A series of five papers argues that psilocybin primarily functions as a conserved intercellular signaling molecule coordinating growth within mycelial networks, not as a chemical defense. Human psychedelic experiences arise from cross-kingdom receptor compatibility, where fungal signals activate mammalian 5-HT2A receptors, producing coherent fractal visual phenomenology as neural tissue executes an ancient growth instruction. The signaling hypothesis is supported by reclassification of Physarum polycephalum to Amoebozoa, pushing tryptophan-based indole signaling back 1.4–1.6 billion years to the last common ancestor of Amoebozoa and Opisthokonta.
As legal psilocybin services expand, this paper addresses gaps in clinical protocols and mechanistic explanations for psychedelic experiences. A dual-drift model (Mystification Drift and Messiah Drift) with a five-step anchoring protocol is introduced for facilitators managing archetypal responses during integration. The mechanistic hypothesis posits that psilocybin functions as an intercellular signaling molecule within mycelial networks, with human experiences resulting from cross-kingdom receptor compatibility—fungal coordination molecules activating mammalian 5-HT2A receptors through evolutionarily conserved indolamine architecture. Experiences are self-generated but operate under altered constraint regimes, explaining coherence without external information transfer. Testable predictions include temporal precedence, spatial topology mapping, and coordination impairment upon blocking.