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

| Source: PNAS

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

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 ( + 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.

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