| Sumario: | Simple Summary: Chemotherapy can cause adverse chemotoxicity, and some patients with colorectal cancer are more vulnerable than others. We aimed to determine whether a person's biological age—how old their body appears based on routine blood tests, rather than their actual age—can help predict who is at higher risk for chemotoxicity. Using blood test data from 1129 colorectal cancer patients, we examined changes in biological aging over six months of chemotherapy, identified its risk factors, and explored how it relates to chemotoxicity. We found that chemotherapy tends to accelerate biological aging, and those with greater age acceleration were more likely to experience chemotoxicity. Accelerated biological aging over time was observed in both younger and older adults and was influenced by social factors, including area-level disparities. Our findings suggest that biological age could serve as a useful tool to identify high-risk patients and support more personalized cancer treatment planning. Background: Biological aging influences cancer outcomes, but its changes during chemotherapy and impact on chemotoxicity in colorectal cancer (CRC) remain underinvestigated. We examined (1) trajectories of biological aging (using Levine Phenotypic Age) during six months of chemotherapy, (2) sociodemographic and clinical risk factors for biological aging, and (3) links between biological aging and chemotoxicity. Methods: Using data from electronic health records (2013–2019) from 1129 adult CRC patients, we computed biological aging (raw Levine Phenotypic Age and its age acceleration [Levine Phenotypic Age–chronological age]) from routine blood tests (e.g., complete blood counts, hepatorenal/inflammatory markers). Chemotoxicity was identified primarily via International Classification of Diseases (ICD-9 and -10) codes. Results: Chemotherapy accelerated biological aging over time. Biological aging at baseline and changes over time predicted chemotoxicity. However, changes in biological aging over time showed stronger associations than baseline biological aging. Advanced cancer stages, higher comorbidity burden, and socioeconomic disadvantage (especially area-level deprivation) were associated with accelerated biological aging at baseline and over time. Biological aging occurred across both young and older adults. Conclusions: Levine Phenotypic Age, computed from routine blood tests in EHRs, offers a feasible clinical tool for aging-related chemotoxicity risk stratification. Validation in diverse cohorts and the development of predictive models are needed.
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