Among 6,526 U.S. adults tracked over two decades, telomere length—widely regarded as a cellular aging biomarker—did not mediate the persistent mortality disparities between racial groups. Black Americans with higher education still faced 38% elevated mortality risk compared to similarly educated White Americans, while education provided no mortality protection for Mexican Americans at all. The finding challenges a prominent hypothesis in health disparities research. Telomeres, the protective DNA caps that shorten with age and stress, have been extensively studied as potential biological pathways through which social disadvantage becomes embedded in cellular aging. The mechanism seemed plausible: chronic stress from discrimination and socioeconomic hardship accelerates telomere shortening, which then drives premature mortality. This large-scale analysis definitively rules out that pathway. The results underscore how structural racism operates through biological mechanisms we don't yet understand, making simple biomarker explanations inadequate. For longevity research, this represents a significant negative finding that redirects attention from telomeres toward other molecular pathways linking social determinants to biological aging and mortality risk.