Paw paws. Source: My yard. Destination: Recycle bin.
We have a couple of paw paw trees in our yard. The are nice-looking trees, with large glossy green leaves. I have the vague recollection that we put them in for butterfly habitat, as they are critical for the reproduction of the zebra swallowtail.
We rarely get any edible fruit from them, as the fruit always seem to go from rock hard to “the deer got them” in a matter of days.
And, as it turns out, that may have been a lucky break.
But this year, possibly as a consequence of my various deer deterrence devices (e.g., Post #G07), we have had some ripe ones fall off the tree. I picked up the ripe ones, ate one, and have been looking forward to eating the rest.
But some of my wife’s acquaintances on the Vienna plant FaceBook group have requested seeds. And as is my habit, I thought I’d do a bit of research first.
If you just want butterfly habitat and an ornamental tree, you can grow one from seed. But if you want fruit, you need two different trees, genetically distinct, and I’m not sure that two seeds from the same tree will give you that. So I was going to warn the potential seed takers that, down the road, they might not get any fruit.
Turns out, that may be lucky, too.
The issue is the presence of a potent neuro-toxin in the fruit. Is that a myth, is it true, and, if true, how dangerous is it? (Knowing full well that it can’t be too dangerous, as you’ve never heard a paw-paw related death making the evening news.)
First, paw paw fruit absolutely does contain a neurotoxin, based on reputable research. And there is some indirect evidence that heavy consumption of fruits of this type may have led to a high incidence of atypical Parkonsonism on one tropic island.
Well, that’s enough for me to swear off them. Despite the fact that they’re yummy, I believe I have eaten my last paw-paw. Unless and until starvation conditions occur out here in the ‘burbs.
The only thing left is to figure out how much damage was done in eating one last night.
The dosage of the key neurotoxin, sufficient to cause brain lesions in rats, is given as 3.8 mg/kg/day, for 28 days (cited in Wikipedia). Or a cumulative dose of about 100 mg/kg of body weight. Paw paw pulp contains about 0.07 mg/g of the key neurotoxin (reference). My last ripe paw paw weighs in at just over 200 grams, of which I’d guess less than half is edible pulp. So call that 100 grams per fruit.
The rest is just math. One paw paw contains about 7 mg of neurotoxin. At my weight, I’d need about 12 grams of it. So my consumption of one ripe paw paw so far amounts to about 0.0006 of the estimated known neurotoxic dose. Inverting that, I’d need to eat about 1700 paw paws to achieve the estimated known neurotoxic dose.
(That needs to be tempered by understanding that a) the dose in the rat study should be viewed as an upper bound, i.e., it was sufficient to generate lesions large enough to be observed. That doesn’t rule out significant brain damage occurring at smaller doses, b) that was rats, which may or may not translate to humans, but, unfortunately, scientists have not intentionally poisoned a sufficiently large enough sample of humans to provide us with a better estimate of the dose that’s toxic to humans, and c) the dose per paw paw will almost certainly vary with the specific variety and with growing conditions. Nevertheless, 1700 is a comfortingly large number, even with those caveats.)
So, no harm done. The toxin in a single paw-paw is fairly minimal. But — how to put this — I don’t lick my fingers after putting down rat poison, so I think I’ll give up on eating paw paws. My brain function is deteriorating plenty fast enough on its own, thanks. I don’t need to help that along.