Biological aging does not always progress at the same rate as chronological age. (Credit: University of Jyväskylä)
Some Teens Age Faster Later in Life, and Genetics May Be Why
In A Nutshell
- Teens with a stronger genetic tendency toward high body weight showed measurably faster biological aging that carried into their 40s and 50s.
- Starting the teen years already heavier mattered more than how fast the weight increased afterward.
- A genetic test offered support for a real causal link, though the strength of the evidence varied depending on which aging measure and which genetic marker was used.
- Researchers say the findings add to the case for paying attention to elevated BMI and related health risks earlier in life.
Teenagers who carry extra weight may deal with repercussions decades later, according to a study out of Finland published in the International Journal of Obesity. Researchers found that teens with a stronger genetic tendency toward high body weight showed measurably faster biological aging that carried into their 40s and 50s.
Scientists tracked thousands of people from childhood into middle age, checking in three separate times over the decades to draw blood and measure chemical changes in DNA that reveal how “old” a person’s cells look compared to their actual birthday. The teenage years look like they matter for long-term health well beyond adolescence itself, with higher body weight in those years sticking with the body long after they end.
Using genetic tools, the researchers pushed further to test whether that pattern actually reflects cause and effect rather than coincidence. What they found offers real support for a causal link, though the strength of the evidence varied depending on which aging measure and which genetic marker was used, a detail that matters for how doctors might think about early weight in the teen years.
Decades of Blood Tests Track Biological Aging
This data came from the Young Finns Study, a research project that has followed the same group of people since 1980, when they were between 3 and 18 years old. Researchers stayed in touch with participants for decades, checking in as recently as 2018 to 2020, by which point many were in their 40s and 50s.
To measure biological aging, scientists drew blood and looked at chemical changes in DNA that build up over time, a signal that can be turned into what’s known as an aging clock. Two people can share the same birthday but land on very different points on this clock depending on how their bodies have actually aged. The study used two versions of this clock, checked at three points across participants’ lives: as teenagers and young adults, in their 30s and 40s, and again in their 40s and 50s. A little over 2,000 people had at least one of these aging measurements taken.
Alongside the aging clocks, researchers calculated genetic risk scores, tallies built from hundreds of gene variants that estimate how strongly someone’s DNA pushes them toward high body weight. One score focused on genetic risk for adult BMI, built from 941 gene variants, while the other estimated genetic risk for childhood body size, using 286 variants. Participants’ actual BMI was tracked at ages 9, 12, 15 and 18, letting the team map out individual weight patterns through the teen years.
Higher Teen BMI Linked to Faster Biological Aging
Genetic risk for higher BMI was consistently tied to faster biological aging across nearly every checkpoint measured, using both aging clocks. But the more interesting question came next: did this genetic risk work directly on the body, or through actual higher body weight during the teen years?
It turned out that having a higher BMI in adolescence explained part of the connection between genetic risk and faster aging. How quickly someone’s weight climbed during the teen years mattered far less. In other words, starting the teen years already heavier carried more long-term weight, in every sense, than how fast the pounds piled on afterward.
A Genetic Test Points to a Causal Link
Then came the test for cause and effect. Because it’s hard to know from observation alone whether higher teen BMI actually causes faster aging or just travels alongside it, researchers used a genetic method called Mendelian randomization, which uses inherited gene variants as stand-ins for BMI itself, since those variants are set at birth and untouched by later lifestyle choices. If genetically predicted higher BMI lines up with faster aging, that strengthens the case for a causal relationship rather than a simple association.
Using this method, the team found a positive causal effect from genetically predicted teen BMI on faster biological aging, an effect that held up most clearly for one aging clock, called DunedinPACE, when paired with the genetic score for adult BMI. The estimated effect suggested that for every one-unit increase in genetically predicted BMI during adolescence, participants’ pace of aging ticked up by about 0.02 years for every calendar year that passed, both in 2011 and again in 2018. That effect was less consistent with the other aging clock, called PC-GrimAge, and it also did not hold up clearly when researchers used the childhood body size genetic score instead of the adult BMI score.
Genetic Risk and Early Weight Add Up Over Time
For context on how much weight patterns have shifted, only about 7 to 10 percent of participants were overweight and roughly 1 percent had obesity when they were teenagers in this study. By the time the group reached their 40s, that had jumped to 40 percent with overweight and somewhere between 21 and 28 percent with obesity, depending on the year measured.
This is one of the first studies to trace that genetic thread from the teen years all the way into measurable signs of cellular aging decades later, using data drawn directly from participants rather than population-wide estimates. The researchers put it plainly in their conclusion, writing that “high BMI in adolescence may accelerate biological aging, especially in individuals with a genetic predisposition to high BMI.” The researchers say the findings add to the case for paying attention to elevated BMI and related health risks earlier in life.
Disclaimer: This article summarizes findings from a peer-reviewed observational study and is intended for general informational purposes only. It is not medical advice. Anyone with questions about their own weight, health risks, or aging should speak with a qualified health care provider.
Paper Notes
Limitations
The researchers were upfront about several caveats. Because teen BMI and later biological aging could both be shaped by early-life factors that weren’t measured, such as conditions before birth, unmeasured factors could bias the results. The childhood body size score relied on adults’ memories of their own body size as children, which is prone to inaccurate recall. BMI itself doesn’t capture body composition, so it’s an imperfect stand-in for body fat. Sample sizes were smaller at certain checkpoints, particularly the earliest one in 1986 and the most recent genetic analysis in 2018, which may have limited the study’s ability to detect effects. The study also relied only on participants with European ancestry from a single Finnish cohort, limiting how broadly the findings can be applied to other populations.
Funding and Disclosures
The study authors reported no competing interests. Individual authors disclosed research support from sources including the Juho Vainio Foundation and the Academy of Finland. The Young Finns Study itself has received funding over the years from the Academy of Finland, the Social Insurance Institution of Finland, several Finnish foundations, and European Union research funding programs, among other sources listed in the paper’s funding section.
Publication Details
The study, titled “Adolescent weight gain trajectories and their associations with biological aging: a genetically informed study,” was published in the International Journal of Obesity. The authors include Anni Pitkänen, Anna Kankaanpää, Emma Raitoharju, Saara Marttila, Leo-Pekka Lyytikäinen, Pashupati P. Mishra, Nina Mononen, Tuija Tammelin, Juha Mykkänen, Katja Pahkala, Suvi Rovio, Laura Joensuu, Miina Ollikainen, Jorma Viikari, Olli Raitakari, Terho Lehtimäki and Elina Sillanpää, with corresponding author Elina Sillanpää. The paper’s DOI is https://doi.org/10.1038/s41366-026-02194-0.







