A Dopamine-Serotonin Theory of Consciousness

TL;DR

This paper introduces a mathematical theory of consciousness based on neurochemical interactions, explaining various conscious states and phenomena through dopamine and serotonin regulation, supported by clinical data analysis.

Contribution

It presents a novel neurochemical framework for consciousness, integrating mathematical formalism with clinical data to explain diverse conscious states and paradoxical phenomena.

Findings

Significant interaction between medication and disease severity in Parkinson's patients.

Model's prediction of non-linear, state-dependent neurochemical dynamics.

Explanation of consciousness spectrum from sleep to psychosis.

Abstract

This work presents a comprehensive theory of consciousness grounded in mathematical formalism and supported by clinical data analysis. The framework developed herein demonstrates that consciousness exists as a continuous, non-monotonic function across a high-dimensional neurochemical space, with dopamine serving as the primary intensity regulator and serotonin (5-HT2A) as the complexity modulator. This work offers mechanistic explanations for the full spectrum of conscious states, from deep sleep and psychosis to the ultimate collapse in neural death. The theory explains paradoxical phenomena such as prefrontal cortex hypoactivity during seizures, the evolutionary persistence of psychosis-prone individuals, and why controlled administration of classical 5-HT2A agonists shows a comparatively low incidence of serious medical events (< 0.01 % in modern clinical trials), while dopaminergic excess proves rapidly lethal. The framework is tested using 70,290 sleep nights from 242 Parkinson's disease patients, using disease severity (UPDRS) as a proxy for system integrity and medication (LEDD) as a proxy for dopaminergic input. The analysis reveals a significant LEDD x UPDRS interaction (beta=-1.7, p<.0001), confirming the model's prediction of state-dependent, non-linear dynamics.