It's not "every" human brain. It's just "most" human brains.
Be that as it may, you might consider asking Gemini such a question. Of course, answers from AI aren't guaranteed to be accurate, but answers from random posters on Slashdot come with even less of a guarantee.
But here, let me save you the effort by posting Gemini's reply:
While researchers are still isolating the exact chemical compound inside Lanmaoa asiatica—which is unique and unrelated to classical psilocybin "magic mushrooms"—neuroscience and psychiatry offer a fascinating framework for why a chemical can cause such a highly specific, repeatable flaw in human perception.
1. The Disruption of "Size Constancy"
To understand why the people are tiny, we look at a neurological concept called size constancy. Your brain continuously performs complex mathematics to ensure that when a friend walks away from you, you perceive them as moving further away, rather than physically shrinking—even though the actual image hitting your retina is getting smaller. This relies on a highly calibrated feedback loop between the primary visual cortex (V1), which processes raw shapes, and the visual association cortices, which interpret depth, distance, and context. When a toxin disrupts this communication channel, it causes a specific sensory distortion called micropsia. If the brain tries to project an object or a memory into the visual field while the size-constancy machinery is offline, the object defaults to a drastically scaled-down size (often measured at exactly 1 to 2 centimeters by patients).
2. The Brain's "Pareidolia" and Object-Recognition Hardware
Why does the brain specifically manufacture human figures instead of just shrinking the existing room? Human brains possess hyper-specialized, dedicated neural architecture designed to recognize faces and bodies, primarily located in the fusiform face area (FFA) and the extrastriate body area (EBA). This hardware is so sensitive that it causes pareidolia—making us see faces in electrical outlets or burnt toast. When a psychoactive compound overstimulates or uncouples these specific regions, the visual system begins firing "spontaneously." Because these circuits are hardwired exclusively to process human attributes, the hallucination cannot be an abstract geometric pattern. The brain is forced to piece together the chaotic neural static using its strongest, most deeply ingrained template: the human form.
3. The "Release Phenomenon" (Deafferentation)
Lilliputian hallucinations are not exclusive to mushrooms; they are also the hallmark of Charles Bonnet Syndrome (where people losing their eyesight see tiny people) and certain stages of Parkinson’s disease. The leading neurological theory for both is the release phenomenon: Under normal conditions, a steady stream of real-world data from your eyes acts as an "inhibitory" brake, keeping your visual association cortices from running wild. If a toxin suddenly blocks or alters this sensory input, the brain's internal dream-generation software is "released" from its brakes. Left to its own devices, the visual cortex starts pulling random information from memory and projecting it into the physical room. Because the interactive physics engine of the brain is still online, 97% of these hallucinations interact realistically with the environment—marching across actual tables or ducking under tablecloths.
The Neuro-Chemical Frontier: Classical psychedelics like psilocybin primarily bind to serotonin $5\text{-HT}_{2\text{A}}$ receptors, causing geometric distortions and emotional shifts. Because Lanmaoa asiatica causes a clinical syndrome completely distinct from a typical psilocybin trip, scientists believe its active compound targets entirely different pathways—likely involving acetylcholine or gabaergic networks, which directly control attention, reality-monitoring, and visual gating.