On June 4, 2018, The Atlantic published Michael Pollan’s account of studying “magic” mushrooms alongside world-famous mycologist Paul Stamets. According to the story, Stamets took Pollan hunting for the Psilocybe azurescens mushroom in its native Pacific Northwest habitat. P. azurescens (or “azzies”) mushrooms were originally discovered by Stamets. These mushrooms are commonly considered the most potent psilocybin-containing mushrooms in the world.
During their foray, Stamets and Pollan discussed one “troubling” feature of eating P. azurescens: temporary paralysis. See Wood Lover Paralysis. Here is the section of The Atlantic article that summarized the conversation:
“And azzies have one potential side effect that some people find troubling.”
“Temporary paralysis,” he said matter-of-factly. He explained that some people on azzies find they can’t move their muscles for a period of time. That might be tolerable if you’re in a safe place, he suggested, “but what if you’re outdoors and the weather turns cold and wet? You could die of hypothermia.” Not much of an advertisement for azurescens, especially coming from the man who discovered the species and named it. I was suddenly in much less of a hurry to try one.
Stamets offered a similar description of wood lover paralysis in 2016. Michael W. Beug’s Mushroom Poisoning in North America cites a personal communication from Stamets in October of 2016. At that time Stamets had received reports from several individuals suffering from temporary paralysis after consuming some of the very potent wood-loving species P. azurescens. According to Stamets, “The concern here is that someone might consume these mushrooms out in the field on a cold, rainy day and suffer hypothermia before they can walk again.” Arguably, there could be some other concerns about losing all voluntary motor function.
Stamets attributes wood lover paralysis to the dose of mushrooms consumed by the user. He also notes in The Atlantic article: “I find azurescens almost too strong.” These two pieces don’t quite add up. If a mushroom is especially “strong,” i.e., potent, wouldn’t an experienced user simply consume less in order to achieve the desired dose? And, wouldn’t people taking large doses of other magic mushrooms (e.g., psilocybe cubensis) experience paralysis?
Notably, wood lover paralysis is not observed in people dosed with pure psilocybin. Moreover, wood lover paralysis is not observed in people taking high doses of other psilocybin-containing mushrooms, thereby controlling for the relatively high potency of Psilocybe azurescens. The paralysis symptoms cannot be explained according to the amount of psilocybin or psilocin consumed. The phenomenon is only observed in P. azurescens and P. cyanescens.
What is the Cause of Wood Lover Paralysis?
Nobody knows the cause of wood lover paralysis. Most likely, wood lover paralysis is caused by the presence (or absence) of certain molecules (other than psilocybin and psilocin) in P. azurescens and P. cyanescens. In other words, psilocybin and psilocin are probably not responsible for the paralysis. Most likely, other psilocybin derivatives cause the paralysis. This is an important point as the world moves forward towards embracing the benefits of psilocybin. Opponents of psilocybin therapies would probably jump at the opportunity to blame psilocybin for the paralysis observed after eating certain kinds of “magic” mushrooms.
Potential Harms Created by Ignoring the True Cause of Wood Lover Paralysis
Continuing to lump all of the molecules together leads to two problems:
- First, attributing wood lover paralysis to psilocybin and psilocin takes the focus away from the actual cause — which is probably some other molecule(s) present in P. azurescens and P. cyanescens but not present in other species, like P. cubensis.
- Second, attributing wood lover paralysis to psilocybin and psilocin will ultimately blame those molecules for the “dangerous” wood lover paralysis symptoms. (See above regarding potential for dying of hypothermia because of unwanted paralysis side-effects).
Where to Look: Aeruginascin?
Several varieties of magic mushrooms contain the psilocybin derivative aeruginascin. This molecule was first found in magic mushrooms in 1989 by Gartz.1 Recently, the correct biosynthetic pathway for psilocybin synthesis was published which demonstrates sequential methylation of norbaeocystin to make baeocystin, psilocybin, and aeruginascin.2 The fungus adds one, two, and then three methyl groups, respectively, to synthesize the chemicals.
According to Stamets, P. azurescens have high amounts of baeocystin. How does consuming baeocystin compare to consuming psilocybin? No one knows. Arguably, the difference between these molecules (a single methyl group) could be important in much the same way that methamphetamine (crystal meth) produces a different effect from amphetamine (Adderall). (Amphetamine and methamphetamine differ by the presence/absence of a single methyl group).
From a chemical standpoint, aeruginascin is very different from norbaeocystin, baeocystin, and psilocybin. Aeruginascin has a quaternary ammonium salt, which would be expected to dramatically influence the way it interacts with different receptors.
- The paralysis observed by people taking magic mushrooms is not caused by the dose of psilocybin.
- The paralysis observed by people taking magic mushrooms is unique to mushrooms that grow on wood substrates.
- The paralysis observed by people taking magic mushrooms is probably due to different molecules that are unique to P. azurescens and P. cyanescens.
- Studying aeruginascin seems like a good starting point for figuring out the cause of wood lover paralysis. The molecule is found along with psilocybin and known to affect different serotonin receptors such as 5-HT3 versus 5-HT2A.
- The community needs to focus on the chemistry underlying magic mushrooms — not just the mushrooms themselves.
** If you have information or insight that could help us find the cure for wood lover paralysis, please share them using the comments section below.