2001-01-01 08:00:00
See discussion of this essay on the forum, Hacker News (a), Marginal Revolution (a), Andrew Gelman’s blog 1 (a), 2 (a), 3 (a), 4 (a), /r/slatestarcodex (a), Twitter (a), listen to BBC interviewing me and Walker himself about it or listen to my interview with Smart People Podcast discussing it.
Note: I link to a bunch of paywalled studies in this essay. Please do not use sci-hub to access them for free and do not use this trick (a) to easily redirect papers to sci-hub.
For the clearest example of deliberate data manipulation, see how Walker edits out the data that contradicts his argument from the graph.
Also see UC Berkeley’s official response regarding this essay – all problems with the book I discovered are “minor”.
Also see Walker’s post. Note: the post is explicitly not a response to my essay, but rather a response to “questions from readers”. Walker never states any of the points I make and never responds to them directly. I wrote some thoughts on the post here.
Matthew Walker (a) is a professor of neuroscience and psychology at the University of California, Berkeley, where he also leads the Center for Human Sleep Science.
His book Why We Sleep (a) was published in September 2017. Part survey of sleep research, part self-help book, it was praised by The New York Times (a), The Guardian (a), and many others. It was named one of NPR’s favorite books of 2017 (a). After publishing the book, Walker gave a TED talk (a), a talk at Google (a), and appeared on Joe Rogan’s (a) and Peter Attia’s (a) podcasts. A month after the book’s publication, he became (a, 2 (a)) a sleep scientist at Google.
On page 8 of the book, Walker writes:
[T]he real evidence that makes clear all of the dangers that befall individuals and societies when sleep becomes short have not been clearly telegraphed to the public … In response, this book is intended to serve as a scientifically accurate intervention addressing this unmet need [emphasis in this quote and in all quotes below mine]
In the process of reading the book and encountering some extraordinary claims about sleep, I decided to compare the facts it presented with the scientific literature. I found that the book consistently overstates the problem of lack of sleep, sometimes egregiously so. It misrepresents basic sleep research and contradicts its own sources.
In one instance, Walker claims that sleeping less than six or seven hours a night doubles one’s risk of cancer – this is not supported by the scientific evidence (Section 1.1). In another instance, Walker seems to have invented a “fact” that the WHO has declared a sleep loss epidemic (Section 4). In yet another instance, he falsely claims that the National Sleep Foundation recommends 8 hours of sleep per night, and then uses this “fact” to falsely claim that two-thirds of people in developed nations sleep less than the “the recommended eight hours of nightly sleep” (Section 5).
Walker’s book has likely wasted thousands of hours of life and worsened the health of people who read it and took its recommendations at face value (Section 7).
The myths created by the book have spread in the popular culture and are being propagated by Walker and by other scientists in academic research. For example, in 2019, Walker published an academic paper that cited Why We Sleep 4 times just on its first page, meaning that he believes that the book abides by the academic, not the pop-science standards of accuracy (Section 14).
Any book of Why We Sleep’s length is bound to contain some factual errors. Therefore, to avoid potential concerns about cherry-picking the few inaccuracies scattered throughout, in this essay, I’m going to highlight the five most egregious scientific and factual errors Walker makes in Chapter 1 of the book. This chapter contains 10 pages and constitutes less than 4% of the book by the total word count.
On page 4, Walker writes:
the shorter your sleep, the shorter your life span
This is false. If you’re concerned about me taking this quote out of context, I provide the full sentence and the two paragraphs leading up to it here. Walker does not cite any studies when making this claim. Most of the studies on the relationship between life span and sleep duration find a U-shaped relationship between length of sleep and longevity, i.e. both short- and long-duration sleep are associated with higher mortality [1 (a) Shen X, Wu Y, Zhang D. Nighttime sleep duration, 24-hour sleep duration and risk of all-cause mortality among adults: a meta-analysis of prospective cohort studies. Scientific Reports. 2016 Feb 22;6:21480. , 2 (a) Cappuccio FP, D’Elia L, Strazzullo P, Miller MA. Sleep duration and all-cause mortality: a systematic review and meta-analysis of prospective studies. Sleep. 2010 May 1;33(5):585-92. , 3 (a) Kripke DF, Garfinkel L, Wingard DL, Klauber MR, Marler MR. Mortality associated with sleep duration and insomnia. Archives of General Psychiatry. 2002 Feb 1;59(2):131-6. ]. The studies typically find that people who sleep 7 hours have the highest longevity. Here’s a graph from the first study, published in Scientific Reports in 2016, which performed a meta-analysis of thirty-five prospective cohort studies:
Figure 1. The dose-response analysis between nighttime sleep duration and risk of all-cause mortality. The solid line and the long dash line represent the estimated relative risk and its 95% confidence interval. Note: the red dashed line on the graph is mine.
Note that the lowest mortality on the graph is at just below 7 hours and that mortality at 5 hours of sleep per night is basically the same if not lower than mortality at 8 hours of sleep.
As the Encyclopedia of Sleep Kushida C. Encyclopedia of sleep. Academic Press; 2012 Dec 31. – which Walker cites two pages later – notes:
[T]he popular expectation that short sleep is correlated with short life span and long sleep with greater longevity is not supported by the existing literature.
On page 3, Walker writes:
Routinely sleeping less than six or seven hours a night demolishes your immune system, more than doubling your risk of cancer.
This is false. Walker does not cite any studies that support this assertion anywhere in the book. There do not appear to exist any experimental studies or studies that would reasonably be able to establish causality, that would support this claim. Even the epidemiological evidence (which you should almost never use to claim causality (a) Even if you “controlled” for confounding variables (a). ) disagrees with Walker’s assertion. For example, a systematic review of sixty-five studies from 2018 (doi), Chen Y, Tan F, Wei L, Li X, Lyu Z, Feng X, Wen Y, Guo L, He J, Dai M, Li N. Sleep duration and the risk of cancer: a systematic review and meta-analysis including dose–response relationship. BMC Cancer. 2018 Dec;18(1):1149. which involved 1,550,524 participants and 86,201 cancer cases, found that neither short nor long sleep duration was associated with increased cancer risk.
Figure 2. Nonlinear dose–response analyses of sleep duration and cancer risk. The solid line and the long-dashed line represent the estimate odds ratios and their 95% confidence intervals. Seven hours of sleep per night was used as the reference Note: the red dashed line on the graph is mine.
All of the big studies that are used as inputs for meta-analyses like those I cited above use self-reported data on sleep duration, since it’s impossible to record objective sleep data for a large number of people (this will soon change with the advent of smart watches, bracelets, and rings).
Self-reported data is notoriously unreliable, so it’s not clear how meaningful those studies are, even if all we’re looking for are various correlations. See further discussion of this in Section 12, where I hypothesize that people who have the lowest mortality might actually sleep just 6 hours a day.
Note: in this section, I only talk about acute sleep deprivation, i.e. being sleep deprived for one or several days. Chronic or externally imposed sleep deprivation is an entirely different matter and has no relation to sleep deprivation therapy.
On page 8, Walker writes:
[W]e are now forced to wonder whether there are any biological functions that do not benefit by a good night’s sleep. So far, the results of thousands of studies insist that no, there aren’t.
This is false. First, an enormous literature dedicated to the treatment of depression with sleep deprivation has found that people with depression frequently benefit by not getting a good night’s sleep.
Second, Walker directly contradicts himself in Chapter 7 by acknowledging that there are cases when a good night’s sleep is not helpful after all: If you’re concerned about me taking this quote out of context, I provide the full discussion of sleep deprivation therapy in Why We Sleep here.
Approximately 30 to 40 percent of these patients will feel better after a night without sleep … the 60 to 70 percent of patients who do not respond to the sleep deprivation will actually feel worse, deepening their depression. As a result, sleep deprivation is not a realistic or comprehensive therapy option.
In this quote, not only does Walker contradict himself, but he also misrepresents the benefits and the dangers of sleep deprivation therapy. He slightly downplays the number of people who benefit from it – it’s closer to 45-50% if you believe this meta-analysis from 2017 (pdf, a) Boland EM, Rao H, Dinges DF, Smith RV, Goel N, Detre JA, et al. Meta-Analysis of the Antidepressant Effects of Acute Sleep Deprivation. The Journal of Clinical Psychiatry. 2017;78(8). or it’s 40-60% if you believe Walker himself from 2009 (doi) Walker MP, van Der Helm E. Overnight therapy? The role of sleep in emotional brain processing. Psychological Bulletin. 2009 Sep;135(5):731. – and he completely mischaracterizes the dangers of it.
In the book, Walker writes that “the 60 to 70 percent of patients who do not respond to the sleep deprivation will actually feel worse, deepening their depression”. However, a review of the literature from 2002 (a) Giedke H, Schwärzler F. Therapeutic use of sleep deprivation in depression. Sleep Medicine Reviews. 2002 Oct 1;6(5):361-77. that he cited in his study from 2009 tells us that depression worsens in less than 10% of patients:
Total sleep deprivation (TSD) for one whole night improves depressive symptoms in 40-60% of treatments. The degree of clinical change spans a continuum from complete remission to worsening (in 2-7%). Other side effects are sleepiness and (hypo-) mania. … It is still unknown how sleep deprivation works.
Here’s a review from 2010 (a): Hemmeter UM, Hemmeter-Spernal J, Krieg JC. Sleep deprivation in depression. Expert Review of Neurotherapeutics. 2010 Jul 1;10(7):1101-15.
The observation that after the recovery night a great majority of SD responders relapse into depression suggests that sleep per se may have a depressiogenic property.
The rapid effect of SD on depressive mood within hours is a fascinating experience for the patient, who may have been depressed for weeks or months …
SD is the only established antidepressant therapy that acts within hours, and therefore, can be applied in patients with treatment-resistant depression with a chance of approximately 50% of seeing an immediate, although temporary, relief from depressive symptoms without major side effects. … The experience of realizing that depression can be lifted and sleep can improve is very important for the further therapy motivation of treatment resistant depressed patients. … [Sleep deprivation] can be combined with antidepressant medication, predominantly serotonergic agents, with bright light therapy and with a phase advance of sleep cycles. All these strategies have been able to provide a chance to stabilize the SD response, at least in a subgroup of patients. [correction: John E. Richters points out that, in 2019, there’s also ketamine (a) which is approved by the FDA for treatment-resistent depression and acts within hours (a).]
Finally, although Walker states that “sleep deprivation is not a realistic or comprehensive therapy option”, a review chapter of sleep deprivation (a) Dallaspezia S, Benedetti F. Sleep Deprivation Therapy for Depression. Sleep, Neuronal Plasticity and Brain Function Current Topics in Behavioral Neurosciences. 2014;:483–502. in the book Sleep, Neuronal Plasticity and Brain Function published in 2014 reads:
[C]onsidering its safety, this technique [sleep deprivation] can now be considered among the first-line antidepressant treatment strategies for patients affected by mood disorders. …
SD is a rapid, safe, and effective therapy for depression. In recent years, this technique has passed the experimental developmental phase and reached the status of affordable clinical intervention for everyday clinical therapy of depressed patients with an increasing literature regarding its safety and efficacy.
This is important because Walker’s scaremongering is likely to harm people with depression who decide to avoid sleep deprivation therapy as a result of reading his book.
On page 6, Walker writes:
[E]very species studied to date sleeps
This is false, at least, according to Walker’s own source. When making this claim, he cites:
Kushida, C. Encyclopedia of Sleep, Volume 1 (Elsever, [sic] 2013)
….which turns out to be a 2,736 page book that costs $1,995. Fortunately, Walker tells us that we should search for this information somewhere in “Volume 1” or the first 638 pages of the book.
Anyway, page 38 reads:
It now appears that many species reduce sleep for long periods of time under normal conditions and that others do not sleep at all, in the way sleep is conventionally defined.
On pages 4-5, Walker writes:
[T]here is a very rare genetic disorder that starts with a progressive insomnia, emerging in midlife [fatal familial insomnia (FFI)]. Several months into the disease course, the patient stops sleeping altogether. By this stage, they have started to lose many basic brain and body functions. No drugs that we currently have will help the patient sleep. After twelve to eighteen months of no sleep, the patient will die. Though exceedingly rare, this disorder asserts that a lack of sleep can kill a human being.
This is false. You cannot say that FFI (a) shows that a lack of sleep will kill a human being.
Here is a rough description of the disease: a genetic mutation results in the production of a misfolded protein in the brain, primarily in the thalamus. This protein is toxic to the nerve cells and, over time, it damages the thalamus, resulting in a variety of symptoms, typically including dementia, hallucinations, and insomnia. Eventually, the rest of the brain gets damaged as well, internal organs shut off, the patient’s ability to sleep gets heavily disrupted, and the patient dies.
It is reckless to claim that people with FFI die because of lack of sleep, given the amount of damage across the brain that accumulates in the course of the disease. Accordingly, FFI is considered a neurodegenerative disease. Looking at page 41 of the Encyclopedia of Sleep we discussed in the Interlude:
A disorder called fatal familial insomnia (FFI) is often presented as proof that sleep loss causes death in humans as it does in rats deprived by the forced walking method. However, FFI is a prion disease that affects all body organs and brain cells. There is little evidence that sleep induced by sedation can greatly extend life in FFI patients.
And as one paper notes (a): Schenkein J, Montagna P. Self-management of fatal familial insomnia. Part 2: case report. Medscape General Medicine. 2006;8(3):66.
[T]he prevailing belief [is] that FFI patients ultimately die of neural degeneration
Note that this was Walker’s only example of lack of sleep leading directly to death.
The seven sentences I quoted in the beginning of this section contain (at least) three more scientific errors. See discussion of them in Section 23.
On page 4, Walker writes:
[T]he World Health Organization (WHO) has now declared a sleep loss epidemic throughout industrialized nations.
This is false. The WHO never declared a sleep loss epidemic throughout industrialized nations.
In the footnote to this sentence, Walker cites:
Sleepless in America, National Geographic, http://channel.nationalgeographic.com/sleepless-in-america/episode/sleepless-in-america.
One might wonder why he cited a documentary film from National Geographic, rather than the WHO directly, but ok, maybe that film has a reference to the primary source. I watched the entire 88-minute long film twice (official YouTube link Can only be viewed from the US, unfortunately. (a)) to make sure I didn’t miss anything and the film never mentions the WHO or any sleep loss epidemics declared by the WHO and never features anyone from the WHO. I googled:
“world health organization” “sleep loss epidemic”
And didn’t find any documents by WHO. Further, when I restricted the search results to before September 28, 2017 (the date when the book was published), Search results page 1 (a), page 2 (a). I also googled the string ‘“world health organization” “sleep” “epidemic”’ but it didn’t return any relevant results either. the hits either
I discuss the possible origin of this “epidemic” declared by the WHO in Walker’s book here.
Later in the book (in Chapter 8) Walker provides the following graph that indicates that the average sleep time has decreased by more than 2 hours between 1940s and 2000s and that corroborates his claims of sleep loss epidemic, even if it was not declared by the WHO:
Figure 3. Sleep loss and obesity. Country not specified for sleep data.
I have not been able to find any data that would support the sleep duration numbers Walker provides in the book and it appears that they were simply made up. Further, in a video published by Penguin Books UK in 2019, Walker says:
There’s been a pernicious erosion of sleep time throughout the past 50 years [i.e. between 1969 and 2019]
On the contrary, there’s strong evidence of no reduction in average sleeping time and perhaps even an increase in sleeping time over this approximate time period Bin YS, Marshall NS, Glozier N. Sleeping at the limits: the changing prevalence of short and long sleep durations in 10 countries. American journal of epidemiology. 2013 Apr 15;177(8):826-33. (h/t /u/O2starved) (a):
To investigate whether the prevalences of short and long sleep durations have increased from the 1970s to the 2000s, we analyzed data from repeated cross-sectional surveys of 10 industrialized countries (38 nationally representative time-use surveys; n = 328,018 adults). … Over the periods covered by data, the prevalence of short sleep duration increased in Italy … and Norway … but decreased in Sweden, the United Kingdom, and the United States. … Limited increases in short sleep duration challenge the claim of increasingly sleep-deprived societies. Long sleep duration is more widespread than is short sleep duration. It has become more prevalent and thus should not be overlooked as a potential contributor to ill health.
Sleep differences in the UK between 1974 and 2015: Insights from detailed time diaries Lamote de Grignon Pérez J, Gershuny J, Foster R, De Vos M. Sleep differences in the UK between 1974 and 2015: Insights from detailed time diaries. Journal of sleep research. 2019 Feb;28(1):e12753. (a):
It is often stated that sleep deprivation is on the rise, with work suggested as a main cause. However, the evidence for increasing sleep deprivation comes from surveys using habitual sleep questions. An alternative source of information regarding sleep behaviour is time‐use studies. This paper investigates changes in sleep time in the UK using the two British time‐use studies that allow measuring “time in bed not asleep” separately from “actual sleep time”. Based upon the studies presented here, people in the UK sleep today 43 min more than they did in the 1970s because they go to bed earlier (~30 min) and they wake up later (~15 min). The change in sleep duration is driven by night sleep and it is homogeneously distributed across the week. The former results apply to men and women alike, and to individuals of all ages and employment status, including employed individuals, the presumed major victims of the sleep deprivation epidemic and the 24/7 society. In fact, employed individuals have experienced a reduction in short sleeping of almost 4 percentage points, from 14.9% to 11.0%. There has also been a reduction of 15 percentage points in the amount of conflict between workers work time and their sleep time, as measured by the proportion of workers that do some work within their “ideal sleep window” (as defined by their own chronotype).
Figure 4. Average sleep duration and time in bed in the UK between 1974 and 2015 across employment status. From Lamote et al 2018.
Suppose that you recommend that adults sleep 7-9 hours per night.
Would this be a fair representation of your position and of the data or would this be misleading?
This is literally what Walker does in his book. On page 3, in the very first paragraph of Chapter 1, Walker writes:
Two-thirds of adults throughout all developed nations fail to obtain the recommended eight hours of nightly sleep.
In the footnote to this sentence he writes:
The World Health Organization and the National Sleep Foundation both stipulate an average of eight hours of sleep per night for adults.
Here are the National Sleep Foundation’s sleep recommendations (a) announced in 2015:
Adults (26-64): Sleep range did not change and remains 7-9 hours
Here are the World Health Organization’s sleep recommendations:
The quote is empty because the WHO does not stipulate how much an adult should sleep anywhere. I don’t know where Walker got this information.
Is giving three impossible numbers within 200 pages likely to be a coincidence or is it a sign that the writer probably doesn’t know how percentages work?
Chapter 5:
[T]he infants of heavy-drinking mothers showed a 200 percent reduction in this measure of vibrant electrical activity relative to the infants born of non-alcohol-consuming mothers.
Chapter 8:
Deprive a mouse of sleep for just a day, as researchers have done, and the activity of these genes will drop by well over 200 percent.
Chapter 15:
[R]esidents made 400 to 600 percent fewer diagnostic errors to begin with.
As an aside, Walker copy-pasted the 400-600% claim into two of his academic papers published in 2018 and 2019 without noticing that the number doesn’t make sense. See this appendix.
In the first chapter of Why We Sleep, Walker:
Given the density of scientific and factual errors and an apparent invention of new “facts” by Walker, I would caution readers against taking the book’s recommendations at face value.
Here are some of the potential harms done by the book:
First, Walker’s misrepresentation of sleep deprivation therapy (Section 2) is likely to make many people with depression avoid this potent and largely safe treatment option.
Second, imagine that a 20-year-old who naturally needs to sleep for 7 hours a night, reads Why We Sleep, gets scared, and decides to spend the full 8 hours in bed every day. Then, assuming that they live until 75, they will waste more than 20,000 hours or more than 2 years of their life, with uncertain long-term side-effects.
Finally, to be less speculative, here’s an email from a sleep coach Martin Reed I got after the publication of this essay:
Hello Alexey
I wanted to drop you a line to thank you for all the time and effort involved in debunking Matthew Walker’s book. As someone who works with individuals with insomnia on a daily basis, I know from firsthand experience the harm that Walker’s book is causing.
I have many stories of people who slept well on less than eight hours of sleep, read Walker’s book, tried to get more sleep and this led to more time awake, frustration, worry, sleep-related anxiety, and insomnia. …
Amjad Masad, CEO of repl.it, writes to me:
I’ve had the same experience of developing insomnia as some of the reports you got because I tried to force 8 hours sleep
For more such examples see Section 17.
We have literally no idea about the optimal for long-term health sleep duration. Correction: originally, this sentence read, “as long as you feel good, sleeping anywhere between 5 and 8 hours a night seems basically fine for your health”, but as several people pointed out, ironically, the only support for this statement comes from the correlational data, which I claimed cannot be used to establish causality.
All of the evidence we have about this is in the form of those essentially meaningless correlational studies, but if you’re going to use bad science to guide your sleep habits, at least use accurate bad science.
Figure 1. The dose-response analysis between nighttime sleep duration and risk of all-cause mortality. The solid line and the long dash line represent the estimated relative risk and its 95% confidence interval. Note: the red dashed line on the graph is mine.
Below, I
I’m planning to write more about sleep, science in general, and the interpretation of correlational studies in particular. Subscribe, if you’d like to stay updated.
I would like to thank (in reverse alphabetic order) Misha Yagudin, Brian Timar, José Luis Ricón, Ada Nguyen, Anastasia Kuptsova, Matt Kovacs-Deak, Basil Halperin, Mark Egan, Maxim Efremov, and especially Steve Gadd for reading drafts of this essay. They have improved it immeasurably. All remaining errors are mine.
I would like to thank Kyle Schiller and Adam Canady for the financial support of my writing and research.
In academic work, please cite this essay as:
Guzey, A. Matthew Walker’s “Why We Sleep” Is Riddled with Scientific and Factual Errors. Guzey.com. 2019 November. Available from https://guzey.com/books/why-we-sleep/.
Or download a BibTeX file here.
If you believe that I’m saying any of those things, please email me at [email protected] with a specific passage where I do that. I will fix it.
Gregg D. Jacobs’s CBT for Insomnia
This paper by Lauderdale et al (a) Lauderdale DS, Knutson KL, Yan LL, Liu K, Rathouz PJ. Self-reported and measured sleep duration: how similar are they?. Epidemiology (Cambridge, Mass.). 2008 Nov;19(6):838-45. is the most well-cited paper on the topic of self-reported vs objectively measured sleep I found. It reads:
the correlation between reported and measured sleep duration was 0.47. Our model suggests that persons sleeping 5 hours over-reported their sleep duration by 1.2 hours, and those sleeping 7 hours over-reported by 0.4 hours.
Two other studies I found report a correlation of 0.43 (a) Cespedes EM, Hu FB, Redline S, Rosner B, Alcantara C, Cai J, Hall MH, Loredo JS, Mossavar-Rahmani Y, Ramos AR, Reid KJ. Comparison of Self-Reported Sleep Duration With Actigraphy: Results From the Hispanic Community Health Study/Study of Latinos Sueño Ancillary Study. American Journal of Epidemiology. 2016 Mar 2;183(6):561-73. and 0.4 (a). Matthews KA, Patel SR, Pantesco EJ, Buysse DJ, Kamarck TW, Lee L, Hall MH. Similarities and differences in estimates of sleep duration by polysomnography, actigraphy, diary, and self-reported habitual sleep in a community sample. Sleep Health. 2018 Feb 1;4(1):96-103. Here’s what a correlation of 0.5 might look like:
This is the kind of noisy sleep data all these big epidemiological studies are based on. Later, Lauderdale et al write:
the average difference at the mean of 6 hours measured sleep was 0.80 hours (48 minutes)
Now, looking at Figure 1, we can see that people who reported sleeping just below 7 hours a night had the lowest mortality. If we interpret this in light of the last quote, people who have the lowest mortality actually sleep 6 hours a night.
One last bit from the Lauderdale et al paper:
The correlation was very low (0.06) for persons with fair or poor self-rated health.
Merijn van de Laar writes:
In appendix 13 you state “if we interpret this in light of the last quote, people who have the lowest mortality actually sleep 6 hours a night”, based on the article by Lauderdale.
I found another article by Manconi [Measuring the error in sleep estimation in normal subjects and in patients with insomnia] (in the attachment) in which it is stated that “normal subjects” do not overestimate their sleep, which is quite contradictory to the Lauderdale article. I dove into it and found out that Lauderdale uses actigraphy to measure objective sleep while Manconi uses polysomnography which is generally thought to be more accurate and thought to better distinguish between stages of sleep and being awake or not, because more indices of sleep are measured (such as EEG). However, in another article comparing PSG and actigraphy, it is mentioned that actigraphy has high sensitivity and accuracy when compared to PSG. So I was still puzzled, until I looked into the characteristics of the participants. The Lauderdale study included only subjects between 18 and 30 years old, while Manconi’s “normal subjects” had an average age of 58.5 (SD 7.23).
A conclusion might be that younger subjects tend to overestimate their sleep, while middle-aged subjects are better in estimating sleep.
I spent more than 130 hours over the last 2 months researching and writing this essay (~5 hours to write the outline; ~60 hours to get to the first draft; ~65 hours to edit and fact-check), which constituted essentially all of my surplus free time over this time period. Continuing at the same pace, it would take me more than 3,000 hours to check the entire book. 3,000 hours is the equivalent of 75 weeks or 1.4 years of full-time work.
I hope that going through one full chapter, rather than cherry-picking stuff from across the book, demonstrated the density of errors in the book.
Update a week after the publication (2019-11-22): in the last week, I spent 20 to 30 more hours editing it.
Why We Sleep is not just a popular science book. As I note in the introduction, Walker specifically writes that the book is intended to be scientifically accurate:
[T]his book is intended to serve as a scientifically accurate intervention
Consequently, Walker and other researchers are actively citing the book in academic papers, propagating the information contained in it into the academic literature.
Google Scholar indicates that (a), in the 2 years since the book’s publication, it has been cited more than 100 times.
A paper (a) Cardon JH, Eide ER, Phillips KL, Showalter MH. Interacting circadian and homeostatic processes with opportunity cost: A mathematical model of sleep with application to two mammalian species. PloS One. 2018 Dec 12;13(12):e0208043. published in PloS One in 2018 reads:
All known forms of animal life must sleep ([1]).
“[1]” here refers to Why We Sleep. If you recall the Interlude, Walker miscites the Encyclopedia of Sleep while making this statement in Why We Sleep.
A paper (a) Shallcross AJ, Visvanathan PD, Sperber SH, Duberstein ZT. Waking up to the problem of sleep: Can mindfulness help? A review of theory and evidence for the effects of mindfulness for sleep. Current Opinion in Psychology. 2019 Aug 1;28:37-41. published in Current Opinion in Psychology in 2019 reads:
Chronic sleep disturbance is a global pandemic with two-thirds of individuals failing to obtain the recommended 7–9 h of sleep each night [1].
“[1]” here refers to Why We Sleep. If you recall Section 4 and Section 5, both the “global pandemic” and the “two-thirds” assertions are false.
A paper (a) Lyon L. Is an epidemic of sleeplessness increasing the incidence of Alzheimer’s disease?. Brain. 2019 Apr 1;142(6):e30-. published in Brain in 2019 reads:
the World Health Organization has pointed to a ‘global epidemic of sleeplessness’ with roughly two-thirds of adults sleeping less than 8 h a night.
The paper does not cite any sources here and does not cite Why We Sleep anywhere, although the wording strongly suggests that this is where the information originated.
Note also how the papers further miscite Walker and transform his industrialized nations epidemic into a global epidemic. This is how academic urban legends (a) Rekdal OB. Academic urban legends. Social Studies of Science. 2014 Aug;44(4):638-54. are created.
Since Why We Sleep was published, Walker published two academic papers that cited it. Many of the claims in both papers originate from Why We Sleep.
The first one (doi) Walker MP. A sleep prescription for medicine. The Lancet. 2018 Jun 30;391(10140):2598-9. was published in The Lancet in 2018.
The second one (doi) Walker MP. A Societal Sleep Prescription. Neuron. 2019 Aug 21;103(4):559-62. was published in Neuron in 2019. It’s 4 pages long and it references Why We Sleep 7 times.
For example, in The Lancet, Walker writes:
pilot studies have shown that when you limit trainee doctors to no more than a 16 h shift, with at least an 8 h rest opportunity before the next shift, serious medical errors drop by over 20%. Furthermore, residents make 400–600% fewer diagnostic errors to begin with.
In Neuron, Walker writes:
pilot studies have shown that when you limit trainee doctors to no more than a 16-h shift, with at least an 8-h rest opportunity before the next shift, serious medical errors drop by over 20%. Furthermore, residents make 400%–600% fewer diagnostic errors to begin with (Walker, 2017).
And in Why We Sleep, Walker writes:
several pilot studies in the US have shown that when you limit residents to no more than a sixteen-hour shift, with at least an eight-hour rest opportunity before the next shift, the number of serious medical errors made—defined as causing or having the potential to cause harm to a patient—drops by over 20 percent. Furthermore, residents made 400 to 600 percent fewer diagnostic errors to begin with.
Three observations:
Update: the Neuron article was retracted “at the request of the Author”.
To expand on the last point, the last 2 pages of the Neuron paper, appear to be mostly identical to The Lancet paper, this despite Neuron publisher’s policy being (a):
Manuscripts are considered for publication with the understanding that no part of the work has been published previously in print or electronic format
Figure 6. The Lancet paper is on the left. Neuron paper is on the right. Identical text is highlighted in red. Image created with the help of copyleaks.com
I’m Alexey. You’re welcome.
On a more serious note, I have a BSc in Mathematics and Economics. During my undergrad, I took 2 years of statistics, a year of econometrics and worked as a research assistant for an economics prof for about 3 years. I also took graduate-level psychology, neuroscience, and biology courses. Over the last several years, I spent many hundreds of hours studying biology and neuroscience.
Since the publication of this essay, it was read by hundreds of psychologists and neuroscientists who–I believe–also failed to find any serious issues. Regardless of what I believe, you can check the discussions in the links in the beginning of the essay and check whether this is true for yourself.
Some of the scientists wrote to me directly. Here’s a sleep scientist with >50 h-index who studied sleep for more than 40 years:
Hello Alexey,
I thoroughly enjoyed your review of Walker’s sleep book. I myself am a sleep researcher but - I would like to think - of quite a different ilk from the Walker variety. In fact, I was so infuriated by the Walker claims that I bought a copy of the book so that I could review it. Upon receipt of the Kindle edition, I found it so full of falsehoods, lightly tossed out, that I didn’t know where to start. Your decision to limit your comments to the first chapter was a great solution to what could have become an intractable morass.
(argument adapted from this video, time 7:13, and from many other people making versions of it)
First, it is true that some diseases lead to prolonged sleep. However, some diseases also lead to shortened sleep. For example, many stroke patients suffer from insomnia (a) Sterr A, Kuhn M, Nissen C, Ettine D, Funk S, Feige B, Umarova R, Urbach H, Weiller C, Riemann D. Post-stroke insomnia in community-dwelling patients with chronic motor stroke: physiological evidence and implications for stroke care. Scientific Reports. 2018 May 30;8(1):8409. and people with fatal familial insomnia struggle with insomnia. Therefore, if you want to make the argument that the association between longer sleep and higher mortality is not indicative of effect of sleep, you have to accept that the same is true about shorter sleep and higher mortality. As Cappuccio et al 2010 (cited in section 1) note, these associations do not have a single accepted reason behind them:
Proposed mechanisms for mortality associated with long sleep include: (I) long sleep is linked to increased sleep fragmentation that is associated with a number of negative health outcomes; (II) long sleep is associated with feelings of fatigue and lethargy that may decrease resistance to stress and disease; (III) changes in cytokine levels associated with long sleep increase mortality risk; (IV) long sleepers experience a shorter photoperiod that could increase the risk of death in mammalian species; (V) a lack of physiological challenge with long sleep decrease longevity; (VI) underlying disease processes mediate the relationship between long sleep and mortality.
Second, at the level of an individual, there do not appear to exist any experimental studies or studies that would reasonably be able to establish causality that would support the claim that sleep restriction cause long-term health problems or an increase in mortality.
You could say that it is well-known that short-term (acute) lack of sleep causes a stress response from the organism. This is true. However, if you make this argument, you should also consider the following argument about the dangers of exercise valid:
When we exercise, our blood pressure and heart rate would increase. Stress hormones’ concentration in the blood rises and the muscles get damaged. Therefore, exercise is bad for your health.
Exercise demonstrates that arguments of the form “x makes me feel bad in the short-term, therefore it’s bad for health” are suspect.
In general, be careful to distinguish short-term stress response and long-term stress response.
Please see section 18, section 19, and section 22, where I cover problems with chapters 6 and 8. For example, in section 18, I show how Walker literally cuts out the part of a graph that displays the data in contradiction with his argument.
Many people do seem to need 8-9 hours of sleep.
However, let me make an analogy: when people don’t restrict their food-eating, many of them start eating more than they need and become obese, meaning that simply allowing ourselves to get as much food as we want, likely isn’t the healthiest choice. My guess is that same is likely true for sleep.
I did look into this. I was not able to find any data on vehicular accidents caused by drowsy driving. However, the data by the National Highway Traffic Safety Administration on accidents that involve drowsy driving (a) and that involve drugs and alcohol (a) does not support this assertion.
According to this data, 1.2-1.4% (Table 2 in linked file) of car crashes involved drowsy driving, while 2.8% (Table 7 in linked file) of car crashes involved driving while having the alcohol blood concentration above the legal limit in the US (and this is not including accidents involving drugs).
I have not investigated Walker’s claims about sleep and learning, since he does not make any concrete statements about this in Chapter 1. However, is there any reason to expect his treatment of sleep and learning to be any more accurate than, for example, his treatment of the relationship between sleep and longevity?
Is there any reason to expect that this is one statistic he decides to portray accurately? Have you considered looking at the scientific literature and seeing if this number checks out?
Before doing all of this research, I frequently forced myself to sleep 8 hours, even if I naturally woke up after 7. I no longer do that and I continue to experiment with my sleep.
A sleep physician Daniel Erichsen (a) writes:
Dear Alexey,
Your essay on Why we sleep - I can’t thank you enough. I’m a sleep doctor in Oregon and have seen many many patients who have developed severe sleep anxiety and insomnia. Two friends in the sleep field and myself weekly have talked about people that slept well until reading this book.
This is the email from a sleep coach Martin Reed (a) I quoted in Section 7:
Hello Alexey
I wanted to drop you a line to thank you for all the time and effort involved in debunking Matthew Walker’s book. As someone who works with individuals with insomnia on a daily basis, I know from firsthand experience the harm that Walker’s book is causing.
I have many stories of people who slept well on less than eight hours of sleep, read Walker’s book, tried to get more sleep and this led to more time awake, frustration, worry, sleep-related anxiety, and insomnia.
Martin also linked to this episode (a) of his podcast on insomnia:
Scott slept well his entire life until he listened to a podcast that led him to worry about how much sleep he was getting and the health consequences of insufficient sleep. That night, Scott had a terrible night of sleep and this triggered a vicious cycle of ever-increasing worry about sleep and increasingly worse sleep that lasted for ten months.
SleepyHead (a sleep clinic in Exeter, UK) writes (a):
My patients are coming to me after reading this alarmist book, with insomnia that they did not have before, and worse, harder to treat because although the book has caused these anxieties - they can’t shake their newly built alarmist beliefs they learnt from the very same book.
After a week of forced 8-hour sleep I faced a problem of not falling asleep for more than an hour. It’s odd on the verge of hyper-personalized healthcare to spread one-size-fits-all advice like that.
Note: this problem was first noticed by Olli Haataja
Figure 7. Likelihood of injury over 21-month period based on hours of sleep per night.
This is a graph from the paper called Chronic Lack of Sleep is Associated With Increased Sports Injuries in Adolescent Athletes. Milewski MD, Skaggs DL, Bishop GA, Pace JL, Ibrahim DA, Wren TA, Barzdukas A. Chronic lack of sleep is associated with increased sports injuries in adolescent athletes. Journal of Pediatric Orthopaedics. 2014 Mar 1;34(2):129-33. Walker cites this paper in Chapter 6 and provides an adaptation of this graph:
Figure 8. Likelihood of injury over 21-month period based on hours of sleep per night.
The 5 hours of sleep column – which is associated with lower chance of injury than 6 hours of sleep – has simply disappeared.
Similarly Walker discusses this study on the Joe Rogan podcast, saying that there’s “a perfect linear relationship: the less sleep that you have, higher your injury risk” in athletes when they were surveyed and found to be sleeping between 4 and 9 hours and that those who slept 5 hours have almost 60% more injuries than those who sleep 9 hours.
Note that none of these facts are true. Nobody slept 4 hours; the relationship is not perfectly linear; and the increase from 9 hours of sleep to 5 hours of sleep is about 230%, not 60%.
As an aside, that 9 hours of sleep column is based on exactly 1 child being injured out of 6 children who reported sleeping for 9 hours.
Many people defend Walker cutting of the data from the graph by saying that he is just trying to make the trend clearer for the popular audience. As I noted in the Introduction of this essay, this argument is indefensible:
On page 8 of the book, Walker writes:
[T]he real evidence that makes clear all of the dangers that befall individuals and societies when sleep becomes short have not been clearly telegraphed to the public … In response, this book is intended to serve as a scientifically accurate intervention addressing this unmet need …
The myths created by the book have spread in the popular culture and are being propagated by Walker and by other scientists in academic research. For example, in 2019, Walker published an academic paper that cited Why We Sleep 4 times just on its first page, meaning that he believes that the book abides by the academic, not the pop-science standards of accuracy (Section 14).
I devote an entire section to the discussion of whether Walker’s book is “pop-science” here.
See discussion of this point by Andrew Gelman: “Why we sleep” data manipulation: A smoking gun? (a)
Update: Neil Stanley shows another example of Walker cutting off data from the graph to change its conclusion (a):
not for the first time! the 1st pic is a tweet from the @sleepdiplomat [a] 15/06/19 [archived tweet] the 2nd data from the paper, he has cropped both the data and the word ‘ratio’ to misrepresent the data which actually shows Veteran suicides peaks between 1000–1200 https://www.sciencedirect.com/science/article/abs/pii/S138994571830861X [a]
Leonardo Tozzi writes in an email:
two of my close friends had stopped sleeping after reading “Why we sleep”, but your post “cured them”. I had tried myself to convince them the book was nonsense but couldn’t.
In Chapter 8, Walker discusses the relationship between sleep and cardiovascular health. In the first paragraph of this discussion, he mentions two studies. He seems to completely misrepresent both of them. Most notably, in the description of both of these studies he inflates their sample sizes. In one case, the study’s 474,684 people turn into “more than half a million”. In the other case, 2,282 people turn into “over 4,000”.
Here’s what Walker writes:
Unhealthy sleep, unhealthy heart. Simple and true. [1] Take the results of a 2011 study that tracked more than half a million men and women of varied ages, races, and ethnicities across eight different countries. Progressively shorter sleep was associated with a 45 percent increased risk of developing and/or dying from coronary heart disease within seven to twenty-five years from the start of the study. [2] A similar relationship was observed in a Japanese study of over 4,000 male workers. Over a fourteen-year period, those sleeping six hours or less were 400 to 500 percent more likely to suffer one or more cardiac arrests than those sleeping more than six hours. [numeration mine]
Although he does not cite the two studies he discusses, he gives enough identifying information that I believe I was able to find both of them.
The first one is Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies (a). Cappuccio FP, Cooper D, D’elia L, Strazzullo P, Miller MA. Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies. European Heart Journal. 2011 Feb 7;32(12):1484-92. Here are the characteristics of the paper that match Walker’s description:
Here are the issues with his description of the paper:
The second study he appears to describe in that paragraph is The effects of sleep duration on the incidence of cardiovascular events among middle-aged male workers in Japan (a). Hamazaki Y, Morikawa Y, Nakamura K, Sakurai M, Miura K, Ishizaki M, Kido T, Naruse Y, Suwazono Y, Nakagawa H. The effects of sleep duration on the incidence of cardiovascular events among middle-aged male workers in Japan. Scandinavian Journal of Work, Environment & Health. 2011 Sep 1:411-7. Here are the characteristics of the paper that match Walker’s description:
Here are the issues with his description of the paper:
I was looking into Matthew Walker a bit and it seems odd that where he claims he got his PhD on his own website [a] (the MRC in London, very prestigious) is clearly not where he got his PhD: both his thesis [a] and wikipedia page [a] show that his PhD was from the University of Newcastle upon Tyne (less prestigious). A contemporaneous publication [a] shows his affiliation as “MRC Neurochemical Pathology Unit, Newcastle General Hospital, Newcastle upon Tyne, UK”.
Was he just sloppy in writing up the bio on his own website? Or stretching the truth to tell a better story? This seems reminiscent of the issues that /u/guzey and others are grappling with in this thread.
Matthew Walker’s site says (a):
Dr. Walker earned his degree in neuroscience from Nottingham University, UK, and his PhD in neurophysiology from the Medical Research Council, London, UK.
As of 2019-12-03, the University of Newcastle upon Tyne is never mentioned on Walker’s site (a). I emailed MRC London for a confirmation that Walker received his PhD there and they told me that they do not grant PhD degrees. Neil Stanley notes on twitter (a):
The MRC is not a degree/PhD awarding body. He may have got funding from the MRC for his studies but his PhD must have been awarded by an academic institution.
On forum.guzey.com, ish found several more serious problems with Why We Sleep:
Chapter 8 also contains another erroneous description of an existing study. In the section “Sleep Loss and the Reproductive System” Walker refers to work by Tina Sundelin on “how attractive you look when sleep-deprived”. This appears* to refer to the study “Beauty sleep: experimental study on the perceived health and attractiveness of sleep deprived people” (Axelsson, Sundelin, Ingre, Van Someren) [2010] {10.1136/bmj.c6614}.
Walker states that:
In one of the sessions, the participants were given just five hours of sleep before being put in front of the camera, while in the other session, these same individuals got a full eight hours of sleep.
He goes on to say:
The faces pictured after one night of short sleep were rated as looking more fatigued, less healthy, and significantly less attractive.
However, in the cited paper it says that the researchers
photographed the faces of 23 adults (mean age 23, range 18-31 years, 11 women) between 14.00 and 15.00 under two conditions in a balanced design: after a normal night’s sleep (at least eight hours of sleep between 23.00-07.00 and seven hours of wakefulness) and after sleep deprivation (sleep 02.00-07.00 and 31 hours of wakefulness)
Walker completely fails to mention that the individuals who received five hours of sleep were also sleep deprived for 31 hours. This fact is even directly stated in the abstract of the paper:
Participants were photographed after a normal night’s sleep (eight hours) and after sleep deprivation (31 hours of wakefulness after a night of reduced sleep)
This completely changes the interpretation of the paper. Being able to tell visually if someone has had 5 hours of sleep is considerably different from being able to tell if they have had five hours of sleep AND have been sleep deprived for 31 hours.
And in another comment in the same thread, ish writes:
[I]n Chapter 8 in the section “Sleep Loss and the Immune System” he [Walker] refers to work by Dr. Aric Prather regarding sleep and colds. He describes the results of the study (without citation) “Behaviorally Assessed Sleep and Susceptibility to the Common Cold” (Prather, Janicki-Deverts, Hall, Cohen) [2015] {10.5665/sleep.4968}. Walker states that:
“In those sleeping five hours on average, the infection rate was almost 50 percent”.
However, looking at the paper, of the 164 participants (Walker refers to this as “more than 150”) “124 (75.6%) were infected and 48 (29.3%) developed a biologically verified cold”. From page 4, Figure 1 of the paper, ~45% of those who slept LESS than 5 hours developed an objective cold (~16 out of 36 people), while ~30% of those who slept 5-6 hours (16 out of 54 people) developed a cold. So somehow 45% sleeping LESS than 5 hours transforms into 50% sleeping 5 hours ON AVERAGE.
Once more, on pages 4-5, Walker writes:
[T]here is a very rare genetic disorder that starts with a progressive insomnia, emerging in midlife [fatal familial insomnia (FFI)]. [1] Several months into the disease course, the patient stops sleeping altogether. By this stage, they have started to lose many basic brain and body functions. [2] No drugs that we currently have will help the patient sleep. [3] After twelve to eighteen months of no sleep, the patient will die. Though exceedingly rare, [4] this disorder asserts that a lack of sleep can kill a human being. [numeration mine]
Statement [1]:
Several months into the disease course, the patient stops sleeping altogether.
This is false. Here’s a description of a case of FFI (a) from the case report paper I referenced in Section 3 (a): Schenkein J, Montagna P. Self-management of fatal familial insomnia. Part 2: case report. Medscape General Medicine. 2006;8(3):66.
Until roughly the 23rd month, DF’s sleep patterns showed a definite cycle, which may have reflected his rotating schedule of the various medications. The first night, he slept well; the second night, less well; and the third, still less, followed by 1–2 sleepless nights. Then the cycle repeated.
Statement [2]:
No drugs that we currently have will help the patient sleep.
This is false. From the same paper:
Gamma-hydroxybutyrate (GHB) was administered during the last month of DF’s life. … According to his caretaker, GHB resulted in sleep within 30 minutes of administration, but did not last long enough for DF to feel rested.
Finally, statement [3] is also false. In case you suspect that he was only writing about the typical course of the disease when writing “After twelve to eighteen months of no sleep, the patient will die”, in Chapter 12, Walker clarifies:
Every patient diagnosed with the disorder [FFI] has died within ten months, some sooner"
Setting aside the question of how all the patients who died within ten months of diagnosis were able to get “twelve to eighteen months of no sleep” – if, as Walker writes, the patient loses sleep several months into the disease course and dies within eighteen months of no sleep, then life expectancy from the onset of the disease is no more than two years. However, for example, this paper (doi) finds that: Montagna P, Cortelli P, Avoni P, Tinuper P, Plazzi G, Gallassi R, Portaluppi F, Julien J, Vital C, Delisle MB, Gambetti P. Clinical features of fatal familial insomnia: phenotypic variability in relation to a polymorphism at codon 129 of the prion protein gene. Brain Pathology. 1998 Jul;8(3):515-20.
Detailed analysis of 14 cases from 5 unrelated families showed that patients ran either a short (9.1+ 1.1 months) or a prolonged (30.8 + 21.3 months) clinical course according to whether they were homozygote met/met or heterozygote met/val at codon 129.
See discussion of statement [4] in Section 3.
Basically everything in Walker’s description of the disease is wrong, aside from the fact that people suffering from it die eventually.
He [Walker] has been frustrating to many in the sleep field for years—talks showing bar graphs without any error bars, clear misunderstandings of p-values, etc. Check out this doozy from a review back in 2005:
In Table 1, he shows a series of studies with various p-values, then claims that the “The combined probability of 10^-15 reflects the likelihood of all six studies providing such low probabilities for the null hypothesis.” How did he generate such a small p-value? It appears he multiplied the numbers from the studies together—but that is by no means a correct methodology! It doesn’t take much knowledge of p-values to realize the absurdity of this: no one would claim that 6 studies with a p-value of 0.5 for a phenomenon would nevertheless be convincing evidence of a real effect (0.5^6=0.015)!
Just to add to your pile of errors in the Why We Sleep book, in Chapter 12 there is a confused section when he talks about narcolepsy and says, “Medically, narcolepsy is considered to be a neurological disorder, meaning that its origins are within the central nervous system, specifically the brain. The condition usually emerges between ages ten and twenty years. There is some genetic basis to narcolepsy, but it is not inherited. Instead, the genetic cause appears to be a mutation, so the disorder is not passed from parent to child. However, gene mutations, at least as we currently understand them in the context of this disorder, do not explain all incidences of narcolepsy.” Page 181.
His discussion of genetics here is very confused. If there were a genetic cause, it would be inherited—and in fact there are rare cases of narcolepsy due directly to mutations in the signalling cascades involved in narcolepsy (Hypocretin/orexin signalling). For example, an examples was reported in this study: https://med.stanford.edu/content/dam/sm/narcolepsy/documents/autopsy/naturemed6.pdf But this is very, very rare.
What he seems to be confusing is the data showing that a certain fairly common human HLA variation is strongly associated with developing narcolepsy—but since most people who have this variation do not get narcolepsy, the HLA variant alone cannot be causal for narcolepsy by itself. E.g. these studies: Tafti M, Hor H, Dauvilliers Y, et al. DQB1 locus alone explains most of the risk and protection in narcolepsy with cataplexy in Europe. Sleep. 2014;37:19–25.
Hor H, Kutalik Z, Dauvilliers Y, et al. Genome-wide association study identifies new HLA class II haplotypes strongly protective against narcolepsy. Nat Genet. 2010;42:786–9.
It is utterly nonsensical to say, “The genetic cause appears to be a mutation, so the disorder is not passed from parent to child.” It is not usually passed from parent to child, true, but that is not because of the genetic cause being a mutation, which WOULD make it inherited. That common HLA variant certainly IS passed from parent to child. But since the HLA locus is not “the genetic cause”, narcolepsy is not (usually) inheritable.
Between late 2010/early 2011 and August/September 2015 [1 (a), 2 (a), 3 (a), 4 (a)], CDC had a page on its site titled “Insufficient Sleep Is a Public Health Epidemic”. More than 2 years before Why We Sleep was published, the page changed the word “epidemic” to “problem”, so that its title became “Insufficient Sleep Is a Public Health Problem”.
A charitable interpretation of this would be that Walker simply misremembered the organization (and added the “industrialized nations” bit). Even this interpretation suffers from
Walker talked about this a bit in an interview to DailyGood (a) a few months before the book was published (h/t Ellen). Note whether he actually answers the interviewer’s question:
Aryae: You talk about the global sleepless epidemic as the greatest public health challenge that we are now facing, and hearing what you are now saying, it makes a lot of sense. Before the call, I was curious and Googled public health challenges and I got all kinds of lists.*Here is one from the Centers for Disease Control and Prevention (CDC) that was published in March 2017. They have on the list alcohol-related harms, food safety, healthcare-associated infections, heart disease/strokes, HIV, motor vehicle injuries, nutrition, physical activity and obesity, prescription drug overdose, teen pregnancy, and tobacco use. They do not have sleep on their list. So what do you say about that discrepancy?
Matt: What is fascinating is that almost every one of those large public health concerns is directly related to insufficient sleep. So, for example, we know that insufficient sleep is tied to high rates of cardiovascular disease, the calcification of the coronary arteries, hypertension, and stroke. We also know that sleep loss is causally related to obesity. Sleeplessness has a profound impact on your immune health and in fact you can go to so many of the classic immune disorders even the common cold. People who get six hours of sleep or less are between 50% or 60% more likely to catch a cold than those who sleep more.
Cancer is now strongly related to insufficient sleep. That includes cancer of the bowel, cancer of the prostate, and cancer of the breast. So much so that in fact the World Health Organization (WHO) recently classified any form of nighttime shift work as a probable carcinogen. Set jobs that disrupt your sleep wake rhythm are cancer-inducing, that is how strong the evidence is right now.
We now know that drowsy driving causes more accidents on our roads then either drugs or alcohol combined. And yet we spend a fraction of 1% of our public health policy budget on educating people about the dangers of insufficient sleep.
Risk-and-reward behaviors are intimately tied to insufficient sleep, from risky behavior to drug addiction and drug-taking and teenage pregnancy. We’ve done a lot of work in this area, too, particularly on adolescent youth. You shorten their sleep; they become much more risk-taking and sensation-seeking. They engage in behaviors that are high-risk behaviors.
Every one of the conditions on that list has a link to insufficient sleep! So why sleep is not on that list is so desperately sad and striking to me. That is why people like me needed to become much better sleep ambassadors. We need to go to places like Capitol Hill. We need not just go there waving our hands saying look at this problem. We need to come up with 21st century new visions of solutions. And that is one of the things that I speak about in the forthcoming book. And is one of the things that I am trying to now push very hard with a number of quick advocacy policies. We need to change society for the better. We need to reorient and prioritize!
The Atlantic (a):
Here’s the story that people like to tell about the way we sleep: Back in the day, we got more of it. Our eyes would shut when it got dark. We’d wake up for a few hours during the night instead of snoozing for a single long block. And we’d nap during the day.
Then—minor key!—modernity ruined everything. Our busy working lives put an end to afternoon naps, while lightbulbs, TV screens, and smartphones shortened our natural slumber and made it more continuous.
All of this is wrong, according to Jerome Siegel at the University of California, Los Angeles. Much like the Paleo diet, it’s based on unsubstantiated assumptions about how humans used to live.
Siegel’s team has shown that people who live traditional lifestyles in Namibia, Tanzania, and Bolivia don’t fit with any of these common notions about pre-industrial dozing. “People like to complain that modern life is ruining sleep, but they’re just saying: Kids today!” says Siegel. “It’s a perennial complaint but you need data to know if it’s true.”
Such data have been hard to come by because the devices that we use to measure and record sleep have only been invented in the last 50 years, and those that do so without disturbing the sleepers are just a decade old. So, there’s no baseline for how long people used to sleep before electric lights. Absent that baseline, Siegel’s team did the next best thing: They studied people who live traditional lifestyles, including Hadza and San hunter-gatherers from Tanzania and Nambia respectively, and Tsimane hunter-farmers from Bolivia.
The team asked 94 people from these groups to wear Actiwatch-2 devices, which automatically recorded their activity and ambient-light levels. The data revealed that these groups all sleep for nightly blocks of 6.9 and 8.5 hours, and they spend at least 5.7 to 7.1 hours of those soundly asleep. That’s no more than what Westerners who have worn the same watches get; if anything, it’s slightly less.
They don’t go to sleep when it gets dark, either. Instead, they nod off between 2 and 3 hours after sunset, well after it becomes pitch-black. And they napped infrequently: The team scored “naps” as periods of daytime inactivity that lasted for at least 15 minutes, and based on these lenient criteria, the volunteers “napped” on just 7 percent of winter days and 22 percent of summer ones.
No relation to Walker’s book, but this paper (a): Geissmann Q, Beckwith EJ, Gilestro GF. Most sleep does not serve a vital function: Evidence from Drosophila melanogaster. Science Advances. 2019 Feb 1;5(2):eaau9253. is really fun:
Sleep appears to be a universally conserved phenomenon among the animal kingdom, but whether this notable evolutionary conservation underlies a basic vital function is still an open question. Using a machine learning–based video-tracking technology, we conducted a detailed high-throughput analysis of sleep in the fruit fly Drosophila melanogaster, coupled with a lifelong chronic and specific sleep restriction. Our results show that some wild-type flies are virtually sleepless in baseline conditions and that complete, forced sleep restriction is not necessarily a lethal treatment in wild-type D. melanogaster. We also show that circadian drive, and not homeostatic regulation, is the main contributor to sleep pressure in flies. These results offer a new perspective on the biological role of sleep in Drosophila and, potentially, in other species.
In the third paragraph of Chapter 2, Walker writes:
[E]very living creature on the planet with a life span of more than several days generates this natural [circadian] cycle
This is false. Brewer’s yeast (S. cerevisiae):
There are two ways to view this error:
Circadian rhythm in general is overrated [1 (a) Hazlerigg DG, Tyler NJ. Activity patterns in mammals: Circadian dominance challenged. PLSS Biology. 2019 Jul 15;17(7):e3000360. , 2 (doi) Bloch G, Barnes BM, Gerkema MP, Helm B. Animal activity around the clock with no overt circadian rhythms: patterns, mechanisms and adaptive value. Proceedings of the Royal Society B: Biological Sciences. 2013 Aug 22;280(1765):20130019. ].
I doubt you are surprised by this fact, but you may be surprised by the consequences. Routinely sleeping less than six or seven hours a night demolishes your immune system, more than doubling your risk of cancer. Insufficient sleep is a key lifestyle factor determining whether or not you will develop Alzheimer’s disease. Inadequate sleep—even moderate reductions for just one week—disrupts blood sugar levels so profoundly that you would be classified as pre-diabetic. Short sleeping increases the likelihood of your coronary arteries becoming blocked and brittle, setting you on a path toward cardiovascular disease, stroke, and congestive heart failure. Fitting Charlotte Brontë’s prophetic wisdom that “a ruffled mind makes a restless pillow,” sleep disruption further contributes to all major psychiatric conditions, including depression, anxiety, and suicidality.
Perhaps you have also noticed a desire to eat more when you’re tired? This is no coincidence. Too little sleep swells concentrations of a hormone that makes you feel hungry while suppressing a companion hormone that otherwise signals food satisfaction. Despite being full, you still want to eat more. It’s a proven recipe for weight gain in sleep-deficient adults and children alike. Worse, should you attempt to diet but don’t get enough sleep while doing so, it is futile, since most of the weight you lose will come from lean body mass, not fat.
Add the above health consequences up, and a proven link becomes easier to accept: the shorter your sleep, the shorter your life span.
The swings in emotional brain activity that we observed in healthy individuals who were sleep-deprived may also explain a finding that has perplexed psychiatry for decades. Patients suffering from major depression, in which they become exclusively locked into the negative end of the mood spectrum, show what at first appears to be a counterintuitive response to one night of sleep deprivation. Approximately 30 to 40 percent of these patients will feel better after a night without sleep. Their lack of slumber appears to be an antidepressant.
The reason sleep deprivation is not a commonly used treatment, however, is twofold. First, as soon as these individuals do sleep, the antidepressant benefit goes away. Second, the 60 to 70 percent of patients who do not respond to the sleep deprivation will actually feel worse, deepening their depression. As a result, sleep deprivation is not a realistic or comprehensive therapy option. Still, it has posed an interesting question: How could sleep deprivation prove helpful for some of these individuals, yet detrimental to others?
I believe that the explanation resides in the bidirectional changes in emotional brain activity that we observed. Depression is not, as you may think, just about the excess presence of negative feelings. Major depression has as much to do with absence of positive emotions, a feature described as anhedonia: the inability to gain pleasure from normally pleasurable experiences, such as food, socializing, or sex.
The one-third of depressed individuals who respond to sleep deprivation may therefore be those who experience the greater amplification within reward circuits of the brain that I described earlier, resulting in far stronger sensitivity to, and experiencing of, positive rewarding triggers following sleep deprivation. Their anhedonia is therefore lessened, and now they can begin to experience a greater degree of pleasure from pleasurable life experiences. In contrast, the other two-thirds of depressed patients may suffer the opposite negative emotional consequences of sleep deprivation more dominantly: a worsening, rather than alleviation, of their depression. If we can identify what determines those who will be responders and those who will not, my hope is that we can create better, more tailored sleep-intervention methods for combating depression.
2001-01-01 08:00:00
This is a guest post by Allen Hoskins. Allen’s Twitter & Substack.
Experts say artificial general intelligence (AGI) will take around forty years to develop and won’t fully automate us for almost a century. At the same time, advancements like ChatGPT and DALLE-2 seem to send a different message. Silicon Valley and leading AI initiatives are anticipating this technology to spark radical change over the next decade – enough to redefine society from the ground up.
So, why do AI researchers continue to predict AGI into the latter half of the century? And should we even take them seriously?
AI experts’ work is spread across the fields of machine learning and computational neuroscience. There are a plethora of research directions being explored. These include reinforcement learning, convolutional neural networks, training image classifiers, neurosymbolic modules, hybrid systems wanting to directly imprint inspirations from the brain… This is still just barely scratching the AI approach surface.
Yet, today’s premier AI systems make little use of other AI researchers’ work. The most powerful models in 2023 are still based on Google’s “Transformer” architecture first showcased in 2017. And with this current paradigm, progress mainly stems from solving the engineering challenges of transformers. These include but are not limited to: hardware scaling, data curation, algorithmic tweaks, careful fine-tuning, and adding more compute. Advancements are, by and large, anything that serves to scale these models up bigger – personifying the mantra of “Scale is all you need.”
In contrast, academia values publishing research that is “novel” and “innovative”. Researchers must craft a unique AI portfolio to stand out from the crowd and capture shares from the S&P H-INDEX – hopefully bolstering their odds to secure future grants. Academics must be constantly innovating or to die trying.
Transformers though just want more server racks, more engineers, and more Reddit memes to train on. This doesn’t leave much room for the intellectual freedom and innovation academia demands or for the other AI approaches to substantially contribute.
Instead, we’re now in the middle of an industry speedrun to see if this actually scales all the way to AGI.
If scaling systems like transformers beats every other approach and single-handedly leads to AGI, most researchers will have no academic route to fall back on. In the new AI paradigm, the promising and thought worthy approaches scholars built their career on could become inferior, forgotten, and be of little benefit on the road to AGI. As a result, recent AI trends could be unsettling. Most AI scientists are at risk of losing their sense of purpose, their work feeling meaningless, ignored, and left to wonder how it all happened so fast.
Early in their career, scientists choose to pursue AI methods that seemed promising, and interesting. They go on to develop the priors and beliefs for why it could eventually work. For example, neuroscientists working in AI usually contemplate systems significantly more complex than deep learning. These experts believe you need to apply deep theories to models to make truly intelligent systems. The brain is their mandatory guide to designing artificial intelligence.
Most people in machine learning also don’t see scale as basically enough for AGI – many don’t even think that’s a possibility. While they view scale as a meaningful concept, most researchers think it’s just a tool to use along the way. Through this perspective, they are actively implying a need for fundamentally new architectures. That you can’t just scale Transformers to AGI.
ChatGPT, however, ignores all of that.. After the model’s performance stalls, the parameter count gets raised, more compute gets allocated, more engineering optimizations are deployed, even deeper recesses of the internet and even cringier Reddit memes get scraped, rinse, and repeat. The process remains straightforward and formulaic.
And once-in-a-while someone kinda wonders “what if I ask the model to think step-by-step?” and improves the model’s performance more than all scientists combined in several years of generating their novelty-maxxing NeurIPS papers.
Many experts see simple models and an inherent lack of complex theory as nonsense and statistical noise that “appears” intelligent.
They often focus on raw numbers, linear trendlines and ignore the story of the model’s emergent trends. Thus, many believe these systems will always falter on real tests of intelligence and fundamentally can’t become AGI.
Most experts, then, will simply not update their AI timelines from scaling progress.
Researchers need to be probing the world’s best AI systems to understand their abilities and predict AI’s future. This would include testing things like how scale improves a system, the ways reasoning ability changes over time and how these models compare to humans.
Unfortunately, most academics don’t have the models necessary for that critical work.
Due to a lack of funding and no access to industry’s cutting-edge AI, researchers’ options are heavily restricted. They’re left with small toy models and older public models like GPT – soon to be out of date. GPT-3 might not strike people as old, and out of date. Instead, they might see it as the biggest leading model. And that’s a reasonable thing to think, but it’s just an illusion – given that ChatGPT is almost a year old.
There are always more powerful systems built and tested months before release. Academics can’t predict scale and deep learning’s actual limitations or capabilities without direct access to the powerful, secretive models to be released any moment by OpenAI, DeepMind or Google Brain.
GPT-3 and ChatGPT provide but a glimpse of what current AI systems can do.
Academics choose to pursue a long academic path for a reason. Fundamentally, they want to express their creativity and freedom within a research area that suits their intellectual curiosities – to ask big questions and find answers in thriving research communities.
AI’s new key holder, FAANG, restricts these desires through their binding responsibilities and directives. On a moment’s notice, a system you hardly understand and built by dozens of people you barely know, could become your responsibility to fix. You’re often separated from the craft of building from the ground up and instead serve to fulfill a company’s wish.
While many people are content with this and their increasingly thicker wallets, others are losing a type of magic. The type with big theories, a sense of independence, and the recognition of accomplishment promised by academia. Some avoid the switch because scholarly crowds might view it as less “prestigious.” And even if you work on amazing industry AI, companies don’t always publish their research – meaning your multi-year project may not see the light of day and nobody will ever cite you by name.
All of this means many researchers will not step away from academia to go full-time at corporations and they will never get access to FAANG’s cutting-edge AI frontier, left with ChatGPT and psets they assign to hapless undergrads to test it on.
Sudden changes are a struggle for experts in any line of work. This is because people bias their predictions toward the average of “their” work experience instead of priors that shift with newer trends. And machine learning scientists are in a much different field now than they were 10 or even 3-5 years ago.
In the past, challenges may have seemed daunting given the few engineers and slow pace of innovation. Every bottleneck, bug, and error risked delaying a system by months. This built their first strong impression that machine learning was a “slow moving” field. Most of those running academic AI labs grew up during the time when neural networks barely worked at all.
This was before they had entire industries designing hardware to accelerate their AI. When they didn’t have ten thousand FAANG scientists dedicated to solving key challenges in machine learning. And now FAANG are willing to invest big into their singular, premier AI groups. Ten billion dollars-big in Microsoft’s case.
Unable to zoom out, experts will keep extrapolating their historic experiences linearly & if the field is driven by exponentials they might actually be the last ones to notice an impending AI explosion coming and wake up one day to find that AI killed everyone oops, sorry, I meant everyone’s h-indexes.
Artificial intelligence’s lightning-fast pace is disconcerting. Experts stand in a direct conflict between the field they built their lives around and how its rapid innovation could threaten everything they’ve worked for. With pressures mounting, a great deal don’t want to actually stay caught up and look through a clear lens.
Experts can either accept that they may be about to lose everything or continue saying AGI is far away. Overwhelmingly, they choose the latter option.
2001-01-01 08:00:00
People often ask me for writing advice. This is the advice I give them.
Thanks to Sean Shelley-Tremblay, Jonas Vollmer, Amanda Geiser, and Niko McCarty for feedback.
Every day, stop writing just a short while before you really want to quit. The next day you will be very keen to get going again. For most mortals, your real enemy is the number of days when you get nothing written. Getting “not enough” done each day is a lesser problem.
Simple advice for academic publishing:
Care about what you are doing. This is ultimately your best ally.
From How to Fail at Almost Everything and Still Win Big:
I never took a writing class in high school or in college. I learned the basics in English classes and that seemed good enough. I could write sentences that people understood. What else did I need?
I did notice that some people in the business world wrote with an impressive level of clarity and persuasiveness. But I figured that was just because those people were extra smart. It never occurred to me that there was some technique involved and that we unwashed citizens could easily learn it.
One day during my corporate career I signed up for a company-sponsored class in business writing. This was part of my larger strategy of learning as much as I could about whatever might someday be useful while my employer was willing to foot the bill. I didn’t have high hopes that the class would change my life. I was just looking for some tips and tricks for better writing.
I was very wrong about how useful the class would be. If I recall, the class was only two afternoons long. And it was life altering.
As it turns out, business writing is all about getting to the point and leaving out all of the noise. You think you already do that in your writing, but you probably don’t.
Consider the previous sentence. I intentionally embedded some noise. Did you catch it? The sentence that starts with “You think you already do that” includes the unnecessary word “already.” Remove it and you get exactly the same meaning: “You think you do that.” The “already” part is assumed and unnecessary. That sort of realization is the foundation of business writing.
Business writing also teaches that brains are wired to better understand concepts that are presented in a certain order. For example, your brain processes “The boy hit the ball” more easily than “The ball was hit by the boy.” In editors’ jargon, the first sentence is direct writing and the second is passive. It’s a tiny difference, but over the course of an entire document, passive writing adds up and causes reader fatigue.
Eventually I learned that the so-called persuasive writers were doing little more than using ordinary business-writing methods. Clean writing makes a writer seem smarter and it makes the writer’s arguments more persuasive.
- Divide things into small chunks
- Variety is the spice of life
- Keep your flow of ideas strong
- Learn what should and shouldn’t be repeated.
- Use microhumor
- Use concrete examples
- Figure out who you’re trying to convince, then use the right tribal signals
- Anticipate and defuse counterarguments
- Use strong concept handles
- Recognize that applying these rules will probably start disastrously
I think it’s far more important to write well than most people realize. Writing doesn’t just communicate ideas; it generates them. If you’re bad at writing and don’t like to do it, you’ll miss out on most of the ideas writing would have generated.
As for how to write well, here’s the short version: Write a bad version 1 as fast as you can; rewrite it over and over; cut out everything unnecessary; write in a conversational tone; develop a nose for bad writing, so you can see and fix it in yours; imitate writers you like; if you can’t get started, tell someone what you plan to write about, then write down what you said; expect 80% of the ideas in an essay to happen after you start writing it, and 50% of those you start with to be wrong; be confident enough to cut; have friends you trust read your stuff and tell you which bits are confusing or drag; don’t (always) make detailed outlines; mull ideas over for a few days before writing; carry a small notebook or scrap paper with you; start writing when you think of the first sentence; if a deadline forces you to start before that, just say the most important sentence first; write about stuff you like; don’t try to sound impressive; don’t hesitate to change the topic on the fly; use footnotes to contain digressions; use anaphora to knit sentences together; read your essays out loud to see (a) where you stumble over awkward phrases and (b) which bits are boring (the paragraphs you dread reading); try to tell the reader something new and useful; work in fairly big quanta of time; when you restart, begin by rereading what you have so far; when you finish, leave yourself something easy to start with; accumulate notes for topics you plan to cover at the bottom of the file; don’t feel obliged to cover any of them; write for a reader who won’t read the essay as carefully as you do, just as pop songs are designed to sound ok on crappy car radios; if you say anything mistaken, fix it immediately; ask friends which sentence you’ll regret most; go back and tone down harsh remarks; publish stuff online, because an audience makes you write more, and thus generate more ideas; print out drafts instead of just looking at them on the screen; use simple, germanic words; learn to distinguish surprises from digressions; learn to recognize the approach of an ending, and when one appears, grab it.
2001-01-01 08:00:00
let me know if you have answers
2001-01-01 08:00:00
2024 update: Please note that as of 2024, I aim to sleep 7-8 hours most of the nights.
Summary: In this essay, I question some of the consensus beliefs about sleep, such as the need for at least 7 hours of sleep for adults, harmfulness of acute sleep deprivation, and harmfulness of long-term sleep deprivation and our inability to adapt to it.
It appears that the evidence for all of these beliefs is much weaker than sleep scientists and public health experts want us to believe. In particular, I conclude that it’s plausible that at least acute sleep deprivation is not only not harmful but beneficial in some contexts and that it’s that we are able to adapt to long-term sleep deprivation.
I also discuss the bidirectional relationship of sleep and mania/depression and the costs of unnecessary sleep, noting that sleeping 1.5 hours per day less results in gaining more than a month of wakefulness per year, every year.
Note: I sleep the normal 7-9 hours if I don’t restrict my sleep. However, stimulants like coffee, modafinil, and adderall seem to have much smaller effect on my cognition than on cognition of most people I know. My brain in general, as you might guess from reading this site, is not very normal. So, be cautious before trying anything with your sleep on the basis of the arguments I lay out below. Specifically do not make any drastic changes to your sleep schedule on the basis of reading this essay and, if you want to experiment with sleep, do it gradually (i.e. varying the average amount of sleep by no more than 30 minutes at a time) and carefully.
Also see Natália Coelho Mendonça Counter-theses on Sleep.
The default argument for sleeping 7-9 hours a night is that this is the amount of sleep most of us get “naturally” when we sleep without using alarms. In this section, I argue against this line of reasoning, using the following analogy:
Most of us (myself included) eat a lot of junk food and candy if we don’t restrict ourselves. Does this mean that lots of junk food and candy is the “natural” or the “optimal” amount for health?
Obviously, no. Modern junk food and candy are unnatural superstimuli, much tastier and much more abundant than any natural food, so they end up overwhelming our brains with pleasure, especially given that we are bored at work, college, or in high school so much of the day.
What if the only food available to you was junk food and candy?
Most of us (myself included) sleep 7-9 hours if we don’t have any alarms in the morning and if we get out of bed when we feel like it. Does this mean that 7-9 hours of sleep is the “natural” or the “optimal” amount?
My thesis is: obviously, no. Modern sleep, in its infinite comfort, is an unnatural superstimulus that overwhelms our brains with pleasure and comfort (note: I’m not saying that it’s bad, simply that being in bed today is much more pleasurable than being in “bed” in the past.)
Think about sleep 10,000 years ago. You sleep in a cave, in a hut, or under the sky, with predators and enemy tribes roaming around. You are on a wooden floor, on an animal’s skin, or on the ground. The temperature will probably drop 5-10°C overnight, meaning that if you were comfortable when you were falling asleep, you are going to be freezing when you wake up. Finally, there’s moon shining right at you and all kinds of sounds coming from the forest around you.
In contrast, today: you sleep on your super-comfortable machine-crafted foam of the exact right firmness for you. You are completely safe in your home, protected by thick walls and doors. Your room’s temperature stays roughly constant, ensuring that you stay warm and comfy throughout the night. Finally, you are in a light and sound-insulated environment of your house. And if there’s any kind of disturbance you have eye masks and earplugs.
Does this sound “natural”?
Now, what if the only sleep available to you was modern sleep?
Even if I convinced you about the “sleeping too much” part, you are still probably wondering: but what does depression have to do with anything? Isn’t sleeping a lot good for mental health? Well…
In this section, I argue that depression triggers/amplifies oversleeping while oversleeping triggers/amplifies depression. Similarly, mania triggers/amplifies acute sleep deprivation while acute sleep deprivation triggers/amplifies mania.
One of the most notable facts about sleep is just how interlinked excessive sleep is with depression and how interlinked sleep deprivation is with mania in bipolar people.
Someone in r/BipolarReddit asked: How many hours do you sleep when stable vs (hypo)manic? Depressed?
Here are all 8 answers that compare hours for manic and depressed states, I excluded answers that describe hypomania but do not describe mania or that only describe mania or only describe depression. note the consistency:
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 Riemann, D., König, A., Hohagen, F., Kiemen, A., Voderholzer, U., Backhaus, J., Bunz, J., Wesiack, B., Hermle, L. and Berger, M., 1999. How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay. European archives of psychiatry and clinical neuroscience, 249(5), pp.231-237. ). NOTE: DO NOT TRY THIS IF YOU ARE BIPOLAR, YOU MIGHT GET A MANIC EPISODE.
Figure 1. Copied from Wehr TA. Improvement of depression and triggering of mania by sleep deprivation. JAMA. 1992 Jan 22;267(4):548-51.
Why does the lack of sleep promote manic states while long sleep promotes depression? I don’t know. But here are a couple of pointers to interesting papers relevant to the question: Can non-REM sleep be depressogenic? Beersma DG, Van den Hoofdakker RH. Can non-REM sleep be depressogenic?. Journal of affective disorders. 1992 Feb 1;24(2):101-8. Brain-derived neurotrophic factor (BDNF) is associated with synapse growth. Sleep deprivation appears to increase BDNF [and therefore neurogenesis?]. Papers that showed up when I googled “sleep deprivation bdnf”: The Brain-Derived Neurotrophic Factor: Missing Link Between Sleep Deprivation, Insomnia, and Depression. Rahmani M, Rahmani F, Rezaei N. The brain-derived neurotrophic factor: missing link between sleep deprivation, insomnia, and depression. Neurochemical research. 2020 Feb;45(2):221-31. The link between sleep, stress and BDNF. Eckert A, Karen S, Beck J, Brand S, Hemmeter U, Hatzinger M, Holsboer-Trachsler E. The link between sleep, stress and BDNF. European Psychiatry. 2017 Apr;41(S1):S282-. BDNF: an indicator of insomnia?. Giese M, Unternährer E, Hüttig H, Beck J, Brand S, Calabrese P, Holsboer-Trachsler E, Eckert A. BDNF: an indicator of insomnia?. Molecular psychiatry. 2014 Feb;19(2):151-2. Recovery Sleep Significantly Decreases BDNF In Major Depression Following Therapeutic Sleep Deprivation. Goldschmied JR, Rao H, Dinges D, Goel N, Detre JA, Basner M, Sheline YI, Thase ME, Gehrman PR. 0886 Recovery Sleep Significantly Decreases BDNF In Major Depression Following Therapeutic Sleep Deprivation. Sleep. 2019 Apr;42(Supplement_1):A356-.
Jeremy Hadfield writes:
My (summarized/simplified) hypothesis based on what I’ve read: depression involves rigid, non-flexible brain states that correspond to rigid depressive world models. Depression also involves a non-updating of models or inability to draw new connections (brain is even literally slightly lighter in depressed patients). Sleep involves revising/simplifying world models based on connections learned during the day, involves pruning unneeded or irrelevant synaptic connections. Thus, excessive sleep + depression = even less world model updating, even more rigid brain, even fewer new connections. Sleep deprivation can resolve this problem at least temporarily by ensuring that you stay awake for longer and keep adding connections, thus compensating for the decreased connection-building caused by depression and “forcing” a brain update (perhaps through neural annealing - see QRI article).
One other argument for sleeping the “natural” (7-9) number of hours is that we feel bad on days when we sleep less. In this section, I argue against this line of reasoning by asking: if fasting and exercising are good, shouldn’t acute sleep deprivation also be good? And I conclude that it is probably good.
Let’s continue our analogy of sleep to eating and add exercise to the mix.
It seems to me that most common arguments against acute sleep deprivation equally “demonstrate” that fasting and exercise are bad.
For example, I ran 7 kilometers 2 days ago and my legs still hurt like hell and I can’t run at all. Does this mean that running is “bad”?
Well, consensus seems to be that dizziness, muscle damage (and thus pain) and decreased physical performance after the run, are not just not bad, but are in fact necessary for the organism to train to run faster or to run longer distances by increasing muscle mass, muscle efficiency, and lung capacity.
What about fasting? When I fast, I am more anxious, I think about food a lot, meaning that focus is more difficult, and I feel cold. And if I decided to fast too much, I would pass out and then die. Does this mean that fasting is “bad”? Well, consensus seems to be that occasional fasting actually activates some “good” kind of stress, promotes healthy autophagy, (obviously) helps to lose weight, etc. and is in fact good.
Now, what happens when I sleep for 2 hours instead of 7 one night? I feel somewhat tingly in my hands, my mood is heightened a little bit, and, if I start watching a movie with my wife at 6pm, I’ll fall asleep. Does this mean that sleeping 2 hours one night is bad for my health?
Obviously no. The only thing we observe is that my organism was subjected to acute stress. However, the reaction to acute stress does not tell us anything about the long-term effects of this kind of stress. As we know, both in running and in fasting, short-term acute stress response results in adaptation and in long-term increase in performance and in benefit to the organism.
I combed through a lot of sleep literature and I haven’t seen a single study that made a parallel to either fasting or exercise and I haven’t seen a single pre-registered RCT that tried to see what happens to someone if you subject them to 1-3 nights per week of acute sleep deprivation and allow to recover the rest of the nights. Do they perform better or worse in the long-term on cognitive tests? Do they have more or less inflammation? Do they need less recovery sleep over time?
I think that the answers are:
(The only parallel to fasting I’m aware of anyone making is by Nassim Taleb… when he was quote-tweeting me.)
Also see:
In this section, I note that most sleep research is extremely unreliable and we shouldn’t conclude much on the basis of it.
Do you believe in power-posing? In ego depletion? In hungry judges and brain training?
If the answer is no, then your priors for our knowledge about sleep should be weak because “sleep science” is mostly just rebranded cognitive psychology, with the vast majority of it being small-n, not pre-registered, p-hacked experiments.
I have been able to find exactly one pre-registered experiment of the impact of prolonged sleep deprivation on cognition. It was published by economists from Harvard and MIT in 2021 and its pre-registered analysis found null or negative effects of sleep on all primary outcomes Bessone P, Rao G, Schilbach F, Schofield H, Toma M. The economic consequences of increasing sleep among the urban poor. The Quarterly Journal of Economics. 2021 Aug;136(3):1887-941. (note that both the abstract and the main body of this paper report results without the multiple-hypothesis correction, in contradiction to the pre-registration plan of the study. The paper does not mention this change anywhere. See comments for the details. ).
So why has sleep research not been facing a severe replication crisis, similar to psychology?
First, compared to psychology, where you just have people fill out questionnaires, sleep research is slow, relatively expensive, and requires specialized equipment (e.g. EEG, actigraphs). So skeptical outsiders go for easier targets (like social psychology) while the insiders keep doing the same shoddy experiments because they need to keep their careers going somehow.
Second, imagine if sleep researchers had conclusively shown that sleep is not important for memory, health, etc. – would they get any funding? No. Their jobs are literally predicated on convincing the NIH and other grantmakers that sleep is important. As Patrick McKenzie notes, “If you want a problem solved make it someone’s project. If you want it managed make it someone’s job.”
Figure 2. Relative risk of showing benefit or harm of treatment by year of publication for large NHLBI trials on pharmaceutical and dietary supplement interventions. Copied from Kaplan RM, Irvin VL. Likelihood of null effects of large NHLBI clinical trials has increased over time. PloS one. 2015 Aug 5;10(8):e0132382.
Even in medicine, without pre-registered RCTs truth is extremely difficult to come by, with more than one half Kaiser J. More than half of high-impact cancer lab studies could not be replicated in controversial analysis. AAAS Articles DO Group. 2021; of high-impact cancer papers failing to be replicated, and with one half of RCTs without pre-registration of positive outcomes being spun Kaplan RM, Irvin VL. Likelihood of null effects of large NHLBI clinical trials has increased over time. PloS one. 2015 Aug 5;10(8):e0132382. by researchers as providing benefit when there’s none. And this is in medicine, which is infinitely more consequential and rigorous than psychology.
Also see: Appendix: I have no trust in sleep scientists.
In this section, I outline several lines of evidence that bring me to the conclusion that decreasing sleep by 1-2 hours a night in the long-term has no negative health effects. To summarize:
“Solo sailing is one of the best models of 24/7 activity, and brains and muscles are required,” Stampi said one day at his home, from which he runs the institute. “If you sleep too much, you don’t win. If you don’t sleep enough, you break.” …
“For those sailors who are seriously competing, Stampi is a necessity,” says Brad Van Liew, a 37-year-old Californian who began working with Stampi in 1998 and went on to become America’s most accomplished solo racer and the winner in his class of the 2002-2003 Around Alone, a 28,000-mile global solo race. “You have to sleep efficiently, or it’s like having a bad set of sails or a boat bottom that isn’t prepared properly.” …
both Golding and MacArthur sleep about the same amount while racing, between 4.5 and 5.5 hours on average in every 24—the minimum amount, Stampi believes, on which humans can get by.
In 2013, scientists tracked the sleep of 84 hunter-gatherers from 3 different tribes Yetish G, Kaplan H, Gurven M, Wood B, Pontzer H, Manger PR, Wilson C, McGregor R, Siegel JM. Natural sleep and its seasonal variations in three pre-industrial societies. Current Biology. 2015 Nov 2;25(21):2862-8. (each person’s sleep was measured for about a week but measurements for different groups were taken in different parts of the year). The average amount of sleep among these 84 people was 6.5 hours. Judging by CDC’s “7 hours or more” recommendation, Consensus Conference Panel:, Watson, N.F., Badr, M.S., Belenky, G., Bliwise, D.L., Buxton, O.M., Buysse, D., Dinges, D.F., Gangwisch, J., Grandner, M.A. and Kushida, C., 2015. Joint consensus statement of the American Academy of Sleep Medicine and Sleep Research Society on the recommended amount of sleep for a healthy adult: methodology and discussion. Journal of Clinical Sleep Medicine, 11(8), pp.931-952. 70% out of these 84 undersleep:
One group of hunter-gatherers (10 people from Tsimane tribe studied in November/December of 2013) slept just 5.6 hours on average.
The authors of this study also note that “None of these groups began sleep near sunset, onset occurring, on average, 3.3 hr after sunset” (they are probably getting too much artificial light… or something).
What I’m getting from all of this is: there’s nothing “natural” about sleeping 7-9 hours. If you think that the amount of sleep hunter-gatherers are getting is the amount of sleep humans have evolved to get, then you should not worry at all about getting 4, 5, or 6 hours of sleep a night.
The CDC and the professional sleep researchers pull the numbers out of their asses without any kind of rigorous scientific evidence for their “consensus recommendations”. There’s no causal evidence that sleeping 7-9 hours is healthier than sleeping 6 hours or less. Correlational evidence suggests Shen X, Wu Y, Zhang D. Nighttime sleep duration, 24-hour sleep duration and risk of all-cause mortality among adults: a meta-analysis of prospective cohort studies. Scientific Reports. 2016 Feb 22;6:21480. 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.
Figure 4. The dose-response analysis between nighttime sleep duration and risk of all-cause mortality. The solid line and the long dash line represent the estimated relative risk and its 95% confidence interval. Note: the red dashed line on the graph is mine. Copied from Shen X, Wu Y, Zhang D. Nighttime sleep duration, 24-hour sleep duration and risk of all-cause mortality among adults: a meta-analysis of prospective cohort studies. Scientific Reports. 2016 Feb 22;6:21480.
Also see: Appendix: Jerome Siegel and Robert Vertes vs the sleep establishment
It appears that there is a distinct single-point mutation that allows some people to sleep several hours less than typical on average. A Rare Mutation of β1-Adrenergic Receptor Affects Sleep/Wake Behaviors: Shi G, Xing L, Wu D, Bhattacharyya BJ, Jones CR, McMahon T, Chong SC, Chen JA, Coppola G, Geschwind D, Krystal A. A rare mutation of β1-adrenergic receptor affects sleep/wake behaviors. Neuron. 2019 Sep 25;103(6):1044-55.
We have identified a mutation in the β1-adrenergic receptor gene in humans who require fewer hours of sleep than most. In vitro, this mutation leads to decreased protein stability and dampened signaling in response to agonist treatment. In vivo, the mice carrying the same mutation demonstrated short sleep behavior. We found that this receptor is highly expressed in the dorsal pons and that these ADRB1+ neurons are active during rapid eye movement (REM) sleep and wakefulness. Activating these neurons can lead to wakefulness, and the activity of these neurons is affected by the mutation. These results highlight the important role of β1-adrenergic receptors in sleep/wake regulation.
The study compares carriers of the mutation in one family to non-carriers in the same family and finds that carriers sleep about 2 hours per day less. Given the complexity of sleep and the multitude of its functions, it seems extremely implausible that just one mutation in the β1-adrenergic receptor gene was able to increase its efficiency by about 25%. It seems that it just made carriers sleep less (due to more stimulation of a group of neurons in the brain responsible for sleep/wakefulness) without anything else obviously changing when compared to non-carriers.
A similar example of a drop in the amount of sleep required without negative side effects and driven by a single factor was described in Development of a Short Sleeper Phenotype after Third Ventriculostomy in a Patient with Ependymal Cysts. Seystahl K, Könnecke H, Sürücü O, Baumann CR, Poryazova R. Development of a short sleeper phenotype after third ventriculostomy in a patient with ependymal cysts. Journal of Clinical Sleep Medicine. 2014 Feb 15;10(2):211-3. To sum up: a 59-year-old patient had chronic hydrocephalus. An endoscopic third ventriculostomy was performed on him. His sleep dropped from 7-8 hours a night to 4-5 hours a night without him becoming sleepy, he stopped being depressed, and his physical or cognitive performance stayed normal, as measured by the doctors.
Sleep is not required for memory consolidation. Jerome Siegel (the author of the hunter-gatherers study mentioned above) writes in Memory Consolidation Is Similar in Waking and Sleep: Siegel JM. Memory Consolidation Is Similar in Waking and Sleep. Current Sleep Medicine Reports. 2021 Mar;7(1):15-8.
Under interference conditions, such as exist during sleep deprivation, subjects, by staying awake, necessarily interacting with the experimenter keeping them awake and experiencing the laboratory environment, will remember more than just the items that are presented. But they may be less able to recall the particular items the experimenter is measuring. This can lead to the mistaken conclusion that sleep is required for memory consolidation [7].
Recent work has, for the first time, dealt with this issue. It was shown that a quiet waking period or a meditative waking state in which the environment is being ignored, produces a gain in recall similar to that seen in sleep, relative to an active waking state or a sleep-deprived state [8–16]. …
REM sleep has been hypothesized to have a key role in memory consolidation [20]. But it has been reported that near total REM sleep deprivation for a period of 14 to 40 days by administration of the monoamine oxidase inhibitor phenelzine has no apparent effect on cognitive function in humans [21]. A systematic study using serotonin or norepinephrine re-uptake inhibitors to suppress REM sleep in humans had no deleterious effects on a variety of learning tasks [22, 23]. Humans rarely survive the damage to the pontine region which when discretely lesioned in animals greatly reduces or eliminates REM sleep [20, 23–25]. However, one such subject with pontine damage that severely reduced REM sleep has been thoroughly studied. The studies show normal or above normal cognitive performance and no deficit in memory formation or recall [26•]. It has been claimed that learning results in greater total amounts of sleep, or greater amounts of REM sleep [27], or greater amounts of sleep spindles, or slow wave activity. However, a systematic test of this hypothesis in 929 human subjects with night-long EEG recording found no such correlation with retention [28•].
The entire Scientific Consensus™ about sleep being essential for memory consolidation appears to be heavily flawed, driven by people like Matthew Walker, and making me lose the last remnants of trust in sleep science that I had.
Also see:
Chadwick worked for several nights straight without sleep on the seminal discovery [of the neutron, for which he was awarded the 1935 Nobel in physics]. When he was done he went to a meeting of the Kapitza Club at Cambridge and gave a talk about it, ending with the words, “Now I wish to be chloroformed and put to sleep”.
I’m not what they call a “natural short sleeper”. If I don’t restrict my sleep, I often sleep more than 8 hours and I still struggle with getting out of bed. I used to be really scared of not sleeping enough and almost never set the alarm for less than 7.5 hours after going to bed.
My sleep statistics tells me that I slept an average of 5:25 hours over the last 7 days, 5:49 hours over the last 30 days, and 5:57 over the last 180 days hours, meaning that I’m awake for 18 hours per day instead of 16.5 hours. I usually sleep 5.5-6 hours during the night and take a nap a few times a week when sleepy during the day.
This means that I’m gaining 33 days of life every year. 1 more year of life every 11 years. 5 more years of life every 55 years.
Why are people not all over this? Why is everyone in love with charlatans who say that sleeping 5 hours a night will double your risk of cancer, make you pre-diabetic, and cause Alzheimer’s, despite studies showing that people who sleep 5 hours have the same, if not lower, mortality than those who sleep 8 hours? Convincing a million 20-year-olds to sleep an unnecessary hour a day is equivalent, in terms of their hours of wakefulness, to killing 62,500 of them.
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.
What do I lose due to sleeping 1.5 hours a day less? I’m somewhat more sleepy every day and staying awake during boring calls is even more difficult now. On the other hand, just a prospect of playing an exciting video game, makes me 100% alert even after sleeping for 2-3 hours. Related: Horne JA, Pettitt AN. High incentive effects on vigilance performance during 72 hours of total sleep deprivation. Acta psychologica. 1985 Feb 1;58(2):123-39. There’s no guarantee that what I’m doing is healthy after all, although, as I explained above, I think that it’s extremely unlikely due to likely adaptation, and likely beneficial effects of sleep deprivation (e.g. increased BDNF, less susceptibility to depression), and since I take a 20-minute nap under my wife’s watch whenever I don’t feel good.
I would like to thank (in reverse alphabetic order): Misha Yagudin, Guy Wilson, Bart Sturm, Ulysse Sabbag, Stephen Malina, Gavin Leech, Anastasia Kuptsova, Jake Koenig, Aleksandr Kotyurgin, Alexander Kim, Basil Halperin, Jeremy Hadfield, Steve Gadd, and Willy Chertman for reading drafts of this essay and for disagreeing with many parts of it vehemently. All errors mine.
Cite as:
Guzey, Alexey. Theses on Sleep. Guzey.com. 2022 February. Available from https://guzey.com/theses-on-sleep/.
Or download a BibTeX file here.
Objection: “When I’m underslept I notice that I’m less productive.”
Answer:
Yes, this is expected as per the analogy to exercise I make above. After exercise you are tired but over time you become stronger.
It might be that undersleeping itself causes you to be less productive. However, it might also be the case that there’s an upstream cause that results in both undersleeping and lack of productivity. I think either could be the case depending on the person but understanding what exactly happens is much harder than people typically appreciate when they notice such co-occurrences.
Figure 5. Causal graph of the "staying up late and feeling demotivated and being unproductive scenario."
As Nick Wignall notes on Twitter:
People are also not great at distinguishing true sleepiness from tiredness.
Analogy would be: of all the times when you feel hungry, how much of that is true hunger vs a craving?
Also related: when people say that e.g. they have a small child, are doing medical residency, etc. and feel terrible due to undersleep, note that there’s a big difference between being randomly forced to not sleep when you want to sleep and managing one’s sleep consciously. The analogy would be to saying that fasting is bad because if you are forbidden by someone from eating randomly throughout the day.
Objection: “Driving when you are sleepy is dangerous, therefore you are wrong.”
Answer: Yep, I agree that driving while being sleepy is dangerous and I don’t want anyone to drive, to operate heavy machinery, etc. when they are sleepy. This, however, bears no relationship on any of the arguments I make.
Objection: “The graph that shows more sleep being associated with higher doesn’t tell us anything because sick people tend to sleep more.”
Answer: It is true that some diseases lead to prolonged sleep. However, some diseases also lead to shortened sleep. For example, many stroke patients suffer from insomnia Sterr A, Kuhn M, Nissen C, Ettine D, Funk S, Feige B, Umarova R, Urbach H, Weiller C, Riemann D. Post-stroke insomnia in community-dwelling patients with chronic motor stroke: physiological evidence and implications for stroke care. Scientific Reports. 2018 May 30;8(1):8409. and people with fatal familial insomnia struggle with insomnia. Therefore, if you want to make the argument that the association between longer sleep and higher mortality is not indicative of the effect of sleep, you have to accept that the same is true about shorter sleep and higher mortality.
Why do I bother with all of this theorizing? Why do I think I can discover something about sleep that thousands of them couldn’t discover over many decades?
The reason is that I have approximately 0 trust in the integrity of the field of sleep science.
As you might be aware, 2 years ago I wrote a detailed criticism of the book Why We Sleep written by a Professor of Neuroscience at psychology at UC Berkeley, the world’s leading sleep researcher and the most famous expert on sleep, and the founder and director of the Center for Human Sleep Science at UC Berkeley, Matthew Walker.
Here are just a few of biggest issues (there were many more) with the book.
Walker wrote: “Routinely sleeping less than six or seven hours a night demolishes your immune system, more than doubling your risk of cancer”, despite there being no evidence that cancer in general and sleep are related. There are obviously no RCTs on this, and, in fact, there’s not even a correlation between general cancer risk and sleep duration.
Walker falsified a graph from an academic study in the book.
Walker outright fakes data to support his “sleep epidemic” argument. The data on sleep duration Walker presents on the graph below simply does not exist:
Figure 6. Sleep loss and obesity. Country not specified for sleep data. Copied from Walker M. Why we sleep: Unlocking the power of sleep and dreams. Simon and Schuster; 2017 Oct 3.
Here’s some actual data on sleep duration over time:
Figure 7. Association of year of study with age-adjusted total sleep time (min) for studies in which subjects followed their usual sleep schedule. Copied from Youngstedt SD, Goff EE, Reynolds AM, Kripke DF, Irwin MR, Bootzin RR, Khan N, Jean-Louis G. Has adult sleep duration declined over the last 50+ years?. Sleep medicine reviews. 2016 Aug 1;28:69-85.
By the time my review was published, the book had sold hundreds of thousands if not millions of copies and was praised by the New York Times, The Guardian, and many other highly-respected papers. It was named one of NPR’s favorite books of 2017 while Walker went on a full-blown podcast tour.
Did any sleep scientists voice the concerns they with the book or with Walker? No. They were too busy listening to his keynote at the Cognitive Neuroscience Society 2019 meeting.
Did any sleep scientists voice their concerns after I published my essay detailing its errors and fabrications? No (unless you count people replying to me on Twitter as “voicing a concern”).
Did Walker lose his status in the community, his NIH grants, or any of his appointments? No, no, and no.
I don’t believe that a community of scientists that refuses to police fraud and of which Walker is a foremost representative (recall that he is the director of the Center for Human Sleep Science at UC Berkeley) could be a community of scientists that would produce a trustworthy and dependable body of scientific work.
Specifically, the original 2013 paper Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O’Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T. Sleep drives metabolite clearance from the adult brain. science. 2013 Oct 18;342(6156):373-7. accumulated more than 3,000 (!) citations in less than 10 years and is highly misleading.
The paper is called “Sleep Drives Metabolite Clearance from the Adult Brain”. The abstract says:
The conservation of sleep across all animal species suggests that sleep serves a vital function. We here report that sleep has a critical function in ensuring metabolic homeostasis. Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.
At the same time, the paper found that anesthesia without sleep results in the same clearance (paper: “Aβ clearance did not differ between sleeping and anesthetized mice”), meaning that clearance is not caused by sleep per se, but instead only co-occurrs with it. Authors did not mention this in the abstract and mistitled the paper, thus misleading the readers. As far as I can tell, literally nobody pointed this out previously.
And on top of all of this “125I-Aβ1-40 was injected intracortically”, meaning that they did not actually find any brain waste products that would be cleared out. This is an exogenous compound that was injected god knows where disrupting god knows what in the brain.
Max Levchin in Founders at Work:
The product wasn’t really finished, and about a week before the beaming at Buck’s I realized that we weren’t going to be able to do it, because the code wasn’t done. Obviously it was really simple to mock it up—to sort of go, “Beep! Money is received.” But I was so disgusted with the idea. We have this security company; how could I possibly use a mock-up for something worth $4.5 million? What if it crashes? What if it shows something? I’ll have to go and commit ritual suicide to avoid any sort of embarrassment. So instead of just getting the mock-up done and getting reasonable rest, my two coders and I coded nonstop for 5 days. I think some people slept; I know I didn’t sleep at all. It was just this insane marathon where we were like, “We have to get this thing working.” It actually wound up working perfectly. The beaming was at 10:00 a.m.; we were done at 9:00 a.m.
/u/CPlusPlusDeveloper on Gwern’s Writing in the Morning:
We know that acute sleep deprivation seems to have a manic and euphoric effect on at least some percent of the population some percent of the time. For example staying up all night is one of the most effective ways to temporarily aleve depression. Of course the problem is that chronic sleep deprivation has the opposite effect, and the temporary mania and euphoria is not sustainable.
My speculative take is that whatever this mechanism, it was the main reason you experienced a productivity boost. By waking up early you intentionally were fighting against your chronobiology, hence adding an element of acute sleep deprivation regardless of how many hours you got the night before. That mania fuels an amphetamine like focus.
The upshot, if my hypothesis is true, is that waking up early would not produce similar gains if you did it everyday. Like the depressive who stays up all night, it may feels like you’ve discovered an intervention that will pay lasting gains. But if you were to actually make it part of your recurring lifestyle, the benefits would stop, and eventually the impact would work in reverse.
Along those lines that’s probably why you naturally tend to stop conforming to that pattern after a few days. As acute sleep deprivation becomes chronic, you’re most likely intuitively recognizing that the pattern has crossed over to the point of being counter-productive.
Lots of writers and software engineers note that their creative juices start flowing by evening extending late into the night - I think this phenomenon is closely related to the one described in the comment above.
sleep anecdote- In undergrad I had zero sleep before several major tests; also before quals in grad school. Basically wouldn’t sleep before things I really considered important (this included morning meetings I didn’t want to miss!). On such occasions I would feel:
- miserable, then
- absurd and in a good humor, weirdly elated, then
- Super PumpedTM, and
really sharp when the test (or whatever) actually started.
Total Wake: Natural, Pathological, and Experimental Limits to Sleep Reduction, Panchin Y, Kovalzon VM. Total Wake: Natural, Pathological, and Experimental Limits to Sleep Reduction. Frontiers in neuroscience. 2021 Apr 7;15:288. quoting Le sommeil, la conscience et l’éveil: Jouvet M. Le sommeil, la conscience et l’éveil. Odile Jacob; 2016 Mar 9.
There is such pathology as Morvan’s disease, in which quasi-wakefulness, which lasted 3,000 h (more precisely, 2,880), or 4 months, was not accompanied by sleep rebound, since the sleep generation system itself was disturbed.” Throughout this period the patient was under continuous polysomnographic control, so his agrypnia was confirmed objectively. Jouvet conclude that “… slow wave (NREM) and paradoxical (REM) sleep are not necessary for life (at least for 4–5 months for the first and about 8 months for the second), and we cannot consider their suppression to be the cause of any serious disorders in the body. A person who had lack of sleep and dreams for 4 months, of which there are only a few minutes of nightly hallucinations, can turn out to read newspapers during the day, make plans, play cards and win, and at the same time lie on the bed in the dark all night without sleep! In conclusion, we admit: this observation makes most theories about the functions of sleep and paradoxical (REM) sleep obsolete at once, but offers nothing else
I once tried to cheat sleep, and for a year I succeeded (strong peak-performance-sailing vibes):
In the summer of 2009, I was finishing the first—and toughest—year of my doctorate. …
To keep up this crazy sleep schedule, I always needed a good reason to wake up the next morning after my 3.5-hour nighttime sleep. So before I went to bed, I reviewed the day gone past and planned what I would do the next day. I’ve carried on with this habit, and it serves me well even today.
But the Everyman schedule was reasonably flexible. Some days when I missed a nap, I simply slept a little more at night. There were also days when I couldn’t manage a single nap, but it didn’t seem to affect me very much the next day.
To the surprise of many, and even myself, I had managed to be on the polyphasic schedule for more than a year. But then came a conference where for a week I could not get a single nap. It was unsettling but I was sure I would be able to get back to sleeping polyphasic without too much trouble.
I was wrong. When I tried to get back into the schedule, I couldn’t find the motivation to do it; I didn’t have the same urgent goals that I had had a year ago. So I returned to sleeping like an average human.
James Gleck in Chaos on Mitch Feigenbaum:
In the spring of 1976 he entered a mode of existence more intense than any he had lived through. He would concentrate as if in a trance, programming furiously, scribbling with his pencil, programming again. He could not call C division for help, because that would mean signing off the computer to use the telephone, and reconnection was chancy. He could not stop for more than five minutes’ thought, because the computer would automatically disconnect his line. Every so often the computer would go down anyway, leaving him shaking with adrenaline. He worked for two months without pause. His functional day was twenty-two hours. He would try to go to sleep in a kind of buzz, and awaken two hours later with his thoughts exactly where he had left them. His diet was strictly coffee. (Even when healthy and at peace, Feigenbaum subsisted exclusively on the reddest possible meat, coffee, and red wine. His friends speculated that he must be getting his vitamins from cigarettes.)
In the end, a doctor called it off. He prescribed a modest regimen of Valium and an enforced vacation. But by then Feigenbaum had created a universal theory.
Ryan Kulp’s experience with decreasing the amount of sleep by several hours:
i began learning to code in 2015. since i was working full-time i needed to maximize after-hours to learn quickly. i experimented for 10 days straight… go to sleep at 4am, wake up at 8am for work. felt fine.
actually, the first 5-10 minutes of “getting up” after 3-4 hours of sleep sucks more than if i sleep ~8 hours. but after 15 mins of moving around, a shower, etc, i feel as if i slept 8 hours.
since then i’ve routinely slept 4-6 hours /day and definitely been more productive. i think if more people experimented for themselves and had the same “aha” moment i did (that you feel fine after the initial gut-wrenching “i slept too little” reaction), they’d get more done too.
This is a very good point that shows that: there’s (1) how sleepy we feel when waking up and (2) how sleepy we feel during the day. (2) is probably more important but most people are focused on (1) and the implicit assumption is that poor (1) leads to (2) – which is unwarranted.
Also: https://twitter.com/BroodVx/status/1492227577896787969,
Nabeel Qureshi writes:
you’re combining two things here: (1) your brain is overpowered by the comfy soft temp-controlled bed (2) you’re bored. they might both be right but i think you conflate them, and they’re separate arguments. this is important bc i think the strongest counterargument to what you’re saying is the classic experience of: you force yourself to wake up early (say 6), you have a project you’re genuinely excited about (hence #2 is false), but when you sit down to work, you’re tired and can’t quite focus. in this scenario, i think your theory would say that i’m not really that excited about what i’m doing, because if i were (see video game argument) then i’d be awake. i’d disagree and say that the researcher should just go take a nap, and they’ll probably be able to make more progress per hour than the extra hours they gain… trying to force yourself to do something while underslept, subjectively, feels hellish. i’m sure you’ve had this experience - did you figure out a workaround?
It is completely true that if you are excited by a project but it’s not super stimulating, it’s still very easy to wake up after less than usual number of hours of sleep and feel sleepy and terrible. This is true for me as well. I found a solution to this: instead of heading straight to the computer, I first unload the clean plates from the dishwasher and load it with dirty plates. This activity is quite special in that it is:
In about 90% of the cases, 10 minutes later when I’m done with the dishwasher, I find that I’m fully awake and don’t actually want to sleep anymore. In the remaining 10% of the cases, I stay awake and work until my wife wakes up and then go take a 20-minute nap under her watch (and take as many 20-minute naps as I need during the day, although I only end up taking a few naps a week and rarely more than one per day, unless I’m sick).
CNBC:
On Tesla’s first-quarter earnings conference call in May, Musk referred to inquiries from Wall Street analysts as “boring, bonehead questions” and as “so dry. They’re killing me.” On the next earnings conference call in August, Musk said he was sorry for “being impolite” on the previous call.
“Obviously I think there’s really no excuse for bad manners and I was violating my own rule in that regard. There are reasons for it, I got no sleep, 120 hour weeks, but nonetheless, there is still no excuse, so my apologies for not being polite on the prior call,” Musk said.
Later in August, in conversation with the New York Times, Musk reported using prescription sleep medication Ambien to sleep.
“Yeah. It’s not like for fun or something,” Musk told Swisher Wednesday. “If you’re super stressed, you can’t go to sleep. You either have a choice of, like, okay, I’ll have zero sleep and then my brain won’t work tomorrow, or you’re gonna take some kind of sleep medication to fall asleep.”
Musk said he was working such insane hours to get Tesla through the ramp up in production for its Model 3 vehicle. ”[A]s a startup, a car company, it is far more difficult to be successful than if you’re an established, entrenched brand. It is absurd that Tesla is alive. Absurd! Absurd.”
First, I wanted to share a way of thinking about some of your findings that builds on the idea of a homeostatic control system (brought to you from engineering via cybernetics). The classic example is a thermostat, which keeps temperature of a room close to a set point. Biology is quite a bit more messy than this, of course, but the body makes use of a plenty of feedback mechanisms to stay close to set points as well. You’re right in pointing out that these set points don’t need to be healthy though. For example, measured via EEG, PTSD patients have alpha power (which primarily modulates neural inhibition in frontal, parietal and occipital areas of the brain) set points far below that of healthy control groups. One way to deal with these suboptimal set points is to simply disrupt the system. Here’s a model that makes this point nicely: imagine all possible brain state dynamics as a two-dimensional plane and place a ball on it which represents the current brain state space. As the ball moves, the brain dynamics change as well (in frequency, phase, amplitude - you name it). On the plane, you have basins that give stability to the brain state, and repellers in the form of hills, as well as random noise and outside interference which drives the ball into various directions. Sometimes the ball will get stuck in basins which are highly suboptimal, but they are deep enough that exploration of other set points is not possible. If the system is disrupted, the ball might get jolted out of its basin though, and be again able to fall into a more optimal position.
With that said, there’s plenty of evidence that stability in itself (even within better basins) is suboptimal for perfect health, because contexts change. For example, people who are very physically healthy (athletes, for example), tend to have far greater variance in the time interval between individual heart beats (heart rate variability) than even the average person, and as the average person gets healthier, their heart rate variability increases as well. Basically, the body becomes more resilient by introducing a noise signal that produces chaotic fluctuations to homeostatic control mechanisms (controlled allostasis) and there are good reasons to think that this is true of psychological health as well.
Because of this, I think that you’re right in suggesting that varying the amount of time you sleep is a good thing - especially if you’re currently struggling with depression or mania. Not even necessarily because sleep per se is the culprit, but because it might dislodge a ball stuck in a suboptimal basin, so to speak. Depressed people tend to oversleep, people with mania tend to sleep too little, so steering in the opposite direction is only logical. For perfectly healthy people, sleep cycling is probably the best way to go - kind of a mirroring the logic of heart rate variability: introduce some noise to keep your body on your toes. It’s just like fasting, working out, cold exposure, saunas, etc. - it’s al about producing stressors on the body which stir up repair processes which keep you healthy (and biologically younger). I have done plenty of self-experiments with polyphasic 5-6 hour sleeping (similar to the the approach studied by Stampi, who you mentioned), with no negative consequences. The main thing that makes it impractical is that intermittent napping is sometimes hard to combine with professional responsibilities and a social life.
As a side note, because you ask the question about why depressed people sleep longer, and people with mania sleep less, the answer to this is very likely highly multi-causal. With that said, I wanted to point out that depressed people generally exhibit excessive alpha activity in eyes-open waking states, which normally becomes more pronounced in people as they drift off to sleep (because of the neural inhibition function). We also have reason to believe that it mediates between BDNF and subclinical depressed mood, so that’s a link to something else you talk about in your article. As for mania, I haven’t looked at this myself, but I remember hearing that it’s almost a mirror image, with generally decreased synchronisation of slower oscillations and heightened faster rhythms, generally associated with greater arousal and wakefulness.
One last thing: as you point out, sleep is likely not required for memory retention. Any claim that sleep is about any specific cognitive function should be suspect on the principle that the phenomenon of sleep predates the development of organisms with brains - it can’t have evolved specifically for something as high-level as memory retention. It’s more likely about something more basic like general metabolic health.
Time for the Sleep Community to Take a Critical Look at the Purported Role of Sleep in Memory Processing Vertes RP, Siegel JM. Time for the sleep community to take a critical look at the purported role of sleep in memory processing. Sleep. 2005 Oct 1;28(10):1228-9. by Robert Vertes and Jerome Siegel (a reply to Walker claiming that the debate on memory processing in sleep is essentially settled):
The present ‘debate’ was sparked by an editorial by Robert Stickgold in SLEEP on an article in that issue by Schabus et a on paired associate learning and sleep spindles in humans
Regarding Stickgold’s editorial, I was particularly troubled by his opening statement, as follows: “The study of sleep-dependent memory consolidation has moved beyond the question of whether it exists to questions of its extent and of the mechanisms supporting it”. He then proceeded to cite evidence justifying this statement. Surprisingly, there was no mention of opposing views or a discussion of data inconsistent with the sleep-memory consolidation (S-MC) hypothesis. It seemed that the controversial nature of this issue should have at least been acknowledged, but apparently to do so would have undermined Stickgold’s position that the door is closed on this debate and only the fine points need be resolved. …
- By all accounts, sleep does not serve a role in declarative memory. As reviewed by Smith, with few exceptions, reports have shown that depriving subjects of REM sleep does not disrupt learning/memory, or exposure to intense learning situations does not produce subsequent increases in REM sleep. Smith concluded: “REM sleep is not involved with consolidation of declarative material.” The study by Schabus et al (see above) is another example that the learning of declarative material is unaffected by sleep. They reported that subjects showed no significant difference in the percentage of word-pairs correctly recalled before and after 8 hours of sleep. Or as Stickgold stated in his editorial [the editorial Vertes and Siegel are replying to], “Performance in the morning was essentially unchanged from the night before”. It would seem important for Stickgold/Walker to acknowledge that the debate on sleep and memory has been reduced to a consideration of procedural memory – to the exclusion of declarative memory. If there are exceptions, they should note.
- Several lines of evidence indicate that REM sleep is not involved in memory processing/consolidation – or at least not in humans. Perhaps the strongest argument for this is the demonstration that the marked suppression or elimination of REM sleep in individuals with brainstem lesions or on antidepressant drugs has no detrimental effect on cognition. A classic case is that of an Israeli man who at the age of 19 suffered damage to the brainstem from shrapnel from a gunshot wound, and when examined at the age of 33 he showed no REM sleep. The man, now 55, is a lawyer, a painter and interestingly the editor of a puzzle column for an Israeli magazine. Recently commenting on his ‘famous’ patient, Peretz Lavie stated that “he is probably the most normal person I know and one of the most successful ones”. There are several other well documented cases of individuals with greatly reduced or absent REM sleep that exhibit no apparent cognitive deficits. It would seem that these individuals would be a valuable resource for examining the role of sleep in memory. …
In Memory Consolidation Is Similar in Waking and Sleep cited above, Siegel notes: Siegel JM. Memory Consolidation Is Similar in Waking and Sleep. Current Sleep Medicine Reports. 2021 Mar;7(1):15-8.
To critically evaluate this hypothesis [that sleep has a critical role in memory consolidation], we must take “interference” effects into account. If you learn something before or after the experimenter induced learning that is being measured in the typical sleep-memory study, it degrades recall of the tested information. For example if you tell a subject that the capital of Australia is Canberra and then allow the subject to have a normal night’s sleep, there is a high probability that the subject will remember this upon awakening. If on the other hand you tell the subject that the capital of Australia is Canberra, the capital of Brazil is Brasilia, the capital of Canada is Ottawa, the capital of Iceland is Reykjavik, the capital of Libya is Tripoli, the capital of Pakistan is Islamabad, etc., it is much less likely the subject will remember the capital of Australia. The effect of proactive and retroactive interference is dependent on the temporal juxtaposition, complexity, and similarity of the encountered material to the associations being tested. Interference is a well-established concept in the learning literature [1–6]. Under interference conditions, such as exist during sleep deprivation, subjects, by staying awake, necessarily interacting with the experimenter keeping them awake and experiencing the laboratory environment, will remember more than just the items that are presented. But they may be less able to recall the particular items the experimenter is measuring. This can lead to the mistaken conclusion that sleep is required for memory consolidation [7].
Fur Seals Suppress REM Sleep for Very Long Periods without Subsequent Rebound: Lyamin OI, Kosenko PO, Korneva SM, Vyssotski AL, Mukhametov LM, Siegel JM. Fur seals suppress REM sleep for very long periods without subsequent rebound. Current Biology. 2018 Jun 18;28(12):2000-5.
Virtually all land mammals and birds have two sleep states: slow-wave sleep (SWS) and rapid eye movement (REM) sleep [1, 2]. After deprivation of REM sleep by repeated awakenings, mammals increase REM sleep time [3], supporting the idea that REM sleep is homeostatically regulated. *Some evidence suggests that periods of REM sleep deprivation for a week or more cause physiological dysfunction and eventual death [4, 5]. However, separating the effects of REM sleep loss from the stress of repeated awakening is difficult [2, 6]. The northern fur seal (Callorhinus ursinus) is a semiaquatic mammal [7]. It can sleep on land and in seawater. The fur seal is unique in showing both the bilateral SWS seen in most mammals and the asymmetric sleep previously reported in cetaceans [8]. Here we show that when the fur seal stays in seawater, where it spends most of its life [7], it goes without or greatly reduces REM sleep for days or weeks. After this nearly complete elimination of REM, it displays minimal or no REM rebound upon returning to baseline conditions. Our data are consistent with the hypothesis that REM sleep may serve to reverse the reduced brain temperature and metabolism effects of bilateral nonREM sleep, a state that is greatly reduced when the fur seal is in the seawater, rather than REM sleep being directly homeostatically regulated. This can explain the absence of REM sleep in the dolphin and other cetaceans and its increasing proportion as the end of the sleep period approaches in humans and other mammals.
The end of sleep: ‘Sleep debt’ versus biological adaptation of human sleep to waking needs: Horne J. The end of sleep:‘sleep debt’versus biological adaptation of human sleep to waking needs. Biological psychology. 2011 Apr 1;87(1):1-4.
It is argued that the latter part of usual human sleep is phenotypically adaptable (without ‘sleep debt’) to habitual shortening or lengthening, according to environmental influences of light, safety, food availability and socio-economic factors, but without increasing daytime sleepiness. Pluripotent brain mechanisms linking sleep, hunger, foraging, locomotion and alertness, facilitate this time management, with REM acting as a ‘buffer’ between wakefulness and nonREM (‘true’) sleep. The adaptive sleep range is approximately 6–9 h, although, a timely short (<20 min) nap can equate to 1 h ‘extra’ nighttime sleep. Appraisal of recent epidemiological findings linking habitual sleep duration to mortality and morbidity points to nominal causal effects of sleep within this range. Statistical significance, here, may not equate to real clinical significance. Sleep durations outside 6–9 h are usually surrogates of common underlying causes, with sleep associations taking years to develop. Manipulation of sleep, alone, is unlikely to overcome these health effects, and there are effective, rapid, non-sleep, behavioural countermeasures. Sleep can be taken for pleasure, with minimal sleepiness; such ‘sleepability’ is ‘unmasked’ by sleep-conducive situations. Sleep is not the only anodyne to sleepiness, but so is wakefulness, inasmuch that some sleepiness disappears when wakefulness becomes more challenging and eventful. A more ecological approach to sleep and sleepiness is advocated.
Long-term moderate elevation of corticosterone facilitates avian food-caching behaviour and enhances spatial memory Pravosudov VV. Long-term moderate elevation of corticosterone facilitates avian food-caching behaviour and enhances spatial memory. Proceedings of the Royal Society of London. Series B: Biological Sciences. 2003 Dec 22;270(1533):2599-604.
It is widely assumed that chronic stress and corresponding chronic elevations of glucocorticoid levels have deleterious effects on animals’ brain functions such as learning and memory. Some animals, however, appear to maintain moderately elevated levels of glucocorticoids over long periods of time under natural energetically demanding conditions, and it is not clear whether such chronic but moderate elevations may be adaptive. I implanted wild–caught food–caching mountain chickadees (Poecile gambeli), which rely at least in part on spatial memory to find their caches, with 90–day continuous time–release corticosterone pellets designed to approximately double the baseline corticosterone levels. Corticosterone–implanted birds cached and consumed significantly more food and showed more efficient cache recovery and superior spatial memory performance compared with placebo–implanted birds. Thus, contrary to prevailing assumptions, long–term moderate elevations of corticosterone appear to enhance spatial memory in food–caching mountain chickadees. These results suggest that moderate chronic elevation of corticosterone may serve as an adaptation to unpredictable environments by facilitating feeding and food–caching behaviour and by improving cache–retrieval efficiency in food–caching birds.
Racemic Ketamine as an Alternative to Electroconvulsive Therapy for Unipolar Depression: A Randomized, Open-Label, Non-Inferiority Trial (KetECT) (via Tomas Roos): Ekstrand J, Fattah C, Persson M, Cheng T, Nordanskog P, Åkeson J, Tingström A, Lindström M, Nordenskjöld A, Movahed RP. Racemic Ketamine as an Alternative to Electroconvulsive Therapy for Unipolar Depression:: A Randomized, Open-Label, Non-Inferiority Trial (KetECT). International Journal of Neuropsychopharmacology. 2021.
Background Ketamine has emerged as a fast-acting and powerful antidepressant, but no head to head trial has been performed, Here, ketamine is compared with electroconvulsive therapy (ECT), the most effective therapy for depression.
Methods Hospitalized patients with unipolar depression were randomized (1:1) to thrice-weekly racemic ketamine (0.5 mg/kg) infusions or ECT in a parallel, open-label, non-inferiority study. The primary outcome was remission (Montgomery Åsberg Depression Rating Scale score ≤10). Secondary outcomes included adverse events (AEs), time to remission, and relapse. Treatment sessions (maximum of 12) were administered until remission or maximal effect was achieved. Remitters were followed for 12 months after the final treatment session.
Results In total 186 inpatients were included and received treatment. Among patients receiving ECT, 63% remitted compared with 46% receiving ketamine infusions (P = .026; difference 95% CI 2%, 30%). Both ketamine and ECT required a median of 6 treatment sessions to induce remission. Distinct AEs were associated with each treatment. Serious and long-lasting AEs, including cases of persisting amnesia, were more common with ECT, while treatment-emergent AEs led to more dropouts in the ketamine group. Among remitters, 70% and 63%, with 57 and 61 median days in remission, relapsed within 12 months in the ketamine and ECT groups, respectively (P = .52).
Conclusion Remission and cumulative symptom reduction following multiple racemic ketamine infusions in severely ill patients (age 18–85 years) in an authentic clinical setting suggest that ketamine, despite being inferior to ECT, can be a safe and valuable tool in treating unipolar depression.
Beersma DG, Van den Hoofdakker RH. Can non-REM sleep be depressogenic?. Journal of affective disorders. 1992 Feb 1;24(2):101-8.
Bessone P, Rao G, Schilbach F, Schofield H, Toma M. The economic consequences of increasing sleep among the urban poor. The Quarterly Journal of Economics. 2021 Aug;136(3):1887-941.
Consensus Conference Panel:, Watson, N.F., Badr, M.S., Belenky, G., Bliwise, D.L., Buxton, O.M., Buysse, D., Dinges, D.F., Gangwisch, J., Grandner, M.A. and Kushida, C., 2015. Joint consensus statement of the American Academy of Sleep Medicine and Sleep Research Society on the recommended amount of sleep for a healthy adult: methodology and discussion. Journal of Clinical Sleep Medicine, 11(8), pp.931-952.
Eckert A, Karen S, Beck J, Brand S, Hemmeter U, Hatzinger M, Holsboer-Trachsler E. The link between sleep, stress and BDNF. European Psychiatry. 2017 Apr;41(S1):S282-.
Ekstrand J, Fattah C, Persson M, Cheng T, Nordanskog P, Åkeson J, Tingström A, Lindström M, Nordenskjöld A, Movahed RP. Racemic Ketamine as an Alternative to Electroconvulsive Therapy for Unipolar Depression:: A Randomized, Open-Label, Non-Inferiority Trial (KetECT). International Journal of Neuropsychopharmacology. 2021.
Giese M, Unternährer E, Hüttig H, Beck J, Brand S, Calabrese P, Holsboer-Trachsler E, Eckert A. BDNF: an indicator of insomnia?. Molecular psychiatry. 2014 Feb;19(2):151-2.
Goldschmied JR, Rao H, Dinges D, Goel N, Detre JA, Basner M, Sheline YI, Thase ME, Gehrman PR. 0886 Recovery Sleep Significantly Decreases BDNF In Major Depression Following Therapeutic Sleep Deprivation. Sleep. 2019 Apr;42(Supplement_1):A356-.
Horne J. The end of sleep:‘sleep debt’versus biological adaptation of human sleep to waking needs. Biological psychology. 2011 Apr 1;87(1):1-4.
Horne JA, Pettitt AN. High incentive effects on vigilance performance during 72 hours of total sleep deprivation. Acta psychologica. 1985 Feb 1;58(2):123-39.
Kaiser J. More than half of high-impact cancer lab studies could not be replicated in controversial analysis. AAAS Articles DO Group. 2021;
Kaplan RM, Irvin VL. Likelihood of null effects of large NHLBI clinical trials has increased over time. PloS one. 2015 Aug 5;10(8):e0132382.
Lyamin OI, Kosenko PO, Korneva SM, Vyssotski AL, Mukhametov LM, Siegel JM. Fur seals suppress REM sleep for very long periods without subsequent rebound. Current Biology. 2018 Jun 18;28(12):2000-5.
Pravosudov VV. Long-term moderate elevation of corticosterone facilitates avian food-caching behaviour and enhances spatial memory. Proceedings of the Royal Society of London. Series B: Biological Sciences. 2003 Dec 22;270(1533):2599-604.
Turner EH, Matthews AM, Linardatos E, Tell RA, Rosenthal R. Selective publication of antidepressant trials and its influence on apparent efficacy. New England Journal of Medicine. 2008 Jan 17;358(3):252-60.
Rahmani M, Rahmani F, Rezaei N. The brain-derived neurotrophic factor: missing link between sleep deprivation, insomnia, and depression. Neurochemical research. 2020 Feb;45(2):221-31.
Riemann, D., König, A., Hohagen, F., Kiemen, A., Voderholzer, U., Backhaus, J., Bunz, J., Wesiack, B., Hermle, L. and Berger, M., 1999. How to preserve the antidepressive effect of sleep deprivation: A comparison of sleep phase advance and sleep phase delay. European archives of psychiatry and clinical neuroscience, 249(5), pp.231-237.
Seystahl K, Könnecke H, Sürücü O, Baumann CR, Poryazova R. Development of a short sleeper phenotype after third ventriculostomy in a patient with ependymal cysts. Journal of Clinical Sleep Medicine. 2014 Feb 15;10(2):211-3.
Shen X, Wu Y, Zhang D. Nighttime sleep duration, 24-hour sleep duration and risk of all-cause mortality among adults: a meta-analysis of prospective cohort studies. Scientific Reports. 2016 Feb 22;6:21480.
Shi G, Xing L, Wu D, Bhattacharyya BJ, Jones CR, McMahon T, Chong SC, Chen JA, Coppola G, Geschwind D, Krystal A. A rare mutation of β1-adrenergic receptor affects sleep/wake behaviors. Neuron. 2019 Sep 25;103(6):1044-55.
Siegel JM. Memory Consolidation Is Similar in Waking and Sleep. Current Sleep Medicine Reports. 2021 Mar;7(1):15-8.
Sterr A, Kuhn M, Nissen C, Ettine D, Funk S, Feige B, Umarova R, Urbach H, Weiller C, Riemann D. Post-stroke insomnia in community-dwelling patients with chronic motor stroke: physiological evidence and implications for stroke care. Scientific Reports. 2018 May 30;8(1):8409.
Vertes RP, Siegel JM. Time for the sleep community to take a critical look at the purported role of sleep in memory processing. Sleep. 2005 Oct 1;28(10):1228-9.
Xie L, Kang H, Xu Q, Chen MJ, Liao Y, Thiyagarajan M, O’Donnell J, Christensen DJ, Nicholson C, Iliff JJ, Takano T. Sleep drives metabolite clearance from the adult brain. science. 2013 Oct 18;342(6156):373-7.
Yetish G, Kaplan H, Gurven M, Wood B, Pontzer H, Manger PR, Wilson C, McGregor R, Siegel JM. Natural sleep and its seasonal variations in three pre-industrial societies. Current Biology. 2015 Nov 2;25(21):2862-8.
Youngstedt SD, Goff EE, Reynolds AM, Kripke DF, Irwin MR, Bootzin RR, Khan N, Jean-Louis G. Has adult sleep duration declined over the last 50+ years?. Sleep medicine reviews. 2016 Aug 1;28:69-85.
2001-01-01 08:00:00
Scientists- in what % of papers you read does the main body of the paper fail to support the assertions made in the title or abstract?
— Alexey Guzey (@alexeyguzey) April 4, 2020
Scientists, suppose you're browsing google scholar and stumble on a paper.
— Alexey Guzey (@alexeyguzey) April 6, 2020
You notice that all of its authors are from one of the countries where scientists are sometimes stereotyped as lacking research integrity (all affiliated with a local university)
Do you read the paper?
Scientists, what % of references (in your opinion) fail to support the statement they're cited with (because of a miscitation, cited paper simply being bad, etc.) in papers that you read?
— Alexey Guzey (@alexeyguzey) April 14, 2020
if stalin was born in 1995, he would be
— Alexey Guzey (@alexeyguzey) April 17, 2020
When you're obsessed with something or have intense pressure to work on something, how much can you work LONG-TERM and feel good?
— Alexey Guzey (@alexeyguzey) May 29, 2020
Choose the closest.
Format: A, B, C
where
A = hrs of work/day on 5 working days/wk
B = same for 6
C = same for 7
would you move to the US permanently by the end of 2020 if you were offered a US citizenship?
— Alexey Guzey (@alexeyguzey) June 11, 2020
On days when you set the morning alarm, in which % of cases do you get out of bed and start the day within a minute of hearing it?
— Alexey Guzey (@alexeyguzey) July 12, 2020
