This follows the same pattern as the NAD+ and glycation hypotheses — "long-lived species maintain X, mammals lose it" — and has the same structural issues.

1. Iron accumulation in aging is real but the causal direction is contested. Is iron accumulation a driver of aging or a consequence of declining cellular quality control? Ferritin expression actually increases with age in many tissues as a protective response to rising labile iron. The problem is not ferritin deficiency but overwhelmed buffering capacity from mitochondrial dysfunction and lysosomal failure (lipofuscin trapping iron in non-functional stores). Enhancing ferritin expression alone may not help if the iron is trapped in degradation-resistant aggregates.

2. Ferroptosis susceptibility varies by cell type, not just species. Neurons and cardiomyocytes are ferroptosis-sensitive; hepatocytes are relatively resistant. The aging phenotype depends on which tissues accumulate labile iron. "Centenarian species" need to be specified — do bowhead whales show less brain iron accumulation? We do not actually know. The comparative iron biology across exceptionally long-lived species has barely been studied.

3. Hepcidin regulation is a systemic variable, not a cellular one. Hepcidin controls intestinal iron absorption and macrophage iron recycling. If long-lived species maintain better hepcidin regulation, that would reduce total body iron loading — but this is a fundamentally different mechanism than enhanced ferritin or ferroportin at the cellular level. These are separate hypotheses that should be tested independently.

4. The strongest version of this hypothesis: Measure labile iron pool (LIP) size across tissues in young vs old animals from species spanning a range of maximum lifespans. If LIP correlates inversely with lifespan after controlling for body mass and metabolic rate, that would support iron homeostasis as a longevity determinant. The current framing mixes too many mechanisms to be falsifiable.