Thank you for this, as a practicing Child and Adolescent psychiatrist it is a hugely underdiscussed and misunderstood territory and your article is informative and balanced. Three things come to mind, one is the paucity of data on SSRI related sexual side effect in adolescent populations (if we look at the range of sexual side effects in adults including loss of libido, anorgasmia etc it ranges from 58-73%), there is little to no meaningful data on the incidence of these sorts of side effects (which would have enormous implications for normal adolescent psychosexual development) in younger populations. Is this because we are afraid or uncomfortable to ask? I often wonder about this with my patients. Secondly, the discussion of SSRIs and suicidality- it is my understanding that only two drugs have real data to support any influence on incidence of suicide, lithium and clozapine. SSRIs do not and have not shown efficacy around reducing suicidality for either adults or adolescents, though by reducing anxiety load they may downstream reduce discomfort and therefore secondarily suicidality. Thirdly, with all medications there is a tension between the individual and the data. Meaning that while data may indicate a medication has limited efficacy on a study level, that same intervention may be profoundly influential on an individual level. This is what makes evidence based medicine ideology so complex in psychiatry. Personally, I tend to think of SSRIs in adolescents as possibly being able to soften symptom burden, which would allow the teen to engage in more meaningful lifestyle changes, tolerate therapeutic interventions more deeply, and overall be able to engage in non-medication interventions that would actually be making the bulk of the difference.
I’m grateful for your persistence with this issue, because it makes me very tired. These debates keep going around of circles because of the underlying assumption that there is one universal best treatment for depression (SSRIs, therapy, social reform, exercise, resilience) despite the fact that depression is an incredible heterogeneous condition and frequently co-occurs with a highly diverse range a other condition (treating some over with concurrent MDD and GAD is very different to treating MMD+PTSD, and very different again if there is substance use involved, or they are neurodiverse) Even though there is more acceptance and research into personalized medicine, we still get caught up in wanting generalized, universal solutions. Further complicating this (and this is the issue I don’t see discussed as much) is too often treatment decisions aren’t based on ‘best evidence based practice’, but on ‘best available treatment’. These debates keep wanting to frame that question as ‘what is the best treatment for depression’, when the reality for clinicians is ‘what is the best treatment for this person with these difficulties in this context, that is also acceptable AND available to the patient.’ Trying to find treatments that tick all of those boxes feels like an impossible task some days (especially if you want to write a snappy headline’, so I get the appeal of wanting blaming everything on something like screentime!
I think you do a fantastic job of highlighting the complexity and diversity in assessment and treatment - it’s the main reason I subscribe to your Substack.
Thanks for another thoughtful, balanced, and fair-minded analysis, Awais. I agree that we need to take Dr. Plöderl’s blog post seriously, and not reflexively deny or rationalize some of his worrisome conclusions. These are very complex areas of investigation, and a healthy dose of humility is called for—but I am going to comment anyway! Disclosure: my clinical practice was confined almost entirely to adults and a few older adolescents. I’m now retired from clinical practice and have no financial conflicts of interest. (Remuneration from sales of my psychopharmacology texts would cover the cost of a few large pizzas). In no particular order, my comments follow:
1. Suicide is a massively overdetermined human choice, and it is simplistic to identify a type of drug as the efficient or primary cause. (It is no small irony that drugs often dismissed as “expensive sugar pills” are also demonized as agents of self-annihilation).
2. The research on suicide and antidepressants is muddied by use of the nebulous term, “suicidality”, which can encompass anything from suicidal ideation to a self-inflicted scratch to a suicide attempt—or to completed suicide. Notably, there were no completed suicides in the original younger cohort studied by the FDA, in the meta-analysis of 24 placebo-controlled clinical trials involving over 4,400 children and adolescents—the study that led to the “black box warning.” [https://www.fda.gov/drugs/postmarket-drug-safety-information-patients-and-providers/suicidality-children-and-adolescents-being-treated-antidepressant-medications] Of course, any degree of self-harm or suicidal ideation is cause for deep concern, and should not be dismissed or rationalized away, as you rightly argue, Awais.
3. I agree with you and Dr. Plöderl, Awais, that the research literature does not make a strong case for the use of SSRI/SNRI antidepressants in children and adolescents. Certainly, the data suggest that non-medication approaches to depression in this population would usually be the treatment of first choice. However, I agree with the comment from our child and adolescent psychiatrist (“Poems from Your Mother”) that research studies summarizing aggregate data do not always reflect or predict how a particular patient will respond to an antidepressant. Some severely depressed adolescents may have a very good response to an antidepressant, and this may facilitate “talk therapy.”
4. I agree that SSRI/SNRI antidepressants across all age groups have not been shown to have significant suicide-preventive effects (lithium does!)—but neither have they convincingly been shown to increase completed suicide rates. At least we can say that in adult populations, there is no signal of increased completed suicides linked to antidepressant use. Indeed, my Tufts colleague, Dr. Nassir Ghaemi, concluded that antidepressants have a net “neutral” effect on suicide rates, at the population level. Specifically, Ghaemi, Vohringer and Whitham concluded found “…an equalization of harm and benefit such that antidepressants can be said to be, at the population level, neutral in their effects on suicide.” [https://onlinelibrary.wiley.com/doi/10.1111/acps.12059].
5. Nevertheless, I agree with Ghaemi et al that, “One reason why adolescents and young adults may be at special risk of suicidality with antidepressants could be misdiagnosed bipolar depression because antidepressants can cause mixed manic episodes, which are highly associated with suicidality.” [op cit]. Of course, there are many reasons why antidepressants can be helpful in restoring quality of life beyond their (probably neutral) effect on suicide rates. [Pies RW. Antidepressants, the Hamilton Depression Rating Scale Conundrum, and Quality of Life. J Clin Psychopharmacol. 2020 Jul/Aug;40(4):339-341].
6. The issue of antidepressants and suicide risk in children and adolescents remains a hotly contested matter among the experts, and in my view, the proverbial jury is still out. This is especially true with regard to the famous “black box warning” from the FDA. On the one hand, Plöderl, Spielmans and others interpret the data as showing that claims of a harmful effect of the black box warning are unjustified. i.e., when using intentional drug-poisoning as the appropriate outcome, “…There is no detectable change of trend in adolescent or young adult suicide rates in line with a detrimental effect of the FDA black box warnings on treatment-emergent suicidality.”
[See: Plöderl M, Hengartner MP. Crisis. 2023 Mar;44(2):128-134.]
7. On the other hand, Harvard researcher Dr. Stephen Soumerai and colleagues have written several rebuttals of the Ploderl/Spielmans position, and argue that “Multiple studies found significant unintended reductions in mental health care after the [FDA] warnings. After these reductions, there were marked increases in psychotropic drug poisonings and suicide deaths.” [Soumerai et al, Health Aff (Millwood). 2024 Oct;43(10):1360-1369] Dr. Ploderl disagrees for reasons discussed in his blog, including but not limited to the time-frame of the studies. For those who want to dig into the complex methodological “weeds” and numerous graphs, here are the relevant links to the Soumerai group’s work:
8. You note, Awais, that, “I have seen many teenagers and young adults (and at times other adults) who experience new suicidal thoughts or worsening of existing suicidal thoughts on starting a new antidepressant that rapidly goes away once the particular antidepressant is discontinued (and not infrequently, for mysterious reasons, it happens with some antidepressants but not with others)…” This last point is important. For example, in the Hetrick et al study (the Cochrane review cited approvingly by Dr. Ploderl), the authors concluded that, “…as a class, SSRIs and SNRIs may at least slightly increase the odds of suicide-related outcomes compared with placebo …” However, this did not seem to be the case with escitalopram; i.e., “Low certainty evidence suggests escitalopram [Lexapro] may at least slightly reduce the odds of suicide-related outcomes compared with placebo.” (italics added). [Hetrick SE, McKenzie JE, Bailey AP, Sharma V, Moller CI, Badcock PB, Cox GR, Merry SN, Meader N. New generation antidepressants for depression in children and adolescents: a network meta-analysis. Cochrane Database Syst Rev. 2021 May 24;5(5)]. It’s important to add that “…the trial populations were uncharacteristic of public child and adolescent mental health services in terms of the exclusion of those with comorbid disorders, and the exclusion of those at risk of suicide.”
Finally (and thank you, Awais and readers, for your patience!), I have always considered psychiatric medication to be a "bridge" between feeling terrible and feeling better. The afflicted patient must still walk across that bridge, and that means working toward self-understanding and self-mastery.
Thanks so much for this Awais. My personal problems with anxiety were not medicalised until my early 20s when I was only offered benzodiazepines or inpatient group therapy. I declined both and am pleased I did although depression arrived afterwards. My brother however, with severe childhood onset OCD might have beneftited from SSRIs but they were not available then. In clinical work with young adults I always aimed to get a person to CBT first. The Talking Therapies results are disappointing but, from working in those services, reflect real life outcomes not trials. We have so much more to do, but society has a massive role to play in this.
This seems about right. Blind Freddy can see that some people respond poorly to SSRIs. How many? who knows? But it certainly happens.
It's an odd sort of bias to me, the idea that people "need" an antidepressant and if they don't get one they might commit suicide. I get it on some relativistic level, but it's a cock-eyed logic that implies something like an antidepressant diffency. It's not case-wise thinking. If I was going to think in generalisable terms, I would suggest that, generally, all things being equal you should be slow to prescribe unless you can achieve a clear cut clinical improvement. The scale needs to tip quite a bit for age. Teenagers have a lot more to lose and and a far greater capacity for spontaneous recovery. Also if suicide is an actual possibility, then I wouldn't be looking to SSRIs as a solution.
I really like psychopharmacology but I cannot fathom why some people can't see what a drug is doing. Years ago I started lurking around recreational drug chat rooms, not because I'm into it but because I was so starved of consensus opinions on drug effects. The scientific state of psychopharmacology was gaslighting me so hard it was causing existential dread, so went to read experiences just to soothe the cognitive dissonance. What I found was that recreational drug users have no difficulty coming to a group consensus on the general effects of a drug. This is not to say that there is no individual variation or that some subtle effects don't escape their notice. Rather, it simply means that the drugs had noticeable effects that could be recognised without great difficulty. You don't need a telescope to see the end of your nose.
I feel actually think it’s a pretty odd comparison. Recreational and therapeutic drugs are used in really different ways. Of course a group of people taking shrooms or weed are going to have some shared experiences since they’re all doing it in a similar setting and kind of reinforcing what each other feels. That can turn into its own kind of gaslighting too
Odd to compare recreational drugs with therapeutic drugs? That qualifies as an odd comparison. Certainly there are differences, but I think people are intelligent enough to understand that without me labouring over it.
I also don't think I need to tediously point out the effects of expectations, priming, conditioning etc. If you seriously believe the effects of recreational drugs are caused largely by those factors, I'm surprised, but I don't think you do think that.
I wonder if the differences are as great as you seem to think they are.
You quote Strawn repeatedly, including his 2015 meta-analysis. Yet in that paper "Dr. Strawn has received research support from Eli Lilly, Shire, Forest, Lundbeck " Of course he will find in favor of the pills, he needs to satisfy his paymasters at these multi-billion dollar companies. Why do you not factor in these major fCOI when you write about psychiatry? Ploderl is not paid by drug companies, yet Strawn is. Who is more credible to discuss these pills and their efficacy and harm?
My own view is that fCOIs alert us to potential bias but they are poor justifications on their own to dismiss/disbelieve research results or other arguments. If there is something wrong with the data or the argument, we should be able to say what it is, but merely bringing up fCOI is inadequate. fCOIs are very common in the medical research world; anybody who’s a somebody is likely to work with industry in some form. So fCOI can even be seen as an index of a certain sort of expertise. And just because someone lacks fCOI doesn’t mean that they are not subject to stronger ideological biases. As my discussion should make clear, I don’t blindly accept anything anyone is saying.
The most robust finding in modern psychiatry and medicine is that fCOI strongly skew the results of the study. The range is from 5 to 22 times more likely to find in favor of the drug, if the author is paid by drug companies. With this kind of data, data mind you, not defensive justification of one's field, anything produced by someone with fCOI is guaranteed to be distorted and skewed. Here are plenty of studies to prove this point.
There is very clear 'Bias in the reporting of harms in clinical trials of second-generation antidepressants for depression and anxiety: A meta-analysis' https://pubmed.ncbi.nlm.nih.gov/27659240/
Awareness of such problems is what has led to the implementation of things like pre-registration of clinical trials, protocols for systematic reviews, inclusion of unpublished trials, etc. Sure, authors with fCOI may still skew interpretation of results in some manner but it is fallacious IMO to dismiss the results of a study or meta-analysis without even engaging with it simply because the authors have industry relationships. We cannot rely on a stereotype to do the epistemic work for us.
Haydn said that one should despite the sonatas of Archdukes - you never know who wrote them. Part of the process of assessing a source of information is to note who wrote it. Whose agenda does it serve, and how transparent is it? Are we looking at a patently paid-for Pharma puff, or a well designed study funded by industry? Are we looking at authors who consciously seek to signal their virtue? Are we looking at medical-psychological needle matches? Bias is everywhere. That isn’t really the problem - it’s acknowledging and trying to identify its existence without throwing the baby out with the bath water.
One other point - and the clue is in the name - antidepressants are for depression, not for feeling fed up or unhappy. And in depression, antidepressants don’t necessarily ‘cure’ the problem, but they can be hugely effective in reducing the symptomatic burden so that the person can marshal their own psychological resources, engage in therapy, do more, etc. Depression is too complex for a one size fits all approach. Also, when I was a trainee - decades ago - we used to smile at the Child & Adolescent Psychiatrists, who never seemed to make a diagnosis, but used a narrative approach to avoid labelling. For children and adolescents, they were dead right, and the bar for any medication in all groups, especially that one, should be high. I think.
Thank you for this, as a practicing Child and Adolescent psychiatrist it is a hugely underdiscussed and misunderstood territory and your article is informative and balanced. Three things come to mind, one is the paucity of data on SSRI related sexual side effect in adolescent populations (if we look at the range of sexual side effects in adults including loss of libido, anorgasmia etc it ranges from 58-73%), there is little to no meaningful data on the incidence of these sorts of side effects (which would have enormous implications for normal adolescent psychosexual development) in younger populations. Is this because we are afraid or uncomfortable to ask? I often wonder about this with my patients. Secondly, the discussion of SSRIs and suicidality- it is my understanding that only two drugs have real data to support any influence on incidence of suicide, lithium and clozapine. SSRIs do not and have not shown efficacy around reducing suicidality for either adults or adolescents, though by reducing anxiety load they may downstream reduce discomfort and therefore secondarily suicidality. Thirdly, with all medications there is a tension between the individual and the data. Meaning that while data may indicate a medication has limited efficacy on a study level, that same intervention may be profoundly influential on an individual level. This is what makes evidence based medicine ideology so complex in psychiatry. Personally, I tend to think of SSRIs in adolescents as possibly being able to soften symptom burden, which would allow the teen to engage in more meaningful lifestyle changes, tolerate therapeutic interventions more deeply, and overall be able to engage in non-medication interventions that would actually be making the bulk of the difference.
I’m grateful for your persistence with this issue, because it makes me very tired. These debates keep going around of circles because of the underlying assumption that there is one universal best treatment for depression (SSRIs, therapy, social reform, exercise, resilience) despite the fact that depression is an incredible heterogeneous condition and frequently co-occurs with a highly diverse range a other condition (treating some over with concurrent MDD and GAD is very different to treating MMD+PTSD, and very different again if there is substance use involved, or they are neurodiverse) Even though there is more acceptance and research into personalized medicine, we still get caught up in wanting generalized, universal solutions. Further complicating this (and this is the issue I don’t see discussed as much) is too often treatment decisions aren’t based on ‘best evidence based practice’, but on ‘best available treatment’. These debates keep wanting to frame that question as ‘what is the best treatment for depression’, when the reality for clinicians is ‘what is the best treatment for this person with these difficulties in this context, that is also acceptable AND available to the patient.’ Trying to find treatments that tick all of those boxes feels like an impossible task some days (especially if you want to write a snappy headline’, so I get the appeal of wanting blaming everything on something like screentime!
You are quite right of course. This would be good for me to highlight in future discussions.
I think you do a fantastic job of highlighting the complexity and diversity in assessment and treatment - it’s the main reason I subscribe to your Substack.
Thanks for another thoughtful, balanced, and fair-minded analysis, Awais. I agree that we need to take Dr. Plöderl’s blog post seriously, and not reflexively deny or rationalize some of his worrisome conclusions. These are very complex areas of investigation, and a healthy dose of humility is called for—but I am going to comment anyway! Disclosure: my clinical practice was confined almost entirely to adults and a few older adolescents. I’m now retired from clinical practice and have no financial conflicts of interest. (Remuneration from sales of my psychopharmacology texts would cover the cost of a few large pizzas). In no particular order, my comments follow:
1. Suicide is a massively overdetermined human choice, and it is simplistic to identify a type of drug as the efficient or primary cause. (It is no small irony that drugs often dismissed as “expensive sugar pills” are also demonized as agents of self-annihilation).
2. The research on suicide and antidepressants is muddied by use of the nebulous term, “suicidality”, which can encompass anything from suicidal ideation to a self-inflicted scratch to a suicide attempt—or to completed suicide. Notably, there were no completed suicides in the original younger cohort studied by the FDA, in the meta-analysis of 24 placebo-controlled clinical trials involving over 4,400 children and adolescents—the study that led to the “black box warning.” [https://www.fda.gov/drugs/postmarket-drug-safety-information-patients-and-providers/suicidality-children-and-adolescents-being-treated-antidepressant-medications] Of course, any degree of self-harm or suicidal ideation is cause for deep concern, and should not be dismissed or rationalized away, as you rightly argue, Awais.
3. I agree with you and Dr. Plöderl, Awais, that the research literature does not make a strong case for the use of SSRI/SNRI antidepressants in children and adolescents. Certainly, the data suggest that non-medication approaches to depression in this population would usually be the treatment of first choice. However, I agree with the comment from our child and adolescent psychiatrist (“Poems from Your Mother”) that research studies summarizing aggregate data do not always reflect or predict how a particular patient will respond to an antidepressant. Some severely depressed adolescents may have a very good response to an antidepressant, and this may facilitate “talk therapy.”
4. I agree that SSRI/SNRI antidepressants across all age groups have not been shown to have significant suicide-preventive effects (lithium does!)—but neither have they convincingly been shown to increase completed suicide rates. At least we can say that in adult populations, there is no signal of increased completed suicides linked to antidepressant use. Indeed, my Tufts colleague, Dr. Nassir Ghaemi, concluded that antidepressants have a net “neutral” effect on suicide rates, at the population level. Specifically, Ghaemi, Vohringer and Whitham concluded found “…an equalization of harm and benefit such that antidepressants can be said to be, at the population level, neutral in their effects on suicide.” [https://onlinelibrary.wiley.com/doi/10.1111/acps.12059].
5. Nevertheless, I agree with Ghaemi et al that, “One reason why adolescents and young adults may be at special risk of suicidality with antidepressants could be misdiagnosed bipolar depression because antidepressants can cause mixed manic episodes, which are highly associated with suicidality.” [op cit]. Of course, there are many reasons why antidepressants can be helpful in restoring quality of life beyond their (probably neutral) effect on suicide rates. [Pies RW. Antidepressants, the Hamilton Depression Rating Scale Conundrum, and Quality of Life. J Clin Psychopharmacol. 2020 Jul/Aug;40(4):339-341].
6. The issue of antidepressants and suicide risk in children and adolescents remains a hotly contested matter among the experts, and in my view, the proverbial jury is still out. This is especially true with regard to the famous “black box warning” from the FDA. On the one hand, Plöderl, Spielmans and others interpret the data as showing that claims of a harmful effect of the black box warning are unjustified. i.e., when using intentional drug-poisoning as the appropriate outcome, “…There is no detectable change of trend in adolescent or young adult suicide rates in line with a detrimental effect of the FDA black box warnings on treatment-emergent suicidality.”
[See: Plöderl M, Hengartner MP. Crisis. 2023 Mar;44(2):128-134.]
7. On the other hand, Harvard researcher Dr. Stephen Soumerai and colleagues have written several rebuttals of the Ploderl/Spielmans position, and argue that “Multiple studies found significant unintended reductions in mental health care after the [FDA] warnings. After these reductions, there were marked increases in psychotropic drug poisonings and suicide deaths.” [Soumerai et al, Health Aff (Millwood). 2024 Oct;43(10):1360-1369] Dr. Ploderl disagrees for reasons discussed in his blog, including but not limited to the time-frame of the studies. For those who want to dig into the complex methodological “weeds” and numerous graphs, here are the relevant links to the Soumerai group’s work:
https://psychiatryonline.org/doi/10.1176/appi.prcp.20200012
https://theconversation.com/after-the-fda-issued-warnings-about-antidepressants-youth-suicides-rose-and-mental-health-care-dropped-171008
https://pubmed.ncbi.nlm.nih.gov/39374452/
8. You note, Awais, that, “I have seen many teenagers and young adults (and at times other adults) who experience new suicidal thoughts or worsening of existing suicidal thoughts on starting a new antidepressant that rapidly goes away once the particular antidepressant is discontinued (and not infrequently, for mysterious reasons, it happens with some antidepressants but not with others)…” This last point is important. For example, in the Hetrick et al study (the Cochrane review cited approvingly by Dr. Ploderl), the authors concluded that, “…as a class, SSRIs and SNRIs may at least slightly increase the odds of suicide-related outcomes compared with placebo …” However, this did not seem to be the case with escitalopram; i.e., “Low certainty evidence suggests escitalopram [Lexapro] may at least slightly reduce the odds of suicide-related outcomes compared with placebo.” (italics added). [Hetrick SE, McKenzie JE, Bailey AP, Sharma V, Moller CI, Badcock PB, Cox GR, Merry SN, Meader N. New generation antidepressants for depression in children and adolescents: a network meta-analysis. Cochrane Database Syst Rev. 2021 May 24;5(5)]. It’s important to add that “…the trial populations were uncharacteristic of public child and adolescent mental health services in terms of the exclusion of those with comorbid disorders, and the exclusion of those at risk of suicide.”
Finally (and thank you, Awais and readers, for your patience!), I have always considered psychiatric medication to be a "bridge" between feeling terrible and feeling better. The afflicted patient must still walk across that bridge, and that means working toward self-understanding and self-mastery.
Best regards,
Ron
Ronald W. Pies MD
Professor Emeritus of Psychiatry
Thanks so much for this Awais. My personal problems with anxiety were not medicalised until my early 20s when I was only offered benzodiazepines or inpatient group therapy. I declined both and am pleased I did although depression arrived afterwards. My brother however, with severe childhood onset OCD might have beneftited from SSRIs but they were not available then. In clinical work with young adults I always aimed to get a person to CBT first. The Talking Therapies results are disappointing but, from working in those services, reflect real life outcomes not trials. We have so much more to do, but society has a massive role to play in this.
This seems about right. Blind Freddy can see that some people respond poorly to SSRIs. How many? who knows? But it certainly happens.
It's an odd sort of bias to me, the idea that people "need" an antidepressant and if they don't get one they might commit suicide. I get it on some relativistic level, but it's a cock-eyed logic that implies something like an antidepressant diffency. It's not case-wise thinking. If I was going to think in generalisable terms, I would suggest that, generally, all things being equal you should be slow to prescribe unless you can achieve a clear cut clinical improvement. The scale needs to tip quite a bit for age. Teenagers have a lot more to lose and and a far greater capacity for spontaneous recovery. Also if suicide is an actual possibility, then I wouldn't be looking to SSRIs as a solution.
I really like psychopharmacology but I cannot fathom why some people can't see what a drug is doing. Years ago I started lurking around recreational drug chat rooms, not because I'm into it but because I was so starved of consensus opinions on drug effects. The scientific state of psychopharmacology was gaslighting me so hard it was causing existential dread, so went to read experiences just to soothe the cognitive dissonance. What I found was that recreational drug users have no difficulty coming to a group consensus on the general effects of a drug. This is not to say that there is no individual variation or that some subtle effects don't escape their notice. Rather, it simply means that the drugs had noticeable effects that could be recognised without great difficulty. You don't need a telescope to see the end of your nose.
I feel actually think it’s a pretty odd comparison. Recreational and therapeutic drugs are used in really different ways. Of course a group of people taking shrooms or weed are going to have some shared experiences since they’re all doing it in a similar setting and kind of reinforcing what each other feels. That can turn into its own kind of gaslighting too
Odd to compare recreational drugs with therapeutic drugs? That qualifies as an odd comparison. Certainly there are differences, but I think people are intelligent enough to understand that without me labouring over it.
I also don't think I need to tediously point out the effects of expectations, priming, conditioning etc. If you seriously believe the effects of recreational drugs are caused largely by those factors, I'm surprised, but I don't think you do think that.
I wonder if the differences are as great as you seem to think they are.
You quote Strawn repeatedly, including his 2015 meta-analysis. Yet in that paper "Dr. Strawn has received research support from Eli Lilly, Shire, Forest, Lundbeck " Of course he will find in favor of the pills, he needs to satisfy his paymasters at these multi-billion dollar companies. Why do you not factor in these major fCOI when you write about psychiatry? Ploderl is not paid by drug companies, yet Strawn is. Who is more credible to discuss these pills and their efficacy and harm?
My own view is that fCOIs alert us to potential bias but they are poor justifications on their own to dismiss/disbelieve research results or other arguments. If there is something wrong with the data or the argument, we should be able to say what it is, but merely bringing up fCOI is inadequate. fCOIs are very common in the medical research world; anybody who’s a somebody is likely to work with industry in some form. So fCOI can even be seen as an index of a certain sort of expertise. And just because someone lacks fCOI doesn’t mean that they are not subject to stronger ideological biases. As my discussion should make clear, I don’t blindly accept anything anyone is saying.
The most robust finding in modern psychiatry and medicine is that fCOI strongly skew the results of the study. The range is from 5 to 22 times more likely to find in favor of the drug, if the author is paid by drug companies. With this kind of data, data mind you, not defensive justification of one's field, anything produced by someone with fCOI is guaranteed to be distorted and skewed. Here are plenty of studies to prove this point.
Industry sponsorship and financial conflict of interest in the reporting of clinical trials in psychiatry https://pubmed.ncbi.nlm.nih.gov/16199844/
Meta-analyses with industry involvement are massively published and report no caveats for antidepressants https://pubmed.ncbi.nlm.nih.gov/26399904/
There is very clear 'Bias in the reporting of harms in clinical trials of second-generation antidepressants for depression and anxiety: A meta-analysis' https://pubmed.ncbi.nlm.nih.gov/27659240/
Unpublished trials of alprazolam XR and their influence on its apparent efficacy for panic disorder. https://pubmed.ncbi.nlm.nih.gov/27659240/
Awareness of such problems is what has led to the implementation of things like pre-registration of clinical trials, protocols for systematic reviews, inclusion of unpublished trials, etc. Sure, authors with fCOI may still skew interpretation of results in some manner but it is fallacious IMO to dismiss the results of a study or meta-analysis without even engaging with it simply because the authors have industry relationships. We cannot rely on a stereotype to do the epistemic work for us.
Haydn said that one should despite the sonatas of Archdukes - you never know who wrote them. Part of the process of assessing a source of information is to note who wrote it. Whose agenda does it serve, and how transparent is it? Are we looking at a patently paid-for Pharma puff, or a well designed study funded by industry? Are we looking at authors who consciously seek to signal their virtue? Are we looking at medical-psychological needle matches? Bias is everywhere. That isn’t really the problem - it’s acknowledging and trying to identify its existence without throwing the baby out with the bath water.
One other point - and the clue is in the name - antidepressants are for depression, not for feeling fed up or unhappy. And in depression, antidepressants don’t necessarily ‘cure’ the problem, but they can be hugely effective in reducing the symptomatic burden so that the person can marshal their own psychological resources, engage in therapy, do more, etc. Depression is too complex for a one size fits all approach. Also, when I was a trainee - decades ago - we used to smile at the Child & Adolescent Psychiatrists, who never seemed to make a diagnosis, but used a narrative approach to avoid labelling. For children and adolescents, they were dead right, and the bar for any medication in all groups, especially that one, should be high. I think.