5 ms·

> Best way to manage the withdrawal would be to dramatically reduce them being prescribed in the first place. No, that will just hurt more people up front for

by burnte 1mo ago

> Best way to manage the withdrawal would be to dramatically reduce them being prescribed in the first place. No, that will just hurt more people up front for longer. The truth is antidepressants have a larger effect on mental health than actually gets reported because of how improvements are measured. If you look at a patient who doesn't get out of bed, is in trouble at work/school for performance, doesn't spend social time with friends, etc, and 6 months after starting an SSRI they're indistinguishable from other people but still have other issues, we call that a "mild impact" because they self-report other problems. The truth is we took someone from being passively suicidal to functioning normally, and we fail to look at the self-reported problems, we just report them. The self reported problems tend to change from "I don't care about anything" to "I'm unhappy at my job" or "I'm stressed at how much I have to do with work and my kids and home." These are actually major improvements, the patient has gone from being actually clinically depressed to significant improvement but continued unhappiness with life circumstances as opposed to unhappiness with life in general. Antidepressants are amazing, we need to improve therapists and how they deal with medicated patients. Too many therapists dismiss meds and too many psychiatrists dismiss therapy. I've been in this space for a long time now, healthcare IT in the mental/behavioral health space. We're engaged in a long erm research study to help demonstrate the value of a tightly integrated therapy/psych team and more advanced treatments and when you get everyone in the room pulling in the same direction patient outcomes are amazing. One actual issue that antidepressants face is that they're not the only treatment, but many doctors are reluctant to move to TMS or esketamine, despite the amaing success rates they have with patients who have not had success with two or more drugs. If two drugs failed you, the third has a 14% chance of helping. The 4th is single digits. But you pivot to TMS and you see 60-80 percent improvement rates. Esketamine is close too. ADs aren't the problem, it's that we don't take mental health as serious as we take physical health.

D-Machine 1mo ago
> The truth is antidepressants have a larger effect on mental health than actually gets reported because of how improvements are measured. The truth is actually exactly the opposite, and I provided very high-quality evidence demonstrating this to be the case. You have nothing but bald assertions.
- keepupnow 1mo ago
  [dead]
- burnte 1mo ago
  No, I have proof, I work in mental health, I'm part of our research committee's board, I see the actual data from our patients, other studies, the discussions about the data, etc. You simply completely ignored my core statement. I spelled out why different studies report different outcomes, and they're genuinely big problems. You don't have to like it or agree with it but don't try to dismiss me, you linked 4 studies you don't even understand because you misrepresented the data they report. One of them actually PROVES my point. Another is a metastudy which is only useful for indicating future research avenues, not drawing clinical decisions. And lastly one proves my point about multi-drug failures requiring a change in treatment. Antidepressants save lives and I will fight tooth and nail to preserve their access by patients.
  - D-Machine 1mo ago
    > You simply completely ignored my core statement. Most of it was junk, or included stuff about TMS which has zero relevance to antidepressants. Here's the junk: > The truth is we took someone from being passively suicidal to functioning normally, and we fail to look at the self-reported problems, we just report them. The self reported problems tend to change from "I don't care about anything" to "I'm unhappy at my job" or "I'm stressed at how much I have to do with work and my kids and home." These are actually major improvements, the patient has gone from being actually clinically depressed to significant improvement but continued unhappiness with life circumstances as opposed to unhappiness with life in general. Sorry, but, no, going from passively suicidal to normal function (including not getting out bed) would move HAM-D and almost other other depression rating scales massively, so we would see this in studies, but we don't. This doesn't pass the sniff test. Could antidepressants help with other symptoms that are milder than suicidality, but which are not measured? Plausibly, but why would I trust you, a faithful zealot (literally: you will "fight tooth and nail", and "antidepressants are amazing")? Where are the papers? You are too biased to take at word. > We're engaged in a long term research study to help demonstrate the value of a tightly integrated therapy/psych team and more advanced treatments and when you get everyone in the room pulling in the same direction patient outcomes are amazing. Great, when it is published, I look forward to reading it. Doctors have felt this way since the dawn of time though, and since you are a zealot, I don't care until I see the paper. That being said, yes, there is broad evidence that combination treatments (e.g. antidepressants + psychotherapy) are generally better than either alone, and it is quite reasonable when there is proper, regular communication amongst those teams that it is a bit better still. There are studies looking at this, but again, you find average effect sizes that really fail to meet anything like a minimally important difference. And again in these cases it remains unclear how much of the patients that do experience clinically meaningful change are changing because of the antidepressants (or how much of the meaningful difference can be attributed to the antidepressants). It's the same basic problem, the science here is really, really poor. > a metastudy [which] is only useful for indicating future research avenues, not drawing clinical decisions Nonsense, you'd better be thinking about and looking at these kinds of things when making clinical decisions. > You linked 4 studies you don't even understand because you misrepresented the data they report. One of them actually PROVES my point You've shown me nothing to indicate you have a better understanding, none of them prove anything you are saying. Best you can say is some interpretations of some studies looking at the distribution of the treatment effect might be consistent with more individuals receiving antidepressants having large positive effects, but, as I said, this is remains only weakly supported in general, i.e. it isn't a clear finding and just remains a "maybe". The MID issue is huge, and that you work in this area on a research committee board and can't deal with this, and appeal to authority without seeming to understand the basic measurement issues at hand here, is deeply concerning. As a true believer, your beliefs about the efficacy of esketamine are also widely overstated, and, we can be sure, ignore the MID issue as usual. Nice try though. EDIT: Okay, since burnte is too lazy to do the work, I did some looking for proper MID-based responder analyses. There are a some, and one is with eskatimine [1], and finds: > By Day 28, 86.5% of patients reached or exceeded the PHQ-9 [MID] in the esketamine/AD group compared to 70% in the placebo/AD group. The most appropriate [MID] for the MADRS was -10 points. By Day 28, 78.2% of patients reached or exceeded the MADRS [MID] in the esketamine/AD group compared to 65.0% in the placebo/AD group. So this is real research! And maybe esketamine really is something new. But then, why is competent research nearly impossible to find and results always presented in a way that aren't clinically interpretable and/or prevent seeing the distributions in a way that could easily answer these questions? Hmmm, maybe because the placebo vs. treatment distributions look so similar, like this: https://www.nature.com/articles/s41398-022-01882-5/figures/1 https://www.nature.com/articles/s41398-022-01882-5/figures/1 [1] https://pubmed.ncbi.nlm.nih.gov/33261932/ https://pubmed.ncbi.nlm.nih.gov/33261932/
tredre3 1mo ago
> But you pivot to TMS and you see 60-80 percent improvement rates. Esketamine is close too. I have received both rTMS and esketamine and the providers themselves told me they saw roughly a 30-40% response rate (not remission, that's even lower!). Upon researching the topic myself, I found that the meta analysis usually agreed with this 30% figure, but recent research papers mark eskatamine even lower. Both treatments can be miraculous for a few select people and it makes a good headline, but it's a total failure for the majority of people. I agree with you that those treatments should be easier to access, though. > Too many therapists dismiss meds and too many psychiatrists dismiss therapy. This is the only factually true statement in your entire comment.
- burnte 1mo ago
  In the practices in which I've worked, proper screening and expertise in treatment delivery boost outcome rates significantly. We see well over 60% success rates with the first round. > This is the only factually true statement in your entire comment. You read something you disagree with so you decided to call me a liar rather than discuss. I'm not wasting any more on time on you.
nabukodonozor 1mo ago
Well I think that we do not know enough about genesis of depression and other mental issues. So this is just symptomatic therapy. And as such it should be prescribed only for very short terms. Analogy: how would you perceive someone who prescribed his febrile patient paracetamol for 10 years just because it works? And in his defense he/she claims that febrile condition has well known metabolic chain and that paracetamol lowers fever mainly by interrupting the COX → PGE₂ part of the fever pathway in the brain.
jaggederest 1mo ago
The problem with the entire argument that you're making is that the natural rate of remission in uncomplicated major depressive episodes is very close to the rate that SSRIs create, individually, and very close in terms of timing. If you do something more like STAR-D you see higher rates, but that also takes so long that many people naturally remit.
- deleted 1mo ago
  [deleted]
elil17 1mo ago
> You look at a patient who doesn't get out of bed, is in trouble at work/school for performance, doesn't spend social time with friends, etc, and 6 months after starting an SSRI they're indistinguishable from other people but still have other issues, we call that a "mild impact" because they self-report other problems. This really lines up with what I've seen anecdotally. My partner literally doesn't remember how bad things were before he took antidepressants because depression impacted his ability to form memories. He self reports that antidepressants had a mild impact, but from an outside perspective nearly everything about his life changed.

by burnte 1mo ago

D-Machine 1mo ago

> The truth is antidepressants have a larger effect on mental health than actually gets reported because of how improvements are measured. The truth is actually exactly the opposite, and I provided very high-quality evidence demonstrating this to be the case. You have nothing but bald assertions.

keepupnow 1mo ago
[dead]
burnte 1mo ago
No, I have proof, I work in mental health, I'm part of our research committee's board, I see the actual data from our patients, other studies, the discussions about the data, etc. You simply completely ignored my core statement. I spelled out why different studies report different outcomes, and they're genuinely big problems. You don't have to like it or agree with it but don't try to dismiss me, you linked 4 studies you don't even understand because you misrepresented the data they report. One of them actually PROVES my point. Another is a metastudy which is only useful for indicating future research avenues, not drawing clinical decisions. And lastly one proves my point about multi-drug failures requiring a change in treatment. Antidepressants save lives and I will fight tooth and nail to preserve their access by patients.
- D-Machine 1mo ago
  > You simply completely ignored my core statement. Most of it was junk, or included stuff about TMS which has zero relevance to antidepressants. Here's the junk: > The truth is we took someone from being passively suicidal to functioning normally, and we fail to look at the self-reported problems, we just report them. The self reported problems tend to change from "I don't care about anything" to "I'm unhappy at my job" or "I'm stressed at how much I have to do with work and my kids and home." These are actually major improvements, the patient has gone from being actually clinically depressed to significant improvement but continued unhappiness with life circumstances as opposed to unhappiness with life in general. Sorry, but, no, going from passively suicidal to normal function (including not getting out bed) would move HAM-D and almost other other depression rating scales massively, so we would see this in studies, but we don't. This doesn't pass the sniff test. Could antidepressants help with other symptoms that are milder than suicidality, but which are not measured? Plausibly, but why would I trust you, a faithful zealot (literally: you will "fight tooth and nail", and "antidepressants are amazing")? Where are the papers? You are too biased to take at word. > We're engaged in a long term research study to help demonstrate the value of a tightly integrated therapy/psych team and more advanced treatments and when you get everyone in the room pulling in the same direction patient outcomes are amazing. Great, when it is published, I look forward to reading it. Doctors have felt this way since the dawn of time though, and since you are a zealot, I don't care until I see the paper. That being said, yes, there is broad evidence that combination treatments (e.g. antidepressants + psychotherapy) are generally better than either alone, and it is quite reasonable when there is proper, regular communication amongst those teams that it is a bit better still. There are studies looking at this, but again, you find average effect sizes that really fail to meet anything like a minimally important difference. And again in these cases it remains unclear how much of the patients that do experience clinically meaningful change are changing because of the antidepressants (or how much of the meaningful difference can be attributed to the antidepressants). It's the same basic problem, the science here is really, really poor. > a metastudy [which] is only useful for indicating future research avenues, not drawing clinical decisions Nonsense, you'd better be thinking about and looking at these kinds of things when making clinical decisions. > You linked 4 studies you don't even understand because you misrepresented the data they report. One of them actually PROVES my point You've shown me nothing to indicate you have a better understanding, none of them prove anything you are saying. Best you can say is some interpretations of some studies looking at the distribution of the treatment effect might be consistent with more individuals receiving antidepressants having large positive effects, but, as I said, this is remains only weakly supported in general, i.e. it isn't a clear finding and just remains a "maybe". The MID issue is huge, and that you work in this area on a research committee board and can't deal with this, and appeal to authority without seeming to understand the basic measurement issues at hand here, is deeply concerning. As a true believer, your beliefs about the efficacy of esketamine are also widely overstated, and, we can be sure, ignore the MID issue as usual. Nice try though. EDIT: Okay, since burnte is too lazy to do the work, I did some looking for proper MID-based responder analyses. There are a some, and one is with eskatimine [1], and finds: > By Day 28, 86.5% of patients reached or exceeded the PHQ-9 [MID] in the esketamine/AD group compared to 70% in the placebo/AD group. The most appropriate [MID] for the MADRS was -10 points. By Day 28, 78.2% of patients reached or exceeded the MADRS [MID] in the esketamine/AD group compared to 65.0% in the placebo/AD group. So this is real research! And maybe esketamine really is something new. But then, why is competent research nearly impossible to find and results always presented in a way that aren't clinically interpretable and/or prevent seeing the distributions in a way that could easily answer these questions? Hmmm, maybe because the placebo vs. treatment distributions look so similar, like this: https://www.nature.com/articles/s41398-022-01882-5/figures/1 https://www.nature.com/articles/s41398-022-01882-5/figures/1 [1] https://pubmed.ncbi.nlm.nih.gov/33261932/ https://pubmed.ncbi.nlm.nih.gov/33261932/

tredre3 1mo ago

> But you pivot to TMS and you see 60-80 percent improvement rates. Esketamine is close too. I have received both rTMS and esketamine and the providers themselves told me they saw roughly a 30-40% response rate (not remission, that's even lower!). Upon researching the topic myself, I found that the meta analysis usually agreed with this 30% figure, but recent research papers mark eskatamine even lower. Both treatments can be miraculous for a few select people and it makes a good headline, but it's a total failure for the majority of people. I agree with you that those treatments should be easier to access, though. > Too many therapists dismiss meds and too many psychiatrists dismiss therapy. This is the only factually true statement in your entire comment.

burnte 1mo ago
In the practices in which I've worked, proper screening and expertise in treatment delivery boost outcome rates significantly. We see well over 60% success rates with the first round. > This is the only factually true statement in your entire comment. You read something you disagree with so you decided to call me a liar rather than discuss. I'm not wasting any more on time on you.

nabukodonozor 1mo ago

Well I think that we do not know enough about genesis of depression and other mental issues. So this is just symptomatic therapy. And as such it should be prescribed only for very short terms. Analogy: how would you perceive someone who prescribed his febrile patient paracetamol for 10 years just because it works? And in his defense he/she claims that febrile condition has well known metabolic chain and that paracetamol lowers fever mainly by interrupting the COX → PGE₂ part of the fever pathway in the brain.

jaggederest 1mo ago

The problem with the entire argument that you're making is that the natural rate of remission in uncomplicated major depressive episodes is very close to the rate that SSRIs create, individually, and very close in terms of timing. If you do something more like STAR-D you see higher rates, but that also takes so long that many people naturally remit.

deleted 1mo ago
[deleted]

elil17 1mo ago

> You look at a patient who doesn't get out of bed, is in trouble at work/school for performance, doesn't spend social time with friends, etc, and 6 months after starting an SSRI they're indistinguishable from other people but still have other issues, we call that a "mild impact" because they self-report other problems. This really lines up with what I've seen anecdotally. My partner literally doesn't remember how bad things were before he took antidepressants because depression impacted his ability to form memories. He self reports that antidepressants had a mild impact, but from an outside perspective nearly everything about his life changed.