Why Extending Healthspan Without Lifespan Is a Misguided Goal for Aging Science

A fashionable mantra has taken hold in the world of aging research: the goal, we are told again and again, is to extend healthspan, not lifespan. The slogan sounds sensible, even virtuous. Who would not want more years of good health rather than more years of illness? But according to a provocative new opinion paper published in the journal GeroScience, this phrase has hardened into a cliché that is scientifically incoherent and ethically troubling. David Gems and Ekaterina R. Iijima of University College London, together with João Pedro de Magalhães of the University of Birmingham, argue that the slogan arose from a confusion between two very different disciplines, and that clinging to it risks undermining one of the most promising enterprises in modern biology: the effort to slow human aging itself.

The term healthspan, defined as the period of life spent in good health, free from the chronic diseases and disabilities of aging, has a longer history than many realize. It appeared in geriatric medicine as early as the 1960s and gained traction after an influential 1987 paper on successful aging, but its use in the scientific literature only soared during the 2010s. That surge coincided with the rise of the geroscience agenda, championed by the US National Institute on Aging and echoed by initiatives such as the Saudi Hevolution Foundation. Alongside this shift came statements like the influential claim that life extension should no longer be the primary goal of medicine for people over 65, and that the extension of healthspan should instead be the principal metric of success. The authors do not dispute that emphasizing healthspan is reasonable, uncontroversial, and pragmatic in terms of public relations and research funding politics. Their complaint is that the message has been misconstrued, often by colleagues in the field itself, as meaning that life extension should no longer be a goal of aging research at all.

To understand how this misconception took root, Gems and his colleagues invite us to contrast the aspirations of two groups of young trainees: those entering geriatric medicine and those entering biogerontology, the study of the biology of aging. The geriatrician faces a sobering reality. Every patient will eventually die from the condition that ails them, namely the process of senescence itself. Within that constraint, the visionary geriatrician James Fries articulated an inspiring goal: because human longevity appears to have an upper ceiling, a conclusion supported by evidence that worldwide records of maximum lifespan plateaued in the 1990s, late-life medicine should aim to compress morbidity. Thanks to a century of public health improvements, population survival curves have become increasingly rectangular, with more people surviving to old age. Fries argued that the morbidity curve could be rectangularized too, shrinking the proportion of later life spent in poor health.

Central to Fries’s vision is the role of frailty. Very late in life, frailty can increase to the point that death comes easily and quickly from even minor insults, a fall or a bacterial infection. Drawing on an essay by Lewis Thomas, Fries likened such a death to the fabled one-hoss shay of Oliver Wendell Holmes’s poem, a carriage that went to pieces all at once, just as bubbles do when they burst. The image suggests the possibility of death without prolonged illness, though the authors are careful to note that frailty is itself the product of widespread pathology and functional impairment across many physiological systems. There is, strictly speaking, no natural death from pure aging without pathology. Within this geriatric framework, recommendations to focus on healthspan rather than lifespan are well founded, and the point is reinforced by the mathematics of life table entropy: with advancing age, reductions in mortality rates yield ever smaller increases in life expectancy.

The vision of biogerontology, however, is fundamentally different. Its central premise is that the aging process as a whole might be decelerated or even reversed. That this is not fantasy is demonstrated by decades of animal research. Caloric restriction extends life in rodents, mutations that reduce growth hormone signaling do the same, and a number of drugs have proven life-extending in the rigorous testing program run by the National Institute on Aging. Aging also shows enormous plasticity in evolution, with mammalian lifespans ranging from a few years in short-lived rodents to several hundred years in bowhead whales. When aging is slowed in an animal model, both healthspan and lifespan typically increase, and with them what the authors call gerospan: the later-life phase spent in diminished health. A deceleration of the entire adult trajectory, such as that produced by lowering temperature in fruit flies, expands healthspan and morbidity proportionally, leaving the relative share of life in decrepitude unchanged. Other outcomes are possible too, including relative compression or expansion of late-life illness.

Here the authors deliver their sharpest argument. In medical terms, the ultimate goal of biogerontologists is the same as that of any medical specialty: to alleviate illness, reduce disease burden, and save lives. Some treatments restore full health; many do not. Surgery for a ruptured bowel that threatens fatal peritonitis may leave a patient with a colostomy bag, yet no one questions its value. In the United States, from the late 1960s until around 2000, death rates after age 60 declined steadily, particularly from cardiovascular disease. That success likely increased deaths from competing risks such as cancer and Alzheimer’s disease, meaning some individuals traded an earlier, quicker death for a later, slower one, increasing the proportion of life spent in poor health. Yet no ethical framework could justify denying people cardiovascular treatments merely to avoid a longer period of ill health at the end of life. A doctor’s duty is to treat illness and save lives, even when the result is a longer life in diminished health.

The same logic, the authors insist, applies to anti-aging medicine. Interventions that slow aging will always reduce disease, and they may extend lifespan, but whether they compress or expand morbidity is likely to be, to some extent, a matter of chance. Rapamycin, for example, extends both lifespan and many aspects of healthspan in mice, yet also causes testicular atrophy and cataracts. Treatment development involves discovering what is possible rather than predetermining outcomes. For a biogerontologist to declare that their work must never expand morbidity is as strange as an oncologist making the same demand of cancer therapy. Treatments that compress morbidity are certainly preferable, but specifying that as the sole legitimate goal is, in the authors’ words, an impotent claim that can easily be read as unrealistic or bogus.

Why, then, do so many researchers repeat the healthspan-not-lifespan formula? Gems and his colleagues identify several anxieties. Biogerontologists fear being tarred with the same brush as the snake-oil salesmen who make false claims about curing aging, or being accused of contributing to overpopulation and the burden of aging societies on healthcare systems. The authors counter that extending lifespan is a good thing, that every medical specialty hopes to add years of good or tolerable health, and that population growth is partly a product of healthcare successes that are not viewed as insidious. They point to the UK’s National Institute for Health and Care Excellence, which judges new treatments by the quality-adjusted life years they deliver, a metric that explicitly includes added years of life. What matters most, they argue, is the humanistic rather than the economic dimension: whether an individual prefers life, in whatever condition, to death. Many people, including some of advanced age, live enjoyable and meaningful lives despite disability, something that person-centered care can help assure.

The authors acknowledge the genuine crisis facing healthcare systems from aging populations, described vividly as a silver tsunami or a healthcare asteroid hurtling toward Earth. Public health programs that keep people healthy into late life, through good nutrition, avoidance of obesity, and anti-smoking measures, remain crucial. But they warn that lurking within the healthspan agenda is the old, anti-humanistic philosophy of apologism, the notion that it is somehow beneficial for people to age and die. Against this, one of the authors has recently argued that slowing human aging, including extending longevity, is an ethical imperative. The paper concludes with a direct call: biogerontologists should frankly state their goals of understanding and intervening in aging, pursue both improvements to late-life health and the saving of lives through life extension, and abjure the healthspan-not-lifespan cliché. Denying a patient a life-saving intervention because it would leave them alive in moderately diminished health, they write, is not part of any ethical reality.

Subject of Research: The debate over whether biogerontology should aim to extend healthspan, lifespan, or both

Article Title: Against the “extend healthspan but not lifespan” cliché

Article References: Gems, D., Iijima, E. R., & de Magalhães, J. P. (2026). Against the “extend healthspan but not lifespan” cliché. GeroScience. https://doi.org/10.1007/s11357-026-02577-1

Image Credits: AI Generated

DOI: 10.1007/s11357-026-02577-1

Keywords: biogerontology, healthspan, lifespan, geroscience, compression of morbidity, geriatric medicine, aging research, rapamycin, frailty, research ethics, longevity science, Against