Transferrin is the primary iron-transport protein in blood. Its role in longevity is indirect but mechanistically plausible: iron is essential for many enzymes, yet excess free iron drives oxidative stress and cellular damage—key drivers of aging. Low transferrin levels (high iron saturation) are epidemiologically linked to increased mortality and age-related diseases such as cardiovascular disease, neurodegeneration, and cancer. Conversely, moderate iron restriction (e.g., via phlebotomy or diet) extends lifespan in animal models. However, transferrin is not a validated direct longevity biomarker in clinical practice. Evidence comes from observational studies and mechanistic research, not from large-scale human intervention trials. Genetic variants in the transferrin gene (e.g., TF C2) have been studied for iron status but lack proven predictive value for individual longevity. For personalized iron management, measuring ferritin, transferrin saturation, and inflammatory markers (CRP) is more actionable. In summary, transferrin is a relevant piece of the iron–aging puzzle, but its standalone role in human longevity remains moderate and mechanistic.
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