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Risks of myocardial infarction, stroke, heart failure, and other debilitating cardiovascular diseases may be directly influenced by adolescent sugar intake.
Restricted sugar intake during childhood is correlated to reduced risks of myocardial infarction, stroke, and heart failure, according to recent research.1
Several prior trials have spotlighted the first 1000 days as a critical period for biological susceptibility, during which dietary patterns, pathogenic exposures, and socioeconomic conditions, among other conditions, exert a significant and lasting effect on predisposition to disease. Nutritional interventions during this period also show greater cost efficiency and long-term health benefits than managing non-communicable diseases in adulthood.2
“We hypothesized that sugar rationing during the first 1000 days reduced the risks of cardiovascular outcomes and delayed their onset and that longer durations of constrained exposure provided progressively greater protection,” wrote Jiazhen Zheng, a doctoral student at the Bioscience and Biomedical Engineering Thrust at the Hong Kong University of Science and Technology, and colleagues. “Additionally, we incorporated cardiac magnetic resonance imaging indices to explore subclinical cardiac alterations.”1
The team analyzed data from the end of UK sugar rationing in 1953, which they noted as triggering a significant increase in sugar consumption without affecting other food types. Participants were drawn from the UK Biobank born between October 1951 and March 1956. The first 1000 days after conception were specifically highlighted, using exposure to national sugar rationing policies as a proxy for sugar intake in early life. This allowed the team to compare adults exposed to sugar rationing early in life to those who were not.2
Of the 74,213 UK Biobank participants born within the study’s timeframe, 10,616 were excluded due to prevalent cardiovascular disease, heart failure, or atrial fibrillation (n = 1612), being born outside of the UK (n = 6540), being from multiple births (n = 2398), or being adopted (n = 66). After an additional 164 patients withdrew, 63,433 participants remained for analysis. Of these, 40,063 had been exposed to sugar rationing and 23,370 had not.2
Patients then participated in a questionnaire collecting variables including gender, age, ethnicity, education level, smoking, alcohol consumption, physical activity, and other key factors. Participants were classified as having hypertension if they used antihypertensive drugs, had a systolic blood pressure >140 mm Hg, diastolic blood pressure >90 mm Hg, or self-reported hypertension. High cholesterol was defined by self-reported diagnosis, the use of lipid-lowering drugs, or a serum total cholesterol concentration ≥200 mg/dL.2
Primary outcomes for the study included incident cardiovascular disease, myocardial infarction, heart failure, atrial fibrillation, stroke, and cardiovascular disease mortality, determined via linked health records. Cox and parametric hazard models were used to determine hazard ratios, adjusted for demographic, socioeconomic, lifestyle, parental health, and genetic factors.2
The hazard ratio for cardiovascular disease was 0.89 (95% CI, 0.82-0.97) for exposure in utero only, 0.86 (95% CI, 0.79-0.95) for in utero plus 1 year, and 0.8 (95% CI, 0.73-0.9) for in utero plus 2 years (P <.001). Risk in the utero plus 2 group was reduced for myocardial infarction (HR, 0.75; 95% CI, 0.63-0.9), heart failure (HR, 0.74; 95% CI, 0.59-0.95), atrial fibrillation (HR, 0.76; 95% CI, 0.66-0.92), stroke (HR, 0.69; 95% CI, 0.53-0.89), and cardiovascular disease mortality (HR, 0.73; 95% CI, 0.54-0.98).2
Additionally, patients exposure to rationing in utero exhibited progressively longer delays in age of onset for cardiovascular outcomes versus those not exposed to rationing. The delay increased from 0.98 (95% CI, 0.66-1.3) years for in utero exposure to 2.53 (95% CI, 2.25-2.81) years for in utero exposure plus 2 years. This trend was repeated across the various outcomes, with investigators finding the longest delay in age of onset observed in heart failure (2.96; 95% CI, 2.43-3.49 years) in people exposed in utero plus 2 years.2
Although the study is observational in nature and no conclusive statements can be made regarding causation, Zheng and colleagues also acknowledge that this study allowed them to assess the effects of different exposure periods and explore the pathways that may be linking sugar rationing and cardiovascular outcomes.1
“Our results underscore the cardiac benefit of early life policies focused on sugar rationing,” Zheng and colleagues wrote. “Further studies should investigate individual level dietary exposures and consider the interplay between genetic, environmental, and lifestyle factors to develop more personalized prevention strategies.”1