease) will also come down. If you take antibiotics those other elevated risks won’t come down, I’m also sure. And I wonder how likely it is if you take antibiotics to get rid of h. pylori that you will become reinfected within a year after you stop the antibiotics? It really is a duct-tape solution. Not the only one, to be sure.
I don’t agree about people being so different (“the genetic makeup of their group . . . is different”). There are plenty of broad truths about how to be healthy. See any nutrition textbook. For another example, I’m quite sure everyone needs regular ingestion of bacteria to be healthy (to have a well-functioning immune system).
Maybe you’ve heard that chimps and humans share 96% of their genes. This implies that two randomly chosen humans must share much more than 96% of their genes. Because two randomly-chosen humans diverged genetically much more recently than chimps and humans.
First, I agree that we are rewarding the wrong research in many cases: “sexy” or “prestigious” and not necessarily fundamental. (Though in the case of h. pylori, I am happy because of how hard they had to fight the voodoo consensus that had preceded their research.)
But the fact that humans share more than 96% of their DNA doesn’t impress me. There are how many inherited diseases that I don’t have, even though I only differ from millions of sufferers by less than 4%? (Not to mention the two other alternatives: inherited benefits, and inherited “doesn’t make enough difference in function that anybody has bothered to look into it”.) And what about the tens of thousands of people who suffer severe side effects from the dozens of medications I’ve taken in my lifetime, from which I’ve never suffered any of those side effects?
My suspicion would be that the DNA argument is like saying that, in the grand scheme of machines, automobiles share 96% of their designs. And sure, they share a lot of common characteristics, like they don’t do well if submerged in salt water. But even though they all have fuse boxes, I wouldn’t assume that the fuse box is in the same location, nor that I could replace the third fuse from the top in all cars and get the same results.
I am allergic to milk, my wife is not. But she is lactose intolerant, while I am not. I’ve learned over the years that chemicals (including medicines) affect me much more rapidly than most people. Obviously, my neurons work like yours, but my brain is wired differently than yours, both in the sense of wiring due to learning and I would suspect how it was originally laid out. And my immune system has also learned differently from yours, and we haven’t even gotten into mental attitude and health. (I’ve heard, and believe, that many people in mental institutions are there because of the effects of bitterness, for example.)
So I would agree with CTB that there are a lot of meaningful differences within the overall human population. And I think that current medicine is in an awkward gap: lured away from general healthy principles, but not yet able to be specific enough (in terms of both the mechanisms by which medicines work and in terms of a particular person’s needs/reactions) to be well-targeted.
I agree with some of your observations about things like butter, but when you then justify them as being sensible in light of historical human life, I am skeptical that your vision of historic human life is accurate. And perhaps the real explanation is that it works for a subset of people who share a particular gene or two, a particular environment, etc. That’s a major point of self-experimentation, isn’t it: what works for others may not work for you?
I’m an avid reader of your blog — learned about it from Andrew Gelman’s site, I believe — and I hope that this doesn’t come across as harsh.
“I don’t think more molecular data will show us what lifestyle factors make a big difference.”
Transcription factors are small pieces of DNA which bind to gene promotors and can regulate the activity of multiple genes. PPAR is a group of these factors, some of which can promote insulin sensitivity by increasing uptake of glucose and fatty acids by adipose tissue (thus lowering blood sugar and bettering lipid profiles). The glitazone drugs which were developed to treat diabetes, work, in part, by activating PPAR. When this factor was discovered, investigators looked for ‘natural’ ligands and found that polyunsaturated fatty acids also stimulated PPAR. Saturated and monounsaturated fatty acids do not.
“I don’t agree about people being so different”
The cytochrome P450 oxidases are a huge family of enzymes which metabolize ‘foreign’ compounds to make them more soluble so that they can be eliminated by the body. These enzymes are the bane of pharmaceutical companies because multiple variations of each enzyme occurs in the population, so that the population runs the gamut from slow- to fast-oxidizers in each category. Still others carry mutations that result in no oxidation. Most medicines are metabolized by these enzymes, which helps explain in part why some people need a much larger dose of drug than the next person, or why some have side-effects that others do not. In other cases the medicines will only work if the patient has the needed oxidizing enzyme to actually activate the drug, so patients are genotyped before treatment. For example, I’ve read that tamoxifen will not work in women who are negative for CYP2D6 activity.
I agree with Wayne that the reason for self-experimentation is to find out what works for you. At the clinical level, this is what ‘personalized medicine’ is all about. We’re just not there yet. Yes, there are broad truths…e.g., eating more fruits and vegetables seems to help…but look what happens when they give people supplements of known nutrients. Sometimes there are good results…sometimes the results are contradictory. Other times you get things like beta-carotene actually being harmful in smokers with lung cancer, or calcium supplements without vitamin D causing increased heart attacks in women. But these harmful effects are not in all the subjects…just some…and we don’t know why yet. But the effect will be because of some interaction at the molecular level…and we need to keep plugging at the research which illuminates it.