Are We Actually Aging More Slowly Than Our Parents Did?

Ricky Martin is 54 years old. Kristen Wiig is 52. If you’ve been watching them on Apple TV’s Palm Royale, set in the glittering excess of 1960s Palm Beach, you might find those numbers hard to believe. Martin looks like he could still be headlining the 1999 Grammy Awards, and when he performed at the 2025 Super Bowl halftime show, social media collectively lost its composure over the fact that a man in his mid-fifties could move and look like that.

They’re not alone. When Anne Hathaway starred in The Idea of You last year, playing a 40-year-old divorced mother who falls for a younger pop star, viewers complained not that she was too old for the part but that she was too young and too attractive to play someone her own age. She was 41 at the time.

Nicole Kidman, at 57, played a CEO engaged in an affair with a 20-something intern in Babygirl and no one blinked at the casting. Twenty years ago, both of those roles would have gone to actresses in their thirties.

Something has clearly shifted. But is this just better skincare and favorable lighting, or is something deeper going on? A growing body of research suggests that at least some of us really are aging more slowly than previous generations, at the level of our cells and organ systems, and that the reasons for this extend well beyond Hollywood budgets.

The science of measuring biological age has advanced considerably in the last decade

The gap between chronological age and biological age has fascinated researchers for decades, but only recently have they developed tools precise enough to quantify it. Dr. Daniel Belsky and colleagues at Columbia University developed DunedinPACE, a DNA methylation-based algorithm that functions like a speedometer for aging, measuring how quickly biological deterioration is occurring in real time. Their foundational work came from the Dunedin Study, a landmark longitudinal study tracking 1,037 people born in 1972-73 from birth through midlife. Even though every participant was chronologically 38 at the time of assessment, their biological ages ranged from 28 to 61, with some people aging nearly three years for every calendar year while others were aging close to zero.

Study members with advanced biological age had poorer physical function, worse cognitive performance, and were rated as looking older by independent observers who had no information about their actual age. Biological aging, in other words, is real and measurable, and it shows up both in blood work and in how people are perceived by others.

The landmark study on this question found that Americans are biologically younger than they used to be

In 2018, Dr. Morgan Levine and Dr. Eileen Crimmins published a study in Demography with the provocative title “Is 60 the New 50?” Using nationally representative data from over 21,500 Americans across two waves of the National Health and Nutrition Examination Survey (NHANES III from 1988-1994 and NHANES IV from 2007-2010), they examined how biological age changed over two decades. They calculated biological age using eight biomarkers spanning metabolic, cardiovascular, inflammatory, kidney, liver, and lung function.

The results were unambiguous. Biological age was lower in the more recent period across essentially all groups. Older adults experienced the greatest improvement, and men showed greater declines in biological age than women. Dr. Crimmins called this the first evidence of delayed aging among a national sample of Americans. Dr. Levine made an important conceptual distinction in the paper between simply keeping sick people alive longer and genuinely slowing the rate at which people deteriorate, noting that only the latter leads to lower healthcare costs and better quality of life.

Several other studies have reinforced this finding across different populations and measurement approaches

The Levine and Crimmins paper was not an isolated result. A large analysis using the Health and Retirement Study tracked Americans born between 1904 and 1966 and found a steady trend of health improvements, with health deficits declining on average by about 1% for each year of later birth. That pattern held across regions and for both men and women, though it was significantly weaker for African Americans compared to Caucasians.

In Finland, researchers compared community-dwelling adults aged 75-95 every ten years across three decades and found that frailty prevalence decreased in later-born cohorts at ages 75, 80, 85, and 90. The trend did not hold for those aged 95, suggesting that at the very extremes of age, biology eventually catches up regardless of generational advantages. Frailty declined more in men than women.

A Swedish cohort study used identical measurement methods to compare 75-year-olds born in 1911-12 with those born in 1930, finding that the later-born group was measurably less frail. And data from the English Longitudinal Study of Ageing found that frailty at each age had been decreasing over time, though the trend was less pronounced for those with lower wealth.

Perhaps most notably, the Seattle Longitudinal Study found that later-born cohorts showed cognitive differences of up to half a standard deviation and less steep rates of cognitive decline on all measured abilities between ages 50 and 80. To put that in practical terms, 70-year-olds in recent cohorts performed cognitively like 65-year-olds did a generation earlier.

A 2025 global analysis revealed that these improvements are concentrated in wealthy countries

A study published in 2025 using Global Burden of Disease data from 1990-2019 found that the biological age of a chronologically 65-year-old man varied between 61 and 74 years depending on the country. The global trend, however, was not uniformly positive. The improvements were driven by diverging trajectories, with biologically old people in rich countries becoming biologically younger while biologically young people in Africa were becoming biologically older. Whether “people are aging more slowly” depends entirely on where you live and what resources you have access to.

Declining death rates alone do not prove the rate of aging has slowed

Dr. S. Jay Olshansky has argued that there are important distinctions between living longer and actually aging more slowly. He examined three separate hypotheses about whether the rate of human aging has already been modified, and concluded that declining death rates across generations are not sufficient evidence that people are biologically aging at a slower pace. Most of the gains in survival, he noted, are better explained by reductions in risk factors for fatal diseases and by advances in medical technology rather than by changes in the underlying aging process itself. However, his position is not taking into account the aforementioned biological clock data. He accepted that delayed aging is the most likely explanation for why exceptionally long-lived people, particularly centenarians who may carry “protective genes,” experience less disease and survive far longer than the general population. If genetic heritability explains a meaningful share of current variation in longevity, he argued, that opens the door to therapeutic interventions that could confer those advantages more broadly.

Other data suggests younger generations may be aging faster than their predecessors

Perhaps the most striking counterpoint comes from work led by Dr. Yin Cao at Washington University School of Medicine. Her team presented findings at the 2024 AACR Annual Meeting showing that among 148,724 individuals aged 37-54 in the UK Biobank, people born in or after 1965 had a 17% higher likelihood of accelerated biological aging compared to those born between 1950 and 1954. They calculated each participant’s biological age using nine biomarkers found in blood including albumin, alkaline phosphatase, creatinine, C-reactive protein, glucose, mean corpuscular volume, red cell distribution width, white blood cell count, and lymphocyte proportion. This accelerated aging was linked to significantly higher risks of early-onset cancers. Each standard deviation increase in accelerated aging was associated with a 42% increased risk of early-onset lung cancer, a 22% increased risk of early-onset gastrointestinal cancer, and a 36% increased risk of early-onset uterine cancer.

These findings were presented at a conference, not yet peer reviewed in a scientific journal, so take this with a grain of salt. We are also comparing apples to oranges, with different ways of measuring biological age in different cohorts. The Levine PhenoAge clock measures biological age a bit differently than the Dunedin pace clock, which is different than Dr. Cao’s clock, which can significantly change the results. See my article “What is biological age?” for more details on clocks.

The increased cancer findings in younger cohorts are worrying, regardless of how you measure biological age.

Dr. James Kirkland at the Mayo Clinic observed that these markers of accelerated aging are appearing in younger generations even after accounting for smoking rates and obesity, suggesting there may be environmental factors we have not yet identified. He cited increased air travel, radiation exposure, and PFAS (so-called “forever chemicals”) as potential culprits worth investigating. See my article “What’s leaching into your beans?” for more details on PFAS.

Two behavioral shifts help explain why some people look so much younger today

Whatever is happening at the epigenetic level, two population-wide changes in behavior have almost certainly contributed to the visible differences between generations.

The decline in smoking has been enormous in scale. Gallup data show that 41% of American adults smoked when the question was first asked in 1944, reaching a peak of 45% in the mid-1950s. By 2024, that number had fallen to 11%, matching the lowest rate in eight decades of tracking. CDC data confirm a drop from 42.4% in 1965 to 11.6% in 2022. Among young adults, the decline has been even more dramatic, from 35% in 2001-2003 to roughly 10% by 2019-2023. Smoking damages collagen and elastic fibers in the skin while causing chronic vasoconstriction, and the cumulative effect of decades of exposure leaves a visible mark. A 50-year-old today who never smoked and was rarely exposed to secondhand smoke will look fundamentally different from a 50-year-old in 1975 who grew up in a household of smokers and lit up through their twenties and thirties.

The other major shift involves sun protection. Research published in Photodermatology, Photoimmunology & Photomedicine confirms that UV radiation is responsible for the majority of visible facial aging, including wrinkling, sagging, and uneven pigmentation. The first commercial sunscreens were not available until the 1920s-1930s, and SPF was not recognized by the FDA as a standard until 1978. A randomized controlled trial found that daily sunscreen users showed no detectable increase in skin aging after 4.5 years, with 24% less aging compared to those who used sunscreen only at their own discretion. The cultural shift from baby oil and tanning beds to daily SPF has been profound, and because photoaging accumulates over decades, the full visual benefit of this change is still unfolding.

These are not merely cosmetic improvements. The same mechanisms that drive photoaging and smoking-related skin damage, including oxidative stress, collagen degradation, DNA damage, telomere shortening, and chronic inflammation, also drive systemic aging throughout the body, including in the brain.

The real picture depends on who you are and where you live

The synthesis of this research is that the answer to “are people biologically younger than past generations?” is both yes and no, depending on which generation, which biomarkers, and which socioeconomic stratum you examine.

For people currently in their 60s through 80s who are health-conscious, well-resourced, and never smoked heavily, the evidence is fairly consistent. Multiple studies across different countries and measurement approaches show improvements in biological age, frailty, and cognitive function compared to earlier cohorts at the same chronological age. The CALERIE trial demonstrated that even modest caloric restriction can measurably slow the pace of biological aging in healthy adults, with a 2-3% reduction in the pace of aging that translates to a 10-15% reduction in mortality risk, an effect comparable in size to smoking cessation. These processes are modifiable.

It is worth noting, however, that modifying biomarkers of aging and actually extending lifespan are not necessarily the same thing, and we do not yet have proof that the former reliably produces the latter in humans.

Dr. Roy Walford, a UCLA pathologist, pioneered caloric restriction research in mice in the 1970s, showing that CR could extend their lifespan by 10 to 50 percent. He practiced severe CR himself at roughly 1,600 calories per day, wrote The 120 Year Diet in the 1980s, and co-founded the Calorie Restriction Society International in 1994. His stated goal was to live to 120.

Members of his society, known as “CRONies” (for Calorie Restriction with Optimal Nutrition), have been voluntarily restricting their caloric intake by 30 to 40 percent for years and in some cases decades, and studies of these individuals show impressive metabolic profiles, including lower blood pressure, reduced inflammation, and cardiovascular function comparable to people 16 to 20 years younger. But no mortality data have been published showing that CRONies live longer than the general population. It’s unclear to me why this data is not available.

There are two conflicting primate studies on caloric restriction (CR) for healthspan and lifespan extension, but perhaps that conversation deserves its own post. Suffice it to say that the data are not conclusive that CR extends lifespan in organisms higher up the phylogenetic than mice.

Walford himself died of ALS at 79. His death was likely unrelated to his diet, but it underscores the gap between surrogate endpoints and actual longevity outcomes. The science of biological aging measurement has advanced considerably since Walford’s era, and the CALERIE results are far more rigorous than anything that preceded them. We can now measure aging better than ever and we can show that interventions move those measurements in the right direction, and yet we do not yet know with certainty whether that translates into more years of life.

Even setting aside that uncertainty, the picture is further complicated by the fact that for younger cohorts born after the mid-1960s, the trajectory may be reversing. Rising rates of obesity, earlier and more pervasive exposure to ultra-processed foods, environmental chemical exposures, and sedentary lifestyles appear to be accelerating biological aging in ways that may offset the gains from reduced smoking and better sun protection.

I have serious regrets about all of the fake food of my childhood from TV dinners, to supposedly healthy but actually terrible, Snackwell cookies, to Cheetos, soda, and candy bars. My typical breakfast in highschool was a vending machine Dr. Pepper and a Snickers bar. Breakfast of champions. We basically ate fiberless, nutritionless, sugar-drenched, plastic-filled, garbage half the time. I am thankful for the home cooked mediterranean meals that partially offset all of that nonsense food.

And across all generations, the benefits of slower aging are strikingly unequal. Nearly every study that examined the question found that the improvements were smaller or absent among women with lower educational attainment, among those with lower wealth, and among racial and ethnic minorities. The biological age gap between a well-resourced 55-year-old and a disadvantaged 55-year-old may be wider today than it was a generation ago.

We need far more data on what may be accelerating aging in younger generations

The Cao findings raise an urgent and largely unanswered question. If younger generations are showing signs of accelerated biological aging (at least for cancer) even after accounting for known risk factors like smoking and obesity, something else is driving the process, and we do not yet know what it is. The list of suspects includes PFAS and other endocrine-disrupting chemicals that have become pervasive in food packaging and water supplies, microplastics that have been found in human blood and organs, ultra-processed foods that now constitute the majority of caloric intake for many Americans, and exposures to environmental pollutants that earlier generations simply did not encounter at the same scale or duration.

We need longitudinal studies that track biological aging markers alongside environmental exposure data in people from their twenties onward, not just in retrospective cohorts who are already in midlife. We need standardized measurement protocols so that findings from different research groups using different epigenetic clocks and biomarker panels can be meaningfully compared. And we need these studies to be demographically inclusive enough to disentangle the effects of environmental pollution from the effects of socioeconomic disadvantage, because those two exposures overlap in ways that make it difficult to identify which factor is doing the damage.

The science of biological aging measurement has matured rapidly, with tools like DunedinPACE and second-generation epigenetic clocks now demonstrating consistent associations with disease risk, mortality, and functional decline. What has not matured at the same pace is our understanding of modifiable environmental exposures that are accelerating the process in populations that should, by all other measures, be aging better than their grandparents.

Healthspan extension should not be a luxury good

The most consistent finding across this entire body of research is that the benefits of slower biological aging are stratified by wealth, education, and race. The people who are aging most slowly are the people who already have the most resources. Meanwhile, the CALERIE trial and other intervention studies have shown that the pace of aging is modifiable through behavioral changes that are neither exotic nor expensive. Caloric moderation, physical activity, avoidance of tobacco and excessive UV exposure, and management of metabolic risk factors are interventions that work and that have been validated in randomized controlled trials.

The barrier is not scientific knowledge, it’s access. Preventive health infrastructure, nutritional quality, environmental safety, and the time and stability required to maintain health-promoting behaviors are distributed unequally across the population. Extending healthspan to more people is not only a matter of fairness but also a matter of fiscal survival for governments facing the economic consequences of population aging.

The economic case for universal healthspan investment is already well-documented

Economists have quantified what it would mean to slow biological aging across the population, and the numbers are staggering. A 2021 analysis published in Nature Aging by Dr. Andrew Scott, Dr. Martin Ellison, and Dr. David Sinclair estimated that slowing aging enough to increase life expectancy by just one year would be worth $37 trillion to the U.S. economy. A 10-year improvement, roughly equivalent to making 70-year-olds biologically resemble today’s 60-year-olds, would generate an estimated $367 trillion in economic value, or about $7.2 trillion annually, representing more than a third of U.S. GDP.

An earlier analysis by Dr. Dana Goldman and colleagues in Health Affairs estimated that delayed aging, modeled on the most promising animal research, would generate $7.1 trillion in economic value over 50 years, with little additional government cost if Social Security and Medicare eligibility were indexed to life expectancy gains. Recent work from the IMF reinforced these projections, finding that even a 20% reduction in the incidence of six major chronic diseases among adults aged 50-64 would increase GDP by 1.5% within a decade through higher labor force participation alone.

Consider the scale of what we currently spend managing the consequences of biological aging rather than preventing it. Alzheimer’s care alone cost an estimated $360 billion in 2024, with projections approaching $1 trillion annually by 2050. Cardiovascular disease costs $254 billion per year in direct medical expenses, plus another $168 billion in lost productivity. Arthritis-attributable costs exceeded $300 billion in 2013. These are not abstract numbers. They represent the fiscal weight of a healthcare system organized around treating age-related disease after it appears rather than slowing the aging process that produces it.

If governments invested in giving all citizens, not just the affluent and well-educated, equal access to the conditions and interventions that produce 10 biologically younger years, the return would dwarf the investment. We need to gather the political will to treat healthspan extension as public infrastructure rather than a private luxury, and to recognize that every year of biological aging we prevent across the population is a year of productivity gained, a year of disability avoided, and a year of healthcare expenditure that never needs to be spent.