Why Aging Is a Disease — And Could We Actually Cure It?

Whether aging counts as a disease sounds like a quibble over vocabulary, but it decides how research is funded, which trials regulators will accept, and whether a drug that slows several age-related illnesses at once can ever be approved as such. The World Health Organization's ICD-11 coding system touched the question in 2022 and left it unresolved. Meanwhile, the biology has moved: researchers have mapped the mechanisms that drive aging, extended lifespan in mice, and started small human trials. This article separates what has been shown from what has only been promised.

Educational content, not medical advice. Talk to your doctor before changing any medication, treatment, or routine. Information here reflects current research but every person's situation differs.

Key takeaways

• Aging is the accumulation of molecular and cellular damage over time, and it is the largest single risk factor for cancer, heart disease, diabetes, and neurodegeneration.
• A 2013 review in Cell proposed nine hallmarks of aging; a 2023 update expanded the list to twelve.
• In mice, clearing senescent cells, giving rapamycin late in life, and telomerase gene therapy have each extended lifespan or survival in published studies, with gains in the range of roughly 9 to 36 percent depending on the measure.
• Human evidence is thin: the senolytic trials are tiny, the metformin trial (TAME) is a proposed six-year study, and no consensus biomarker of aging exists.
• Whether aging is a "disease" is a classification dispute, not a lab result, and regulators currently do not accept aging itself as a treatable indication.

What it means to call aging a disease

A disease, in the usual medical sense, is a departure from normal function with an identifiable cause and a set of symptoms. Aging fails the "departure from normal" test in an obvious way: everyone does it. That is the core of the argument against the label, and it is made seriously. A 2024 review in Cureus by Mendoza-Núñez and colleagues, for example, calls aging "a process inherent to living beings" and warns that classifying it as a disease can feed ageism (Europe PMC).

The argument for the label is practical rather than philosophical. Age is the strongest predictor of nearly every chronic illness, so a drug that slows a shared mechanism might delay many of them together. Under current rules, the US Food and Drug Administration and the European Medicines Agency approve drugs for diseases or conditions, and aging itself is not currently a recognized indication, as a 2023 Nature Communications review of geroscience trials points out (Rolland et al., 2023). A company cannot simply run a trial to show that a pill "slows aging" and expect an approval at the end.

Think of it like the difference between treating rust and treating each leaking pipe, hinge, and rivet on an old bridge. Conventional medicine repairs the leaks one at a time, and does it well. Geroscience, the field that studies the biology of aging in order to delay age-related disease, asks whether slowing the rusting would reduce all the leaks at once.

Where ICD-11 actually stands

Popular accounts say the WHO "classified aging as a disease" in 2018. The record is messier. The Cureus review reports that the proposal to include aging and old age was approved in 2019 and took effect in 2022. The code MG2A, originally titled "old age," sits among general symptoms and signs, which drew broad objections from geriatricians and gerontologists. The WHO then reworded it as "ageing associated decline in intrinsic capacity," and a separate extension code, XT9T ("ageing-related"), was retained (Mendoza-Núñez et al., 2024).

The authors of that review read these choices as the WHO treating aging as a disease; others read the symptom-chapter placement as exactly the opposite. Both readings agree on one point: ICD-11 did not create a treatable "aging disease" that a drug can be approved for. That regulatory gap is the real obstacle for the field.

The hallmarks: aging as a list of mechanisms

If aging is not one process, what is it? The most cited answer is the 2013 paper "The Hallmarks of Aging" in Cell by Carlos López-Otín, Maria Blasco, Linda Partridge, Manuel Serrano, and Guido Kroemer. It proposed nine tentative hallmarks shared across organisms: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication (López-Otín et al., 2013).

A decade later the same group published "Hallmarks of aging: An expanding universe" in Cell (January 2023). It proposes twelve hallmarks and sets three criteria for each: it appears with age, making it worse experimentally speeds up aging, and treating it can slow, halt, or reverse aging (López-Otín et al., 2023). The added entries are disabled macroautophagy, chronic inflammation, and dysbiosis, an imbalance in the community of gut microbes.

Hallmark	What goes wrong	Where the intervention research stands
Genomic instability	DNA damage outpaces repair	Mostly basic research
Telomere attrition	Chromosome caps shorten with division	Telomerase gene therapy in mice
Epigenetic alterations	Chemical marks on DNA drift	Epigenetic clocks; partial reprogramming in mice
Loss of proteostasis	Misfolded proteins accumulate	Linked to neurodegeneration research
Disabled macroautophagy	Cellular self-cleaning slows	Rapamycin and fasting studies
Deregulated nutrient sensing	mTOR and related pathways stay switched on	Rapamycin in mice; metformin trials proposed
Mitochondrial dysfunction	Energy output falls	NAD+ precursor trials
Cellular senescence	Cells stop dividing but persist	Senolytics in mice, pilot human trials
Stem cell exhaustion	Tissue repair declines	Cell-therapy trials, early stage
Altered intercellular communication	Signaling between cells degrades	Anti-inflammatory strategies
Chronic inflammation	Low-grade, persistent immune activity	Observational and mechanistic work
Dysbiosis	Gut microbial balance shifts	Microbiome research

The table should be read with one caution. A hallmark is a hypothesis about where to intervene, not proof that intervening extends human life. For a closer look at one of the hallmarks, the aging biology explainer walks through the damage-accumulation picture in more detail.

Senescent cells: the hallmark drawing the most attention

Cellular senescence is a state in which a cell stops dividing but does not die. Such cells are often called "zombie cells," and they are not inert: they secrete a mix of inflammatory proteins, growth factors, and tissue-degrading enzymes known as the senescence-associated secretory phenotype, or SASP. In small numbers, senescence helps wound healing and blocks the growth of damaged cells that might become cancerous. The trouble is accumulation: senescent cells build up with age, and their secretions can irritate neighbors.

How does senescence differ from the better-known cell death process? Apoptosis is a tidy, programmed self-destruction. Senescent cells resist it, so they persist, which is exactly what makes them a drug target.

What the mouse studies found

The strongest early evidence comes from a mouse study led by Jan van Deursen's group at the Mayo Clinic. In 2016 in Nature, they reported that using the INK-ATTAC transgene to clear cells expressing p16Ink4a, starting at one year of age, extended median lifespan in both male and female mice across two genetic backgrounds. It also delayed tumor formation and slowed age-related decline in the kidney, heart, and fat tissue without obvious side effects (Baker et al., 2016). This used a genetic trick to delete the cells, which cannot be applied to people.

The drug route came two years later. A 2018 paper in Nature Medicine from James Kirkland's group at the Mayo Clinic tested dasatinib (a cancer drug) plus quercetin (a plant flavonoid) in mice. Intermittent treatment improved physical function in naturally aged mice, and treated animals showed a 36 percent increase in post-treatment survival and a reduction in mortality hazard to 65 percent of controls (Xu et al., 2018). Drugs that selectively kill senescent cells are called senolytics.

What the human data show

The human data are far smaller. In a 2019 open-label phase 1 pilot in EBioMedicine, nine adults with diabetic kidney disease (mean age 68.7 years) took dasatinib 100 mg and quercetin 1,000 mg orally for three days. Eleven days later, fat-tissue biopsies showed fewer cells expressing the senescence markers p16 and p21, and several circulating SASP factors, including interleukin-6, had dropped (Hickson et al., 2019).

That result is meaningful and also modest. It had no control group, nine participants, and it measured senescent-cell markers, not survival, disease progression, or quality of life. A reduction in a biomarker is a reason to run a larger trial, not a reason to take the drugs.

Telomeres: the timekeepers that are not the whole clock

Every time a cell divides it must copy its chromosomes, and the copying machinery cannot fully replicate the very ends. Those ends, the telomeres, shorten a little with each division. They work like the plastic tips on a shoelace: they protect the functional material inside from fraying. When telomeres get critically short, a cell typically enters senescence or dies. The telomere and telomerase explainer covers the mechanics.

The enzyme telomerase can rebuild telomeres. It is active in stem cells and germline cells but largely silent in most body cells, and many cancers switch it back on, which is one reason that broad activation is a double-edged idea.

In 2012, Maria Blasco's group in Madrid published a gene-therapy experiment in EMBO Molecular Medicine. Using adeno-associated virus vectors to deliver the telomerase gene (TERT) to mice, they raised median lifespan by 24 percent in animals treated at one year of age and by 13 percent in animals treated at two years, with no increase in cancer compared with controls. A version of TERT without catalytic activity produced none of the benefits (Bernardes de Jesus et al., 2012).

It is a striking result, with two limits. Mice have much longer telomeres than humans and are less limited by telomere shortening, so a result in mice does not map cleanly onto people. And the cancer-free outcome applies to that mouse design and follow-up, not to every context in which telomerase might be switched on.

Epigenetic clocks and the idea of rewinding cells

The epigenome is the layer of chemical marks on DNA and its packaging proteins that tells a cell which genes to read. Methylation, the addition of small methyl groups at specific DNA sites, changes predictably with age. In 2013, Steve Horvath, then at UCLA, published a multi-tissue predictor of age in Genome Biology, trained on about 8,000 samples from 82 datasets covering 51 tissues and cell types and using 353 sites in the genome (Horvath, 2013). The estimate it produces is often called DNA methylation age or "epigenetic age."

Two features of Horvath's paper deserve mention. The predicted age was close to zero in embryonic and induced pluripotent stem cells, which suggests the clock can be reset. And all 20 cancer types analyzed showed significant age acceleration, averaging 36 years, which shows the clock is picking up something biological rather than just calendar time.

Partial reprogramming

If methylation marks drift with age, can they be pushed back? In 2016, Alejandro Ocampo, Juan Carlos Izpisua Belmonte, and colleagues reported in Cell that short, cyclic expression of the four Yamanaka factors (Oct4, Sox2, Klf4, and c-Myc, the genes that can convert adult cells into stem-like cells) improved cellular and physiological signs of aging and extended lifespan in a mouse model of premature aging. The same treatment improved recovery from metabolic disease and muscle injury in older normal mice (Ocampo et al., 2016). The Yamanaka experiments explainer describes how those factors were first discovered.

The word "partial" matters: the aim is to rejuvenate cells without erasing what makes them a liver cell or a neuron. Running the program too long risks turning cells into tumors, and the mouse model used in that study ages unusually fast, so it is an imperfect stand-in for ordinary human aging. Think of it like pressing a car's undo button just a few steps rather than reverting it to a factory-fresh chassis.

Eating less, mTOR, and rapamycin

The most reproducible lifespan intervention in animal biology is eating less without malnutrition. Caloric restriction extends lifespan in yeast, worms, flies, and rodents. In primates the evidence is split, which is a useful reminder of how hard it is to transfer findings to humans.

A 20-year study at the Wisconsin National Primate Research Center, published in Science in 2009, found that moderate restriction in rhesus monkeys lowered age-related deaths: 80 percent of restricted animals survived at the time reported versus 50 percent of controls. Restricted animals also had fewer cases of diabetes, cancer, cardiovascular disease, and brain atrophy (Colman et al., 2009). A parallel study by the National Institute on Aging, published in Nature in 2012, found that calorie restriction (10 to 40 percent below normal intake) did not improve survival, though the authors argued differences in diet composition and husbandry between the studies might explain the discrepancy (Mattison et al., 2012).

The mTOR connection

Much of the interest in restriction comes from a nutrient-sensing pathway built around a protein called mTOR (mechanistic target of rapamycin). When nutrients are plentiful, mTOR is active and pushes the cell toward growth. When they are scarce, mTOR activity falls and the cell shifts toward maintenance, including autophagy, the process that recycles damaged components. Rapamycin, a drug first used to prevent organ transplant rejection, inhibits mTOR.

The test that made rapamycin famous came from the NIA Interventions Testing Program. In a 2009 Nature paper, David Harrison, Richard Miller, and colleagues gave rapamycin to genetically diverse mice starting at 600 days of age, roughly late middle age. Lifespan rose by about 14 percent in females and about 9 percent in males, and the result reproduced at three independent sites (Harrison et al., 2009). The authors noted the drug could be working by delaying cancer deaths, by slowing aging mechanisms, or both, and that ambiguity has not fully gone away.

For humans, rapamycin and related drugs suppress the immune system at transplant doses and have side effects, so the benefit-risk balance at lower doses is an open question. A related idea is that metformin, a decades-old diabetes drug thought to act partly through the AMPK energy-sensing pathway, might delay several age-related conditions at once. The proposed TAME trial (Targeting Aging with Metformin) is designed as a six-year study of about 3,000 people aged 65 to 80, with the primary endpoint being time to any of five major age-related conditions or death (Rolland et al., 2023). Its main purpose is to show regulators that aging-related outcomes can be a legitimate trial endpoint.

For the dietary angle, the intermittent fasting evidence review covers what time-restricted eating has and has not shown in people.

NAD+, sirtuins, and the supplement question

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme involved in energy metabolism and in the activity of sirtuins, a family of proteins that influence DNA repair, inflammation, and mitochondrial function. NAD+ levels are reported to fall with age in several tissues, which led to interest in precursors such as NMN (nicotinamide mononucleotide) and NR (nicotinamide riboside), both sold as supplements. The mitochondria explainer gives the background on why cells need this molecule at all.

What do human trials show? One recent, relatively typical example: a randomized, placebo-controlled trial of 60 older adults published in GeroScience in 2024 gave 250 mg of NMN daily for 12 weeks. Blood NAD+ levels rose and walking times and sleep quality improved at 12 weeks, but the pre-specified primary stepping test showed no difference between the groups (Morifuji et al., 2024). A 2025 mouse study in Science Advances found that most orally given NMN and NR was converted by gut microbes into nicotinic acid before the liver used it to make NAD+ (Yaku et al., 2025), which complicates the simple "take a precursor, raise NAD+" story.

The fair summary is that raising a blood biomarker is easy and showing a clinical benefit is not. Anyone considering a supplement should discuss it with a clinician, particularly if they take other medications.

Why mouse results do not automatically become human medicine

Almost every dramatic headline in this field starts with a mouse, a worm, or a fly. Those organisms are useful because they live for months or weeks, so an experiment finishes in a reasonable time. They are risky guides for the same reason: their biology, lifespans, and cancer risks differ from ours.

Intervention	Strongest evidence	Human evidence so far
Caloric restriction	Rodents; one of two primate studies	Short-term biomarker studies; no lifespan data
Rapamycin	9 to 14% lifespan gain in mice, started late in life	No lifespan data
Senolytics (dasatinib + quercetin)	36% post-treatment survival gain in aged mice	Nine-person pilot, biomarkers only
Telomerase gene therapy	13 to 24% median lifespan gain in mice	None
Partial reprogramming	Lifespan gain in progeroid mice	None
NMN / NR	Mouse models	Small trials, mixed outcomes
Metformin	Observational signals in diabetes	TAME trial proposed

A task-force discussion in the 2023 Nature Communications review is blunt about the state of the art: most geroscience trials are small and short, so they cannot show progression from robust to frail, and there are no consensually accepted biomarkers of aging (Rolland et al., 2023). Epigenetic clocks are promising, but a clock that predicts risk is not the same as a clock that tells you whether a drug worked.

Is there a ceiling on human lifespan?

The oldest verified person, Jeanne Calment of France, died in 1997 at the age of 122. In 2016, Xiao Dong, Brandon Milholland, and Jan Vijg published a Nature analysis of demographic data arguing that gains in survival at advanced ages fade after about age 100 and that the age at death of the world's oldest person had not risen since the 1990s. They concluded that the maximum human lifespan is probably fixed by natural constraints (Dong et al., 2016).

Not everyone reads the data that way. In 2018 in Science, Elisabetta Barbi, James Vaupel, and colleagues analyzed 3,836 documented Italians aged 105 or older and found mortality rates that were essentially flat beyond 105, rather than climbing steadily. They presented this as evidence for a mortality plateau, which is hard to square with a hard ceiling (Barbi et al., 2018). The two papers use different methods and data, a published comment in Science challenged the Italian analysis, and the debate is still active.

Why does a ceiling matter for the "cure aging" question? Because every intervention in the tables above, if it works, works at the margin: it might add years of healthy life, not rewrite the maximum. The centenarian ranking and the life expectancy ranking show how far populations have moved on average, which is a different thing from moving the maximum.

Longevity escape velocity and other speculation

Ray Kurzweil and Aubrey de Grey popularized the idea of longevity escape velocity: if medicine improved fast enough that each year of research added more than a year to remaining life expectancy, people could in principle outrun aging. It is an arithmetic argument about rates, not a biological finding, and nothing in the current evidence shows that the rate condition is close to being met.

The idea also carries a quiet assumption, that the hallmarks can be repaired independently. Many of them are tangled together: senescent cells feed inflammation, inflammation damages stem cells, damaged mitochondria produce more reactive molecules, and those damage DNA. Fixing one without the others may deliver only partial gains. For a more speculative look at what radical lifespans would imply, see what if humans could live to 1,000 years.

Why evolution did not select for longer lives

If aging were purely harmful, natural selection should have removed it. The standard evolutionary answer is that selection weakens with age. A gene that does harm only after the organism has done most of its reproducing is barely visible to selection, and a gene that helps early but harms late may even be favored. Aging, on this view, is not a program that evolution designed but an absence of maintenance that evolution did not need to fund.

Comparative biology supports the idea that maintenance is adjustable. Species vary enormously in lifespan relative to body size, and some long-lived animals have unusual tumor-suppression or repair biology. The longest-living animals and the naked mole-rat cancer resistance articles show where researchers look for lessons.

What the evidence supports today

Setting the drug pipeline aside, the best-documented ways to be healthier for longer are not exotic. In a 2018 Circulation analysis of the Nurses' Health Study (78,865 women) and the Health Professionals Follow-up Study (44,354 men), with up to 34 years of follow-up, people who met five low-risk lifestyle criteria (never smoking, a body mass index of 18.5 to 24.9, at least 30 minutes a day of moderate-to-vigorous activity, moderate alcohol intake, and a high-quality diet) had a hazard ratio for all-cause mortality of 0.26 compared with those who met none. Estimated life expectancy at age 50 was about 14.0 years longer for women and 12.2 years longer for men (Li et al., 2018).

These are observational data, so they show association rather than proof of cause, and people who follow healthy habits may differ in other ways. A second large source is the pooled analysis of 661,137 adults by Hannah Arem and colleagues in JAMA Internal Medicine (2015): people meeting the minimum guideline for leisure-time activity had about a 31 percent lower mortality risk than inactive people, and benefits leveled off at roughly three to five times the minimum (Arem et al., 2015).

Further reading on the individual pieces: the science of exercise, sleep and health, and the broader longevity interventions review.

Frequently asked questions

Q: Is there a maximum human lifespan? A: The oldest verified person, Jeanne Calment, died at 122 in 1997. A 2016 analysis in Nature argued the maximum is fixed by natural limits, while a 2018 study in Science of Italians aged 105 and older found mortality rates that flatten out rather than rise. The question is unresolved.

Q: Is aging officially a disease? A: Not in a way that creates an approved treatment target. ICD-11, in effect since 2022, includes the code MG2A, now worded as ageing-associated decline in intrinsic capacity, in its symptoms chapter, plus an extension code, XT9T. Scholars disagree on whether that amounts to calling aging a disease, and regulators do not currently accept aging itself as a drug indication.

Q: Are anti-aging supplements worth taking? A: Evidence in humans is limited. A 12-week trial of NMN in 60 older adults raised blood NAD+ levels but showed no difference on its primary walking test. Whether a supplement is appropriate depends on individual health and medications, so it is a question for a clinician rather than a general recommendation.

Q: Have senolytic drugs been shown to work in people? A: Only at the biomarker level so far. A 2019 pilot gave dasatinib and quercetin to nine adults with diabetic kidney disease and found fewer senescent cells in fat tissue after eleven days. There was no control group and no measure of clinical outcomes, so larger trials are needed.

Q: Why did evolution not select for longer lifespans? A: Natural selection acts weakly on traits that appear after reproduction. A gene that causes harm late in life is hard for selection to remove, and a gene that helps early but harms late can even spread. Aging reflects limited investment in long-term maintenance rather than a designed program.

Q: Would much longer lives be desirable? A: That is a social and ethical debate, not a scientific one. Proponents argue that treating aging reduces suffering. Critics raise unequal access, pressure on pensions and health systems, and slow turnover in institutions. Researchers generally acknowledge these concerns, and they are part of why the trial endpoints chosen for geroscience matter.

The bottom line

Calling aging a disease is a way of asking whether its mechanisms can be treated the way we treat disease mechanisms. The hallmarks give researchers a map, and animal studies show that several of those mechanisms can be moved: clearing senescent cells, inhibiting mTOR, activating telomerase, and partially reprogramming cells have each extended lifespan or healthspan in mice. What is missing is human proof. The senolytic trials are pilots, the metformin trial is a design, and no accepted biomarker tells us a treatment worked before the outcomes arrive. The honest position is neither "aging is solved" nor "nothing can be done": the science is real, the timeline is unknown, and the best-supported human interventions remain the ordinary ones.

Sources

• López-Otín C, et al. "The hallmarks of aging." Cell 2013: Europe PMC record
• López-Otín C, et al. "Hallmarks of aging: An expanding universe." Cell 2023: Europe PMC record
• Rolland Y, et al. "Challenges in developing Geroscience trials." Nature Communications 2023: Europe PMC record
• Mendoza-Núñez VM, et al. "Is Aging a Disease? A Critical Review Within the Framework of Ageism." Cureus 2024: Europe PMC record
• Harrison DE, et al. "Rapamycin fed late in life extends lifespan in genetically heterogeneous mice." Nature 2009: Europe PMC record
• Hickson LJ, et al. Senolytics in diabetic kidney disease. EBioMedicine 2019: DOI
• Dong X, Milholland B, Vijg J. "Evidence for a limit to human lifespan." Nature 2016: Europe PMC record

Related Reading

• Why We Age — The Biology of Getting Old
• Why Do We Age? The Science of Aging Explained
• Longevity Interventions: What Actually Works
• The Gut Microbiome Explained
• Why Do We Yawn — and Why Is It Contagious?
• The Science of Exercise — Why It Works and How Much You Actually Need
• The Science of Sleep — Why You Need It and What Happens Without It
• The Vitamin D Paradox — Why It's So Important and So Misunderstood
• The Science of Mental Health — What We Actually Know