Rousting me out of my recent blog-post drought was some click-bait I saw about the growing popularity of a fruit called paw-paw.
So-named because of its outward resemblance to papaya, paw-paw grows on trees both wild and cultivated, in the eastern US and Canada. The flesh is sweet and creamy, like a banana, and can be consumed in many forms. Maybe the only reason it’s not more popular is that the fruit is easily bruised during shipping. It’s one of the faves of the locavore, farm-to-table movement in eastern North America. So, what’s not to like?
Here’s what: Paw paw contains a mitochondrial toxin called “annonacin.” It’s not only on the seeds, leaves and roots, where toxins exist in many plants with harmless fruit, but also in the fruit itself. The toxin inhibits the action of “complex I,” a critical part of the process in the mitochondria that makes energy from sugars and oxygen. It seems likely that the toxin serves the plant as a defense against insects, whose mitochondria, like ours, are susceptible to it.
Annonacin first reached the attention of scientists studying neurodegeneration after the 2002 publication of a description of a tauopathy endemic on the Caribbean island of Guadeloupe. A third of the people with that disease met diagnostic criteria for PSP. The others had falling, frontal cognitive loss and disinhibited emotional responses, but not the eye movement palsy of PSP. Compared with people on Guadeloupe with typical Parkinson’s disease or healthy controls, those with “Guadeloupean tauopathy,” as it came to be called, were far more likely to have consumed a tropical fruit called soursop. You guessed it: soursop turns out to have harbor annonacin, like paw-paw.
Prompted by that information, scientists in Germany injected annonacin intravenously into rats. The result was a tauopathy that resembled PSP in the rats’ motor behavior and in the appearance of their brain cells under the microscope. The same group subsequently found that annonacin can cause tauopathy by a very different mechanism as well.
Shortly thereafter, I did a dietary risk factor survey among my patients with PSP, comparing them to controls with non-degenerative neurological diseases from our clinic. So few had ever eaten paw-paw (or soursop) that the study didn’t have the statistical power to answer the question and I never published it. (The more common foods included in the questionnaire gave no statistically significant results, either, in case you were wondering.)
Bottom line: There’s probably not enough annonacin in paw-paw to cause PSP or other tauopathies after only occasional consumption. But over decades? And what about people with a genetic predisposition to develop tauopathy? Or people who just love paw-paw and eat them like candy? (There are some!) I think more research and some careful thinking by the FDA is needed before paw-paw becomes more widely marketed and consumed alongside apples, bananas and oranges.