> SSRIs have an NNT around 7, depending on the study you look at [...] Which sounds terrible if you know nothing about NNT. But when you learn that Tylenol has an NNT of almost 5 and even a powerful drug like Xanax has an NNT of 4, you realize that NNT is a difficult measure of drug efficacy
This kind of comparison is utterly meaningless (like saying a Cohen's d of 0.3 is large for phenomena X, so if we see 0.4 in phenomena Y, it is large in Y), and is just one part of why NNT as usually reported is basically deceptive for antidepressants.
What qualifies as an effective "treatment" has to be anchored to a minimal important difference, and this is what antidepressants really don't clearly have, on average. I.e. saying the NNT of SSRIs is around 7 is not really practically interpretable, because they tend not to base NNTs here on the amount of patients that actually experienced a clinically meaningful change, they just count the number that exceed some arbitrary (usually purely statistical) threshold.
If you reformulate NNT competently to count number of people needed to be treated to ensure one has (on expectation) a minimally important difference in the depression scales, then the NNT gets even larger than is typically reported.
This is why the denialism about differences in visual experience are so indefensible: they basically require an assumption that the whole world is out to lie and deceive.
Like, so, people just say things like "I see it in my mind's eye", and insist it is not a metaphor... why, exactly? If the typical mind fallacy assumption of denialists was correct, then no one would have any incentive to use such metaphors, because they would feel false. So clearly minds do in fact differ.
To state otherwise is a kind of narcissism / solipsism, or at least there is something monstrous about this kind of denial. "Everyone else is clearly wrong about their experience and their descriptions of it. I know better".
In fact, the term typical mind fallacy was born from aphantasia [1]:
> Galton gave people some very detailed surveys, and found that some people did have mental imagery and others didn't. [...] Though another psychologist, Dr. Berman, did, at that time, come up with a name for the masking behavior, called the Typical Mind Fallacy: the human tendency to believe that one's own mental structure can be generalized to apply to everyone else's.
Yup, sadly the absolute denialists saying "it is just semantic confusion" don't really have a tenable position, as a quick read through this whole thread would instantly reveal.
Yeah, this is a valid critique of the whole internal monologue idea, but interestingly aphantasia has been quite empirically confirmed and the simple apple test has been validated!
The self-report objection has been tested, though. Aphantasics show no imagery priming in binocular rivalry, no pupil constriction when asked to imagine bright shapes, and flat skin conductance to frightening text while responding normally to frightening pictures. A questionnaire that predicts autonomic responses nobody can fake is doing more than semantics.
I don't consider self-reported nonsense to be empirical confirmation. There can be correlations between different self-reports, that doesn't mean that our idea of why those correlations exist is correct.
There are plenty of examples multiple times in this thread that show that what is self-reported is demonstrated in non-self-reported phenomena, so those self-reports are clearly not nonsense, basically by definition.
The aphantasia theory is clear and parsimoniously makes sense of all this, but your "it's all just semantics" does not, and additionally requires rather other extreme acrobatics with regards to much of the entirety of human experience and discourse. Scholarly research also basically says this.
Your mind is clearly closed and you do not have any serious interest in understanding anything here.
There are measurable practical differences, besides differences in fMRI responses and pupil dilations as mentioned in the thread, there are also the ones I mention here (https://news.ycombinator.com/item?id=49471908) that involve different skin conductance responses, less response to image priming, less ability to produce image visual details from memory, and etc.
They just aren't obvious practical differences, because cognition or neural plasticity seems so flexible that we can compensate pretty impressively for surprisingly different sensory experiences, overall.
There are plenty of competent meditation approaches that don't really require visualization of any kind. Most Western "mindfulness" meditations don't require visualizations, nor does e.g. shi-ne / opening awareness, nor most forms of concentration meditations (e.g. transcendental where you focus on a sound like "ohm", meditations that have you focus on your breath, etc).
Best way to manage the withdrawal would be to dramatically reduce them being prescribed in the first place.
The linked article says they have "small to moderate effectiveness", but this is being far too generous. The correct way to measure drug effectiveness is if the treatment meets the standard of a minimal important difference. I.e. you measure depression on various rating scales, like the 17-point HAM-D, and research suggests a minimal important difference (i.e. one patients and clinicians can actually notice) needs to be about 3-5 points. But the average effects of almost all antidepressants do not meet these thresholds, i.e. the effect actually appears practically invisible. [1]
Then you'll get waffling like "oh, but it really has a big effect for some people", but, well, no, we've looked at that too, and the placebo groups get just as miraculous "big effects", i.e. evidence supporting the idea "they really help some people" is also largely lacking [2-3]. All the other attempted saves ("oh, but eventually you find one that works for you") are also not really well supported either [4].
Like, maybe they really help some people, but it is far, far less clear than most assume, and should be balanced with concerns like withdrawal and serious side effects like emotional blunting and sexual dysfunction.
EDIT: And just to be clear to anyone doing a drive-by downvote thinking this is about recent asinine US politics, it emphatically isn't. There are serious methodological concerns here that desperately need to be communicated to the public.
> 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.
> 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.
> 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.
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.
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.
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.
> 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.
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.
> 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
You have the better argument, and could just leave it at the last comment before this. (I'm not the boss of you, but I hate seeing the better argument taunted into writing like this.)
So did you take them and have a bad time? Because they definitely work for me and I doubt a placebo could have such a large effect on the 48 hour stomach pains I used to get alongside my frequent panic attacks.
I find it funny that people complain about emotional blunting when that is the entire purpose of the drug. I would prefer not to live on the razors edge ever again. I’ve had chronic anxiety and depression ever since I was a child, though.
For some people the emotional blunting is desirable, especially as you said, if the problem is chronic anxiety. But for many other people, their depression is defined by a lack of positive affect and anhedonia, meaning that emotional blunting is literally making things worse.
Depression is highly heterogenous, and I am glad the medication helped you.
SSRIs have much more clinical evidence of efficacy for addressing anxiety disorders vs a placebo than depression. The effect size is ~0.7 vs 0.2 in meta studies.
Totally agree, they really shouldn't be called antidepressants at all. Important to add tho that for many with depression they have comorbid anxiety and often the anxiety is harder to tolerate than depression, so removal of anxiety symptoms can be hugely beneficial.
Also, IME they are dosed completely wrong. So many people seem to be on very low doses, which has no improvement on placebo in the studies I've read.
Whereas, higher doses are _hugely_ better than placebo, especially for anxiety.
What's worse is a lot/most studies on SSRIs in general often don't adjust for dose. Which seems like an enormous oversight to me.
> I find it funny that people complain about emotional blunting when that is the entire purpose of the drug.
The ideal would be to blunt the negatives but not the positives. The effect of some of the older antidepressants can be to blunt both, across the board.
Some of the newer atypical antidepressants can address depression without making everything flat.
"As effective as placebo" does not mean worthless. As you point out, placebo antidepressants are fairly effective.
It's a terrible bind. Patients want a pill to fix things, but if they know it's just a sugar pill, it doesn't work. It has to have active ingredients that might work. That's why there's little desire to change the status quo on antidepressants much. Anyone who reads the medical literature knows they're statistically underwhelming, but the experienced reality is that they help people a lot.
Talking therapies, CBT, exercise are all good alternatives but they take time and effort that a depressed person might not be able to manage. An antidepressant prescription they can get in 15 minutes.
> As you point out, placebo antidepressants are fairly effective.
This is a misunderstanding of concepts like regression to the mean, and also the active placebo elements involved.
> but the experienced reality is that they help people a lot
And the evidence is that the reality people think they are experiencing is wrong, i.e, they are improving and factually experiencing improvement, but misattributing the cause to the drug.
> "As effective as placebo" does not mean worthless
In one sense of worthless, perhaps, but since drugs have larger costs relative to placebo, well, we can argue they are worse than worseless in another.
Better instead to talk about cost-benefit tradeoffs, number-needed-to-treat vs number-needed-to-harm and etc though, and try to get better at prescribing more carefully to those they clearly benefit.
It’s unethical to prescribe a patient a placebo in a way that suggests that what they are receiving is scientifically proven.
In a clinical trial setting, you can prescribe a placebo, because the patient is fully aware and clearly consenting to the fact that they may receive a placebo. Lying to a patient, in a clinical setting, from a position of authority, is a completely different matter. The informed consent would be completely absent, the patient’s ability to make informed choices about their own healthcare would be undermined and withheld, and the provider would be deriving financial benefit from the patient and / or through insurance claims for what amounts to a scam.
The patient, who would be seeking a treatment from a trusted expert, would believe that they are receiving proven treatments in exchange for their time, patience, money, reduced quality of life due to side effects, and opportunity costs in terms of not going to a different provider or trying something else, but in reality their provider would be misleading them. Some patients would even die as a result of taking a particular placebo and depending on it—either because of side effects or due to the lack of effectiveness—when they tragically would have been better off trying a different approach or medication. How could a patient possibly give informed consent in such a scenario, for one thing? How could they meaningfully compare treatment options and make their own informed choices when the advice they receive includes lies?
Alas, some providers believe in placebo effects so much more strongly than their patients’ right to autonomy that when faced with complaints of side effects, they will just lie more and more to their patients in hopes that the side effects will go away, but that’s really just more gaslighting to people who are already in difficult situations.
On an academic level, we have reined in much of the excess enthusiasm in antidepressants that was courtesy of 90s-era pharmaceutical reps and ad men, but I don't think this revision ever occurred in the cultural consciousness at large.
See also: The Serotonin Theory of Depression: a Systematic Umbrella Review of the Evidence (2022). It's worth reading the introduction and results in full, but here are two important quotes (footnote markers removed):
> Our comprehensive review of the major strands of research on
serotonin shows there is no convincing evidence that depression
is associated with, or caused by, lower serotonin concentrations or
activity. Most studies found no evidence of reduced serotonin
activity in people with depression compared to people without,
and methods to reduce serotonin availability using tryptophan
depletion do not consistently lower mood in volunteers. High
quality, well-powered genetic studies effectively exclude an
association between genotypes related to the serotonin system
and depression, including a proposed interaction with stress.
> The chemical imbalance theory of depression is still put forward
by professionals, and the serotonin theory, in particular, has
formed the basis of a considerable research effort over the last few
decades. The general public widely believes that depression
has been convincingly demonstrated to be the result of serotonin
or other chemical abnormalities, and this belief shapes
how people understand their moods, leading to a pessimistic
outlook on the outcome of depression and negative expectancies
about the possibility of self-regulation of mood. The idea
that depression is the result of a chemical imbalance also
influences decisions about whether to take or continue anti-depressant medication and may discourage people from dis-continuing treatment, potentially leading to lifelong dependence
on these drugs.
Personally, I both agree that SSRI antidepressants were likely overprescribed early on, and disagree with the notion that the chemical imbalance theory is unsupported. N = 1, they can absolutely work. It took a few to find one that really did, hence I am certain it is not a placebo effect.
The idea that simple serotonin deficiency is the whole entirety of all depressions is 100% discredited and completely incoherent in the face of current evidence, but yes, for sure it remains clear and plausible that some forms or aspects of depression involve a serotonin deficiency.
However, tianeptine is serotonin reuptake enhancer and also can help with depression, so any simple deficiency hypothesis also doesn't look good either.
Broadly, the "chemical imbalance" theory, left vague and unspecified, is still basically sane (though not specific enough to be super useful).
>1. Selective serotonin reuptake inhibitors versus placebo in patients with major depressive disorder. A systematic review with meta-analysis and Trial Sequential Analysis. Conclusions: SSRIs might have statistically significant effects on depressive symptoms, but *all trials were at high risk of bias and the clinical significance seems questionable*. SSRIs significantly increase the risk of both serious and non-serious adverse events. The potential small beneficial effects seem to be outweighed by harmful effects.
>2. The trouble with antidepressants: why the evidence overplays benefits
and underplays risks. Widespread prescribing has not reduced mental disability or suicide, raising questions about the assessment of evidence on effectiveness and safety of antidepressants
>3. In search of a dose–response relationship in SSRIs—a systematic review, meta-analysis, and network meta-analysis. Conclusions: There is no conclusive level I or level II evidence of a clinically meaningful dose–response relationship of SSRIs as a group or of single substances. High SSRI doses are not recommended as routine treatment.
>4 The serotonin theory of depression: a systematic umbrella review of the evidence "We did not identify *any* trials using ‘active placebo’ or ‘no intervention’ as control interventions. "
The "chemical imbalance" theory is objectively wrong, but still useful in that it conveys the fact that mental disorders have physical causes. It's a purposeful simplification.
Many people take SSRIs and other medications because they believe the serotonin imbalance theory to be the modern scientific consensus. A doctor would be fired and ostracized for using the four humours, but can prescribe life-altering medication after five minutes to correct chemical imbalance, a theory which has never had much support within the scientific community.
Indeed, a rebuttal [1] to that paper starts with:
> Moncrieff et al. report in a review of reviews that depression is not generally linked with serotonin deficiency. This is hardly news to neuropharmacologists, which Moncrieff et al. tacitly admits, as they justify their review by citing examples of laity and general practitioners believing depression is caused by a “chemical imbalance”, i.e., in serotonin. For instance, already in 1986 did Depue and Spoont point out that serotonin deficiency may not be a general cause of depression or other psychiatric illness. Further, that increasing extracellular serotonin—e.g., with selective serotonin reuptake inhibitors (SSRIs)—treats depression does not mean decreased serotonin causes depression.
I have a lot of trust in the science of medicine, but almost none in healthcare. It seems like the research is totally divorced from the medieval treatments I see doctors give all the time. "This is hardly news to neuropharmacologists" vs "laity and general practitioners believe ..." indeed.
Note that it's not uncommon for even more widely prescribed medication to have no firmly established mechanism of action. Acetaminophen/paracetamol is probably the best example.
Ultimately medication is prescribed based on evidence from clinical trials, whether or not the mechanism of action is fully understood. SSRIs work to help with depression in clinical trials when compared to placebo, so they get prescribed.
Because the 1 in 10 stat I find seems a bit low, at least in my circle, and those are the ones who are open about it.
And the people I know have been on them approximately a decade. What baffles me is that a fair number of them triggered their own depressive episodes, and likely did need therapy and something at the time - but have all long since move past those "moments".
Yup, I would agree. The meta-research / methodological research and awareness here is really quite impressive, even though its conclusions are a bit grim and not well-known.
A good book on this is Mind Fixers: Psychiatry's Troubled Search for the Biology of Mental Illness. Describing the history of how many of these classes of drugs came about is pretty eye opening, I would say the book is pretty nuanced in its conclusions.
My anecdotal experience going on and off Paxil is that it does work for me, and no matter how badly I want to live Rx-free, I consistently devolve into a moody mess without them.
What's your opinion of the claim that antidepressants have small impact on people with mild to moderate depression, but significantly more impact on people with severe depression [1]?
I ask as a nonexpert because this is a view I've read a few times from people I trust more than most, and I know two people who suffered from severe depression who credited SSRIs for getting them through.
Wait, I finally found a paper that properly presents the results in a way that lets you decide for yourself! See figure 2 here: https://pmc.ncbi.nlm.nih.gov/articles/PMC9344377/#f2, you want to focus on the second plot with the dotted and dashed lines.
Basically, both placebo and drugs can have huge responses, but basically, for severe depression, yes, it looks like the drug is more likely to have a large positive effect than the placebo is likely to have a large positive effect.
There are still a lot of limitations, main one being that study criteria generating the data for this would exclude most cases of really high severity actually seen in practice. Also "blinding" is mostly BS in these kinds of studies, and antidepressants have massive, noticeable effects, so the proper comparison is really an active placebo, and we really can't be sure the whole apparent antidepressant effect is basically just "woah, I can really feel this doing shit", basically, at some level, and this is still bad because the placebo vs. drug difference is still super tiny and below what we would consider typical minimal clinically important differences.
So still hard to say. But, yeah, there is a good chance the drugs are more effective in severe cases, and, technically, you should definitely treat in a severe case.
Honestly, every time I look into if the "treatment by severity effect" is clearly established, I feel I come away only able to shrug. It is at least plausible, but hasn't been clearly established or refuted.
What does seem clear to me is that the whole cost-benefit considerations change in favor of anti-depressants when the depression is severe. I wouldn't say anti-depressants should be first-line treatments for ordinary depression, but for severe depression, I think they are a very reasonable first-line option.
Sure, they still might not help, but the costs / harms don't seem so bad compared to the potential costs / harms of leaving the severe major depression untreated, and the other options look all pretty terrible here too.
I tend to feel the same way. The medication is obviously useful in some cases and for some conditions, but there's also a pushback against the notion that it isn't the best solution for other cases and conditions. There are cases where other solutions might be healthier, especially in the long term, but the availability of a potential pharmaceutical fix interferes.
And look at the new batch of weight-loss drugs. It's a similar circumstance. It's a wonder drug in many ways, helps so many people that wouldn't have been helped otherwise. Yet, also being used in some cases as a shortcut to avoid a behavioral change that would be advantageous for a person to do.
It is important to remember that there are people for whom these drugs are literal lifesavers. And at the same time, there are those for whom the drugs enable avoidance of fixing a root cause.
Agreed. They have to be significantly helping at least some, but we can't say who these people are for certain yet, or how many there really are.
And yes, in some cases, no other options are possible, so even if the evidence is pretty dismal for their effectiveness, they are still broadly safe enough to definitely be worth a try. They probably just shouldn't be the first-line approach.
I don’t get why people are so negative about drugs. They’re just a medical treatment, with pluses and minuses. If they help and they’re not too costly then what’s the big deal? Half the population is addicted to caffeine and nobody cares. A huge number of people need medical intervention for other things and we don’t get this quasi moralistic opposition to them.
Agreed. The problem is largely that the pluses of antidepressants have been quite significantly overstated, and the minuses have been understated, meaning the cost-benefit equation is unfortunately quite different than what the general public assumes.
We don't want to get rid of them, we just need to recalibrate prescribing, and also to properly assess cessation at intervals more frequently than we have been.
Yeah, I’m open to the idea that their effectiveness may have been overestimated and they’re overprescribed as a result. But this “I can’t believe we’ve normalized antidepressants” “there are better solutions than drugs” stuff is just moralizing.
I suppose it can be moralizing, and probably is in the parent comment.
For me I still feel the surprise because I've followed the evidence carefully for well over a decade, and the methodological problems and lack of evidence for meaningful effectiveness have always been clear. I.e. it is clear standardized effect sizes are meaningless, and you need to determine important differences, as this is just basic science, but only a tiny handful of papers ever bothered.
So it feels very much like "how can we have normalized something so incredibly scientifically shaky", i.e. for me the moralizing is not "drugs are bad, how are we normalizing drugs" it is "how can an entire medical field and society so recklessly adopt something so obviously weakly supported". I.e. my dismay is more about the weak epistemic standards of society than it is about drugs.
The downsides to these drugs are pretty well understood and not generally that bad, right? Can we really say it's "reckless" to attempt to treat people with something that's fairly safe and see if it helps them?
This is what really rubs me the wrong way and makes me call it moralizing. There's this implicit foundation of "drugs bad" that's basically straight out of D.A.R.E. You're supposed to avoid drugs, but we might make an exception if they treat a serious problem and there are no alternatives.
Once in a while I'll take Tylenol or ibuprofen for a headache. Do they actually help? Hell if I know. Is it "reckless" to do this when I don't know if it actually does anything? Absolutely not. Antidepressants aren't as safe as those are, but at least some of them seem like they're safe enough to say, let's give this a try and see how it goes.
> I’m not trying to discount mental health, I just think there are better solutions than drugs to fix your state of mind.
Find one that's as effective on the general population.
I mean, sure, perhaps lifestyle changes are better. Can you get a higher percentage to change them and improve people's lives than we currently can with drugs?
As a top performer in school, I definitely think (and still point out), that you can get fantastically high results in SAT/GRE without paying any test prep service. I and many of my peers did it. There are better solutions than paying those services. But how many who don't pay do as well as those who do? I can tell them how to study as much as I can, but the reality is that statistically, people who attend will do better than if they don't.
From a medical standpoint, telling people to change how they live and think has a fairly low success rate. The best options usually don't work on the masses.
There's hundreds of years of "depression isn't real and even if it was real the only treatment is to take a walk in the woods!!" and like a decade of "man, ssris are great, they really helped me".
Public responses have probably not finished overcorrecting.
But imo the issue with that might be that “just man up and go take a walk” may still be better advice than “hey kid with your underdeveloped brain… take this maybe psychoactive drug that absolutely changes your brain chemistry in ways we absolutely do not understand causing almost certain addiction with effectively zero supervision unless you self-report murderous and psychotic tendencies! Don’t mind that I’m making kickbacks on every subscription!!”
In terms of possible damage to self and others. And to long term society.
Almost certainly there is also a "latent" representation that isn't just based on sensory imagery (i.e. some kinds of logical relations).
But it is also not likely that an absence of sensory imagery is without impact, i.e. that only the latent representations matter. You can see this in studies where aphantasics can't be subconsciously primed by images as easily [1], have skin conductance responses to visual stimuli less to imagery compared to normal people [2], and miss more visual details when attempting to redraw complex images from memory [3]. I.e. the visualizations are likely important in some cases, with the latent (non-visual) representations alone being deficient in some very particular cases, at least.
This kind of comparison is utterly meaningless (like saying a Cohen's d of 0.3 is large for phenomena X, so if we see 0.4 in phenomena Y, it is large in Y), and is just one part of why NNT as usually reported is basically deceptive for antidepressants.
What qualifies as an effective "treatment" has to be anchored to a minimal important difference, and this is what antidepressants really don't clearly have, on average. I.e. saying the NNT of SSRIs is around 7 is not really practically interpretable, because they tend not to base NNTs here on the amount of patients that actually experienced a clinically meaningful change, they just count the number that exceed some arbitrary (usually purely statistical) threshold.
If you reformulate NNT competently to count number of people needed to be treated to ensure one has (on expectation) a minimally important difference in the depression scales, then the NNT gets even larger than is typically reported.
reply