Weight gain during puberty increases the risk of heart disease

The risk of developing coronary heart disease (CHD) – which includes heart attacks and angina pectoris – begins to build much earlier in life than previously assumed. Although these conditions have long been associated with old age, new research suggests that the foundations are laid already in childhood and early adolescence.

When researchers follow individuals from childhood into adult life, a clear pattern emerges. Adults who had overweight as children but achieved normal weight by young adulthood are no more likely to develop CHD than those who had normal weight throughout their childhood. This suggests that the body can, to some extent, compensate for overweight in childhood – but not if weight gain first occurs during puberty.

Those who had normal weight as children but became overweight during puberty and remained overweight as young adults had the highest risk. They face a markedly higher risk of CHD than both those who had normal weight throughout and those who had overweight both as children and as young adults – even after the researchers accounted for differences in socioeconomic conditions.

The findings challenge a common simplification in both research and prevention: that the risk of heart disease is largely set early in childhood. Instead, the results suggest that how weight develops during puberty and into young adulthood plays a particularly important role.

“Overall, the study shows that the risk of CHD is not determined once and for all in childhood. What matters is how weight develops towards young adulthood, and our data suggest no additional risk among those who have normal weight as young adults, even if they had overweight as children,” says Jenny M. Kindblom, Senior Physician in Clinical Pharmacology at Sahlgrenska University Hospital and Professor at the University of Gothenburg, Sweden.

“This research finding is very encouraging, and communicating it widely is important. It suggests that we can prevent children from developing serious heart disease as adults by preventing overweight during puberty.”

Mining old school records for weight data

The suspicion that heart disease in adulthood is linked to having overweight early in life goes back decades. Doctors have repeatedly encountered middle-aged people with heart attacks or angina pectoris who could recall having had overweight as children or adolescents. But memory is unreliable, and diet, physical activity and other habits are difficult to reconstruct accurately many years later. To investigate the connection properly, researchers needed a more dependable trail back to childhood.

Here, the relationship between height and weight proved crucial. Height and weight are measured systematically throughout childhood and can be combined into an age- and sex-specific body-mass index (BMI), showing whether a child’s weight is within the normal range or indicates overweight. For that reason, these measurements are among the very few childhood data that can be meaningfully compared across generations.

Jenny M. Kindblom and colleagues therefore used weight development as a key and turned to historical records to understand how childhood and puberty relate to heart disease later in life. In municipal school health records, they found decades of routine height and weight measurements collected through school health services.

For men, these data were supplemented with measurements from the mandatory conscription examination in young adulthood. Together, these sources made it possible to follow weight development from childhood into early adult life and after diagnoses of coronary heart disease in national health registers, along with socioeconomic information.

Drawing on these records, the research team assembled a large cohort of 103,232 men and women born in the 1940s, 1950s and 1960s who could be followed from childhood into midlife. For each participant, weight was assessed at two key points: at 7–8 years of age and again in young adulthood – at age 18 years for women and 20 years for men.

Based on these measurements, the researchers calculated BMI and classified participants as having either normal weight or overweight, using thresholds corresponding to a BMI of 25 or higher for adults and age- and sex-specific cutoffs for children.

Four weight trajectories from childhood to young adulthood

For each participant, weight was assessed both in childhood and in young adulthood. Participants were then assigned to one of four weight trajectories: normal weight both as a child and as a young adult; overweight as a child but normal weight as a young adult; normal weight as a child but overweight as a young adult (i.e. pubertal onset); or overweight in both childhood and young adulthood.

These weight trajectories were then linked to Swedish health registries, in which diagnoses of CHD are recorded. The researchers followed participants from young adulthood onwards and were thus able to identify who later developed CHD.

Jenny M. Kindblom emphasises that the study is purely register-based, relying on medical records and registered diagnoses. The analyses are therefore based exclusively on objective, prospectively collected measurements and registry data. This enables researchers to follow very long life-courses without having to depend on memory or self-reporting.

“Nevertheless, we can follow the same individuals from school age into adulthood by linking old school records with modern health registries via Sweden’s personal identity number. In this way, we can turn back time and see how weight gain during puberty reappears in the life-courses that end in CHD,” she says.

Puberty as a particularly vulnerable period

Jenny M. Kindblom notes that the finding that weight gain during puberty carries the greatest risk of CHD suggests a particular vulnerability in those years. However, the study cannot determine what drives this vulnerability with certainty.

“We are working with medical records. We have not had the opportunity to perform physical examinations or to measure biomarkers and other relevant indicators. So here I can only speculate,” she says.

Her interpretation is that overweight arising during puberty places a greater strain on the heart than overweight earlier in childhood because the weight gain coincides with major biological changes. The body begins producing sex hormones, metabolism shifts and several physiological systems undergo rapid reorganisation. The combination of hormonal changes and increased fat mass may trigger processes of atherosclerosis that only manifest as disease many years later.

She also emphasises that the results relate primarily to overweight and moderate overweight. Very few children had obesity in the generation studied, which reflects growing up in the mid-20th century, when both lifestyles and weight patterns differed markedly from those of today.

“In practical terms, the study reveals when weight seems to place the greatest strain on the heart but not the processes that lead to damage. The specific biological mechanisms will have to be clarified by other, more experimental studies,” says Jenny M. Kindblom.

From childhood weight to future prevention efforts

Although the study cannot explain the biological mechanisms behind the link, it provides a solid starting-point for exploring other aspects of the heart’s vulnerability. The same cohort, with historical weight data and decades of follow-up in health registries, can be used to investigate more than CHD alone.

According to Jenny M. Kindblom, the research group is already working on new studies that link weight in childhood and adolescence to other diseases and conditions. Early analyses suggest that not only the degree of excess weight but also how long it persists and when in life it occurs may matter – and that these patterns do not necessarily follow the same logic as CHD. In this way, the cohort is beginning to paint a more nuanced picture of how various heart conditions are connected to weight development early in life.

In the longer term, she hopes that understanding when in life weight places the greatest strain on the heart will help target both prevention and treatment more effectively and shift efforts further upstream. This could, for example, involve earlier lifestyle interventions in childhood as well as identifying children and adolescents who should be monitored more closely because their weight trajectory makes them particularly vulnerable.

For Jenny M. Kindblom, the findings are ultimately about understanding – and preventing – where heart disease truly begins. Its roots, she says, are often laid long before the first prescription, in the environments children grow up in and the everyday places where they are measured, weighed and cared for.

“Prevention of heart disease must be built on decisions made at the societal level. This is a responsibility for politicians, authorities and those who plan the healthcare system,” she says, stressing that prevention must extend beyond individual encounters between doctor and patient.

She therefore sees the results as a strong argument for cardiologists, general practitioners, school doctors and health visitors to think about prevention across age groups. “Ultimately, this involves moving efforts to where they have the greatest impact: to the years when the heart is still being shaped, long before the first chest pain appears,” she says.