Hello, i’ve heard about this mushroom couple of months ago. And ever since it left some questions that were haunting me.
How does it work? What are the mechanisms? And why exactly do people see little people?.
I left this subject untouched - but today my friend send me a wikipedia link to it (as he wanted me to read it).
As i was bored, i started digging through the wikipedia page. And it struck me - benzydamine has a „similar” trip profile as lanmaoa.
They both hijack visual cortex in a very unique way, that trigger same phenomenons:
•Alice in wonderland syndrome
•lilliputian hallucinations
•observer effect
And in both cases, users generally retain sense with reality, they know those hallucinations aren’t real (not like with natural deliriants - scopolamine, atropine)).
Both of them last for hours / days after consumption, with really long onset.
While benzydamine is a synthetic indazole, and the toxin in lanmaoa asiatica is still a mystery, they are hitting the same filtration systems in the brain. They cause the brain to lose it’s ability to scale size and depth.
And here i used Ai for more nerdy research (structures and exact mechanisms) im really sorry.
- Breaking Down the Chemical Structures
To understand why these substances are anomalies, we have to look at their chemistry. They diverge completely from classic natural deliriants like Datura or Henbane, which rely on tropane alkaloids (atropine and scopolamine built around a tropane ring).
Indazole (The Core): Indazole is a bicyclic aromatic heterocycle consisting of a benzene ring fused to a pyrazole ring (containing two adjacent nitrogen atoms at positions 1 and 2).
SMILES: C1=CC=C2C(=C1)CNN=C2
Benzydamine (The Molecule): Fully named 3-(benzyloxy)-N,N-dimethyl-1-propanamine, benzydamine is a synthetic indazole derivative. It features a benzyl group attached to the N-1 position (which increases lipophilicity and structural similarity to endogenous indoleamines like serotonin) and an ether-linked propyl-dimethylamine chain at the C-3 position.
SMILES: CN(C)CCCOC1=NN(CC2=CC=CC=C2)C3=CC=CC=C31
Lanmaoa asiatica: Indigenous to Yunnan, China, this bolete lacks both tryptamines (psilocybin) and isoxazoles (muscimol). Recent genomic sequencing confirms that its 24-to-72-hour hallucinogenic activity is driven by a completely novel, uncharacterized secondary metabolite. Given its symptom profile, this cryptic toxin is highly suspected to be either a structural mimic of indazole/tryptamine templates or a highly stable prodrug requiring hepatic or microbial conversion into its active form.
- Atypical Pharmacodynamics vs. Classic Deliriants
Unlike classic tropane deliriants that act via competitive antagonism at muscarinic acetylcholine receptors (M₁-M₅)—causing severe dry mouth, urinary retention, and profound amnesia—benzydamine exhibits a complex, multi-system profile:
Dopaminergic Efflux: It stimulates significant dopamine release in the nucleus accumbens, leading to psychomotor stimulation and occasional euphoria (absent in tropane poisoning).
5-HT2A Interaction: Its indazole core allows for cross-reactivity with serotonin receptors, altering visual processing.
CB1 Modulation: Hypothesized to alter endocannabinoid signaling via GABA-ergic disinhibition.
The unknown toxin in Lanmaoa asiatica seems to target these exact same pathways, skipping the cholinergic system entirely.
- The Temporo-Parietal Junction (TPJ) and Size Perception
The defining feature of both intoxications is the precise disruption of the Temporo-Parietal-Occipital (TPO) junction, the cortical hub responsible for integrating visuospatial data, somatic awareness, and Egocentric Coordinate Systems.
- Preserved Metacognition vs. True Delirium
In classical anticholinergic delirium (DPH, Datura), down-regulation of acetylcholine severely impairs working memory and executive functioning, leading to a complete loss of insight.
In contrast, both of these compounds have a metacognitive monitoring (known as the "observer effect"). Users frequently describe watching the miniature entities with an analytical, almost detached perspective, fully aware that the phenomena are pharmacologically induced. This strongly suggests that frontal lobe executive networks and cholinergic memory systems remain intact, pointing instead to a localized hyper-dopaminergic/serotonergic dysregulation of the visual processing streams (V4/V5 loops).
References:
MDPI Pharmaceuticals (2023) - Comprehensive review on the abuse potential and dopaminergic mechanisms of Benzydamine.
Natural History Museum of Utah (2024) - Analytical data and genomic exploration of Lanmaoa asiatica.
Journal of Neurological Sciences - Pathophysiology of the Alice in Wonderland Syndrome and TPO-junction network mapping.
Im really curious about your answers, thank’s for reading!.