Transferrin is a key iron-transport protein in the blood. Its link to longevity is hypothesized through iron homeostasis: chronically elevated iron levels promote oxidative stress and inflammation, which can accelerate aging. Low transferrin (e.g., in iron deficiency) is associated with anemia and reduced function, also potentially shortening lifespan. Observational studies suggest that balanced iron regulation—neither excess nor deficiency—correlates with healthier aging. However, the evidence is largely correlational, not causal. Genetic variants in the transferrin gene (TF) or related genes (e.g., HFE) can modulate iron absorption, but their effect on lifespan is small and overshadowed by diet, inflammation, and other lifestyle factors. Therefore, transferrin alone is not a reliable longevity biomarker. Consumer DNA tests reporting transferrin-related variants lack clinical context (e.g., ferritin, CRP) and should not be used for health decisions. In summary, transferrin is indirectly linked to aging via iron metabolism, but the evidence is moderate and insufficient for personalized longevity advice.
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