Content warning: discussion of allergy attacks.
Epistemic warning: I know very little and this is total
speculation. Don't do anything in this post unless this becomes the
recommended way of dealing with allergy attacks.
Imagine you're walking in a remote area with someone who has a severe
allergy to bee stings, and they get stung. They don't have their
autoinjector), there's no one else around, and you're far from
everything. There's clearly not time for an ambulance, and they start
going into anaphylactic shock. I think it's possible that the best
response is to try to kill them.
Well, not actually try to kill them, but make them think you're trying
to kill them. Specifically, triggering the "fight-or-flight"
or "acute stress" response to make their body release epinephrine
(adrenalin), the standard emergency treatment for anaphylaxis.
One question is whether their body would release enough epinephrine
that this would actually work. Being stung by a bee when you know you
have a life-threatening allergy seems terrifying already, which
probably induces some amount of acute stress response, and that's
clearly not enough to stop anaphylaxis. Perhaps the problem is that
the amount of epinephrine released in acute stress is just much lower
than what you get from an Epi-Pen?
I tried to look up numbers, and found Adrenomedullary response to maximal stress in
humans (Wortsman 1984). They looked at blood samples from fifteen
patients undergoing cardiac arrest, which is about as stressful as you
can get. All were either not given external epinephrine, or their
blood was sampled before they were. They measured a mean peak value
of 10.3 ± 2.9 ng/ml of epinephrine in the samples. They also
Resuscitation after cardiac arrest is associated with
the highest endogenous epinephrine concentration ever
recorded: 35.6 ng/ml. This finding supports our a priori
assumption that the stress of cardiac arrest produces
maximal adrenomedullary stimulation.
To compare to an auto-injector, I found Epinephrine
0.3 mg Bioavailability Following a Single
Injection with a Novel Epinephrine Auto-injector, e-cue, in Healthy
Adults, with Reference to a Single Injection using EpiPen 0.3 mg
(Edwards 2012) which compared the Epi-Pen to the Auvi-Q (then called
e-cue). They found a mean peak blood epinephrine concentration of 0.52
ng/ml with the Epi-Pen and 0.49 ng/ml with the Auvi-Q.
Those levels are about 20x lower than the ones measured during cardiac
arrest, which tells us that the body is capable of releasing
sufficient epinephrine to handle anaphylaxis.
The main remaining questions are (a) can someone reliably induce an
acute stress response in a friend and if so how? and (b) does
friend-induced response cause the body to release sufficient
Overall this sounds plausible, and I'm very curious what someone who
knows more about this than I do would think.
Comment via: facebook
I expect that knowing you're having anaphylaxis without a solution is already reasonably close to the upper end of psychological stress, and you can't add that much more. The reason the epinephrine concentrations are so much higher in cardiac arrest patients is not because cardiac arrest is psychologically stressful, it's because epinephrine release is triggered by hypoxia.
This suggests that blocking the ability of the person to breath for a minute might be a way to push epinephrine concentrations.
Doesn't anaphylaxis already do this?
I'm not sure that it does it fast enough. You likely need high CO2 blood concentration to get your epinephrine and I'm not sure you get that in the normal anaphylaxis.
At the moment I have another open question about whether anaphylaxis shock might happen in situations where the body somehow doesn't produce as much epinephrine as it should and therefore a feedback process in the body gets out of wrack.