Thanks for the taking the time to look into my essay.
Mendonça’s claim 1: Guzey’s /r/BipolarReddit evidence is misleading
Here’s what Mendonça writes in her first point that so conclusively demonstrates that the point I make is “misleading”:
[Guzey’s] evidence from bipolar disorder patients is not representative of what you see in the general population: both long and short sleep duration are associated with depression
The paper Mendonça cites looks at long-term long sleep and long-term short sleep, with their association with depression. My claim and my evidence (from bipolar people) are concerned with short-term long sleep and short-term short sleep. That is, Mendonça’s paper is simply not overlapping with with what I write about or what the evidence she calls “misleading” is concerned about. It is further puzzling that in her refutation of my argument she:
completely ignores the relationship between sleep and mania (i.e. she ignores one half of my argument and only discusses the part about depression).
completely ignores the fact that in ~50% of ALL people with depression (not just bipolar), short-term short sleep relieves depression.
I am similarly puzzled by a later accusation:
Guzey claims that “most sleep research is extremely unreliable and we shouldn’t conclude much on the basis of it,” but there are problems with that. Firstly because he doesn’t seem to believe that about sleep research that favors his hypotheses. Guzey, after all, uses sleep research to show that Matthew Walker’s book is terrible and fraudulent. So it seems that he wants to trust sleep research when it says that sleep deprivation is not as bad as Walker shows, but doesn’t want to trust it when it says that sleep deprivation is not harmless.
I wrote that most sleep research is extremely unreliable. And indeed, this is what I believe and this is why I’m so selective with the kind of evidence I use, preferring to show my readers Reddit comments left by bipolar people, instead of meta-analyses, and why, when I do use meta-analyses, I use them very cautiously. For example, in the essay, I used a meta-analysis exactly once when I noted in a point I dedicated to a paper about a study of hunter-gatherers that “There’s no causal evidence that sleeping 7-9 hours is healthier than sleeping 6 hours or less. Correlational evidence [from a meta-analysis] suggests that people who sleep 4 hours have the same if not lower mortality as those who sleep 8 hours and that people who sleep 6-7 hours have the lowest mortality.”
What Mendonça seems to miss more generally is that meta-analyses, which she is relying on heavily, do not reflect reality: they reflect the consensus of an academic field. And if the academic field is confused and the majority of the papers published in it are garbage, then meta-analyses are going to be confused garbage as well.
Mendonça’s claim 2: Chronic sleep deprivation might be associated with *decreased* BDNF expression, as shown by Guzey’s own sources
I believe that it is similarly confused. I write about sleep deprivation causing increase in BDNF. What does Mendonça have that contradicts my writing, supposedly by papers I cited myself?
1:
Chronic sleep deprivation and insomnia can act as an external stressors and result in depression, characterized by hippocampal BDNF downregulation along with disrupted frontal cortical BDNF expression, as well as reduced levels and impaired diurnal alterations in serum BDNF expression.
This quote talks about depression (due to chronic sleep deprivation and stress) being characterized by BDNF downregulation. This is not about sleep deprivation per se because sleep deprivation does not necessarily lead to depression.
2:
significantly decreased serum BDNF levels compared with sleep-healthy controls (n=24; F(1)=5.017; P=0.03; Figure 1a). In addition, serum BDNF levels were significantly correlated with severity of insomnia in all paricipants (n=50; rp=−0.409; P=0.004; Figure 1). [...] We found subjective sleep impairment to be associated with lower serum BDNF levels, whereas reported good sleep was related to higher serum BDNF levels, as shown for those suffering from current insomnia compared with sleep-healthy subjects.
This quote talks about people with insomnia having decreased BDNF. People with insomnia have all kinds of health issues and are famous for underestimating how much they sleep (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277880/) and using them to argue about the relationship between sleep deprivation and BDNF is misleading.
I regret citing this paper in my essay but it’s indicative of the overall depth of Mendonça’s arguments: instead of noting that using insomniacs as evidence is simply inappropriate for the point I was making and writing that I’m using inappropriate evidence, she doesn’t note any issues with it and simply notes that it contradicts my point.
3:
[O]ur findings are in line with the hypothesis of an increased stress vulnerability due to sleep loss which may lead to a decrease in BDNF. [...] While we report a reduction of BDNF levels linked to sleep disturbance reflecting chronic stress on the one side, we and others consistently showed that prolonged wakefulness caused by SD (partial or total), which can be considered as an acute stressor for the brain, leads to a rapid increase of BDNF
This quote again talks about stress due to sleep loss, not sleep loss per se and specifically notes “we and others consistently showed that prolonged wakefulness caused by SD (partial or total), which can be considered as an acute stressor for the brain, leads to a rapid increase of BDNF”, so I’m very confused by Mendonça uses it to contradict me.
I don’t have the ability to go through every claim in the post and show what exactly is wrong with them, but my read that the rest are similarly confused: they seem to be somewhat related to what I wrote but mostly misinterpreted with their misinterpretations being “refuted” or shown “misleading”.
The paper Mendonça cites looks at long-term long sleep and long-term short sleep, with their association with depression. My claim and my evidence (from bipolar people) are concerned with short-term long sleep and short-term short sleep.
Your specific claim about depression was “depression triggers/amplifies oversleeping while oversleeping triggers/amplifies depression.” Nowhere in the section did you specify your claim was about short-term long sleep.
Your evidence, too, barely concerns short-term long sleep: depressive episodes last about five or six months on average, which is often not what people have in mind when they think about “short-term” oversleeping, and it’s common for them to last a year or more.
It is further puzzling that in her refutation of my argument she:
completely ignores the relationship between sleep and mania (i.e. she ignores one half of my argument and only discusses the part about depression).
completely ignores the fact that in ~50% of ALL people with depression (not just bipolar), short-term short sleep relieves depression.
I don’t disagree with you on the claim that sleep restriction or deprivation often causes mania, and can adequately treat depression in some cases. I also mentioned the relationship between sleep and mania elsewhere in my post.
It was not my intention to respond to every single one of your claims, or to mount a comprehensive takedown of every aspect of your post. I’ll repeat what AllAmericanBreakfast said to you after you made a similar argument in your previous comment:
Natália doesn’t set out to disprove all of your theses, but rather to put forth some counter-theses. She says:
I decided to write a post pointing out several of the mistakes I think he’s made, and reporting some of what the academic literature on sleep seems to show.
Read carefully, she neither claims that every point you’ve made is mistaken, nor to give a comprehensive review of the academic literature. [...] She’s critiquing those theses of yours which she found weak, not issuing a comprehensive point-by-point criticism of your entire original post.
Guzey:
I wrote that most sleep research is extremely unreliable. And indeed, this is what I believe and this is why I’m so selective with the kind of evidence I use
Yes, I wasn’t claiming that you said that all sleep research was bad, but that the sleep research you’re willing to trust is also, suspiciously, seemingly exclusively research that indicates that sleep is not as important as people think, when there doesn’t seem to be a difference in quality between the research you cite as evidence and the research I do. You use evidence from experimental studies to show that acute sleep deprivation often relieves depression, and I use evidence from experimental studies to show that sleep restriction seems to cause cognitive impairment and overeating, and you haven’t elaborated on why the research you cite is more trustworthy.
In other words, I understand that you do not think that all sleep research is bad. However, I was, and remain, skeptical that you had a consistent and rigorous standard for what research you thought was admissible and what research you thought was not.
What Mendonça seems to miss more generally is that meta-analyses, which she is relying on heavily, do not reflect reality: they reflect the consensus of an academic field. And if the academic field is confused and the majority of the papers published in it are garbage, then meta-analyses are going to be confused garbage as well.
Why can’t I say the same about e.g. the “enormous literature” you use as evidence that sleep deprivation helps depression? [1] Why does that reflect reality, but not my meta-analyses? (These are not rhetorical questions, I’d like to know what you see as the difference). It’s not the case that, as you claim in the original post, the kind of evidence I use is “like cognitive psychology” and is only not suffering from a replication crisis because sleep studies are hard; the findings I talk about do get replicated. It’s also not as if my evidence is inconsistent with people’s experiences.
Also, it’s instructive to note that academic fields are not monolithic things, as Scott Alexander explains in this essay. As he points out, a lot of correct contrarians were in fact supported by academic research when they made their “contrarian” points. Knowledge just doesn’t propagate that quickly among people who work in the same field. As an example, some clinical psychiatrists promote the serotonin theory of depression, but the academic research body on psychiatry does not support it. Lumping clinicians and the research body together as a monolithic “psychiatric field” obscures this.
1:
Chronic sleep deprivation and insomnia can act as an external stressors and result in depression, characterized by hippocampal BDNF downregulation along with disrupted frontal cortical BDNF expression, as well as reduced levels and impaired diurnal alterations in serum BDNF expression.
This quote talks about depression (due to chronic sleep deprivation and stress) being characterized by BDNF downregulation. This is not about sleep deprivation per se because sleep deprivation does not necessarily lead to depression.
[...]
3:
[O]ur findings are in line with the hypothesis of an increased stress vulnerability due to sleep loss which may lead to a decrease in BDNF. [...] While we report a reduction of BDNF levels linked to sleep disturbance reflecting chronic stress on the one side, we and others consistently showed that prolonged wakefulness caused by SD (partial or total), which can be considered as an acute stressor for the brain, leads to a rapid increase of BDNF
This quote again talks about stress due to sleep loss, not sleep loss per se
These quotes simply say that chronic sleep deprivation may lead to decreased BDNF expression through a certain mechanism (depression and stress, respectively).
[The quote starting with “[O]ur findings are in line[...]”] specifically notes “we and others consistently showed that prolonged wakefulness caused by SD (partial or total), which can be considered as an acute stressor for the brain, leads to a rapid increase of BDNF”, so I’m very confused by Mendonça uses it to contradict me.
I’m not contradicting you on the acute effects of sleep deprivation on BDNF. I specifically said,
These sources agree that acute sleep deprivation increases BDNF expression, but they also say that the opposite may happen when sleep deprivation is chronic
2:
significantly decreased serum BDNF levels compared with sleep-healthy controls (n=24; F(1)=5.017; P=0.03; Figure 1a). In addition, serum BDNF levels were significantly correlated with severity of insomnia in all paricipants (n=50; rp=−0.409; P=0.004; Figure 1). [...] We found subjective sleep impairment to be associated with lower serum BDNF levels, whereas reported good sleep was related to higher serum BDNF levels, as shown for those suffering from current insomnia compared with sleep-healthy subjects.
This quote talks about people with insomnia having decreased BDNF. People with insomnia have all kinds of health issues and are famous for underestimating how much they sleep (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277880/) and using them to argue about the relationship between sleep deprivation and BDNF is misleading
Thanks for pointing out that I had an incorrect assumption; I realize now that it’s unclear whether insomniacs sleep less than other people. I’ll edit the post.
instead of noting that using insomniacs as evidence is simply inappropriate for the point I was making and writing that I’m using inappropriate evidence, she doesn’t note any issues with it and simply notes that it contradicts my point.
Hm, I had assumed that you were simply showing a random sample of the first papers that you found when searching “sleep deprivation bdnf.” You simply said
In the interest of simplicity, I’m going to look at individual pieces of your and Natalia’s counterarguments. I won’t do it all at once, but I’ll try to be thorough over time. I’ll be separating my analyses into separate comments.
To start with, you say:
Here’s what Mendonça writes in her first point that so conclusively demonstrates that the point I make is “misleading”:
[Guzey’s] evidence from bipolar disorder patients is not representative of what you see in the general population: both long and short sleep duration are associated with depression
The paper Mendonça cites looks at long-term long sleep and long-term short sleep, with their association with depression. My claim and my evidence (from bipolar people) are concerned with short-term long sleep and short-term short sleep. That is, Mendonça’s paper is simply not overlapping with with what I write about or what the evidence she calls “misleading” is concerned about.
To break this into parts:
My claim and my evidence (from bipolar people) are concerned with short-term long sleep and short-term short sleep.
Bipolar I Disorder is defined by manic episodes that last at least seven days (most of the day, nearly every day) or when manic symptoms are so severe that hospital care is needed. Usually, separate depressive episodes occur as well, typically lasting at least two weeks. Episodes of mood disturbance with mixed features (having depression and manic symptoms at the same time) are also possible.
Bipolar II Disorder is defined by a pattern of depressive episodes and hypomanic episodes, but not the full-blown manic episodes described above.
None of the respondants from the r/BipolarReddit thread you quoted specify if they have BP I or BP II. However, if some have BP I, then the length of their depressive episodes fit within the diagnostic criteria for atypical depression.
Two or more of the following features, present for most of the time, for at least two weeks:
Increased appetite
Increased sleep
Leaden paralysis (i.e., heavy, leaden feelings in arms or legs)
Interpersonal rejection sensitivity (not limited to episodes of mood disturbance) resulting in significant social or occupational impairment
You say:
The paper Mendonça cites looks at long-term long sleep and long-term short sleep, with their association with depression. That is, Mendonça’s paper is simply not overlapping with with what I write about.
The paper Natalia cites is the one I just quoted. It specifically covers sleep in bipolar I patients with atypical depression, which is directly overlapping with your topic.
Your argument in this section is setting up a model in which depression/long sleep and mania/short sleep are at two ends of a sliding scale in the general population. Your BipolarReddit anecdotes are meant to establish the polar ends of this scale, and the use of sleep deprivation as a depression treatment is meant to establish the causal role of sleep length in moving us from one end to the other of the scale in the general population. Natalia’s counterargument is that there doesn’t exist a simple depression/high sleep—mania/low sleep scale in the general population. Using bipolar patients gives a misleading impression that there is such a simple scale.
I think, however, that the most important point you’re trying to make here is that “less sleep can be good for you,” using the example of sleep as depression treatment as an example, as well as the existence of atypical depression. Here, the simple scale does generate useful results. There’s evidence (accessible on sci-hub) that sleep deprivation works better as a treatment for depression with melancholic features (coinciding with shortened sleep and sleep disturbance) than for depression with atypical features.
Researchers and clinicians agree that the effect of SD is most favorable in patients with the classical ‘endogenous (endogenomorphic)’ depressive syndrome. In terms of DSM-IV these patients fulfil the criteria of a major depressive episode (with melancholic features). Less favorable SD effects have been observed in dysthymic patients (formerly neurotic depression). However, these differences are not very pronounced according to the metaanalysis published by Wu and Bunney (1990); who determined a response rate of 67% in endogenous depression compared with 48% in neurotic depression...
So even for patients not sleeping very much (those with melancholic features), the right move can be a careful regimen of getting even less sleep. A simple “depression → healthy” scale works when we consider this specific sleep intervention. If sleep deprivation can also trigger manic episodes in bipolar patients, as you both seem to agree it does, we also have a “healthy → manic” piece of the scale as well.
Sleep compression and restriction is also used as a treatment for insomnia. From the sleep foundation (not a great source, but I think this is an OK as a description of the technique):
Sleep restriction and compression: These two methods aim to improve sleep quality and quantity by reducing the amount of time a person lies in bed. A CBT-i practitioner can use records from a patient’s sleep diary to determine how much time they sleep each night compared to the amount of time they lie in bed awake. Sleep restriction involves a sharp curtailing of time in bed while sleep compression is a more gradual process, but both techniques are intended to achieve the same goal: less time in bed awake each night.
I think this highlights that we need to distinguish between “spending more time in bed” and “getting more sleep.” More on this later.
None of the respondants from the r/BipolarReddit thread you quoted specify if they have BP I or BP II. However, if some have BP I, then the length of their depressive episodes fit within the diagnostic criteria for atypical depression.
Two or more of the following features, present for most of the time, for at least two weeks:
Increased appetite
Increased sleep
Leaden paralysis (i.e., heavy, leaden feelings in arms or legs)
Interpersonal rejection sensitivity (not limited to episodes of mood disturbance) resulting in significant social or occupational impairment
The difference between BP II and BP I doesn’t matter in respect to this. You need to have depressive episodes at least 2 weeks in length to be diagnosed with BP II.
Thanks for the taking the time to look into my essay.
Mendonça’s claim 1: Guzey’s /r/BipolarReddit evidence is misleading
Here’s what Mendonça writes in her first point that so conclusively demonstrates that the point I make is “misleading”:
The paper Mendonça cites looks at long-term long sleep and long-term short sleep, with their association with depression. My claim and my evidence (from bipolar people) are concerned with short-term long sleep and short-term short sleep. That is, Mendonça’s paper is simply not overlapping with with what I write about or what the evidence she calls “misleading” is concerned about. It is further puzzling that in her refutation of my argument she:
completely ignores the relationship between sleep and mania (i.e. she ignores one half of my argument and only discusses the part about depression).
completely ignores the fact that in ~50% of ALL people with depression (not just bipolar), short-term short sleep relieves depression.
I am similarly puzzled by a later accusation:
I wrote that most sleep research is extremely unreliable. And indeed, this is what I believe and this is why I’m so selective with the kind of evidence I use, preferring to show my readers Reddit comments left by bipolar people, instead of meta-analyses, and why, when I do use meta-analyses, I use them very cautiously. For example, in the essay, I used a meta-analysis exactly once when I noted in a point I dedicated to a paper about a study of hunter-gatherers that “There’s no causal evidence that sleeping 7-9 hours is healthier than sleeping 6 hours or less. Correlational evidence [from a meta-analysis] suggests that people who sleep 4 hours have the same if not lower mortality as those who sleep 8 hours and that people who sleep 6-7 hours have the lowest mortality.”
What Mendonça seems to miss more generally is that meta-analyses, which she is relying on heavily, do not reflect reality: they reflect the consensus of an academic field. And if the academic field is confused and the majority of the papers published in it are garbage, then meta-analyses are going to be confused garbage as well.
Mendonça’s claim 2: Chronic sleep deprivation might be associated with *decreased* BDNF expression, as shown by Guzey’s own sources
I believe that it is similarly confused. I write about sleep deprivation causing increase in BDNF. What does Mendonça have that contradicts my writing, supposedly by papers I cited myself?
1:
This quote talks about depression (due to chronic sleep deprivation and stress) being characterized by BDNF downregulation. This is not about sleep deprivation per se because sleep deprivation does not necessarily lead to depression.
2:
This quote talks about people with insomnia having decreased BDNF. People with insomnia have all kinds of health issues and are famous for underestimating how much they sleep (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277880/) and using them to argue about the relationship between sleep deprivation and BDNF is misleading.
I regret citing this paper in my essay but it’s indicative of the overall depth of Mendonça’s arguments: instead of noting that using insomniacs as evidence is simply inappropriate for the point I was making and writing that I’m using inappropriate evidence, she doesn’t note any issues with it and simply notes that it contradicts my point.
3:
This quote again talks about stress due to sleep loss, not sleep loss per se and specifically notes “we and others consistently showed that prolonged wakefulness caused by SD (partial or total), which can be considered as an acute stressor for the brain, leads to a rapid increase of BDNF”, so I’m very confused by Mendonça uses it to contradict me.
I don’t have the ability to go through every claim in the post and show what exactly is wrong with them, but my read that the rest are similarly confused: they seem to be somewhat related to what I wrote but mostly misinterpreted with their misinterpretations being “refuted” or shown “misleading”.
Your specific claim about depression was “depression triggers/amplifies oversleeping while oversleeping triggers/amplifies depression.” Nowhere in the section did you specify your claim was about short-term long sleep.
Your evidence, too, barely concerns short-term long sleep: depressive episodes last about five or six months on average, which is often not what people have in mind when they think about “short-term” oversleeping, and it’s common for them to last a year or more.
I don’t disagree with you on the claim that sleep restriction or deprivation often causes mania, and can adequately treat depression in some cases. I also mentioned the relationship between sleep and mania elsewhere in my post.
It was not my intention to respond to every single one of your claims, or to mount a comprehensive takedown of every aspect of your post. I’ll repeat what AllAmericanBreakfast said to you after you made a similar argument in your previous comment:
Guzey:
Yes, I wasn’t claiming that you said that all sleep research was bad, but that the sleep research you’re willing to trust is also, suspiciously, seemingly exclusively research that indicates that sleep is not as important as people think, when there doesn’t seem to be a difference in quality between the research you cite as evidence and the research I do. You use evidence from experimental studies to show that acute sleep deprivation often relieves depression, and I use evidence from experimental studies to show that sleep restriction seems to cause cognitive impairment and overeating, and you haven’t elaborated on why the research you cite is more trustworthy.
In other words, I understand that you do not think that all sleep research is bad. However, I was, and remain, skeptical that you had a consistent and rigorous standard for what research you thought was admissible and what research you thought was not.
Why can’t I say the same about e.g. the “enormous literature” you use as evidence that sleep deprivation helps depression? [1] Why does that reflect reality, but not my meta-analyses? (These are not rhetorical questions, I’d like to know what you see as the difference). It’s not the case that, as you claim in the original post, the kind of evidence I use is “like cognitive psychology” and is only not suffering from a replication crisis because sleep studies are hard; the findings I talk about do get replicated. It’s also not as if my evidence is inconsistent with people’s experiences.
Also, it’s instructive to note that academic fields are not monolithic things, as Scott Alexander explains in this essay. As he points out, a lot of correct contrarians were in fact supported by academic research when they made their “contrarian” points. Knowledge just doesn’t propagate that quickly among people who work in the same field. As an example, some clinical psychiatrists promote the serotonin theory of depression, but the academic research body on psychiatry does not support it. Lumping clinicians and the research body together as a monolithic “psychiatric field” obscures this.
These quotes simply say that chronic sleep deprivation may lead to decreased BDNF expression through a certain mechanism (depression and stress, respectively).
I’m not contradicting you on the acute effects of sleep deprivation on BDNF. I specifically said,
Thanks for pointing out that I had an incorrect assumption; I realize now that it’s unclear whether insomniacs sleep less than other people. I’ll edit the post.
Hm, I had assumed that you were simply showing a random sample of the first papers that you found when searching “sleep deprivation bdnf.” You simply said
So I wasn’t expecting all of those papers to be appropriate for the point you were making.
Not that I would want to say that; I don’t disagree with Guzey on the effects of sleep deprivation on depression.
In the interest of simplicity, I’m going to look at individual pieces of your and Natalia’s counterarguments. I won’t do it all at once, but I’ll try to be thorough over time. I’ll be separating my analyses into separate comments.
To start with, you say:
To break this into parts:
There are several types of bipolar, including bipolar I and bipolar II.
None of the respondants from the r/BipolarReddit thread you quoted specify if they have BP I or BP II. However, if some have BP I, then the length of their depressive episodes fit within the diagnostic criteria for atypical depression.
You say:
The paper Natalia cites is the one I just quoted. It specifically covers sleep in bipolar I patients with atypical depression, which is directly overlapping with your topic.
Your argument in this section is setting up a model in which depression/long sleep and mania/short sleep are at two ends of a sliding scale in the general population. Your BipolarReddit anecdotes are meant to establish the polar ends of this scale, and the use of sleep deprivation as a depression treatment is meant to establish the causal role of sleep length in moving us from one end to the other of the scale in the general population. Natalia’s counterargument is that there doesn’t exist a simple depression/high sleep—mania/low sleep scale in the general population. Using bipolar patients gives a misleading impression that there is such a simple scale.
I think, however, that the most important point you’re trying to make here is that “less sleep can be good for you,” using the example of sleep as depression treatment as an example, as well as the existence of atypical depression. Here, the simple scale does generate useful results. There’s evidence (accessible on sci-hub) that sleep deprivation works better as a treatment for depression with melancholic features (coinciding with shortened sleep and sleep disturbance) than for depression with atypical features.
So even for patients not sleeping very much (those with melancholic features), the right move can be a careful regimen of getting even less sleep. A simple “depression → healthy” scale works when we consider this specific sleep intervention. If sleep deprivation can also trigger manic episodes in bipolar patients, as you both seem to agree it does, we also have a “healthy → manic” piece of the scale as well.
Sleep compression and restriction is also used as a treatment for insomnia. From the sleep foundation (not a great source, but I think this is an OK as a description of the technique):
I think this highlights that we need to distinguish between “spending more time in bed” and “getting more sleep.” More on this later.
The difference between BP II and BP I doesn’t matter in respect to this. You need to have depressive episodes at least 2 weeks in length to be diagnosed with BP II.
From the DSM-5, which you can find on libgen:
Thanks for pulling that up. This makes the point you and I are making even stronger in this area.