What information has surprised you most recently?

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Dec 9, 2012

Information that surprises you is interesting as it exposes where you have been miscalibrated, and allows you to correct for that.

I suspect the users of LessWrong have fairly similar beliefs, so it is probable that information that has surprised you would surprise others here, so it would be useful for them if you shared them.

Example: In a discussion with a friend recently I realised I had massively miscalibrated on the percentage of the UK population who shared my beliefs on certain subjects, in general the population was far more conservative than I had expected.

In retrospect I was assuming my own personal experience was more representative than it was, even when attempting to correct for that.

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36 points

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Sex education (including non-abstinence) may not work at all, and if it does work it works only in a very weak and limited way.

Eating cholesterol doesn't cause high blood cholesterol. Eating saturated fat probably doesn't cause higher blood cholesterol. High blood cholesterol levels are protective against cancer and the mortality gain here probably outweighs any mortality loss from cardiovascular disease. The entire science of cholesterol is confused and terrible and practically every statement you have ever heard that includes the word "cholesterol" is very likely a lie. (link to a readable blog post with some of this, but you can also find it all in big-name medical journals)

The (good!) effect of drinking alcohol on life expectancy is super strong. Drinking wine a few times a week is correlated with up to four years gain in lifespan (effect mostly found in the middle-aged, might not be such a good idea in young), and people who are smart and understand that correlation isn't always causation have amassed some decent evidence that at least some of this might be causal.

Labeling the amount of calories in food (for example on McDonald's restaurant menus) totally fails to change people's eating behaviors at all, no matter how hard people study it. Article here, credit to SarahC for pointing this out to me.

I hate all of these facts and wish they were not true, which makes me a credible source for them.

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I'm a fifth year med student from Finland, a long time lurker, and you provoked me to post the first time. Thank you for that, I'm a terrible procrastinator. I'm a also big fan of many of your submissions. The alcohol fact seems right and the other two I can't comment on, so I'll focus on cholesterol. In this case I'm surprised of seeing no criticism.

If the information you present about cholesterol is true, I am highly surprised too, and I hope you're right because otherwise the information is potentially very deadly. The effect, whatever the direction, is amplified by you being a high status member of this community. If there were no other comments on this, I wouldn't bother either.

I would like to see the sources that REALLY changed your mind, and the link you provide doesn't seem to contain any good sources at a glance. The post that Kresser links to has sources that are ancient. I looked up on Chris Kresser, and he is a licenced acupuncturist trained in some version of chinese medicine. This doesn't exactly make me trust him as a source of medical information.

From what I've read, in big-name medical journals you can find that the case about cholesterol is hardly settled for good, but the mainstream medical opinion still is that LDL is very bad for you. Pretty much all mainstream arterial disease risk calculators implement this fact. If I have a patient who has high cholesterol and I don't react, I'm considered a bad doctor by at least 99 % of my colleagues and every single one of my professors. Every textbook I know of can tell you that LDL is bad for you. The only doctor in my country that I know of who recommends raising your LDL is a quack selling overpriced supplements. This is the level of consensus at least in Finland.

How am I supposed to update? Edit: see in the following comments how difficult this is Distrusting my entire field in my country in any circumstance doesn't seem feasible. Understand that I'm not a scientist, and not trained in statistics. I'm a doctor and trained to implement science. I think this is the most feasible division of work given the volume of current knowledge. Currently my time is spent at lectures, at the clinic and reading textbooks, and reading journals doesn't seem like a low hanging fruit most of the time.

Please provide proper sources before you spread any medical information. If your provide the goodies, I'm ready to read. Otherwise as an extortion I will treat my future patients with statins like the rest of the medical community :P

This is an important topic to me, and as I said misinformation is deadly. I hope you can forgive whatever indignation I couldn't eliminate.

A couple of sources that medical people consider reliable: www.cochrane.org, heart disease The Framingham Heart Study

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Yes, I understand your indignation and I should not have been as quick to spurt that out without more information. I've tried to justify everything I've said above with data from Framingham and the Cochrane Collaboration, but I hope you'll forgive me if I have to lapse into a few sources from less hallowed publications once in a while.

"Eating cholesterol doesn't cause high blood cholesterol."

Since only citing things from Framingham or Cochrane is a hard constraint to keep I am forced to commit the minor sin of citing a work not published in a peer-reviewed journal and refer you to the Framingham Diet Study, a subpart of the Framingham Heart Study whose methodology was published appropriately but whose results for some reason weren't. A guy who tracked down the results reports on them here and finds that

"With one exception there was no discernible association between reported diet intake and serum cholesterol level in the Framingham Diet Study Group. The one exception was a weak negative association between caloric intake and serum cholesterol level in men. [As to] coronary heart disease–was it related prospectively to diet. No relationship was found."

If you'll allow me to step out of Framingham and Cochrane for a moment I can also link to a review on egg consumption and LDL which found that in most of the population there's no relationship.

"Eating saturated fat probably doesn't cause higher blood cholesterol."

This claim can also be supported by the Framingham data above finding no link between diet and serum cholesterol.

You may also be interested in a Cochrane review that finds no effect reducing dietary fat consumption on cardiovascular events, cardiovascular mortality or total mortality, and finds that changing the type of fat slightly decreases cardiovascular events (look how close that confidence interval gets to 1!), but not cardiovascular mortality or total mortality. And here's a non-Cochrane meta-analysis saying pretty much the same thing.

If those are true, either the fat -> blood cholesterol or the blood cholesterol -> CVD connections have to be flawed; I'd say at this point it's more likely the former.

"High blood LDL probably doesn't cause heart disease."

That was irresponsibly speculative as written; I have now edited it out of the original post lest it cause exactly the confusion you worry about. I am impressed by arguments suggesting that the association between cholesterol and heart disease may be more correlational than causal, or at least super-complicated and modulated by weird factors we don't understand like subtype of LDL, but at this point I can't support that with Framingham or Cochrane and it would be irresponsible to say so too loudly.

But I think it's weird how randomized trials keep finding that a lot of drugs that change cholesterol don't change disease risk. The ENHANCE trial of ezetimibe finds it successfully reduced LDL cholesterol but didn't decrease (and may increase) cardiovascular events. The AIM-HIGH trial of niacin finds it successfully raises HDL cholesterol and lowers LDL cholesterol but didn't decrease cardiovascular events. Fibrates may prevent CVD but have no effect on all-cause mortality. The only lipid-lowering drugs that seem to be consistently awesome are, of course, the statins, but they seem to work equally well in high and low cholesterol populations leading some to think they also have non-cholesterol-related effects.

I also just think LDL is a lousy biomarker. A majority of heart attack patients have LDL levels considered normal; this is especially impressive considering the high results of high cholesterol even in the general population.

But in general you're right and I apologize for asserting this one until I can back it up better.

"High blood cholesterol levels are protective against cancer and the mortality gain here probably outweighs any mortality loss from cardiovascular disease."

Framingham found that mortality increased with increasing cholesterol in people younger than 50. In people older than 50 (ie 90% of heart attack victims) it found no relationship (other sources say low cholesterol led to higher mortality in these age groups, but I can't access the paper to check.)

In other studies, the relationship between cholesterol and noncardiovascular mortality has indeed been clearly protective.The article I linked to tries to explain this as people with hidden catabolic diseases (eg cancer) having decreased cholesterol levels. This has become less plausible as longitudinal studies show low cholesterol long precedes disease; see for example Schatz 2001.

Overall I am not as confident in my claim above as I was when I wrote it. I wrote it right after reading Good Calories, Bad Calories, but before double-checking everything in it to avoid effects of confirmation bias. I continue to think the statements above are mostly true, in the vague and weasel-ish way that medical statements are true (true in most subgroups, if you hold risk factors constant, so on). But I suggest reading Good Calories, Bad Calories and doing some more research and checking for yourself: I would be really interested to know what another rationalist who's interested in medicine thinks of it.

I would suggest (not "recommend", I'm nowhere near high-status or high-information enough to "recommend") that you use a better source of monitoring cardiovascular risk than LDL (ApoA/ApoB ratios seem to work), that you suggest an Obvious Healthy Diet Without Twinkies Or Coca-Cola and leave it at that unless you want to wade into the monster-infested radioactive swamp that is nutrition science, and that you continue prescribing statins where indicated.

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That was fast. This is why I love you and the rest of the community.

Before I say anything else, let me remind everyone of something. Atherosclerosis is a systemic disease. When we're talking about arterial disease, mortality is not the only endpoint we're interested in. Most of the time a cardiovascular event will not kill you, it will leave you disabled. It's also a hell of a painful way to die. A stroke very rarely kills you, but most of the time leaves you less functional. Microinfarctions in the brain will cause dementia, but you might not die of it. Atherosclerosis in the leg will first make you lose sensation and function in the leg, and later you might lose the whole leg. That will probably not be lethal either. It would of course be intellectually dishonest to say that these events are not correlated with mortality, however.

Since only citing things from Framingham or Cochrane is a hard constraint to keep I am forced to commit the minor sin of citing a work not published in a peer-reviewed journal and refer you to the Framingham Diet Study, a subpart of the Framingham Heart Study whose methodology was published appropriately but whose results for some reason weren't. A guy who tracked down the results reports on them here and finds that....

I'm sorry. I'm not trying to be extra difficult, but where is the original source? Is it authentic? (Edit: Here, unfortunately not accessible, thank you Yvain)

If you'll allow me to step out of Framingham and Cochrane for a moment I can also link to a review on egg consumption and LDL which found that in most of the population there's no relationship.

Permission granted ;) I accept that the effect of dietary intake varies between individuals. Even this review recognizes that there are "hyperresponders" to dietary cholesterol. I also think that for a motivated individual measuring their response to diet would be optimal compared to just blindly switching. Measuring lipid profiles and other risk factors is cheap. I'm not sure how to measure subtypes of LDL, however, and to be honest I know nothing about their clinical relevance.

You may also be interested in a Cochrane review that finds no effect reducing dietary fat consumption on cardiovascular events, cardiovascular mortality or total mortality, and finds that changing the type of fat slightly decreases cardiovascular events (look how close that confidence interval gets to 1!), but not cardiovascular mortality or total mortality.

As I said, mortality is not the only interesting endpoint. Also the CI upper bound for CVD is not over 1, not matter how hard we want to push it. The other review does support your conclusions. It doesn't however support increasing dietary saturated fat or changing nutritional guidelines in any other way.

The only lipid-lowering drugs that seem to be consistently awesome are, of course, the statins, but they seem to work equally well in high and low cholesterol populations leading some to think they also have non-cholesterol-related effects.

That statins work equally well in high and low cholesterol populations is to me the most interesting claim that you make. Can you provide a source for it? It is commonly accepted that they have benefits on top of them affecting lipids, but that the effect is completely isolated is contrary to my knowledge. The reason for the bonus effect is also a mystery. The other drugs you mention have common annoying side effects that mostly reduce compliance, and I wouldn't be surprised if some of the side effects increased mortality. In Finland they are also usually prescribed by a specialist and are never a first line treatment.

I also just think LDL is a lousy biomarker. A majority of heart attack patients have LDL levels considered normal; this is especially impressive considering the high results of high cholesterol even in the general population.

We have guidelines to measure lipid profiles after 48 hours of an ischemic vascular event. Within this time period, the LDL levels plummet, but then they rise again. Since this is a very recent guideline, it might explain the finding you present. Then again, it also might not. If I skimmed correctly there was no mention of the timing of the measurements. Look below for Edit2 for a better explanation.

Framingham found that mortality increased with increasing cholesterol in people younger than 50. In people older than 50 (ie 90% of heart attack victims) it found no relationship (other sources say low cholesterol led to higher mortality in these age groups, but I can't access the paper to check.)

Atherosclerosis is mostly a nonreversible progressive disease that can start as early as in late adolescence, so it makes sense that hypercholesterolemia before age 50 is most important for its development. All it takes for a plague to rupture after tens of years of accumulation is that the endothelium covering it fails, it doesn't necessarily have to grow anymore. (Edit: see additional explanations in the next comment) I'm definately more critical about these issues in older age groups and probably should read more about them. We're taught that statins are useful even in people over 75, but maybe this has nothing to do with cholesterol. If you can tell me what the other source is, I can look it up. I might have access ;) Edit: Apparently neither of us do.

Only standard labs are readily available to me in clinical practice. We have a mostly public health care system, and nonstandard labs are usually ridiculously pricey. Of course LDL is hardly the only measurement we take, and is combined with all the other risk factors when assessing total arterial disease risk.

I hope I have provided a POV of how background knowledge can change the way we interpret study findings, and how much easier it makes sceptiscism about them. I apologize that I don't have english sources ready at hand for the claims I make, and I know that you will not take them on authority. It is impossible to me to keep record of most of my sources, and most of them are in finnish language.

I will check out the book you recommend, I'm chillin' after all. I think there are far too few rationalists in medicine. The education methods are authoritative and many times frustratingly ineffective. Unfortunately I don't know how to change it (yet), and will do my best with what I have.

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I'm sorry. I'm not trying to be extra difficult, but where is the original source? Is it authentic?

If I understand correctly, the original source is this. I can't find any way to access it online, but everyone who talks about it says the results mentioned in that blog post and no one says otherwise, so I'm assuming they didn't just make it up.

As I said, mortality is not the only interesting endpoint. Also the CI upper bound for CVD is not over 1, not matter how hard we want to push it. The other review does support your conclusions. It doesn't however support increasing dietary saturated fat or changing nutritional guidelines in any other way.

I see where you're coming from. On the other hand, there is a $40 billion diet industry telling people to eat less fat and causing a spectacular amount of mental anguish around this idea (I don't know if this is true in Finland; it's definitely a big deal in America). That eating less fat has literally zero effect on any outcome seems like something we should be trying to make more widely known, whether or not the small effect of changing fat types on events but not mortality holds up.

That statins work equally well in high and low cholesterol populations is to me the most interesting claim that you make. Can you provide a source for it?

Apparently not; I know I've heard this but my attempts to Google a study in humans failed. I did find something in rabbits showing effects regardless of cholesterol, but even that wasn't a direct comparison.

The other drugs you mention have common annoying side effects that mostly reduce compliance, and I wouldn't be surprised if some of the side effects increased mortality. In Finland they are also usually prescribed by a specialist and are never a first line treatment.

Right, but the studies on niacin and ezetimibe showed that they decreased cholesterol (ie were being used successfully and correctly) but failed to decrease cardiovascular endpoints.

We have guidelines to measure lipid profiles after 48 hours of an ischemic vascular event. Within this time period, the LDL levels plummet, but then they rise again. This might be caused by a ruptured atherosclerotic plague releasing its contents in the blood stream. Since this is a very recent guideline, it might explain the finding you present. Then again, it also might not. If I skimmed correctly there was no mention of the timing of the measurements.

You're right that the measurements were taken within 24 hours, but I've heard this isn't such a big deal, and according to the full-text version of the Fonarow study (sorry, didn't find it until this morning) they agree with me. Also, if I'm reading their table right patients having acute coronary events had higher, not lower, cholesterol than those coming in with chronic complaints, and if the effect were really only 5-15% it wouldn't significantly affect the main finding of the paper by much.

If you can tell me what the other source is, I can look it up. I might have access ;)

It's the same Framingham paper. I can only reach the abstract (my medical school doesn't give me electronic access that far back) and I'm relying on reviews and comments to tell me what's inside.

Atherosclerosis is mostly a nonreversible progressive disease that can start as early as in late adolescence, so it makes sense that hypercholesterolemia before age 50 is most important for its development. All it takes for a plague to rupture after tens of years of accumulation is that the endothelium covering it fails, it doesn't necessarily have to grow anymore.

Right, this makes sense, I'm just saying it's the opposite of what Framingham shows. Framingham says that "there is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels"

I hope I have provided a POV of how background knowledge can change the way we interpret study findings, and how much easier it makes sceptiscism about them

Yes, I agree with this. But the thesis of Good Calories, Bad Calories is that this allows enough degrees of freedom to be able to back up infinite amounts of confirmation bias. That is, if you see a study that supports your hypothesis, you say "Great, studies have proven we're right!" And if you see a study that opposes your hypothesis, you say "in light of my background knowledge that my hypothesis is right, we can't take this study at face value", then seize on the first flaw you find in the study and use it to throw it all out. Kind of the "one person's modus ponens is the other person's modus tollens" thing people here keep talking about.

My new favorite study ever is the Biblically-named Lee, Lord, and Lepper, which asked people to evaluate the methodology of a study on the death penalty. They found that regardless of its actual methodology, if the experimenters wrote the conclusion such that it supported the opinions of the evaluators, the evaluators said it had good methodology. If the experimenters changed the conclusion so that it disagreed with the opinions of the evaluators, the evaluators were - surprise! - able to find a bunch of problems with the methodology and reasons why the study didn't apply to anything.

I have no idea to what degree that's happening in medicine these days; I'm really only beginning to seriously engage with the literature beyond a boring student level. I read Good Calories, Bad Calories on the advice of a bunch of other Less Wrongers, it was a really interesting book and has gotten me worried enough that I wanted to vent - as you pointed out, this wasn't the best place for it and I apologize.

But I do think that further investigation beyond the level of just agreeing we can use background knowledge to interpret away findings is necessary at this point. At the very least, you have to admit the Cochrane review showing restricting dietary fat had no effect on anything means that something has gone atrociously wrong somewhere between what doctors say to their patients and reality (actually, I don't know how that works in Finland; in the US dietary fat is a pretty big deal).

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If I understand correctly, the original source is this. I can't find any way to access it online, but everyone who talks about it says the results mentioned in that blog post and no one says otherwise, so I'm assuming they didn't just make it up.

I'm impressed. I took a look at various sources, and it seems like you can't even buy a used copy of that book anymore - it only exists in various academic libraries, and in many of them, it's stored only as microfiche/microfilm.

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If I understand correctly, the original source is this. I can't find any way to access it online, but everyone who talks about it says the results mentioned in that blog post and no one says otherwise, so I'm assuming they didn't just make it up.

Perhaps I don't trust people enough on the internet. Especially when they're trying to sell books of their own. See down below. Perhaps most of the people who talk about it haven't seen it themselves, but are happy to spread the good message anyway. Perhaps the guy who sold it forged it. There are many points where someone could be lying, so you don't have to blame a guy you like. There are some very dishonest people in my personal life so maybe this is a bias. It's also pretty amazing to me that google gives only 563 results for "Framingham Diet Study", because I guess this should be kind of a big deal. I'd really like to get my hands on it.

Right, but the studies on niacin and ezetimibe showed that they decreased cholesterol (ie were being used successfully and correctly) but failed to decrease cardiovascular endpoints.

I agree it's very weird, but again the decrease in cholesterol not helping is hardly the only explanation for the results. Confounding factors are not fiction. Unfortunately I don't have time to scrutinize them, as I'm not going to prescribe these drugs. (EDITED)

I see where you're coming from. On the other hand, there is a $40 billion diet industry telling people to eat less fat and causing a spectacular amount of mental anguish around this idea (I don't know if this is true in Finland; it's definitely a big deal in America).

Living in Finland might indeed be the source of my confusion. Since most of the studies come from the US, I should update that this industry affects our nutrition more than I'd currently like to think. Nutrition here is a frequent topic, but excluding a couple of cases I've never come across the emotional turmoil that it seems to cause in americans. Isn't there an industry pushing back too, and how are these people not just trying to make money?

You're right that the measurements were taken within 24 hours, but I've heard this isn't such a big deal, and according to the full-text version of the Fonarow study (sorry, didn't find it until this morning) they agree with me. Also, if I'm reading their table right patients having acute coronary events had higher, not lower, cholesterol than those coming in with chronic complaints, and if the effect were really only 5-15% it wouldn't significantly affect the main finding of the paper by much.

Thank you, definately saving them. Edit: The first study says "Although fasting blood samples were not mandated on the admission baseline test, subsequent samples collected on days 2 and 4 were in the fasting state. " This means the baseline probably seems higher than it should. See the chapter "Limitations" in the Fonarow study. I can't see how they agree with you (See Edit3 below, though).

The chronic cases receive statins after the disease has mostly developed so I guess that should explain the results. 30 % of the chronics received lipid lowering medication. 20 % of the admitted patients overall received lipid lowering medication. In the fifth table, lipid lowering medication is the strongest predictor of lower LDL. Edit2 This might also better explain why admitted patients overall have lower LDL than the general population, and can also be combined with the acute effect observed. It just means that patients at risk are properly recognized and treated, although probably too late.Edit3 Read more thoroughly and did some unit conversions from mg/dl to mmol/l, it doesn't. However what is considered normal varies from risk group to risk group, and can be as low as 70 mg/dl. The authors of this study are supporting lowering the limits of what is considered normal, and I suppose you wouldn't agree with this.

Framingham says that "there is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels"

In people over 50 years, if I understand correctly. Might be an english issue or then the issue is really with my understanding. So if people have more diseases (or they have progressed further) after 50 years that cause starvation (or some other mechanism that lowers cholesterol you can agree with) ie. IBD, depression, dementia, heart failure AND CVD mortality (edit), it makes sense that mortality follows falling cholesterol levels in that age group. Combine this with what I said before. As they speculate, "After age 50 years the association of mortality with cholesterol values is confounded by people whose cholesterol levels are falling--perhaps due to diseases predisposing to death." They only ruled out CVD and cancer after all. I'd like to find the full copy for free because I have slight difficulty parsing the abstract. Of course it's the study itself versus their speculation based on some "background knowledge" so I have to admit that your position is the stronger one here.

Yes, I agree with this. But the thesis of Good Calories, Bad Calories is that this allows enough degrees of freedom to be able to back up infinite amounts of confirmation bias.

Now I definately have to read this book! I promise.

At the very least, you have to admit the Cochrane review showing restricting dietary fat had no effect on anything means that something has gone atrociously wrong somewhere between what doctors say to their patients and reality

Our national guidelines already say that the effect of recommended diet (and exercise!) on cholesterol is tiny, but positive. After this discussion I'm even less enthusiastic about giving dietary advise. Concerning diabetes the guidelines might be even more wrong, but lets not open that can of worms this time!

And if you see a study that opposes your hypothesis, you say "in light of my background knowledge that my hypothesis is right, we can't take this study at face value", then seize on the first flaw you find in the study and use it to throw it all out.

Yeah, this culture is very prevalent in medicine, but of course varies from person to person. University hospital doctors are very status oriented people. I've read Heuristics and Biases, and as I understand knowing about biases doesn't help much. Then again, I don't think it's only (dis)confirmation bias, but caution (a bias in itself), and I think everyone has difficulty differentiating these two. To be honest at this level of my education if I seriously start questioning my elders about everything I'll be scared shitless in my daily work.

While time allows for additional studies, I feel like I can only concentrate on a few topics to master them. I was previously interested in a few fringes of neurology, mainly MS, but I'm starting to see that this is hardly rational from a utilitarian perspective.

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the Cochrane review showing restricting dietary fat had no effect on anything

Restricting dietary fat keeping carbs and proteins constant (decreasing total calorie intake), or restricting dietary fat keeping total calorie intake constant (increasing carbs and/or proteins)? Or something in between?

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Jayson_Virissimo

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Have you ever seen any research showing alcohol consumption to be beneficial in non-humans? I am currently a non-drinker, but an animal study would defeat my true rejection.

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Labeling the amount of calories in food (for example on McDonald's restaurant menus) totally fails to change people's eating behaviors at all, no matter how hard people study it.

The effect may be too small to measure, but I can personally attest that it is at least 1 in 7.057 billion.

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While my grocery shopping is strongly determined by nutritional label content, my behavior at restaurants only weakly is, and I think this is related to the fact that so few restaurants offer that service in the first place. If I'm going to a restaurant at all, I'm in the habit of taking for granted that I will only be able to guess at the nutritional content of the meal I'm ordering, and will therefore be taking a break from deciding on the basis of labeling (as an aside, I have an enormous appetite, and can eat a meal meant for three and have room for dessert afterwards despite weighing under 75 kg. I'm used to eating until I'm only fractionally full, but will sometimes have "break" meals at restaurants or on holidays, so my restaurant eating isn't that indicative of my usual diet.)

If restaurants routinely listed caloric content of their menu items, instead of the places that do so mostly being fast food chains which I tend to avoid in the first place due to their reputations for low quality and unhealthy food, it might be a significantly stronger determining factor in what I order.

ETA: When I was mostly reliant on a college cafeteria for food (which is in many ways more similar to a restaurant than a grocery,) I was strictly dependent on nutrition labels to choose what I ate, and if anything was unlabeled, or I suspected it was mislabeled, I wouldn't eat it.

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I checked this book out of the library recently, and most of the information in it pretty much fits into my models even if the specifics are news to me. I was quite surprised though, to find that Warren Buffett in particular directs his holdings to a lot of deliberate competition stifling and price gouging on captive customers. I had gotten used to thinking of him as the Big Good of the investment world, and I was surprised to realize that even if he puts his own personal fortune to benevolent uses, he doesn't have any particular qualms about deliberately concentrating wealth rather than producing it, in order to maximize profits. That didn't reflect the traditional capitalist values I imagined him to hold.

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someonewrongonthenet

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The divorce rate in India is 1.1%, and people in arranged marriages report greater love for partners than people in love marriages.

Some suggest that it has something to do with previous findings that being given more choices makes you less satisfied about the choice that you ultimately make.

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I have been miscalibrating how much people at my workplace like or dislike me. I've gotten it wrong in both directions recently.

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I was surprised by news of the Toyota labs replication of the Mitsubishi Low Energy Nuclear Transmutation experiment. Nuclear physics is nowhere near my field of expertise, but I am surprised and confused that phenomena similar to LENR are possible and are not being exploited left, right and centre.

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Disclaimer: this post contains personal informations and (very mild) generalizations about gender behaviour. If you think you cannot handle it properly, please avoid it.

Unfortunately, the most surprising information I had recently has been my February break-up: this girl I was dating and was madly in love with exhibited all behaviours of being in love with me too... There were some problems that prevented us getting together, but I thought they weren't so determining. It turned out I was deadly wrong: she started dating a guy that was nearer to her home and had more free time, and after two weeks I was dumped. A month later they were engaged. I have thus increased the probability of correlation between behaviours signalling love (signs of affection, sex, gifts, etc.) and predatory behavious (securing a mate for resources). Which is another way to say that now I'm less trustful towards women :/

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someonewrongonthenet

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Well, that's interesting...unless you are bisexual, you don't and won't ever have such bad experiences with men.

So from a rationalist perspective, does it make sense to use this evidence to update your beliefs about the trustworthiness of women, but not your beliefs about the trustworthiness of men? (This is a real, not rhetorical question)

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The fact that you were deeply in love with her suggests that you aren't in a position where you can see the facts of the situation clearly.

Do you think it's a good idea to update based on that understanding of the situation?

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Do you think it's a good idea to update based on that understanding of the situation?

Well, I've asked myself this for a long time. Sure I was deeply in love, but for what I could see all my behaviours were reciprocated. Also other people (besides her friends, apparently) were surprised (ranging from very surprised to downright furious) for her 'change'. I still don't know how much I could have foreseen this in advance, but this doesn't change the fact that I must be a lot more aware the next time.

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I've found that paying attention to how much "signs of love" and "access to me for resources" correlate is useful in my relationships. But I'm also polyamorous so distance tends not to be nearly as big an obstacle as it seems to be for monogamy (coincidentally, if you're not aware, distance? Is a HUGE factor for a lot of people)

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I've found that paying attention to how much "signs of love" and "access to me for resources" correlate is useful in my relationships.

Yeah...

But I'm also polyamorous so distance tends not to be nearly as big an obstacle as it seems to be for monogamy

How do you implement that? You just simply tell a girl you like that you have multiple relationships?

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I usually say I'm polyamorous, because most polyamorous people know the term, but otherwise yeah. I also live in Portland, and hang out with crowds where this is more common than normal. I did end up dating one monogamous girl, but she was completely okay with it - work occupied 90% of her life, and having a partner that didn't mind seeing her once or twice a month worked out very nicely for her.

I generally bring this up well before asking someone out, so that I can get a good feel for their reaction (often first or second meeting - just talking about my life makes it pretty clear I date multiple people. "Oh, today I hung out with girlfriend A and watched Farscape, then got a haircut with girlfriend B")

I also tend to emphasize my particular style of polyamory, which centers on honesty and the idea "It's not cheating if everyone involved has agreed to play by different rules". I've found signalling "I'm poly, NOT someone cheating on their spouse" is important :)

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someonewrongonthenet

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Have I ever mentioned how envious I am of people who live in Portland...

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Even simple "obvious" insights often don't occur to us. But they become clear in hindsight or after being pointed out by others.
Humans don't have general intelligence. This became clear after watching a video of John Tooby, Evolutionary speaking humans have evolved subsystems for solving specific problems like navigating the social landscape. But we don't have general intelligence. This explains a lot.

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Could you give a brief summary of why we don't have general intelligence?

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First there is some contention in this and I'm basically reflecting Toobys opinion here. He says that there was no selection pressure to develop general intelligence and instead we have specialized subsystems that help us navigate our world.

IIRC the video was the following:John Tooby: Can discovering the design principles governing natural intelligence unleash breakthroughs in AI?

As evidence consider the Wason selection task, although a very simple logic puzzle most people fail at it, but can do it when the same problem is presented in a social context instead.

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Pablo_Stafforini

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What has surprised me the most recently is reading this THINK document about the huge effects that self-improvement can have on one's ability to change the world for the better.

I was also surprised to learn that 25% of the philosophers that responded to Brian Leiter's 'Philosophers, Eating, Ethics' poll said they were vegetarian and an additional 8% said they were vegan. In other words, a whopping one third of respondents reported being either vegans or vegetarians. The proportion of vegetarians in this sample is about eight times larger than that of the general American population; the proportion of vegans is 10-20 times larger.

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The thing that first comes to mind is recently realizing that even I was infected by a dangerous memeplex directly decended from christianity.

I've always been an atheist and wondered what it was like to realize that there is no god, or what it's like to strongly believe some obviously false thing just because it's what people you grew up with believed. I remember thinking "well, I'm right on the big things like god and psychic powers and such, I guess epistemic rationality is a solved problem"

Now I'm like "holy crap, I (we) really suck at this, and could be way better".

NOt sure if this is what you're looking for.

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Not saying which it is is pretty obnoxious, but I'll have to assume you've been bitten by the moldbug

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I feel like there's an Edgar Allen Poe parody just waiting to happen here.

"Dis i' real bad, mistah. He bin bitten ba de moole-bug."

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Gender is much more biologically determined and less socially constructed than I had previously thought. http://whyevolutionistrue.wordpress.com/2011/01/31/evolutionary-psychology-gender-construction/

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Having some predictions on record helps answering this kind of question. The following are from my GJP forecasts:

the announcement of Mario Monti's imminent resignation; I'd been very sure (95% probability) he'd stay in power until the election, as that was only a few months away
the peace talks between Ansar Dine and the Malian government; I'd been skeptical (35% probability) that anyone would want to talk with such a ragtag bunch, and yet the talks just took place

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