Entanglement-Enabled Information Processing Implies Human Consciousness Mechanism

Quantum information processing of EPR-generated entangled proton qubits exhibited by rat and human genomes falsifies the in vivo anti-entanglement hypothesis. An EPR-entangled proton qubit algorithm explains “probabilistic” genomic growth ― over the past ~ 3.6x109 y ― from primordial duplex RNA–ribozyme segments, into a DNA double helix of ~ 6.8x109 bp. Homo sapiens' consciousness is thus considered a consequence of ~3.6x109 y of entanglement-enabled evolution. The evolved human brain acquired sensory “biological files” for vision, acoustics, vocal, olfactory, touch, taste, balance, self-motion, pain, emotion, language, analytical, music, imagination, “truth” and “fantasy”. Sensory files are interfaced with, initially vacant, “hard drive” memory files that acquire input data from one or all sensory files. Each “new” experience (stimulus) generates input for “hard drive” memory. This stimulus creates an entanglement state between the “measured”, entangled groove-proton “qubit-pair” and Grover's enzyme quantum processor , which executes quantum information processing , Δt́≤ 10‒14 s, before proton decoherence, τD < 10‒13 s. The sequence of acquired input events, e.g., successfully riding a bicycle, is “permanently” stored. When EPR-generated entangled proton qubit-pairs populate DNA sequences not evolutionarily selected for normal quantum information processing in neurological cells, heritable neurological diseases ― e.g., Huntington's disease and congenital myotonic dystrophy ― are exhibited, thereby protecting the gene pool against evolutionary extinction. Anesthetics inhibit Grover's quantum-reader enzyme from quantifying quantum informational content within EPR-generated entangled proton qubits. This absence of quantum information processing instructions disallows normal consciousness, yielding unconsciousness. Significance of entanglement is illustrated by age-related cancer data (ages 10 to 80 y). “Accurate” evaluation by a “corrected” Muller's constant “mutational load” expression, i.e., dN/dt = λ + βt – where βt (β ≈ 2.2x10–23 s –2) is an EPR-entanglement term – yields assessments that clearly identify EPR-entanglement terms, Σjβj t 4, as solely responsible for age-related cancer manifestation, but classical contributions – Σi λi t3, “passenger mutations” – do not contribute to disease.