Lifespan vs Healthspan: Which Should We Prioritise?
There has been considerable debate within the healthy longevity community of late: should we speak of longevity — how long we live — or focus on healthspan — how long we live without serious disease? I’ve found myself very much in the minority, favouring healthspan over lifespan or longevity, and so I thought I would devote this newsletter to the question. I also suspect the choice is sometimes framed too sharply — yet in practice, R&D design, policy priorities and public messaging often force us to prioritise one over the other. Perhaps the most interesting ground lies between the two positions.
First, though, why does it matter? Some would say it doesn’t — anything that achieves longer lifespan must surely delay disease, and anything that delays disease will inevitably boost lifespan. That is not quite true. Anti-ageing therapies are unlikely to eliminate cancers, a meaningful fraction of which arise from stochastic replication errors. Likewise, treatments that delay or prevent specific diseases may not significantly affect how long we live, which is influenced by many other factors, especially genetics.
Prostate cancer is a case in point. Detecting and treating aggressive cancer early in life will indeed benefit both healthspan and lifespan. However, the USPSTF recommends against routine PSA screening after age 70, because at that point detecting cancer through PSA testing may trigger painful biopsies and potentially impotence-causing surgery for a tumour that may never cause the patient’s death (“dying with prostate cancer, not from it”). That, however, is a statistical finding, and not one that determines the fate of any individual. I will still take the test.
But back to whether the question matters. I believe it does, for several reasons. While few would argue that reducing or compressing morbidity is undesirable, many challenge the desirability of extending lifespan. Their concerns range from fears of global overpopulation to the belief that longevity treatments will disproportionately benefit the wealthy and thereby increase inequality. Many of these objections are addressed very effectively in a recent paper I would recommend: The Ethics Case for Longevity Science, published in Ageing Research Reviews.* The authors examine most of the common objections to increasing longevity and dismiss them on ethical or practical grounds.
My reasons for preferring healthspan over longevity, however, are not those discussed in that paper — overpopulation, societal stagnation, loss of meaning, boredom or inequality. They are more practical.
First, as we develop anti-ageing therapies, demonstrating life extension as a primary endpoint is far more demanding than demonstrating reductions in disease burden or risk factors such as inflammaging. All-cause mortality requires very large cohorts followed for decades. By contrast, trials using composite disease endpoints, functional outcomes or validated ageing biomarkers can deliver actionable results far sooner.
Second, we face a communication challenge. We are developing therapies to target something many people consider a “natural” process. It is all too easy for the public to conclude that success will primarily benefit billionaires or powerful leaders. Framing the goal as compressing morbidity and improving functional years may prove both more ethically persuasive and politically defensible.
Third — and I readily admit this reflects my stage of life — the idea of extending a life already burdened by arthritis, frailty or cognitive decline becomes less attractive as the sixties become seventies and the seventies become eighties. If there were a therapy that allowed someone with painful arthritis or declining cognition to return to how they were — and how they felt — twenty years earlier, who would refuse it? But such a pill seems distant. Starting interventions earlier likely flattens the slope of age-related decline, though meaningful functional gains at older ages are certainly possible. Even so, strategies to make “80 the new 60” will probably be most effective when initiated in the 30s, 40s or 50s, so that later decades are characterised by vigour rather than disability.
In practical terms, does this choice affect R&D strategy? Yes. Slowing or reversing key mechanisms of ageing — through senolytics, epigenetic reprogramming and related approaches — will likely influence both disease onset and ultimate lifespan. However, the clinical trials we design — the age of participants, the biomarkers we select and the endpoints we prioritise — will differ depending on whether we aim primarily to delay metabolic dysfunction, dementia or inflammatory disease, or instead to extend the lives of individuals already in their seventies, when much of the cumulative damage may already be present.
Finally, it may be reassuring to remember that the most effective tools currently available to promote healthy longevity — exercise, diet, sleep and social connection — positively influence both targets. If integrated into our lives, they delay disease, enhance quality of life and, on average, extend lifespan with less pain and distress.
So the distinction may not dramatically alter how we live day to day. But it may shape how we prioritise research, regulation and investment in the years ahead.
If you had to prioritise one as the primary focus for the next decade of healthy longevity research and policy, which would it be? Lifespan or Healthspan?
We will share the results and explore what they imply for clinical trial design, regulation and investment priorities in a forthcoming edition.
* Han, Z.Z. & de Magalhães, J.P. (2026). The Ethics Case for Longevity Science. Ageing Research Reviews. DOI: 10.1016/j.arr.2026.103054.
