Anthropics of Aluminum-26 Decay and Biological Homochirality

TL;DR

This paper explores the hypothesis that biomolecular homochirality originates from beta decay of aluminum-26, providing new constraints on fundamental particle parameters and suggesting the fine structure constant may be environmentally variable in the multiverse.

Contribution

It offers new constraints on particle masses based on aluminum-26 decay's role in biological homochirality and argues for the fine structure constant as an environmental parameter.

Findings

Aluminum-26 decay could explain biomolecular homochirality.

New tighter constraints on electron and quark masses.

Evidence suggests the fine structure constant varies across the multiverse.

Abstract

Results of recent experiment reinstate feasibility to the hypothesis that biomolecular homochirality originates from beta decay. Coupled with hints that this process occurred extraterrestrially suggests aluminum-26 as the most likely source. If true, then its appropriateness is highly dependent on the half-life and energy of this decay. Demanding that this mechanism hold places new constraints on the anthropically allowed range for multiple parameters, including the electron mass, difference between up and down quark masses, the fine structure constant, and the electroweak scale. These new constraints on particle masses are tighter than those previously found. However, one edge of the allowed region is nearly degenerate with an existing bound, which, using what is termed here as `the principle of noncoincident peril', is argued to be a strong indicator that the fine structure constant must be an environmental parameter in the multiverse.