Counter-theses on Sleep

[Natália]

Alexey Guzey’s Theses on Sleep gained a lot of popularity and acclaim on LessWrong and among people I follow on social media, despite largely consisting of what I think were weak arguments and misleading claims. I found that a bit surprising, so 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.

Sleep deprivation is associated with *both* depression *and* mania

One of Guzey’s theses is that “depression triggers/​amplifies oversleeping while oversleeping triggers/​amplifies depression.” The first piece of evidence he uses to support that is people on /​r/​BipolarReddit saying that they sleep a lot when depressed, and sleep very little when manic. However, there’s a big problem with using that as evidence.

Guzey’s /​r/​BipolarReddit evidence is misleading

The DSM-5 specifies subtypes of depression that have opposing relationships with sleep. Depression with melancholic features is associated with early morning awakening, whereas depression with atypical features is associated with hypersomnia.

Guzey’s evidence is misleading because people with bipolar disorder are disproportionally prone to having atypical features during their depressive episodes. So, unsurprisingly, his 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 (and, relevantly, suicide as well, in adults as well as adolescents).

I’m surprised no one in the comments of this post brought up this objection – it only takes a very quick Google Scholar search to see that the relationship between sleep duration and depression is not linear.

Chronic sleep deprivation might be associated with *decreased* BDNF expression, as shown by Guzey’s own sources

Guzey hypothesizes that

Sleep deprivation appears to increase BDNF [and therefore neurogenesis?]

He then proceeds to link to a few papers that showed up when he Googled “sleep deprivation bdnf”. These sources agree that acute sleep deprivation increases BDNF expression, but some also say that the opposite may happen when sleep deprivation is chronic, which Guzey fails to mention in his post.

From The Brain-Derived Neurotrophic Factor: Missing Link Between Sleep Deprivation, Insomnia, and Depression:

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.

Guzey also links to The link between sleep, stress and BDNF, which seems to be only an abstract. After a bit of searching, I found this full-text paper with some of the same authors, which appears to have an almost identical abstract (?). It concludes with the following:

[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 (1,36).

Our priors about sleep research should be high

I feel grumpy, dumb and distractable every time I sleep less than 7 or so hours. I can’t do things that require focused attention like solving physics homework problems very effectively, and I don’t get nearly as much pleasure when I attempt doing so. My memory becomes very poor: after a recent night of <6 hours of sleep, I somehow forgot the reasoning behind several Manifold Markets trades I had made the prior evening and just stared at them in utter confusion for several minutes before remembering.

I have the impression that most people have a similar experience. Guzey has a cute explanation of how this is consistent with his thesis that sleep deprivation doesn’t make you grumpy or dumb, but the fact that I and others I know have this experience with sleep deprivation obviously makes it so that I have a high prior that it’s harmful to cognition and mood. It sounds a lot more plausible that sleep deprivation being harmful in those ways is causing both my personal experience with it to be terrible and academic research to find that it’s harmful, instead of a different factor explaining each thing. Guzey has to add quite a few epicycles to his theory to explain the evidence.

To the extent that you and the people you know feel the same way I do after a night of sleep deprivation, your prior should be high as well.

Most of Guzey’s arguments against trusting sleep research are bad

Guzey claims that “most sleep research is extremely unreliable and we shouldn’t conclude much on the basis of it,” but there are problems with that. Firstly because he doesn’t seem to believe that about sleep research that favors his hypotheses. Guzey, after all, uses sleep research to show that Matthew Walker’s book is terrible and fraudulent. So it seems that he wants to trust sleep research when it says that sleep deprivation is not as bad as Walker shows, but doesn’t want to trust it when it says that sleep deprivation is not harmless.

Secondly, he bases that assertion on a claim that sleep science is “mostly just rebranded cognitive psychology” (and that it is only not facing a severe replication crisis because sleep experiments are expensive), which is very misleading. Unlike the famously unreliable cognitive science results, the finding that sleep deprivation is harmful for cognition (1) in fact gets replicated a lot (see the section below on meta-analyses of sleep restriction studies, as well as this meta-analysis of total sleep deprivation studies) and (2) is consistent with a lot of people’s experiences (for examples, see this addendum.) So it’s hard to see how Guzey’s criticisms apply.

Moderate sleep restriction impairs cognition

Guzey says, in his post:

I wrote large chunks of this essay having slept less than 1.5 hours over a period of 38 hours. I came up with and developed the biggest arguments of it when I slept an average of 5 hours 39 minutes per day over the preceding 14 days. At this point, I’m pretty sure that the entire “not sleeping ‘enough’ makes you stupid” is a 100% psyop. It makes you somewhat more sleepy, yes. More stupid, no. I literally did an experiment in which I tried to find changes in my cognitive ability after sleeping 4 hours a day for 12-14 days, I couldn’t find any. My friends who I was talking to a lot during the experiment simply didn’t notice anything.

I don’t think that “feeling smart after sleep deprivation” (or any of those other things) is nearly enough evidence to make you conclude that “ ‘not sleeping ‘enough’ makes you stupid’ is a 100% psyop” if you start out with even a halfway reasonable prior, and especially if you appropriately update on what the sleep literature says.

I looked for meta-analyses that investigated the effect of experimental or quasi-experimental nighttime sleep restriction on cognition. I found three, and am quoting the relevant conclusions from them:

The neurocognitive consequences of sleep restriction: A meta-analytic review:^[1]

The current meta-analytic review revealed that restricted sleep results in significant neurocognitive deficits (g = −0.383) in a sample of 1688 participants derived from 71 different study populations. This effect was apparent across multiple cognitive domains, with the largest effects being observed on measures of sustained attention (g = −0.409) and EF (g = −0.324), and within these domains, attentional lapses and (g = −0.516) and behavioural inhibition (g = −0.464) specifically.

[...]

Meta-regression analyses indicated that age-adjusted sleep deficit (β=-.206, p=.033), cumulative days of restricted sleep (days; β=-.015, p=.019),^[2] subjective sleepiness (β=-.040, p=.016), biological sex (β=.0318, p=.009), and sleep latency (β=.012, p=.013) accounted for a significant proportion of the variance in the observed effect of sleep restriction on overall cognitive abilities.

Sleep Loss and Performance in Residents and Nonphysicians: A Meta-Analytic Examination:

Chronic partial sleep loss also resulted in a significant reduction in cognitive performance, with a correct d value of -.886.

A Meta-Analysis of the Effect of Experimental Sleep Restriction on Youth’s Attention and Hyperactivity (on people under 18 years old only):

A total of 13 samples (N = 268) examined the difference in youth’s attention performance between baseline (control) sleep and restricted sleep. The overall effect size of −0.19 was significant (95% CI: −0.34−0.03; p = .02); Q(13) = 21.98, p = .04, I 2 = 45.40% (see Figure 2). The I^2 index of 45.40% indicates a small to moderate amount of heterogeneity in effect sizes across studies (Card, 2012). However, the trim and fill method for addressing publication bias (Duval & Tweedie, 2000a; Duval & Tweedie, 2000b) revealed asymmetry in the funnel plots for the difference in attention outcomes between sleep restricted and baseline sleep. One study to the left of the mean was unmatched. The counterpart of this study was imputed to the right of the mean, resulting in a non-significant and small adjusted effect size of −0.14 (95% CI: −0.32–.04).

Six samples (N = 279) examined the difference in attention between extended sleep (sleep extension) and sleep restriction. The overall effect size of −0.37 was significant (95% CI: −0.55 to −0.19, p < .0001) and represents a small to medium effect size (Lipsey & Wilson, 2001), though this effect was heterogeneous between studies Q(5) = 15.29, p = .009, I 2 = 67.30% (see Figure 2). The I 2 index of 67.30% indicates a moderate to large amount of heterogeneity in effect sizes across studies (Card, 2012). Based on trim-and-fill analyses, asymmetry was also present for attention outcomes between restricted and extended sleep, with two studies to the left of the mean unmatched, resulting in a significant adjusted effect size of −0.26 (95% CI: −0.46 to −0.05), which is considered a small to medium effect (Lipsey & Wilson, 2001).

The average age-adjusted sleep deficit in the first meta-analysis was 3.83 hours (SD = 1.25). (This is in comparison with the median recommended amount of sleep for each age group (so 8 hours per night for non-elderly adults), not the average amount of sleep people in each age group actually get.) I couldn’t find information about the other ones, but I have a high credence that they examined studies with a roughly similar protocol; I’ve combed through a lot of individual sleep restriction studies before and they rarely seem to involve making people sleep for < 3.5 hours.

I also found a meta-analysis investigating the effects of napping, and it finds that it’s beneficial, which is probably relevant:

Effects of a Short Daytime Nap on the Cognitive Performance: A Systematic Review and Meta-Analysis:

Overall cognitive performance did not differ at baseline (t0) between groups (effect size −0.03, 95% CI −0.14 to 0.07), and improved in the nap group following the nap (t1) (0.18, 0.09 to 0.27), especially for alertness (0.29, 0.10 to 0.48). Sensitivity analyses gave similar results comparing only randomized controlled trials, and after exclusion of outliers.

There’s also (weaker) evidence that, contrary to what Guzey hypothesizes, there is no cognitive adaptation to chronic sleep restriction. From this article:

Contrary to a popular belief that healthy adults can acclimate to sleep loss, the effects of chronic partial sleep loss appear to be cumulative.^9-11 Specifically, sleepiness has been found to increase⁹ and performance on tests of vigilance and mathematical calculations to decline across 7 days of 5 and even 7 hours of sleep per night.^10,11 Subjects often underestimate their own degree of sleep-related impairments in vigilance after 1 week of partial sleep restriction.^9,12 Thus, they may mistakenly believe that they have acclimated to sleep deprivation.

In addition to reduced vigilance, verbal processing and complex problem solving^13,15 are impaired with both short-term and chronic partial sleep loss.

See also footnote 2 (^[2]) on the matter of cognitive adaptation.

---

I do recognize that even meta-analyses of experimental studies can obviously be very problematic, and so this section is not conclusive evidence that moderate sleep restriction impairs cognition (and not only because conclusive evidence is not a thing). But it’s not as if Guzey has any better evidence to argue that “ ‘not sleeping ‘enough’ makes you stupid’ is a 100% psyop.”

Occasionally stubbing your toe is good for health and promotes more efficient toe healing

One of Guzey’s theses is that “[o]ccasional acute sleep deprivation is good for health and promotes more efficient sleep.” His argument supporting that thesis is pretty much that, because some types of acute stress (such as exercising and fasting) are good, and acute sleep deprivation causes acute stress, then acute sleep deprivation is also good. (Yes, that does seem to actually be the entirety of his argument in that section. You can read it yourself.)

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.

Short-term != long-term

In this section, Guzey lists lines of evidence that bring him to the conclusion that “decreasing sleep by 1-2 hours a night in the long-term has no negative health effects.” The lines of evidence are:

1. A sleep researcher who trains sailors to sleep efficiently in order to maximize their race performance believes that 4.5-5.5 hours of sleep is fine.

2. 70% of 84 hunter-gatherers studied in 2013 slept less than 7 hours per day, with 46% sleeping less than 6 hours.

3. A single-point mutation can decrease the amount of required sleep by 2 hours, with no negative side-effects.

4. A brain surgery can decrease the amount of sleep required by 3 hours, with no negative-side effects.

5. Sleep is not required for memory consolidation.

Apart from (2), we don’t have any indication of the long-term outcomes of the groups of people he mentioned. So I don’t know how these points could be more than weak and circumstantial evidence of this section’s thesis.

(For that matter, barely any of those even rigorously measure the health effects of short sleep at all. In a sense, they confirm that these people are not immediately dying or getting very acutely sick or something, and I guess I can interpret Guzey as merely wanting to claim that, but it’s not exactly a novel or surprising claim.)

(Also, the 5th line of evidence doesn’t even seem to be related to health.)

Experimental sleep restriction seems to cause short-term detriments to metabolic health

I searched Embase for meta-analyses on the effect of experimental sleep restriction on a host of health-related variables, and this is what I found.

Effects of sleep manipulation on markers of insulin sensitivity: A systematic review and meta-analysis of randomized controlled trials:

Whole-body insulin sensitivity was also reduced after short sleep when measured by the hyperinsulinemic euglycemic clamp, but peripheral insulin sensitivity was not affected. In addition, circadian misalignment and slow wave sleep suppression negatively affected insulin sensitivity, while rapid eye movement sleep disturbance and sleep fragmentation had no effect.

Effects of sleep restriction on metabolism-related parameters in healthy adults: A comprehensive review and meta-analysis of randomized controlled trials:^[3]

Participants consumed 252.8 more kcal/​d (p = 0.011) under sleep restriction than under normal sleep. Partial sleep restriction resulted in a 0.34 kg weight gain (p = 0.003). Sleep restriction also decreased insulin sensitivity (standardized mean difference = −0.70, p < 0.01). Significant changes in brain activity in response to food stimuli were observed under sleep restriction, particularly regions related to cognitive control and reward.

Sleep Restriction Effects on BP: Systematic Review & Meta-analysis of RCTs:

Overall, sleep restriction did not result in significant changes in systolic blood pressure (SBP) or diastolic blood pressure (DBP) and heart rate (HR). The respective weighted mean difference (MD) was 1.0 mmHg (95%CI, −2.3-4.2; p = 0.57), −0.4 mmHg (95%CI, −3.2-2.4; p = 0.80), and 2.0 bpm (95%CI, −2.2-6.2; p = 0.34).

Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation:

Experimental sleep deprivation, either for partial or total night, was not associated with CRP [...], IL-6 [...], or TNFα [...]. Likewise, sleep restriction over several days was not associated with CRP [...], IL-6 [...], or TNFα [...].

(Eyeballing each of those meta-analyses’ lists of studies, it seems that, in most of them, time in bed was restricted to 4-5 hours, with the range being from ~3.5 to ~5.5.)

So experimental sleep restriction (presumably during short periods of time) seems to impair things like insulin sensitivity and the regulation of satiety, but not blood pressure or inflammatory markers.

Importantly, the metabolic effects of sleep restriction found in the first two meta-analyses seem consistent with the finding that short sleep duration is associated with weight gain in observational studies (particularly in younger persons), which perhaps indicates that the adverse metabolic effects of sleep restriction don’t wane with time.

These changes seem pretty bad. It’s unclear to what extent they translate to long-term health effects (see the section below) but those are things you perhaps should not ignore when investigating whether sleep deprivation is bad for your health.

The evidence for a U-shaped association between sleep and mortality is actually pretty weak

Guzey doesn’t talk about the supposedly U-shaped association between sleep and mortality on Theses on Sleep itself, but he has brought it up in a couple of other places (in the conclusion of his takedown of Walker’s Why We Sleep, and on a comment in the EA Forum) so I thought I’d tackle it here.

For those who don’t know, a lot of epidemiological studies seem to show that the association between sleep duration and mortality is something like this:

(This specific chart comes from Shen 2016).

But Kurina et al.’s “Sleep duration and all-cause mortality: a critical review of measurement and associations” finds that this U-shaped association is suspiciously restricted to a very specific type of study (emphasis mine):

One interesting pattern among studies using survey sleep measures is that all of the studies reporting U-shaped associations measured sleep duration with questions about typical nighttime sleep or 24-hour sleep (Table 2). None of the studies that asked about usual bedtimes and waking times reported a U-shaped association; rather, they reported either no association [12,22,23] or only a long sleep association [6,9,34,99], or, in the case of two studies of young to middle-aged Japanese men, only a short sleep association [12,22]. That the U-shaped associations are exclusively found in studies asking about usual sleep duration may be informative and suggests the possibility of systematic response biases, with people in generally good health more likely to give a “normative” response (i.e., 7 or 8 hours) and those in worse health more likely to give a “non-normative” (shorter or longer duration) response.

It seems that you can’t take people’s reports of how many hours they sleep at face value. Further evidence of that is that studies have shown that people seem to give the same answers when asked how many hours they sleep and how many hours they spend in bed. Also, a substantial fraction of older adults (47% in this study) report sleeping >=8 hours a night, but when their sleep is actually measured, very few of them do, as pointed out in Kurina et al.’s paper.

Kurina et al. look into studies that actually measure people’s total sleep time, and report the following:

A study employing actigraphy among women 50 to 81 years of age (n = 444) concluded that the relationship between sleep duration and mortality was U-shaped [… but] death rates by more detailed sleep categories do not show a dose response for either side of the duration distribution. The top and bottom categories (<4.5 or >7.5 hours) have relatively low mortality, albeit with small numbers, and the highest mortality risk was observed in women sleeping either 4.5—5 hours or—interestingly—between 7 and 7.5 hours.

Neither of the two studies employing polysomnography reported significant associations between sleep duration and mortality [27,36]. In both studies, sleep duration was dichotomized at fewer than 6 and 6 or more hours, precluding the possibility of finding a U-shaped effect.

This isn’t exactly strong evidence that sleeping too much or too little is not harmful. This review only mentions three studies examining the effect of measured sleep on mortality, and two of those didn’t record sleep duration in a way that would make them able to find a U-shaped relationship. Moreover, all of these naturalistic studies probably have substantial range restriction — they mostly involve elderly or middle-aged subjects, many of whom can probably sleep as much as they want, and it’s fairly plausible that very few of those people manage to consistently sleep so much or so little that it’s harmful. Also, they measured sleep for one night only, and the study equipment might have disrupted the sleep of subjects.

However, this review does provide evidence against six hours of sleep being associated with the lowest mortality, as Guzey has hypothesized before (as well as evidence against eight hours of sleep being associated with the lowest mortality, of course). And thus, most importantly, it also provides evidence against moderately short or moderately long sleep being harmful.

Conclusion

So here are my credences on a few relevant object-level claims:

• Shorter-than-average sleep is associated with both depression and mania: 95%

• Modulo weird edge cases like abolishing REM sleep exclusively, a single night with 4.5 to 6 hours of sleep has a negative impact on cognition the following day: 96%

  • Conditional on this, cognition does not return to baseline levels after several months of sleep restriction: 83%

• Also modulo weird edge cases, consistently sleeping between 4.5 and 6 hours per night as a non-elderly adult has some long-term negative health effects: 75%

• It’s not worth it to stress out about how much you’re sleeping, as long as you feel comfortable and productive (and you’re not (getting) manic)^[4]: 63%

I’d be happy to bet on reasonable operationalizations of those statements at those odds (unless I change my mind, in which case I’ll probably edit the credences listed here).

Addenda

Mania is really, really bad, and can be triggered by sleep restriction

I thought I’d bring this up, since it affects how harmful we should expect sleep deprivation to be in expectation. Two years after being hospitalized for a manic episode, less than half of people regain their premorbid occupational and residential status, and the hospitalization rate of mania is pretty high, so manic episodes seem to screw people over really badly for a long time.

And sleep deprivation might risk triggering mania if you have bipolar or a high risk of getting it. 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.

Given how bad mania is, it might be a good idea to try to decrease even a relatively small chance of getting it, so those at a high risk of getting bipolar disorder should probably consider these effects before experimenting with sleep restriction.

Amusing r/​NewParents anecdotes about sleep deprivation

I collected a few amusing anecdotes about sleep deprivation from r/​NewParents.

From this thread, titled “Tell me you’re sleep deprived without telling me you’re sleep deprived..”:

I just unzipped my 1 month old’s sleeper to expose his nipple so I could feed him…… 🤨

My husband attempted to hand me a cat to nurse.

“There was 120ml in the bottle, there is now 50ml in the bottle, so she’s drank...

Okay, this isn’t that hard, there was 120 in the bottle, there is now 50 in the bottle so she’s had...

Right the bottle has 50ml, she’s drank 120 so there should be.. no, she’s drank 50 there’s 120 left so, NO!

there was 120 in the bottle, there is now 50 and it goes 50, 60, 70, 80, 90, 100, 110, 120 so she’s had 120.

NO! ”

i genuinely gave up and used a calculator

From “Finish the sentence: I was so sleep deprived I....”:

Filled the dryer full of wet clothes and tried to turn it on via the microwave sat above it

...ran into a laundry basket and said “excuse me” to it.

Turned on the Keurig to make my coffee and walked away without noticing that I forgot to put my mug under it. The worst part is I’ve done this 3 or 4 times now.

Forgot to put a new diaper on after taking dirty one off. Baby went commando for a while.

From “Funniest thing you’ve said while sleep deprived in the dead of night”:

Nothing will ever top my husband waking me up saying “please take the baby I can’t stay awake any longer” and gently passing me a very pissed off cat that had been asleep on his lap. Note, cat weighed twice what our newborn weighed. When I told him that was a cat he looked terrified and went “but then where’s the baby?!”

My husband and I woke up to our 5-month old crying and he said, “Is that ours??” Yes, my good sir, that is in fact our baby.

It was my turn to wake up for a feed and my wife woke up first so said “babe, wake up she’s crying” and I responded “what? who the hell would be crying in our house?” It was 2 weeks after our daughter got home and she’s our first 🙃

Errata

(Let me know if you think something should be added here that hasn’t been.)

• I used to have an additional quote in the section about BDNF, saying that insomniacs had lower levels of BDNF than sleep-healthy controls in a study. Guzey noted that insomniacs often underestimate how much they sleep; which prompted me to look up the objective sleep duration of insomniacs and not find much evidence that they sleep less than other people. So I removed the quote.

• The last paragraph of my section about mortality used wording that seemed to imply that Guzey had hypothesized that sleeping 6 hours per night was causally optimal, in the sense that people should sleep that much if they want to have the lowest mortality. Guzey did not actually hypothesize that. He pointed that out and I reworded the paragraph.

1. ^

   This study looks for publication bias in the literature and says the following about what they found: “Evidence for publication bias was observed for the overall effect and the effect on measures of sustained attention; see Table 3. However, the impact of such publication bias on the effect appears to be minimal as another 75 studies with an effect size <0.0 would have to be added to result in a small overall effect size (g < −0.200).”

   Orwin’s fail-safe N was used to calculate that number.

2. ^

   Note that the β for cumulative days of restricted sleep is negative, providing evidence against Guzey’s hypothesis that cognitive adaptation occurs after several days of restricted sleep, at least in the timespans investigated in the studies included in that meta-analysis.

3. ^

   Importantly, although this meta-analysis included total sleep deprivation studies, the numbers reported in the sentences I quoted are for partial sleep restriction only.

4. ^

   This is a very important caveat. People with mania will feel perfectly comfortable and productive while sleeping very little.

[Heron]

The references to research for the clarification and countering of assertions, made in a previous piece on sleep, allows for useful knowledge sharing. And the examples of the effects of sleep deprivation are mostly hilarious!

[Angela Pretorius]

70% of 84 hunter-gatherers studied in 2013 slept less than 7 hours per day, with 46% sleeping less than 6 hours.

The study in question also found that the hunter gatherers spent 8-9 hours in bed each night. Sleep duration was measured using those Fitbit trackers that always tell you that you only slept four hours when you’re sure you slept about eight hours. If you move around in your sleep then the tracker assumes that you are awake.

[ChristianKl]

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.

[Natália]

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.

[Dustin]

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.

[DirectedEvolution]

I love the thought and research you’ve put into this, and I’m excited to see this dialogue continue.

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?

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 think it would be valuable to read some measured reviews of individual sleep research metastudies.

Based on my experience with these two meta-analyses, simply being shown additional meta-analyses in this field finding a cognitive impairment effect doesn’t update me much in the direction of there being a real issue. I would need to be confident that the studies it chose to analyze were relevant to the question at hand.

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.

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!).

[Natália]

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.

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? 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)

[DirectedEvolution]

I didn’t notice that it was you I was originally responding to—I apologize for the oversight! I also want to emphasize that I agree with you on some of your responses to Guzey. I think a lot of his arguments are weak, his Reddit- and self-supplied supporting evidence shouldn’t be stacked up against peer-reviewed controlled sleep studies, and some of the argumentation comes off as a conspiratorial strawman (i.e. “At this point, I’m pretty sure that the entire “not sleeping ‘enough’ makes you stupid” is a 100% psyop.”).

In the first of the meta-analyses you posted (Lowe, Safati, and Hall), I see some supporting evidence for your position, and some complicating factors. From the abstract:

This effect held for executive functioning (g = −0.324, p < 0.001), sustained attention (g = −0.409, p < 0.001), and long-term memory (g = −0.192, p = 0.002). There was insufficient evidence to detect an effect within the domains of attention, multitask, impulsive decision-making or intelligence.

So first, let’s acknowledge that they found significant, moderate effects in two areas that we may very well care quite a lot about! However, the long-term memory effect would be conventionally categorized as “small, not visible to the naked eye.” As a note, it’s hard to interpret effect sizes intuitively. They also point out that these effect sizes are highly variable across studies.

Let’s also talk publication bias. They do an Egger Funnel Plot and do find evidence of bias (p<0.001 for the overall effect).

Limitations include the possibility of publication bias, which was observed across almost all cognitive domains...

However, the impact of such publication bias on the effect appears to be minimal as another 75 studies with an effect size <0.0 would have to be added to result in a small overall effect size (g < −0.200).

Read literally, I’m not sure what to make of this caveat. First, isn’t it the number of subjects, rather than the number of studies, that’s relevant here? Perhaps they mean “average-size” studies? Second, I don’t know what they mean by “with an effect size <0.0.” Effect sizes that are lower than zero (as this refers to) are those that show a cognitive impairment. To give a precise statement on the number of (subjects or average-sized studies) needed to bring the total effect size to 0.2, we’d need to know a specific effect size that those studies would need to have. Mathematically, the statement just doesn’t make sense. I’ve read meta-analyses where the researchers at least try to find unpublished work, and it’s disappointing that the authors not only don’t do that here, but write about this issue in a way that seems to show a lack of care around the issue.

Most importantly, median and average sleep across studies was 4.3 and 4.6 hours, respectively—and this includes a few studies on young children, such as one in which “sleep deprivation” meant 8.1 hours of sleep. So the effects found by this meta-analysis, which seem relatively modest to me, required an amount of sleep deprivation that to me seems rather extreme.

So we have to ask two questions.

1. Is there some meta-analytic evidence of a statistically significant effect of an average of 3.5 hours of SD on at least some measures of cognitive function? The answer is yes.

2. Does that evidence paint a picture of an effect that warrants concern over a more modest 1-2 hour SD regimen over the long term, considering effect sizes and the scope of impairment across cognitive domains? This meta-analysis is both weak (due to bias and limited effect sizes) and flawed (due to publication bias) in regards to this specific research question.

There’s no perfect meta-analysis, and despite the flaws I see in this one, it’s still useful to investigate. But when I think through its shortcomings, it does not leave me worried about a consistent 6 hours of sleep per night, or even the occasional 4-5 hour night of sleep.

And note that these are the results without making any efforts to optimize for a shortened sleep schedule. What if you had a coach to help establish a rejuvenating 5 hour long-term sleep regimen? What about modafinil? Does impairment continue to degrade indefinitely over time, or do you eventually just get used to it? What if you’re motivated to do whatever activity’s keeping you awake, rather than doing a bunch of psych tests in a sleep lab? Is sleep debt a thing, or can you balance out 5x5-hour nights of sleep with a 2x9-hour nights of sleep, netting a total of 6 extra waking hours per week = 16 waking days per year?

I’m not complaining at all that these questions aren’t addressed in this meta-analysis. But the point is that the deck is somewhat stacked in favor of the “SD bad” hypothesis. That should be kept in the back of our minds when we take the additional step of synthesizing our interpretation of a particular meta-analysis into our overall view of, as Walker puts it, why we sleep.

[Natália]

Read literally, I’m not sure what to make of this caveat. First, isn’t it the number of subjects, rather than the number of studies, that’s relevant here? Perhaps they mean “average-size” studies? Second, I don’t know what they mean by “with an effect size <0.0.” Effect sizes that are lower than zero (as this refers to) are those that show a cognitive impairment. To give a precise statement on the number of (subjects or average-sized studies) needed to bring the total effect size to 0.2, we’d need to know a specific effect size that those studies would need to have. Mathematically, the statement just doesn’t make sense. I’ve read meta-analyses where the researchers at least try to find unpublished work, and it’s disappointing that the authors not only don’t do that here, but write about this issue in a way that seems to show a lack of care around the issue.

The article specifies that it used Orwin’s fail-safe N to calculate the number of missing studies required to reach a small effect size. It’s not as good as the standard trim-and-fill method I’ve seen a lot in meta-analyses. But it makes mathematical sense and provides evidence.

[DirectedEvolution]

Ah, perhaps the “<” is a typo.

[Natália]

(Quick reply, will go into more depth later)

So first, let’s acknowledge that they found significant, moderate effects in two areas that we may very well care quite a lot about! However, the long-term memory effect would be conventionally categorized as “small, not visible to the naked eye.”

I think the small effect sizes are not as important for predicting overall cognition as the larger ones. If damage happens to a specific part of the brain and not others (as in e.g. most non-fatal strokes), that causes a lot more functional impairment than you would expect if you focused on all of the many parts of the brain that weren’t damaged.

They also point out that these effect sizes are highly variable across studies.

A lot of the variability in the effect sizes is caused by perfectly reasonable things like variations in sleep deficit and cumulative days of restricted sleep, as I explicitly pointed out in the post, and the type of cognitive test used is probably responsible for a substantial fraction of the variability too.

Most importantly, median and average sleep across studies was 4.3 and 4.6 hours, respectively—and this includes a few studies on young children, such as one in which “sleep deprivation” meant 8.1 hours of sleep. So the effects found by this meta-analysis, which seem relatively modest to me, required an amount of sleep deprivation that to me seems rather extreme.

The meta-analysis itself tells you the average sleep deficit across the studies compared with age-adjusted sleep recommendations, as I pointed out in my post, and that number is probably more relevant than those averages.

when I think through its shortcomings, it does not leave me worried about a consistent 6 hours of sleep per night, or even the occasional 4-5 hour night of sleep.

Note that one of my meta-analyses found that (the absolute value of) the effect size of sleep restriction on attention is higher when the comparison group undergoes sleep extension rather than when it undergoes no intervention. This is at least weak evidence that the dose-response relationship between sleep duration and cognition doesn’t flatten out once you get to the average amount of time people sleep.

(This is consistent with me own experience; I started taking less time on assignments and getting better grades in college after I started forcing myself to sleep longer than my previous higher-than-average baseline.)

[DirectedEvolution]

I think the small effect sizes are not as important for predicting overall cognition as the larger ones. If damage happens to a specific part of the brain and not others (as in e.g. most non-fatal strokes), that causes a lot more functional impairment than you would expect if you focused on all of the many parts of the brain that weren’t damaged.

If I’m understanding you correctly, you’re saying that you think that a 1-2 statistically significant moderate effect sizes are more worrisome than if this research had discovered statistically significant but small effect sizes in every category. You expect that functional impairment on real-world tasks would be serious and wide-ranging as a consequence of moderate impairment in a single cognitive domain.

First, I think this is a great crux, and highlights the importance of carefully framing a research question.

Second, I think we ought to consider a few possible functional performance scenarios:

1. Tasks that stretch cognitive capacity to the maximum extent, often by design. Example: a chess championship or math exam.

2. Tasks that typically use limited cognitive capacity, but in which mistakes can have severe consequences and rare emergencies can occur at any time that will result in much higher cognitive demands than normal. Example: jet pilots, soldiers on patrol.

3. Tasks that use limited cognitive capacity, allow for corrections and adjustments, and are primarily bottlenecked by time, skill, and material resources. Example: most jobs, tasks of daily living, sailing competitions.

I think that scenarios (1) and (2) are the best candidates for the hypothesis of greater functional impairment effects relative to limited and modest cognitive function deficits, and scenario (3) is best for the hypothesis that modest and limited cognitive function deficits aren’t too concerning.

Some challenges might even be mixed. For example, we could imagine that in school coursework, learning is bottlenecked by hours of study in general. However, on exams, for well-prepared students, hours of sleep might become the limiting factor on their performance. Hence, an idealized study strategy might want to routinely sacrifice some sleep in exchange for more study time, but then increase sleep on the days leading up to an exam.

Under this mixed framework, a strategic sleep regimen would be flexible, based on the specific performance demands the person in question was facing.

Note that one of my meta-analyses found that (the absolute value of) the effect size of sleep restriction on attention is higher when the comparison group undergoes sleep extension rather than when it undergoes no intervention. This is at least weak evidence that the dose-response relationship between sleep duration and cognition doesn’t flatten out once you get to the average amount of time people sleep.

I’ll check into this when I have time—it’s interesting!

The meta-analysis itself tells you the average sleep deficit across the studies compared with age-adjusted sleep recommendations, as I pointed out in my post, and that number is probably more relevant than those averages.

The sleep times I referred to track closely with the average age-adjusted sleep deprivations, but you are right that it would have been more apt to choose the latter instead of the former. I simply find it more intuitive to gauge what X hours of sleep feels like than Y hours of sleep deprivation.

Edit:

As a followup, I’m not sure how to think about the relationship between single-factor cognitive effects and broad functional effects.

At first glance, it seems to me that if we hypothesize that a single-factor cognitive deficit corresponds to broad functional impairment, that we’re essentially saying that you’re held back by whatever cognitive faculty is furthest below baseline. That in turn would indicate that any single-factor cognitive improvements obtained by sleep extension (i.e. alertness) would not correspond to functional improvements, if any cognitive factors fail to be improved by sleep extension.

On the other hand, it could be that, in either direction, the cognitive factors that are harmed/​helped by sleep adjustments happen to be the load-bearing factors for most activities. Maybe executive function and sustained attention are the limiting cognitive resource for most people at baseline, and alertness is the typical limiting cognitive resource above that. If that were true, we’d expect to see broad functional improvements or impairments across wider ranges of sleep adjustment.

I’m most inclined toward the idea that tasks have a heterogeneous relationship with particular cognitive capacities, and thus with the impact of sleep. This suggests that people can reap the most benefit by tailoring their sleep schedule to their particular requirements.

Busy parents with regular jobs that aren’t too cognitively demanding or hazardous might benefit most from a couple extra hours of wakefulness every day to get things done, and indeed, they often seem to opt for that strategy. By contrast, airlines apparently have strict policies for how long pilots must sleep before a shift, and I’ve also heard an anecdote from a biologist in a BSL4 facility that they don’t do inoculations unless they’re in absolutely tip-top cognitive shape. If they got bad sleep, or woke up with a crick in their neck, they reschedule.

My guess is that many people are modestly strategic about their sleep budget. But if this hypothesis is correct, there may be substantial gains to be reaped by individualized, flexible tailoring of the sleep schedule, rather than issuing a blanket recommendation of X hours of sleep across the board.

[Natália]

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.

[Elizabeth]

I am also interested, especially in “what tools can help people develop data for themselves, that can be aggregated in useful ways?”

One way I think sleep science and most everything else goes wrong is in looking for the modal human answer, ignoring how the right amount of sleep/​nutrient X/​exercise/​etc vary between humans and for the same human over time.

[DirectedEvolution]

Excellent. Will do. I’m also reaching out to Guzey. Maybe we can get a bit of a community effort going!

[moridinamael]

I wear an Oura ring and and Apple Watch with a sleep app. Both of these devices agree on when I’m underslept, and they are both correct; when my watch says I’m underslept, I feel stupid and tired and my chess.com scores plummet. My chronic pain condition is also much worse when I’m underslept. Additionally, I do not use an alarm clock, so my body will claw back the sleep it needs. If I only get 6 hours two nights in a row, I will sleep 9 hours the following night, but I habitually wake up after 7-8 hours. I can observe these patterns in my recorded sleep data, and they are robust over long stretches of time.

I say all of the above because frankly my own personal experience and data tracking is sufficient evidence for me to basically disregard any sort of thesis claiming that I need less sleep. Maybe you need less sleep, I don’t know. Do the experiment, try to sleep less for a couple of days, see if you physically implode. I would put money on the “you will probably learn that you were already pretty in tune with your body’s needs” outcome.

[Elizabeth]

I think Natalia brings up a lot of important, true, points here, and I’m really glad she wrote this post. I also stand by what I said when I curated Alexey’s post, that while I was doubtful on any particular conclusion I thought he was pointing at real deficits in current models and I was excited to see those explored so they could be eventually filled in. My current guess (having not deeply investigated the evidence for either post) is that this post is closer to the literal truth, and Alexey’s post is pointing in a more useful direction (but we will get there in part by people pointing on the parts that are false, via posts like this).

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, I agree with AllAmericanBreakfast that it’s more like scurvy before the vitamin C paradigm. There’s a real thing there, but without the paradigm it looks incredibly fake and exactly like epicycles. 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.

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.

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

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

  • Or more formally, the evidence on depression Natalia links

• Alexey acknowledges that sleep deprivation makes people much worse drivers but doesn’t seem to think that has implications for anything else?

• In a 1:1 conversation with me he argued that medication never increases the actual need for sleep, merely perceived need.

[Natália]

[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

[DirectedEvolution]

1. Copper tubing and environmental exposure does destroy vitamin C

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

At first glance, I thought you were claiming that copper tubing and air exposure does not destroy vitamin C, but now I think I read you backwards. I think you are claiming that they do destroy vitamin C, and that copper and O2 destruction of vitamin C was the only reason that “lime juice” was failing to prevent scurvy (and that the differences between lemons vs. limes had nothing to do with it). Just to emphasize that vitamin C is susceptible to destruction by copper and environmental exposure, here’s the Australian Ministry of Health:

Vitamin C is very labile [easily broken down or displaced] and its content in foods varies. Vitamin C content can be affected by season, transport, shelf life, storage time, cooking practices and chlorination of water. Cutting, bruising, heating and exposure to copper, iron or mildly alkaline conditions can destroy ascorbate.

2. Liver and vitamin C

Polar bear liver contains massive amounts of vitamin A, enough to kill humans (1, 2). When the Idle Words essay on which the SMTM post is based says “Eat a bear liver every few weeks and scurvy will be the least of your problems,” the proper response is “because you’ll be dead of vitamin A poisoning.” However, the IW post vascillates between saying that the vitamin C in the polar bear comes from “meat,” “liver,” and “kidneys,” and I don’t trust that the author carefully investigated the nutritional value of each of these organs.

However, I did find a source that talks more about the Inuit and early European arctic explorer diet.

In the 1920s, the explorer Vilhjalmur Stefansson threw a wrench in “fresh fruits and vegetables” theory when he reported that the Inuit, who rarely ate plant foods, also did not suffer from scurvy. As it turns out, their Vitamin C came from animal organs: liver, adrenal glands, roe [egg masses in the ovaries], and tongue, to name a few. Traditional cooking methods also helped: Vitamin C is present in raw muscle meat, but harsh cooking destroys it. So by cooking their meat very lightly, the Inuit were preserving the Vitamin C in it. In a year-long experiment, Stefansson and a friend lived entirely on raw or lightly-cooked meat without showing any signs of scurvy.

Raw bear meat has a little more vitamin C (2mg/​100g). So this would require eating 500g bear meat/​day (about 650 calories, or 1.1lb per day) to get an adequate quantity to prevent scurvy indefinitely, or less merely to prevent it for the duration of the voyage. Scurvy takes 3 months to set in if vitamin C intake is extremely low.

I think we have adequate evidence to say that bear meat could have prevented scurvy in Arctic explorers if lightly cooked.

3. Sourcing the claims on limes vs. lemons

I found a source containing the claim of lemons being 4x as powerful an antiscorbutic as limes, which may be the origin of the IW/​SMTM claim. In fact, it contains several of the essential points in the story conveyed by these blog posts. The source is The Prevention of Scurvy in the Navy by Surgeon-Commander J. L. PRISTON, M.B., M.R.C.P., D.P.H., R.N., from 1926. Unfortunately, neither SMTM nor Idle Words appear to cite this document.

In spite of this [better diet provided after a 1797 mutiny], scurvy continued to be a common disease for many years until, with the introduction of steam, voyages became shorter and fresh food was supplied as a matter of course, not as a rare privilege.

About the year 1860 the Admiralty gave up trying to get good supplies from the Mediterranean and began to use lime juice prepared from the sour lime in the West Indies. It is now known that the fresh lemon is four times as powerful an antiscorbutic as the fresh sour lime. Moreover, the method of preserving Navy lime juice destroys all the vitamin C, so that the Navy lime juice as now supplied has no antiscorbutic power at all.

The name “lime juice” had always been applied indiscriminately both to lemon juice and lime juice.

Arctic explorers, however, noticed from time to time as a puzzling fact that lime juice did not prevent scurvy.

We don’t really know what “fresh” means. Does it mean that both the limes and lemons were recently picked? Or only recently squeezed in the scientist’s lab, perhaps after several weeks in the ice-packed hull of a transport ship? And moreover, we don’t really know whether the “antiscorbutic power” of a citrus fruit scales linearly with vitamin C content, using whatever methods of processing and measurement they applied to generate this finding. Sadly, Priston also does not cite his source when he makes this claim.

Now let’s talk modern data. Is it possible that lemons contain, in some meaningful sense, about 4x the vitamin C of limes?

Key limes weigh about 1oz. Some random poster on a cooking forum says that a pound of key limes gives about ²⁄₃ of a cup of juice, so you’d need 1.5 pounds = 24 oz of key limes to get a cup.

I’ve found varying estimates for how much juice is in a large lemon, but 3-5 tbsp seems to be about the range. Here’s a source for 5 tbsp. A 52mg/​100g vitamin C lemon would have 1.7x the vitamin C content of an equivalent amount of lime juice, so you’d only need 0.6 cup, or 9.6 tbsp, to get the same amount. Rounding to 10, this would be the juice of two lemons, weighing in at about 8 oz.

By these figures, per unit weight of fresh fruit (as opposed to juice), fresh lemons might have 3x the vitamin C of fresh key limes. We can also imagine that if the scientist who conducted this old study was using lemons and limes purchased in their local market, those fruits might have been picked at different times. If the lemons were a bit fresher, perhaps more of the vitamin C was still stable. If Surgeon-General Priston was rounding up, or if random chance favored the lemon somewhat in the study, it’s possible to imagine a scientific result that at the time showed a pound of lemons being 4x as effective as a pound of key limes at preventing scurvy.

4. Conclusion

Note that these weird, subtle distinctions and epistemic challenges are precisely the point of the sleep/​vitamin C comparison. Even if the early scientists studying the antiscorbutic power of lemons and limes wrongly found that lemons are 4x better than limes, this is precisely the point! Without both careful scientific investigation, using multiple lines of converging evidence (including the anecdotes of weirdos like arctic explorers), as well as a mechanistic understanding, it’s very easy for the real complexities of a system to be disguised by intuitive human categorization schemes that wildly miss the mark.

Another comparison is pica. We know that the body can generate cravings for “nutrients” that it does not need, or that are actively destructive (as in addiction or disordered eating), while also failing to give us cravings for nutrients that we do need. So we should keep our minds wide-open to the possibility that we are fundamentally misunderstanding the role of sleep in cognition and functional capacity.

[Natália]

At first glance, I thought you were claiming that copper tubing and air exposure does not destroy vitamin C, but now I think I read you backwards. I think you are claiming that they do destroy vitamin C, and that copper and O2 destruction of vitamin C was the only reason that “lime juice” was failing to prevent scurvy (and that the differences between lemons vs. limes had nothing to do with it).

Yeah, your current interpretation is correct.

This article finds that Musk limes have less than half the vitamin C of lemons, just to gesture in that direction.

It’s not that different from the raw limes in USDA’s data. In the titration method, that article found that musk limes had 42.3% as much vitamin C as lemons, and in the HPLC method, 53.5%. The average of those is 47.9%. My data on non-musk limes suggest they have 54.7% as much vitamin C as lemons.

The quote you gave for lemon vitamin C is the minimum value listed in the source. The maximum is 43.3mg/​100g

I’m confused. The number I listed for lemon vitamin C was 53mg/​100g.

I think we have adequate evidence to say that bear meat could have prevented scurvy in Arctic explorers if lightly cooked.

To be clear, I wasn’t arguing against that. I was just pointing out that it’s misleading to claim that polar bear meat is more like lemons than limes are. All 3 of those things seem able to prevent scurvy when they’re fresh and consumed in reasonable quantities; even ¹⁄₄ of the vitamin C concentration of fresh lemon juice is 23.22mg per cup. It’s possible that a citrus species has an abnormally low vitamin C concentration, and it’s possible that 10mg of vitamin C from lime juice is not the same as 10mg of vitamin C from fresh meat. But SMTM was asserting as a known fact that Sicilian lemons are more like polar bear meat than they are like West Indian limes in their ability to treat scurvy, which in expectation causes people who read the post to be worse at predicting the data we found than they would be if they had never read it, and that is what I was objecting to.

[DirectedEvolution]

Apologies, I missed several of these points in your OP at first, and edited my post to correct it. Sorry you saw it before it was fixed!!!

I was just pointing out that it’s misleading to claim that polar bear meat is more like lemons than limes are.

I agree with your characterization of SMTM’s argument. It’s hard to parse, given the reference to his own made-up dialog that’s partly to make (supposedly) factual claims and partly to illustrate the challenges of analyzing complex scientific data. However, I read this as SMTM in their authorial voice defending the claim that key limes don’t contain vitamin C and polar bear meat does. We both agree this claim is false. Here’s the relevant quote:

Frolich: Maybe some citrus fruits contain the antiscorbutic [scurvy-curing] property and others don’t. Maybe the British Royal Navy used one kind of lime back when Lind did his research but gave a different kind of lime to Nares and the others on their Arctic expeditions. Or maybe they did something to the lime juice that removed the antiscorbutic property. Maybe they boiled it, or ran it through copper piping or something, and that ruined it.

Maybe there are different kinds of citrus. Maybe some animals need this mystery ingredient and others don’t. Maybe polar bear meat is, medically speaking, more like citrus fruit from Sicily than like citrus fruit from the West Indies. Really???

This looks a lot like special pleading, but in this case, the apparent double standard is correct. All of these weird exceptions he suggests were actually weird exceptions. And while our hypothetical version of Frolich wouldn’t have any way of knowing, these were the right distinctions to make.

I think that SMTM got this fact wrong. However, I think that the essential point of the SMTM article holds, and by extension the analogy I am drawing between vitamin C and sleep.

Thank you for your patience with my original slip-ups in noticing the full content of your preceding comment.

[Natália]

There was also another relevant passage:

“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.

[DirectedEvolution]

Followup: SMTM points out that differences in fertilization and propagation (clonally or by seed) mean that we don’t know whether or not historical key limes had enough vitamin C to cure scurvy. I notice in myself a certain tendency to say oh puh-leeze in response to this, but at the same time, I think the broader point of the original SMTM piece is that it’s precisely this reaction that we ought to be suspicious of. After all, we don’t necessarily know that the arctic explorers who found that lime juice didn’t cure their scurvy were drinking it out of copper tubes, or that the vitamin C in the lime juice they were drinking was oxidized.

Reality is surprisingly complex.

[Natália]

SMTM points out that differences in fertilization and propagation (clonally or by seed) mean that we don’t know whether or not historical key limes had enough vitamin C to cure scurvy.

Hm, that would still make the post misleading — “Sicilian lemons really ARE more like polar bear meat than they are like West Indian limes, at least for the purposes of treating scurvy” is a very different claim from “we don’t know whether or not historical key limes had enough vitamin C to cure scurvy.”

Thanks for contacting them, though!

[DirectedEvolution]

Agreed!

[DirectedEvolution]

I will see if I can get in touch with SMTM and IW, I’d be curious what they have to say about this.

[Natália]

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.

[Elizabeth]

Sounds like we agree a lot- I think he got a lot of stuff wrong and was glad to see you correct it. I think he wildly overextrapolated from his own data. My opinion on mainstream sleep researchers is closer to his than yours, but agree he overextrapolated from the sailing sleep coach.

I spend a lot of time going “that person’s big idea is built on a foundation of factually inaccurate sand”, so it’s novel for me to be the one going “yes, mostly, but I still want to follow up”. I feel this way due to a combination of thinking Alexey brings up a lot of legit problems with existing sleep research, and that he put serious time into generating new data (although I was extremely disappointed in his data collection, and would have found even writing down his subjective score each day an improvement over nothing).

[Natália]

My opinion on mainstream sleep researchers is closer to his than yours

I feel this way due to a combination of thinking Alexey brings up a lot of legit problems with existing sleep research

Could you elaborate on what you mean by “mainstream sleep researchers” and/​or “existing sleep research,” and what, in your view, the legit problems with the latter are? (Modulo Walker). These terms can mean many things and refer to very different sets of models. Researchers, the organizations that set guidelines, and clinicians in a certain field can often have very mistaken views about what the research in their field actually shows if they’re not personally involved in it. For example, some clinical psychiatrists promote the serotonin theory of depression even though the research body does not support it. Lumping together the clinicians with the research body as a monolithic “psychiatric field” obscures this. (I’m not sure that that’s what’s going on here but discussing what you mean specifically could be helpful.)

Some of Guzey’s points on Theses on Sleep and Matthew Walker’s “Why We Sleep” Is Riddled with Scientific and Factual Errors are genuinely both counterintuitive to the general public (and some/​most sleep researchers, guidelines-setters, and clinicians) and true. But Guzey’s evidence for those points didn’t come out of the ether (and most of it did not come from his own experiment). It largely came out of the academic research body on sleep, the same place in which I found evidence that sleep duration e.g. affects cognition but barely has a clear association with mortality. So it seems reasonable to me to dissociate the research body from the opinions of most people in the field.

(Also, I think it’s very unclear what view you’re ascribing to me in the first quote, but I suspect that I do not endorse it. I don’t expect sleep scientists to be that good at predicting reality in subfields or sub-subfields they’re not personally involved in.)

[Natália]

[An earlier version of this comment said “do endorse it” when I meant the opposite, sorry for the confusion.]

[DirectedEvolution]

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.

[jimmy]

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.

[Natália]

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.

[Elizabeth]

makes me unsurprised that some people remain astonishingly productive for years on very little sleep.

I’m surprised to hear you say this and am now less sure what you’re arguing against.

[Natália]

I think mainstream sleep models don’t fail to predict that some people remain astonishingly productive for years on very little sleep. The meta-analyses I included showed moderate effect sizes for the impacts of sleep restriction on cognition, which aren’t enough to decrease a large baseline advantage in cognitive performance that much.

[Elizabeth]

okay. It sounds like the words “sleep deprivation” are doing a lot of work in the original post. You don’t mean “sleeping much less than the average”, but literally “depriving yourself of sleep you need”?

Regardless of what mainstream science says, what gets filtered out to the public is very much “get N hours or you’re going to die”, if sleep scientists have the concept of standard deviation in their models I’ll be impressed.

[DirectedEvolution]

My interpretation is something like this:

1. Let’s say that long-term sleep deprivation costs 15 IQ points (1 standard deviation) in terms of cognitive function.

2. Furthermore, let’s imagine Bob is a researcher with a baseline IQ of 145, while his coworkers have IQs of 115. Bob is chronically sleep deprived, so his functioning IQ is 130.

3. Bob’s functioning IQ is still above that of his coworkers, and he’s also able to work more hours, and therefore will be astonishinly productive relative to his coworkers.

4. However, it may still be that his productivity would be higher still if he slept better. What he lost in time, he’d more than make up for in productivity per hour of work.

5. Therefore, the existence of rare, astonishingly productive, sleep-deprived workers is compatible with sleep deprivation being harmful to cognitive function and net negative to productivity even for these workers.

Let’s assume that at a research university, the mean IQ of faculty is 115, still with a standard deviation of 15 IQ points. In this case, Bob would merely be in the top 5% for IQ relative to his colleagues. At a major research university, with 5,000 faculty, there would be 250 faculty like Bob. We can imagine that their level of sleep deprivation would be normally distributed as well, and so we could find quite a few examples of people like Bob just by looking around.

Natália, is that a fair representation of the point you’re making here?

[Elizabeth]

I think that makes sense (and wasn’t what Natalia was saying, but is compatible with it. Bob could be smater than average, have a lower optimal sleep length, and have fewer consequences per hour of foregone sleep ). I want to highlight that there are many tasks that don’t benefit from the additional 15 IQ points, and if your total output depends more on those than on tasks that benefit from every last IQ point, then trading IQ points for more hours in the day can be the optimal move. But if Bob got smarter co-workers or became less resilient to sleep loss the trade-off might be different, and it’s beneficial for him to check the trade-offs periodicially.

I don’t think that’s what Alexey or Natalia were arguing, and it ignores health effects, but what I’m excited about in this discussion is rendering these kinds of trade-offs able to reasoned about

[DirectedEvolution]

I agree about your point on making trade-offs possible to reason about. I’ve found that in discussing this away from LW, people will talk as if extra hours of sleep don’t come at the expense of waking hours. To them, at first glance, the decision is between “activity X, Y, and Z with 6 or 8 hours of sleep” rather than between “activity X and Y with 8 hours of sleep, or activity X, Y, and Z with 6 hours of sleep.”

When I point this out, the follow-up is “but what if the lost sleep makes activity Z a negative experience?” When we eventually anchor on that being the question at hand, rather than the assumption by default, the conversation can become productive and interesting.

I also agree with your bottlenecks-based framing. I think some tasks are bottlenecked by cognitive function (chess competitions), others usually aren’t but can be in rare/​emergency circumstances that therefore require full-time high cognitive function (airline pilots), and many others aren’t bottlenecked by cognition (sailing races).

[gbear605]

One counterpoint to that framing is that activities usually don’t take a fixed amount of time. There are many things that I’ve done where I’ll take a quarter of the time or less if I’m in a productive state rather than a non-productive state. Sometimes it might really be a trade off between “activity X, Y, and Z with 6 or 8 hours of sleep”, or even “activity X, Y, and Z with 8 hours of sleep, or activity X and Y with 6 hours of sleep”. I’ve also found that I’m less distracted with more sleep, so it could be “be productive for the most of the day with 8 hours of sleep, or browse social media for most of the day with 6 hours of sleep”. This all has been most obvious when I’ve been working on intellectual activities, like writing or developing software, but I also tend to have slower reflexes when I’ve been sleeping less, so physical activities are also relevant.

My personal sleep logs show that productive states are strongly correlated with the amount of hours of sleep I’ve gotten over the last month and the previous night. I don’t have proof that the math really works out, but I strongly suspect it does. Over longer term periods where I’ve had more or fewer hours of sleep, I’ve gotten more positive outside feedback (grades, feedback in monthly reviews) in the the periods with more sleep. But of course I have no proof that this applies to everyone, it’s correlation instead of causation, and it’s certainly no double blind study.

And of course the hardest problem is beating the akrasia to go to bed when I want to, but that’s a separate issue.

[DirectedEvolution]

Agree! I think we are coming to a model where N hours of SD results in an average of X% loss in productivity per hour, and a change from Y to Z daily productive hours. We want to know the sign of XZ—Y.

Here, you may be arguing both that the performance loss is so great as to more than cancel out the increased number of working hours. You may also be arguing that we actually lose productive hours with sleep deprivation, despite being awake longer, because the loss of executive function makes us unable to focus on our work.

Alternatively, it may be that the additional productive hours from SD can be put into low-demand but time-consuming life maintenance or pleasurable occupations that otherwise might get neglected. For example, we can imagine a busy student choosing between 8 hours of sleep, or 6 hours of sleep plus 2 hours of socializing. Or between 8 hours of sleep, or 7 hours of sleep plus a trip to the grocery store. Or between 8 hours of sleep and 7 hours of sleep plus 1 hour of exercise.

Sacrificing sleep for efficiency-compounding tasks and meaningful occupations may cancel out or even reverse the cognitive impacts of SD itself. It may be that the worst effects of SD can be mitigated with a combination of practice, organizational supports, and stimulating activities and caffeine. It may also be that for some people, their baseline need for sleep is below the level recommended by sleep researchers, so that for them, reduced sleep comes at no cognitive cost.

So the question is twofold. Does non-strategic mild-to-moderate SD lead to net positive or net negative results on some outcome, like productivity, pleasure, health, or meaningful experiences? Furthermore, to what extent can an SD-management strategy mitigate the negative impacts of mild SD?

The stakes are rather significant. Consider that 2 hours of daily SD from age 20-60 adds up to 3.3 years of additional wakefulness, distributed across the most productive and healthy part of the lifespan. If it ruins the experience of life and damages productivity, that is an enormous detriment. On the other hand, if long-term strategically managed SD can be made neutral to positive, then that is the only intervention we currently have to more or less add healthy years to the natural lifespan.

Given the obvious complexities of managing sleep, even for adults people who are attempting to get a full 7-8 hours per night, it seems worth puzzling through it up front in order to establish an optimal sleep routine, given one’s individual preferences, bodily needs, and demands of life.

[Natália]

It sounds like the words “sleep deprivation” are doing a lot of work in the original post. You don’t mean “sleeping much less than the average”, but literally “depriving yourself of sleep you need”?

I tried to be explicit about the average number of hours slept in the studies included in these meta-analyses of experimental studies. Usually, it’s about 4 to 5 hours, with the average seeming to be closer to 4. I also tried to be explicit about how many hours of sleep per night my claims refer to in my conclusion (except for the first claim, which I specified was about “shorter-than-average” sleep, and the last one, which is a harder-to-operationalize claim, but still didn’t explicitly refer to “sleep deprivation”).

if sleep scientists have the concept of standard deviation in their models I’ll be impressed.

Standard deviations are used very often; I would be surprised if they weren’t used in 5% or more of the sleep studies I’ve read.

[Elizabeth]

Sorry yes, of course they’re including SD calculations in their papers. What I meant was that medical papers (or popular coverage thereof) almost never consider the implications of the fact that 0.3% of people will be >=3 standard devs out, and with a large enough population that’s a lot of people.

[DirectedEvolution]

I’ve been meditating on the broader relationship of this post, and Guzey’s, to the idea of instrumental rationality and the question of what rationality is good for. A idea is that instrumental achievement is bottlenecked by akrasia.

When we study sleep, we’re really studying one aspect of fatigue, which is similar if not identical to akrasia. We can think of fatigue as being subdivided into physical and experiential components. Like other forms of fatigue, sleep pressure manifests both in physical brain structures and in our conscious, felt experience.

Sleep may be a specific solution to a specific physical or felt need, and our sense of sleep pressure may be well-tuned by evolution to indicate the amount of sleep required for optimal function. Sleep may also be a nonspecific solution to these needs, and sleep pressure may be only marginally attuned to the timing and duration of required sleep.

More broadly, we have agentic goals. To accomplish them, we generally must maintain our minds and bodies in order to work efficiently and maintain motivation, while also freeing up time to do that work.

It is possible to carefully calibrate many of our routines. For our diets, we can count calories, ensure our daily intake of vital nutrients, prepare delicious or easy-to-cook meals. For exercise, we have access to a wide variety of exercise equipment and clothing, have several rich theories of how to build strength, flexibility, and endurance, and tools to monitor and plan our workouts.

Yet for managing fatigue, our theories, tools, and equipment often seem far less robust, precise, and thoughtful. Activities that seem relevant to fatigue management, including sleep, meditation, passive entertainment, and taking breaks from work, are often thought of as entirely different spheres of human activity (i.e. sleep, spirituality/​therapy, and entertainment). It is not considered unusual, and is indeed considered admirable, to invest a great deal of time, money, and care into developing a healthy and well-considered diet and exercise routine. Why is fatigue management not thought of in the same way?

Fatigue management seems like a concept where rationalists have an opportunity to make real progress. What’s needed is a set of terms and frameworks for naming, relating, and making predictions about how our behaviors, experience of fatigue, and capacity for productive work interrelate.

For example, I noticed today a drop in my energy level for several hours in the middle of my day. I felt low energy, low motivation, and was making many mistakes in my math homework. I had a lot of work still to do, and hadn’t been up and working for all that long. In addition, I was worried that if I stopped, that I would get sucked into leisure activities for the rest of the day. After trying to push on and continuing to make little progress, I stopped.

Instead, I watched a couple episodes of TV, went to the grocery store, and cooked myself dinner. When I was finished, several hours later, I found that my head had cleared, and I was once again able to make progress.

Without a considered relationship with fatigue management, the decisions to stop or continue work get made in an impulsive fashion, and do not result in an increased understanding of how my behaviors intersect with fatigue. Because I did engage in conscious fatigue management today, I got a piece of data about how significant fatigue feels, the effect it has on my in-the-moment productivity, and an upper bound on how long it takes to treat that fatigue with food and rest.

Learning to notice fatigue-related performance loss, and to identify which behaviors seem to most efficiently cause or treat fatigue, seems like it could result in a realistic strategy for reducing akrasia over time, being more productive, feeling better, and knowing what to do in order to have better control over one’s mind and body.

[guzey]

(I’ll reply in more substance by the end of the week—have a big deadline coming up this Thursday)

From skimming the post, three parts stand out to me

1. the fact that acute sleep deprivation relieves depression in ~50% of people with depression seems completely unaddressed and Natália’s section about bipolar people seems to imply that this would not be happening. I specifically noted in this the section Natália addresses by writing:

Lack of sleep is such a potent trigger for mania that acute sleep deprivation is literally used to treat depression. Aside from ketamine, not sleeping for a night is the only medicine we have to quickly – literally overnight – and reliably (in ~50% of patients) improve mood in depressed patients

2.

One of Guzey’s theses is that “[o]ccasional acute sleep deprivation is good for health and promotes more efficient sleep.” His argument supporting that thesis is pretty much that, because some types of acute stress (such as exercising and fasting) are good, and acute sleep deprivation causes acute stress, then acute sleep deprivation is also good. (Yes, that does seem to actually be the entirety of his argument in that section. You can read it yourself.)

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.

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.

3. Natália misquotes me at the end of the piece. I never wrote that 6 hours of sleep is optimal. I have no idea how many hours of sleep is optimal and I believe (please let me know if this is not the case) I never stated that a particular amount of sleep is optimal.

What I wrote in the appendix of the Why We Sleep piece Natália linked to was: “people who have the lowest mortality actually sleep 6 hours a night”. Earlier in that article (which, it is clear that Natália read carefully), I specifically wrote “we should almost never use [epidemiological evidence] to claim causality”.

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, but, as noted above, I will reply in more detail in a few days.

[DirectedEvolution]

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!

[Matthew Barnett]

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.

FWIW, I don’t think the stubbed toe example is integral to the argument. The stubbed toe example was almost certainly just an analogy, not a knockdown argument, in regards to the more general point that the link between acute stress and health benefit seems to be weak.

I think a better way of phrasing this crux is that it’s unclear why this form of acute stress is beneficial, where this refers to sleep deprivation. It would be nice to get specific evidence regarding why sleep deprivation is the right type of acute stress to promote health, when the relationship does not hold in general.

I don’t think I’m objecting to your current summary of the debate necessarily, but I do think focusing on the stubbed toe example is mostly a distraction, and all parties are better off relying on different arguments.

[DirectedEvolution]

I agree that stubbed toes needn’t be a central example of “acute stress,” and I would hope that most people are just using it as you suggest—a convenient analogy for a minor but pretty-clearly-bad form of injury, one that stands in contrast to plausibly beneficial stressors like exercise.

[Natália]

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.

[DirectedEvolution]

Here, I think it was clear that I pointed out the antidepressant effects of sleep deprivation in at least some subjects (before the “and”). So I think it’s misleading to suggest that this section implied that the antidepressant effect does not exist.

I don’t quite follow. The closest you come in the quote is that it can “trigger full-blown mania,” not that it is a depression treatment.

Guzey says:

Lack of sleep is such a potent trigger for mania that acute sleep deprivation is literally used to treat depression. Aside from ketamine, not sleeping for a night is the only medicine we have to quickly – literally overnight – and reliably (in ~50% of patients) improve mood in depressed patients (until they go to bed, unless you keep advancing their sleep phase ). NOTE: DO NOT TRY THIS IF YOU ARE BIPOLAR, YOU MIGHT GET A MANIC EPISODE.

I did not interpret this as saying sleep deprivation treats depression by causing mania. Instead, I think Guzey is suggesting that sleep deprivation treats depression through a neurological pathway that can also lead to mania in bipolar patients. I think it’s fine to ignore this point if you’re not interested in addressing it, but I don’t think it’s fair to characterize your reference to “trigger full-blown mania” as a clear acknowledgement of sleep deprivation’s therapeutic benefits for some depressed patients. If that was indeed your conscious intent, then my feedback is that your writing was illegible in this area.

As a caveat, it seems like you might have inferred from Guzey’s overall post that he has a positive impression of mania. I think this is belied by phrases like “DO NOT TRY THIS IF YOU ARE BIPOLAR, YOU MIGHT GET A MANIC EPISODE,” but not an impossible takeaway.

Overall, I don’t think the errors you pointed out so far were particularly glaring… 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 agree with your assessment, and Guzey really ought to read your article in depth before throwing shade on it. I think your commitment to constructive dialog is admirable here.

[Natália]

Switching to mania from depression usually (though not always) means that the depressive symptoms went away. But I agree that my phrasing was poor and I’ll edit it.

[guzey]

Hi Natália,

I want to apologize for lack of proper engagement with the post and lack of replies to you as well as a high level of combativeness in the comments I did leave.

This stuff makes me anxious and I feel like I’m just unable to properly explain what makes me disagree so much with you.

My best attempt is that my takes are some combination of:

1. Academic literature is a highly adversarial playing field and although it’s very tempting for smart outsiders to think that they can just go on Google Scholar and figure out what’s going on, I don’t think this is possible for the vast majority of fields of science and this is certainly not possible for sleep literature. It seems that this surface-area survey is basically what you tried to do and my understanding is that you

   1. never studied biology or neuroscience with critical discussions with specialists in the field

   2. never discussed the papers in-depth with people in the field

   3. never tried to holistically assess the quality of the literature

   4. never studied the history of science in-depth and the dynamics of scientific progress in general

2. very deep skepticism of sleep literature and the knowledge of how entire fields of science can be led astray and become detached from reality with me becoming convinced that this is indeed what happened with sleep science, thus me being extremely selective with the kind of evidence I take seriously (I tried to explain this in https://​​guzey.com/​​theses-on-sleep/​​#our-priors-about-sleep-research-should-be-weak).

   1. Thus, I have absolutely no issue with me disagreeing with meta-analyses in the field. They very barely count as real evidence for me in fields like sleep science.

   2. The “successful replications” you appeal to similarly just don’t count for me. I have a pretty simple model of how they happen: sleep scientists sit around and come up with an experiment to do. Then if the experiment shows something in line with “sleep good, no sleep bad” they publish it; otherwise they try to make it seems like it’s “sleep good, no sleep bad” or just don’t publish it.

      1. Why would I think that such a strange thing happens? Because I think that the field is dominated by people who have the view “sleep good, no sleep bad” and publishing anything else is way more difficult + people usually become sleep scientists because they think that sleep is very important.

         1. Mass preference falsification is real https://​​www.youtube.com/​​watch?v=PW2kxREtdCs, mistaken consensus is real.

3. personal experience (very deep conviction that brains are totally fucked up and try to trick us all the time while also being incredibly liable to both self- and external psyops e.g. https://​​guzey.com/​​personal/​​my-journal/​​, e.g. my video game addiction, e.g. me literally falling asleep when I become anxious or really bored, e.g. me sometimes sleeping 3 hours and feeling fine without any stimulants and sometimes sleeping 8 hours and feeling sleepy, me knowing how much the expectations affect the mental state and how the video game addiction can be literally get expunged from my brain and be brought down to 0 by saying a single sentence to my wife [it is “I will not play video games for {duration}”]; me personally literally jumping out of bed without an alarm after 3 hours of sleep if i’m allowed to play video games and at the same time ability to sleep 8-9 hours in most other cases)

   1. You called some of my explanations of self and external psyops “epicycles” (in particular, the picture with how lack of sleep per se doesn’t actually lead to lack of productivity) but I’m very confident that brains do stuff like this to us all the fucking time (my one certainly does). Most people are just not very good at introspection and don’t notice this.

   2. mass psychogenic illness is real https://​​en.wikipedia.org/​​wiki/​​Mass_psychogenic_illness

4. 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.

   1. (Sleep deprivation can certainly increase energy/​decrease brain fog/​etc. both on depressed non-bipolar people and bipolar people in general and it seems that people in general are affected (e.g. https://​​www.reddit.com/​​r/​​slatestarcodex/​​comments/​​9tpk94/​​writing_in_the_morning/​​?st=jozurz3y&sh=4c0150e1).)

   2. 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?

5. to continue the previous points. The evidence I take seriously is:

   1. trusted personal experience

      1. where the way “trusted” experience are chosen relies on lots of heuristics, background knowledge, intuition, etc. and for an outsider it might look like cherry-picking, “epicycles”, etc. (this also applied to 5.2 and 5.3 below)

   2. trusted anecdotes

   3. trusted field observations

   4. n-of-1-proof-by-contradiction-style arguments

      1. e.g. “A single-point mutation can decrease the amount of required sleep by 2 hours, with no negative side-effects” and “A brain surgery can decrease the amount of sleep required by 3 hours, with no negative-side effects” from my theses are good examples of this. My take is that just these two examples invalidate large chunks of the sleep literature by showing that normal people can have something tweaked just a little bit, radically decrease the amount of required sleep but remain the same otherwise, which simply would not have been possible if these 2-3 hours of sleep they lost were essential for anything important.

      2. Similarly with anecdotes of people sleeping very little for days on end yet being very functional because they are very stressed out/​caffeinated/​etc. The brains just keep working! Here (https://​​www.youtube.com/​​watch?v=3xtwu0xOrls), for example, you can see a 2004 UK TV show in which volunteers slept an average of 1.5-2 hours a night for about a week competing for 100,000 pounds. Yes, they become pretty sleepy over time and the cognition of some of them becomes pretty fucked up. But then, many of them remain close to 100% functional even after many days of super severe sleep deprivation (they don’t have bipolar or anything like this—just normal people), as you can see from the later episodes. Again, this TV show from 2004 for me invalidates probably like 90% of published sleep literature because according to the sleep literature consensus people should become almost incapacitated under such conditions and yet they just don’t when they are sufficiently motivated.

      3. Similarly with Walker. I believe that he’s a charlatan. He doesn’t know the most basic facts about sleep (as the single most outrageous example for me, in paragraph 2 of chapter 1 of his book he wrote “Routinely sleeping less than six or seven hours a night demolishes your immune system, more than doubling your risk of cancer.”), if you watch his talks, it’s very clear that he just has no ability to evaluate evidence critically or just doesn’t care. The fact that a charlatan directs the Center for Human Sleep Science at UC Berkeley and that he gives premier talks to neuroscience conferences tells me that that the entire field is deeply deeply broken. This, even with n-of-1 simply should not happen and shows that there are no well-functioning error-correction mechanisms in the field.

6. 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”.

7. BDNF thing is, I think, much stronger than you appreciate because: sleep literature is SUPER pro sleep. For everything under the sun they try to show that sleep is good, no sleep bad. The very fact that there’s an open debate with lots of papers showing that BDNF is increased when you are sleep deprived, tells me that there’s something super interesting going on, as otherwise the entire literature would very quickly converge on “oh yeah, just like with everything else good under the soon, BDNF decreases with lack of sleep”

Coincidentally, I wrote this comment after less than 3 hours of sleep today (had 100 mg of caffeine 5 hours ago and another 100 mg of caffeine 3 hours ago).

[Cobblepot]

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!

[Rafael Harth]

I’m pretty surprised at Guzey’s tone in responding; even this last response starting with an apology makes arguments that suggest argument motivated by some sort of psychological trigger rather than rational consideration.

I don’t know if this generalizes, but my experience with tone is that it’s mostly unintentional. There’ve been many instances where I’ve written something that seemed perfectly appropriate to me at the time, only to be horrified at how sound when I read it a month later (and the result pattern-matches to guzey’s comment). It also does not require a psychological trigger, it just happens by default when arguing with someone in text form (and it happens more easily when it’s about something status-related like who made better arguments). Took a lot of deliberate effort to change the default to sounding respectful.

I agree that it’s bad enough to be worth mentioning, but I’d be quite surprised if it’s the result of a strategic effort rather than of an unconscious signaling-related instinct.

[Dustin]

I agree with you.

I’ve found that I’ve lessened this experience of reading something I’ve wrote and being horrified at its tone by going back and reading my comments at various sites. At least once a year I find myself going to my profile page at LW or some other site and just spending a couple of hours reading what I’ve wrote in the past. I think this has helped me be more aware of what my tone is conveying.

[Natália]

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.

I have a tentative guess on why he’s doing that, based on Scott Alexander’s post about trapped priors.

I’ll give an example of the basic problem outlined in the post myself, to spare you from having to read all of it before understanding my comment. Suppose that a physicist spends two hours trying to convince you that the Earth is flat. Would you see that as strong evidence that the Earth is flat? Personally, I’d see that as extremely weak evidence. Instead of updating much that the Earth is flat, the conversation would instead make me seriously consider the following more-plausible-to-me hypotheses:

• The physicist really enjoys pulling very elaborate pranks on people.

• It’s April fools or something similar and I for some reason just haven’t realized it yet.

• The physicist currently has some sort of untreated psychosis.

• Any physics department the physicist has studied or worked on is extremely terrible and ought not to be trusted in the future.

• I am hallucinating, or otherwise have perceptions of the world that don’t track reality. Perhaps I’m in a dream, perhaps I have extremely-early-onset Alzheimer’s, perhaps I’m on a potent perception-altering drug.

Similarly, if I saw a lot of studies claiming to show something absurd like that prohibited-by-the-laws-of-physics “psychic” phenomena are real, I won’t need to read their methodology to conclude that there’s something wrong with them. And if a group of people claims to have such psychic powers, I won’t think twice before dismissing their personal experience as unreliable. And, at the same time, I’ll accept, without batting an eye, studies and anecdotes claiming that such powers are not possible.

So dismissing arguments from experts, studies, and personal anecdotes as horribly flawed and no more than weak evidence — even before trying to assess their quality — is perfectly reasonable and Bayesian if they’re claiming something that you think is absurd. But clearly, if you have that attitude towards a belief of yours that does not reflect the territory, that will be problematic.

Guzey’s attitude towards sleep research and anecdotes seems compatible with him having a prior that it’s outright absurd that sleep restriction could be harmful. And, like, it’s not an epistemological sin to be born with that prior. But it does mean that what he sees as very weak evidence against his theses won’t necessarily be very weak evidence for people with different priors, if he can’t explain why he thinks that sleep restriction being harmful is absurd.

(I’m not claiming that that is what is going on here. I just thought that the idea of trapped priors was probably relevant.)

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.

My main objection to Guzey’s response would be a bit different than yours here. I’d point out that I haven’t argued anywhere that “sufficient sleep” is required for “proper functioning,” and that the meta-analyses I quoted don’t purport to show that either. Rather, they report the magnitude and direction of the effect of experimental sleep restriction on e.g. cognitive ability across a variety of different studies, and the magnitude of the effect they show, although substantial, is a far cry from being enough to outright incapacitate you from most everyday tasks. Guzey seems to be responding to a claim like “people do worse on math exams when they’re tipsy compared to when they’re sober” with “but have you talked to tipsy people? They act almost entirely normally!”

[Benquo]

If a physicist were to spend two hours trying to explain to me how they knew that the earth was flat, I’d expect to come away from that conversation with a better understanding of the physical world or the social construction of physics knowledge, which would better help me navigate my life, even if I ended up wronger on the bottom-line answer—because that’s how epistemically persuasive explanations work, they have to show an ability to win bets either more often or with less computational cost than alternative hypotheses.

[Vaniver]

I feel sort of weird about the ‘trapped prior’ point, because I think it’s more reasonably pointed at academic fields than individual people? Like, it is not that surprising for an academic field to have ‘core beliefs’ that everyone who disagrees with is ‘not in the field’, given the forces that people in the field can exert on each other. One fun example of this is PhilGoetz’s post Too Good To Be True, wherein he points to a claim that out of 60 studies studying vaccines and autism, none of them find any link, and then observes that by standard frequentist analysis, ~3 of them should have been significant at the p=0.05 level, and getting none of them significant at that level is pretty unlikely without suppression. And it’s obvious why there would be suppression; no one wants to give ammunition to the enemy.

Separately, it feels like it doesn’t really distinguish ‘justified priors’ from ‘unjustified priors’. If you tell me that a psychology experiment found evidence of psychic effects, I will basically just not believe it. But hopefully if you transported my mind to a universe where psychics were real, I would believe the corresponding studies in those universes—because I had seen things like dowsing being used by oil companies in that universe. This is, from the perspective of a new study, ‘my prior’, but that prior is built out of all of the evidence that I’ve seen before. It’s kind of fair to call my position on psychics a “trapped prior” but it feels more fair to call it “a mountain of evidence”.

[Yonatan Cale]

I’m pretty surprised at Guzey’s tone in responding; even this last response starting with an apology makes arguments that suggest argument motivated by some sort of psychological trigger rather than rational consideration.

Maybe better to assume good intentions? (And even if someone is biased or motivated by “impure” motives, we try to turn this into a high quality discussion if we can?)

[Cobblepot]

Fair point, although I wasn’t assuming any bad intentions, more like a hard-to-explain emotional intensity that seemed out of character for someone whose writing I am familiar with. But perhaps expressing my genuine surprise was not constructive—thanks. I removed this intro from my post.

[guzey]

I think that if you ask anyone who knows me in-person they will tell you that I’m an unusually emotionally intensive person. My writing is also usually very emotionally intense but it tend to go through getting feedback from like 20 people who tell me to remove all of the excessive language and to tone it down before publication, so it ends up sounding normal. Comment do not go through this kind of process.

[Natália]

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, and (3) in this comment. 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).

[guzey]

I don’t think you’re engaging with the substance of the argument.

The crux is:

Also, notice that I could have written a post just like yours, with the same kinds of evidence that you use, but instead arguing that sleep deprivation impairs cognition and can worsen mood.

This is incorrect. If you argue that “proper sleep is necessary for x” and I show you a counterexample where a person has x but doesn’t have proper sleep, then however many studies or arguments you give for why “proper sleep is necessary for x”, the argument will remain invalidated, which I claim 4, 5.4.1., and 5.4.2. (which you do not represent accurately in your comment—the participants were able to perform complex mental tasks and function in general at what appears to be ~full-capacity, not just “able to perform basic tasks”) all demonstrate.

[Natália]

I don’t recall having argued that “proper sleep is necessary for x.” ^[1]

I’ve argued that sleep restriction impairs cognition, is associated with negative mood and suicidality (not only positive mood) and causes overeating. Not that you need a certain minimum amount of sleep to perform competently at something. So I still don’t think that the kind of evidence that you bring up is asymmetric.

I’ll come up with an example to explain the difference. Suppose that, after 8 hours of sleep, humans complete a task with an average accuracy of 83%. After 6 hours of sleep, the average accuracy decreases to 71%. And even after a full night of sleep deprivation, accuracy is still 60%, substantially better than a dart-throwing monkey (which would have, say, a 10% accuracy at the task). Suppose that accuracy above 50% is considered acceptable. You point out that the average accuracy of the sleep-restricted/​deprived groups is still pretty good, and argue that this shows that sleeping 8 hours per night, or sleeping at all the previous night, is not necessary to complete the task acceptably. And obviously, you’ll be right — but that wouldn’t be an argument against the claim that sleep restriction impairs performance on that task.

you do not represent accurately in your comment—the participants were able to perform complex mental tasks and function in general at what appears to be ~full-capacity, not just “able to perform basic tasks”

I edited my comment. Notice, however, that it’s still unclear how people in the show would be doing in a rigorous assessment of cognition not subject to learning effects, and, as far as I know, we don’t know how well they did on their tasks compared to their baseline performance.

1. ^

   Claims of that sort would not be very general, and their truth-value would obviously depend on what you mean by “necessary,” so I don’t think they’re that interesting. Also, in some tasks there’s probably a very big difference between acceptable performance and peak performance.

[wslafleur]

Does anybody know if there have been any sleep-deprivation studies that attempt to control for belief effects? I’m think about this sort of thing. The knock-on ramifications in either direction seem like they could be potentially significant. Among other things, belief effects could help to explain the swaths of contradictory studies around this topic.

[Natália]

This isn’t as important as my previous reply (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 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).

[ChristianKl]

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).

Domain experts usually do learn not only from public information. When it comes to the question of whether or not to believe a scientific paper domain experts usually learn the skills from talking with their collegues.

I had one bioinformatics professor who made a point of saying something in every lecture about how we shouldn’t just believe the literature and how there’s a lot of mistaken papers out there.

One of your disagreements with guzey is whether “X is true because a meta-analysis says so” is a reasonable argument.

(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]).

Talking to people is a good way to understand how untrustworthy they are.

[Ben Pace]

Thanks for this post, I’ve curated it! Reason why include:

• In general when we curate a post (e.g. Theses on Sleep) I like curating thoughtful critique of the original post.

• While I got a useful new mental model from Theses on Sleep about how to think about sleep, this post has done the valuable work of bringing up a lot of the counterarguments. I didn’t put in the time to do it myself, so seeing the strength of them and critiques of various specific lines of reasoning in the prior post gives me a far better sense of how strong the arguments were in that post.

• This post brought together a bunch of different types of reasoning that I really like, not only digging into the literature but also concluding with a series of claims-plus-probabilities, and also a ton of quotes from subreddits to show the first-person experience of sleep deprivation. It was also pretty clearly written and readable, which is rare when doing a dive into scientific literature.

• The discussion in the comments has continued to be pretty high quality and helpful, I’m especially thinking about AllAmericanBreakfast’s contributions.

[DirectedEvolution]

Conditional on this, cognition does not return to baseline levels after several months of sleep restriction: 78%

Does this mean you’re conditionally claiming that several months of sleep restriction results in permanent damage to cognitive faculties, irreversible even after long-term restoration of normal sleep?

[Natália]

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.

[DirectedEvolution]

Thank you for clarifying!

[Foop]

Anecdotally, since reading Guzey’s post a month ago, I cut down my sleep from ~7.25 hours (5 nights 7.5 hours + 1 night 6 hours) to around 6.33-6.5 hours (1 night 7.5 + 2-3 nights 6). I found that doing just 6 hours 4+ days in a row led to noticeable tiredness, although I never tried just pushing through and seeing if I can get used to it.

Regardless, with the current sleep load, I feel pretty good, and I plan to continue it. However, I have noticed some rare working memory slip-ups, maybe one per day or every other day, that I don’t think were as common before I dropped the sleep, although this isn’t severe enough to make me want to stop.

[Elizabeth]

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

[Viktor Rehnberg]

There is something about Natália’s and Guzey’s interaction through your posts and in the comment section that doesn’t feel right to me. I haven’t been able to pin down exactly why I get this feeling but my best guess is that it seems like you are missing your actual disagreement.

To me it seems like you are both agreeing on the existing evidence is week. You bring up evidence that point in different directions sure but neither of you seem to bring up strong evidence.

However, you seem to have quite different beliefs on the matter. Natália says:

Our priors about sleep research should be high

I feel grumpy, dumb and distractable every time I sleep less than 7 or so hours. I can’t do things that require focused attention like solving physics homework problems very effectively, and I don’t get nearly as much pleasure when I attempt doing so. My memory becomes very poor: after a recent night of <6 hours of sleep, I somehow forgot the reasoning behind several Manifold Markets trades I had made the prior evening and just stared at them in utter confusion for several minutes before remembering.

and high priors would explain quite high odds (19:1 in two cases) given for the posterior despite what seems to be fairly week evidence^[1]. However, note that the reason for this prior seem to be based on personal observations and on abrupt changes in sleep schedule. I agree about the observation that reducing the amount of sleep does impair my cognitive capacity in the short term, but then the same applies to the week after adding or removing daylight saving times from which I do cope quite well after that week. It seems unclear to me if a gradual change in the amount of sleep would have a significant impact without some good data.

On the other hand, Guzey also seem to put most weight into anecdotal evidence. It seems to me that one real possibility that there are large individual differences which would explain that your different priors and why you can find anecdotal evidence both for that little sleep is bad for you and that you can get by with less sleep than otherwise claimed.

The competing hypothesis is that most people are bad at judging how much sleep they need and how their sleep amounts affect their health. This would mean that priors based on own experiences and similar experiences from some other people should not carry much weight when applied to people in general. Furthermore, that the few existing studies with reasonable methodologies measuring effects which are not just reported by subject’s experiences are relatively more important.

1. ^

   Most of the stated posteriors in the conclusion are something I find reasonable when applied to myself but I wouldn’t use so strong posteriors when applied to people in general.

[DirectedEvolution]

Another odd discrepancy.

The largest single study in the Lowe meta-analysis is Banks (2010), which had 159/​1688 of the participants (9.4%). 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. In addition, I don’t understand how they would have incorporated effect sizes into their meta-analytic procedure.

Given that this single study is a large proportion of their total participants, and that the meta-analysis analyzes the mediating effect of days of cumulative sleep restriction on cognitive function, I think this is potentially important to understand better. I’ve emailed the author to ask about this. If and when I hear back, I’ll let you know.

[Natália]

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.

]

[DirectedEvolution]

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

I’m not sure why that’s relevant to my question? They still did 5-6 days (depending on whether you count the recovery day, on which many SR subjects got even less sleep than before) of sleep restriction in total. Unless Lowe is only counting the results from the first day of sleep restriction, which is possible but seems unlikely, describing this as 1 day of cumulative sleep restriction duration seems inaccurate. However, I will withhold judgment until I hear back from Lowe.

[Natália]

Huh. I had assumed they might have been only including the first day, but you’re right that that’s unlikely. Probably a typo.

That wouldn’t change their overall meta-analytic effect sizes, though, since they aggregate across different durations of sleep restriction when calculating it.

[DirectedEvolution]

Dr. Lowe did get back to me briefly to say she’s looking into it. I’ll post an update when I hear back.

[DirectedEvolution]

If it was indeed a typo (there is at least one more in the same table—Saleh (2003) is duplicated when there should be one entry for 2003 and one for Saleh 2011). On the other hand, it’s possible it was miscoded or misinterpreted. I’d be surprised if that were the case, but it’s hard to see, for example, how they came up with a number for “mean hours of sleep deprivation” given the 6 different cases for the recovery day sleep in the experimental group, or whether they code an effect size for the group that was sleep deprived for 5 days and then got 10 hours of sleep on the recovery day.

[guzey]

Thanks for the taking the time to look into my essay.

Mendonça’s claim 1: Guzey’s /​r/​BipolarReddit evidence is misleading

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. 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 am similarly puzzled by a later accusation:

Guzey claims that “most sleep research is extremely unreliable and we shouldn’t conclude much on the basis of it,” but there are problems with that. Firstly because he doesn’t seem to believe that about sleep research that favors his hypotheses. Guzey, after all, uses sleep research to show that Matthew Walker’s book is terrible and fraudulent. So it seems that he wants to trust sleep research when it says that sleep deprivation is not as bad as Walker shows, but doesn’t want to trust it when it says that sleep deprivation is not harmless.

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, preferring to show my readers Reddit comments left by bipolar people, instead of meta-analyses, and why, when I do use meta-analyses, I use them very cautiously. For example, in the essay, I used a meta-analysis exactly once when I noted in a point I dedicated to a paper about a study of hunter-gatherers that “There’s no causal evidence that sleeping 7-9 hours is healthier than sleeping 6 hours or less. Correlational evidence [from a meta-analysis] suggests that people who sleep 4 hours have the same if not lower mortality as those who sleep 8 hours and that people who sleep 6-7 hours have the lowest mortality.”

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.

Mendonça’s claim 2: Chronic sleep deprivation might be associated with *decreased* BDNF expression, as shown by Guzey’s own sources

I believe that it is similarly confused. I write about sleep deprivation causing increase in BDNF. What does Mendonça have that contradicts my writing, supposedly by papers I cited myself?

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.

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.

I regret citing this paper in my essay but it’s indicative of the overall depth of Mendonça’s arguments: 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.

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 and 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 don’t have the ability to go through every claim in the post and show what exactly is wrong with them, but my read that the rest are similarly confused: they seem to be somewhat related to what I wrote but mostly misinterpreted with their misinterpretations being “refuted” or shown “misleading”.

[Natália]

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 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 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.

[DirectedEvolution]

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 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.

[DirectedEvolution]

Sleep compression and restriction is also used as a treatment for insomnia. From the sleep foundation (not a great source, but I think this is an OK as a description of the technique):

Sleep restriction and compression: These two methods aim to improve sleep quality and quantity by reducing the amount of time a person lies in bed. A CBT-i practitioner can use records from a patient’s sleep diary to determine how much time they sleep each night compared to the amount of time they lie in bed awake. Sleep restriction involves a sharp curtailing of time in bed while sleep compression is a more gradual process, but both techniques are intended to achieve the same goal: less time in bed awake each night.

I think this highlights that we need to distinguish between “spending more time in bed” and “getting more sleep.” More on this later.

[Natália]

None of the respondants from the r/​BipolarReddit thread you quoted 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:

[DirectedEvolution]

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

[skot523]

I think the value was in the interesting idea rather than being particularly rigorous

[DirectedEvolution]

The effects of napping found by the meta-study you linked are more complex than your quote suggests:

The literature reports that the benefits of daytime napping may last 2.5 h [68], with conflicting results during the sleep inertia period, i.e., after awakening [55,69]. These findings were in accordance with results from our study, in which the positive effects of the nap were mainly 30–120 min following awakening. For the 30 min after napping, results were mitigated and variable, depending on sensitivity analyses, reflecting putative effects of sleep inertia [16]. Even if we did not find an influence on the duration of the nap, the literature suggests that short naps may benefit more on cognitive performance—possibly because napping more than 30 min produces sleep inertia, making nap benefits obvious only after a delay [55]. Sleep inertia reflects a transition from a sleep state to a waking state [19] and is characterized by a reduction in the ability to think and perform upon awakening due to sleep [55]. This period is a state of grogginess, confusion [70] and lowered arousal [71,72]. The magnitude of sleep inertia is mostly dependent on the quantity of slow-wave sleep contained within the nap [73]. Sleep inertia is greater following longer naps that typically contain more slow-wave activity than shorter naps [11,74,75]. So, to avoid sleep inertia, naps should be short (20–30 min), and should not occur at the bottom of the circadian phase [76,77]. Paradoxically, in older adults [78] and not in middle-aged workers, napping might both increase morbidity [79,80,81,82,83]—cardiovascular disease, falls and cognitive impairment—and mortality [84,85,86,87]. Daytime napping could also diminish the quality of sleep at night [8].

You didn’t explicitly claim that napping has no ill effects, but since one important thrust of your counterargument and complaint is that Guzey’s selectively reporting those aspects of the research that favor his claim, I think that you should subject yourself to the same standard.

Note that I haven’t read anything else from this meta-analysis; my only objective in reporting this is to highlight the omission. I can’t vouch for whether or not the meta-analysis is high-quality, and I’m conflicted about whether or not the costs and benefits of napping seem important to the overall debate.

[Natália]

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.

[DirectedEvolution]

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.

[Natália]

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:

[DirectedEvolution]

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.

[Natália]

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.

[DirectedEvolution]

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

[Shmi]

I’m surprised that tinkering with sleep is even an area of interest in LW circles. It’s a classic Chesterton’s fence not to mess with. Short-term sleep deprivation is fine and happens all the time, chronic sleep deprivation is bad, don’t do it, focus on some other ways to squeeze more time out of the day, if that’s what one is after. Leave the sleep research to the professionals, it’s not a low-hanging fruit.

(Unless you intentionally sleep deprive to trigger bipolar hypomania and are reckless enough to risk it turning into a full mania.)

[DirectedEvolution]

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.

[Shmi]

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 :)

Indeed. And sleep is one of those, erected by evolution, pervasive across species, but with no clear reasons. Playing with it without clear understanding of what is going on is bound to backfire. Yes, as a pure exercise in rationality it is interesting. It is also called “science of sleep” and best done professionally. As a way to save time or to do self-experimenting, it’s definitely not the way to go.

[DirectedEvolution]

Your advice here is too imprecise to be debatable. What’s the line between normal sleep variation, individual sleep differences, and “playing with it?” If we don’t feel tired (as in mania), are we “playing with sleep” if we simply stay awake, as we feel inclined to do, or are we “playing with sleep” if we indulge in staying up late?

When you say that it’s “bound to backfire,” can you turn this into a claim precise enough to make into a bet?

When you say it’s “best done professionally,” do you mean that we should leave it to professional sleep researchers to run such studies, or that we should simply get the FDA-recommended amount of sleep and not ask why?

If you can make your claims precise enough to match the level of care, thought, and rigor on display here and in guzey’s original post, I’d love to engage further!

[Shmi]

Can’t promise the “level of care, thought, and rigor on display here and in guzey’s original post” in a single comment. Seems like asking a lot. But, to answer some of your questions:

• In mania you are not playing with it, it is playing with you, and you have little control of what is going on. It is also known to be unhealthy in various ways.

• By “playing with sleep” I mean not going with the flow by staying up or staying awake, but methodical deliberate attempts to change one’s sleeping patterns.

• “Bound to backfire”: it is well established that chronic sleep deprivation leads to various side effects that are discussed in the OP (and also argued against by Alexey). One pitfall is that it is not just the side effects, but the inability to tell that something goes wrong as a result of sleep deprivation, thus destroying an essential feedback mechanism.

• “Best done professionally” means exactly that, “professional sleep researchers”. Someone who is qualified and is not sleep deprived while doing the research on willing subjects, or on those who are stuck with unusual or poor sleep. “we should simply get the FDA-recommended amount of sleep and not ask why” seems silly enough that I have trouble believing you actually considered that as something I might have suggested.

Not sure if this is up to your standards, but I guess I tried.

[DirectedEvolution]

This definitely helps, so thank you.

• By “playing with sleep” I mean not going with the flow by staying up or staying awake, but methodical deliberate attempts to change one’s sleeping patterns.

It surprises me that you’d find relatively impulsive and ill-considered modifications of one’s sleep routine to be preferable to a carefully thought-through approach. Can you say a little more as to why you hold this opinion?

• “Bound to backfire”: it is well established that chronic sleep deprivation leads to various side effects that are discussed in the OP (and also argued against by Alexey). One pitfall is that it is not just the side effects, but the inability to tell that something goes wrong as a result of sleep deprivation, thus destroying an essential feedback mechanism.

I think we all pretty much agree here that sleep deprivation comes with downsides. It’s really the magnitude of those downsides, potential for upsides, the impact of those downsides on things like health and functional performance that are in question, and how the downsides weigh against the benefits of ~12% additional waking hours that’s in question. While it’s fine to point out that downsides exist, your tone seems to imply that you believe that the existence of downsides settles the matter, while it seems to me that the whole point of broaching the discussion in the first place is that Guzey and I (and others) think it’s worth discussing.

• “Best done professionally” means exactly that, “professional sleep researchers”. Someone who is qualified and is not sleep deprived while doing the research on willing subjects, or on those who are stuck with unusual or poor sleep. “we should simply get the FDA-recommended amount of sleep and not ask why” seems silly enough that I have trouble believing you actually considered that as something I might have suggested.

I don’t think it’s silly to have interpreted you that way. After all, nobody here has suggested actually running any sort of formal sleep study. What we’re all clearly doing is discussing the published results, along with anecdata and our own ideas. You might have been referring to our own personal choices about how much sleep to get as a form of “sleep research,” but given the fact that people vary and try to optimize and improve their sleep all the time, saying that people should not do this sort of “sleep research” would seem silliest of all to me, so I assumed that was not what you meant. Perhaps you could be more specific about what activity you’re recommending people avoid when you say to “leave the sleep research to the professionals?”

[Shmi]

From a bunch of downvotes I assume that people don’t want to see the types of comments I have made about tinkering with sleep being unwise, I think I said enough, anyway.

[DirectedEvolution]

Up to you! I’ve been upvoting you, though. My main concern in this thread is that I don’t want to see an opportunity for constructive debate stifled by people’s feelings getting hurt, or by frustrating levels of imprecision. So I find it annoying that people are downvoting you when you’re making an effort to provide an alternative perspective. If you’d like to PM with other thoughts, please do.

[frankybegs]

I don’t think your ‘our priors about sleep research should be high’ argument holds, for the simple reason that everyone knows, now, that you’re supposed to be tired and grumpy when you get less than “your eight hours”. There is almost certainly a placebo effect in play, which means that you may well be allowing the sleep research itself to affect your priors about the plausibility of the sleep research!

[Elizabeth]

This doesn’t undercut the rest of the post, but I do think “Occasionally stubbing your toe is good for health and promotes more efficient toe healing” is unfair. 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. Of course those beliefs could be wrong, or sleep could not be a member of the set, but if the hypothesis were incorrect I think it would be a normal kind of incorrect, not something as ridiculous as “breaking a bone is good for you”.

[Matthew Barnett]

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?

[DirectedEvolution]

I agree with Elizabeth that it intuitively feels like SD fits more with things like exercise and infection than things like toe-stubbing. I did not have a ready-made answer before you asked the important question “why?,” and I think that means you should discount this somewhat as rationalization. With that caveat, here goes!

First, let’s look at some of the underlying physiological impacts of these potentially “good stressors.”

• Exercise: tear and repair of muscle fibers results in altered morphology

• Infection: repeated exposure results in death of dysfunctionally reactive immune cells

• Fasting: hormone changes in response to change in metabolism (I’m handwaving to the max!)

• Extreme temperatures: one impact is that elevated body temperature causes the release of heat shock proteins, which directly impact immune system function, such as by increasing MHC class I loading (this is an important role of fever in fighting off infections). It also affects the material properties of proteins, which could impact things like flexibility but also enzyme reaction rates (though not necessarily in a straightforward way, since the body attempts to create homeostasis and there are all kinds of feedback loops).

Let’s start not with a stubbed toe, but with breaking a bone. What does this lack that excludes it from the potentially “good stressor” category, or what does it include that puts it in the “bad stressor” category?

Clearly, bone breaking is incredibly, durably painful. It potentially permanently alters the physical shape of bones in a way that can easily destroy their ability to naturally regain their original shape. Since the body depends on the skeleton to operate muscles effectively, strength, flexibility, and dexterity may be impacted as well. Furthermore, bone breakage may cause large-scale tearing of soft tissue and generate a massive infection site, potentially concomitant with tearing of blood vessels and solid organ puncture. These large-scale physical impacts are what put bone breaking into the “bad stressor” category, and I think it’s safe to say nobody in their right mind would hope to find some countervailing positive effect that’s worth this massive cost.

As we scale down the magnitude and duration of pain, the extent of physical tissue destruction, the destruction of the skin’s barrier against infection, we overall scale down many of the things that put an acute stressor into the “bad” category, potentially allowing any benefits it may have to become relevant.

Since sleep deprivation entails no tissue destruction, except insofar as it impacts synaptogenesis or axonal pruning (a field of study where our knowledge is quite patchy!), we can’t start from a physical assumption that it’s obviously bad.

Now, let’s compare with the stubbed toe, and also with exercise.

Exercise, unlike a stubbed toe, is a natural consequence of human activity that’s necessary for life. As such, if there are inherently damaging aspects of exercise, we can expect that evolution has had an enormous amount of time to work on mitigating them. Biomechanical cues impacting development are all over the place in the body. Because it’s metabolically expensive to maintain unnecessary girth, we can interpret the body’s ability to respond to cues saying “grow more and bigger cells here, we’re obviously using them” as a helpful regulatory feature, one that might be evolutionarily advantageous.

By contrast, we also expect nature to put highly aversive pain signals in place where they’re most useful, since pain comes with costs. A stubbed toe isn’t a signal that we’re “using that toe,” but a signal to adjust how we’re walking and of potential injury. There’s again a straightforward biomechanical interpretation to be found.

Although sleep pressure is often aversive, this aversion comes from an entirely different physical system, and it’s not clear that it means the same thing. In addition, I can control my sleep aversion to an extent that’s impossible without drugs when it comes to pain. The controllability, modest extent, origin from a source other than tissue trauma, and context as part of the normal pattern of behavioral variation in organisms on a day-to-day basis set sleep deprivation apart from a stubbed toe and in the category of exercise, exposure to pathogens and chemicals, fasting, and temperature variation.

None of this necessarily means that sleep deprivation (or any of these other “relatively normal, non-injurious” interventions) is good for you.

If they were, though, we might offer a unified meta-reason. In general, all these sources of variation may be ways to supply useful regulatory cues to the body.

Now, let’s zoom in on sleep. Even when we look specifically at sleep research, as opposed to work-related fatigue, we have a confounder that I suspect may not be adequately addressed.

This is light. Where I am, it’s 1:20 AM, and I have the slights on blazing bright while staring into my computer screen. In addition to my wakefulness, my body us receiving a cue about when light is available. Returning to the evolutionary biology lens, this would be ancestrally correlated with my ability to hunt, my concerns about predators, social activity, the season, and so on. Potentially, more sleep goes with more darkness goes with less abundant food and social opportunity goes with hibernation. More wakefulness would be ancestrally associated with more abundance and opportunity and fewer predation threats. This is aside from the fact that we can actually do more while awake, which may have additional benefits if we use our time wisely.

So this is a candidate for a reason why sleep deprivation could have some benefits. It could either be entirely due to light exposure during additional hours of wakefulness, or to wake and sleep being used as proxies for opportunities while awake. The idea that light cues and circadian rhythms are important controllers of our behavior and experience are already well-established (light therapy is a depression treatment, as is sleep deprivation).

A second possibility is that sleep deprivation could, on its own, diminish bad forms of mental and emotional stress. Hear me out! Usually, when people are sleep deprived, it’s because they’re trying to cope with some very stressful circumstances—a new baby, a demanding job, an upcoming exam, jet lag, a war or other stressful environment. So it is associated with high stress, and often perceived to be at least a contributing cause of it.

However, it’s easy to picture how sleeping for fewer hours, in these situations, is often a way to reduce and manage that stress. You are able to take care of activities that need to be done with those additional waking hours, thereby removing sources of worry and discomfort that would otherwise bother you while you’re trying to sleep.

So imagine if regular folks, without any extreme stressors, chose to take a couple extra hours awake to take care of random lingering sources of discomfort or stress. A couple extra hours per day could easily be the difference between “I have only just enough time to get everything done” and “I have plenty of time to relax and make improvements to the conditions of my life.” In this case, we’d see sleep deprivation reducing people’s stress over time.

Note that neither of these hypotheses are out of the bounds of our familiar experience. Plenty of people have said “oh, if only I had an extra hour or two in my day.” We already use both sleep deprivation and light therapy as depression treatments, and they fit naturally into the category of environmental and behavioral cues regulating physiological processes.

In fact, the real mystery is why sleep deprivation should be bad for us, not why it should be neutral-to-good for us. Not all animals sleep, and amount of sleep isn’t really correlated with cognitive capacity as far as I remember (I’m being lazy and not looking up the relevant study, sorry!). We also have a great alternative explanation for why animals sleep: to reduce metabolic demands during times of high threat and low light, as in hibernation.

One physiological reason to think sleep might in fact be important is that the brain, like other organs, may need to physically alter its morphology in order to accomplish maintenance tasks. These might include learning-central tasks like synaptogenesis, but it also might just entail things like clearance of fluids. I think it’s fairly well-established that this does happen during sleep. In addition, I understand that it’s not just the physical connectivity of synapses, but also the overall flow of electrical potential throughout the brain as a whole, that governs thought. So it’s plausible that sleep is necessary to perform essential maintenance tasks that degrade the physical ability of the brain to function properly if they aren’t done. Alternatively, it might be that these maintenance tasks will intrude into the waking hours, disrupting cognition in an unpleasant fashion, if they don’t happen during sleep.

[Elizabeth]

Broadly, they train your body’s homeostasis mechanisms to handle a wider range of conditions, which lets it cope better with aging.

For the immune system in particular, it’s pretty well demonstrated that childhood disease load is setting expectations for future disease load.

Muscles are strengthened via tiny tears that heal. Tears are stress, too large tears are damage, but small tears are the only way to grow the muscle.

Fasting triggers some hormonal changes that maybe include some housecleaning and repair mechanisms, although I know less about this.

[Elizabeth]

A better answer: in the course of a week, you will naturally spend time eating and not eating, moving and not moving, and sleeping and not sleeping. Calling something “fasting” (as opposed to “not eating right this second”), “excess exercise” (as opposed to “moving”), or “sleep deprivation” (as opposed to “being awake”) is begging the question. It assumes you know the correct balance and are describing a departure from that balance. Meanwhile, stubbing a toe is always a worse state than not having stubbed a toe. The correct amount of toe-stubbing is zero, we can assume any deviation is bad (but then argue about what is slow-motion assault and what is deeply useful trigger point massage therapy).

[The immune system is not a member of the “all things in balance” class. Having zero pathogens and being adapted to an environment with zero pathogens is obviously superior, but the trade-offs are made weird by being an adversarial game with lock-in]

My model is that the finding balance between eating/​not-eating, moving/​not-moving, and sleeping/​not-sleeping, is not always trivial. Your body sends imperfect signals, the right answer varies based on the environment, which changes a lot, and you’re making trade-offs you might not endorse if you had more info. Mild-to-moderate departures from your current balance can be informative in helping you find the correct balance and learn the trade-offs you’re making, even if the experiment ends up being net negative in the short term

You might argue that Alexey specifically used the words “sleep deprivation”. I think that’s a poor phrasing resulting from a bad model being embedded in the language, but if he comes back and says “no, I definitely meant deprivation-as-in-bad-for-you”, it won’t change my belief in this model.

[Natália]

A better answer: in the course of a week, you will naturally spend time eating and not eating, moving and not moving, and sleeping and not sleeping. Calling something “fasting” (as opposed to “not eating right this second”), “excess exercise” (as opposed to “moving”), or “sleep deprivation” (as opposed to “being awake”) is begging the question. It assumes you know the correct balance and are describing a departure from that balance. Meanwhile, stubbing a toe is always a worse state than not having stubbed a toe.

There is something that is similar to eating, moving and sleeping in that respect: exhaling. Over the course of a minute, you will naturally spend time exhaling and not exhaling. The correct amount of time to spend not exhaling is not zero. And failing to exhale acutely stresses your body. But it doesn’t seem to follow from those things that holding your breath once in a while is beneficial.

[DirectedEvolution]

In exercise, breathing, eating, and sleeping, we can perhaps roughly model the system as being driven by an oscillatory forcing function, with some amplitude and frequency, such as of the form Acos(w*t). The point is that although instinct, intuition, and imitation allow us to find parameters compatible with life/​cognitive function/​acceptable performance, we don’t have the data to determine whether or not these parameters are optimal, achievable, or sustainable, nor under what conditions this is or is not true.

We should carefully reserve the word “optimal” and “optimize” for situations where we have some sort of proof or evidence relative to the claim. It’s preferable to use words like “target” or “conventional” or “standard” when we’re discussing parameters that seem likely to work, or that have been shown to work, but that haven’t been clearly shown to be the best for our use case.

We know that a standard sleep length of 8 hours per day for adults is compatible with cognitive function, life, and health, but the argument we are all having here is over whether the evidence is sufficient to say that this is robustly optimal.

[Natália]

My point here is just that the argument “X-to-a-greater-than-usual-extent is an acute stress, and therefore it is good for health” (which was Guzey’s argument) is bad even if X is something we naturally do to a nonzero extent.

I’m probably about as uncertain as you are about whether sleeping 8 hours per night is optimal. (Though my comment was indeed unclear about that before I edited it, so thanks for pointing that out).

[DirectedEvolution]

I think we should understand Guzey’s argument as a gesture in the direction of saying “we should try to establish the base rate for these sorts of stressors [i.e. purposeful behaviors with a normal range of variation in frequency and intensity]” He’s pointing out a few salient behaviors in this reference class (diet and exercise), pointing out that what we might call “sensible variation” is believed to be good for you, and then noting that sleep also belongs in this reference class. You’ve also noted that breathing belongs in this reference class, and we can also find extensive traditions of breath work that are at least meant to promote health.

I agree with others here that toe-stubbing and other injury does not belong in this reference class, because they aren’t purposeful behaviors.

A stronger counterargument is that we may be suffering from availability bias in identifying members of this reference class. We receive lots of messages to breath deep, get exercise, and eat less. What about sensory stimulation vs. lack of stimulation, emotional variation vs. calm, social contact vs. solitude, focus vs. distraction? Do we expect that there’s a “normal range” here that gives you health benefits with “sensible variation?” For example, do we think that people receive health benefits from periodic meditation retreats due to the unusual level of social isolation, calm, and lack of stimulation? Or that they receive health benefits from attending a music festival (sober), due to the unusual level of social contact, excitement, and sensory stimulation?

My uncertainty here is that I don’t know whether we’re restricting this to physical health, and also that I don’t feel confident on what health impacts these additional sorts of reference class members tend to have. intuitively, it seems good for you to get some variety in your life, but on the other hand, will going to the occasional rock concert really improve my heart health (any dancing I might do aside)?

I think that getting some evidence here would be beneficial. However, I also suspect that most of the research is on extremes (i.e. attending too many loud concerts is bad for your hearing), rather than on moving from “moderate” to “sensibly going a little above or below moderate for a while.”

But a few examples of “clearly good for you” in the reference class along with a bunch of examples of “not sure” still puts the valence of “sensible variation” for a member of this reference class as on average positive, though with not much more than 50% confidence.

On the other other hand, the evidence we do have about the impact of sleep on cognitive function is not encouraging. Anyway, the more I think about it, the less clarity I have on how to even think about this question. It doesn’t seem likely to result in a knock-down argument either way, no matter how much we might research it. Too fuzzy.

[Ansel]

I think it’s useful to point out that training muscles for strength/​size results in a well documented phenomenon called supercompensation. However, training for other qualities like speed doesn’t really work the same way. There’s lots of irrational training done because people make an inferential leap from the supercompensation they see in strength training and apply it to cases which intuitively seem like they might be analogues (e.g., weighted sprints don’t make you faster).

I think counterexamples are relevant because sometimes intuition points out real analogues, and sometimes fake ones, so we should value evidence and mechanistic explanation over analogies and cultural beliefs.

Sorry if this is a little incoherent, I wrote it when I was really sleepy.

[Natália]

I feel like there’s much stronger evidence that those things are beneficial than that acute sleep deprivation is. So it’s not clear to me how sleep deprivation is a lot more like those things than like stubbing your toe really hard.

[Elizabeth]

My impression is that people who are used to sleep deprivation (new parents, military, shift workers) are not as impaired by it as people encountering the same level of deprivation for the first time- even when the former group is running on a prolonged sleep deficit, and the latter is going into sleep deprivation fully rested. You never stop being impaired, but past deprivation lets you cope with it better. This pattern matches to me with e.g. fasting will always make you dumb eventually, but people with fasting experience can go much longer before getting dumb.

[Natália]

I agree that this sort of adaptation probably occurs, but I don’t see how this makes sleep deprivation a lot more like those other things you mentioned than to stubbing your toe. Guzey also claimed that “[o]ccasional acute sleep deprivation is good for health,” not only that it promotes more efficient sleep, and for each of your examples of things that are more like sleep deprivation than toe-stubbing is (fasting, exercise, and infections in some cases) the claim does not seem to be that those things impair you but just less so with time.

(For that matter, I would guess that there is also some adaptation to stubbing your toe. It shouldn’t ever stop hurting or lightly and temporarily damaging you, but if you do it a lot you’ll probably find a way to cope with it better, and go back to doing work five minutes later rather than ten.)

[Elizabeth]

you’re right, it’s not quite analogous. I still low-confidence believe in the homeostasis disruption thing, but this isn’t evidence of that.

[jimmy]

This clearly isn’t fair. For one, the “really hard” modifier is completely made up (did Guzey ever imply that the way to train sleep deprivation resilience is to go “really hard” at not-sleeping rather than easing into it?), and for two, physical stress to ones toes is clearly a much more local thing than caloric or sleep deprivation so the hypothesis would be “kicking things in a controlled fashion strengthens the thing you’re impacting with”.

And I’m not sure if it’s true or not, but it’s definitely a thing that professional fighters do, and it does not at all strike me as “obviously false”.

[mikbp]

[Disclaimer: I’m not a doctor and by far I’m not an specialist on health]

First of all, I don’t think the use of “acute” is correct here. Unless I’m misreading the meaning of “acute” in medical jargon [edit: yes, it seems I did. I use acute to mean sever in this comment], acute stress in all these cases is bad for your health and going too far can even cause death. I think it is a (mild to) moderate stress that is good.

It seems to me that the model for “good stresses” are (evolutionarily-) common moderate stresses that produce some minor damage which the body takes advantage of to improve something. The lack of these stresses implies lack of (or lower?) improvement. The same type of stress but of a high enough magnitude starts being detrimental. I think this is what inspired Taleb for the concept of antifragility, where a stress within some limits is advantageous for a system instead of a harmful.

I also think stubbing a toe is not a good counter example (in a relatively short time, it would produce callus that would ultimately protect from the hits). The breaking a bone example seems better. I think the main difference is that breaking a bone actually is an acute stress rather than a moderate one. That’s an stress that is beyond the threshold the body can stand.

This way to model it is not very helpful here, cause we don’t seem to know yet whether short-time lack of sleep brings us any kind of improvement. But it makes 2 things obvious: (1) it seems very plausible that short-time lack of sleep is at least not too bad, as humans may have had occasional all-nighters during our evolution (e.g. to escape predators or other humans); (2) short-time lack of sleep is not an acute stress, so it could fall into the category of good stresses.

Besides acute stresses (obviously bad) and good stresses, there is at least one other relevant category of stresses: mild to moderate stresses the effects of which are cumulative (enough accumulation in a long enough life has bad consequences). I am not sure if this category can be further broken into 2 categories as well, because at least in some instances these stresses make the body somehow resilient to higher doses of the stressor (e.g. heavy drinkers develop a tolerance to the effects of alcohol). Probably there are more categories of stress but I am not aware of them.

Now the issue is still open to which category of stress do short-time and chronic lack of sleep lay in. I’m very interested to know it! My guess is that short-term lack of sleep can very well be beneficial in some way and that the accumulation of lack of sleep is probably bad in the long term.

[Elizabeth]

I’m using acute to mean “of short duration”, independent of severity, which I think is not how you are using it.

[mikbp]

Ah, ok sorry. Yes, I thought it means sever.

[remizidae]

Re the point that mania is very bad, I agree, but people should know that not all mania is associated with bipolar disorder.

[mikbp]

Sleep is not required for memory consolidation.

That’s very puzzling to me. Why do babies need so much sleep then? I assume memory consolidation is a central part of the learning process, is it not? Or do babies need to sleep a lot for other reasons than learning stuff? Of course what a baby’s brain goes through is pretty massive, but is it not the same (at least partly) as what an adult’s brain goes through when learning something, just at a different scale?

[ChristianKl]

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

[mikbp]

I don’t understand you; they have to literally learn everything.

[ChristianKl]

Human children learn a lot of things during the first year of life slower than other species. It’s possible that there are benefits to a certain learning speed.

[mikbp]

Ok, I see. But I still don’t see why we need to sleep that much. It must have some other benefit then, and it cannot only be saving resources, as then babies should be able to trade sleep for food, no?

I checked, and it seems that land mammals’ babies also sleep more than gown ups, which would imply that learning slower than other species is probably not the reason why babies sleep that much. Interestingly, marine mammals’ babies seem to sleep less than grown ups.

[Sniffnoy]

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.

[mikbp]

That makes total sense, true.

[mikbp]

70% of 84 hunter-gatherers studied in 2013 slept less than 7 hours per day, with 46% sleeping less than 6 hours.

Does this really count all sleep time (including naps) or only night sleep? It sounds strange if it counts all sleep time. At least in conjunction with the claim that hunter-gatherers “worked” fewer hours than modern humans (I, of course, assume that modern hunter-gatherers have a life similar to ancient ones). In addition, there doesn’t seem to be much to do when it is dark -even when you have fire-; it is very unlikely not to fall asleep if you are in any way not well rested, no?

If the studies include naps, it points to me to something I have thought a bit about: sleep and idle-resting/​some-kind-of-meditation may have non-trivial overlap. If hunter-gatherers can spend enough idle time during the day, this effectively would decrease their need for sleep. So, even if they had the opportunity to easily sleep longer, they wouldn’t. Modern life effectively brings idle time close to zero, so it would be no wonder why we need more sleep. Is there any data on sleep time for different kind of meditators?

Another explanation could be that modern life implies a much intensive use of our brain, we’d need to think much more than hunter-gatherers. In my experience, when I don’t think much I really don’t have a problem sleeping less than usual (although I cannot recall if I feel sleepy anyway or not). And when I need to really think hard I do need more sleep than usual (actually, when I started to study in the uni I was not able to go to bed early -external forces + lack of willpower- and it went pretty bad until I decided not to take any class before 10h). Does that sound plausible?

[jmh]

Currently not in a frame of mind for focus but want to ask about two related questions. A quick search didn’t seems to find some key words so don’t think you discussed in the post (but again, not well focused right now so maybe fit better with some of the quotes you conclude with ;-)

First, seems like there might be a opposing result related to limiting sleep and the reverse flow for cleaning out toxin accumulation in the brain. Did you find any mention of that aspect?

Second, and I have zero basis for the thought other than it was something that popped into my hear the other day when something got me thinking about “why sleep?”. The brain has huge energy demands but we have limited energy production (I think) systemically. That got me thinking that perhaps sleep is more about consuming energy output for non-mental repair/​growth related needs of the body. If so then there seems we might want to look at balancing between the two demands. I would think different people will find different optimal points (and we probably see that naturally).