Key result
Dual parental obesity is linked to an ~4-fold higher risk of offspring obesity.
Why the study?
Evidence regarding the association of parental obesity with longitudinal cardiometabolic disease progression in offspring remains limited.
Does parental obesity increase the risk of adverse cardiometabolic trajectories and incident obesity or hypertension in offspring from childhood to adulthood?
Cohort (n=4,982)
Yes
Does parental obesity increase the risk of adverse cardiometabolic trajectories and incident obesity or hypertension in offspring from childhood to adulthood?
Hazard Ratio: 3.72 (95% CI 1.73–7.99)
Parental obesity, particularly when both parents are affected, is strongly associated with higher baseline cardiometabolic risk and substantially higher risk of incident obesity in offspring from childhood to adulthood.
May guide family-based monitoring of at-risk offspring; leaves open causal effects on hypertension and intervention impact.
Objectives Parental obesity is a strong risk factor for childhood adiposity. However, evidence regarding its association with longitudinal cardiometabolic disease progression in offspring remains limited. We aimed to examine whether parental obesity is associated with adverse cardiometabolic trajectories in offspring from childhood to adulthood. Methods We analyzed prospective data from the China Health and Nutrition Survey (1989–2015). Offspring aged ≥2 years were categorized according to parental overweight/obesity status: neither parent affected (Group 1, reference), only father affected (Group 2), only mother affected (Group 3), and both parents affected (Group 4). We used linear mixed-effects models with polynomial age terms to estimate longitudinal trajectories and annual changes in body mass index, waist circumference, and blood pressure. Cox proportional hazards models were used to assess hazard ratios for incident overweight/obesity, central obesity, and hypertension. Results Among 4,982 offspring, those with both parents affected (group 4) had the highest baseline levels; however, annual rates of increase were not consistently higher. Male offspring in group 4 had the highest risks for incident overweight/obesity (HR = 3.72; 95% CI, 1.73–7.99) and central obesity (HR = 2.46; 95% CI, 1.31–4.62); the association with hypertension was elevated but did not reach statistical significance (HR = 1.55; 95% CI, 0.86–2.77). Female offspring in group 4 had the highest risk for incident overweight/obesity (HR = 4.60; 95% CI, 1.93–10.94). Formal interaction tests for sex × parental obesity were not significant for any outcome (all P interaction > 0.05). Conclusions Parental obesity, particularly when both parents are affected, is associated with higher baseline cardiometabolic risk levels and substantially higher disease risk in offspring, though the annual rates of increase do not consistently differ across groups. These findings underscore the family unit as a critical target for early preventive strategies.
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Qian et al. (2026) conducted a cohort in Cardiometabolic trajectories (overweight/obesity, central obesity, hypertension) (n=4,982). Parental obesity (both parents affected) vs. Neither parent affected (normal weight) was evaluated on Incident overweight/obesity in male offspring (HR 3.72, 95% CI 1.73-7.99). Having both parents affected by obesity substantially increased the risk of incident overweight/obesity in offspring, with hazard ratios of 3.72 in males and 4.60 in females compared to having neither parent affected.
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