I haven't really gone deep on the MRI side, but I'm interested in citations for empirical work.
This one (Hagerty et. al., 2013: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659471/) seems to get at the quesiton Scott is posing about which reward machinery is being triggered, using MRI to investigate. In particular they substantiate this hypothesis:
> H5: Jhanas should show increased activation compared to the rest state in the dopamine reward system of the brain (NAc in the ventral striatum and medial OFC). A broad range of external rewards stimulate this system (food, sex, beautiful music, and monetary awards), so extreme joy in jhana may be triggered by the same system (the VTA is also part of this system, but is too small to image with standard fMRI methods, but see [35] for successful imaging methods).
> Now, what does the released dopamine do? In PFC (via the mesocortical pathway), it draws attentional resources to the surprising stimulus and its plausible causes, gating out the processing of other, less relevant stimuli. Simultaneously, in NAc, it strengthens connections between PFC inputs and the endorphin-releasing cells, thereby wiring together the hedonic features of the reward and the sensory features of any cues predictive of it. This imbues the cue with the ability to release the GABAergic brake on VTA DA neurons all by itself. Phenomenologically, it results in us "liking" the cue as much (or nearly as much) as we like the reward (this is what allows, e.g., animal trainers to reinforce behavior with only the sound of a clicker that has previously been paired with food).
So, speculatively, if Jhana is somehow short-circuiting NAc to trigger without specific signals from PFC, are we weakening the existing connections from PFC that previously triggered NAc? Something like normalizing the weights over a bunch of input signals, but with the new input signal being "non-causal / Jhanic stimulation"? Thus reducing the weight of other causal hedonic pleasures (like casual sex in this example)? So these signals from PFC would not elicit as much dopamine response through NAc activation as they did pre-Jhana.
Perhaps there is also something here viz the second part:
> But once the brain learns that a reward is reliably predicted by a cue, the reward ceases to elicit a surprise signal. This means it no longer increases VTA DA neuron firing rate. It may still cause endorphin release and thus keep the GABAergic brake off, but if there's no surprise signal driving phasic firing, dopamine release will be minimal.
> That is to say: We still enjoy expected rewards; we just don't much *care* about our enjoyment of them.
If you can reliably produce the Jhanic pleasure state, perhaps this condition eventually obtains as well; it's no longer "surprising" that you can experience this bliss state, and therefore it's not addictive/appealing. But, maybe it's still a strong-enough stimulus in the NAc system to continue to reduce the weight of the other, more-surprising NAc activations from the PFC, so it's also displacing those surprisingly-pleasurable states from firing.
I haven't really gone deep on the MRI side, but I'm interested in citations for empirical work.
This one (Hagerty et. al., 2013: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659471/) seems to get at the quesiton Scott is posing about which reward machinery is being triggered, using MRI to investigate. In particular they substantiate this hypothesis:
> H5: Jhanas should show increased activation compared to the rest state in the dopamine reward system of the brain (NAc in the ventral striatum and medial OFC). A broad range of external rewards stimulate this system (food, sex, beautiful music, and monetary awards), so extreme joy in jhana may be triggered by the same system (the VTA is also part of this system, but is too small to image with standard fMRI methods, but see [35] for successful imaging methods).
Ok, now what does this mean for Scott's quesitons? I'm far from an expert here, but stitching this together with https://astralcodexten.substack.com/p/highlights-from-the-comments-on-unpredictable :
> Now, what does the released dopamine do? In PFC (via the mesocortical pathway), it draws attentional resources to the surprising stimulus and its plausible causes, gating out the processing of other, less relevant stimuli. Simultaneously, in NAc, it strengthens connections between PFC inputs and the endorphin-releasing cells, thereby wiring together the hedonic features of the reward and the sensory features of any cues predictive of it. This imbues the cue with the ability to release the GABAergic brake on VTA DA neurons all by itself. Phenomenologically, it results in us "liking" the cue as much (or nearly as much) as we like the reward (this is what allows, e.g., animal trainers to reinforce behavior with only the sound of a clicker that has previously been paired with food).
So, speculatively, if Jhana is somehow short-circuiting NAc to trigger without specific signals from PFC, are we weakening the existing connections from PFC that previously triggered NAc? Something like normalizing the weights over a bunch of input signals, but with the new input signal being "non-causal / Jhanic stimulation"? Thus reducing the weight of other causal hedonic pleasures (like casual sex in this example)? So these signals from PFC would not elicit as much dopamine response through NAc activation as they did pre-Jhana.
Perhaps there is also something here viz the second part:
> But once the brain learns that a reward is reliably predicted by a cue, the reward ceases to elicit a surprise signal. This means it no longer increases VTA DA neuron firing rate. It may still cause endorphin release and thus keep the GABAergic brake off, but if there's no surprise signal driving phasic firing, dopamine release will be minimal.
> That is to say: We still enjoy expected rewards; we just don't much *care* about our enjoyment of them.
If you can reliably produce the Jhanic pleasure state, perhaps this condition eventually obtains as well; it's no longer "surprising" that you can experience this bliss state, and therefore it's not addictive/appealing. But, maybe it's still a strong-enough stimulus in the NAc system to continue to reduce the weight of the other, more-surprising NAc activations from the PFC, so it's also displacing those surprisingly-pleasurable states from firing.