The research drew on one of the world’s most remarkable longitudinal resources, the Copenhagen School Health Records Register. For decades, school physicians in Copenhagen measured the height and weight of virtually every schoolchild in the city, creating a meticulously preserved archive of childhood body size. The investigators harnessed this register to follow 66,906 females and 71,479 males born between 1952 and 1996, all of whom had weight and height measurements recorded between the ages of 6 and 15 years. By linking these childhood records to Danish national registers of hospital diagnoses and causes of death, the team could track which individuals later developed coronary heart disease, defined as diagnoses occurring at age 25 or beyond.

A central methodological strength of the study lies in how it characterized childhood growth. Rather than relying on a single measurement at one age, the researchers used latent class trajectory modelling, a statistical technique that identifies groups of individuals who share similar patterns of change over time. Five sex-specific childhood BMI trajectories emerged from the data, ranging from trajectories that remained within the lower average range to those tracking toward overweight and obesity. This approach captures the dynamics of growth, recognizing that a child whose BMI climbs steadily through the school years may carry a different cardiovascular risk profile than a child whose BMI stays stable, even if their measurements at any single age look similar.

During the follow-up period, 1,642 females and 3,456 males were diagnosed with coronary heart disease. The team then asked a question that had never been answered at this scale: does a parental history of cardiovascular disease modify the relationship between childhood BMI trajectories and early-onset heart disease? Family history is a well-established risk factor in its own right, and previous studies have shown that offspring of parents with cardiovascular disease face higher risks themselves. It was plausible that inherited or shared familial factors might amplify the harm of excess childhood adiposity, or alternatively that a strong family history might dominate risk to the point of overshadowing childhood body size.

The answer was a clear and somewhat surprising negative. Parental cardiovascular disease did not modify the associations between childhood BMI trajectory and later coronary heart disease. In other words, the increased risk conveyed by an overweight or obese childhood trajectory operated independently of whether a child’s parents had experienced heart disease. This statistical independence carries an important clinical message: a child with no family history of cardiovascular disease who follows an obese BMI trajectory is not protected from the cardiovascular consequences of childhood obesity. Excess adiposity in childhood appears to be a risk factor in its own right, not merely a marker that matters only in genetically susceptible families.

The magnitude of the associations was substantial. In models adjusted for parental cardiovascular disease, and compared with children following the average BMI trajectory, females on the overweight trajectory had a 65 percent higher hazard of coronary heart disease at ages 25 to 44 years, with a hazard ratio of 1.65 and a 95 percent confidence interval of 1.21 to 2.26. Females on the obesity trajectory fared worse still, with a hazard ratio of 2.28, meaning their hazard of early-onset disease was more than doubled. The corresponding estimates for males were strikingly similar: 1.70 for the overweight trajectory and 2.23 for the obesity trajectory, both statistically significant. These are large effects for a risk factor measurable in childhood, decades before any symptoms appear.

The age-stratified analysis revealed a pattern with real biological and public health significance. The elevated hazards were concentrated in the youngest age bands. Among both sexes, associations were strongest and clearest at ages 25 to 44 years. Among males, the associations remained evident at ages 45 to 54 years, but by age 55 and beyond, no associations between childhood BMI trajectory and coronary heart disease were found in either sex. This fading of the signal at older ages likely reflects the interplay of competing risks and the accumulation of other exposures across the life course. As people age, smoking, hypertension, diabetes, and adult weight change increasingly shape coronary risk, and the predictive power of childhood body size diminishes relative to these later-life factors. The finding underscores that childhood adiposity is a particularly potent driver of the early-onset form of the disease, precisely the form that is rising and that strikes people in the prime of working and family life.

The study’s conclusions land at a moment of global alarm over early-onset cardiovascular disease. Worldwide analyses have documented that cardiovascular disease remains the leading cause of death, and that rates of heart disease in younger adults have been climbing in many countries. At the same time, childhood obesity has surged: pooled analyses covering 222 million children and adolescents show that obesity has risen sharply since 1990, and in the United States the prevalence of obesity among children aged 2 to 19 has continued to increase through 2023. The Danish findings suggest these two trends are connected. If excess childhood adiposity more than doubles the hazard of coronary heart disease before middle age, then the current generation of children growing up with obesity may face a future wave of heart attacks and other coronary events occurring decades earlier than in their parents’ generation.

Mechanistically, the evidence that childhood obesity leaves lasting cardiovascular fingerprints is not new. Autopsy studies from the Bogalusa Heart Study, conducted decades ago, revealed fatty streaks and early atherosclerotic plaques in the coronary arteries of children and young adults, demonstrating that atherosclerosis begins in childhood. Subsequent cohort studies have linked childhood and adolescent BMI to cardiovascular mortality in midlife, to atrial fibrillation, to ischemic stroke, and to type 2 diabetes and obesity-related cancers. What the new study adds is the demonstration that this childhood risk is not contingent on family history. Children with obese BMI trajectories carry their risk with them regardless of the cardiovascular health of their parents, which strengthens the argument that childhood body size is an independent, modifiable determinant of lifelong cardiovascular health.

The public health implications are difficult to overstate. Clinical risk assessment has traditionally focused on middle-aged and older adults, and family history is often used to decide which younger patients deserve closer scrutiny. These results suggest that childhood BMI deserves a place in that conversation, and that prevention efforts aimed at childhood obesity are, in effect, coronary prevention campaigns with a lead time of several decades. Because the associations were independent of parental cardiovascular disease, interventions need not be targeted only at children with a family history; the entire population of children on elevated BMI trajectories stands to benefit. The authors emphasize that their findings highlight excess childhood adiposity as an important contributor to the early origins of coronary heart disease and reinforce the urgency of addressing the growing burden of childhood obesity. With early-onset cardiovascular disease on the rise worldwide, the trajectory a child’s BMI follows between the ages of 6 and 15 may quietly help determine whether that child, as an adult, becomes one of the growing number of people struck by heart disease in the prime of life.

Subject of Research: Childhood BMI trajectories and early-onset coronary heart disease risk

Article Title: Are associations of childhood body mass index trajectories with early-onset coronary heart disease modified by parental history of cardiovascular disease?

Article References: Aarestrup, J., Andersen, E. W., Twig, G., Jacobsen, R. K., Johnson, W., Bjerregaard, L. G., & Baker, J. L. (2026). Are associations of childhood body mass index trajectories with early-onset coronary heart disease modified by parental history of cardiovascular disease?. International Journal of Obesity. https://doi.org/10.1038/s41366-026-02239-4

Image Credits: AI Generated

DOI: 10.1038/s41366-026-02239-4

Keywords: childhood obesity, body mass index, coronary heart disease, early-onset cardiovascular disease, parental history, Copenhagen School Health Records Register, BMI trajectories, epidemiology, cohort study, risk factors, cardiovascular prevention, Denmark