We added roughly two decades to the average human life over the course of the twentieth century, a public health achievement with almost no historical parallel. About ten of those extra years, in the average high-income country, are not spent in good health. That gap between how long people live and how long they live well is the quiet scandal of longevity science, and it is growing.
Why This Matters
If you ask most people whether they would rather live to 85 in good health or to 95 confined to a chair, nearly everyone chooses 85. I have asked my parents this question every few years since I started caring about aging science. Their answer has never changed, and I don't think it ever will.
And yet the longevity conversation in 2026 is still mostly about extending lifespan. Billionaires fund rejuvenation companies. Supplement ads promise more years. Headlines celebrate centenarian populations. Almost none of the popular story centers the question that actually matters to real people, which is not "how long will I live" but "how long will I be able to walk to the corner store and back."
That second question has a name. Scientists call it healthspan, and the gap between healthspan and lifespan turns out to be the most important number in aging research. Recent data says the gap is getting wider, not narrower, almost everywhere in the world. The country leading the widening is the United States.
This is the piece I wanted to read when I started taking aging seriously.
The Two Numbers That Usually Get Confused
Lifespan is the total number of years you live. It is the number on your tombstone. At the population level, it is usually reported as life expectancy at birth. In 2024, global life expectancy at birth was about 73.3 years. In the United States, it was about 78.4.
Healthspan is the portion of life you spend in good health, meaning free from serious disease and disability. The World Health Organization reports this as Healthy Life Expectancy, abbreviated HALE. Globally in 2019, HALE was about 63.7 years.
Subtract healthspan from lifespan and you get the gap. This is the period at the end of a typical life spent managing chronic conditions, losing independence, and waiting.
For a long time, aging researchers assumed the gap would stay roughly constant or shrink as medicine got better. The data does not support that assumption. In the largest analysis yet, published in JAMA Network Open in December 2024 by Armin Garmany and Andre Terzic at the Mayo Clinic, the global mean gap was 9.6 years. In 2000, it was 8.5 years. That is a 13 percent increase in two decades, in the wrong direction.
The paper covered all 183 WHO member states. The country with the largest gap was the United States at 12.4 years. Australia came in second at 12.1, New Zealand at 11.8, the UK at 11.3, Norway at 11.2. The countries with the smallest gaps were mostly poor nations with short lifespans, where people simply do not live long enough to accumulate the decade of chronic disease. Lesotho had a gap of 6.5 years. The Central African Republic had 6.7.
That pattern alone should tell you what is going on. The healthspan-lifespan gap is a disease of success. Rich countries have beaten infectious disease and acute injury so effectively that people now live long enough to get the slow chronic conditions that used to kill almost no one: type 2 diabetes, coronary disease, dementia, osteoarthritis, COPD, chronic kidney disease. The price of surviving the first seventy years is spending the next ten to fifteen accumulating them.
How the Gap Got This Big
To understand the gap, you have to understand what happened to lifespan first.
In 1900, global life expectancy at birth was about 31 years. In the United States, it was 47. Most of that shortfall came from childhood mortality. Infectious disease, childbirth complications, and acute illness killed enormous numbers of people before they ever reached their thirties. When a ten-year-old died of diphtheria, it pulled the average down hard.
The twentieth century changed this. Clean water, sanitation, vaccines, antibiotics, improved obstetric care, and better nutrition removed most of the things that used to kill children and young adults. By 2000, global life expectancy had more than doubled to about 66 years. That is arguably the greatest public health achievement in human history. None of it was about aging biology. It was about not dying young.
But once people routinely reach their seventies and eighties, a different problem appears. The biology of aging catches up. Cells accumulate damage. Blood vessels stiffen. Insulin signaling breaks down. Immune systems misfire. This is the territory covered by the 12 hallmarks of aging, and it is what modern longevity science is actually trying to address.
The twentieth century extended how long people live by fighting the acute killers. It did not extend how long people stay biologically young. So the extra years got tacked onto the end of life, and most of them went to managing the diseases of aging rather than to climbing mountains.
This is the part of the longevity story that rarely makes it into the headlines.
How We Actually Measure Healthspan
Healthspan sounds simple until you try to measure it. What counts as "healthy" depends on what you are measuring.
The most widely used metric is the WHO's Healthy Life Expectancy (HALE). HALE subtracts years lost to disease and disability from total life expectancy, weighted by severity. A year spent with mild hypertension counts more than a year spent bedridden. HALE is the number cited in most cross-country comparisons, including the Garmany and Terzic work.
Researchers also use disability-free life expectancy, which asks a simpler question: how many years can a person perform basic activities of daily living without help? Bathing, dressing, preparing meals, walking across a room. When you lose the ability to do these things, your disability-free life has ended even if you are still breathing.
A third approach is disease-free life expectancy, which counts years before the diagnosis of major chronic conditions. This one tends to give the most pessimistic numbers, because most people over 60 have at least one chronic diagnosis on their chart.
These three metrics do not always agree. A 2022 paper in Demography by Zheng and colleagues at the Max Planck Institute for Demographic Research looked at US birth cohorts from 1998 to 2016 and found that disability-free years were slowly expanding for some subgroups, while morbidity-free years (counting chronic disease diagnoses) were contracting for nearly everyone. People were staying functionally independent a little longer, but they were doing it while carrying more disease labels.
That apparent contradiction is part of why the field uses the word "healthspan" a bit loosely. When a longevity podcaster says "healthspan is declining," they might be citing any of these metrics, and the answer depends on which one.
For the rest of this article, when I say healthspan I mean the HALE definition, because that is the one the Garmany and Terzic data uses and the one most relevant to the global picture.
The Compression of Morbidity Debate
In 1980, a Stanford rheumatologist named James Fries published a paper in the New England Journal of Medicine called "Aging, natural death, and the compression of morbidity." Fries proposed a hopeful thesis. He argued that as medicine improved, the onset of chronic disease and disability would get pushed later and later in life, while the maximum human lifespan would stay roughly fixed somewhere around 85 to 100 years. The result, he predicted, would be a compression of sickness into the final brief period before death. People would live almost their entire lives in good health, then decline and die relatively quickly.
Fries's compression hypothesis was genuinely beautiful. If it were true, the longevity project would eventually solve itself: lifespan would plateau, healthspan would catch up, and the gap would shrink toward zero.
The data since 1980 has been a mixed response to Fries, leaning toward disappointment. Eileen Crimmins, a demographer at the University of Southern California who has spent four decades tracking these questions, published a clear assessment in 2015 in The Gerontologist. Her conclusion was blunt. The United States had not, by any reasonable measure, experienced much compression of morbidity. The age of onset of major chronic diseases had barely moved. People were not getting sick later. They were just dying later while sick.
A 2024 paper in the Journals of Gerontology: Series A by Cai and colleagues, titled "Are We Adding Pain-Free Years to Life? A Test of Compression Versus Expansion of Morbidity," tested Fries's hypothesis directly using contemporary US data. The answer was that pain-free years have expanded for some groups and contracted for others, with substantial disparities by race, sex, and socioeconomic status. For the population as a whole, the picture is closer to what researchers call "dynamic equilibrium" than to Fries's optimistic compression.
Dynamic equilibrium is the gentler version of bad news. It means that as lifespan grows, sickness grows along with it, and the ratio stays about the same. More years, proportionally more bad years. The total stack gets taller without getting healthier.
The starkest evidence against Fries is the Garmany and Terzic 2024 paper itself. If compression were happening globally, the gap should be shrinking. It is not. It is growing.
What Actually Moves Healthspan
If the longevity project is really about healthspan, the practical question becomes: what interventions actually compress the sick years and not just the rest?
The honest answer is that only a handful of things have strong evidence for expanding healthspan in humans, and almost none of them come in a bottle.
Physical activity, especially cardiorespiratory fitness
The single most consistent finding in human healthspan research is that people who maintain higher aerobic capacity into later life have both longer lives and longer disability-free lives. Linda Fried, former dean of the Columbia Mailman School of Public Health and one of the founders of frailty research, has argued that physical activity is the closest thing we have to a real healthspan drug. Her 2016 review in JAMA made the case that structured exercise can delay or prevent the frailty cascade that turns independent 70-year-olds into dependent 80-year-olds.
The effect sizes are larger than anything in the supplement literature. A person in the top 25 percent of cardiorespiratory fitness in their age group has a lower risk of all-cause mortality than a person in the bottom 25 percent by a factor of roughly 2 to 3 in most cohort studies. That gap has been shown across the Cooper Institute cohort, the HUNT study in Norway, and the Aerobics Center Longitudinal Study. The relationship holds after controlling for smoking, diet, body weight, and genetics.
For more on why this particular number, VO2 max, matters so much, we have a dedicated piece.
Muscle mass and strength, especially after 60
Sarcopenia, the age-related loss of muscle, is one of the strongest predictors of losing independence. Grip strength alone, measured with a cheap hand dynamometer, predicts disability and mortality in older adults better than most blood-based biomarkers. Resistance training remains the only intervention that reliably reverses sarcopenia. This is covered in more detail in our piece on exercise and longevity.
Metabolic health
People who maintain normal glucose regulation and blood pressure into their seventies have dramatically lower rates of the diseases that drive the healthspan-lifespan gap: type 2 diabetes, coronary disease, stroke, chronic kidney disease, and some forms of dementia. The intervention stack is not glamorous, and you can read more about it in our primer on metabolic health.
Sleep
Chronic short sleep, below about six hours per night sustained over years, is associated with higher risk of nearly every chronic disease that contributes to the gap. This is a strong signal in observational studies and a mechanistically plausible one given what sleep does for memory consolidation, metabolic clearance, and immune function. The full story, with the trials, is in our sleep and aging piece.
Social connection
This one surprises people. Loneliness and social isolation have roughly the same effect on mortality as smoking fifteen cigarettes a day in some meta-analyses. That is not a metaphor. It is what the effect sizes look like. Social connection appears to affect healthspan through stress physiology, behavior (people who live alone are less likely to exercise and more likely to skip meals), and probably some mechanisms we have not worked out yet. See our piece on social connection and longevity for the full picture.
The ones that do not clearly belong on this list yet
Notice what is not here: most of the supplements that dominate the longevity conversation. NAD+ precursors, metformin in healthy adults, resveratrol, rapamycin in humans. Some of these may eventually prove to compress morbidity. As of 2026, none of them has shown a clear healthspan benefit in a well-designed long-term human trial. For the specific case of NAD+ precursors, see our article on NAD+ supplements.
The Part Nobody Wants to Say
The cleanest way to compress morbidity is to prevent the diseases that cause it in the first place, and prevention is boring, unprofitable, and requires time people feel they do not have.
If you could take every adult in a high-income country and get them to walk 7,000 steps a day, sleep seven hours, keep their waist circumference below a healthy threshold, and maintain one or two close social relationships, the population healthspan-lifespan gap would probably shrink by years. Not because of any single intervention, but because each of those inputs pushes back simultaneously on several of the diseases that create the gap. There is no molecule in a bottle that does this. There is no procedure a clinic can bill for. There is no investor pitch. So the conversation goes somewhere else.
The other uncomfortable thing about the gap is that it has a social gradient. Within the United States, the healthspan-lifespan gap is substantially larger for people with less education and lower income. The same dataset that shows the US at 12.4 years average hides a range within the country that is almost as big as the range across countries. If you are a college-educated American with stable housing, your gap is much closer to Norway's. If you are not, it is closer to the national average. The "longevity revolution" some of the wealthier corners of this field talk about is, at the population level, almost entirely a story of who gets access to the basics.
Bottom Line
Here is what I would say to someone deciding what to focus on, based on the evidence as it stands in 2026.
Lifespan is not the right target. The right target is healthspan, or more specifically, the gap between the two. Extending lifespan without extending healthspan just means more years of being sick. The 9.6-year global gap is not a small problem. It is the actual problem.
The gap is shaped almost entirely by chronic diseases of aging, and those diseases have a well-understood prevention stack that starts with cardiorespiratory fitness, muscle mass, metabolic control, sleep, and social connection. These are unglamorous and they work, and their effect sizes in real human populations dwarf anything in the supplement literature.
The interventions that get the most attention right now, including most molecular longevity therapies, do not yet have human evidence for compressing morbidity. They might in the future. They do not now. If you are choosing where to put your time and money, the boring stack is where the data is.
The American gap of 12.4 years is the largest in the world among wealthy countries, and it is getting worse. That is not a biology problem. It is a public health problem layered on top of a biology problem. No pill fixes it.
What I try to optimize for, and what I would suggest to someone who asked, is the question behind the question. Not "how long will I live" but "what do I want to be able to do at 80, and what do I need to do now so that will still be possible." The answer, for almost everyone, involves more walking than pills, more sleep than supplements, and more friends than clinic visits.
Frequently Asked Questions
What is the difference between lifespan and healthspan? Lifespan is the total number of years a person lives. Healthspan is the number of years a person lives in good health, free from significant disease and disability. The difference between the two is called the healthspan-lifespan gap, and it represents the period at the end of life spent managing chronic conditions and losing independence.
How big is the gap between healthspan and lifespan? A 2024 study in JAMA Network Open analyzing data from 183 WHO member states found the global mean gap is 9.6 years. That means the average person lives roughly a decade in a state that qualifies as "not in good health" at the end of their life. The gap grew from 8.5 years in 2000 to 9.6 years in 2019, a 13 percent increase.
Which country has the biggest healthspan-lifespan gap? The United States. According to Garmany and Terzic's 2024 analysis, the US has a healthspan-lifespan gap of 12.4 years, the largest of any country studied. Australia (12.1), New Zealand (11.8), the UK (11.3), and Norway (11.2) are close behind. The pattern largely reflects the burden of chronic noncommunicable diseases in wealthy countries.
Why do women have a bigger gap than men? Women on average live longer than men, but the extra years are disproportionately spent in poor health. The Garmany and Terzic data found a 2.4-year larger gap for women worldwide, associated with a higher burden of chronic musculoskeletal, autoimmune, and mental health conditions. Women gain more lifespan than healthspan, on average.
What is compression of morbidity? Compression of morbidity is a hypothesis proposed by James Fries in a 1980 New England Journal of Medicine paper. It argues that as medicine improves, the onset of chronic disease will get pushed later and later in life, while maximum lifespan stays roughly fixed, squeezing sickness into a shorter period at the end of life. The evidence since 1980 has been mixed. For the US population as a whole, compression has not clearly occurred.
What is HALE? HALE stands for Healthy Life Expectancy, the metric used by the World Health Organization to measure healthspan. It subtracts years lived with disability or disease from total life expectancy, weighted by severity. HALE is the most common cross-country healthspan measure and is reported for every WHO member state.
What interventions actually extend healthspan? Based on human evidence as of 2026, the interventions with the strongest support for compressing morbidity are cardiorespiratory fitness (especially maintaining high VO2 max into later life), resistance training to preserve muscle mass and strength, metabolic health (normal blood pressure, glucose, and lipids), adequate sleep, and social connection. The effect sizes for these are larger than anything currently shown for supplements or longevity drugs in humans.
Do NAD+ supplements or rapamycin extend healthspan? Not based on the current human evidence. NAD+ precursors like NR and NMN reliably raise blood NAD+ levels but have not shown healthspan benefits in well-designed human trials. Rapamycin has extended healthspan in mice but no adequately powered long-term human healthspan trial has been completed. Both remain research questions, not answered questions.
Is healthspan a real scientific concept or a marketing term? Both. Healthspan is a real concept with a measurable definition (HALE or disability-free life expectancy), and it is also used loosely in wellness marketing to justify products that have no demonstrated effect on it. The University of Washington aging scientist Matt Kaeberlein has argued that the healthspan concept needs sharper definitions to prevent this kind of dilution. The strict, measurable version is what drives real research.
Sources
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Garmany, A., and Terzic, A. (2024). "Global Healthspan-Lifespan Gaps Among 183 World Health Organization Member States." JAMA Network Open. Link
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Garmany, A., and Terzic, A. (2025). "Healthspan-lifespan gap differs in magnitude and disease contribution across world regions." Communications Medicine. Link
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Fries, J.F. (1980). "Aging, natural death, and the compression of morbidity." New England Journal of Medicine. 303(3):130-135. Link
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Crimmins, E.M. (2015). "Lifespan and Healthspan: Past, Present, and Promise." The Gerontologist. 55(6):901-911. Link
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Cai, Y., Zimmer, Z., et al. (2024). "Are We Adding Pain-Free Years to Life? A Test of Compression Versus Expansion of Morbidity." The Journals of Gerontology: Series A. Link
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Zheng, H., Choi, Y., Ramirez, J., and Crimmins, E.M. (2022). "Expansion, Compression, Neither, Both? Divergent Patterns in Healthy, Disability-Free, and Morbidity-Free Life Expectancy Across U.S. Birth Cohorts, 1998-2016." Demography. 59(3):949-973. Link
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Kaeberlein, M. (2018). "How healthy is the healthspan concept?" GeroScience. 40(4):361-364. Link
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Olshansky, S.J. (2018). "From Lifespan to Healthspan." JAMA. 320(13):1323-1324. Link
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Olshansky, S.J., Perry, D., Miller, R.A., and Butler, R.N. (2006). "In Pursuit of the Longevity Dividend." The Scientist. 20(3):28-36. Link
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Fried, L.P. (2016). "Interventions for Human Frailty: Physical Activity as a Model." Cold Spring Harbor Perspectives in Medicine. 6(6):a025916. Link
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World Health Organization. (2024). "Healthy Life Expectancy (HALE) at Birth." Global Health Observatory. Link
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Holt-Lunstad, J., Smith, T.B., Baker, M., Harris, T., and Stephenson, D. (2015). "Loneliness and Social Isolation as Risk Factors for Mortality: A Meta-Analytic Review." Perspectives on Psychological Science. 10(2):227-237. Link
Funding Transparency
LSD is editorially independent. We receive no funding from pharmaceutical, supplement, or longevity companies. Here is what we found about the funding relationships behind the research cited above:
- Source 1 and 2 (Garmany and Terzic) were authored by researchers at the Mayo Clinic. The work was supported by intramural Mayo Clinic funds and the Marriott Family Foundation. The authors declared no commercial conflicts related to supplement or longevity companies.
- Source 3 (Fries 1980) was published without external commercial funding. James Fries was a tenured Stanford rheumatologist.
- Source 4 (Crimmins 2015) was supported by the National Institute on Aging at the NIH. Eileen Crimmins is a tenured professor at the University of Southern California Davis School of Gerontology.
- Source 5 (Cai et al. 2024) was supported by the National Institute on Aging. No commercial funding was disclosed.
- Source 6 (Zheng et al. 2022) was supported by the National Institute on Aging and the Max Planck Institute for Demographic Research. No commercial funding.
- Source 7 (Kaeberlein 2018) was a commentary piece without external funding. Matt Kaeberlein is a longevity scientist who has been publicly critical of hype in the supplement space and who runs the Dog Aging Project, which receives NIH funding.
- Source 8 and 9 (Olshansky) were supported by academic and foundation sources. S. Jay Olshansky is a professor at the University of Illinois Chicago and has published repeatedly against rejuvenation and age-reversal marketing claims, which is relevant context for how to read his perspective on healthspan.
- Source 10 (Fried 2016) was supported by the National Institute on Aging. Linda Fried runs the Columbia University Mailman School of Public Health's aging research program.
- Source 12 (Holt-Lunstad et al. 2015) was supported by the Brigham Young University Family Studies Center. No commercial funding.
The pattern here is that nearly all of the research underlying the healthspan-lifespan gap literature comes from publicly funded academic groups, primarily the NIH's National Institute on Aging. This is very different from the NAD+ precursor literature, where commercial involvement is pervasive. It is one of the reasons the healthspan data tends to be more reliable than the supplement data.
Related Reading
- The 12 Hallmarks of Aging - The underlying biology that makes the healthspan-lifespan gap grow in the first place
- Exercise and Longevity: Zone 2 Training - The single intervention with the strongest healthspan evidence and the largest effect sizes in human trials
- VO2 Max: First Principles - Why cardiorespiratory fitness is the most predictive number for healthy aging and how to actually improve yours
- Sleep and Aging - Chronic short sleep is one of the strongest behavioral predictors of the diseases that widen the gap
- Metabolic Health Fundamentals - The upstream system that, when it breaks, drives most of the chronic disease burden of late life
- Social Connection and Longevity - The healthspan input that nobody expected to matter and every large study keeps finding
- NAD+ Supplements: What the Evidence Actually Shows - A worked example of what it looks like when a longevity intervention has not yet shown healthspan benefit in humans
- Your Body's Biomarkers - How to measure where you actually stand on the healthspan curve rather than guessing
Written with the help of AI tools, shaped and verified by humans who care about getting this right.
This is not medical advice. Consult your healthcare provider before making major changes to your diet, exercise, supplementation, or sleep routine, especially if you have existing medical conditions.