I’ll try rephrasing, somewhat overstating the strength of the reasoning (taking it from probabilistic to logical) in case that causes a basic idea to be clearly communicated that was obscured by probabilism.
If an increase in calorie intake was itself sufficient to produce an increase in fat mass in otherwise metabolically high-functioning adults, we’d have seen a different result from pre-obesity-epidemic experiments in overfeeding. This rules out the direction of causality “mere overeating” → “obesity”.
Any hypertrophy of fat cells, in turn, will causally require more nutritional intake to feed the hypertrophy, just like a cancer growing, or any other body part growing, will require more nutritional intake. So once you observe a cancer or a huge fat cell mass or any other diseased body part growing, you already know the person already took in that much food, both to grow the cancerous body part and sustain it; you shouldn’t be surprised to look back at the cancer patient’s caloric consumption record and find an excess; so finding that excess consumption shouldn’t update you at all about the cause of the malevolently growing body part.
You’re taking causality that must at least run from “fat cell hypertrophy” → “excess consumption” and already fully explains away the presence of an observed correlation, and then adding on a causal postulate that runs the other way—a direction of causality that would be theoretically possible in a world with no overfeeding experiments one way or the other, though not supported even there, since there is no otherwise unexpected observation which it explains; but which in our world is ruled out by the results of overfeeding experiments, which tested the results of experimental-intervention-produced excess calorie consumptions in metabolically healthy individuals before the obesity epidemic.
To further oversimplify the oversimplification: the logic you’re deploying for obesity would also work to conclude that overeating causes cancer, and therefore Proves Too Much.
The only reason why “overeating caused this huge fat mass to grow inside my body” sounds more plausible than “overeating caused this huge tumor to grow inside my body” is that the former theory follows the Sin Theory of Obesity in which obesity is a punishment for the sin of gluttony, while the latter theory is incongruent with simple just-world hypotheses as of the 21st century in Western societies. Both are ruled out by experiments showing that (in metabolically healthy individuals before the obesity epidemic) a randomized experimental intervention to add overeating does not produce obesity any more than it produces tumors.
The only reason why “overeating caused this huge fat mass to grow inside my body” sounds more plausible than “overeating caused this huge tumor to grow inside my body” is that the former theory follows the Sin Theory of Obesity
I think the first sounds more plausible because the story “humans store caloric excess as fat in times of plenty and burn it off in times of scarcity” is the kind of thing that we should have as a hypothesis-under-consideration before we look at the link between calorie intake and body mass. Whereas “humans store caloric excess as cancer” (or as fetuses) isn’t. And if that story is true, then “eating lots of caloric excess causes lots of fat to be stored” isn’t automatically true, but again it’s definitely something we should have under consideration.
So if your line here is meant to be taken a priori—that is, if you’re saying “even without actually looking at the link between caloric intake and body mass, there’s no reason to believe overeating-causes-fat any more than you’d believe overeating-causes-cancer”, then it seems just wrong.
Maybe you meant it a posteriori? Something like “okay but overeating studies show that eating lots of caloric excess doesn’t by default cause lots of fat to be stored, so you no longer have a plausible explanation”?
But then at least two other reasons come to mind for why overeating-causes-fat might still seem more plausible than overeating-causes-cancer. One is that someone might not believe that studies show what you think they show. Another is that someone might just be bad at propagating updates. Currently, these both seem more likely to me than your “sin theory” theory.
I strongly disagree with this interpretation of those overfeeding studies. From what I can tell (though I couldn’t access every study SMTM cites), “overfeeding” is usually defined relative to the output of one of the typical BMR/TDEE estimation formulas given a person’s parameters, not based on actual measurement of a subject’s TDEE. Those formulas are fine for a baseline guess, but even the most accurate ones are going to be substantially off in either direction for a fair number of people! Some of the difference is unaccounted-for NEAT, some of it is differences in absorption efficiency, some of it is probably other factors we don’t understand yet. Given the known reality of interpersonal variation in what your actual calories in and out are relative to their naive estimates, some subjects not gaining weight while “overfeeding” is exactly what you’d expect to see.
A fun fact: my estimated “effective TDEE” is (averaged over months) pretty consistently around 3300 cal/day for the past 18 months—rarely more than +/- 100 cal/day off in either direction—whereas the best formula I could find (using my body fat %, as actually-measured by a DEXA scan) says it should be something more like 2600-2800 cal/day. This is based on weighing my body daily and recording the caloric intake from actually-everything I eat, almost always weighing food when necessary rather than coming up with estimates.
I think I understood what you’re saying the first time around and again I agree that your account of things is certainly possible, but even in your case the tumor or fat mass has to be sustained by calorie consumption from the outside. The increase in calorie intake we’ve seen is about the amount we would have expected if someone had just told us that people are 15% fatter on average without any increase in exertion or heat dissipation to compensate for that.
Another way to say this is that I’m just making a claim about the conditional expectation E[average body mass increase | average calorie consumption increase = 20%] and pointing out this expectation is not far off from the actual observed body mass increase we see. In that sense the increase in calorie intake can account for the increase in body mass in correlational terms. The question of why both of these variables went up, though, is difficult and their level is obviously not determined by this argument.
Externally, why people feel the need to keep eating until they become obese is not a question with a clear (to me) answer. It could be because there is some process that’s operating in the body that’s taking priority over other activities and hoarding a lot of the energy intake to produce fat cells, which I think is your story. However, it could also be that some part of the brain is malfunctioning and leading the lipostat to be poorly calibrated. It could also be that the food you’re eating messes with the natural feedback loops in your body that are supposed to make you feel full when you’ve eaten enough.
I think this question is interesting and your account is logically possible. I just think that
I don’t have any special insight into which account is right, and
I don’t think your particular explanation is favored that much over other competing explanations.
I don’t think the overfeeding experiments provide strong evidence for your scenario, though I agree that they should be a Bayesian update in favor of accounts in that broad neighborhood. What would convince me is experiments which involve smaller increases in calorie intake but sustained over much longer periods of time, on the order of a year or so. If such experiments failed to find an effect that would be a strong update for me towards your view. Right now I buy the cancer analogy on conceptual grounds but I don’t think we have enough evidence to conclude obesity is like cancer in this regard, though it very well could be the case.
To give an analogy of my own, the overfeeding studies look similar to attempts to settle disputes about which programming languages are best for productivity by asking undergraduates to complete some simple tasks in them over the course of a few weeks. What really matters is how you do when you’re working with big and complex software in the real world that has to be developed and maintained by large teams with turnover for years, sometimes decades; but that obviously doesn’t lend itself to a simple experimental design so people still keep arguing about it.
“Pregnancy” probably isn’t a thing. “Pregnant” people eat around 500 more calories per day. This is sufficient to explain all the weight gain from “pregnancy” without supposing anything other than thermodynamics at work—anyone who eats an extra 500 calories per day will probably gain that much weight over the course of 40 weeks.
I think Ege’s alleging that SMTM presented two causal graphs:
calories → ? → weight gain
calories → weight gain
Ege’s saying that 2 is simpler and sufficient, so we don’t need to posit a ? in the middle.
You’re pointing out that we still need to address a third causal graph:
? → calories → weight gain
Edit: And maybe that there’s also a scenario where ?, calorie intake, and weight gain are all in some complex interrelationship. Maybe contaminants cause more fat deposition and less energy and more hunger, thereby increasing weight gain per calorie, increased calorie intake, and increased contaminant intake via food. Or something.
Ege’s agreeing with you, but wants to emphasize that this is compatible with criticism of SMTM’s alleged emphasis on graph 1.
Note: I say “alleged” only because I’m sidestepping evaluating the truth of Ege’s claim. Just trying to clarify what it is (AFAICT).
I don’t agree with this presentation of what I’m saying.
I’m not terribly sure what SMTM means when they say “the increase in calorie intake is small”, but all possible interpretations of their claim seem wrong. For instance, one plausible interpretation in causal graph lingo is “if you applied the do operator on calorie intake and raised it by 20%, we would have seen an increase in body mass that’s significantly smaller than what we’ve actually seen”. I think this claim is wrong, basically for long-run energy balance reasons.
I’m not saying anything else about the structure of the causal graphs, which could be arbitrarily complicated and involve arbitrarily many nodes and dependencies. I’m just saying that if you apply the do operator on calorie intake and raise it by 20% then you’d get an increase in mean body mass that’s about as big as what we’ve seen.
Thanks for clarifying that I misrepresented your view. Based on your response here, you’re pointing out that there’s a strong correlation between increased caloric intake at the population level, and increased obesity. You are also saying that the explanations you’ve read from SMTM for why this correlation exists seem wrong, and also that they underestimate the magnitude or importance of the caloric intake.
WRT Eliezer’s arguments, you seem to be agreeing that there may be some underlying force(s) causing that increased caloric intake. However, you are very uncertain about which, if any, of the hypothesized forces(s) are the true causes of increased caloric intake.
Eliezer and others seem to be perhaps mistakenly interpreting you as denying the existence of, or “need for,” a deeper explanation for increased caloric intake and consequent weight gain. You are confused about why they are making this mistake.
I’m not sure who is “to blame” for the miscommunication but I suspect I simply was not clear enough in my top comment. Now it’s likely too late to clear up the issue for most readers as they won’t be following the developments in this thread.
I’m just saying that if you apply the do operator on calorie intake and raise it by 20% then you’d get an increase in mean body mass that’s about as big as what we’ve seen.
This is “assuming there’s no link “increased calorie intake → increased energy expenditure”″, right? I think one of the things Eliezer is saying is that there seems to have been such a link in the past and now there isn’t / it’s much weaker.
That’s not quite true—there is at least the naive link that a higher equilibrium body mass leads you to expend more energy in daily activities even if you exercise the same amount as before. In my very naive model I assume these are directly proportional, but Natalia cites some better research that does a log-linear regression of calorie expenditure on equilibrium (I think? I didn’t check this part) body mass which seems to be more accurate empirically.
I think it’s unclear whether we had the link you mention in the past, too. We definitely had a correlational link: people who did hard labor and ended up exercising a lot every day took in much more calories, as we would expect, and they were generally not obese. However, I think my argument would work just as well in the past if you just applied the do operator on calorie intake per day and looked at the causal impact on equilibrium body mass, as I don’t think there’s evidence that there’s a big downstream link from calorie intake per day to exercise.
I don’t understand why you’re “retrying”. I already agree with your point and you not saying “yes, you already agree with me” is quite confusing to me. As I say in my comment:
Externally, why people feel the need to keep eating until they become obese is not a question with a clear (to me) answer. It could be because there is some process that’s operating in the body that’s taking priority over other activities and hoarding a lot of the energy intake to produce fat cells, which I think is your story.
Do you think this characterization of your position is unfair or wrong? If so, why?
As far as I can see the only object-level point I disagree with you about is that I don’t think the evidence for obesity being like cancer or pregnancy is as strong as you seem to think it is. It’s definitely possible for it to be like that but I would bet against it at even odds. I explain this here:
I don’t think the overfeeding experiments provide strong evidence for your scenario, though I agree that they should be a Bayesian update in favor of accounts in that broad neighborhood. What would convince me is experiments which involve smaller increases in calorie intake but sustained over much longer periods of time, on the order of a year or so. If such experiments failed to find an effect that would be a strong update for me towards your view. Right now I buy the cancer analogy on conceptual grounds but I don’t think we have enough evidence to conclude obesity is like cancer in this regard, though it very well could be the case.
On top of that I also have a separate disagreement with you about emphasis in the context of my comment, since the point of my top comment is to draw attention to 400 kcal/day not being a small increase in calorie intake. You agree with me about this but you just don’t think it’s worth focusing on, probably because you think it’s a trivial observation. I still think it’s something that should be corrected given that SMTM explicitly said that it’s a small increase.
As far as I can see the only object-level point I disagree with you about is that I don’t think the evidence for obesity being like cancer or pregnancy is as strong as you seem to think it is.
Some people certainly are obese because of literal cancer and literal pregnancy. We seem to have strong evidence for that.
The interesting question is about how much of the obesity pandemic is explainable by such factors and not whether evidence for such factors exists.
We certainly don’t see enough pregnancy and cancer to explain the obesity epidemic but there might be other factors that are similar but harder to see. Thermodynamic arguments don’t help us rule out other effects that are similar to pregnancy/cancer.
I agree with everything you said, so again I’m confused why you thought you should make this comment.
I feel like I don’t really disagree with most of the commenters but they either think I do disagree with them or that I did a very bad job of communicating exactly what my point was. It’s hard for me to understand.
I still stand by this claim, again with the caveat that you take it as a correlational use of the word “explain” (which is not at all uncommon e.g. when talking about “fraction of explained variance” and so forth) and not one that suggests a causal explanation of the form “people wanted to eat more food, so they ate more food, so they got fatter as a result”.
Ok. My main point is just to clarify that other people are reading you as talking about explanation in general, not just strictly correlational explanation (if that’s what’s happening).
I do also think that’s not a great use of the word “explain” and “mystery”, because it’s not why the colloquial word is useful. The colloquial words “explain”/”mystery” are useful because they index “more information and ideas given/needed about this”. So just because X correlationally explains Y, and X is true, doesn’t mean there’s no mystery about Y.
I never said there’s no mystery about Y, just that there’s no mystery about Y being true conditional on X being true.
It’s a fair point that my usage of “explain” and “mystery” confused some people but I’m not too sure how else I would have made my point. Should I have said “people today are eating about as much more compared to the past as we would expect given how much fatter they’ve gotten”?
Someone may have made this point somewhere else already, but there’s really no mystery in Americans getting fatter if we condition on the trajectory of mean calorie intake.
Read literally, this says: There’s a mystery of why intake went up. Conditioned on intake up, there’s no mystery of why fat went up. I think this isn’t right. If we agreed that sustained high intake implies weight increase, it’s still not right. That’s because conditional probability isn’t the same as explanation, and if there’s a mystery, what we’re after is explanation. That’s one of the points of the tumor example: If fat causes intake, then saying “there’s no mystery about fat” is pointing away from the explanation of intake, which is that fat causes intake and something causes fat.
They later tried to address this because people picked up on it and eventually said “well, even if the 20% increase explains the obesity epidemic, that still leaves the question of why people are eating more open”. I think this is bizarre: to me it’s quite obvious that in the long run more calorie intake has to lead to higher body mass, though not necessarily in a proportional way as I’ve idealized above. They should have been focusing on the causal channel going through calorie intake from the start. Instead, it seems like to them this was a secondary channel to fall back on.
Taken literally, this seems to be consistent with beliefs of people who disagree with you? It’s just that they have different conclusions about the causality going through calorie intake. Interpreted that way, I don’t see how this statement is consistent with saying “there’s really no mystery in Americans getting fatter”.
I don’t understand your objection. I never made any claims about causality. My whole argument is about energy balance, which says nothing about causality.
On the other hand, I think it’s just true that conditioned on the increase in calorie intake there’s no mystery in the increase in body mass. I don’t understand why you’re disputing this point. You can say this is not an interesting observation (which I agree with, though as far as I can tell SMTM did not, which is why I wrote my comment) but I don’t see how you can say it’s not right.
My impression is that some people are engaging in a bizarre combination of steelmanning SMTM’s point while strawmanning my own. SMTM didn’t make the best version of the claim they could have made, they made the actual claim that I quote in my post. I think their claim is wrong. Do you disagree with this or not?
Meta: my interest here is to see if there are miscommunications here that I can clear up. I’m not carefully following the object-level debate. (In particular, I think that you Ege should feel extremely free to ignore what I’m saying as unhelpful to you; if I’m not helping you understand what’s happening in the thread then I’m not doing what I’m trying to do.)
I don’t understand your objection. I never made any claims about causality. My whole argument is about energy balance, which says nothing about causality.
On the other hand, I think it’s just true that conditioned on the increase in calorie intake there’s no mystery in the increase in body mass. I don’t understand why you’re disputing this point.
(Note: you did mention causality in the passage I quoted: “They should have been focusing on the causal channel going through calorie intake from the start.” That’s not a claim about what causes what, but it is a claim about what questions are the right questions to ask.)
I’m pointing at the word “mystery”. I’m saying that to me, “mystery” means “explanation wanted”. I’m saying that just because P(X|Y) is high, doesn’t mean Y is a good explanation of X. (For a silly example, setting Y=”X and 2+1=3″ makes P(X|Y) = 1 and is obviously doesn’t explain anything.) I agree (based on my preconceptions, ~0 independent data) that P(body mass high | high sustained intake in the wild) is high. My read of some of the comments on your comment, e.g. Yudkowsky’s, is that they are taking you to be saying “high intake explains fat, such that there is no further interesting question about fat, though there may be further questions about why high intake”, based on the passages from your comment I quoted. Reading your comment closely, you didn’t actually say that, if by “conditional on Y, there’s no mystery about X” you mean “P(X|Y) is high”. In fact, what you said is consistent with believing that “Alice is fat” explains (in the contextually relevant sense) that “Alice has high intake”, and you recommend that if you believe this then you should “focus[] on the causal channel going through calorie intake”, i.e. investigate why Alice is fat in order to explain her high intake.
SMTM didn’t make the best version of the claim they could have made, they made the actual claim that I quote in my post. I think their claim is wrong. Do you disagree with this or not?
I don’t know. I think your argument makes sense, but the actual situation is going to be more complicated.
Do you know, if we also observe an obesity-epidemic in the subgroup of people who average 25k+ in daily steps? That step-requirement is a good, high standard of “metabolically healthy” to isolate. I belong in that group these days and it feels natural, relaxed and I feel far more energetic than when I was averaging 7k daily steps and was the sedentary nerd cliché, about a year ago. Now I am a nerd, who takes two walks per day, almost never sits and either stands or uses his office treadmill when on the computer. Even before, I never really got fat. But I feel, that I might not have been “metabolically healthy”, because now I feel better. So I strongly suspect that a far higher than average step-count is a hard requirement for being “metabolically healthy”.
I hear that “pregnant” people also do less mountain-climbing, even if they were exercising healthily before. No wonder they gain weight! Do we even need to postulate “pregnancy” as a condition, when their caloric intake and reduced exercise seems adequate to explain all of the observed weight gain?
I was not responding to your pregnancy-argument, but to your post higher up in this subthread from 3 days ago. The threading makes this a bit confusing. Also should have specified what I was responding to the last paragraph: ”Both are ruled out by experiments showing that (in metabolically healthy individuals before the obesity epidemic) a randomized experimental intervention to add overeating does not produce obesity any more than it produces tumors.”
Is there actually an obesity epidemic among people who walk more than 25k steps per day? (or is something like that currently known).
EDIT: I suppose my hypothesis is: Living a non-sedentary lifestyle meaning less than 20 minutes of sitting per day, 25k-ish steps per day somewhat equally spread out over all waking hours makes the “weight-gain -=> obesity”-phenomenon impossible, because it’s a sufficient requirement for robust metabological health. If that was true, it might not answer what is behind the obesity epidemic. But that’s what I would study, to check if it’s a cure or reliable prevention.
I’d say 90% chance of this being true, but mostly on intuition and with high model uncertainty. And I don’t know, if we know enough to answer this question, because non-sedentary lifestyles like that are fairly niche in all Western societies. But I recently figured out, that they’re not all that hard to adopt.
EDID2: Actually, I’d say the 90% applies to it being “reliable prevention”. No clue, how curative that would be. I never had to really lose more than a couple kg of fat. [and “had to” is really exaggerating a lot] From what I observe, it seems somehow impossible for really fat people to become not fat, despite heroic struggles which have always been strange to observe from the outside.
Is there any solid evidence that walking 25k steps per day will solve the obesity epidemic? I ask this because it’s genuinely a remarkable claim, one that if verified and implemented would save huge numbers of lives and hundreds of billions in medical expenses. The literature mostly seems to indicate that increased exercise doesn’t have dramatic effects on obesity.
There is not. That’s why I was asking him if he knows. I was not interested in the effect of exercise. Exercise means, you do some activity a couple times per week. I’m interested whether the obesety epidemic only affects the sedentary populatrion. And if being or becoming non-sedentary is protective or curative. 25k steps for me means, that my treadmill is running constantly when I’m on my computer. This is not really exercise. Movement is just my default state.
In that way, I have become closer to what an EAA-hunter-gatherer, than to a sedentary office worker does with his body. [or I would, if this had been my lifetime norm instead of something I still get used to] If the human body was sold as a machine, the sedentary lifestyle probably would void your warranty, because it’s rather extreme (dis)usage. Sedentary people being unhealthy is not surprising. It’s surprising that some sedentary people aren’t.
Anyway, “being in near-constant motion” is too specific/complicated a metric. So I’d just look for a step count high enough, that’s only feasibly doable by a non-sedentary person like me. Though, I guess any daily jogger can probably match or exceed 25k steps per day. The group of people whose 80th quantile waking hour still has >1k steps. That’s probably the better proxy, come to think of it.
All right, here’s my crack at steelmanning the Sin of Gluttony theory of the obesity epidemic. Epistemic status: armchair speculation.
We want to explain how it could be that in the present, abundant hyperpalatable food is making us obese, but in the past that was not so to nearly the same extent, even though conditions of abundant hyperpalatable food were not unheard of, especially among the upper classes. Perhaps the difference is that, today, abundant hyperpalatable food is available to a greater extent than ever before to people in poor health.
In the past, food cultivation and preparation were much more labor intensive than in the present, so you either had to pay a much higher price for your hyperpalatable food, or put in the labor yourself. Furthermore, there were fewer opportunities to make the necessary income from sedentary work, and there wasn’t much of a welfare state. Thus, if you were in poor health, you were much more likely in the past than today to be selected out of the class of people who had access to abundant hyperpalatable food. Obesity is known to be a downstream effect of various other health problems, but only if you are capable of consuming enough calories, and have access to food that you want to overeat.
Furthermore, it is plausible that some people, due to genetics or whatever, have a tendency to be in good health when they lack access to abundant hyperpalatable food, and to become obese and thus unhealthy when they have access to abundant hyperpalatable food. Thus there is a feedback loop where being healthier makes you more productive, which makes hyperpalatable food more available to you, which makes you less healthy, which makes you less productive, which makes hyperpalatable food less available to you. Plausibly, in the past, this process tended towards an equilibrium at a much lower level of obesity than it does today, because of today’s greater availability of hyperpalatable food to people in poor health.
It is also plausible that our technological civilization has simply made considerable progress in the development of ever more potent gustatory superstimuli over the past century. This is a complex optimization problem, and it’s not clear why we should have come close to a ceiling on it long before the present, or why just contemplating the subjective palatability of past versus present-day food would give us conscious awareness of why we are more prone to overeating the latter.
Both of these proposed causes are consistent with pre-obesity-epidemic overfeeding studies of metabolically healthy individuals failing to cause large, long-term weight gain: They suggest that the obesity epidemic is concentrated among metabolically unhealthy people who in the past simply couldn’t afford to get fat, and that present-day food is importantly different.
I’ll try rephrasing, somewhat overstating the strength of the reasoning (taking it from probabilistic to logical) in case that causes a basic idea to be clearly communicated that was obscured by probabilism.
If an increase in calorie intake was itself sufficient to produce an increase in fat mass in otherwise metabolically high-functioning adults, we’d have seen a different result from pre-obesity-epidemic experiments in overfeeding. This rules out the direction of causality “mere overeating” → “obesity”.
Any hypertrophy of fat cells, in turn, will causally require more nutritional intake to feed the hypertrophy, just like a cancer growing, or any other body part growing, will require more nutritional intake. So once you observe a cancer or a huge fat cell mass or any other diseased body part growing, you already know the person already took in that much food, both to grow the cancerous body part and sustain it; you shouldn’t be surprised to look back at the cancer patient’s caloric consumption record and find an excess; so finding that excess consumption shouldn’t update you at all about the cause of the malevolently growing body part.
You’re taking causality that must at least run from “fat cell hypertrophy” → “excess consumption” and already fully explains away the presence of an observed correlation, and then adding on a causal postulate that runs the other way—a direction of causality that would be theoretically possible in a world with no overfeeding experiments one way or the other, though not supported even there, since there is no otherwise unexpected observation which it explains; but which in our world is ruled out by the results of overfeeding experiments, which tested the results of experimental-intervention-produced excess calorie consumptions in metabolically healthy individuals before the obesity epidemic.
To further oversimplify the oversimplification: the logic you’re deploying for obesity would also work to conclude that overeating causes cancer, and therefore Proves Too Much.
The only reason why “overeating caused this huge fat mass to grow inside my body” sounds more plausible than “overeating caused this huge tumor to grow inside my body” is that the former theory follows the Sin Theory of Obesity in which obesity is a punishment for the sin of gluttony, while the latter theory is incongruent with simple just-world hypotheses as of the 21st century in Western societies. Both are ruled out by experiments showing that (in metabolically healthy individuals before the obesity epidemic) a randomized experimental intervention to add overeating does not produce obesity any more than it produces tumors.
I think the first sounds more plausible because the story “humans store caloric excess as fat in times of plenty and burn it off in times of scarcity” is the kind of thing that we should have as a hypothesis-under-consideration before we look at the link between calorie intake and body mass. Whereas “humans store caloric excess as cancer” (or as fetuses) isn’t. And if that story is true, then “eating lots of caloric excess causes lots of fat to be stored” isn’t automatically true, but again it’s definitely something we should have under consideration.
So if your line here is meant to be taken a priori—that is, if you’re saying “even without actually looking at the link between caloric intake and body mass, there’s no reason to believe overeating-causes-fat any more than you’d believe overeating-causes-cancer”, then it seems just wrong.
Maybe you meant it a posteriori? Something like “okay but overeating studies show that eating lots of caloric excess doesn’t by default cause lots of fat to be stored, so you no longer have a plausible explanation”?
But then at least two other reasons come to mind for why overeating-causes-fat might still seem more plausible than overeating-causes-cancer. One is that someone might not believe that studies show what you think they show. Another is that someone might just be bad at propagating updates. Currently, these both seem more likely to me than your “sin theory” theory.
I strongly disagree with this interpretation of those overfeeding studies. From what I can tell (though I couldn’t access every study SMTM cites), “overfeeding” is usually defined relative to the output of one of the typical BMR/TDEE estimation formulas given a person’s parameters, not based on actual measurement of a subject’s TDEE. Those formulas are fine for a baseline guess, but even the most accurate ones are going to be substantially off in either direction for a fair number of people! Some of the difference is unaccounted-for NEAT, some of it is differences in absorption efficiency, some of it is probably other factors we don’t understand yet. Given the known reality of interpersonal variation in what your actual calories in and out are relative to their naive estimates, some subjects not gaining weight while “overfeeding” is exactly what you’d expect to see.
A fun fact: my estimated “effective TDEE” is (averaged over months) pretty consistently around 3300 cal/day for the past 18 months—rarely more than +/- 100 cal/day off in either direction—whereas the best formula I could find (using my body fat %, as actually-measured by a DEXA scan) says it should be something more like 2600-2800 cal/day. This is based on weighing my body daily and recording the caloric intake from actually-everything I eat, almost always weighing food when necessary rather than coming up with estimates.
I think I understood what you’re saying the first time around and again I agree that your account of things is certainly possible, but even in your case the tumor or fat mass has to be sustained by calorie consumption from the outside. The increase in calorie intake we’ve seen is about the amount we would have expected if someone had just told us that people are 15% fatter on average without any increase in exertion or heat dissipation to compensate for that.
Another way to say this is that I’m just making a claim about the conditional expectation E[average body mass increase | average calorie consumption increase = 20%] and pointing out this expectation is not far off from the actual observed body mass increase we see. In that sense the increase in calorie intake can account for the increase in body mass in correlational terms. The question of why both of these variables went up, though, is difficult and their level is obviously not determined by this argument.
Externally, why people feel the need to keep eating until they become obese is not a question with a clear (to me) answer. It could be because there is some process that’s operating in the body that’s taking priority over other activities and hoarding a lot of the energy intake to produce fat cells, which I think is your story. However, it could also be that some part of the brain is malfunctioning and leading the lipostat to be poorly calibrated. It could also be that the food you’re eating messes with the natural feedback loops in your body that are supposed to make you feel full when you’ve eaten enough.
I think this question is interesting and your account is logically possible. I just think that
I don’t have any special insight into which account is right, and
I don’t think your particular explanation is favored that much over other competing explanations.
I don’t think the overfeeding experiments provide strong evidence for your scenario, though I agree that they should be a Bayesian update in favor of accounts in that broad neighborhood. What would convince me is experiments which involve smaller increases in calorie intake but sustained over much longer periods of time, on the order of a year or so. If such experiments failed to find an effect that would be a strong update for me towards your view. Right now I buy the cancer analogy on conceptual grounds but I don’t think we have enough evidence to conclude obesity is like cancer in this regard, though it very well could be the case.
To give an analogy of my own, the overfeeding studies look similar to attempts to settle disputes about which programming languages are best for productivity by asking undergraduates to complete some simple tasks in them over the course of a few weeks. What really matters is how you do when you’re working with big and complex software in the real world that has to be developed and maintained by large teams with turnover for years, sometimes decades; but that obviously doesn’t lend itself to a simple experimental design so people still keep arguing about it.
Retrying again:
By the same reasoning:
“Pregnancy” probably isn’t a thing. “Pregnant” people eat around 500 more calories per day. This is sufficient to explain all the weight gain from “pregnancy” without supposing anything other than thermodynamics at work—anyone who eats an extra 500 calories per day will probably gain that much weight over the course of 40 weeks.
I think Ege’s alleging that SMTM presented two causal graphs:
calories → ? → weight gain
calories → weight gain
Ege’s saying that 2 is simpler and sufficient, so we don’t need to posit a ? in the middle.
You’re pointing out that we still need to address a third causal graph:
? → calories → weight gain
Edit: And maybe that there’s also a scenario where ?, calorie intake, and weight gain are all in some complex interrelationship. Maybe contaminants cause more fat deposition and less energy and more hunger, thereby increasing weight gain per calorie, increased calorie intake, and increased contaminant intake via food. Or something.
Ege’s agreeing with you, but wants to emphasize that this is compatible with criticism of SMTM’s alleged emphasis on graph 1.
Note: I say “alleged” only because I’m sidestepping evaluating the truth of Ege’s claim. Just trying to clarify what it is (AFAICT).
I don’t agree with this presentation of what I’m saying.
I’m not terribly sure what SMTM means when they say “the increase in calorie intake is small”, but all possible interpretations of their claim seem wrong. For instance, one plausible interpretation in causal graph lingo is “if you applied the do operator on calorie intake and raised it by 20%, we would have seen an increase in body mass that’s significantly smaller than what we’ve actually seen”. I think this claim is wrong, basically for long-run energy balance reasons.
I’m not saying anything else about the structure of the causal graphs, which could be arbitrarily complicated and involve arbitrarily many nodes and dependencies. I’m just saying that if you apply the do operator on calorie intake and raise it by 20% then you’d get an increase in mean body mass that’s about as big as what we’ve seen.
Thanks for clarifying that I misrepresented your view. Based on your response here, you’re pointing out that there’s a strong correlation between increased caloric intake at the population level, and increased obesity. You are also saying that the explanations you’ve read from SMTM for why this correlation exists seem wrong, and also that they underestimate the magnitude or importance of the caloric intake.
WRT Eliezer’s arguments, you seem to be agreeing that there may be some underlying force(s) causing that increased caloric intake. However, you are very uncertain about which, if any, of the hypothesized forces(s) are the true causes of increased caloric intake.
Eliezer and others seem to be perhaps mistakenly interpreting you as denying the existence of, or “need for,” a deeper explanation for increased caloric intake and consequent weight gain. You are confused about why they are making this mistake.
Is that a more accurate account of your position?
Yes, this summary is accurate.
I’m not sure who is “to blame” for the miscommunication but I suspect I simply was not clear enough in my top comment. Now it’s likely too late to clear up the issue for most readers as they won’t be following the developments in this thread.
Feel free to adapt, or copy/paste, the summary into your parent comment if you like.
This is “assuming there’s no link “increased calorie intake → increased energy expenditure”″, right? I think one of the things Eliezer is saying is that there seems to have been such a link in the past and now there isn’t / it’s much weaker.
That’s not quite true—there is at least the naive link that a higher equilibrium body mass leads you to expend more energy in daily activities even if you exercise the same amount as before. In my very naive model I assume these are directly proportional, but Natalia cites some better research that does a log-linear regression of calorie expenditure on equilibrium (I think? I didn’t check this part) body mass which seems to be more accurate empirically.
I think it’s unclear whether we had the link you mention in the past, too. We definitely had a correlational link: people who did hard labor and ended up exercising a lot every day took in much more calories, as we would expect, and they were generally not obese. However, I think my argument would work just as well in the past if you just applied the do operator on calorie intake per day and looked at the causal impact on equilibrium body mass, as I don’t think there’s evidence that there’s a big downstream link from calorie intake per day to exercise.
You left out weight gain->calories, as in the pregnancy example, and calories ← X → weight gain.
I don’t understand why you’re “retrying”. I already agree with your point and you not saying “yes, you already agree with me” is quite confusing to me. As I say in my comment:
Do you think this characterization of your position is unfair or wrong? If so, why?
As far as I can see the only object-level point I disagree with you about is that I don’t think the evidence for obesity being like cancer or pregnancy is as strong as you seem to think it is. It’s definitely possible for it to be like that but I would bet against it at even odds. I explain this here:
On top of that I also have a separate disagreement with you about emphasis in the context of my comment, since the point of my top comment is to draw attention to 400 kcal/day not being a small increase in calorie intake. You agree with me about this but you just don’t think it’s worth focusing on, probably because you think it’s a trivial observation. I still think it’s something that should be corrected given that SMTM explicitly said that it’s a small increase.
Some people certainly are obese because of literal cancer and literal pregnancy. We seem to have strong evidence for that.
The interesting question is about how much of the obesity pandemic is explainable by such factors and not whether evidence for such factors exists.
We certainly don’t see enough pregnancy and cancer to explain the obesity epidemic but there might be other factors that are similar but harder to see. Thermodynamic arguments don’t help us rule out other effects that are similar to pregnancy/cancer.
I agree with everything you said, so again I’m confused why you thought you should make this comment.
I feel like I don’t really disagree with most of the commenters but they either think I do disagree with them or that I did a very bad job of communicating exactly what my point was. It’s hard for me to understand.
(The thread continues to look to me like what I described here https://www.lesswrong.com/posts/7iAABhWpcGeP5e6SB/it-s-probably-not-lithium?commentId=NxzEfuyGfuao25mrx
i.e. Yudkowsky is responding to the part of your original comment where you said
)
I still stand by this claim, again with the caveat that you take it as a correlational use of the word “explain” (which is not at all uncommon e.g. when talking about “fraction of explained variance” and so forth) and not one that suggests a causal explanation of the form “people wanted to eat more food, so they ate more food, so they got fatter as a result”.
Ok. My main point is just to clarify that other people are reading you as talking about explanation in general, not just strictly correlational explanation (if that’s what’s happening).
I do also think that’s not a great use of the word “explain” and “mystery”, because it’s not why the colloquial word is useful. The colloquial words “explain”/”mystery” are useful because they index “more information and ideas given/needed about this”. So just because X correlationally explains Y, and X is true, doesn’t mean there’s no mystery about Y.
I never said there’s no mystery about Y, just that there’s no mystery about Y being true conditional on X being true.
It’s a fair point that my usage of “explain” and “mystery” confused some people but I’m not too sure how else I would have made my point. Should I have said “people today are eating about as much more compared to the past as we would expect given how much fatter they’ve gotten”?
That’s clearer to me, yeah. It’s unambiguous that it’s about conditional prediction (“we would expect given”) rather than explanation-in-general.
In your original comment, you wrote:
Read literally, this says: There’s a mystery of why intake went up. Conditioned on intake up, there’s no mystery of why fat went up. I think this isn’t right. If we agreed that sustained high intake implies weight increase, it’s still not right. That’s because conditional probability isn’t the same as explanation, and if there’s a mystery, what we’re after is explanation. That’s one of the points of the tumor example: If fat causes intake, then saying “there’s no mystery about fat” is pointing away from the explanation of intake, which is that fat causes intake and something causes fat.
Taken literally, this seems to be consistent with beliefs of people who disagree with you? It’s just that they have different conclusions about the causality going through calorie intake. Interpreted that way, I don’t see how this statement is consistent with saying “there’s really no mystery in Americans getting fatter”.
I don’t understand your objection. I never made any claims about causality. My whole argument is about energy balance, which says nothing about causality.
On the other hand, I think it’s just true that conditioned on the increase in calorie intake there’s no mystery in the increase in body mass. I don’t understand why you’re disputing this point. You can say this is not an interesting observation (which I agree with, though as far as I can tell SMTM did not, which is why I wrote my comment) but I don’t see how you can say it’s not right.
My impression is that some people are engaging in a bizarre combination of steelmanning SMTM’s point while strawmanning my own. SMTM didn’t make the best version of the claim they could have made, they made the actual claim that I quote in my post. I think their claim is wrong. Do you disagree with this or not?
Meta: my interest here is to see if there are miscommunications here that I can clear up. I’m not carefully following the object-level debate. (In particular, I think that you Ege should feel extremely free to ignore what I’m saying as unhelpful to you; if I’m not helping you understand what’s happening in the thread then I’m not doing what I’m trying to do.)
(Note: you did mention causality in the passage I quoted: “They should have been focusing on the causal channel going through calorie intake from the start.” That’s not a claim about what causes what, but it is a claim about what questions are the right questions to ask.)
I’m pointing at the word “mystery”. I’m saying that to me, “mystery” means “explanation wanted”. I’m saying that just because P(X|Y) is high, doesn’t mean Y is a good explanation of X. (For a silly example, setting Y=”X and 2+1=3″ makes P(X|Y) = 1 and is obviously doesn’t explain anything.) I agree (based on my preconceptions, ~0 independent data) that P(body mass high | high sustained intake in the wild) is high. My read of some of the comments on your comment, e.g. Yudkowsky’s, is that they are taking you to be saying “high intake explains fat, such that there is no further interesting question about fat, though there may be further questions about why high intake”, based on the passages from your comment I quoted. Reading your comment closely, you didn’t actually say that, if by “conditional on Y, there’s no mystery about X” you mean “P(X|Y) is high”. In fact, what you said is consistent with believing that “Alice is fat” explains (in the contextually relevant sense) that “Alice has high intake”, and you recommend that if you believe this then you should “focus[] on the causal channel going through calorie intake”, i.e. investigate why Alice is fat in order to explain her high intake.
I don’t know. I think your argument makes sense, but the actual situation is going to be more complicated.
Do you know, if we also observe an obesity-epidemic in the subgroup of people who average 25k+ in daily steps? That step-requirement is a good, high standard of “metabolically healthy” to isolate.
I belong in that group these days and it feels natural, relaxed and I feel far more energetic than when I was averaging 7k daily steps and was the sedentary nerd cliché, about a year ago. Now I am a nerd, who takes two walks per day, almost never sits and either stands or uses his office treadmill when on the computer.
Even before, I never really got fat. But I feel, that I might not have been “metabolically healthy”, because now I feel better. So I strongly suspect that a far higher than average step-count is a hard requirement for being “metabolically healthy”.
I hear that “pregnant” people also do less mountain-climbing, even if they were exercising healthily before. No wonder they gain weight! Do we even need to postulate “pregnancy” as a condition, when their caloric intake and reduced exercise seems adequate to explain all of the observed weight gain?
I was not responding to your pregnancy-argument, but to your post higher up in this subthread from 3 days ago. The threading makes this a bit confusing.
Also should have specified what I was responding to the last paragraph:
”Both are ruled out by experiments showing that (in metabolically healthy individuals before the obesity epidemic) a randomized experimental intervention to add overeating does not produce obesity any more than it produces tumors.”
Is there actually an obesity epidemic among people who walk more than 25k steps per day? (or is something like that currently known).
EDIT:
I suppose my hypothesis is:
Living a non-sedentary lifestyle meaning less than 20 minutes of sitting per day, 25k-ish steps per day somewhat equally spread out over all waking hours makes the “weight-gain -=> obesity”-phenomenon impossible, because it’s a sufficient requirement for robust metabological health.
If that was true, it might not answer what is behind the obesity epidemic.
But that’s what I would study, to check if it’s a cure or reliable prevention.
I’d say 90% chance of this being true, but mostly on intuition and with high model uncertainty.
And I don’t know, if we know enough to answer this question, because non-sedentary lifestyles like that are fairly niche in all Western societies. But I recently figured out, that they’re not all that hard to adopt.
EDID2: Actually, I’d say the 90% applies to it being “reliable prevention”. No clue, how curative that would be.
I never had to really lose more than a couple kg of fat. [and “had to” is really exaggerating a lot]
From what I observe, it seems somehow impossible for really fat people to become not fat, despite heroic struggles which have always been strange to observe from the outside.
Is there any solid evidence that walking 25k steps per day will solve the obesity epidemic? I ask this because it’s genuinely a remarkable claim, one that if verified and implemented would save huge numbers of lives and hundreds of billions in medical expenses. The literature mostly seems to indicate that increased exercise doesn’t have dramatic effects on obesity.
There is not. That’s why I was asking him if he knows. I was not interested in the effect of exercise. Exercise means, you do some activity a couple times per week.
I’m interested whether the obesety epidemic only affects the sedentary populatrion.
And if being or becoming non-sedentary is protective or curative.
25k steps for me means, that my treadmill is running constantly when I’m on my computer.
This is not really exercise. Movement is just my default state.
In that way, I have become closer to what an EAA-hunter-gatherer, than to a sedentary office worker does with his body.
[or I would, if this had been my lifetime norm instead of something I still get used to]
If the human body was sold as a machine, the sedentary lifestyle probably would void your warranty, because it’s rather extreme (dis)usage. Sedentary people being unhealthy is not surprising.
It’s surprising that some sedentary people aren’t.
Anyway, “being in near-constant motion” is too specific/complicated a metric.
So I’d just look for a step count high enough, that’s only feasibly doable by a non-sedentary person like me. Though, I guess any daily jogger can probably match or exceed 25k steps per day.
The group of people whose 80th quantile waking hour still has >1k steps.
That’s probably the better proxy, come to think of it.
All right, here’s my crack at steelmanning the Sin of Gluttony theory of the obesity epidemic. Epistemic status: armchair speculation.
We want to explain how it could be that in the present, abundant hyperpalatable food is making us obese, but in the past that was not so to nearly the same extent, even though conditions of abundant hyperpalatable food were not unheard of, especially among the upper classes. Perhaps the difference is that, today, abundant hyperpalatable food is available to a greater extent than ever before to people in poor health.
In the past, food cultivation and preparation were much more labor intensive than in the present, so you either had to pay a much higher price for your hyperpalatable food, or put in the labor yourself. Furthermore, there were fewer opportunities to make the necessary income from sedentary work, and there wasn’t much of a welfare state. Thus, if you were in poor health, you were much more likely in the past than today to be selected out of the class of people who had access to abundant hyperpalatable food. Obesity is known to be a downstream effect of various other health problems, but only if you are capable of consuming enough calories, and have access to food that you want to overeat.
Furthermore, it is plausible that some people, due to genetics or whatever, have a tendency to be in good health when they lack access to abundant hyperpalatable food, and to become obese and thus unhealthy when they have access to abundant hyperpalatable food. Thus there is a feedback loop where being healthier makes you more productive, which makes hyperpalatable food more available to you, which makes you less healthy, which makes you less productive, which makes hyperpalatable food less available to you. Plausibly, in the past, this process tended towards an equilibrium at a much lower level of obesity than it does today, because of today’s greater availability of hyperpalatable food to people in poor health.
It is also plausible that our technological civilization has simply made considerable progress in the development of ever more potent gustatory superstimuli over the past century. This is a complex optimization problem, and it’s not clear why we should have come close to a ceiling on it long before the present, or why just contemplating the subjective palatability of past versus present-day food would give us conscious awareness of why we are more prone to overeating the latter.
Both of these proposed causes are consistent with pre-obesity-epidemic overfeeding studies of metabolically healthy individuals failing to cause large, long-term weight gain: They suggest that the obesity epidemic is concentrated among metabolically unhealthy people who in the past simply couldn’t afford to get fat, and that present-day food is importantly different.