Hi, thanks very much to Gualtiero for allowing me to post here. Last summer, I published an article in the journal Neuroethics discussing the possibility of genetically engineering livestock that lack the affective or “suffering” component of pain. New Scientist magazine picked up on the story and this generated a little flurry of media activity. It was fun getting a lot of feedback on the paper, but as you might imagine, much of the discussion revolved around people’s pretheoretical intuitions on the subject, so I’ve been looking forward to the possibility of getting some feedback from the Philosophy of Brains community.
Anyway, the basic idea of the article (which can be found here) is as follows: I think the question “Will we be able to get rid of intensive factory farming in the near future?” is an empirical question. It’s a complicated empirical question since it ultimately depends upon many people’s ethical decisions, but nevertheless there are ways of evaluating whether it is a realistic possibility. Based on the evidence I’ve seen, I’d say it’s extremely unlikely that our society will change our habits enough in the near future to eliminate the practice of factory farming. Given this, and since factory farming is responsible for a huge amount of suffering, I argue that we ought to genetically engineering animals that lack the ability to feel pain (or rather, the ability to feel a particular component of pain).
Furthermore, I think we’re actually very close to being able to do so. In order to say why, I need to briefly review some facts about the pain system in mammals. Scientists have identified two distinct pathways from nociceptors to higher brain regions. The sensory pathway (which travels from the thalamus to the primary and secondary somatosensory cortex) underlies our ability to localize pain, to estimate it’s intensity, and to describe what type of a pain it is (sharp, dull, burning, etc). The affective pathway (which travels from the thalamus to the anterior cingulate cortex and the insula) underlies subjects’ judgments of how unpleasant the pains are, or how much the pains are minded. Humans who have damaged affective pathways (particularly the anterior cingulate) will report that they still feel pain but no longer mind it. As such, lesioning the anterior cingulate (ACC) is used in rare cases to treat debilitating chronic pain. The role of the ACC in human pain has been further verified by fMRI studies, single-unit recordings (yes, in humans), and pharmacological interventions.
In nonhuman mammals, a similar pattern of results is observed. Rats with damage to the ACC will still show immediate reactions to noxious stimuli, but will no longer change their preferences as a result of this stimulation. Morphine, which disproportionately acts on the affective pathway in the brain, causes similar effects. Furthermore, increasing neural activation in the ACC will cause rats to avoid certain environments even in the absence of noxious stimulation, while blocking ACC activity will prevent rats from avoiding these environments even in the presence of noxious stimulation. Thus, I argued in a previous paper, it appears that the ACC plays a similar role in pain perception in other mammals as it does in humans.
But what’s really interesting, from my perspective, is that researchers have been learning a huge amount about the cellular neurobiology of the ACC in recent years. Min Zhuo’s lab at Toronto has identified neurons in cortical layers II/III of the ACC that change their synaptic connections as a result of painful stimulation. Blocking long-term potentiation in these neurons results in rats that show the immediate reaction to painful stimulation but lack the symptoms of chronic pain found in controls. In fact, the lab has performed several genetic knockouts on the rats that appear to selectively block the affective dimension of pain.
More research needs to be done, but given that scientists appear to be able to locate specific genes that influence the affective dimension of pain, it looks to me that creating pain affect knockouts in other mammals, such as those that are used as livestock, would not be an especially difficult endeavor. We already know what genes to look for, and have a good idea of what kinds of tests could be used to look for similar effects. Thus, I argue, we are very close to being able to create livestock that can still have an immediate reaction to pain while lacking the unpleasant sensation that seems to constitute the suffering of pain.
If we are able to do this, and if there’s no indication that we will be getting rid of factory farming in the near future, shouldn’t we take steps to mitigate the suffering of millions of animals every year?