A 1-year increase in is associated with a 68% increased risk of incident stroke.
Obesity, biological age acceleration, and cardiovascular disease are significantly linked.
The risk of heart disease increases by 35% with each 1-year increase in biological age acceleration.
Biological age acceleration mediates the relationship between various obesity measurements and cardiovascular disease.
Mediation proportions for these associations range from 10.03% to 25.46%.
Significant mediation effects were mostly observed in individuals aged 45-65 years.
Sex differences were noted, with mediation mechanisms varying between males and females.
Simplified
BACKGROUND: Recent basic biological research found that obesity accelerates biological aging and increases cardiovascular disease (CVD) risk. However, there is still a lack of real-world population evidence. This study aimed to explore the potential mediation roles of in the associations between different dimensions of obesity characterization and incident CVD.
METHODS: This international multi-cohort study included participants aged over 45 years with 3 waves longitudinal data from China Health and Retirement Longitudinal Study (CHARLS). China Health and Nutrition Survey (CHNS) was used to develop Klemera-Doubal method-biological age (KDM-BA), and the validation analysis was performed in UK Biobank (UKB) and Hongguang Elderly Health Examination Cohort (HEHEC). including body mass index (BMI), waist circumference (WC), waist height ratio (WtHR), body roundness index (BRI) for body shape; Chinese visceral adiposity index (CVAI), lipid accumulation product (LAP) for visceral fat accumulation; triglyceride-glucose index (TyG) and its derivatives (TyG-BMI, TyG-WC, TyG-WtHR) for metabolic function were used to measure obesity across different dimensions. Biological age acceleration was evaluated by the classic KDM-BA acceleration (KDM-BAacc). Causal mediation analyses assessed the role of biological age acceleration in mediating obesity and incident CVD.
RESULTS: In CHARLS, the median follow-up period was 9.00 years, with a baseline age of 58 (52, 65) years. Obesity, KDM-BAacc, and CVD were all significantly associated with each other. For each 1-year increase in KDM-BAacc, the risk of incident stroke, heart disease and CVD increased by 68% (OR 1.68, 95% CI 1.35-2.09), 35% (OR 1.35, 95% CI 1.15-1.59), and 44% (OR 1.44, 95% CI 1.25-1.65), respectively. KDM-BAacc mediated the associations between BMI, WC, WtHR, BRI, CVAI, LAP, TyG-BMI, TyG-WC, TyG-WtHR, with CVD, with the mediation proportions ranging from 10.03 to 25.46%. However, the mediating effect was significant mostly in middle-aged individuals aged 45-65 years. Furthermore, sex differences existed in the mediation mechanisms. Biological age acceleration strongly mediated body shape indices and incident CVD in males, whereas in females, it predominantly mediated visceral fat accumulation and metabolic function dimensions with incident CVD. Similar main results were found in UKB and HEHEC.
CONCLUSIONS: 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.
Key numbers
1.68
Increase in Stroke Risk
Odds Ratio for stroke per 1-year increase in
1.35
Increase in Heart Disease Risk
Odds Ratio for heart disease per 1-year increase in
1.44
CVD Risk Increase
Odds Ratio for cardiovascular disease per 1-year increase in
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