Looking at this and this, I’d guess that it’s just harder to produce super toxic toxins artificially than it is to produce super sweet sweeteners. IIRC the mass of neotame it takes to taste any sweetness is lower than the mass of VX it takes to kill someone.
You are correct. If one estimates that one requires a milliliter of that 0.5% saccharine solution from that paper cited above to detect the sweetness, that would come around to 50mg of sugar. If neotame is 6000 times more potent, that would mean about 800ng. Even if we switch from VX to the more potent botulinum toxin A, we would need a whole whopping microgram per kilogram orally, so perhaps a 100x more than what we need for neotame. (If we change the route of administration to IV, then botox will easily win, of course.)
Of course, this is highly dependent on the ratio of saliva in the mouth (which will dilute the sweetener) to the weight of the organism (which will affect the toxin dose needed). I don’t think this ratio will change overly much when going to elephants or mice, though.
In a way, this should be unsurprising. Both the taste molecule and the neurotoxin interact with very specific receptor molecules. Only in one case, the animal evolved to cooperate with the molecule (by putting the receptors directly on the tongue) while in the other case the evolutionary pressure was very much not to allow random molecules from the environment access to the synapses.
Looking at this and this, I’d guess that it’s just harder to produce super toxic toxins artificially than it is to produce super sweet sweeteners. IIRC the mass of neotame it takes to taste any sweetness is lower than the mass of VX it takes to kill someone.
You are correct. If one estimates that one requires a milliliter of that 0.5% saccharine solution from that paper cited above to detect the sweetness, that would come around to 50mg of sugar. If neotame is 6000 times more potent, that would mean about 800ng. Even if we switch from VX to the more potent botulinum toxin A, we would need a whole whopping microgram per kilogram orally, so perhaps a 100x more than what we need for neotame. (If we change the route of administration to IV, then botox will easily win, of course.)
Of course, this is highly dependent on the ratio of saliva in the mouth (which will dilute the sweetener) to the weight of the organism (which will affect the toxin dose needed). I don’t think this ratio will change overly much when going to elephants or mice, though.
In a way, this should be unsurprising. Both the taste molecule and the neurotoxin interact with very specific receptor molecules. Only in one case, the animal evolved to cooperate with the molecule (by putting the receptors directly on the tongue) while in the other case the evolutionary pressure was very much not to allow random molecules from the environment access to the synapses.
On that note, it looks like people have deliberately engineered artificial sweeteners, but for whatever reason they aren’t in use.
I think people typically use the naturally occurring nondigestible sweeteners anyway, stevia and erythritol mainly