Background: The systemic long-term health effects and underlying biological mechanisms of early-life sugar restriction remain poorly defined. Methods: We exploited a natural experiment created by the abrupt end of UK postwar sugar rationing (September 1953), including 60,768 UK Biobank participants born between October 1951 and March 1956. Exposure to early-life sugar restriction was defined by birth date relative to the policy end. We assessed 27 incident disease outcomes and all-cause mortality. In subsets, we performed plasma proteomic and metabolomic profiling, evaluated 81 adult phenotypes, and applied formal mediation analysis. Findings: Of 60,768 participants (mean age 54.6 years; 56.2% female), 38,453 (63.3%) were exposed to early-life sugar restriction. Longer exposure was associated with dose-dependent risk reductions for infections, cancer, mental and behavioural disorders, nervous system, digestive, musculoskeletal, genitourinary, and skin disorders (adjusted HRs 0.83-0.93), and with lower all-cause mortality (adjusted HR 0.79; 95% CI 0.73-0.87). The exposure was associated with a distinct molecular signature and an adult phenotype marked by higher fat-free mass and lower basal metabolic rate, with no difference in BMI. Mediation analyses identified a modest "molecular memory" pathway (3-9% of effect) and a dominant "physiological programming" pathway (4-13% of effect). Interpretation: Sugar restriction in the first 1,000 days programs multisystem resilience that substantially reduces risk of chronic diseases and later-life mortality. This protection operates through a hierarchical biological architecture dominated by a metabolically efficient physiological phenotype, providing mechanistic support for stricter regulation of added sugars in infant foods.