Pediatric Research Update: Change in Weight Status from Childhood to Young Adulthood and Risk of Adult Coronary Heart Disease

Each month, the OMA Pediatric Committee reviews a pediatric-focused obesity research update to help keep you up to date about the latest findings. 

Article Summary #

This long-term population study examines how changes in weight from childhood to young adulthood relate to adult coronary heart disease risk, highlighting adolescence as a critical period.

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Article Review

Introduction: Coronary heart disease (CHD) remains the leading cause of death worldwide. Although advances in prevention and treatment have reduced CHD mortality in many high-income countries, recent stagnation and reversals raise concern that rising obesity rates may be undermining these gains. From a developmental origin of health and disease (DOHaD) perspective, excess adiposity during sensitive periods of growth may program long-term cardiometabolic risk. While higher childhood BMI is associated with increased adult CHD risk, it is less clear whether this risk reflects permanent early-life programming or whether normalization of weight during later developmental windows can mitigate adverse outcomes.

The BMI Epidemiology Study (BEST) in Gothenburg, Sweden examined whether changes in weight status from childhood through young adulthood influence adult CHD risk. This question is particularly relevant in pediatric endocrinology, where puberty represents a period of profound hormonal, metabolic, and body composition changes that may modify long-term cardiovascular risk trajectories.

Methods: This population-based cohort study included 103,232 individuals (45,965 women and 57,267 men) born between 1945 and 1968. Height and weight measurements were obtained from archived school health records for childhood (age 7 years for girls and age 8 years for boys) and from conscription records for young adulthood (age 18 years for women and age 20 years for men). Childhood BMI categories were defined using International Obesity Task Force cutoffs, while young adult BMI was classified using standard adult thresholds. Individuals with preexisting CHD or missing anthropometric data were excluded.

Weight trajectories were categorized into four groups: never overweight/obese, overweight in childhood only, overweight in young adulthood only, and persistent overweight/obesity across both periods. Cox proportional hazards models were used to estimate the association between BMI trajectories and adult CHD outcomes, adjusting for age, sex, birth cohort, and demographic factors. Sensitivity analyses were performed to assess the robustness of findings, including models accounting for adult socioeconomic status.

Results: In this cohort, 8.7% of girls and 4.4% of boys were overweight in childhood, while 5.1% of women and 7.7% of men were overweight in young adulthood. Over long-term follow-up, 4,438 men and 1,298 women experienced a first CHD event, and 763 men and 168 women died from CHD.

Childhood and Young Adulthood Overweight, Including Obesity, and the Risk of CHD: Both childhood overweight and young adult overweight/obesity were associated with higher adult CHD risk, though no significant differences were seen between sexes. When analyzed together, only young adult overweight remained significantly linked to CHD, suggesting it is a stronger predictor than childhood overweight.

Changes in Weight Status Between Childhood and Young Adulthood and the Risk of CHD: Individuals who were overweight in childhood but normalized by young adulthood had CHD risk like those who were never overweight, indicating reversibility of risk. In contrast, pubertal onset overweight (normal childhood weight but overweight in young adulthood) and persistent overweight (overweight in both periods) were linked to higher CHD risk, with pubertal onset overweight carrying the highest risk, particularly in men. Findings remained consistent after adjusting for adult socioeconomic status.

BMI Percentile Changes Between Childhood and Young Adulthood and the Risk of CHD: Using BMI percentiles, high childhood BMI that normalized by young adulthood did not increase CHD risk, while high young adult BMI, regardless of childhood BMI, was linked to higher CHD risk. The highest risk was seen in individuals with low childhood BMI who became high BMI in young adulthood. Results were consistent across sexes and using different percentile or clinical overweight cutoffs.

Associations Between Continuous BMI Variables and the Risk of CHD: Pubertal BMI change, but not childhood BMI, was significantly associated with adult CHD risk in both women and men. Each 1-unit increase in pubertal BMI change corresponded to a 9–10% higher risk of CHD events and a 12–18% higher risk of fatal CHD, with consistent linear associations and no interaction with childhood BMI.

Discussion: These findings support a developmental model in which adolescence represents a critical window for cardiometabolic risk programming. While excess adiposity in childhood is associated with later obesity, it does not appear to irreversibly program CHD risk if weight normalizes by young adulthood. In contrast, weight gain during puberty: a period characterized by insulin resistance, changes in body fat distribution, and hormonal shifts may have lasting consequences for cardiovascular health.

These results emphasize the importance of monitoring BMI trajectories rather than relying on single time-point measurements. Puberty may represent a particularly vulnerable period during which excess weight gain confers disproportionate long-term risk, even in children who were previously lean.

Strengths of the study include its large, population-based design, objectively measured BMI across multiple developmental stages, and long-term follow-up using national health registries. Limitations include its observational nature, limited data on lifestyle factors such as diet and physical activity, and reduced generalizability beyond predominantly European populations.

Conclusion: This study provides compelling evidence that the cardiovascular risks associated with childhood overweight are not fixed and may be mitigated through normalization of weight by young adulthood. Conversely, excess weight gain during puberty appears to play a critical role in shaping adult CHD risk. These findings underscore the importance of early identification and intervention during key developmental windows, particularly adolescence, to reduce long-term cardiovascular disease risk.