Across 466,864 UK Biobank participants followed a median 13.8 years, Fried-phenotype frailty was linked to higher risk of 458 of 536 tracked chronic diseases after Bonferroni correction. Frail adults accumulated new chronic conditions faster than robust peers (β = 0.941 additional conditions per year, 95% CI 0.936-0.946), and pre-frail adults showed a smaller but significant acceleration (β = 0.266). The effect held at zero, one, and two-plus baseline conditions, and across neurodegenerative, metabolic, and psychiatric disease clusters. Frailty's reach looks systemic rather than disease-specific, which fits the view that it marks reduced physiological reserve. The pre-frailty result matters most for prevention: this stage is potentially reversible, and strength training, adequate protein, and treating low mobility are established levers. Even robust-looking adults with no baseline disease showed the pattern, suggesting grip strength, gait speed, and exhaustion deserve attention before diagnoses appear. Limitations are substantial. Frailty was measured once at baseline, UK Biobank skews healthier and more affluent than the general population, and reverse causation or residual confounding (early undiagnosed illness, socioeconomic factors, smoking) can't be excluded from observational data. Hospital-coded diagnoses also miss milder disease. This is a preprint that has not yet been peer reviewed, so estimates may shift. The finding is confirmatory and incremental, extending known frailty-mortality links into a broad disease-accumulation framework, but it does not show that improving frailty slows multimorbidity; trials are needed for that.