Definitely asks questions related to the strength of the simulation—do people with aphantasia have a more suppressing system? Do people with vivid imaginations have weaker suppression systems?
Is the suppression factor constant for all behaviours/actions of the brain, or can you be more suppressive in one domain than another.
Can we modify this suppressive factor?
Is the suppressive factor a feature of the neural architecture or an extra isolated feature (i.e. paint on the walls vs a new room)? I'd argue it's more the former than the latter, since we would probably have observed the latter in fMRI scans, but it begs the question of how something like that evolved so uniformly given our similarity to non-conscious organisms.
> delusions tend to go with disorganized speech and bizarre behaviors
Interesting article, but this statement is unsupported by real evidence. It's unclear whether there is any correlation at all between "delusions" and incoherent speech. One could reasonably say this statement is itself an assertion, or even a definition of delusion, instead of the observation it pretends to be.
How is this not empiricist-reductionistic? It still relies on reduced and abstracted science. I am sorry but how does it make anything better because it is not "empiricist-reductionistic"? It sounds very smart and philosophical. But does it mean anything useful in this context?
Hi, thanks for commenting. I agree this hypothesis relies on empirical data, ultimately. What I mean to say, but did not articulate well, is that I think that psychiatry has been under-theorized for several decades now, and overly fixated on Data! and Evidence! But this does not mean much without some sort of theory or model that we are trying to test. We collect a lot of data about symptoms and genes and molecular transporters and fMRI activity, but it does not seem to add up to much. People are wary of offering interpretations or theories.
In contrast, a cardiologist can tell you a lot about different heart diseases, and tell you why particular symptoms occur in a given disease and not others, and it all relates to a model of "what the heart is for and how it works." We are not able to do this in psychiatry.
I would argue that this simulation hypothesis is 1) an interpretation of certain data which 2) helps us make sense of other data.
Really interesting work.
Definitely asks questions related to the strength of the simulation—do people with aphantasia have a more suppressing system? Do people with vivid imaginations have weaker suppression systems?
Is the suppression factor constant for all behaviours/actions of the brain, or can you be more suppressive in one domain than another.
Can we modify this suppressive factor?
Is the suppressive factor a feature of the neural architecture or an extra isolated feature (i.e. paint on the walls vs a new room)? I'd argue it's more the former than the latter, since we would probably have observed the latter in fMRI scans, but it begs the question of how something like that evolved so uniformly given our similarity to non-conscious organisms.
Woah. Must read.
> delusions tend to go with disorganized speech and bizarre behaviors
Interesting article, but this statement is unsupported by real evidence. It's unclear whether there is any correlation at all between "delusions" and incoherent speech. One could reasonably say this statement is itself an assertion, or even a definition of delusion, instead of the observation it pretends to be.
“The cabin lights turn on, the mirrors work, the engine revs, the brakes pump, but it’s not going anywhere.”
Too true … too true.
How is this not empiricist-reductionistic? It still relies on reduced and abstracted science. I am sorry but how does it make anything better because it is not "empiricist-reductionistic"? It sounds very smart and philosophical. But does it mean anything useful in this context?
Hi, thanks for commenting. I agree this hypothesis relies on empirical data, ultimately. What I mean to say, but did not articulate well, is that I think that psychiatry has been under-theorized for several decades now, and overly fixated on Data! and Evidence! But this does not mean much without some sort of theory or model that we are trying to test. We collect a lot of data about symptoms and genes and molecular transporters and fMRI activity, but it does not seem to add up to much. People are wary of offering interpretations or theories.
In contrast, a cardiologist can tell you a lot about different heart diseases, and tell you why particular symptoms occur in a given disease and not others, and it all relates to a model of "what the heart is for and how it works." We are not able to do this in psychiatry.
I would argue that this simulation hypothesis is 1) an interpretation of certain data which 2) helps us make sense of other data.
Great response. Thank you for your elaboration.