All of the information on this site was intuited through self-observation and inference from the cascade of drugs the doctors gave me. The science seems to line up, but I need real researchers.
Summary
We propose an active-inference framework for meditative “jhāna” progression and nibbāna as a sequence of precision-modulation events that destabilize maladaptive high-level priors, open a reconsolidation window for alternative generative models, consolidate embodied priors, transiently suppress hierarchical prediction-error signalling, and finally re-establish a reorganized attractor with reduced self-centric prior precision. Mechanistically, this hypothesis predicts a characteristic neuromodulatory trajectory—early phasic NE/DA-marked salience and high prediction-error variance, followed by rising tonic dopaminergic precision supporting policy consolidation, transient attenuation of phasic signalling during a non-narrative attractor, and resumed low-self-referential phasic responses after integration—mediated in concert with serotonergic and cholinergic modulation. Testable outcomes include time-locked changes in EEG variance and event-related potentials, pupil/LC-fMRI signatures of noradrenergic engagement, PET markers of tonic DA shifts, altered DMN–corticostriatal functional connectivity, and enhanced behavioural flexibility and fear-extinction after REM-mediated consolidation. This model yields falsifiable predictions and an empirical program combining neurophysiology, neurochemistry, sleep metrics, and behavioural assays to evaluate whether meditation-induced state transitions correspond to precision reweighting and attractor restructuring as described by active-inference.
Below I map each phase to core predictive-processing concepts (priors, prediction errors, precision weighting, policy selection, hierarchical message passing) and indicate plausible neuromodulatory roles, testable predictions, and simple operational markers you could use in experiments or self-tracking. I keep language provisional — these are plausible mappings, not claims of proof.
Summary:
Phase 1–2 = destabilisation + reconsolidation window.
Phase 3 = consolidation and embodiment of new priors.
Phase 4 = global attractor collapse, seizure-risk stage, suspension of predictive coding.
Phase 5 = reorganisation into a new attractor basin, potentially transformative.
Phenomenology: Heightened awareness of intrusive or maladaptive thoughts (“demons”), experienced as emotionally salient but not yet integrated.
Neural dynamics: Existing high-level priors (self-narratives) lose precision, allowing suppressed or trauma-related memory traces to generate strong prediction errors (PEs).
Neuromodulation: Norepinephrine surges (locus coeruleus activation) heighten salience and arousal; dopamine phasic bursts mark unexpected signals. Tonic dopamine is low, so phasic spikes dominate.
Functional role: Destabilisation of entrenched models; exposure of latent maladaptive priors.
Clinical parallel: Mindfulness-based CBT (observe without engaging; cognitive defusion).
Phenomenology: Strong affect (rapture, desire for release); sense of possible transformation.
Neural dynamics: Candidate new priors are sampled to re-explain previously destabilising PEs. Higher-level models increase in precision, but lower-level error signals remain accessible.
Neuromodulation: Rising tonic dopamine strengthens stability of candidate narratives; serotonin increases to modulate affective tone and safety signalling; norepinephrine drops as vigilance reduces.
Functional role: Window for updating maladaptive priors; memory reconsolidation processes active.
Clinical parallel: Acceptance and Commitment Therapy (allowing thoughts/feelings to unfold without suppression, building new meaning frameworks).
Phenomenology: Reduced volatility of thought; stable equanimity; somatic awareness takes precedence over narrative.
Neural dynamics: Updated priors consolidate into higher levels; prediction errors from previously intrusive sources are down-weighted. Interoceptive and somatosensory channels become dominant evidence sources.
Neuromodulation: Tonic dopamine high (stable motivational baseline); phasic bursts suppressed; serotonin supports affective stability; parasympathetic tone increases.
Functional role: Embodiment of new priors; consolidation of updated generative model.
Clinical parallel: Somatic Experiencing and related body-based trauma therapies.
Fork: For many practitioners, this equanimity stage plus REM sleep re-encoding suffices (“A&P”). In rare cases, additional destabilisation occurs (toward full attractor collapse).
Phenomenology: Timeless stillness; absence of thought chain; “non-moment” experience.
Neural dynamics: Hierarchical message-passing attenuates across multiple levels; prediction errors approach near-zero because high-level priors temporarily over-explain all input. Temporal encoding collapses due to lack of phasic fluctuation. The generative model effectively “goes offline.”
Neuromodulation: Maximal tonic dopamine; phasic signalling minimal; serotonin stabilising; norepinephrine very low.
Functional role: Global attractor collapse — the system suspends ongoing generative activity.
Risk: If inhibitory balance is exceeded, the collapse may manifest as seizure-like paroxysmal activity. This is consistent with rare reports of seizure coinciding with breakthrough experiences.
Clinical parallel: None exact; shares features with deep meditative absorption, certain psychedelic states, and temporal lobe seizure phenomenology.
Phenomenology: Sudden reconstitution of consciousness; bliss, equanimity, absence of self-referential fixation. The sense of “a new baseline.”
Neural dynamics: Following attractor collapse, the system re-stabilises into a novel attractor basin with reorganised priors. Prediction errors return, but their self-referential weighting is reduced. Hierarchical precision assignments are redistributed, weakening the grip of previous maladaptive priors.
Neuromodulation: Post-collapse, phasic signalling resumes but on a reorganised tonic baseline. The balance of dopamine, serotonin, and GABA/glutamate shifts toward more flexible regulation. Endogenous opioids and oxytocin may contribute to bliss and affiliative affect.
Functional role: Network reset; durable reprogramming of generative model; new attractor configuration.
Clinical parallel: No direct analogue. Shares features with reports of mystical experience, spontaneous remission of trauma symptoms, or transformative psychedelic therapy outcomes.