Kerbside Consult

How Long Do You Want to Live?

The science — and business — of longevity

Cyberdoc — writing on medicine since 1995

A longer life is an old wish with a new price list. Biological clocks, experimental drugs and supplements promise more control over how we age. How much of that promise survives the harder question: will it help us live longer, stay well and remain independent?

Kerbside Consult

How old are you?

“How old are you?” used to be an easy question.

Apparently, it no longer is.

There is the age on the birth certificate. Then there is biological age, epigenetic age, vascular age, metabolic age, immune age — and, for a sufficiently large fee, somebody will probably offer to measure most of them.

This is more than a change in vocabulary. For most of medical history, the ambition was to prevent premature death and treat the diseases that arrived with age. A growing field called geroscience asks a more ambitious question: if ageing itself helps drive cardiovascular disease, cancer, diabetes, dementia and frailty, could changing the biology of ageing delay several of them at once?

It is a serious scientific question. It has also become a very large commercial opportunity.

The result is the modern longevity industry: part molecular biology, part preventive medicine, part Silicon Valley optimism and part an ancient human wish with a new price list.

We are living longer. That is not quite the same as living better.

Before dismissing longevity as the latest wellness fashion, it is worth remembering what medicine has already achieved. Clean water, sanitation, vaccination, antibiotics, safer childbirth, cardiovascular treatment and better management of chronic disease have transformed survival. WHO estimates show that global life expectancy rose from 66.8 years in 2000 to 73.1 in 2019. Healthy life expectancy also rose, but by less — from 58.1 to 63.5 years.

That gap matters. It is the difference between lifespan — how long we are alive — and healthspan — how long we remain in reasonably good health and function.

The distinction is especially relevant closer to home. WHO’s Malaysia profile estimated healthy life expectancy at birth at 63.9 years in 2021, a figure also reported by Malaysia’s Department of Statistics, citing WHO. The exact number is modelled and should not be mistaken for an individual prediction. The larger point is harder to dispute: adding years to life is not automatically the same as adding healthy years.

The longevity movement is therefore asking a legitimate question. Can we postpone the period in which disease, disability and dependence accumulate — not merely postpone death?

Is ageing a disease?

Medicine traditionally divides the problems of later life into separate boxes. We treat hypertension, diabetes, coronary disease, osteoporosis, cancer, osteoarthritis, dementia and frailty as different diagnoses, usually with different specialists and different drugs.

Geroscience turns the telescope around. Age is the dominant risk factor for many of these conditions. If several diseases share upstream biological processes, perhaps intervening upstream could delay more than one disease at a time.

The scientific basis is not imaginary. The influential 2023 Cell review “Hallmarks of aging: An expanding universe” described twelve interconnected hallmarks, including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, impaired autophagy, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem-cell exhaustion, altered intercellular communication, chronic inflammation and dysbiosis.

That is an extraordinary advance from simply saying that bodies “wear out”. We can now describe biological pathways that change with age and, in animals, manipulate some of them.

But there is an important leap between understanding a mechanism of ageing and possessing a treatment that safely makes healthy humans live longer. Much of the longevity debate takes place in that gap.

When ageing became a product

Once ageing becomes measurable and potentially modifiable, a market follows almost inevitably.

The modern longevity consumer can buy large biomarker panels, genetic sequencing, continuous glucose monitoring, body-composition scans, biological-age reports and increasingly elaborate imaging. There are supplements intended to support mitochondria, raise NAD⁺, improve autophagy or suppress “inflammaging”. There are hormone programmes, hyperbaric oxygen, cryotherapy, red-light devices and clinics offering packages whose sophistication is often easier to establish than their effect on lifespan, as discussed in a 2025 Cell review of geromedicine.

Some of these technologies are useful in the right patient for the right indication. That is not the same as proving that deploying them broadly in healthy people prolongs life.

This is where preventive medicine and the medicalisation of normal ageing begin to overlap. A test can detect an abnormality. The harder questions are whether the abnormality matters, whether treating it improves an outcome, and whether the benefit exceeds the harms created by testing.

The longevity industry is particularly good at answering the first question. Medicine has to insist on the other three.

The biological-age problem

Few ideas have captured the imagination of longevity medicine as effectively as the biological clock.

Epigenetic clocks use patterns such as DNA methylation to estimate aspects of biological ageing. Other approaches use proteins, metabolites or combinations of routine clinical measurements. Many can predict mortality or age-related outcomes at a population level. That makes them scientifically valuable.

It does not automatically make them clinical endpoints.

A 2024 Nature Medicine review on validation of biomarkers of ageing made the problem explicit: there is still no consensus on how ageing biomarkers should be validated before clinical translation. Predicting risk, responding to an intervention and serving as a trustworthy surrogate for a longer, healthier life are three different achievements.

The CALERIE randomized trial analysis is a useful illustration. Two years of calorie restriction in healthy adults produced a small slowing in one DNA-methylation measure of the pace of ageing, DunedinPACE, but not significant changes in the PhenoAge or GrimAge clocks. The investigators themselves emphasised that proving the geroscience hypothesis ultimately requires long-term outcomes such as chronic disease and mortality.

So if a commercial programme tells me that my biological age has fallen from 68 to 61, I would certainly be interested. I would not yet assume that I have acquired seven additional healthy years.

A clock that predicts ageing is not necessarily a clock that tells us how to stop it.

The longevity pharmacy

The drug cabinet is where the science becomes both most exciting and most vulnerable to overstatement.

Rapamycin. The mTOR pathway is one of the most compelling targets in ageing biology, and rapamycin extends lifespan in several animal models. Human evidence is emerging but remains preliminary. The 48-week randomized PEARL trial tested intermittent low-dose rapamycin in generally healthy adults, primarily examining safety and healthspan-related measures. That is important research. For context, all listed PEARL authors were affiliated with AgelessRx, a company operating in the longevity field. It is not proof that taking rapamycin extends human lifespan.

Metformin. Few drugs have generated more enthusiasm as possible geroprotectors. It is inexpensive, familiar and biologically plausible. But much of the favourable human longevity evidence comes from people with type 2 diabetes and observational data. A 2026 systematic review of healthspan-related outcomes in people with type 2 diabetes found that all 27 eligible studies were observational cohorts; no randomized trial met its criteria. Association is encouraging, but it cannot establish that metformin should be prescribed to healthy non-diabetic people to slow ageing.

Senolytics. Some senescent cells release inflammatory signals and other substances that can disturb surrounding tissue. A 2023 EBioMedicine editorial explains two approaches: senolytics aim to selectively eliminate these cells, while senomorphics aim to suppress their potentially harmful secretions. But senescence also contributes to tissue repair and tumour suppression. Removing senescent cells therefore requires more care than the appealing idea of clearing out worn-out cells might suggest.

Early human trials have begun, but the clinical evidence remains very limited. A 2023 randomized pilot trial of dasatinib plus quercetin in idiopathic pulmonary fibrosis enrolled only 12 participants and was designed mainly around feasibility and tolerability. It found no meaningful between-group differences in the exploratory measures of frailty, lung function or physical function, and was not powered to establish efficacy. The editorial calls for larger, well-conducted trials to clarify benefits and harms. Neither the editorial nor this pilot establishes that senolytics extend human lifespan.

NAD⁺ precursors. NMN and NR have become staples of the supplement conversation. Yet a 2024 meta-analysis of eight randomized NMN trials, involving 342 mainly middle-aged or older adults, found no significant improvement in fasting glucose, insulin, HbA1c, insulin resistance or lipid profiles over the short treatment periods studied.

GLP-1 drugs. These are different because the outcome evidence is already substantial for defined high-risk populations. In the SELECT trial, semaglutide reduced the relative risk of major cardiovascular events by 20% in 17,604 adults with established cardiovascular disease and overweight or obesity but without diabetes. That is excellent preventive medicine. It does not mean semaglutide has been shown to be a general anti-ageing drug for healthy people.

The same discipline should apply to every longevity drug: What is the biological rationale? What has happened in animals? What has happened in humans? And has anyone actually shown that healthy human life is longer or better because of it?

When a pathway becomes a supplement

The supplement market illustrates an old problem in a particularly modern form.

A molecule may participate in a pathway involved in mitochondrial function, oxidative stress, inflammation, autophagy or cellular senescence. That is scientifically interesting. It does not follow that swallowing more of the molecule improves the pathway in a clinically useful way, reaches the relevant tissue at the relevant dose, or changes how long a person remains healthy.

Yet the language of molecular biology is remarkably persuasive marketing. “Supports cellular energy”, “activates longevity pathways” and “promotes healthy ageing” can all sound like clinical outcomes without actually being clinical outcomes.

A plausible mechanism should be the beginning of the evidence chain, not the end of it.

The intervention nobody can patent

After all that molecular biology, the most defensible longevity prescription is almost embarrassingly conventional.

Do not smoke. Move. Maintain muscle. Control blood pressure, lipids and diabetes. Keep excess weight under control. Sleep reasonably. Vaccinate. Use evidence-based screening. Maintain relationships and a reason to get out of bed.

These are not glamorous recommendations, but their evidence base is considerably stronger than that of most commercial anti-ageing programmes. The World Health Organization recommends 150–300 minutes of moderate aerobic activity a week for adults, together with muscle strengthening; for older adults it also emphasises balance and functional activity.

Muscle deserves particular attention. A 2022 systematic review and meta-analysis found that resistance training was associated with lower all-cause mortality, while a randomized trial in 110 adults over 75 (mean age 80) found significant improvements in leg strength with resistance training. Association is not proof of immortality. But preserving strength has an immediate benefit that no epigenetic clock needs to validate: it helps preserve function.

Smoking gives an even clearer comparison. The CDC notes that stopping smoking reduces premature death and can add as much as ten years to life expectancy. There are few longevity interventions with a claim of that magnitude backed by such mature human evidence.

And then there is something no blood test measures particularly well: other people. The 2025 WHO Commission on Social Connection concluded that loneliness and social isolation have serious effects on health and premature mortality. Longevity is not only a biochemical project.

The irony is difficult to miss. We are spending increasingly sophisticated sums to measure ageing while some of the most powerful ways of protecting healthspan remain cheap, familiar and chronically underused.

What the people who actually live to 100 teach us

Centenarians are irresistible to longevity researchers because they are the experiment nature has already performed.

The lesson is not that there is a single centenarian diet, supplement or morning routine. Extreme longevity appears to arise from a mixture of genetics, environment, behaviour and chance. Studies such as the New England Centenarian Study have found that many centenarians delay disability until very late life, providing a real-world example of compressed morbidity.

How much of lifespan is inherited remains actively debated. A 2026 Science analysis argued that the heritability of intrinsic human lifespan may exceed 50% after accounting for deaths from extrinsic causes, considerably higher than older estimates. That finding will undoubtedly stimulate further debate rather than end it.

Genes matter. Behaviour matters. Environment matters. Luck matters. Any industry selling certainty about an outcome produced by all four deserves a little scepticism.

What exactly are we trying to extend?

Suppose medicine offered two futures.

In one, you live to 100 but spend the final fifteen years progressively frail, dependent and cognitively diminished. In the other, you live to 88, remain active and independent until 86, and experience a relatively short final period of illness.

Which is the more successful longevity intervention?

More than forty years ago, James Fries described the idea of “compression of morbidity”: postponing chronic illness and disability so that the period of infirmity occupies a smaller part of life. The concept remains more useful than many modern anti-ageing slogans.

The objective is not necessarily to make death infinitely distant. It is to move frailty, disability and dependency closer to it.

That changes what counts as success. Walking speed matters. Strength matters. Cognition matters. Independence matters. The ability to travel, work, play golf, climb stairs, carry a grandchild, remember a conversation and choose how to spend the day matters.

A longer life is valuable largely because of what can still be done with it.

The longevity gap

There is another uncomfortable aspect to the longevity revolution: access.

The wealthy can increasingly purchase repeated imaging, genomic analysis, personal trainers, dietitians, private physicians, advanced biomarkers and experimental interventions. Some of these may eventually prove useful. But large differences in health and life expectancy already reflect much less exotic factors — including education, income, housing, working conditions, pollution and access to ordinary healthcare, alongside risks such as smoking and obesity. The 2025 WHO World report on social determinants of health equity documents how unequal living and working conditions contribute to avoidable illness and premature death.

There is something strange about discussing whether a wealthy 55-year-old should measure his epigenetic age while another 55-year-old cannot obtain consistent control of hypertension.

If geroscience eventually produces an intervention that genuinely slows human ageing, the scientific achievement will be extraordinary. The next question will be who gets it.

If we really succeed

Imagine that the optimists are right.

Not immortality. Simply a treatment that reliably adds twenty healthy years.

It would be one of the greatest medical advances in history. It would also change retirement, pensions, inheritance, employment, housing, population structure and the relationship between generations. A society built around education in the first two decades, employment for four or five, and retirement thereafter would have to be redesigned.

Longevity therefore stops being merely a medical problem once it succeeds.

Perhaps that is a problem worth having. But it reminds us that “living longer” is not a laboratory endpoint detached from the world around it.

What I would do tomorrow

If someone asked me today how to maximise the chance of a long and healthy life, my prescription would be disappointingly conventional.

I would start with the diseases we already know how to prevent. I would not smoke. I would exercise aerobically and lift weights. I would protect muscle and balance as I grew older. I would know my blood pressure, lipids and glucose and treat them when indicated. I would keep my vaccinations current, use established screening appropriately, sleep adequately, avoid sustained obesity, and remain socially and intellectually engaged.

If I chose to measure a new biomarker or try an experimental longevity intervention, I would ask a more demanding question than whether it changed a number: has this been shown to help people like me live longer, remain healthier, or function better?

That question does not kill innovation. It protects it from marketing.

The science of ageing is advancing rapidly, and some of today’s experiments may become tomorrow’s standard medicine. Rapamycin, senolytics, metabolic drugs, biomarkers and interventions we have not yet imagined deserve serious study.

But perhaps that is the central irony of the longevity revolution.

While we wait for science to discover how to slow ageing, we already know a remarkable amount about how not to accelerate it.