LSD-Induced Increase of Ising Temperature and Algorithmic Complexity of Brain Dynamics

LSD measurably increases the "temperature" of brain dynamics — and that temperature is a precise statistical physics quantity, not a metaphor.

The paper fits an Ising spin model to fMRI data from 15 people who received LSD or placebo in a crossover design. The Ising model, borrowed from condensed-matter physics, treats each of 90 brain regions as a binary spin (active or inactive) and infers a coupling matrix — how strongly each region's activity is tied to every other's — plus a single temperature parameter per person per condition. Temperature here means exactly what it does in physics: high temperature flattens the energy landscape, so the system wanders more freely through its possible states rather than settling near preferred configurations. LSD raises that temperature by about 3.8% on average (p < 0.0001, Cohen's d = 1.35), a small but statistically robust shift toward greater neural disorder.

Two independent complexity measures — Lempel-Ziv compression and the Block Decomposition Method, both upper-bound estimators of Kolmogorov complexity (the length of the shortest program that could reproduce a signal) — confirm the same direction of change. The catch is that real fMRI time series are short and slowly varying, so the empirical complexity numbers are noisy. The authors' solution is elegant: they use the fitted Ising model to generate synthetic data via Metropolis sampling, then measure complexity on that. The synthetic complexity tracks temperature with near-perfect correlation (r > 0.95), validating the temperature parameter as a reliable proxy for algorithmic complexity even when the raw BOLD signal is too short to measure it directly.

A theoretically important finding is where the brain sits on the phase diagram. The Ising model has a critical point — a temperature at which the system is maximally sensitive and structured, analogous to water at the boiling point. Some theories predict that psychedelics push the brain toward this critical point. The data say the opposite: the resting brain under placebo is already above the critical temperature (supercritical, paramagnetic phase), and LSD pushes it further into disorder, not toward criticality. This is a direct empirical challenge to criticality-seeking accounts of psychedelic action. The paper also finds that the inferred Ising coupling matrix recovers the structural connectome measured by diffusion MRI in a separate cohort (r = 0.60), and that LSD selectively reduces interhemispheric homotopic connectivity by roughly 20%, weakly correlated with cortical serotonin 5-HT₂ₐ receptor density — the primary target of LSD.

The broader significance is methodological as much as pharmacological. The paper establishes a pipeline — binarize BOLD, fit maximum-entropy Ising model, extract personalized temperature, generate synthetic data, measure algorithmic complexity — that turns a coarse neuroimaging signal into a quantitative index of brain disorder grounded in both statistical physics and information theory. That pipeline is the empirical foundation for a larger research program linking consciousness, psychedelics, and algorithmic complexity.