# Endogenous Epinephrine for Anaphylaxis?

*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 Epi-Pen ([epinephrine autoinjector](https://en.wikipedia.org/wiki/Epinephrine_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.

Wait, what?

Well, not actually try to kill them, but make them think you're trying to kill them. Specifically, triggering the "[fight-or-flight](https://en.wikipedia.org/wiki/Fight-or-flight_response)" 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](https://www.jefftk.com/wortsman1984.pdf) (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 wrote:

> 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](https://www.jacionline.org/article/S0091-6749(11)02197-X/pdf) (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 epinephrine?

Overall this sounds plausible, and I'm very curious what someone who knows more about this than I do would think.

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