Since you mention pain several times, one pretty significant gap in this discussion is consideration of the dissociation between the sensory and affective components of pain experience. The reported intensity of pain is correlated with the reported unpleasantness of pain, but the two components can be pushed in opposite directions (for example, reported pain intensity can remain constant while pain unpleasantness is increased or decreased). The affective component of pain is presumably what matters morally, and valance is definitionally part of the affective component.
This is important because a lot of your discussion of pain is referencing the reported sensory intensity of pain. For example, the gamma band oscillations appear to be tracking the sensory component of pain (the Yue et al article traces it to the primary somatosensory cortex). This would suggest that even if these oscillations are relatively predictive of pain, they are not good candidates for biomarkers that could be used to tell us something about the moral status of other species, since they occur upstream of the neural activity connected to affect.
This is super interesting...thanks Max!
I haven’t read the books so I assume they deal with this there, but what about cases of blindsight, where people self-report that they don’t see objects in certain parts of their visual field but nevertheless are able to respond above chance on forced choice tasks and even make appropriate grasping motions for objects in that area of the visual field? Wouldn’t those, if true, be cases where we have maps of our surrounding environment that guide behaviour but nevertheless are not phenomenally conscious?
Also, a couple of the things he said about pain seem incorrect to me. He says “I think consciousness can come in degrees, but not in a way related to the invertebrate-versus-vertebrate status. Rather, it relates to the number of sensory receptors possessed. For example,some people have few pain-sensing neurons and are insensitive to pain whereas other people with more pain neurons are more sensitive to pain.” But in all the studies I’ve seen, individual differences in how sensitive people are to pain have to do with neurons *in the brain* not with how many nociceptors in the peripheral nervous system someone has. After all, if all of the information from the peripheral nervous system is funnelled through the spinal cord to specific tracts in the brain, what ultimately matters is the coded information coming from that tract. In other words, if a given spinal neuron passes on the information [50 actions potentials in time span X] to a particular brain region, it doesn’t really matter whether that signal was caused by 1 nociceptor or 100 nociceptors.
Finally, he seems to fall into a inexplicably common mistake of assuming that the difference between “fast pain” (transmitted through A-delta fibres) and “slow pain” (via C fibres) maps onto the difference between sensory and affective pain. I’m not sure why that is such a common move, but it’s not really true...fast pain can lead to pain affect and suffering. I guess since he says that fast pain can lead to “misery,” this suggests that he’s not ruling out all affect, but it seems like an odd definition of suffering to me to restrict it to slow pain.