Introduction
Smoking has long been recognized as a major threat to longevity. Longitudinal cohort studies in the mid-20th century first quantified the toll of tobacco on lifespan, revealing stark differences in survival between smokers and non-smokers.[
1] In the 1950s, life insurance actuaries had already observed significantly shorter life expectancies among smokers.[
2] Subsequent large-scale studies confirmed these early warnings: prolonged cigarette smoking eventually kills over half of persistent smokers and cuts an average of roughly ten years off an individual’s life compared to a never-smoker.[
3] However, with mounting evidence indicating smoking as a leading cause of multiple non-communicable diseases, by the late 20th century public messaging had become focused on disease-specific effects and shifted away from loss of life expectancy. Instead, research and interventions became targeted, such as lung-cancer screening programs or medications for prevention of heart disease in smokers.
Most smoking-attributable deaths stem from a short list of chronic illnesses: cancers (chiefly lung cancer), chronic respiratory diseases (especially chronic obstructive pulmonary disease, COPD), and cardiovascular diseases (such as coronary heart disease and stroke). Global estimates reinforce this: as of 2019, tobacco was responsible for over 7–8 million deaths annually worldwide, with the largest fractions due to lung cancer, COPD, ischemic heart disease, and stroke.[
4] Smokers also face elevated risk for dozens of other conditions – from blindness and osteoporosis to peripheral vascular disease.
If smokers can be persuaded to quit in their 30s–50s, they can regain several years of life expectancy. Jha and colleagues[
5] calculated that smokers who quit by around age 40 years regained 90% of potential life-years lost had they continued smoking. Le and colleagues[
6] found that smokers who had smoked throughout adulthood up to age 35 were predicted to lose 9.1 years of life on average if they continued. However, if they quit smoking at that age, they could regain an average of 8.0 years’ life expectancy. In addition to lifespan, the growing specialty of geroscience explores ways to extend the health span – the healthy, functional years of life – by considering holistically how the aging process drives chronic diseases.[
7] Geroprotective interventions might include drugs and lifestyle changes to address biological rather than chronological age. Yet, despite the systemic aging effects of smoking, the use of tobacco harm reduction (THR) as a gerotherapeutic option has not by widely explored in geroscience studies.
In this paper I explore returning longevity to the focus of smoking cessation strategies and the use of “clean” non-combustible nicotine THR products, such as e-cigarettes, heated tobacco, and oral pouches, with emphasis on the aspect of increased health span. I propose roles for THR products to aid quitting and switching and highlight how geroscience data can support messaging for the public and policymakers.
Insurance Industry Insights
Intriguingly, one of the earliest sectors to act on smoking’s mortality risk was the life insurance industry. Initially, and for several decades despite clear actuarial data on smokers’ shortened lifespan, insurers were reluctant to adjust premiums or publicly acknowledge the risk.[
2] Only after the United States Surgeon General’s landmark 1964 report on smoking and health[
8] did this silence break. In the same year, State Mutual, an insurance company in Massachusetts, MA, became the first insurer to offer a non-smoker discount on life insurance, effectively penalizing smokers with higher premiums.[
2] Before long, differentiated underwriting for smokers and non-smokers became the industry norm. This change incentivized smoking cessation by rewarding quitters with lower rates and signaled that smoking was a quantifiable risk factor with financial implications. Some insurers even experimented with temporary smoker rates that could be lowered after a period of cessation.
Beyond Smoking Cessation – The Nicotine Paradox
Paradoxically, long-term smokers have a significantly lower risk of Parkinson’s disease than never-smokers, with protective effects being suggested for nicotine.[
17,
18] Research suggests that nicotine may have neuroprotective properties: in animal models it reduces neuroinflammation and oxidative stress, and small clinical trials in patients with early Parkinson’s disease or mild cognitive impairment have shown improvements in motor and cognitive performance.[
17] Any potential benefit of nicotine never outweighs the harms of smoking, but it raises the prospect that smoke-free nicotine use could help to preserve brain function in aging individuals. The potential benefits of maintaining nicotine intake should be investigated in geroscience studies as well as smoking cessation.
Geroscience: Targeting Aging Processes for Health Span
The past decade has seen the rise of geroscience, which is an interdisciplinary field that seeks to understand the biology of aging and apply that knowledge to extend health span (the healthy, functional years of life). Geroscience starts from the insight that aging itself is the single biggest risk factor for most chronic diseases, including cancer, heart disease and age-related neurological and cognitive disorders (the very diseases also elevated by smoking). Rather than tackling diseases in isolation, geroscientists aim to slow the aging process, thereby delaying the onset or progression of multiple diseases at once – an appealing strategy. The goals of geroscience range from deciphering fundamental mechanisms, such as cellular senescence, DNA damage, chronic inflammation, and other hallmarks of aging, to developing geroprotective interventions, which might include drugs and lifestyle regimens, that retard those mechanisms and improve resilience. In practical terms, a successful geroscience intervention might allow a person to live to 90 or 100 years in good health instead of suffering multiple morbidities in their 70s or 80s. Notably, geroscience considers aging in terms of biology, meaning that a person might be biologically “older” or “younger” than their chronological age. Interventions aim is to maintain young biological age, slow progression or reduce it.
Several candidate interventions are being tested in humans. A flagship effort is the TAME Trial (Targeting Aging with Metformin), which aims to investigate whether the generic diabetes drug metformin can reduce multimorbidity in older adults. Metformin was chosen due to promising observational data showing beneficial effects in relation to type 2 diabetes (reduced cardiovascular effects and extended lifespan), cancer (reduced incidence and mortality) and possibly cognitive impairment, hinting at broad antiaging effects.[
19] Other compounds, like sirolimus and its derivatives and senolytics that kill senescent cells, are also under study,[
20,
21] although data in humans remain sparse. Nevertheless, momentum in the field is palpable.
New institutional players have emerged, such as the Hevolution Foundation (Riyadh, Saudi Arabia), which is a
$1-billion-plus initiative that funds aging biology and geroscience research globally. In 2022, Hevolution partnered with the American Federation for Aging Research (New York, NY, USA) to launch new investigator awards in aging biology. These fund dozens of young scientists to study topics ranging from cellular senescence to novel gerotherapeutics. For instance, some grants have explicitly encouraged work on compounds like metformin and sirolimus as potential longevity enhancers. Similarly the XPRIZE Healthspan award is offering
$101 million to the team that develops a “proactive, accessible therapeutic that restores muscle, cognition, and immune function” in 10–20 years among people aged 65–80 years.[
22] Smoking cessation and the use of THR may well be one of the most effective ways to achieve these outcomes.
One of the most significant advances in geroscience has been the development of biomarkers of aging – measurable indicators that reflect biological age or functional capacity better than chronological age. These include molecular measures, such as analysis of DNA methylation patterns to estimate biological age (also known as “epigenetic clocks”), protein and metabolite signatures of aging, inflammation markers like (e.g., IL-6), and physical indicators like gait speed or muscle strength. For example, the GrimAge epigenetic clock can predict mortality risk, and has shown that heavy smokers reach an advanced epigenetic age earlier than non-smokers.[
23] Similarly, chronic smokers often exhibit higher levels of inflammatory cytokines and a more rapidly declining lung function than former and never smokers, indicating accelerated aging. On the flip side, these biomarkers offer a way to test the effects of anti-aging interventions in a feasible timeframe. Rather than waiting 30 years to see whether a drug lowers mortality, researchers can see within a 1–2 years if epigenetic aging has slowed.
Composite metrics for functional health are already available. These underpin efforts to address ways of measuring the effects of interventions that increase health span. The World Health Organization proposed the concept of intrinsic capacity as a holistic measure of an individual’s functional age.[
24] Unlike disease diagnoses, intrinsic capacity directly gauges an older person’s functional ability in daily life. Thus, this measurement is essentially a composite of all the physical and mental capacities an individual can draw on. Intrinsic capacity is assessed across multiple domains (cognitive, vitality, locomotor, psychological, and sensory). Research has shown that intrinsic capacity tends to decline with age and, importantly, lifestyle factors significantly influence its trajectory.[
25] Higher physical activity and a healthy body weight correlate with better intrinsic capacity profiles over time. Not surprisingly, tobacco use is associated with worse intrinsic capacity trajectories, reflecting the broad multisystem impairment associated with smoking. A lifelong heavy smoker might have the lung function, cognition, and muscle strength of someone 10 years older. Intrinsic capacity scores, therefore, provide an effective way to link geroscience and public health. It is now being validated as an endpoint for use in longitudinal studies and geroprotective trials.[
26]
Bridging Smoking and Aging Research
There is a compelling case for closer collaboration between the tobacco control and geroscience fields. For one, geroscientists need to account fully for smoking as a key variable that can confound studies of aging. If a cohort study seeks to identify determinants of healthy aging but fails to stratify by smoking status, it may mistake effects of smoking for those of normal aging. Smoking accelerates many aspects of aging – onset of diseases, frailty, and even measurable aging at the cellular level. Smokers not only die younger on average than non-smokers, they also tend to experience age-related disabilities about a decade earlier.[
27] To isolate the true impact of novel antiaging interventions, researchers must either exclude smokers or, better yet, include smoking status in study designs as a critical stratifier, for which adjustments are made in their analyses. Many ongoing aging studies (e.g., epigenetic clock research) do adjust for smoking, and it has been shown that smoking leaves a distinctive epigenetic signature. But, more integration of tobacco epidemiology into geroscience models is needed.
Conversely, tobacco researchers could use geroscience tools to better understand benefits of smoking cessation, including the use of THR products. Traditional smoking studies focus on short-term improvements in disease outcomes, like better lung function within 1 year of quitting. With the addition of geroscience biological age markers and functional measures, recovery may be captured in a more holistic way.
One powerful illustration of what might be learned comes from the seminal work of Jha and colleagues
5 on smoking cessation and life expectancy. In a large cohort in the United States of America, smokers who quit by around age 40 years regained most (90%) of the life-years they would have lost by continuing. Those who quit between ages 35–44 lived about 9 years longer than those who continued smoking, nearly reaching the lifespan of never-smokers. Even quitting at age 50 or 60 still added about 4–6 years of life relative to never quitting. Le and colleagues[
6] presented very similar figures in their study using 2018 census data in the United States. Smokers who had smoked throughout adulthood up to age 35 were predicted to lose 9.1 years of life on average if they continued. However, if they quit smoking at that age, they could regain an average of 8.0 years’ life expectancy. These dramatic benefits underscore that it is never too late to quit smoking. An intriguing question is: what if a smoker doesn’t quit nicotine, but switches to a THR product in mid-life? The intuitive expectation is that switching completely to a non-combustible nicotine source would substantially mitigate risk, since most harm comes from smoke rather than nicotine. Epidemiological data are still emerging, but evidence from snus users in Sweden[
28] and heated tobacco users in Japan[
29] suggests long-term switchers have much lower rates of smoking-related diseases. Quantifying life gain, for instance in a 40-year-old who switches completely to clean nicotine, should be a priority and combine the expertise of epidemiologists and geroscientists.
Measuring Success in New Ways
By incorporating geroscience measures, THR outcomes can be broadened. Traditionally, “success” has been measured by diseases avoided and deaths averted. But studies could also measure outcomes like cognitive aging and physical function. For example, a trial could test whether older smokers who switch to vaping maintain better intrinsic capacity over time (e.g., slower declines in gait speed, memory, or muscle strength) than those who continue smoking. The highlighting of such improvements might resonate with the public and policymakers by linking quitting to positive aging and independence in later life, rather than, for example, quitting being only about preventing a heart attack. It also aligns with WHO’s emphasis on functional ability during aging and echoes calls in medicine to shift focus from simply extending lifespan to improving health span.
Policy Synergies and a Shared Research Agenda
The convergence of geroscience and tobacco control has practical implications for policy and research. First, aging and tobacco studies can integrate data. Large aging cohorts could collect detailed smoking and nicotine-use data and, vice versa, smoking cessation trials could include aging biomarkers and functional assessments. Collaborative analyses could yield new insights, such as identifying whether ex-smokers receiving nicotine-replacement therapy have different aging trajectories from ex-smokers who are completely nicotine-free. Second, regulatory science can evolve: agencies evaluating antiaging therapeutics and those overseeing new nicotine products might harmonize approaches. for instance, by considering biological aging markers as evidence in regulatory assessments of nicotine-only products. Third, insurers might benefit from more nuanced risk stratification using geroscience and THR data. Currently, many insurers still classify users of THR products as “tobacco users,” and charge them the same high premiums as smokers, despite evidence of reduced risk. However, a 2024 industry report highlights the increasing complexities in products, regulations, and patterns of use, and encourages research and inspiration into technologies, biomarkers, and so on, to assess actuarial risk more reliably.[
30]
Public health experts argue that insurers and wellness programs should “accept the science” by treating non-combustible nicotine users more leniently than smokers.[
31] Insurers could even partner with geroscientists to develop aging-based risk metrics, illuminating how a 50-year-old ex-smoker biologically rejuvenates after cessation. In the long run, such incentives could save both lives and health-care costs, as fewer smokers develop expensive chronic diseases in midlife.
Finally, there is a need for shared research protocols and data between the traditionally separate realms of tobacco research and aging research. Tobacco companies and their academic collaborators have conducted many short-term studies of switching to THR products, generating data on biomarkers, lung function, etc. Meanwhile, academic geroscientists have cohorts and trials measuring longevity-related endpoints. The embedding of a THR arm into a geroscience trial or the other way around could greatly accelerate discovery. The private and public sectors both have roles: industry can provide products, technology, and funding while public institutions can ensure unbiased analysis and broad dissemination of findings. With transparency and independent oversight to overcome historical mistrust, the potential gains are huge.
Conclusions
Leveraging lessons from geroscience offers a fresh lens through which to reinvigorate the fight against smoking – shifting expectation away from solely preventing disease and death towards promoting healthy longevity and brain health. With the inclusion of geroscience data, benefits of quitting smoking or switching completely to THR products can be articulated in novel ways that might resonate with the public and policymakers. The synergy goes both ways. For geroscience, smoking remains a critical but controllable accelerant of aging that must be accounted for, and studying “natural” smoking cessation can give insights into resilience and recovery that could inform antiaging therapeutics. For tobacco control, geroscience provides new measures of “success”. As we stand at the intersection of these fields, the message is one of optimism: by applying cutting-edge aging science to the world’s leading preventable cause of death, a transformative innovation could not only add to life but also add life to the later years of millions of people.
Author Contributions
I researched and wrote the article.
Funding Information
No funding.
Ethics Statement
Not applicable.
Conflict of Interest
I am a former executive director in the WHO’s non-communicable diseases cluster, and I had a major role in the development of its international Framework Convention on Tobacco Control. From September, 2017 to October, 2021, I was President and CEO of the Foundation for a Smoke-Free World, a non-profit entity funded by Philip Morris International, with a mandate to support scientific research and development in the battle against smoking.
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