Counter-theses on Sleep

This is an important point. When discussing sleep we have to both look at sleep as measured by devices (that do notice awake times during the night that aren't remembered) and at time in bed. 

It's plausible that 7 hours of sleep are good for the average person while 8 hours in bed are necessary to achieve that for the average person. 

The range the study gave for time in bed was actually 6.9–8.5 hours (not 8-9). But it's a good point that subjective sleep duration reports significantly overestimate actigraph measurements. 

For what it's worth, in my experience there is a wide delta in accuracy between bad fitbit-style sleep trackerse and good fiftbit-style trackers.  

I do not know if this study used good or bad devices.

One of the distinctions Guzey made that I think was important was the difference between work-related fatigue and sleep deprivation. Many SD studies are on resident doctors at the end of 24-hour shifts. They are experiencing both work-related fatigue from a notoriously taxing job and sleep deprivation. As such, if we care about SD as opposed to fatigue, then such studies are hopelessly confounded as far as relevance for our specific research question.

I do think that that's an important distinction. Note that most of the studies included in the sleep restriction meta-analyses I quoted (all but one, in fact) are not on resident doctors, and, as far as I know, they pretty much exclusively examine the effect of sleep restriction (sleeping fewer than 6 or so hours per night) rather than the effect of staying awake for an abnormally long time.  

I didn't look at the meta-analyses you cite here. The ones I did look at, though (Pilcher and Huffcutt on cognitive impairment, and Irwin, Michael R., Richard Olmstead, and Judith E. Carroll on inflammation), for me surprised me with how unconvincing they were when I looked under the hood.

I did actually cite Irwin, but note that my conclusion from it was that sleep duration does not impact inflammation [LW · GW].  

When Guzey posted his "Theses on Sleep," I spent a lot of time going through meta-analyses and considering whether the underlying studies were sound. I talked about what I found in the comments there, and I wonder if you got a chance to read them?

Are you referring to your reply to my comment on Guzey's post [LW(p) · GW(p)]? If so, I did, and I believe that your concerns do not extend to the meta-analyses I cited here (because, as I said, they focus on the effects of sleep restriction rather than staying awake a very long time, and largely do not include physicians). Note that I did not cite Pilcher and Huffcutt, and did not bring it up as evidence, anywhere in this post.

(however, as I acknowledge in the post, these meta-analyses I did cite can have many possible problems & are not conclusive evidence)

My hope is that those of us in and around the rationality community who care about this question enough to spend more than a few hours investigating it carefully (Guzey, you, me, and certainly others) can, over time, enter into a sustained dialog about what the research tells us and how to frame the research questions we care about. I think it would be interesting to put together some kind of shared doc where we could dig into this a bit. Please let me know if that would be of interest at some point in the future. I'm a busy graduate student in biomedical engineering; what I lack in time I hopefully will make up for in some relevant knowledge (and direct experience with lack of sleep!).

I am interested in this, so feel free to contact me if you want to start this.

[ETA: to be clear, I’m not criticizing the thesis of SMTM’s post here, just pointing out a factual error]

The linked SMTM post is misleading. 

Here is the vitamin C content per 100g of some relevant foods, which I found after a few minutes of searching on Google:

• Lime juice: 30mg ^[1]
• Lemon juice: 38.7mg ^[2]
• Raw lemons: 53mg ^[3]
• Raw limes: 29mg ^[4]
• Key limes in particular, which Wikipedia says are the same thing as West Indian limes: 31.3mg ^[5]
• Raw caribou liver: 23.874.9 mg ^[6]
• Raw ringed seal liver: 23.873.8 mg ^[6]
• Raw cattle liver: 71.2mg ^[7]
• Raw buffalo liver: 72.4mg ^[7]
• Raw sheep liver: 77.6mg ^[7]
• Raw goat liver: 76.7mg ^[7]
• Fresh/raw polar bear meat: 1mg ^[8] [9]

I couldn’t find information on the vitamin C density of polar bear livers in particular, but from these values, it seems far from clear that polar bear livers are more similar to lemons than limes in that respect. The vitamin C contents of limes and lime juice do not stand out in that list. 

Moreover, it seems that it only takes about 10mg of vitamin C per day to prevent scurvy, and the Manual of Nutritional Therapeutics says that the same daily quantity is enough to improve scurvy symptoms, with 60-100mg/day being recommended for full recovery. So it seems that a cup (~240g) of fresh lime juice per day is enough to both prevent and enable recovery from scurvy. 

(Scott and Scurvy says that “[t]ests on animals would later show that fresh lime juice has a quarter of the scurvy-fighting power of fresh lemon juice,” but I couldn’t find a source for that, I could find many contradicting it, and the USDA data suggests that it has ~3/4 of the vitamin C density of fresh lemon juice).

So it seems that the lime juice was just not preventing scurvy because it had spent long periods of time open to the air, and had been pumped through copper tubing. And so this paragraph from the post:

“Different kinds of citrus fruits are more like one another than they are like polar bear meat” sounds very reasonable, but in this case it was wrong. Sicilian lemons really ARE more like polar bear meat than they are like West Indian limes, at least for the purposes of treating scurvy.

seems very misleading (especially but not exclusively if you don't interpret “polar bear meat” as referring to a specific polar bear organ, given that my sources say that fresh polar bear meat has 30x less vitamin C than fresh lime juice).

1. ^{^}

   https://fdc.nal.usda.gov/fdc-app.html#/food-details/168156/nutrients

2. ^{^}

   https://fdc.nal.usda.gov/fdc-app.html#/food-details/167747/nutrients

3. ^{^}

   https://fdc.nal.usda.gov/fdc-app.html#/food-details/1102594/nutrients

4. ^{^}

   https://fdc.nal.usda.gov/fdc-app.html#/food-details/168155/nutrients 

5. ^{^}

   https://fdc.nal.usda.gov/fdc-app.html#/food-details/509702/nutrients 

6. ^{^}

   https://doi.org/10.1006/jfca.2002.1053

7. ^{^}

   https://doi.org/10.1111/j.1365-2621.1965.tb00287.x

8. ^{^}

   https://www.jstor.org/stable/40508955

9. ^{^}

   https://escholarship.mcgill.ca/downloads/t148fj883?locale=en

The version of Alexey’s theses I most broadly support is “we treat sleep like one thing, when it is in fact multiple things with multiple purposes”. Natalia calls this epicycles

That sleep is multiple things is not something I am arguing against. (In fact, I don’t recall that being a point in Guzey’s post). What I uncharitably called “epicycles” was the additional complexity Guzey’s model has to have to explain why so many people feel dumber after sleep restriction, and why experimental studies say that sleep loss causes cognitive impairments, when ““not sleeping ‘enough’ makes you stupid” is a 100% psyop.”

It’s pretty clear to me that sleep has multiple effects, and that it might be the case that there’s something with all of sleep’s good effects and none of the bad ones that just hasn’t been discovered yet. Maybe digital people would only have to spend the subjective equivalent of a few seconds per day shut down in order to renormalize their weights or whatever, or might not need to be shut down ever at all to maintain their performance. 

But I don't think that is incompatible with the object-level claims in my post, any more than saying “humans don't live to be 200 years old” is incompatible with knowing that the passage of time has multiple effects or with admitting the possibility of revolutionary life-extension methods being discovered that do allow humans to be 200 years old. 
 

In general I think distinguishing ideas analogous to pre-vitamin-C scurvy from ideas like epicycles is one of the Hamming problems of science, and would cheer development in the area.

I'll take a stab at this.

It seems like the key distinction is separating ideas that are heavily but still inadequately tested (epicycles) from those that are underexplored (pre-vitamin-C scurvy) and those that are thoroughly tested (the pathogen theory of disease).

Researchers are bound by convention, resources, and the limits of their own imagination and enthusiasm. As such, they often wind up using experimental methods that both fail to distinguish empirical confounders and can never yield a better underlying mechanistic account of the phenomena at hand. Instead, they just put out another study as meta-analysis fodder.

Take this sleep research. We can find dozens of studies showing that X hours of sleep deprivation results in Y amount of cognitive deficit. But have the scientists designed studies to test for weird confounds?

Maybe being sleepy doesn't make you cognitively slow, but instead makes you socially anxious. Being around a bunch of strange scientists subjecting you to unusual tests in an unfamiliar environment could trigger anxiety. This in turn could explain some of the cognitive deficits in the sleep research. Sleepiness -> social anxiety -> cognitive deficits around strangers. That hypothesis took me all of 1 minute to come up with, and it might be true, who knows? If resources were unlimited for testing it, we could just go ahead and do it.

If it takes me 1 minute to come up with a probably-untested plausible alternative hypothesis to a field that has produced dozens and dozens of studies, it's a sign that the field is designing its experiments inefficiently, and we should discount the apparent strength of its findings. This doesn't mean that its current hypothesis is wrong, but that it has disguished alternative hypotheses by neglecting to test them and thus created a false impression of consensus.

If it's not possible to test all the hypotheses we'd ideally like to explore, then too bad. Scientists don't get to say they've discovered "the truth" just because they've hit the current limit of their experimental capacities. They just have to admit that they're not sure. In this case, we would start by pointing out that we have extremely limited mechanistic information on exactly how sleep and extended wakefulness physically alter the brain, and how any such alterations turn into cognitive impacts. By contrast, we have abundant (if still far from completely sufficient) physical information about how other complex physiological systems work, such as the immune system.

So in general, we ought to rank our certainty not by how much evidence we've accumulated, but by how many alternative hypotheses we've ruled out (this idea is certainly not original to me). Unfortunately, either there's no good way to quantify this, or there is, and it's just not conventional for scientists to do so when designing their experiments and writing their literature reviews.

Based on my limited experience in the lab environment, I can already see firsthand the degree to which resource constraints, convention, careerism, and an honest assessment of one's own strengths and limitations as a scientist dominate decisions about what to study and how to study it. "Important if true" gives way to other concerns, like "who will pay to find out?."

I think science tends to get the biggest big things right, and that's a profound accomplishment. But if it's a question with significant nuance, in a niche subfield, and doesn't have any really crisp methods and unequivocal metrics, then you're at the frontier, and should retain durable skepticism about the field.

Some evidence I think Alexey’s model fails to explain:

• “do all my friends hate me or do I just need a nap”

I don't think that's much of a problem. People get "hangry" too and that doesn't invalidate the usefulness of fasting nor does it imply that fasting has to be miserable like that.

I think any prolonged discomfort that is unaddressed is going to make people cranky and bias them towards negative explanations of things. Address the discomfort, and the experience can change dramatically. 

Perhaps the most useful thing I got out of experimenting with polyphasic sleep was a recognition of how well I could function when sleep deprived so long as I wasn't constantly battling an unaddressed urge to sleep. Sleep deprivation still made me dumber, but the crankiness and most of the dysfunction was actually a result of trying to ignore (and yet not completely tuning out)  my body screaming at me to sleep. Having a reference experience for being sleep deprived without craving sleep made it a lot easier to function when an hour or two short, and also more willing to go take a nap when I need one.

Some evidence I think is not explained by current mainstream sleep models:

• Naps I have induced in myself via emotional or sensory overload, which have no relationship to how much I slept the night before or will sleep that night. I haven’t looked for studies on this but enough friends report similar things that I’m comfortable claiming the phenomenon definition exists. 
• Depression is sometimes cured through sleep deprivation. 
• Some people remain astonishingly productive for years on very little sleep.

I don't think the last point is not explained by mainstream sleep models.  Around 440,000 people in the United States are 3 standard deviations smarter than the US average.  That, together with the fact that some jobs (even some that are common among those 440,000 people) might have higher marginal returns to hours worked & past experience than to cognitive performance, makes me unsurprised that some people remain astonishingly productive for years on very little sleep.

I'm not sure what would count as "mainstream sleep models" w.r.t sleep deprivation's antidepressive effects, but a lot of studies seem to confirm that acute SD increases BDNF, as Guzey pointed out.

Natália doesn't set out to disprove all of your theses, but rather to put forth some counter-theses. She says:

I decided to write a post pointing out several of the mistakes I think he’s made, and reporting some of what the academic literature on sleep seems to show.

Read carefully, she neither claims that every point you've made is mistaken, nor to give a comprehensive review of the academic literature. So I don't think you can fault her for not addressing the point about the use of sleep deprivation as a depression cure. She's critiquing those theses of yours which she found weak, not issuing a comprehensive point-by-point criticism of your entire original post.

I think that you owe this level of care in interpreting her language, because you're insisting that she offer you that same level of care. You said:

people who sleep just 6 hours a night might have the lowest mortality

And then you complain when she rephrases this as:

six hours of sleep being optimal for mortality, as Guzey has hypothesized before (as well as evidence against eight hours being optimal for mortality, of course).

To my eye, these reflect approximately equal levels of imprecision, thought that's a purely subjective claim. I think you would both be in the right to object to each others' misreporting of your exact claims. To put it in more collegial terms, I think this discussion can and will benefit from precise reading and deep consideration.

The obvious problem with that argument is that the set of things that cause acute bodily stress is much larger than the set of things that cause long-term benefits. Stubbing your toe, for example, causes acute bodily stress. Guzey’s argument works equally well for showing that occasional toe-stubbing is good for health as for showing that occasional acute sleep deprivation is. - Natália

As far as I know, there's no evidence that stubbing depressed people's toes relieves their depression in 50% of the cases, which combined with the relationship with mania in bipolar people, and the analogical reasoning to exercise and fasting leads me to believe that acute sleep deprivation is good. - Guzey

Here, I think that while it's reasonable to desire Natália to have inferred that you think the utility of SD as a depression treatment is supporting evidence for it being a "good stressor," you also did not specifically tie this in as a piece of evidence in the relevant section here. So I think Natália is more or less literally correct when she points out that this is "the entirety of [your] argument in that section" (emphasis mine), even if it's not a maximally charitable synthesis of your post as a whole.

That aside, I think it's clear that this is a crux, as others have brought up the question of why we intuit that some forms of acute stress (i.e. stubbing a toe) are just bad, while others (i.e. exercise and maybe sleep deprivation) can be good. I think it's an interesting question, and worth carrying on the argument, as you're doing here.

I'm looking forward to reading a more extensive response to Natália's post!

1.

Natália's section about bipolar people seems to imply that [sleep deprivation's short-term antidepressant effects] would not be happening.

I disagree. I said,

A night of total sleep deprivation seems to be able to trigger full-blown mania in a substantial percentage of people with bipolar disorder (even those currently depressed) and even cause mania-like behavior in healthy subjects. Moreover, a shift towards mania or hypomania after a short night of sleep seems common in bipolar patients. 

Here, I think it was clear that what I said is consistent with sleep deprivation having antidepressant effects, and it could even be interpreted as implying that it does. So I think it's misleading to suggest that this section implied that the antidepressant effect does not exist.

2. Your section arguing that occasional sleep deprivation is good for health makes no mention of its antidepressant effects, which were addressed separately earlier on in your post. I thought you were making a separate argument in that section, which is why I countered with an appropriate analogy. I merely think that the argument "sleep deprivation causes acute stress, therefore it's good" is weak, and that was my point in that section. My particular analogy might not have been great, however, I agree.

Separately, I don't think that association between sleep deprivation and mania is evidence that sleep deprivation is good rather than bad; as my section in this matter showed, manic episodes very often have severe long-term consequences. 

3. I apologize, I used poor phrasing here that made it seem like I was claiming something I wasn't. I didn't mean to say that you were hypothesizing that 6 hours was causally optimal, in the sense that people should sleep for 6 hours if they want to have the lowest mortality, in that paragraph. I was using the word "optimal" to mean "associated with the lowest mortality." I'll rephrase the paragraph to make it clearer that I was not interpreting you as making a causal claim.

Overall, I don't think the errors you pointed out so far were particularly glaring. The last part of your point (1) seems to be based on a misunderstanding of what I wrote, though perhaps upon further elaboration we'll find that we do actually disagree on something specific here. Point (2) reflects more of a clash of intuitions between us, rather than a mistake on my part; it's reasonable to disagree about the strength of my analogy, but it really wasn't a large part of my argument. Point (3) was merely an error in the sense that I used poor phrasing when describing your position. 

I think it's a little unfair to say "The fact that I spotted these three points after spending ~3 minutes skimming the post do not make me optimistic about the rest of the critique" when your points were individually and together, quite weak. However, I am hopeful that we can have a productive dialogue about this subject soon, and get closer to our cruxes on these issues.

I found this reply unpersuasive.

By numerical point:

1. Speculation on OP's education is irrelevant. You reject lots of studies by PhDs that did study the field. If she misunderstood something, address the specific error.
2. Deep skepticism of the sleep literature is fine, even if you rely on some sleep research yourself, but it's insufficient to respond to the objection of hypocrisy of relying on the sleep literature with "well, I'm really careful about which studies I use". You need to explain why the studies you use somehow avoid the methodological problems that cause you to reject other studies. If you don't, it seems like you are just cherry-picking supporting studies because they support you.
3. It is SO strange to me that you rely so heavily on your personal experience, which is almost the least reliable scientific method available. Who's to say that your experience generalizes? You're a very unusual person. I'm always incredibly skeptical of people who have the position "everyone else's introspection is unreliable, but somehow I'm above all of that" or "you are all brainwashed by consensus, but I can figure out what's true and what's BS because I'm smart, educated, and careful".
4. Your claim here relies on an apparent failure to seriously consider the gap between ordinary language and scientific claims, which is a gap I'm confident that you are aware of in other contexts: "I think that the very fact that acute sleep deprivation sometimes increases energy and mood should make almost everyone almost completely re-evaluate everything they know or think about sleep because this should just not happen under the "sleep is restorative and is necessary for good functioning" paradigm."
   Here's the thing. A common error in science articles is using a non-standard, specific, operationalized definition for a concept in the actual study and then using an ordinary language meaning for the concept in the conclusions, leading to overgeneralization. IF science were formal logic, then yes, one counter-example should cause us to reject a general proposition. BUT, science articles that say "sleep is restorative" aren't claiming "sleep is restorative in every case for every person on every night", they are making a claim about average population effects. THUS, the fact that acute sleep deprivation sometimes increases energy and mood should not make us think that we must reject everything we know about sleep. This also responds to your no-of-1 proof by contradiction point.
   An analogy: cold weather makes us feel cold. The fact that people suffering from hypothermia will, just before death, suddenly feel super-hot and take off their clothes doesn't mean that we should reject everything we know about weather and subjective temperature. It means that a general probabilistic claim doesn't always apply. That's why I'm not persuaded by your personal experience. You live a super atypical lifestyle. Your experience makes me think that reduced sleep times is something worth studying further, but doesn't make me reject existing findings.
5. Some is addressed above, but I am just floored that someone who is skeptical of much of published science due to methodological problems is so willing to be persuaded by "trusted personal experience" and "trusted anecdote". I agree that we should be much more skeptical of popularized scientific findings due to valid methodological criticisms, but the solution is not to embrace lousy methodology. If we embraced trusted personal experience and anecdotes as reliable methods for truth findings, we lose the ability to reject massively harmful alternative medicine and new age movements that are propped up by them. The whole reason we set up scientific methods such as systematic data-gathering and double-blind trials is to prevent self-deception.
6. Again, re: the default claim "sufficient sleep is good and necessary for proper functioning for normal people on the scale of a few days to a week", this is not a formal logic claim about all cases, it is a claim about trends and norms. And I am not convinced that the default claim is limited to the scale of a few days to a week, but is instead about sleep in general.
7. I have no comment on this!

Thanks for engaging. I hope we can figure out what our cruxes are. 

On points 1 and 2: I still think you haven't addressed my counter-argument to points of that nature, which I've raised (1) in the post itself, (2) in my previous reply to you [LW(p) · GW(p)], and (3) in this comment [LW(p) · GW(p)]. To reiterate some of it: you use sleep research to support some of your points, mostly in your review of Walker's book but also in Theses on Sleep, and it's not clear to me why research that shows that sleep deprivation is not as bad as people think is admissible evidence to you but research that shows that sleep deprivation is not harmless is not. I was, and remain, skeptical that you have a consistent and rigorous standard for what research you think is admissible and what research you think is not.

...

Just to reiterate: I believe that the points 4, 5.4.1, and 5.4.2 invalidate large chunks of sleep literature and are simply not possible under the default "sufficient sleep is good and necessary for proper functioning for normal people on the scale of a few days to a week".

Notice that my post does not argue against anything that is invalidated by 4, 5.4.1 or 5.4.2. 

As I elaborated before in my post, 5.4.1 pretty much just shows that sleep deprivation doesn't make you very acutely sick or something, which is (1) not something I'm arguing against, (2) not something the sleep literature is arguing against, (3) not a surprising claim, and (4) not a novel claim. 

Concerning 5.4.2, we don't know how well people in the show would be doing in a rigorous assessment of cognition not subject to learning effects, such as the psychomotor vigilance task or other similar tests. I appreciate that the show is evidence that people are able to perform some tasks even while very sleep-deprived, but again, that's not something I or the sleep literature are arguing against, and it isn't novel or surprising. 

...

even if we only take people with bipolar disorder: how the hell can they go on so few number of hours a night with their brain being manic but not simply breaking down?

Uh, whatever manic people are doing, it's putting them at hospitals and making them unable to functionally recover even 2 years later at incredibly high rates, so they really aren't a good example of a group that sleeps very little consistently without breaking down.

...

Also, notice that I could have written a post just like yours, with the same kinds of evidence that you use — not bringing up any meta-analysis at all —  but instead arguing that sleep deprivation impairs cognition and can worsen mood. The kind of evidence that you use does not asymmetrically favor you. You may have a high prior that all anecdotes about sleep deprivation impairing cognition are untrustworthy, and all anecdotes denying that are trustworthy, but that too isn't asymmetric; why can't I claim that it's the other way around because there's a psyop making people wrongly believe that there are no harms to sleep restriction, fueled by bosses that want their reports to spend more time working and less time sleeping? (This is not something I actually believe, but I'm just pointing out that the kind of evidence that is consistent with your points is not asymmetrically so; you don't elaborate on why we should expect people to be massively wrong about their experiences in that specific direction and not the other). 

This isn’t as important as my previous reply [LW(p) · GW(p)] (in which I address your object-level arguments), but I wanted to perhaps note that most of your points 1.1 through 1.4 sound, to me, more like an attempt to generate an emotional reaction in the reader than a good-faith effort at pointing out mistakes you think I’ve made or investigating object-level disagreements (although I could be wrong). I don’t recall criticizing you for not having an MD or something, or publicly speculating that you have never thought about [important meta-level epistemological consideration]. 

I understand that the fact that I did not take biology or neuroscience classes in college is evidence that I would not have a good understanding of sleep research, but I think it is perhaps important to keep in mind that argument screens off authority [LW · GW] here, and it sounds plausible that, a lot of the time, domain experts in the area would acquire knowledge in it the same way I do (by reading meta-analyses and systematic reviews, or textbooks based on those). They don't have some sort of magical essence that makes them more knowledgeable than everybody else could become. They do original research, but not in every sub-area of their field. If I saw you explaining to someone why a massless particle can carry energy and momentum if it travels at the speed of light, and you were using the same arguments that convinced me why that was the case, I would not object simply because that (probably) wasn't part of your formal education, as it was of mine, or because you didn't talk to a physicist about it. 

(I'm also a bit confused about why you are criticizing me for not talking to people in the field if, in your view, those people are mostly untrustworthy and just want to show that sleep deprivation is bad^[1]). 

1. ^{^}

   Which, in my experience, was not the case — I was able to find many systematic reviews and meta-analyses claiming that sleep deprivation is probably not bad for some things. (For example, blood pressure, inflammation, and mortality, as I've pointed out in the post). 

No. (Thanks for pointing out that that’s not clear). My model is that moderate sleep restriction harms cognition the following a day, regardless of how many nights of it you’ve had before; I’m much more uncertain about whether it causes permanent damage to cognition.

Any updates? how did this work out in the long term?

In table 2, Lowe reports that Banks measured 1 day of sleep restriction. But Banks actually did 5 days of 4hr sleep restriction/4hr time in bed, followed by 1 "recovery" day of 0, 2, 4, 6, 8, or 10 hours of time in bed. It's unclear why Lowe coded it as 1 day of cumulative sleep restriction rather than 5-6.

Banks (2010) conducted neurobehavioral assessments on every day of sleep restriction (including the first one). See Figure 2 in their paper. 

[In case you're wondering how Lowe et al extracted data from Figure 2, apparently there's software for that. From their article:

A Plot Digitizer program (Rohatgi, 2017) was used to estimate means and standard deviations (SD) when data was available in chart form only.

]

The paper Mendonça cites looks at long-term long sleep and long-term short sleep, with their association with depression. My claim and my evidence (from bipolar people) are concerned with short-term long sleep and short-term short sleep. 

Your specific claim about depression was “depression triggers/amplifies oversleeping while oversleeping triggers/amplifies depression.” Nowhere in the section did you specify your claim was about short-term long sleep.

Your evidence, too, barely concerns short-term long sleep: depressive episodes last about five or six months on average, which is often not what people have in mind when they think about “short-term” oversleeping, and it's common for them to last a year or more. 

It is further puzzling that in her refutation of my argument she:

1. completely ignores the relationship between sleep and mania (i.e. she ignores one half of my argument and only discusses the part about depression).
2. completely ignores the fact that in ~50% of ALL people with depression (not just bipolar), short-term short sleep relieves depression.

I don't disagree with you on the claim that sleep restriction or deprivation often causes mania, and can adequately treat depression in some cases. I also mentioned the relationship between sleep and mania elsewhere in my post. 

It was not my intention to respond to every single one of your claims, or to mount a comprehensive takedown of every aspect of your post. I'll repeat what AllAmericanBreakfast said [LW(p) · GW(p)] to you after you made a similar argument in your previous comment:

Natália doesn't set out to disprove all of your theses, but rather to put forth some counter-theses. She says:

I decided to write a post pointing out several of the mistakes I think he’s made, and reporting some of what the academic literature on sleep seems to show.

Read carefully, she neither claims that every point you've made is mistaken, nor to give a comprehensive review of the academic literature. [...] She's critiquing those theses of yours which she found weak, not issuing a comprehensive point-by-point criticism of your entire original post.

Guzey:

I wrote that most sleep research is extremely unreliable. And indeed, this is what I believe and this is why I'm so selective with the kind of evidence I use

Yes, I wasn’t claiming that you said that all sleep research was bad, but that the sleep research you’re willing to trust is also, suspiciously, seemingly exclusively research that indicates that sleep is not as important as people think, when there doesn't seem to be a difference in quality between the research you cite as evidence and the research I do. You use evidence from experimental studies to show that acute sleep deprivation often relieves depression, and I use evidence from experimental studies to show that sleep restriction seems to cause cognitive impairment and overeating, and you haven't elaborated on why the research you cite is more trustworthy.

In other words, I understand that you do not think that all sleep research is bad. However, I was, and remain, skeptical that you had a consistent and rigorous standard for what research you thought was admissible and what research you thought was not.

What Mendonça seems to miss more generally is that meta-analyses, which she is relying on heavily, do not reflect reality: they reflect the consensus of an academic field. And if the academic field is confused and the majority of the papers published in it are garbage, then meta-analyses are going to be confused garbage as well.

Why can't I say the same about e.g. the "enormous literature" you use as evidence that sleep deprivation helps depression? ^[1] Why does that reflect reality, but not my meta-analyses? (These are not rhetorical questions, I'd like to know what you see as the difference). It's not the case that, as you claim in the original post, the kind of evidence I use is "like cognitive psychology" and is only not suffering from a replication crisis because sleep studies are hard; the findings I talk about do get replicated. It's also not as if my evidence is inconsistent with people's experiences.

Also, it's instructive [LW(p) · GW(p)] to note that academic fields are not monolithic things, as Scott Alexander explains in this essay. As he points out, a lot of correct contrarians were in fact supported by academic research when they made their "contrarian" points. Knowledge just doesn't propagate that quickly among people who work in the same field. As an example, some clinical psychiatrists promote the serotonin theory of depression, but the academic research body on psychiatry does not support it. Lumping clinicians and the research body together as a monolithic "psychiatric field" obscures this. 

1:

Chronic sleep deprivation and insomnia can act as an external stressors and result in depression, characterized by hippocampal BDNF downregulation along with disrupted frontal cortical BDNF expression, as well as reduced levels and impaired diurnal alterations in serum BDNF expression.

This quote talks about depression (due to chronic sleep deprivation and stress) being characterized by BDNF downregulation. This is not about sleep deprivation per se because sleep deprivation does not necessarily lead to depression.

[...]

3:

[O]ur findings are in line with the hypothesis of an increased stress vulnerability due to sleep loss which may lead to a decrease in BDNF. [...] While we report a reduction of BDNF levels linked to sleep disturbance reflecting chronic stress on the one side, we and others consistently showed that prolonged wakefulness caused by SD (partial or total), which can be considered as an acute stressor for the brain, leads to a rapid increase of BDNF

This quote again talks about stress due to sleep loss, not sleep loss per se

These quotes simply say that chronic sleep deprivation may lead to decreased BDNF expression through a certain mechanism (depression and stress, respectively). 

[The quote starting with "[O]ur findings are in line[...]"] specifically notes "we and others consistently showed that prolonged wakefulness caused by SD (partial or total), which can be considered as an acute stressor for the brain, leads to a rapid increase of BDNF", so I'm very confused by Mendonça uses it to contradict me.

I'm not contradicting you on the acute effects of sleep deprivation on BDNF. I specifically said,

These sources agree that acute sleep deprivation increases BDNF expression, but they also say that the opposite may happen when sleep deprivation is chronic

2:

significantly decreased serum BDNF levels compared with sleep-healthy controls (n=24; F(1)=5.017; P=0.03; Figure 1a). In addition, serum BDNF levels were significantly correlated with severity of insomnia in all paricipants (n=50; rp=−0.409; P=0.004; Figure 1). [...] We found subjective sleep impairment to be associated with lower serum BDNF levels, whereas reported good sleep was related to higher serum BDNF levels, as shown for those suffering from current insomnia compared with sleep-healthy subjects.

This quote talks about people with insomnia having decreased BDNF. People with insomnia have all kinds of health issues and are famous for underestimating how much they sleep (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277880/) and using them to argue about the relationship between sleep deprivation and BDNF is misleading

Thanks for pointing out that I had an incorrect assumption; I realize now that it's unclear whether insomniacs sleep less than other people. I'll edit the post.

instead of noting that using insomniacs as evidence is simply inappropriate for the point I was making and writing that I'm using inappropriate evidence, she doesn't note any issues with it and simply notes that it contradicts my point.

Hm, I had assumed that you were simply showing a random sample of the first papers that you found when searching “sleep deprivation bdnf.” You simply said

Papers that showed up when I googled “sleep deprivation bdnf”: The Brain-Derived Neurotrophic Factor: Missing Link Between Sleep Deprivation, Insomnia, and Depression. The link between sleep, stress and BDNF. BDNF: an indicator of insomnia?. Recovery Sleep Significantly Decreases BDNF In Major Depression Following Therapeutic Sleep Deprivation.

So I wasn’t expecting all of those papers to be appropriate for the point you were making. 

1. ^{^}

   Not that I would want to say that; I don't disagree with Guzey on the effects of sleep deprivation on depression.

In the interest of simplicity, I'm going to look at individual pieces of your and Natalia's counterarguments. I won't do it all at once, but I'll try to be thorough over time. I'll be separating my analyses into separate comments.

To start with, you say:

Here's what Mendonça writes in her first point that so conclusively demonstrates that the point I make is "misleading":

[Guzey's] evidence from bipolar disorder patients is not representative of what you see in the general population: both long and short sleep duration are associated with depression

The paper Mendonça cites looks at long-term long sleep and long-term short sleep, with their association with depression. My claim and my evidence (from bipolar people) are concerned with short-term long sleep and short-term short sleep. That is, Mendonça's paper is simply not overlapping with with what I write about or what the evidence she calls "misleading" is concerned about. 

To break this into parts:

My claim and my evidence (from bipolar people) are concerned with short-term long sleep and short-term short sleep.

There are several types of bipolar, including bipolar I and bipolar II.

• Bipolar I Disorder is defined by manic episodes that last at least seven days (most of the day, nearly every day) or when manic symptoms are so severe that hospital care is needed. Usually, separate depressive episodes occur as well, typically lasting at least two weeks. Episodes of mood disturbance with mixed features (having depression and manic symptoms at the same time) are also possible.
• Bipolar II Disorder is defined by a pattern of depressive episodes and hypomanic episodes, but not the full-blown manic episodes described above.

None of the respondants from the r/BipolarReddit thread you quoted [LW · GW] specify if they have BP I or BP II. However, if some have BP I, then the length of their depressive episodes fit within the diagnostic criteria for atypical depression.

Two or more of the following features, present for most of the time, for at least two weeks:

• Increased appetite
• Increased sleep
• Leaden paralysis (i.e., heavy, leaden feelings in arms or legs)
• Interpersonal rejection sensitivity (not limited to episodes of mood disturbance) resulting in significant social or occupational impairment

You say:

The paper Mendonça cites looks at long-term long sleep and long-term short sleep, with their association with depression. That is, Mendonça's paper is simply not overlapping with with what I write about. 

The paper Natalia cites is the one I just quoted. It specifically covers sleep in bipolar I patients with atypical depression, which is directly overlapping with your topic.

Your argument in this section is setting up a model in which depression/long sleep and mania/short sleep are at two ends of a sliding scale in the general population. Your BipolarReddit anecdotes are meant to establish the polar ends of this scale, and the use of sleep deprivation as a depression treatment is meant to establish the causal role of sleep length in moving us from one end to the other of the scale in the general population. Natalia's counterargument is that there doesn't exist a simple depression/high sleep - mania/low sleep scale in the general population. Using bipolar patients gives a misleading impression that there is such a simple scale.

I think, however, that the most important point you're trying to make here is that "less sleep can be good for you," using the example of sleep as depression treatment as an example, as well as the existence of atypical depression. Here, the simple scale does generate useful results. There's evidence (accessible on sci-hub) that sleep deprivation works better as a treatment for depression with melancholic features (coinciding with shortened sleep and sleep disturbance) than for depression with atypical features.

Researchers and clinicians agree that the effect of SD is most favorable in patients with the classical ‘endogenous (endogenomorphic)’ depressive syndrome. In terms of DSM-IV these patients fulfil the criteria of a major depressive episode (with melancholic features). Less favorable SD effects have been observed in dysthymic patients (formerly neurotic depression). However, these differences are not very pronounced according to the metaanalysis published by Wu and Bunney (1990); who determined a response rate of 67% in endogenous depression compared with 48% in neurotic depression...

So even for patients not sleeping very much (those with melancholic features), the right move can be a careful regimen of getting even less sleep. A simple "depression -> healthy" scale works when we consider this specific sleep intervention. If sleep deprivation can also trigger manic episodes in bipolar patients, as you both seem to agree it does, we also have a "healthy -> manic" piece of the scale as well.

↑ comment by Natália (Natália Mendonça) · 2022-03-27T19:35:20.578Z · LW(p) · GW(p)

None of the respondants from the r/BipolarReddit thread you quoted [LW · GW] specify if they have BP I or BP II. However, if some have BP I, then the length of their depressive episodes fit within the diagnostic criteria for atypical depression.

Two or more of the following features, present for most of the time, for at least two weeks:

• Increased appetite
• Increased sleep
• Leaden paralysis (i.e., heavy, leaden feelings in arms or legs)
• Interpersonal rejection sensitivity (not limited to episodes of mood disturbance) resulting in significant social or occupational impairment

The difference between BP II and BP I doesn't matter in respect to this. You need to have depressive episodes at least 2 weeks in length to be diagnosed with BP II. 

From the DSM-5, which you can find on libgen:

Replies from: AllAmericanBreakfast

↑ comment by DirectedEvolution (AllAmericanBreakfast) · 2022-03-27T20:38:59.833Z · LW(p) · GW(p)

Thanks for pulling that up. This makes the point you and I are making even stronger in this area.

The effect size I quoted includes studies in which cognitive testing was done in the sleep inertia period (and, in fact, they account for about 30% of the weight), and the mean nap duration among the studies in that meta-analysis was 55.4 ± 29.4 min (quite a bit longer than 20-30 minutes), so I don't think that was selective reporting.

↑ comment by DirectedEvolution (AllAmericanBreakfast) · 2022-03-23T18:12:31.828Z · LW(p) · GW(p)

That's a fair objection.

A second selective reporting complaint that I would make about how the researchers framed their findings is that after outlier exclusion or after analyzing only RCTs, their global effect size drops from 0.18 to 0.07-0.08, with a 95% CI on both sides of 0. However, when describing this result, the researchers consistently, in both the abstract and in the sensitivity analysis section, refer to this as "similar results," without qualification and without reprinting the effect size number.

To be fair, the only RCT model still finds a moderate effect size 61-120 minutes after napping, which tracks with the common sense idea that a nap can temporarily boost cognitive function once the sleep inertial period is over. It's odd, though, that their global model finds that napping provides the biggest benefits to alertness, while their only RCT analysis finds the worst results for napping on alertness, with the central estimate showing a negative impact.

Possibly, this can all be explained if the few RCTs they found focused on testing less than 30 minutes after the nap, so that the apparent effect of napping on performance would be diminished. I haven't looked at them, so I don't want to be too strident in this critique.

Replies from: Natália Mendonça

↑ comment by Natália (Natália Mendonça) · 2022-03-24T21:40:24.421Z · LW(p) · GW(p)

their only RCT analysis finds the worst results for napping on alertness, with the central estimate showing a negative impact

What you mean is that it showed a difference between the napping and control groups at t1 that favored the control group. This seems to have been due to baseline differences between the groups, because when you look at how the mean alertness of each group changed in the RCT analysis, they both improved, with that of the nap group having improved a bit more:

Replies from: AllAmericanBreakfast

↑ comment by DirectedEvolution (AllAmericanBreakfast) · 2022-03-24T22:18:18.446Z · LW(p) · GW(p)

That's a good catch. So it sounds like they're comparing the "effects of a nap" by comparing the control group performance at t1 with the nap group performance at t1, rather than the difference in the magnitude of improvement between the groups from time t0 to t1?

Example:

• Controls score 1 for alertness at time t0, and a 3 at time t1.
• Nappers score a -1 for alertness at time t0, and a 2 at time t1.
• The nappers improved by 3, while the controls only improved by 2.
• Yet the controls scored higher at t1, because they started at higher baseline alertness.

If this is what's going on, my credence in napping being effective is increased. The gains in figure S4 vs. S7 are easy to discern, just by eye.

Replies from: Natália Mendonça

↑ comment by Natália (Natália Mendonça) · 2022-03-25T00:14:12.303Z · LW(p) · GW(p)

So it sounds like they're comparing the "effects of a nap" by comparing the control group performance at t1 with the nap group performance at t1, rather than the difference in the magnitude of improvement between the groups from time t0 to t1?

Yeah, that is what Figure 4 (which you attached in your comment) shows, and what the effect sizes reported in the abstract refer to. There does seem to be a trend towards nap groups across the studies having a bit lower baseline cognitive performance:

Figure S6 directly compares the change in performance of the groups, though the effect sizes are harder to interpret in it.

Replies from: AllAmericanBreakfast

↑ comment by DirectedEvolution (AllAmericanBreakfast) · 2022-03-25T02:02:23.708Z · LW(p) · GW(p)

Thanks for digging out the supplemental figures! Interesting...

Chesterton's fence means that you want to investigate strange-seeming barriers, rules, and norms before tearing them down permanently, not that you should leave them in place unquestioned :) And the claims you make here are precisely the questions we are trying to address.

Sleep research provides an interesting exercise in rationality, because it touches on so many pertinent challenges. There's instrumental reasoning with imperfect information, figuring out how to conceptualize the issue, mechanistic reasoning, critical interpretation of scientific literature -- it's all there. Personally, I think it's a great rationalist exercise.

Lots of people believe that acute stress in the form of exercise, infection, fasting, or extreme temperatures is good for them, and sleep deprivation seems a lot more like those than like stubbing a toe.

Why?

It could be that babies sleep a lot because it's not very useful for them to be awake for longer. 

Why do babies need so much sleep then?

Given that at the moment we don't really understand why people need to sleep at all, I don't think this is a strong argument for any particular claimed function.