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
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.