Is Aging a Disease? A Written Debate

Is aging a disease, or a natural part of life? At first, the question may seem straightforward. But ask researchers whether aging should be classified as a disease, and the answer quickly becomes more complicated. The line between normal aging and disease is not always clear, and where that line is drawn could have far-reaching consequences.

This is not merely an academic issue. Whether aging is officially recognized as a disease could determine which research gets funded, which drugs are approved, what insurers pay for, and how doctors treat their patients. It would shape whether we invest in targeting the biology of aging itself, and whether we consider age-related decline as inevitable or as something that can be slowed, treated, or even prevented.

To explore this question - and others like it - we are launching a series of written debates in Lifespan Magazine. Each debate will pose a question that must be argued from one side or the other. For this opening debate, a coin toss determined the positions: Kelly Rich, Ph.D., will argue that aging is a disease, while Adiv Johnson, Ph.D., will argue that it is not. David Sinclair, A.O., Ph.D., will serve as debate moderator.

David: Does aging meet the fundamental definition of disease?

Kelly: A disease is any pathological process that impairs normal function and increases the risk of death. Aging fits that definition. It has reproducible biological mechanisms, including genomic instability, epigenetic changes, cellular senescence, chronic inflammation, that degrade the functions of cells and organs, driving nearly every major cause of death.

What counts as a “disease” has always been historically contingent. Hypertension, osteoporosis, and cardiomyopathies were once viewed as “just old age” and only later classified as diseases once we understood them and could treat them. Osteoporosis, for example, wasn’t formally labeled a disease by the World Health Organization until the 1990s.¹ If those kinds of conditions eventually earn the label of disease, what disqualifies aging from the same treatment?

Adiv: Disease implies a departure from a normal biological function. Aging, by contrast, is the normal course of human life. It is universal, expected, and deeply integrated into nearly every biological system. That does not mean its harmful effects should be accepted or left untreated. We should prevent cancer, dementia, frailty, and other age-related conditions wherever possible. But susceptibility to disease is not itself a disease. Aging is a life stage, just like childhood. Childhood also carries distinctive biological vulnerabilities, yet we do not classify it as a pathology. Labeling aging a disease risks confusing a natural life stage with the specific disorders that may arise during it, effectively medicalizing life itself.²

Kelly: Sure, aging happens to all humans. In fact, there are lots of universal bodily processes that we label as normal when they work properly, and we label as clearly diseased when they go wrong. For example, the systems that tell cells when to grow and when to die are essential for normal development. When they become mis‑regulated, we get heart failure, cancer or neurodegeneration, and no one doubts those are diseases. So, the key question isn’t “does this happen to everyone?” It’s “does this process damage the body in a way that increases sickness and death, and can we, in principle, change it?” By that standard, aging fits the definition of disease.

Adiv: This is the crux of our disagreement as I do think universality is highly relevant here. Alzheimer’s disease, cancer, stroke, type 2 diabetes, glaucoma, age-related macular degeneration, and other common age-related diseases are not universal. Many people reach old age without ever developing them, which is exactly why we single them out as disease. Aging, by contrast, is something no human being has ever escaped.

David: Some animals have extremely slow aging or appear to “escape” aging. Do these examples prove that aging is not universal and inevitable?

Kelly: Long‑lived species show that aging is a variable trait, not a fixed law of nature. Bowhead whales can live for more than 200 years and Greenland sharks can live for nearly four centuries. Naked mole-rats, ocean quahogs, and some turtles maintain function and show relatively low rates of age-related decline for most of their lives. Hydra and planarian worms can maintain essentially indefinite regenerative capacity under laboratory conditions.³

From a disease perspective, these species demonstrate that the processes we call “aging” in humans are not hard-wired into biology. Evolution can slow or suppress them. We see something similar with diseases. Some organisms, such as elephants, have evolved remarkable resistance to cancer or atherosclerosis because they’ve evolved protective mechanisms. We don’t conclude those conditions aren’t diseases simply because some species are protected. We should conclude that natural “therapies” exist in other species.

Adiv: It’s true that these long-lived animals are mind-boggling. The fact that the ocean quahog clam can survive for half a millennium is hard to wrap your head around. That said, all known long-lived animals eventually die. We also don’t actually know if any animals truly escape aging. “Immortal” jellyfish may very well die, for example, and the reality is that these animals haven’t been thoroughly studied.

Despite the many interventions that can extend lifespan in mice, rats, or other model organisms,⁴ these animals still show age-related decline and die. And even if potentially immortal animals like planarian worms lived forever, there’s a world of difference between a simple worm and a highly complex mammal. The reality is that, among us mammals, aging is universal. A sanguine attitude won’t allow humans to easily recreate the biological advantages of a worm.

Kelly: The fact that these animals don’t literally live forever isn’t the point. The key is that interspecies differences in healthspan track with core mechanisms like DNA repair and cellular senescence. That suggests human “normal aging” is one particular failure mode of complex biology, and much closer to a shared disease process than to a neutral life stage.

Adiv: I have a different interpretation, which is that the presence of long-lived animals further serves as evidence that aging is a modifiable process. However, there are limits to what can be achieved within an animal’s biology. It’s also important to acknowledge that humans are already long-lived animals. The maximum recorded lifespan for humans is 122 years, which is monumental compared to other primates. Orangutans, for instance, have a maximum lifespan of 59 years.⁵ Given that evolution has already optimized human physiology for longevity, it’s not clear how much more this process can be pushed.

Kelly: And that’s exactly why disease framing matters. If humans are already at the long‑lived end of primates, we’re unlikely to get much further by addressing diseases one by one or waiting on evolution to extend our lifespans. Meaningful gains will require deliberately targeting the underlying biological mechanisms of aging, including those that allow other species to age more slowly. In practice, that is exactly what medicine does with any disease: identify its causes and develop ways to intervene.

David: Should aging biomarkers such as Horvath’s DNA methylation clock be used by doctors to predict diseases or guide the treatment of patients?

Adiv: Aging biomarkers are not simple on-or-off indicators of disease, nor were they designed to identify a clearly defined pathological state. Contrast them with fasting glucose or hemoglobin A1c, for which established thresholds can support a diagnosis. Aging biomarkers are better understood as probabilistic risk indicators: they reflect the odds in longitudinal data rather than provide a yes-or-no answer.

Epigenetic clocks, for example, integrate the effects of social, environmental, and behavioral exposures, capturing differences in both health and life history. But elevated risk is not itself a disease. If it were, many other risk-associated characteristics would also qualify as diseases. Living in rural America, for example, is associated with a greater risk of chronic disease and a shorter lifespan.⁶ Yet it would be absurd to diagnose someone with a disease based on geography alone. Aging biomarkers may eventually help doctors assess risk or guide care, but a high molecular age (as predicted by an aging clock) does not, by itself, prove that aging is a disease.

Kelly: Biomarkers start to matter clinically when they reliably tell us something important about people’s future health. Many aging biomarkers now do exactly that. Epigenetic measures such as DunedinPACE, which estimate the pace of biological aging from DNA methylation patterns, can now predict death and major diseases as well or better than many traditional clinical risk factors.⁷

Clinically, we already treat high-risk states as diseases or pre-diseases when the underlying process is understood and modifiable, as with prediabetes or inherited high cholesterol. Aging biomarkers differ mainly in scale: they read out a whole-body pathological process rather than a single organ. Aging biomarkers may be probabilistic and influenced by lifestyle, but so too are things like blood pressure and hemoglobin A1c. We would never say that hypertension or diabetes “don’t count” as diseases just because lifestyle and context influence them. Instead we use those markers to track disease activity and treat an underlying problem. If aging drives late-life illness, its best biomarkers may measure the activity of that process, not merely background risk.

Adiv: You’re right that traditional biomarkers also indicate risk. Someone can have hypertension and never have a heart attack, and the predictive power of many aging biomarkers is impressive. But there is still an important difference: mechanism. Low grip strength predicts future cardiovascular death in adults tracked over time,⁸ but why? Is it inactivity, malnutrition, low muscle mass, or excess visceral fat? High blood pressure, by contrast, damages the heart and blood vessels through well-understood mechanisms. Aging biomarkers may be valuable warning signs, but until we understand what they are measuring, they should not be treated as evidence of a disease.

David: If aging is a disease, do everyday signs of aging, wrinkles, gray hair, less strength, and slower walking speed, count as disease symptoms?

Adiv: Wrinkles and gray hair may bother us cosmetically, but they don’t necessarily harm health or function. People’s hair color, skin texture, or walking speed vary widely no matter how old you are. Calling all of these “symptoms” stretches the idea of disease so far that it becomes almost meaningless. If we claim that reduced strength is symptomatic of disease, then is someone diseased if they lose muscle mass after going on a month-long vacation? What if someone takes a break from running and their aerobic capacity drops? For these examples, “disease” is too strong a label.

Kelly: I agree that gray hair and wrinkles are largely cosmetic. The case for aging as a disease doesn’t rest on labeling every surface change a problem. It instead rests on the fact that symptoms such as declines in strength, balance, and walking speed reflect deeper biological damage. Loss of muscle (sarcopenia) and frailty are linked to chronic inflammation, mitochondrial dysfunction, impaired cellular cleanup, and stem-cell exhaustion, many of the same processes that drive chronic disease.

Adiv’s vacation example is helpful here. If you stop exercising for a few weeks, you can lose some fitness, but that can be temporary. Age-related decline, on the other hand, reflects a persistent failure to maintain proteins, repair tissues, and rebuild muscle. A new gray hair is not a diagnosis. But becoming progressively weaker, slower, and less resilient may be an outward symptom of a deeper condition: aging itself.

David: What are the downstream effects of calling aging a disease? Why is this so important to get right?

Adiv: There is a real risk of hype and overselling “cures for aging” if it’s framed as a disease you can honestly escape. For now, our limited resources and brainpower should be focused on compressing the gap between healthspan and lifespan as well as treating specific conditions that are especially burdensome (e.g., dementia, cancer, etc.). It’s no coincidence that longevity scientists who believe aging is a disease are much more likely to expect radical gains in life expectancy in the near future.⁹ Labeling aging as a disease is connected to the ideas of immortality and transhumanism. It can conjure the idea that, if it’s a disease, it can be cured.

At this time, it should be sufficient to just accept that aging is a targetable process and something that can be substantially modified. We already know this is the case because there are dramatic differences in lifespan and healthspan across the globe.¹⁰ I fail to see why aging needs to be branded as a disease to improve longevity. Is it necessary to call gravity a disease to justify building better parachutes?

Kelly: The consequences are largely regulatory and economic. Because aging is not an approved indication, drugs cannot be approved to treat it specifically, and insurers generally will not cover therapies that target it. Clinical trials must instead focus on individual diseases, even when an intervention targets fundamental aging pathways such as mTOR, cellular senescence, or mitochondrial dysfunction. This fragments research and makes it harder to test therapies that might delay several diseases at once. Without formal recognition, even safe and effective treatments targeting aging could struggle to gain approval or reimbursement.

You are justified in being wary of hype and “cures for aging.” But that is a problem of messaging, not biology. Calling aging a disease should not imply immortality. It simply means aging is something we can, at least in part, change. Refusing to classify aging as a disease is not a neutral choice. It directs resources toward late-stage treatment rather than addressing a shared underlying cause. If aging drives most chronic diseases, then our language and regulations should reflect that reality.

 

Final Thoughts

As you think about this debate, it may help to imagine two futures. In one, aging is formally classified as a disease: regulators, companies, and clinicians treat it as a major drug target and “anti-aging” medicines are developed and reimbursed like any other therapy. In the other scenario, aging as a process remains a background process. We continue to focus on preventing and treating specific diseases like Alzheimer’s and sarcopenia, and treat aging as a major risk factor rather than a diagnosis. Both futures come with tradeoffs – scientific, ethical, economic and social. The real question is: which future would lead to longer, healthier lives?

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Last Updated: Oct 8, 2026 · 13 minute read