D-Machine

> "Nine times" literally means multiplied by nine

Rather, "nine times larger" means multiplied by nine, and "nine times smaller" means divided by nine. This is basic and not particularly awkward, certainly not more so than e.g. positive/negative correlation, or many much more awkward and more common linguistic constructions, IMO.

If you have to edit out words (i.e. context) to argue a phrase doesn't make sense... I am not sure what mental model you have for natural language, exactly, but it certainly isn't a very robust one.

It is a good question because aphantasics that can dream normally are far less likely to engage in the sort of "aphantasia is just semantics" denalism that is largely disproven given modern science and online discourse. I.e. it is a very strong credibility signal that what follows is not just cope / self-delusion, but actually potentially useful and interesting self-report.

The distinction between imagination and seeing is regularly blurred, most commonly in dreams, but also on psychedelics or quasi-psychedelics (e.g. cannabis), and also in altered spiritual states (meditative practices).

The two experiences are different, most of the time, yes, but only "completely 100% different" IMO to aphantasics, or those who are high in aphantasia. I.e. hyperphantasia is a thing, and a normal thing for most people in altered states (and schizophrenia might be seen as involving an extreme form of hyperphantasia intruding where it shouldn't, in some cases).

This is partly why only aphantasics argue for the "it is only semantics" explanation. For anyone else, this explanation makes no sense, because they have at least one vivid example showing otherwise. Only if you have no vivid visual experiences does this argument have any appeal.

Also the well-documented cases of acquired aphantasia are especially troubling for the skeptical "semantic disagreement" cases, given that acquired aphantasia is entirely within-person.

Anyone who doesn't believe this is real needs to explain the well-documented cases of acquired aphantasia. Good luck with that.

Your theory is fairly conclusively disproven, most damningly by acquired aphantasia.

See also my post below: https://news.ycombinator.com/item?id=49707079

There is some truth in this, but evidence sometimes suggests worse visuospatial memory, at least under some very specific operationalizations. E.g. less detail can be remembered overall, even though crucial details remembered are the same: https://pmc.ncbi.nlm.nih.gov/articles/PMC10598423/

More likely than not there are tradeoffs to using strictly visual vs. visual+ vs. strictly non-visual mental models in all domains, and there is no universally optimal strategy (and that teams of mixed cognitive styles are best overall). You know, no free lunch.

> Yes, I am well aware of the bias that only certain people post, as well as the distinct possibility that there are underlying correlations that could lead to our industry abounding in them. Though prior to this I would have thought quite the opposite given the association between visual processing and success in STEM and engineering.

I agree this is an annoying confound, and also that it feels highly intuitive that being able to consciously visualize ought to correlate with better visuospatial (and thus much mathematical) cognitive ability.

I think the solution is recognizing that the reason cognitive deficits are mostly unobserved (visual memory recall studies aside) is recognizing that aphantasia is almost certainly a conscious access problem, i.e. most aphantasics are still using imagery too, just unawares. Last I checked, this is the leading hypothesis / explanation.

Also, plasticity and the ingenuity of the brain is clearly such that an aphantasic can also find other ways (e.g. other sensory modality imagery, pure logical relations, etc) of representing the problems that seem like they should rely on visualization. It seems obvious to me that these other ways can be both advantageous/disadvantageous, depending on the situation / phenomenon.

> I've also wondered whether this entire conversation is just all of us collectively talking past each other for the entire conversation and we all in fact have quite similar experiences

This is fairly conclusively disproven by far more than just fMRI / brain-imaging studies. E.g. aphantasics have problem with visual memory recall, visual priming, pupil dilatory and skin conductance responses when imagining light and/or fearful stimuli, and many other results (especially acquired aphantasia) that don't depend on brain imaging and obviously rule out semantic explanations. Likewise, rejecting the reality of the phenomenon also seems to require believing an extraordinary amount of error and/or conspiracy on the part of highly educated and insightful people that explicitly are saying the issue is not one of semantics / description. This is also not to mention the rich history of visualization practices in much of the worlds religions and esoteric practices (which make basically zero sense if this is all metaphor). See e.g. the discussion in a previous HN thread (https://news.ycombinator.com/item?id=49464414).

> I invite you to feed your own friendly AI these references then ask it to analyze the recent papers [...]

Likewise, an unbiased AI prompt (or two prompts in separate sessions, with opposite biases) will clearly reveal the "semantics denialist" case has very little to stand on here. Yes, there are communication and linguistic issues, but these only cover a subset of ambiguous cases. Rejecting or denying the reality of aphantasia is an extremely strong indicator you are aphantasic, to some considerable degree.

You are wrong, as I didn't limit the analogy specifically to desktop computers only, try reading the rest of what I wrote. The original analogy was obviously hedging against simplistic brain-computer analogies (GP could be read as: "the brain is not a simplistic computer"), so the response demanding to "live with that" citing computational aspects of the brain was misguided and arrogantly wrong.

Multiple other responses also point out the definition given leads to absurdities / triviality (the liver is a computer in this context), so the "correction" with citations is both inept and inapt.

"The brain is not a computer" != "Parts / aspects of the brain do computation".

"A computer" in the first statement is IMO obviously intended in the common usage sense of the term, i.e. the brain is not a desktop computer or smartphone, or Turing machine, or etc, and thinking of it like these things will cause more error than insights. Also, billions of interlinked mini bio quantum computers arguably produce something with emergent properties and behaviour much, much more complex than "a computer". I am with GP, the analogy to "a computer" is not super helpful here unless you highly restrict the meaning.

But yeah, the Shereshevsky case is a super interesting one, thanks for linking!

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.

> 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

[1] https://pubmed.ncbi.nlm.nih.gov/33261932/

> 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.

I am telling you to ask a chatbot because you are saying things so hilariously philosophically incompetent and ignorant that even a retarded LLM will improve your thinking.

You obviously don't care about thinking coherently though, or can't even recognize what coherent thought looks like (mainly because you seem to think something along the lines of "my few minutes of armchair reflections prove all philosophy is vague and retarded"), so this is clearly a waste of time. I will not be engaging further.

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".

> there are obviously no testable hypotheses about subjective descriptions

Clearly false if you take just 30 seconds to scroll through this thread. Embarrassing.

Frankly, it is very hard to tell at times.

If you want to get really kooky, read up on Western Esotericism and Chaos Magic or tantric Buddhist practices and etc. They make basically this exact claim that this is how you "do magic" or similar such things, via sustained, "one-pointedness" and focus of attention and the Will ("gnosis"), and that, yes, often this one-pointedness of mind/attention is what lets you manifest things.

Untrue, of course, but very clearly something people have believed almost universally for centuries.

I can almost always tell the projection and reality are different, but in some very rare and extreme cases (psychedelics, sleep deprivation, extremely protracted and deliberate meditative focus / practice, or e.g. in situations where the projection is properly aligned with the actual stimuli, like seeing a face in the clouds, or in vivid / lucid dreams), the differences can be so small that what allows you to distinguish the two can simply be knowledge of the will / effort involved or e.g. knowledge from laws of physics that what is visualized cannot be present, or, in the case of dreams, an inconsistency with autobiographical memory.

Otherwise, yes, in almost all other cases, I suspect our experiences aren't that much different.

Very cool

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.

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 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.

> 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.

To be polite, it is called "typical-mind fallacy". To be less polite, it is called "cope".

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.

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).

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.