Aging as a Disease: Scientific Evidence and Ethical Implications

Should Aging Be Classified as a Disease?

For most of human history, aging has been viewed as an immutable aspect of existence - as natural and inevitable as birth itself. Yet recent advances in molecular biology, genetics, and gerontology have fundamentally challenged this assumption. Scientists have begun to unravel the specific mechanisms by which cells and tissues deteriorate over time, raising a provocative question: if aging has identifiable biological causes and potentially treatable symptoms, should it be classified as a disease?

This question moved from theoretical to practical in 2018 when the World Health Organization's 11th revision of the International Classification of Diseases (ICD-11) introduced the extension code "Ageing-related" (XT9T) in the causality section (Khaltourina et al., 2020). This represented a significant shift in how the global medical community conceptualizes aging. However, the classification has generated substantial controversy, with critics arguing that it reinforces ageism and could lead to unintended negative consequences in healthcare delivery (Aprahamian et al., 2021).

The stakes of this debate extend far beyond medical taxonomy. By 2050, the number of individuals aged 60 years and older worldwide is projected to reach 2 billion, representing a dramatic demographic transformation (Khaltourina et al., 2020). How we classify and treat aging will profoundly impact quality of life, healthcare costs, and the very nature of human existence in the coming decades.

Main Content

The Biological Foundations of Aging

To understand whether aging qualifies as a disease, we must first examine what aging actually entails at the molecular and cellular levels. In 2013, a landmark paper identified nine hallmarks of aging: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication (López-Otín et al., 2013). These hallmarks were subsequently expanded to twelve in 2023, adding macroautophagy, chronic inflammation, and dysbiosis (López-Otín et al., 2023).

Each of these hallmarks represents a specific, measurable biological dysfunction. Take telomere attrition, for instance. Telomeres are protective caps at the ends of chromosomes that shorten with each cell division. When they reach a critical length, cells enter a state called senescence, ceasing to divide. Research in genetically modified mice has established causal links between telomere loss, cellular senescence, and organismal aging - mice with shortened telomeres exhibit decreased lifespan, while those with lengthened telomeres live longer (López-Otín et al., 2013).

Cellular senescence, another critical hallmark, involves cells that have stopped dividing but remain metabolically active, secreting inflammatory proteins that damage surrounding healthy cells through what is termed the senescence-associated secretory phenotype (SASP). Studies in which mice were genetically engineered to eliminate senescent cells demonstrated remarkable health benefits, including extended lifespan and delayed onset of age-related diseases (Kirkland & Tchkonia, 2020).

These are not abstract theoretical constructs but observable, quantifiable biological processes. They can be diagnosed through frailty indices, functional assessments, and blood-based biomarkers. Moreover, researchers have identified genetic and environmental factors that influence these processes, and several clinically proven interventions can modulate them (Khaltourina et al., 2020).

The Case for Disease Classification

When the World Health Organization developed its definition of disease for the ICD-11 revision, it specified six criteria: symptomatology, underlying mechanism, distinct pattern of development over time, known treatment response, linkage to genetic factors, and linkage to environmental factors (Khaltourina et al., 2020). A comprehensive analysis applying these criteria to biological aging found that aging meets all six requirements.

The symptomatology of aging includes a recognizable pattern of functional decline affecting multiple body systems. Memory, cognition, mobility, sight, hearing, taste, and communication all deteriorate with age in predictable ways. The mechanisms underlying these changes - from DNA damage accumulation to mitochondrial dysfunction - have been extensively characterized. The course follows a distinct temporal pattern, with exponentially increasing vulnerability to disease and death with advancing years.

Regarding treatment response, several interventions show promise. Caloric restriction has been shown to extend lifespan and reduce age-related pathology in numerous species. Pharmacological agents including rapamycin, metformin, and senolytics have demonstrated anti-aging effects in animal models and early human studies (Khaltourina et al., 2020). Rapamycin, an inhibitor of the mechanistic target of rapamycin (mTOR) pathway, has extended lifespan in mice even when treatment began late in life. A recent meta-analysis confirmed that rapamycin, not metformin, significantly mirrors dietary restriction-driven lifespan extension in vertebrates (Ivimey-Cook et al., 2025).

Genetic linkages are also clear. Studies of human centenarians suggest that genetics accounts for approximately 60 percent of the likelihood of reaching age 100, compared to only 20 percent for reaching age 70 (Holstege, cited in Newman, 2024). Specific genetic variants associated with longevity have been identified in populations with exceptional lifespan, though no single genetic profile appears necessary or sufficient.

From this perspective, aging appears to satisfy the clinical definition of disease more completely than some conditions already classified as such. The primary argument for classification is not that old age itself is pathological, but that the biological processes driving aging constitute identifiable dysfunctions that could potentially be treated.

The Case Against Disease Classification

Despite meeting technical criteria, the classification of aging as a disease faces substantial opposition on medical, social, and ethical grounds. The most immediate concern is that equating chronological age with disease reinforces ageism - the systematic stereotyping and discrimination against older adults (Aprahamian et al., 2021).

Ageism is already pervasive, affecting healthcare delivery in profound ways. Studies indicate that approximately one in two people globally harbor ageist beliefs (World Health Organization, 2021). During the COVID-19 pandemic, ageist attitudes contributed to violations of older people's rights to healthcare, with some regions implementing age-based triage protocols for intensive care admission. Classifying aging as a disease could further marginalize older adults and justify discriminatory practices.

Furthermore, chronological age is a poor predictor of individual health status. There is enormous inter-individual variability in how people age - some 80-year-olds are physiologically similar to 50-year-olds, while some 50-year-olds show advanced aging markers. Simply labeling someone as having the "disease" of old age based on their birth date provides little useful diagnostic or prognostic information and could lead to inadequate evaluation of other treatable conditions (Aprahamian et al., 2021).

The framing also raises questions about healthspan versus lifespan. Many researchers argue that the goal should not be to extend the number of years lived but to extend the number of healthy years - what is termed "healthspan." Data from developed nations show that while life expectancy has increased, many additional years are spent with chronic disease, disability, and dependence. Quality of life for individuals over 90 is, on average, significantly compromised by multiple health conditions (Gems, 2015).

Some critics contend that current medical research is already too focused on extending lifespan at the expense of quality of life. A disproportionate amount of funding goes to cancer and cardiovascular research aimed at reducing death rates in the elderly, even though preventing these deaths may simply result in more years lived with dementia, frailty, and other debilitating conditions (Gems, 2015).

Examples of Exceptional Longevity

While debates about classification continue, researchers have identified populations and factors associated with remarkable longevity that offer insights into healthy aging. The so-called "Blue Zones" - regions where people reach age 100 at rates up to ten times higher than in the United States - have received extensive study. These include Sardinia in Italy, Okinawa in Japan, the Nicoya Peninsula in Costa Rica, Ikaria in Greece, and Loma Linda in California (Buettner & Skemp, 2016).

Research in these populations identified common lifestyle factors including natural physical activity integrated into daily life, moderate caloric intake with predominantly plant-based diets, strong social connections, sense of purpose, and stress-reduction practices (Buettner & Skemp, 2016). The Danish Twin Study established that only about 20 percent of lifespan variation is determined by genetics, while approximately 80 percent is influenced by lifestyle and environment - suggesting that behavioral and environmental interventions hold substantial promise.

However, recent scrutiny has raised questions about the validity of some Blue Zones data. Researcher Saul Justin Newman found evidence that many reported centenarians in these regions were actually missing or deceased when studies were conducted, suggesting problems with record-keeping and potentially pension fraud (Newman, 2019). Birth certificate accuracy in historical populations is notoriously unreliable, making precise age validation difficult.

Despite controversies about specific populations, the general principles identified in Blue Zones research - social connection, physical activity, nutritious diet, and life purpose - remain well-supported by independent research on factors promoting healthy aging.

Pharmacological Interventions and Their Promise

The development of drugs targeting aging mechanisms has accelerated dramatically. Three classes of compounds have shown particular promise: mTOR inhibitors (particularly rapamycin), metformin, and senolytics.

Rapamycin's lifespan-extending effects are among the most robust findings in aging research. In preclinical studies, it induces autophagy (cellular self-cleaning), maintains cellular integrity, and has demonstrated the ability to extend lifespan across species from yeast to mammals (Khaltourina et al., 2020). Human trials have shown that even short-term treatment with rapamycin analogs improves immune response to influenza vaccination in older adults. However, rapamycin also has immunosuppressive effects that limit its use for broader anti-aging applications in healthy individuals.

Metformin, a first-line diabetes medication, has attracted attention for its potential anti-aging properties. It activates the AMPK pathway, mimics some effects of caloric restriction, and has been associated with reduced inflammation and oxidative stress. However, a comprehensive meta-analysis found that metformin does not significantly extend lifespan in vertebrates the way rapamycin does (Ivimey-Cook et al., 2025). Human trials are underway to determine whether metformin can prevent frailty in older adults, but results remain preliminary.

Senolytics - drugs that selectively eliminate senescent cells - represent a novel approach. The combination of dasatinib and quercetin has shown the ability to reduce senescent cell burden in humans. Early clinical trials in conditions like idiopathic pulmonary fibrosis and Alzheimer's disease have reported improvements in physical function and safe penetration into the central nervous system (Kirkland & Tchkonia, 2020). Studies in mice found that eliminating senescent cells extended median lifespan by up to 27 percent and reduced cancer mortality.

Despite these promising findings, no pharmaceutical intervention has yet been approved specifically for treating aging in humans. The U.S. Food and Drug Administration does not recognize slowing aging as an approved indication for drugs, creating regulatory obstacles for development of explicit anti-aging therapies.

The Ethical Dimensions of Extended Longevity

Even if science makes radical life extension possible, profound ethical questions remain about whether and how such technology should be deployed. These concerns cluster around issues of justice, resource allocation, overpopulation, and the nature of human experience.

Justice and Access

The most immediate ethical concern is distributive justice. New longevity treatments are likely to be expensive initially, accessible only to wealthy individuals and nations. This could create an unprecedented form of inequality - a caste system based on biological age where the rich live decades longer than the poor (Frances, 2016). While technologies typically become more affordable over time, the interim period could see dramatic health disparities.

Philosophers have debated whether justice requires that everyone have access to life extension if anyone does. Some argue that banning life extension because it cannot be universally provided would be unethical - analogous to banning organ transplants because not everyone can receive them. Others counter that creating a world where fundamental biology divides the haves from the have-nots crosses a moral threshold that justifies restrictions (Davis, 2018).

Overpopulation and Resources

Perhaps the most frequently cited objection to life extension is the specter of overpopulation. If people live substantially longer while continuing to reproduce, wouldn't planetary resources become catastrophically strained?

Demographic analysis suggests this concern may be overstated. Population growth is driven primarily by fertility rates rather than longevity. Countries with the longest life expectancies typically have fertility rates below replacement level. Mathematical modeling indicates that moderate life extension (to age 120) would not significantly increase population at current developed-world fertility rates. Even radical life extension (to age 1,000) could be managed if coupled with reduced fertility rates (Davoudpour et al., 2025).

There is an inverse correlation between fertility and longevity globally - population increases most in countries with the shortest life expectancies. Poverty creates incentives for large families to ensure some children survive and provide elder care. Addressing inequality and improving living standards tends to reduce both mortality and fertility (Maurer, 2022).

Critics of the overpopulation objection also note that opposing life extension to control population is ethically equivalent to opposing improvements in automobile safety or reductions in violent crime for the same reason. If population control is necessary, it should be achieved through reducing births, not maintaining deaths (More, 2004).

Quality Versus Quantity of Life

A subtler ethical question concerns whether extending lifespan without proportionally extending healthspan represents genuine benefit. Some philosophers have argued that extremely long lives might become intolerably boring or that individuals would change so much over centuries that personal identity would be lost (Williams, 1973).

Empirical evidence suggests that healthspan can be extended along with lifespan. Centenarians in Blue Zones and participants in life extension studies often maintain function much longer than average. The goal of geroscience is explicitly to compress morbidity - to keep people healthy longer and reduce the period of decline at the end of life.

Nevertheless, the question remains whether society should prioritize research aimed at extending maximum lifespan versus research aimed at improving quality of life in existing years. The debate over funding allocation - cancer research versus dementia research, disease-specific interventions versus aging interventions - reflects competing visions of what medicine should accomplish.

Meaning and Human Nature

Some critics worry that dramatically extended lifespans could fundamentally alter what it means to be human. Traditional life stages, relationships, careers, and social institutions are structured around expected lifespans. Multigenerational family structures, educational systems, career trajectories, and retirement all depend on assumptions about human lifespan.

Proponents counter that humans have repeatedly adapted to increased longevity. Life expectancy in developed nations has already doubled since 1900, yet society has successfully adjusted. Extended education, second careers, and multigenerational families have emerged without destroying meaning or human nature. There is no reason to expect that further extensions would be fundamentally different.

Policy and Research Implications

The debate over classifying aging as a disease has concrete implications for research funding, drug development, and healthcare policy. If aging is officially recognized as a treatable condition, it could:

Facilitate Drug Development: Pharmaceutical companies could seek regulatory approval for drugs that target aging mechanisms rather than individual age-related diseases. This could accelerate development of therapies with broad benefits across multiple conditions.

Redirect Research Funding: Resources could shift from treating individual age-related diseases to addressing underlying aging processes. This systems-level approach might prove more efficient than the current disease-by-disease paradigm.

Enable Insurance Coverage: Health insurance might cover interventions aimed at slowing aging, not just treating manifest diseases. This could incentivize preventive approaches that reduce overall disease burden.

Improve Statistical Tracking: Better coding of age-related conditions would enable more accurate epidemiological research and international comparisons of population health.

However, these potential benefits must be weighed against risks. Poor implementation could lead to age-based discrimination in healthcare, oversimplification of complex individual health needs, and misallocation of resources away from quality-of-life improvements toward simple lifespan extension.

The WHO ultimately modified its approach in response to widespread criticism. The term "old age" was withdrawn from ICD-11 and replaced with "ageing-associated decline in intrinsic capacity" (Aprahamian et al., 2022). This compromise attempts to acknowledge biological aging processes while avoiding the stigma of labeling chronological age itself as pathological.

Conclusion

Whether aging should be classified as a disease is not merely a question of biological taxonomy but a decision with far-reaching implications for how humanity approaches one of its most fundamental challenges. The evidence clearly demonstrates that aging involves specific, measurable biological processes that meet technical criteria for disease classification. Yet the social, ethical, and practical concerns about such classification are equally substantial.

Perhaps the most productive path forward is to recognize that the question itself may be less important than the research and interventions it motivates. Whether we call it a disease or not, the biological processes of aging cause immense suffering and limit human potential. Understanding these processes, developing interventions to address them, and ensuring equitable access to resulting therapies are worthy goals regardless of semantic categories.

The coming decades will likely see continued tension between competing priorities: extending lifespan versus improving healthspan, individual access versus population sustainability, innovation versus equality, and prevention versus treatment. Navigating these challenges will require not just scientific advancement but wisdom, humility, and a clear-eyed assessment of what we hope to achieve.

If the goal is to enable more people to live longer, healthier, more fulfilling lives - rather than simply to add years regardless of quality - then the question is not whether aging is a disease but how we can most effectively reduce suffering and enhance human flourishing across the entire lifespan. That is a question worth answering, whatever terminology we ultimately choose.

References

Aprahamian, I., Cesari, M., & Landi, F. (2021). Not a disease: A global call for action urging revision of the ICD-11 classification of old age. The Lancet Healthy Longevity, 2(10), e586-e587.

Aprahamian, I., Cesari, M., Landi, F., Schneider, R. H., & Vellas, B. (2022). How "old age" was withdrawn as a diagnosis from ICD-11. The Lancet Healthy Longevity, 3(6), e363-e364.

Buettner, D., & Skemp, S. (2016). Blue Zones: Lessons from the world's longest lived. American Journal of Lifestyle Medicine, 10(5), 318-321.

Davoudpour, S., & Herodotou, C. (2025). Life extension and overpopulation: Demography, morals, and the Malthusian objection. HEC Forum, 37(3), 305-331.

Davis, J. K. (2018). Life extension ethics and the question of harm. The Conversation.

Frances, A. (2016). A debate on the pros and cons of aging and death. Psychology Today.

Gems, D. (2015). Living too long: The current focus of medical research on increasing the quantity, rather than the quality, of life is damaging our health and harming the economy. EMBO Reports, 16(2), 137-141.

Ivimey-Cook, E. R., Sales, K., et al. (2025). Rapamycin, not metformin, mirrors dietary restriction-driven lifespan extension in vertebrates: A meta-analysis. Aging Cell, 24(1), e70131.

Khaltourina, D., Matveyev, Y., Alekseev, A., Cortese, F., & Ioviţă, A. (2020). Aging fits the disease criteria of the International Classification of Diseases. Mechanisms of Ageing and Development, 189, 111230.

Kirkland, J. L., & Tchkonia, T. (2020). Senolytic drugs: From discovery to translation. Journal of Internal Medicine, 288(5), 518-536.

López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.

López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2023). Hallmarks of aging: An expanding universe. Cell, 186(2), 243-278.

Maurer, A. (2022). Overpopulation and immortality. Institute for Ethics and Emerging Technologies.

More, M. (2004). Life extension and overpopulation. Kurzweil Library.

Newman, S. J. (2019). Supercentenarians and the oldest-old are concentrated into regions with no birth certificates and short lifespans. bioRxiv [Preprint].

Williams, B. (1973). The Makropulos case: Reflections on the tedium of immortality. In Problems of the Self (pp. 82-100). Cambridge University Press.

World Health Organization. (2021). Global report on ageism.

Insights, Analysis, and Developments

Author Credentials: Ian is the founder and Editor-in-Chief of Disabled World, a leading resource for news and information on disability issues. With a global perspective shaped by years of travel and lived experience, Ian is a committed proponent of the Social Model of Disability-a transformative framework developed by disabled activists in the 1970s that emphasizes dismantling societal barriers rather than focusing solely on individual impairments. His work reflects a deep commitment to disability rights, accessibility, and social inclusion. To learn more about Ian's background, expertise, and accomplishments, visit his full biography.