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From Li Qingyun to the Modern Body
We spent a long time with Li Qingyun.
The man from Sichuan who claimed to live 250 years. The herbalist who said he had seen dynasties rise and fall. The vegetarian, the meditator, the man who slept little, ate simply, and moved through the world with what his admirers described as a kind of unhurried stillness.
The article series begins with The Immortal: Uncovering the Legend of the 250-Year-Old Man, Li Qingyun
Whether you believe his age or not—and there are good reasons to be skeptical—his story poses a question that refuses to go away: What if the pace at which we age is not fixed? What if it can be slowed or sped up by the way we live?
Li Qingyun’s answer, whatever its literal truth, was a set of practices: restraint in diet, regularity in sleep, moderation in all things, and a deliberate resistance to the frantic pace of ordinary life. He was, in his own way, making a claim about biology. He was saying that the body’s decline is not a simple function of the calendar. It is shaped by how we treat it.
Now fast-forward to the present.
Something strange is happening to the modern body. Faster biological aging is underway—and it is happening fast enough that scientists can now measure it in the blood of people still in their thirties and forties.
Cancer in younger adults is rising. Between 1990 and 2019, cancers diagnosed in people under 50 increased by 24% globally. In the United States, the proportion of colorectal cancers diagnosed before age 55 nearly doubled between 1995 and 2019, from 11% to 20%.
In several countries—including Australia, Canada, the UK, and the US—people born in the 1990s face at least four times the risk of early-onset colorectal cancer compared with those born in the 1960s. In the US, people born around 1985 have roughly twice the risk of uterine cancer as those born before 1950.
These are not small shifts. They are generational shifts—patterns that track with the year you were born, not just how long you’ve lived. And they raise a question that Li Qingyun’s story, however mythologized, anticipated: Are we aging faster than our parents did? And if so, what is doing this to us?
A new study published in Nature Medicine offers a compelling—and somewhat unsettling—answer. The researchers propose that recent generations are biologically aging faster than their chronological ages would suggest, and that this accelerated aging may be contributing to the rise in early-onset cancers.
The modern body, in other words, is carrying a burden that the body of a previous era did not. And that burden is showing up in the blood, metabolism, and tissues of people who are still young.
The contrast with Li Qingyun is almost too neat. He claimed to have slowed his aging through simplicity, restraint, and stillness. The study suggests that we have collectively done the opposite.
We have built a world that accelerates aging—through diet, inactivity, environmental exposures, chronic stress, and the sheer speed and disruption of modern life—and the consequences are appearing earlier and earlier.
This article is about that acceleration. It is about what the science says, what it means, and what it might take to slow it down. And it is, in a sense, a return to the question Li Qingyun posed: Is aging something that happens to us, or something we do to ourselves?
What Is Biological Aging?
We all know people who seem younger or older than their years. A 45-year-old who runs marathons and has the bloodwork of a 30-year-old. A 50-year-old who has already weathered a heart attack, diabetes, and chronic inflammation. These differences aren’t just anecdotal—they reflect a measurable phenomenon known as biological aging.
Biological aging refers to the cumulative wear and tear on the body’s systems over time. It’s shaped by genetics, but also by everything else: diet, exercise, sleep, stress, pollution, infections, socioeconomic conditions, and the broader environment we live in. Unlike chronological age, which ticks forward at the same rate for everyone, biological aging can speed up or slow down.
Scientists have developed tools called aging clocks to estimate biological age from measurable data. Some clocks use blood chemistry—things like albumin, creatinine, glucose, and C-reactive protein. Others use metabolomics (the profile of small molecules in the blood), proteomics (the profile of proteins), or even epigenetic markers on DNA.
The difference between your biological age and your chronological age is called your age gap. A positive age gap means your biology looks older than your birth certificate suggests. A negative age gap means the opposite.
The new study asked a simple but powerful question: Has the age gap been growing across generations? And if so, does that explain why early-onset cancer is rising?
The Study: Two Countries, 164,000 People
To answer this question, researchers turned to two of the largest and most detailed health datasets in the world: the UK Biobank and the All of Us Research Program in the United States.
The UK Biobank includes over 500,000 participants with extensive clinical measurements, genetic data, and long-term follow-up. The All of Us program is a more diverse US cohort of over 450,000 adults, with linked electronic health records.
For this analysis, the researchers focused on 154,169 UK Biobank participants and 10,262 All of Us participants, all under age 55 at baseline—the age range most relevant to early-onset cancer.
The Clocks Used in This Study
The researchers used several different aging clocks, each capturing a different dimension of aging biology:
- PhenoAge, a mortality- and morbidity-based clock built from nine routine blood chemistry markers
- KDM biological age, a clock trained to predict chronological age from eight biochemical markers plus blood pressure and lung function
- Metabolomic aging, based on 54 metabolic markers measured by nuclear magnetic resonance
- Organ-specific aging, based on proteomic data, which estimates aging in individual organs like the lung, immune system, and adipose (fat) tissue
They then asked two questions:
- Did biological age gaps increase across birth cohorts? In other words, are people born later aging faster?
- Was a larger age gap associated with a higher risk of early-onset solid cancers—cancers diagnosed before age 55?
The Findings: Later Birth Cohorts Are Aging Faster
The first finding was striking.
Across both the UK and US cohorts, biological age gaps increased steadily across birth cohorts. In the UK Biobank, people born between 1965 and 1974 had a 23% higher standardized PhenoAge-defined age gap compared with those born between 1950 and 1954.
In the All of Us program, the pattern was even more pronounced: people born between 1990 and 1999 had a 92% higher standardized age gap compared with those born between 1965 and 1969.
In other words, more recent generations are biologically older than their chronological age would predict—and the trend is accelerating.
This pattern held after adjusting for age, sex, race, socioeconomic status, and other factors. It was consistent across multiple aging clocks, including PhenoAge, KDM, and metabolomic aging. And it was evident in both men and women, though the trajectories differed slightly: men tended to have larger baseline age gaps, whereas women showed steeper increases over time.
The researchers also found that non-Hispanic Black and Hispanic participants in the All of Us program had higher average age gaps than non-Hispanic White participants—a finding that likely reflects the cumulative impact of social, economic, and environmental disparities on biological aging.
The Link to Early-Onset Cancer
The second finding was equally important.
Across 953,582 person-years of follow-up in the UK Biobank, a higher PhenoAge-defined age gap was associated with an increased risk of early-onset solid cancers.
For every standard deviation increase in the age gap, the risk of early-onset solid cancer rose by 8%. People in the highest tertile of age gap had a 15% higher risk compared with those in the lowest tertile.
The association was driven primarily by three cancer types:
- Lung cancer: 57% higher risk per standard deviation increase in age gap
- Gastrointestinal cancers (including colorectal): 17% higher risk overall; 14% for colorectal specifically
- Uterine cancer: 31% higher risk
These associations remained robust after adjusting for genetic predisposition to aging and cancer, leukocyte telomere length, and a wide range of lifestyle and health factors. They also held when the analysis was restricted to participants with at least two years of follow-up, reducing the possibility that undiagnosed cancers were causing the accelerated aging rather than the other way around.
Importantly, the associations were weaker for cancers diagnosed after age 55, suggesting that the age gap may be particularly relevant for understanding early-onset disease.
The findings were partially validated in the All of Us program, where a higher PhenoAge-defined age gap was associated with a 22% higher risk of early-onset solid cancer per standard deviation increase. The KDM-defined age gap showed a similar, though weaker, association.
Organ-Specific Aging: A Closer Look
The researchers also used proteomic data to estimate aging in specific organs and tissues. This allowed them to ask whether certain organs were aging faster than others—and whether that mattered for cancer risk.
Two findings stood out:
- Immune aging was associated with early-onset lung cancer. For every standard deviation increase in immune aging, the risk of early-onset lung cancer rose by 89%. This association remained strong even after adjusting for systemic aging, suggesting that immune aging contributes independently to lung cancer risk.
- Adipose tissue aging was associated with early-onset colorectal cancer. For every standard deviation increase in adipose aging, the risk of early-onset colorectal cancer rose by 60%. Again, this association remained robust after adjusting for systemic aging.
These findings align with what scientists know about the biology of these cancers. Lung cancer risk is influenced by chronic airway inflammation and immune remodeling—processes that are closely tied to immune aging.
Colorectal cancer risk, meanwhile, is increasingly linked to metabolic dysfunction, visceral fat, and inflammation—all of which are reflected in adipose tissue aging.
What Might Be Driving Accelerated Aging?
The study doesn’t answer this question definitively, but it offers some clues.
The researchers note that recent generations have experienced earlier and more sustained exposures to a range of factors that are known to accelerate biological aging:
- Obesity and metabolic syndrome: Rates of childhood and adolescent obesity have risen dramatically. Metabolic dysfunction is a well-established driver of accelerated aging.
- Poor diet quality: Diets high in ultra-processed foods, added sugars, and saturated fats promote inflammation and metabolic stress.
- Sedentary behavior: Physical inactivity is independently associated with faster biological aging.
- Circadian disruption: Irregular sleep patterns, night-shift work, and screen exposure may disrupt hormonal and metabolic rhythms.
- Environmental chemicals: Pervasive exposure to endocrine-disrupting chemicals, air pollution, and other environmental toxins can accelerate aging processes.
- Social and economic stressors, including inequality, discrimination, and chronic stress, are linked to accelerated biological aging.
The study also points out that many of these factors co-occur and interact, creating a cumulative burden that may be greater in recent generations than in earlier ones.
Why This Matters for Cancer Prevention
The implications of this study are significant.
First, it suggests that biological aging may be a useful integrative marker for early-onset cancer risk. Rather than trying to measure every individual exposure or risk factor, clinicians could use aging clocks to identify young adults at elevated risk who might benefit from earlier or more intensive screening.
Second, it highlights the importance of life-course prevention. If accelerated aging begins in childhood or adolescence—driven by obesity, poor diet, inactivity, and environmental exposures—then interventions need to start early. Waiting until middle age to address these factors may be too late.
Third, it underscores the need for mechanistic research. The study shows that the age gap is associated with early-onset cancer risk independent of genetic predisposition, telomere length, and traditional risk factors. That means there are biological pathways connecting aging to cancer that we don’t yet fully understand—and that could be targeted for prevention or treatment.
Finally, it raises important questions about health equity. The finding that non-Hispanic Black and Hispanic participants had higher age gaps is consistent with a large body of research showing that marginalized communities experience faster biological aging due to structural inequities.
Addressing these disparities will require not just medical interventions but social and economic policies that reduce exposure to harmful environments and improve access to healthy food, safe housing, and quality healthcare.
Conclusion: The Takeaway
This study provides population-based evidence that biological aging has increased across birth cohorts and is associated with a higher risk of early-onset solid cancers—particularly lung, gastrointestinal, and uterine cancers. The findings suggest that accelerated aging may be a measurable marker of the cumulative impact of emerging generational risk factors, and that addressing these factors early in life could be key to preventing cancer in younger adults.
Li Qingyun, if he existed as described, may have understood something that modern science is only now beginning to quantify: that aging is not a simple matter of time. It is a process shaped by how we live, what we consume, how we move, how we sleep, and what we are exposed to.
His answer was asceticism and stillness. Ours will have to be something else—but the study makes clear that the question is no longer philosophical. It is medical. And it is urgent.
Key Takeaways:
- Biological aging is increasing across generations. People born in recent decades have higher age gaps—meaning their biology looks older than their chronological age—compared with earlier generations.
- Accelerated aging is linked to early-onset cancer. A higher age gap is associated with increased risk of solid cancers before age 55, especially lung, gastrointestinal, and uterine cancers.
- Organ-specific aging matters. Immune aging is linked to early-onset lung cancer; adipose tissue aging is linked to early-onset colorectal cancer.
- The association is independent of genetics. Age gap predicts cancer risk even after accounting for genetic predisposition to aging and cancer.
- Lifestyle and environmental factors likely play a role. Obesity, poor diet, inactivity, circadian disruption, environmental chemicals, and social stressors may all contribute to accelerated aging.
- Prevention must start early. If accelerated aging begins in childhood or adolescence, interventions need to start early—not in middle age.
- Health equity is essential. Marginalized communities experience faster biological aging due to structural inequities; addressing these disparities is critical to reducing cancer risk.
- More research is needed. Longitudinal studies, larger samples, mechanistic research, and intervention trials are needed to confirm these findings and translate them into prevention strategies.
- The Li Qingyun question remains open. If aging can be slowed, the modern world is currently doing the opposite. The study suggests that reversing this trend is not just possible but necessary.
The rise in early-onset cancer is not inevitable. But reversing it will require understanding—and addressing—the biological aging processes that appear to be accelerating in younger generations.
Hundreds of years ago in China, there was a group of people known as the Taoist Immortals—men and women who were said to have transcended the ordinary limits of the human body, living for centuries through practices of breath, stillness, diet, and inner alchemy.
Whether they achieved what the legend claims is a question we cannot answer. But what they believed—and what they practiced—speaks directly to the questions this study raises.
In our next series, we will explore the Taoist Immortals: who they were, what they did, and what their way of life might still teach us about slowing the clock inside us all.
Don’t Get Sick!
About Dr. Jesse Santiano, MD
Dr. Santiano is a retired internist and emergency physician with extensive clinical experience in metabolic health, cardiovascular prevention, and lifestyle medicine. He reviews all medical content on this site to ensure accuracy, clarity, and safe application for readers. This article is for educational purposes and is not a substitute for personal medical care.
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Reference:
- Tian, R., Zong, X., Ren, D. et al. Biological aging and generational shifts in early-onset cancer risk. Nat Med 32, 2983–2990 (2026). https://doi.org/10.1038/s41591-026-04448-w
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