Early-life sugar restriction causally reduces adult cancer incidence and slows biological aging.

Abstract

Excess sugar consumption is implicated in multiple cancers through insulin resistance, chronic inflammation, and metabolic reprogramming, yet whether early-life sugar exposure causally shapes long-term cancer risk remains an open question. We exploit the abrupt end of United Kingdom sugar rationing in September 1953 as a natural experiment, analyzing 64,761 UK Biobank participants born 1951-1956. Cohorts whose first 1,000 d of life fell under rationing exhibit dose-dependent reductions in adult cancer incidence: liver/intrahepatic bile duct (IHBD) (hazard ratio 0.31), rectum (HR 0.60), lung (HR 0.59), prostate (HR 0.48), and breast (HR 0.64). We uncover two pathways through which this early-life exposure propagates across the life course. First, a behavioral pathway: Rationed cohorts consume less sugar, eat smaller quantities, and maintain healthier, more diverse diets five decades later, consistent with persistent taste preferences shaped during a critical developmental window. Second, a biological pathway: Rationed cohorts exhibit longer leukocyte telomere length ([Formula: see text]0.05 SD, approximately 2.2 fewer years of biological aging) and lower Granzyme B, indicating reduced chronic immune activation. These findings provide causal evidence linking early-life sugar intake to cancer and identify a behavioral pathway, consistent with persistent taste preferences, through which early nutritional environments may shape lifelong disease risk. The results carry direct implications for early-life nutrition and added-sugar policy.