Analysis of 433,911 UK Biobank participants reveals that biological age acceleration—measured through PhenoAge and KDM-BA biomarkers—significantly accelerates the progression from single cardiovascular-kidney-metabolic diseases to multimorbidity, dementia, and death. Individuals with accelerated biological aging showed 24% higher risk of developing their first cardiovascular-metabolic condition and 20% increased risk of progressing to multimorbidity. The acceleration shortened disease-free time by 1.09 years and reduced multimorbidity-free survival by an additional 1.75 years. This represents a compelling validation of biological age as a clinical predictor beyond chronological age. The finding bridges two critical gaps in aging research: quantifying how cellular aging drives disease cascades and establishing timeframes for intervention windows. The multistate modeling approach provides unprecedented granularity in tracking disease progression patterns. However, this preprint awaits peer review, and results may change upon scrutiny. The observational design cannot establish causality—biological age acceleration might reflect existing subclinical disease rather than driving progression. Despite these limitations, the consistency across two different aging biomarkers and the large cohort size suggest biological age assessment could revolutionize personalized prevention strategies for middle-aged adults.