Earth's surface acquired necessary life-giving volatile elements carbon, nitrogen, and sulfur from a collision with a Mercury-like planetary embryo ~ 4.4 billion y ago. Icy comets containing hydrocarbons collided with a cooling prebiotic Earth to create impact reactive environments that via classical anthropic causality introduced primordial "ribozyme-like" RNA complexes which could duplicate a few molecular units/24 hrs. Random classical processes introduced energetically accessible duplex RNA segments containing keto─amino (─NH2) hydrogen bonds, where hydrogen bonded amino protons encountered quantum uncertainty limits, Δx Δpx ≥ ħ/2. This introduced probabilities of EPR-arrangements, ketoamino-(entanglement) → enol−imine, where reduced energy product protons are each shared between two different indistinguishable sets of electron lone-pairs belonging to enol oxygen and imine nitrogen on opposite genome strands. Product protons participate in entangled quantum oscillations at ~4×10 13 s −1 (~ 4800m s −1) between near symmetric energy wells in decoherence-free subspaces until measured, δt << 10 −13 s, in a genome groove, ~12 or 22Å, by selected Grover's quantum bio-processors. Analyses imply entanglement origins of the triplet code, 4 3 codons, specifying ~ 22 L-amino acids. Entanglement resources provided a sequence of ~ 12 incremental entanglement-enabled improvements to genome fitness, of the form: RNA-ribozyme → genetic code origin → RNA-protein → DNA-protein. An EPR-entanglement algorithm explains "probabilistic" genomic growth over the past ~ 3.610 9 y from duplex RNA-ribozyme segments, into a DNA double helix of ~ 6.810 9 bp. Entangled proton "qubit pairs" are the smallest "measurable" genetic informational unit, specifying evolution instructions with "measured" quantum information. This EPR-entanglement model accurately predicts microsatellite evolutionary distributions in rat and human genomes. Consistent with preserving "wild-type" gene pool viability, Huntington's and other age-related human diseases are phenotypically expressed by Grover's quantum processors, measuring quantum informational content of entangled proton qubits occupying a "threshold limit".

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 ~ 3.6x10 9 y-from primordial duplex RNA-ribozyme segments, into a DNA double helix of ~ 6.8x10 9 bp. Homo sapiens' consciousness is thus considered a consequence of ~3.6x10 9 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 termyields assessments that clearly identify EPR-entanglement terms, Σjβj t 4 , as solely responsible for age-related cancer manifestation, but classical contributions-Σi λi t 3 , "passenger mutations"-do not contribute to disease. Conceptual Paper Volume 2 Issue 1