Why We Age: Entropy from Space

Human lives differ enormously in genes, environments and histories, yet deaths cluster tightly in age. A random failure process with the observed median would leave one person in ten alive at 269 years; real populations reach this point at about 93 to 95. Aged heart, muscle and brain show the same pattern: sparse failing cells, each dominated by its own mitochondrial DNA deletion. Radiaging proposes that Earth’s background ionizing radiation is the primary physical cause of normal aging in complex life. Every aging experiment has run inside this field, so untreated controls cannot show independence from it. Radiation acts through two pathways. In the Seed Path, a rare radiation-induced deletion of mitochondrial DNA escapes repair and expands over years until its cell loses respiratory function. In the Tax Path, radiation chemistry displaces the electronic state of respiratory cofactors: an iron-sulfur cluster gains an electron or shifts its bond lengths by hundredths of an ångström, and usable energy falls. Incomplete recovery leaves a lasting deficit, the Recovery Debt. In renewing tissue, a Lineage Relay carries retained states into new generations of cells. Mean dose is the wrong measure: over eighty years, about a thousand cosmic-ray muons cross each heart cell, and the geometry of each track decides whether damage is removed or retained. Shielding works in the laboratory and in nature: shielded organisms live longer and lose that gain when a radiation source returns, and within fish lineages longevity rises with ocean depth. A decisive lifetime experiment could refute Radiaging. Files Why_We_Age_preprint_2026-10-12e.pdf: main text Why_We_Age_Supplementary_Notes_2026-10-11d.pdf: Supplementary Notes S1–S4 Why_We_Age_Supplement_Code.zip: Python scripts (standard library only) reproducing the calculations of Supplementary Note S4; see S4.8 Why_We_Age_Figures.zip: Figures 1–11 at full resolution Why_We_Age_graphical_abstract.png: graphical abstract Correspondence: [email protected]

Authors

Publication Details

Journal
Zenodo (CERN European Organization for Nuclear Research)
Published
2026-10-13
DOI
https://doi.org/10.5281/zenodo.23335814
Primary Topic
Genetics, Aging, and Longevity in Model Organisms
Type
preprint
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preprint

Why We Age: Entropy from Space

Homib Mebrahtu
Zenodo (CERN European Organization for Nuclear Research)
Genetics, Aging, and Longevity in Model Organisms
preprint

Why We Age: Entropy from Space

Homib Mebrahtu
preprint en

Abstract

Human lives differ enormously in genes, environments and histories, yet deaths cluster tightly in age. A random failure process with the observed median would leave one person in ten alive at 269 years; real populations reach this point at about 93 to 95. Aged heart, muscle and brain show the same pattern: sparse failing cells, each dominated by its own mitochondrial DNA deletion. Radiaging proposes that Earth’s background ionizing radiation is the primary physical cause of normal aging in complex life. Every aging experiment has run inside this field, so untreated controls cannot show independence from it. Radiation acts through two pathways. In the Seed Path, a rare radiation-induced deletion of mitochondrial DNA escapes repair and expands over years until its cell loses respiratory function. In the Tax Path, radiation chemistry displaces the electronic state of respiratory cofactors: an iron-sulfur cluster gains an electron or shifts its bond lengths by hundredths of an ångström, and usable energy falls. Incomplete recovery leaves a lasting deficit, the Recovery Debt. In renewing tissue, a Lineage Relay carries retained states into new generations of cells. Mean dose is the wrong measure: over eighty years, about a thousand cosmic-ray muons cross each heart cell, and the geometry of each track decides whether damage is removed or retained. Shielding works in the laboratory and in nature: shielded organisms live longer and lose that gain when a radiation source returns, and within fish lineages longevity rises with ocean depth. A decisive lifetime experiment could refute Radiaging. Files Why_We_Age_preprint_2026-10-12e.pdf: main text Why_We_Age_Supplementary_Notes_2026-10-11d.pdf: Supplementary Notes S1–S4 Why_We_Age_Supplement_Code.zip: Python scripts (standard library only) reproducing the calculations of Supplementary Note S4; see S4.8 Why_We_Age_Figures.zip: Figures 1–11 at full resolution Why_We_Age_graphical_abstract.png: graphical abstract Correspondence: [email protected]

Zenodo (CERN European Organization for Nuclear Research)
Genetics, Aging, and Longevity in Model Organisms
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