Even healthy young adults can carry silent heart damage decades before symptoms appear – not because of how they live but because of their parents’ cardiometabolic health. New research shows that inherited risk is already reshaping young hearts by their mid-twenties.
How much of a young person’s risk of heart disease is shaped by their choices – and how much is already written into their biology before adulthood? That question lies at the heart of this research, and it is difficult to answer clinically because damage can remain invisible for decades.
To probe that hidden period before symptoms appear, new research published in the European Journal of Preventive Cardiology examined the physical structure of the heart among apparently healthy young people – and found a disquieting pattern.
One in 60 young people whose parents had common health conditions – such as high blood pressure or high blood sugar – already showed signs of a struggling heart by age 24 years, long before any symptoms would be expected to appear. The risk, in other words, was visible in the heart itself, even though this does not mean these young adults have heart disease.
“While one in 60 may not sound dramatic at the individual level, these risk factors are so widespread in the parents’ generation that their effects quickly accumulate across the population,” says lead author Professor Andrew Agbaje, an pediatric epidemiologist at the University of Eastern Finland in Kuopio.
He emphasises that incremental factors result in the estimated 1 billion young people who will be at risk of cardiometabolic disease by 2030. Governments and healthcare providers cannot afford to ignore “subtle” contributors like these, Andrew Agbaje warns.
Early changes in young hearts
Previous studies have shown that a young person’s own heart health risk factors – such as blood pressure, insulin resistance and high blood sugar – predict future heart disease. But this study asks a different question: what happens to the heart long before disease becomes visible?
But to understand how heart health is inherited, Andrew Agbaje looked to the ALSPAC (Avon Longitudinal Study of Parents and Children) birth cohort: a group of thousands of young people in the United Kingdom whose health was tracked in meticulous detail from birth into young adulthood alongside equally detailed health data from their parents.
Because echocardiograms are expensive and rarely performed on healthy young people, the ALSPAC data offers a rare view of how adolescent hearts change before symptoms appear – revealing structural damage that standard risk scores or questionnaires would miss, Andrew Agbaje says.
Within those scans, he was particularly interested in signs of left ventricular hypertrophy, meaning excessive thickening of muscle in the heart’s main pumping chamber. This cardiac remodelling, or enlargement of the heart muscle, reflects the heart gradually working under extra strain and can appear decades before overt heart failure. In that sense, inheritance shows up not only in genes but in how early the heart begins to adapt.
Crucially, ALSPAC also gathered detailed information on the participants’ parents, including histories of cardiometabolic conditions such as diabetes, high blood pressure, unhealthy cholesterol levels, vascular disease and stiffened arteries.
Parental risk shows up early
To isolate the role of inherited risk, Andrew Agbaje compared the hearts of adolescents whose parents had cardiac risk factors such as high blood pressure or high cholesterol to their peers whose parents had a clean bill of heart health.
He found that young people whose parents had any of these risk factors were about 20% more likely to show cardiac enlargement, even when the adolescents themselves ate well, exercised regularly and had no obvious lifestyle risks – bringing imaging data, parental health history and individual behaviour into the same picture, without implying that lifestyle is irrelevant.
“They still carry their parents’ problems with them,” Andrew Agbaje says.
This is where the story takes a sharper turn. By comparing echocardiograms at ages 17 and 24 years, Andrew Agbaje found that enlargement progressed at roughly twice the speed among those with a parental history of risk factors compared with their peers – turning inherited risk into a measurable trajectory although not a guaranteed outcome.
“If we see one in 60 at age 24 years, that proportion may rise to one in 30 over the next seven years and perhaps one in 15 seven years after that,” Andrew Agbaje says, extrapolating from the accelerated rate of change seen between ages 17 and 24 years.
“Because of their parents’ health, they are already on an accelerated pathway toward heart disease.”
Routine screening could buy precious time
Andrew Agbaje says he was surprised to find that family history has such a strong impact so early in life. “We have previously shown that the individual risk factors of these children were strong enough to drive any cardiac damage, but to now have an additional risk that is beyond the children’s control is striking,” he explains. “It opens our eyes.”
Thirty percent of the young people in the study had parents with at least one of the cardiometabolic risk factors – meaning that imaging-based findings at the individual level could translate into substantial numbers of 24-year-olds with early heart changes at the population level.
Since the ALSPAC study participants are predominantly of European ancestry, Andrew Agbaje strongly believes that more research will be needed in populations of other ethnicities to assess how race affects this pattern.
A chance to intervene earlier
But the findings also point to a window of opportunity. Taken together, they suggest that healthcare providers may need to intervene much earlier – and, since echocardiograms remain out of reach as routine screening tools, rely on familiar risk factors such as blood pressure, cholesterol and blood sugar to identify young people who may be on an “express train to heart disease,” Andrew Agbaje says.
Andrew Agbaje is brainstorming ways to integrate checks for cardiometabolic risk factors into milestones for young people. He points to how many adolescents first realise they need glasses during the vision test for their driver’s licence.
“Perhaps governments can enact laws like this – as part of driving lessons, you need to pass your cholesterol test, you need to pass your blood pressure and blood sugar test. If the test fails, we would have at least 20 years to modify your diet and environment — potentially altering the trajectory of heart disease.”
Andrew Agbaje emphasises that early intervention is a winning proposition from a purely financial perspective. “Prevention is cheaper than cure,” he says. “A single heart failure is very expensive, and you do not really cure it – you manage it for life with drugs and ongoing intervention. The money required to treat one heart failure could instead prevent a hundred cases.”
