How does biological age acceleration mediate the associations of obesity with cardiovascular disease? Evidence from international multi-cohort studies
Authors' conclusion
Biological age acceleration partially mediates the relationship between obesity and incident CVD. This temporal evidence firstly validated the mediation pathway based on international cohorts, emphasizing the importance of addressing biological aging processes in population aged 45-65 years while providing sex-specific obesity intervention strategies to prevent CVD.
Study context
- Population
- Participants aged over 45 years with 3 waves of longitudinal data from China Health and Retirement Longitudinal Study (CHARLS); Klemera-Doubal method-biological age (KDM-BA) developed in China Health and Nutrition Survey (CHNS); validation in UK Biobank and Hongguang Elderly Health Examination Cohort (HEHEC); baseline age 58 (52, 65) years
- Outcome
- Mediation of the associations between obesity indices and incident CVD by biological age acceleration (KDM-BAacc)
- Follow-up
- Median 9.00 years
Methodological detailsinternational multi-cohort, longitudinal, validation in UK Biobank and HEHEC
- International multi-cohort
- Longitudinal
- Validation in UK Biobank and HEHEC
Main finding
As reported in the abstract
KDM-BA acceleration (KDM-BAacc) mediated associations of body mass index (BMI), waist circumference (WC), waist height ratio (WtHR), body roundness index (BRI), chinese visceral adiposity index (CVAI), lipid accumulation product (LAP), TyG-BMI, TyG-WC, TyG-WtHR with cardiovascular disease (CVD); mediation proportions
10.03 to 25.46%
Observational data: associations, not effects.
Further findings
Incident stroke per 1-year increase in KDM-BAacc
- OR
- 1.68 (95% CI 1.35-2.09)
Incident heart disease per 1-year increase in KDM-BAacc
- OR
- 1.35 (95% CI 1.15-1.59)
Incident CVD per 1-year increase in KDM-BAacc
- OR
- 1.44 (95% CI 1.25-1.65)
Original publication
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