Early Life Sugar Rationing Correlates with Better Later Life Health and Slowed Aging in Humans
Rationing of sugar in the United Kingdom in the years immediately following the Second World War forms a natural experiment in the long term effects of changes in human nutrition that can be explored in great detail given the establishment of the UK Biobank. Researchers here show that lower sugar intake in early life correlates with improved later life health, reduced biological age measures, and reduced mortality. A number of other natural experiments around the time of the Second World War have been used to explore the effects of calorie restriction in early life, but this particular episode of rationing is a way to separate lower sugar intake from overall calorie restriction; it is interesting to see positive results.
Excessive intake of free or added sugars is strongly linked to childhood dental caries and is also associated with higher risks of incident obesity, type 2 diabetes (T2D), cardiovascular disease (CVD), obesity-related cancers, and dementia in adulthood. Britain's post-World War II sugar rationing provides a unique natural experiment. Unlike famine, rationing constrained access to added sugars without broad caloric deprivation, offering a rare opportunity to isolate the long-term impact of early-life sugar reduction to determine the impact on a variety of ageing-related outcomes.
Exposure to sugar rationing during the first 1,000 days of life is associated with a 9% lower incidence of hallmark-related disease, with a hazard ratio of 0.91, and a 19% lower risk of all-cause mortality. Mediation analysis indicates that the survival association is statistically mediated, by approximately 60%, through differences in incident hallmark-related disease. Rationed individuals show 1.0-1.2-year younger biological ages across multiple clocks and lower organ ages, particularly in the lung, heart, and liver. Proteomic profiling identifies 47 altered proteins, with enrichment of adenosine monophosphate-activated protein kinase (AMPK) and longevity pathways and suppression of mechanistic target of rapamycin (mTOR) signaling.