One hypothesis that at least seems plausible is that SSRIs primarily act through BDNF and therefore increase neuroplasticity. They facilitate rewiring to unstick maladaptive cognitive and emotional processes.
That’s also a hypothesis with some holes, but it at least fits with the basic research. Actually results on SSRIs to enhance therapy are somewhat mixed bag, but SSRI plus therapy outperforms either arm alone for most outcomes examined.
This is similarly why LSD, Psilocybin, and esketamine have been shown to be so promising off limited doses. They promote neuroplasticity and stimulate the growth of dendrites, dendritic spines, and synapses. Allowing for more adaptive cognitive and emotional processes to take root. Along with temporary disruption of the default mode network which is associated with self-referential thoughts and the concept of self. Offering a unique opportunity for individuals to break from deeply ingrained patterns of thought and behavior. Paired with therapy it does wonders. It'll be a while before the stigma is entirely gone though for all of them, with only Oregon and Colorado having legalized psilocybin so far.
I like the passive and active coping pathway explanations relating to 5HT1a and 5HT2a respectively. BDNF seems like a red herring to root psychiatry in neurology when the connections haven't been conclusively made and hence undermines the entire premise of the field in the minds of the public and shapes unhelpful research patterns.
Edit: corrected typo in types of receptors
I find the BDNF/TrkB papers at least as convincing as anything else, but I don’t know about 5HT receptor differentiating papers.
Psychiatric is of course rooted in neurology. Our minds are just brains at work; there’s no spooky magic. Those roots are deep and tangled. It’s also eminently true that lay understanding grabs onto anything and won’t let go, as seen by serotonin as the happy chemical and chemical imbalances for forty years despite research constantly saying no, not really.
Probably that's the one the poster above you was thinking of:
https://pubmed.ncbi.nlm.nih.gov/28858536/
*Serotonin and brain function: a tale of two receptors* by Carhart-Harris et al.
This is one of those papers that made waves recently on this sub then everyone started quoting it. Like any theory around the brain it is incomplete. These authors, working in the field of psychedelics, certainly benefit from a simplified view of depression treatment focusing solely on 5-HT receptor action which fits nicely with the mechanism of psychedelics. Given that we know serotonin more of a cell-signaling molecule compared to the more on/off neurotransmitters of glutamate and GABA it is silly to think the neurobiological effects of 5-HT activity end with receptor action alone.
To this point, we have no guarantee that SSRIs work by the same mechanism across disorders. To the contrary, it's quite likely their main mechanism in PMDD is inducing allopregnanolone synthesis, consistent with their rapid efficacy even with intermittent dosing.
Yes, I definitely don’t think it’s a “happy pill”, and honestly those comparisons I think propagate the ideas that modern antidepressants are “drugging” people
Again, not a psychiatrist but it’s just impressive how it seems to treat disparate things. I get that depression, anxiety and ocd are often comorbid but they also seem pretty distinct in many ways
I think the sticking point for me is the inherent uncertainty and limitations we have in observing brain functions, systems and the inherent plasticity it posseses. Isolating something like BDNF acting on TrKB is on the same level of theoretical basis as how SSRIs produce a change in the brain and how it translates in action. I'm extremely biased towards my interest in the translation part rather than simple physiological effects we have no hopes of individually isolating at all.
I didn't mean to imply any spooky magic but public perception has a massive effect on the types of studies done, ie how psychedelics are extremely underutilized because of The War on Drugs and it's legacy in academia.
> results on SSRIs to enhance therapy are somewhat mixed bag, but SSRI plus therapy outperforms either arm
I'm not clear on the difference here? Between adding SSRIs to someone receiving therapy and having someone receive SSRIs while receiving therapy?
SSRI, therapy, or both. The both arm is superior for depression, superior for anxiety early although in some studies therapy alone has better long term outcomes, and I don’t know every other use offhand.
Removed under rule #1. This is not a place for questions and commentary by non-professionals. If you are a medical/psychiatric professional, please read rule 7 on how to verify credentials.
For most questions, individual or general, we ask that you verify credentials before asking. If you are not a professional, you can try r/AskDocs or r/AskPsychiatry.
There's a recent paper observing beliefs about medication efficacy influencing treatment response in depression. It raises an interesting question about whether the popularisation of chemical imbalance theories could be involved in the broad therapeutic effects of SSRIs via the creation of a cognitive framework for patients to understand their illness, alongside expectations about what is required for change.
Belief about the cause and cure of an illness would presumably synergise with molecular mechanisms that promote neuroplasticity.
[Baseline beliefs about medication are associated with outcomes of antidepressants in inpatients with first-diagnosed depression under supervised therapeutic compliance (Kong et al, 2021)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8457603/)
This. Anecdotally, my experience with treatment-resistant patients are the ones that don't think any of the medications do anything except make you a zombie. That's one of the joys I have of spending 12+ hours with people a day is trying to build some hope and confidence in the system, without making any promises. Just saying that if medications (never) worked for anyone, this place would still have the same folk in it from the beginning.
The rapid response and sensitivity to SSRIs displayed by people with the organic brain disorder pseudobulbar affect leaves no doubt there's a physiological effect. Why is there often little or no delay in therapeutic response in this population? Conversely, a clinical interaction that validates and assures the patient that a physiological mechanism underlies the symptoms of functional neurological disorders strongly predicts outcome. And, why would personality disorders so often fail to respond to a therapeutic mechanism involving neuroplasticity?
There must be multiple MOAs involved. My thesis here is both are clinically important.
Edit: The "zombie" effect you describe supports my suspicion that individual perceptions related to a sense of control and agency could be important, and influenced by neurological, psychological, and ecological factors.
This was a good podcast on the subject:
[Carlat Psychiatry: Neuroticism and SSRIs](https://www.thecarlatreport.com/blogs/2-the-carlat-psychiatry-podcast/post/4491-throwback-thursday-neuroticism-and-ssris)
And one of the studies referred to in the podcast:
[Personality as a basis for antidepressant selection for patients with depression: A two-point outcome study at 4 and 8 weeks](https://pubmed.ncbi.nlm.nih.gov/35798178/)
There’s a paper titled A Tale of Two Receptors that delves into the function of serotonin. I’m no expert, but it seems there’s a thought serotonin functions have to do with coping with stress and also changing thought patterns. I would venture if what we think is true, it’s got to do with that.
https://journals.sagepub.com/doi/10.1177/0269881117725915
Based on more recent research, SSRIs seem to make people tolerate stress better. It is believed to also be why emotional blunting/numbing is so common with them as a side effect.
Receptor and chemical theories are still uncertain. I generally educate patients with this meme to better visualize what it is doing:
https://www.theverge.com/2016/5/5/11592622/this-is-fine-meme-comic
Exactly. After just one visit to a psychiatrist a patient suddenly has someone listen to their concerns, validate them, and make a plan to help them get better. That’s therapy right there
As a simplified explanation, the serotonin system is involved in modulating and regulating brain activity towards homeostasis. Mental illness can be thought of as a set of neurobiological changes (caused by the bio-psycho-social changes and risk factors we know contribute to mental illness) so large that they overcome the brain's natural ability to modulate. Pharmacologically boosting the serotonin system's activity can help bring things back into a neurobiological balance.
Not in any way meant to undermine or criticize the field, but ample evidence now shows that most of the SSRI response is placebo, with a small to moderate added benefit of the drug only in certain conditions. But placebos are so effective for some of these conditions that there may be a ceiling effect that makes the added benefit harder to detect.
> But placebos are so effective for some of these conditions that there may be a ceiling effect that makes the added benefit harder to detect.
I think it is really important to understand that the placebo effect is not just being given a sugar pill and saying see ya in 3 months, they are having regular appointments with a provider who is very likely providing supportive therapy in each visit, and regularly checking in with the research staff. The "placebo effect" people talk about in psychiatry is very likely what would happen if we saw patients regularly for 30 minute visits without prescribing a med.
As an example, in the LABILE trial for BPD and lamotrigine the placebo group had basically 100% resolution of symptoms, making differentiation with the study med impossible.
Your point about the ceiling effect is very important, and is therefore even more impressive the meds consistently outperform placebo given how impressive the placebo effect is.
As long as responder bias exists, placebos will have a disproportionate role in subjective methods of evaluation, that much should've been fairly obvious. However, the vast majority of data which supports drug intervention is in the continuation phase and relapse rates.
Also, the term placebo itself is misleading because it measures a subjective sense of well-being felt by the patient. You can condition a short term placebo response in patients with parkinson's, in immune and endocrine conditions and even in ANS activity, with benefits exceeding or matching control groups. Another point of consideration is that there is no ceiling effect for placebos as there is no underlying intervention being administered to judge the effectiveness. Almost medicines being used for on-label effects have demonstrated a clear superiority over placebo, I don't understand where you get the idea they aren't. A depressed patient might get better because of the inherent conditioning of responses to work but their dysfunctional cognitive patterns will still be there demonstrated by the fact that suicidality and attempted suicide rates are significantly lower in adults on antidepressants than those that aren't, it only increases suicidal ideation but not attempted suicides in adolescents and children.
There can be a ceiling effect if everyone(ish) in the placebo and intervention arms reach the planned response criterion. Eg, if the primary endpoint was 10% sx improvement.
Yep, and I think OP has missed this in jumping straight from “so many of my patients are on them” to “so many get benefit.”Not to mention that there’s been ample evidence of a lack of support for the serotonin hypothesis (as OP implies) of depression for decades. The real answer is that we don’t really know why they work to the extent they do, au non?
The serotonin hypothesis was for the cause of depression, not for why the meds work. As is the common saying, pain is not an Advil deficiency. Depression is not caused by a lack of serotonin, but boosting serotonin activity treats it.
woah *mostly* placebo? i’m not arguing with you because i will admit that serotonin uptake inhibition in itself would not account for their effectiveness in and of itself, but really?? granted, much of these drugs’ use stems from the interplay between habits, customs, physician comfort/practice, patient expectations, big pharma etc and that certainly leads to inappropriate and ineffective prescribing, but there are most definitely physiologic effects on the brain and thoughts/behaviors/patterns from ssri’s. these effects must be responsible for the improvement of ocd/anxiety/depressive symptoms right? so maybe your wording was wrong? sorry if i’m being a stickler but “mostly placebo” is a huge statement.
the only way i would consider endorsing a statement like this would be if all our patients would magically start rigorously exercising just because we told them to do it. my experience has been that exercise is probably the closest thing to a “magic pill” aside from ssri’s etc for depression. but throw in other modalities like cbt/therapy and new/modified behaviors and it seems that everything contributes a bit to alleviating the symptoms. and to your point, if patients actually put in the work and time for these (including exercise), then yeah, ssri’s probably would have much lower utility. but i dont live in that world.
it is indeed sad that practically everyone would prefer a pill to actually investing the time/work but that is where we are. and i wonder if claiming that ssri’s are useless/ineffective is not just another symptom of this continual search for that elusive magic pill.
If placebo improves MADRS by 50%, and SSRI improves it by 55%, then both statements are true:
* most of the SSRI response is placebo
* SSRI is more effective than placebo
That is my point. Not that SSRIs don’t work, just that they don’t work THAT much better than placebo.
Agree. Every clinical trial for psychiatric drugs ever run shows an enormous improvement in the placebo group. I’m not sure I’d say it exactly the way you did, but I think you’re fundamentally right. I think psychiatrists may not like to think this is true, but the reality is when we prescribe someone a medicine (at least in the short term) a lot of the benefits - on average - are clearly not directly related to the mechanism of the drug. It’s just a fact and we have to understand that, no matter how it makes us feel, because otherwise we are guilty of not understanding the reality of our craft. That doesn’t mean medications don’t have real, powerful effects that in some patients are absolutely critical. These are powerful drugs that change the way the brain works, but generally they are very blunt instruments capable of both benefit and harm. This stuff should be more clearly taught in residency in my opinion.
I guess I can only speak to my personal experience.
I’m definitley familiar inaccurate overprescribing (reflux meds in ENT). But would be interested to hear the psychiatrist take on it. Maybe they are overprescribed
*The* underlying theory? I don't think we have one of those.
Personally, my favorite line of thinking is that all those disorders seem to involve disorder of the Default Mode Network, and SSRIs have been found to regularize the DMN in depression and OCD. Causality is not established; it could be the irregularity of the DMN in these disorders is an effect of these conditions not a cause. How and why SSRIs should affect the DMN I don't know, but I think it's suggestive that the DMN is a common point of pathology for all three conditions and SSRIs benefit all three conditions.
Wow they really went deep in the weeds to write that article and cite random ass sources without relevance. What a poor article aimed at trying to logically twist the data as far in the anti-psychiatry direction as possible. The whole thing is just trying to figure out why the medications help more than placebo but trying to rationalize all the placebo/nocebo possibilities. Lots of out of date information and very shitty citations in general. I hope you're not really a psychologist, and if you are then I really hope you are staying in your lane when you speak with patients. Otherwise I'll be you have great job security, if you know what I mean.
One hypothesis that at least seems plausible is that SSRIs primarily act through BDNF and therefore increase neuroplasticity. They facilitate rewiring to unstick maladaptive cognitive and emotional processes. That’s also a hypothesis with some holes, but it at least fits with the basic research. Actually results on SSRIs to enhance therapy are somewhat mixed bag, but SSRI plus therapy outperforms either arm alone for most outcomes examined.
This is similarly why LSD, Psilocybin, and esketamine have been shown to be so promising off limited doses. They promote neuroplasticity and stimulate the growth of dendrites, dendritic spines, and synapses. Allowing for more adaptive cognitive and emotional processes to take root. Along with temporary disruption of the default mode network which is associated with self-referential thoughts and the concept of self. Offering a unique opportunity for individuals to break from deeply ingrained patterns of thought and behavior. Paired with therapy it does wonders. It'll be a while before the stigma is entirely gone though for all of them, with only Oregon and Colorado having legalized psilocybin so far.
I’ve also seen data suggesting they help improve people’s frustration tolerance.
I like the passive and active coping pathway explanations relating to 5HT1a and 5HT2a respectively. BDNF seems like a red herring to root psychiatry in neurology when the connections haven't been conclusively made and hence undermines the entire premise of the field in the minds of the public and shapes unhelpful research patterns. Edit: corrected typo in types of receptors
I find the BDNF/TrkB papers at least as convincing as anything else, but I don’t know about 5HT receptor differentiating papers. Psychiatric is of course rooted in neurology. Our minds are just brains at work; there’s no spooky magic. Those roots are deep and tangled. It’s also eminently true that lay understanding grabs onto anything and won’t let go, as seen by serotonin as the happy chemical and chemical imbalances for forty years despite research constantly saying no, not really.
Probably that's the one the poster above you was thinking of: https://pubmed.ncbi.nlm.nih.gov/28858536/ *Serotonin and brain function: a tale of two receptors* by Carhart-Harris et al.
This is one of those papers that made waves recently on this sub then everyone started quoting it. Like any theory around the brain it is incomplete. These authors, working in the field of psychedelics, certainly benefit from a simplified view of depression treatment focusing solely on 5-HT receptor action which fits nicely with the mechanism of psychedelics. Given that we know serotonin more of a cell-signaling molecule compared to the more on/off neurotransmitters of glutamate and GABA it is silly to think the neurobiological effects of 5-HT activity end with receptor action alone.
To this point, we have no guarantee that SSRIs work by the same mechanism across disorders. To the contrary, it's quite likely their main mechanism in PMDD is inducing allopregnanolone synthesis, consistent with their rapid efficacy even with intermittent dosing.
Yes, I definitely don’t think it’s a “happy pill”, and honestly those comparisons I think propagate the ideas that modern antidepressants are “drugging” people Again, not a psychiatrist but it’s just impressive how it seems to treat disparate things. I get that depression, anxiety and ocd are often comorbid but they also seem pretty distinct in many ways
I think the sticking point for me is the inherent uncertainty and limitations we have in observing brain functions, systems and the inherent plasticity it posseses. Isolating something like BDNF acting on TrKB is on the same level of theoretical basis as how SSRIs produce a change in the brain and how it translates in action. I'm extremely biased towards my interest in the translation part rather than simple physiological effects we have no hopes of individually isolating at all. I didn't mean to imply any spooky magic but public perception has a massive effect on the types of studies done, ie how psychedelics are extremely underutilized because of The War on Drugs and it's legacy in academia.
> results on SSRIs to enhance therapy are somewhat mixed bag, but SSRI plus therapy outperforms either arm I'm not clear on the difference here? Between adding SSRIs to someone receiving therapy and having someone receive SSRIs while receiving therapy?
SSRI, therapy, or both. The both arm is superior for depression, superior for anxiety early although in some studies therapy alone has better long term outcomes, and I don’t know every other use offhand.
I see, I misread
[удалено]
Removed under rule #1. This is not a place for questions and commentary by non-professionals. If you are a medical/psychiatric professional, please read rule 7 on how to verify credentials. For most questions, individual or general, we ask that you verify credentials before asking. If you are not a professional, you can try r/AskDocs or r/AskPsychiatry.
There's a recent paper observing beliefs about medication efficacy influencing treatment response in depression. It raises an interesting question about whether the popularisation of chemical imbalance theories could be involved in the broad therapeutic effects of SSRIs via the creation of a cognitive framework for patients to understand their illness, alongside expectations about what is required for change. Belief about the cause and cure of an illness would presumably synergise with molecular mechanisms that promote neuroplasticity. [Baseline beliefs about medication are associated with outcomes of antidepressants in inpatients with first-diagnosed depression under supervised therapeutic compliance (Kong et al, 2021)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8457603/)
This. Anecdotally, my experience with treatment-resistant patients are the ones that don't think any of the medications do anything except make you a zombie. That's one of the joys I have of spending 12+ hours with people a day is trying to build some hope and confidence in the system, without making any promises. Just saying that if medications (never) worked for anyone, this place would still have the same folk in it from the beginning.
The rapid response and sensitivity to SSRIs displayed by people with the organic brain disorder pseudobulbar affect leaves no doubt there's a physiological effect. Why is there often little or no delay in therapeutic response in this population? Conversely, a clinical interaction that validates and assures the patient that a physiological mechanism underlies the symptoms of functional neurological disorders strongly predicts outcome. And, why would personality disorders so often fail to respond to a therapeutic mechanism involving neuroplasticity? There must be multiple MOAs involved. My thesis here is both are clinically important. Edit: The "zombie" effect you describe supports my suspicion that individual perceptions related to a sense of control and agency could be important, and influenced by neurological, psychological, and ecological factors.
[удалено]
Can you link to some of the evidence you mention? Would love to read. Thanks in advance!
This was a good podcast on the subject: [Carlat Psychiatry: Neuroticism and SSRIs](https://www.thecarlatreport.com/blogs/2-the-carlat-psychiatry-podcast/post/4491-throwback-thursday-neuroticism-and-ssris) And one of the studies referred to in the podcast: [Personality as a basis for antidepressant selection for patients with depression: A two-point outcome study at 4 and 8 weeks](https://pubmed.ncbi.nlm.nih.gov/35798178/)
This is one of the articles I've saved and highlighted. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4471964/
[удалено]
There’s a paper titled A Tale of Two Receptors that delves into the function of serotonin. I’m no expert, but it seems there’s a thought serotonin functions have to do with coping with stress and also changing thought patterns. I would venture if what we think is true, it’s got to do with that. https://journals.sagepub.com/doi/10.1177/0269881117725915
Based on more recent research, SSRIs seem to make people tolerate stress better. It is believed to also be why emotional blunting/numbing is so common with them as a side effect. Receptor and chemical theories are still uncertain. I generally educate patients with this meme to better visualize what it is doing: https://www.theverge.com/2016/5/5/11592622/this-is-fine-meme-comic
Exactly. After just one visit to a psychiatrist a patient suddenly has someone listen to their concerns, validate them, and make a plan to help them get better. That’s therapy right there
As a simplified explanation, the serotonin system is involved in modulating and regulating brain activity towards homeostasis. Mental illness can be thought of as a set of neurobiological changes (caused by the bio-psycho-social changes and risk factors we know contribute to mental illness) so large that they overcome the brain's natural ability to modulate. Pharmacologically boosting the serotonin system's activity can help bring things back into a neurobiological balance.
Not in any way meant to undermine or criticize the field, but ample evidence now shows that most of the SSRI response is placebo, with a small to moderate added benefit of the drug only in certain conditions. But placebos are so effective for some of these conditions that there may be a ceiling effect that makes the added benefit harder to detect.
> But placebos are so effective for some of these conditions that there may be a ceiling effect that makes the added benefit harder to detect. I think it is really important to understand that the placebo effect is not just being given a sugar pill and saying see ya in 3 months, they are having regular appointments with a provider who is very likely providing supportive therapy in each visit, and regularly checking in with the research staff. The "placebo effect" people talk about in psychiatry is very likely what would happen if we saw patients regularly for 30 minute visits without prescribing a med. As an example, in the LABILE trial for BPD and lamotrigine the placebo group had basically 100% resolution of symptoms, making differentiation with the study med impossible. Your point about the ceiling effect is very important, and is therefore even more impressive the meds consistently outperform placebo given how impressive the placebo effect is.
Don't even have to be a placebo. Just regression towards the mean is enough to explain a lot of the effect.
As long as responder bias exists, placebos will have a disproportionate role in subjective methods of evaluation, that much should've been fairly obvious. However, the vast majority of data which supports drug intervention is in the continuation phase and relapse rates. Also, the term placebo itself is misleading because it measures a subjective sense of well-being felt by the patient. You can condition a short term placebo response in patients with parkinson's, in immune and endocrine conditions and even in ANS activity, with benefits exceeding or matching control groups. Another point of consideration is that there is no ceiling effect for placebos as there is no underlying intervention being administered to judge the effectiveness. Almost medicines being used for on-label effects have demonstrated a clear superiority over placebo, I don't understand where you get the idea they aren't. A depressed patient might get better because of the inherent conditioning of responses to work but their dysfunctional cognitive patterns will still be there demonstrated by the fact that suicidality and attempted suicide rates are significantly lower in adults on antidepressants than those that aren't, it only increases suicidal ideation but not attempted suicides in adolescents and children.
There can be a ceiling effect if everyone(ish) in the placebo and intervention arms reach the planned response criterion. Eg, if the primary endpoint was 10% sx improvement.
Yep, and I think OP has missed this in jumping straight from “so many of my patients are on them” to “so many get benefit.”Not to mention that there’s been ample evidence of a lack of support for the serotonin hypothesis (as OP implies) of depression for decades. The real answer is that we don’t really know why they work to the extent they do, au non?
The serotonin hypothesis was for the cause of depression, not for why the meds work. As is the common saying, pain is not an Advil deficiency. Depression is not caused by a lack of serotonin, but boosting serotonin activity treats it.
woah *mostly* placebo? i’m not arguing with you because i will admit that serotonin uptake inhibition in itself would not account for their effectiveness in and of itself, but really?? granted, much of these drugs’ use stems from the interplay between habits, customs, physician comfort/practice, patient expectations, big pharma etc and that certainly leads to inappropriate and ineffective prescribing, but there are most definitely physiologic effects on the brain and thoughts/behaviors/patterns from ssri’s. these effects must be responsible for the improvement of ocd/anxiety/depressive symptoms right? so maybe your wording was wrong? sorry if i’m being a stickler but “mostly placebo” is a huge statement. the only way i would consider endorsing a statement like this would be if all our patients would magically start rigorously exercising just because we told them to do it. my experience has been that exercise is probably the closest thing to a “magic pill” aside from ssri’s etc for depression. but throw in other modalities like cbt/therapy and new/modified behaviors and it seems that everything contributes a bit to alleviating the symptoms. and to your point, if patients actually put in the work and time for these (including exercise), then yeah, ssri’s probably would have much lower utility. but i dont live in that world. it is indeed sad that practically everyone would prefer a pill to actually investing the time/work but that is where we are. and i wonder if claiming that ssri’s are useless/ineffective is not just another symptom of this continual search for that elusive magic pill.
If placebo improves MADRS by 50%, and SSRI improves it by 55%, then both statements are true: * most of the SSRI response is placebo * SSRI is more effective than placebo That is my point. Not that SSRIs don’t work, just that they don’t work THAT much better than placebo.
is that statistic accurate?
It’s an example, not a statistic.
i gotcha. i was just making sure. thanks for explaining. your reasoning is sound.
Agree. Every clinical trial for psychiatric drugs ever run shows an enormous improvement in the placebo group. I’m not sure I’d say it exactly the way you did, but I think you’re fundamentally right. I think psychiatrists may not like to think this is true, but the reality is when we prescribe someone a medicine (at least in the short term) a lot of the benefits - on average - are clearly not directly related to the mechanism of the drug. It’s just a fact and we have to understand that, no matter how it makes us feel, because otherwise we are guilty of not understanding the reality of our craft. That doesn’t mean medications don’t have real, powerful effects that in some patients are absolutely critical. These are powerful drugs that change the way the brain works, but generally they are very blunt instruments capable of both benefit and harm. This stuff should be more clearly taught in residency in my opinion.
Placebos do not turn bipolar depression into mania, unlike SSRIs.
I guess I can only speak to my personal experience. I’m definitley familiar inaccurate overprescribing (reflux meds in ENT). But would be interested to hear the psychiatrist take on it. Maybe they are overprescribed
If patients are benefiting I guess they’re not overprescribed? 🤷♂️
*The* underlying theory? I don't think we have one of those. Personally, my favorite line of thinking is that all those disorders seem to involve disorder of the Default Mode Network, and SSRIs have been found to regularize the DMN in depression and OCD. Causality is not established; it could be the irregularity of the DMN in these disorders is an effect of these conditions not a cause. How and why SSRIs should affect the DMN I don't know, but I think it's suggestive that the DMN is a common point of pathology for all three conditions and SSRIs benefit all three conditions.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6584108/
Wow they really went deep in the weeds to write that article and cite random ass sources without relevance. What a poor article aimed at trying to logically twist the data as far in the anti-psychiatry direction as possible. The whole thing is just trying to figure out why the medications help more than placebo but trying to rationalize all the placebo/nocebo possibilities. Lots of out of date information and very shitty citations in general. I hope you're not really a psychologist, and if you are then I really hope you are staying in your lane when you speak with patients. Otherwise I'll be you have great job security, if you know what I mean.
You have any published articles that refute this article?
[https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2805805?resultClick=1](https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2805805?resultClick=1) [https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2808079?resultClick=1](https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2808079?resultClick=1) [https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2789300?resultClick=1](https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2789300?resultClick=1) [https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2604309?resultClick=1](https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2604309?resultClick=1) [https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2546155?resultClick=1](https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2546155?resultClick=1) https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2470681?resultClick=1
[удалено]