Note: I broadly have the same question for suffering from the coldness in a cold slurry. i.e. How do we know shrimp suffer more from coldness than stunning? I do want to establish cold slurry vs. stunning but want to focus on asphyxiation right now first.

Why do we think that suffocation would be more painful for shrimp than stunning? What, or how strong, is the evidence that suffocation via asphyxiation is actually a more negatively valenced experience for shrimp (and how do we know air hunger and suffocation is experienced negatively at all for shrimp?). 

As I understand it, there is no evidence that shrimp possess type C nociceptors^[1]. Ischemic and hypoxic tissue accumulates lactate and protons, and that acidosis activates acid-sensing type C nociceptors and this seems to directly lead to the experience of long-term suffering in humans.

A human with congenital insensitivity to pain still experiences air hunger however. Air hunger is a different system entirely. In vertebrates, dyspnea is driven by interoceptive respiratory chemoreception. But patients in a persistent vegetative state breathe spontaneously and mount chemoreflex responses to hypercapnia and hypoxia. The brainstem loop is intact; the experience is absent. So we have direct proof that the ventilatory chemoreflex and the felt state of air hunger are dissociable.

Ergo, asphyxia may plausibly produce two dissociable bad things: air hunger (interoceptive, non-nociceptive) and acidosis-driven nociceptive pain. And it may well be the latter which is important for establishing whether a being actually suffers.

• A living being with type-C nociceptors slowly dies from suffocation:
  • chemoreceptors -> chemoreflex -> maybe this isn't experienced negatively?
  • acidosis -> type C -> more acidosis -> sustained C-fibre firing -> "long pain" that accumulates over minutes
• A living being - like shrimp - without type-C nociceptors slowly dies from suffocation:
  • chemoreceptors -> chemoreflex -> maybe this isn't experienced negatively?
  • acidosis -> detected by acute Aδ channel -> more acidosis -> still detected by the acute channel, but it adapts -> onset burst; no accumulation of "long pain" that we would call suffering^[2]

Massive "wait-a-second" alarm bell for me 

Acute pain like that from electric stunning does not require type C  nociceptor activation. All you need is fast, sharp "first pain" -> the Aδ channel -> which shrimp likely possess^[3], since there is far better evidence that decapods show acute nociceptive-defensive responses than that they have a slow/tonic pain channel. So it seems possible that the benefit SWP assumes is far less certain than advertised, possibly near zero.

Why zero and not negative? Because both stunning and asphyxiation would carry some acute "first pain," but the asphyxiation here lacks the "long pain."

The intuition that asphyxiation is worse rides entirely on duration. But duration only decisively accumulates suffering if there's a sustained "long pain" signal to carry it across the minutes, and that's exactly the channel our current lack of evidence seems to point to shrimp lacking. No type-C -> no "long pain" -> long death is not a long agony.^[4] It's an acute onset-burst and then an adapting channel, structurally like stunning minus the tonic tail. It only tips negative if the stun's brief jolt is more acutely intense than asphyxiation's onset. This is not obvious.

But hold on, dying via acidosis is trivially progressive in a way that exacting shock is not. pH keeps dropping, and a worsening stimulus re-drives even an adapting channel. So there's "acute channels firing multiple times" in asphyxiation which you could argue is trivially worse than "electric stun has the acute channels firing only once." I actually think this aggregation may well hold up. But I am uncertain. Shocking depolarises every axon in its path at once, which is a categorically different kind of event vs from a nociceptor discharging. It may well be that the acute pain from shock is vastly worse than several acute firings from asphyxiation. So we are left still with very real "possibly near zero impact for welfare by SWP.^[5]"

What evidence do we need that could resolve this more decisively?

I think experiments here are genuinely missing? 

Firstly, a) Is hypoxia aversive at all to shrimp?  and b) How does that compare to the stun?

Is Hypoxia aversive at all to shrimp?

1. Do shrimp make motivational tradeoffs? Will a shrimp pay a graded cost like abandoning shelter, cross an aversive bright field, forgo food etc., to leave hypoxic water?^[6]
2. Do shrimp make conditioned place avoidance? Will shrimp avoid a location associated with past hypoxia, in normoxic (ha, learnt a new word) water?
   1. Actually I think Michael St. Jules may have found some evidence for this
3. What about pharmacological modulation? Does anaesthesia or an anxiolytic reduce hypoxia-escape beyond motor effects?

How does that compare to the stun?

1. Will shrimp reveal a preference between the two? Give them a choice between brief shock and progressive hypoxia, or make escaping hypoxia cost a shock, and titrate.
   1. E.g. similar to Elwood's hermit-crab shock-vs-shell work that put two aversives on one scale
2. Does a sub-lethal stun leave a lasting aversive signature? Are there prolonged grooming of the affected area, avoidance of the stun location, or altered predator-risk tradeoffs afterwards; if there is nothing, that bounds how bad the stun is, perhaps in a way that can be directly compared to shrimp that have experienced sub-lethal asphyxiation
   1. I will readily admit I am starting to feel uncomfortable thinking of setting up such an experiment for beings that may well suffer. But this does seem like the hole we have in our evidence.

If existing literature answers these I would appreciate a link!

(I am going to investigate the question of "pain from cold vs shock" next. Stay tuned.)

1. ^{^}

   Crump et al. 2022 rate Criterion 3 (pathways from nociceptors to integrative brain regions) low for every decapod, explicitly on 'the absence of high-quality evidence one way or the other—not on evidence against.' → Crump et al. 2022, Animal Sentience

2. ^{^}

   The one direct acid-sensing test in a penaeid found no behavioural response and no acid-responsive neurons. Granted, Elwood found the opposite in a caridean eyestalk. → Puri & Faulkes 2010, PLOS ONE and Elwood 2019

3. ^{^}

   Crump et al. rate penaeids high on Criterion 1 (nociceptors) — one of only two criteria they score with real confidence. → Crump et al. 2022, Animal Sentience

^{^}

Air hunger is the feeling of wanting to breathe more than you're managing to — so it needs drive that's ramped up and still unmet. Green crabs held in air didn't ramp up: gill pumping dropped within minutes and stayed low for an hour. Weak evidence, since pumping rate can't distinguish "no drive" from "drive that can't be expressed." But it's the only decapod measurement I can find, and it points away from air hunger being a thing in shrimps rather than toward it. → Wood & Po 2022, J Exp Biol

^{^}

matthes has already made a version of this case from the operational side (animal welfare has an evidence problem). Reading the preprint, matthes found that at lower shock voltage/duration, neural activity sometimes increased, only 3/6 animals showed a 90% drop within 30 min, and that group had worse outcomes than 0°C ice slurry alone. His conclusion is that insufficient stunning with proper ice slurry may be worse than ice slurry alone, and stunning without proper ice slurry has real potential for harm. That is a route to "possibly net-negative" that doesn't depend on any of my neurobiology.

^{^}

Baker 2003 (unpublished NCSU thesis) found brown shrimp entered hypoxic water significantly less with an uncaged predator present. But Bell et al. 2009 found blue crab movement rose with any water-oxygen change, hypoxic or not. So there could be a confound; either way, this remains untested in any penaeid. → Baker 2003, Bell et al. 2009

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