My government name is Mack Gallagher. I am a thrift store cashier living in Iowa. Crocker’s Rules. I am an underfunded “alignment” “researcher”. DM me if you’d like to fund my posts.
Lorec
Karma: 16
Interested to hear how you would put this with “research” tabooed. Personally I don’t care if it’s research as long as it works.
I agree that the somatosensory cortex [in the case of arm movements, actually mostly the parietal cortex, but also somewhat the somatosensory] needs to be getting information from the motor cortex [actually mostly the DLPFC, but also somewhat the motor] about what to expect the arm to do!
This necessary predictive-processing “attenuate your sensory input!” feedback signal, could be framed as “A [C]”, such that “weak A [C]” might start giving you hallucinations.
However, in order for the somatosensory cortex to notice a prediction error and start hallucinating, it has to be receiving a stronger [let’s say “D”] signal, from the arm, signifying that the arm is moving, than the “weak A [C]” signal signifiying that we moved the arm.
I don’t think your theory predicts this or accounts for this anyhow?
My “Q/P” theory does.
[ “B” in your theory maps to my “quasi-volition”, ie anterior cortex, or top-down cortical infrastructure.
Every other letter in your theory—the “A”, “C”, and “D”—all map to my “perception”, ie posterior cortex, or bottom-up cortical infrastructure. ]
Thanks for clarifying. The point where I’m at now is, as I said in my previous comment,
if it’s just signal strength, rather than signal speed, why bring “A” [cortico-cortical connections] into it, why not just have “B” [“quasi-volitional” connections] and “C” [“perceptual” connections]?
Thanks for being patient enough to go through and clarify your confusion!
About the pyramidal cells—I should have been more specific and said that prefrontal cortex [as opposed to primary motor cortex] - AFAIK does not have output pyramidal cells in Layer V. Those are Betz cells and basically only the primary motor cortex has them, although Wikipedia (on Betz cells and pyramidal cells) tells me the PFC has any neurons that qualify as “pyramidal neurons”, too; it looks like their role in processing is markedly different from the giant pyramidal neurons found in the primary motor cortex’s Layer 5.
Pyramidal neurons in the prefrontal cortex are implicated in cognitive ability. In mammals, the complexity of pyramidal cells increases from posterior to anterior brain regions. The degree of complexity of pyramidal neurons is likely linked to the cognitive capabilities of different anthropoid species. Pyramidal cells within the prefrontal cortex appear to be responsible for processing input from the primary auditory cortex, primary somatosensory cortex, and primary visual cortex, all of which process sensory modalities.[21] These cells might also play a critical role in complex object recognition within the visual processing areas of the cortex.[3] Relative to other species, the larger cell size and complexity of pyramidal neurons, along with certain patterns of cellular organization and function, correlates with the evolution of human cognition. [22]
This is technically compatible with “pyramidal neurons” playing a role in schizophrenic hallucinations, but it’s not clear how there’s any correspondence with the A vs B [vs C] ratio concept.
Maybe I slightly misunderstood your original theory, if you are not trying to say here, in general, that there is an “action-origination” signal that originates from one region of cortex, and in schizophrenics the major data packet [“B”] and the warning signal [“C”] experience different delays getting to the target.
If you are postulating a priori that the brain has a capability to begin the “B” and “C” signals in different regions of cortex at the same time, then how can you propose to explain schizophrenia based on intra-brain communication delay differentials at all? And if it’s just signal strength, rather than signal speed, why bring “A” into it, why not just have “B” and “C”?
My own view is: Antipsychotics block dopamine receptors. I think you’re right that they reduce a ratio that’s something like your B/A ratio. But I can’t draw a simple wiring diagram about it based on any few tracts. I would call it a Q/P ratio—a ratio of “quasi-volition”, based on dopamine signaling originating with the frontal cortex and basal ganglia, and perception, originating in the back half of the cortex and not relying on dopamine.
Illustration of how the Q/P idea is compatible with antipsychotics reducing something like a B/A ratio in the motor case: Antipsychotics cause “extrapyramidal” symptoms, which are stereotyped motions of the extremities caused by neurons external to the pyramidal [corticospinal] tract. As I understand it, this is because one effect of blocking dopamine receptors in the frontal lobe is to inhibit the activity of Betz cells.
No, when I say “in parallel”, I’m not talking about two signals originating from different regions of cortex. I’m talking about two signals originating from the same region of cortex, at the time the decision is made—one of which [your “B” above] carries the information “move your arm”[/”subvocalize this sentence”] and the other of which [the right downward-pointing arrow in your diagram above, which you haven’t named, and which I’ll call “C”] carries the information “don’t perceive an external agency moving your arm”[/”don’t perceive an external agency subvocalizing this sentence”].
AFAICT, schizophrenic auditory hallucinations in general don’t pass through the brainstem. Neither do the other schizophrenic “positive symptoms” of delusional and disordered cognition. So in order to actually explain schizophrenic symptoms and the meliorating effect of antipsychotics, “B” and “C” themselves have to be instantiated without reference to the brainstem.
With respect to auditory hallucinations, “B” and “C” should both originate further down the frontal cortex, in the DLPFC, where there are no pyramidal neurons, and “C” should terminate in the auditory-perceptual regions of the temporal lobe, not the brainstem.
If you can’t come up with a reason we should assume the strength of the “B” signal [modeled as jointly originating with the “C” signal] here is varying, but the strength of the “C” signal [modeled as sometimes terminating in the auditory-perceptual regions of the temporal lobe] is not, I don’t see what weight your theory can bear except in the special case of motor symptoms—not auditory-hallucination or cognitive symptoms.
Doesn’t this all rely on the idea that
Command to move my arm
and
Signal that I expect my arm to move (thus suppressing the orienting / startle reaction which would otherwise occur when my arm motion is detected)
are sent through separate [if parallel] channels/pathways? What substantiates this?
Something else I later noticed should confuse me:
OK, now let’s look at the sentences in the above excerpt one-by-one:
For the first sentence (on genes): Consider a gene that says “Hey neurons! When in doubt, make more synapses! Grow more axons! Make bigger dendritic trees!” This gene would probably be protective against schizophrenia and a risk factor for autism, for reasons discussed just above. And vice-versa for the opposite kind of gene. Nice!
Why would your theory [which says that schizophrenia is about deficient connections] predict that a gene that predisposed toward a more fully-connected connectome, would protect against schizophrenia?
Great post!
I think schizophrenia is generally recognized as involving more deficiencies in local than long-distance cortex-to-cortex communication. I don’t have any particular knockdown studies for this and your Google Scholar judo seems on a level with mine. But as far as I understand it, autism is the disorder associated with deficits in longer white matter tracts; I believe this is because axons grow too densely and mesh too tightly during fetal development, while in schizophrenia the opposite happens and you end up with fewer axons [also probably fewer neurons because fewer neural progenitor divisions but this wouldn’t a priori affect the shape of the connectome].
I figure, when a neurotypical person is subvocalizing, there’s communication between the motor cortex parts that are issuing the subvocalization commands (assuming that that’s how subvocalization works, I dunno), and the sensory cortex parts that are detecting the subvocalization which is now happening. Basically, the sensory cortex has ample warning that the subvocalization is coming. It’s not surprised when it arrives.
But in schizophrenia, different parts of the cortex can’t reliably talk to each other. So maybe sometimes the sensory cortex detects that a subvocalization is now happening, but hadn’t gotten any signal in advance that this subvocalization was about to be produced endogenously, by a different part of the same cortex. So when it arrives, it’s a surprise, and thus is interpreted as exogenous, i.e. it feels like it’s coming from the outside.
I don’t see how your theory would make this prediction. To me it seems like your theory predicts, if anything, weaker subvocalization in schizophrenics—not subvocalization that’s more perceptible. The “it inhibits the warning shot but not the actual data packet” thing frankly feels like an epicycle.
I don’t see how Dehaene clarifies anything or how your theory here relies on him.
I missed this being compiled and posted here when it came out! I typed up a summary [ of the Twitter thread ] and posted it to Substack. I’ll post it here.
“It’s easier to build foomy agent-type-things than nonfoomy ones. If you don’t trust in the logical arguments for this [foomy agents are the computationally cheapest utility satisficers for most conceivable nontrivial local-utility-satisfaction tasks], the evidence for this is all around us, in the form of America-shaped-things, technology, and ‘greed’ having eaten the world despite not starting off very high-prevalence in humanity’s cultural repertoire.
WITH THE TWIST that: while America-shaped-things, technology, and ‘greed’ have worked out great for us and work out great in textbook economics, textbook economics fails to account for the physical contingency of weaker economic participants [such as horses in 1920 and Native Americans in 1492] on the benevolence of stronger economic participants, who found their raw resources more valuable than their labor.”
As I say on Substack, this post goes hard and now I think I have something better to link people to, who are genuinely not convinced yet that the alignment problem is hard, than List of Lethalities.
Thank you! Someone else noticed! For my part, I’ll update this if I find anything.
As far as I can tell, density-dependent selection is an entirely different concept from what I’m trying to get at here, and operates entirely within the usual paradigm that says natural selection is always optimizing for relative fitness. Yes, the authors are trying to say, “We have to be careful to pay attention to the baseline that selection is relative to”, but I think biologists were always implicitly careful to pay attention to varying baseline populations—which are usually understood to be species, and not ecological at all.
I’m trying to take a step back and say, look, we can’t actually take it for granted that selection is optimizing for reproductive fitness relative to ANY baseline in the first place; it’s an empirical observation external to the theory that “what reproduces, increases in prevalence” that evolution within sexual species seems to optimize for %-prevalence-within-the-species, rather than absolute size of descendants-cone.
Which is?
Have you read Byrnes on how we should expect certain emotional reactions to seemingly prohibitively complex stimuli, to be basically hardcoded?
I think I have learned a certain amount of my eye-contact-aversion, but I also suspect it is hardcodedly unusually difficult for me. When I was younger, my parents and teachers constantly harangued me to “get better at eye contact”, and I really tried [I hated their haranguing!] but the eye contact itself was just too emotionally painful.
When I first went on Ritalin in November of 2020, I immediately noticed that it became much more possible to voluntarily choose to sustain eye contact with most people for ~3-10-second periods; I was excited and thought maybe I could make the whole aversion go away. But that didn’t work either. It stayed effortful, although easier.
I still don’t make much eye contact, and at this point in my life nobody ever remarks on it, and it causes no problem at all. I regularly meet people who are worse at it than I am, and some of them seem to have less of a general social handicap than I do!
Thoughts on Evo-Bio Math and Mesa-Optimization: Maybe We Need To Think Harder About “Relative” Fitness?
Is Bostrom’s original Simulation Hypothesis, the version involving ancestor-simulations, unconvincing to you? If you have decided to implement an epistemic exclusion in yourself with respect to the question of whether we are in a simulation, it is not my business to interfere with that. But we do, for predictive purposes, have to think about the fact that Bostrom’s Simulation Hypothesis and other arguments in that vein will probably not be entirely unconvincing [by default] to any ASIs we build, given that they are not entirely unconvincing to the majority of the intelligent human population.
If a human being doesn’t automatically qualify as a program to you, then we are having a much deeper disagreement than I anticipated. I doubt we can go any further until we reach agreement on whether all human beings are programs.
My attempt to answer the question you just restated anyway:
The idea is that you would figure out what the distant superintelligence wanted you to do the same way you would figure out what another human being who wasn’t being verbally straight with you, wanted you to do: by picking up on its hints.
Of course this prototypically goes disastrously. Hence the vast cross-cultural literature warning against bargaining with demons and ~0 stories depicting it going well. So you should not actually do it.
How would you know that you were a program and Omega had a copy of you? If you knew that, how would you know that you weren’t that copy?
Do you want to fully double-crux this? If so, do you one-box?
Unlike with obvious epistemic predicates over some generality [ eg “Does it snow at 40 degrees N?”, “Can birds heavier than 44lb fly?”—or even more generally the skills of predicting the weather and building flying machines ], to which [parts of] the answers can be usefully remembered as monolithic invariants, obvious deontic predicates over generalities [ eg “Should I keep trying when I am exhausted?”, “Will it pay to fold under pressure?”—and the surrounding general skills ] don’t have generalizable answers that are independent of one’s acute strategic situation. I am not against trying to formulate invariant answers to these questions by spelling out every contingency; I am unsure whether LessWrong is the place, except when there’s some motivating or illustrative question of fact that makes your advice falsifiable [ I think Eliezer’s recent The Sun is big, but superintelligences will not spare Earth a little sunlight is a good example of this ].