When I lived in Northern California, I would often hear stories about people scouring the back country for psychedelic toads. In popular imagination, these toad wranglers would then gather around bonfires and with great ceremony and earnestness, they would lick hapless bufoids until they (the humans) fell into ecstatic trances---and then vomited profusely. These stories, often parroted by local media, would end with the news that toad licking had finally been outlawed by the state. The truth, as usual, is quite a bit more complicated.
Bufotenin, one of many molecules secreted by the skin and parotid glands of some toads of the genus Bufo, is classified by the DEA as a Schedule I drug. This is the same class as heroin, mescaline, cannabis, and other drugs the DEA feels have a high potential for abuse and little or no therapeutic value. Bufotenin is also present in certain mushrooms, so I wouldn't swear that is was outlawed because of a pandemic of toad licking.
But many toads are toxic. While there are few reports in the literature about poisoning due to toad licking, there are plenty of reports of accidental toad poisoning. Toads are a food product in parts of Southeast Asia. There have been many reports of accidental toad poisoning in rural Laos, especially when toad skin and toad eggs are part of a meal.
But there's more than one way to get killed by a toad. A traditional Chinese herbal medicine called ch'an su *, which has been sold as an aphrodisiac, topical anesthetic, and a heart medicine, has been responsible for poisonings both in Asia and the U.S. (one of the versions sold in the U.S. was "marketed" as a topical medication, but was taken internally, perhaps for the hallucinogentic affects).
Some of the chemicals present in toad venom are closely related to cardiac glycosides such as digoxin, a potent naturally-derived heart medication, and intoxication with toad venom closely resembles digoxin poisoning. In fact, blood tests in victims are often positive for digoxin. Given the similarities to digoxing poisoning, investigators have tried treating toad poisoning in a clever way. Digoxin (and toad) poisoning requires intensive medical care. Even with close care, a patient can die of fatal heart arrhythmias. But a couple of decades ago, an antidote was developed for digoxin poisoning. Sheep are injected with digoxin and anti-digoxin antibodies are then isolated from their blood. These antibodies are then chopped up so that only the "Fab" portion is present. When given to a patient with digoxin toxicity, the Fab binds to circulating digoxin, preventing it from binding to other receptors in the body, and allowing it to be harmlessly excreted by the kidney.
Given how closely toad poisoning and digoxin poisoning resemble each other, and that toad toxins are similar enough to digoxin that they show up as digoxin in toxicology tests, it seems reasonable to think that the same antidote may work for both poisons. This has been tested in several cases, with apparently good results (there data are limited by the small number of patients).
Cardiac glycoside poisoning is very dangerous. It would appear that poisoning by sources other than regular medications has a high fatality rate. Given this, it would seem reasonable to treat suspected toxicity with digoxin immune Fab. The only catch is cost and availability. If a kid in New York eats some Chinese toad venom, any hospital can administer the antidote. If a woman in a small Laotian village eats a bad batch of toad soup, the cure may not be available. The cost may also be prohibitive. Each vial costs around $700, and it wouldn't be unusual to give 10 vials.
It may be hard to prevent toad poisoning among rural Laotians without solving societal problems of poverty and hunger. But in this country we can easily avoid consuming potentially deadly herbal remedies.
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