Key result
Direct and parental famine exposure linked to ~4 mmHg greater SBP rise by age 60.
Why the study?
The transgenerational impact of famine on blood pressure trajectories from childhood to adolescence remains poorly understood.
Does famine exposure accelerate blood pressure trajectories in directly exposed individuals and their offspring?
Cohort (n=7,706)
Yes
Does famine exposure accelerate blood pressure trajectories in directly exposed individuals and their offspring?
Famine exposure creates a transgenerational subclinical vascular risk, accelerating blood pressure elevation in directly exposed individuals and their offspring during early adolescence.
Answers are grounded in this paper and cite their sources.
Famine-exposed adolescents may warrant closer BP surveillance; extends prior observations but leaves open causality and clinical translation.
While the transgenerational impact of famine on adult health is well-documented, its impact on blood pressure (BP) trajectories from childhood to adolescence remains poorly understood. We aimed to capture multi-generational BP trajectories and identify the primary drivers of adolescent BP elevation. Utilizing data from the China Health and Nutrition Survey, we analyzed BP trajectories in the F1 ( n = 5,357) and F2 ( n = 2,349) generations. The F1 generation was categorized into 2 groups: famine exposed and non-exposed groups, while the F2 generation was divided into 4 groups: no parental exposure, father-only-exposed, mother-only-exposed, and both-parents-exposed. Linear mixed-effects models and causal mediation analyses were conducted to ascertain BP trajectories and the mediation of parental body mass index (BMI). In the F1 generation, BP of famine-exposed individuals surpassed that of controls after age 40. In the F2 generation, BP trajectory divergence occurred at approximately age 14. By age 18, all exposed groups had significantly higher BP than controls, independent of parental hypertension ( P < 0.01). Notably, the mother-only-exposed group exhibited the highest velocity of BP elevation; however, after excluding offspring with hypertensive parents, the father-only-exposed group exhibited the fastest velocity of BP increase. Mediation analysis revealed that over 85% of this effect was direct, with parental BMI accounting for only 14.51% and 10.08% of the effect for systolic and diastolic BP, respectively. Individuals with direct famine exposure possess higher rate of BP elevation. Furthermore, parental famine exposure programs an accelerated BP velocity in offspring that manifests during early adolescence. These findings suggest that the famine exposure creates a subclinical vascular risk that requires early monitoring, independent of adiposity and hypertension.
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Fanfan Chan (2026) conducted a cohort in Blood pressure trajectories (n=7,706). Famine exposure vs. Non-exposed (born pre-famine 1954-1957 or post-famine 1964-1967) was evaluated on Mean systolic blood pressure change from age 24 to 60 (F1 generation) (p=<0.01). Direct famine exposure accelerated systolic blood pressure elevation by age 60 (27.47 vs 23.01 mmHg increase), and parental exposure programmed faster blood pressure increases in offspring.
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