Why We Age: Causes and Mechanisms of Aging

We age not because the body has a single "aging clock," not because a predetermined number of heartbeats expires, and not only because telomeres shorten. Modern biology views aging as a gradual loss of the ability of cells, tissues, and the entire organism to maintain internal balance, repair damage, and recover from stress. This process simultaneously involves changes in DNA, epigenetic regulation, proteins, mitochondria, autophagy, stem cells, the immune system, intercellular communication, and the microbiome. These processes reinforce each other, so looking for a single "cause of aging" is now considered an oversimplification. [1]

But the question of "why do we age" has another layer. Molecular biology primarily addresses the question of how organisms age, while evolutionary biology addresses the question of why natural selection hasn't created organisms capable of maintaining a youthful state indefinitely. Modern evolutionary models agree that the effects of natural selection become weaker for effects that manifest late in life. Therefore, mutations and genetic programs that are beneficial in youth or have little effect on reproduction can persist even when they later contribute to functional decline. [2]

It turns out that aging isn't simply "wear and tear." A living organism constantly repairs itself, replacing molecules and many cells, and adapting to damage and stress. The problem arises because, over time, the rate of formation and accumulation of disorders, regulatory changes, and declining quality of recovery begin to exceed the body's ability to fully return to its previous state. It is this gradual loss of biological resilience that helps us understand why the same stress, infection, surgery, or period of inactivity are handled differently at age 30 than at age 80. [3]

Aging doesn't start with wrinkles and doesn't start on a specific day.

Aging has no set onset age, such as 25, 30, 40, or 50 years. Different molecular processes begin to change at different times, organs may age at different rates, and changes in two people of the same age may differ significantly. Modern research is even attempting to calculate the separate "ages" of the brain, heart, kidneys, immune system, and other organs, but such methods are still primarily exploratory. [4]

Therefore, statements like "the body begins to age after 25" or "aging accelerates sharply after 40" cannot be considered established biological laws. In 2024, a study in Nature Aging received considerable attention for reporting pronounced waves of molecular changes around 44 and 60 years of age. However, it included only 108 participants, and on July 15, 2026, the editors of Nature Aging posted a special notice that the reliability of some of the analysis used to identify these age peaks had been questioned. Therefore, turning the numbers 44 and 60 into universal "aging spikes" would now be incorrect. [5]

It is much more accurate to think of aging as a long-term trajectory. In some tissues, certain changes appear earlier, in others later; some processes develop almost linearly, while others accelerate or slow down. This trajectory is influenced by heredity, disease, physical activity, nutrition, smoking, environmental exposure, social conditions, and a host of other factors. [6]

Why did evolution allow aging at all?

At first glance, aging appears to be an evolutionary paradox. If a young and well-functioning body is more beneficial than an old one, why hasn't natural selection eliminated aging? The most common modern answer is not that old age is "needed" by anyone, but that natural selection is much more effective at eliminating factors that impair survival and reproduction in youth than problems that arise many years later. A modern review of the evolution of aging characterizes aging primarily as a maladaptive byproduct of evolutionary processes, rather than a specifically selected death program. [7]

One of the classic ideas is mutation accumulation. If a genetic variant causes serious harm to a young organism before or during reproductive life, the likelihood of its removal by natural selection is high. If the negative effect manifests itself primarily in old age, the evolutionary pressure against it is significantly weaker. Therefore, variants with adverse late effects may persist in the genome. [8]

The second concept is antagonistic pleiotropy. The same gene or biological pathway can provide an advantage early in life and become less advantageous later in life. For example, processes that promote growth, repair, and reproductive success in a young organism could theoretically contribute to excessive cellular activity or other adverse changes in later life. Evolution, in this case, "sees" an early advantage much more strongly than a later disadvantage. [9]

A third prominent model is the disposable soma theory, associated with Thomas Kirkwood. An organism has limited resources and allocates them among growth, reproduction, immune defense, cellular repair, and tissue maintenance. From an evolutionary perspective, absolute infallibility of repair over an infinite period of time might be too costly and not provide sufficient reproductive advantage. This does not mean that the organism "saves repairs after age 40" due to some simple switch; the theory describes a fundamental evolutionary tradeoff between longevity and other vital functions. [10]

Today, these models are not necessarily viewed as mutually exclusive. Contemporary research attempts to link mutations, antagonistic pleiotropy, resource allocation, organismal development, and specific molecular mechanisms of aging into a unified system. Therefore, the question of "why we age" does not yet have a single definitive answer, but evolutionary theory provides a good explanation for why natural selection can create extremely complex repair systems and yet does not guarantee their perfect operation indefinitely. [11]

What Exactly Breaks Down in Cells: 12 Signs of Aging

One of the most influential modern models was published in the journal Cell. In the updated version, the authors identify 12 interconnected hallmarks of aging. These do not represent twelve independent diseases, nor do they prove that each is equally important for every person. Rather, they provide a research model that allows for the integration of a vast number of observations into a unified biological system. [12]

A sign of aging	What's happening	Why it can affect the body
Genome instability	DNA damage and maintenance problems accumulate	The likelihood of cellular malfunction increases
Telomere shortening	The protective ends of some chromosomes gradually change and shorten	Some cells are less able to maintain their ability to divide normally
Epigenetic changes	The regulation of gene activity is altered without changing the DNA sequence itself	The cell may be less able to maintain its normal functional profile
Loss of proteostasis	Control of protein formation, folding and removal is reduced	Damaged and misfolded proteins accumulate more easily
Impaired macroautophagy	The cell processes damaged components worse	The efficiency of intracellular “cleaning” is reduced
Nutrient recognition disorder	The functioning of metabolic signaling systems is altered	The balance of growth, repair and energy expenditure is changing
Mitochondrial dysfunction	The functioning of the cell's energy organelles changes	Energy and signaling processes are disrupted
Cellular aging	Some of the damaged cells stop dividing but remain metabolically active.	Such cells are capable of changing the tissue environment.
Stem cell depletion	The regenerative potential of some tissues is reduced	Recovery from injury may be slower
Disruption of intercellular communication	Cells and organs change the nature of signal exchange	The body's systems are coordinated less precisely
Chronic inflammation	A persistent low-level inflammatory background arises	It may support tissue damage and age-related diseases.
Dysbiosis	The structure of the body's microbial communities changes	Immune and metabolic regulation may be altered

Classification source: López-Otín et al., Cell, 2023, DOI: 10.1016/j.cell.2022.11.001. [13]

The strength of this model is that it explains why trying to find a single "aging gene" or single damaged molecule consistently proves insufficient. For example, mitochondrial dysfunction can stimulate inflammatory signals; chronic inflammation can alter stem cell function; impaired autophagy can lead to the accumulation of damaged proteins and organelles; and cellular senescence can affect neighboring cells. This creates feedback loops in which several initially small changes begin to feed into each other. [14]

DNA Damage: Why Perfect Repair Is Impossible

DNA is constantly exposed to internal and external factors. Errors can occur during the copying of genetic material, as a result of exposure to the products of normal cellular metabolism, ultraviolet or ionizing radiation, and other factors. Cells have numerous systems for recognizing and repairing damage, and they successfully correct most problems that arise. Aging, therefore, cannot be thought of as a situation in which the body suddenly "stops repairing DNA." [15]

However, repair is not completely error-free. Over decades of life, individual cells accumulate somatic changes—that is, DNA alterations that were not necessarily present at birth and are not transmitted throughout the organism. Their consequences vary: many are neutral, some lead to cell death, while others can alter cell function or create conditions conducive to tumor growth. Therefore, genomic instability is simultaneously considered both a hallmark of aging and one of the mechanisms linking age with an increased risk of certain diseases. [16]

This also helps explain why the body can't simply endlessly replace damaged cells. A new cell doesn't arise from nothing: it receives genetic material, signals, and conditions from an existing biological system. If the tissue environment, stem cells, immune control, and regulation gradually change, a single cellular renewal doesn't return the entire body to its original state.

Telomeres are indeed linked to aging, but they are not a "life counter"

Telomeres are specialized structures at the ends of chromosomes. As somatic cells divide, they tend to gradually shorten, which is why telomere shortening has long been one of the best-known hypotheses about aging. When telomeres reach a critical point, a cell may stop dividing normally or activate programs that protect the body from potentially dangerous continued division. [17]

But the popular notion that "if a person has 40% of their telomeres remaining, they have 40% of their life left" is incorrect. A systematic review and meta-analysis of 414 samples with data from more than 743,000 people did indeed find a link between age and telomere length, but this association was relatively weak and depended on the tissue type and measurement method. The rate of telomere change was also nonlinear. Therefore, telomere length is a biologically interesting indicator, but not a precise individual timer of death. [18]

There's another biological tradeoff. Telomerase can restore telomeres and is active, for example, in some stem cells, but allowing cells to continually divide without limit is potentially dangerous. Cancer cells often acquire telomere maintenance mechanisms precisely because this helps them avoid normal division limits. Therefore, the simple idea of "activating telomerase in all cells and stopping aging" ignores the fundamental conflict between regeneration and anti-tumor defense. [19]

Epigenetics: DNA can remain the same, but the cell begins to read it differently

Liver cells and neurons contain virtually identical genomes, but they function completely differently because they activate different sets of genes. One mechanism for this control is epigenetics—chemical and structural changes that influence DNA activity without altering the sequence of its letters. With age, the epigenetic profiles of tissues gradually change, which is why epigenetic changes are part of the modern signs of aging. [20]

This gave rise to the popular idea of epigenetic clocks. The algorithm analyzes, for example, the methylation of certain DNA regions and estimates age or the rate of aging. In large study samples, some clocks are indeed associated with disease, mortality, and other outcomes. However, different clocks measure slightly different biological signals, and the causal significance of specific methylation changes often remains unclear. [21]

As of 2026, such tests cannot be considered equivalent to a standard medical blood test that can tell a specific person how much older or younger they are than their passport age and what treatment they require. A 2025 review specifically warns that epigenetic clocks do not yet meet the usual requirements for clinical utility for individual decision-making. Different methods and samples may yield different results, and the reasons for specific deviations are far from always clear. [22]

In a 2026 Nature Medicine review, Tony Wyss-Coray and Eric Topol also consider the biological clock as a promising research tool, potentially useful for assessing the risk and effectiveness of future interventions, but emphasize the need to critically evaluate what exactly each such indicator measures. [23]

Proteins also age: the problem is not only in DNA

Cellular life depends not only on genes but also on a vast number of proteins. Proteins must be properly synthesized, folded into a specific spatial shape, function, and be eliminated in a timely manner. The system that maintains this balance is called proteostasis. With age, the body's ability to maintain protein quality gradually changes. [24]

The importance of proteostasis is particularly evident in neurodegenerative diseases, where pathologically altered protein structures can accumulate. But aging isn't limited to a single protein aggregate. The problem is broader: protein synthesis, quality control systems, proteasomes, and mechanisms for intracellular removal of damaged components are altered. [25]

Autophagy, a system for recycling cellular components, plays a central role. It allows the cell to disassemble and recycle some damaged proteins and organelles. In the updated 2023 classification, impaired macroautophagy was identified as an independent feature of aging, emphasizing the importance of not only the rate of damage formation but also the cell's ability to eliminate it. [26]

Mitochondria: Aging is linked to energy, but the "free radical" theory turned out to be too simple

Mitochondria are often called the cell's powerhouses, although their functions are much broader. They are involved in the production of adenosine triphosphate, metabolism, intracellular signaling, stress response, and the control of cell death. With age, the structure and function of mitochondria can change, which is why mitochondrial dysfunction is one of the hallmarks of aging. [27]

For a long time, the free-radical theory was extremely popular: it was assumed that reactive oxygen species gradually damage molecules and are the primary cause of aging. Today, this explanation is considered insufficient. Reactive oxygen species are indeed capable of damaging cellular structures, but they also perform normal signaling functions, and attempts to reduce the entire aging process to their accumulation are inconsistent with the current body of evidence. A 2024 review of the causality of aging explicitly classifies the classical free-radical model among theories whose influence in modern science has diminished. [28]

This leads to a practical caveat: the idea that "the more antioxidants, the slower aging" doesn't follow from modern biology. Neutralizing all oxidative signals is not only impossible but also undesirable, since some of them are necessary for normal cellular adaptation. This is one reason why research findings on specific antioxidant supplements cannot be generalized to the fanciful idea of a general "treatment for oxidative aging."

The body constantly renews cells - why then does it still age?

This is one of the most intriguing questions about aging. It seems logical: if the epidermis, blood, and intestinal epithelium constantly replace cells, after a while a person should consist of "new parts." But an organism is not a collection of independent cells. Tissue age is also determined by the quality of stem cells, the extracellular matrix, the blood supply, the immune system, intercellular signals, and the architecture of the tissue itself. [29]

Furthermore, the rate of cellular renewal varies greatly. Some cell populations renew rapidly, others much more slowly, and some cells in the body exist for a very long time. Therefore, the statement that "every seven years a person is composed entirely of new cells" is biologically incorrect.

Even a new cell is born within an aging system. If a stem cell receives altered signals, the surrounding tissue contains chronic inflammation, the extracellular matrix is altered, and the metabolic environment differs from that of a young cell, renewal does not return the tissue to its original youthful state. This is why stem cell exhaustion and altered intercellular communication are considered independent components of aging. [30]

Studies of human tissues also reveal an age-related decline in stemness-related characteristics, although the degree of this change varies between tissues. Such findings help explain why regeneration may remain possible with age, but become slower or less complete. [31]

Senescent cells do not necessarily die.

Some cells, when severely damaged, stop dividing but continue to survive and exchange signals with surrounding tissue. This condition is called cellular senescence. Initially, it may serve a beneficial function: stopping the division of a damaged cell reduces the likelihood of its uncontrolled proliferation and plays a role in healing and other physiological processes. [32]

The problem arises when such cells accumulate. Senescent cells are capable of releasing large quantities of biologically active molecules and altering the state of neighboring cells and the immune system. Therefore, cellular senescence can transform from a protective mechanism into a factor in chronic tissue damage. [33]

This is where the idea of senolytics—drugs designed to eliminate specific senescent cells—came from. Some such strategies showed great promise in animals, but translating the results to humans proved significantly more difficult. In a clinical trial of elderly women, a combination of senolytics produced only limited effects on bone tissue, and a review in Nature Aging 2025 emphasized that there is still no clear evidence of the clinical efficacy of senolytics in humans. [34]

Why does chronic inflammation occur with age?

The immune system also undergoes restructuring with age. At the same time, certain specific immune responses may decline, while chronic low-level inflammation increases. This phenomenon is often referred to as inflammaging, or age-associated chronic inflammation. The updated classification of signs of aging identifies chronic inflammation as a distinct component. [35]

The source of this inflammatory state may not be a single event, but a combination of processes: senescent cells, damaged molecules, altered immune regulation, metabolic disturbances, and interactions with the microbiome. In turn, inflammatory signals can affect blood vessels, muscles, the nervous system, and tissue regeneration, creating another cycle of mutual reinforcement. [36]

This doesn't mean that every elevated inflammatory marker in an elderly person should be attributed to "aging." Infections, autoimmune diseases, obesity, cancer, and many other conditions also influence inflammation. The concept of inflammaging describes a population-wide biological process, not a diagnosis that can be made based on a single test.

The microbiome is also becoming part of the picture

In the 2023 version of Hallmarks of Aging, dysbiosis was added as a distinct feature of aging. Microbial communities in the gut and other parts of the body interact closely with the immune system and metabolism, so changes in their composition may be associated with age-related changes in the body. [37]

However, this doesn't mean there's a single "young microbiome" that can be restored with a probiotic and thereby rejuvenate a person. The microbiome is extremely variable and depends on diet, medications, diseases, geography, lifestyle, and many other factors. Its role is currently better established as part of the complex aging system than as a ready-made, stand-alone therapeutic target.

Why can different organs in the same person age at different rates?

Aging is not necessarily distributed evenly throughout the body. Modern research using protein, metabolic, genetic, and imaging data allows us to identify differences in the estimated biological age of individual organs. One person may exhibit more pronounced age-related changes in the cardiovascular system, another in the kidneys, and a third in the brain or metabolism. [38]

The reasons for this discrepancy are still being studied. Genetic differences, diseases, medications, smoking, physical activity, diet, and specific effects on a particular organ may all contribute. Interactions between organs cannot be ruled out either: dysfunction in one system can affect others through inflammatory, metabolic, or hormonal signals. [39]

This is one reason why the concept of a single "biological age" may be overly simplistic. In the future, medicine may speak more about the aging map of individual systems than simply assigning a single number, "You're biologically 47." For now, the organ clock remains a developing research area rather than a standard clinical examination. [40]

Aging and illness are not the same thing.

Aging significantly increases the likelihood of many chronic diseases, but it does not necessarily mean that a person will have a specific disease. The US National Institute on Aging views aging as a key common factor linking cardiovascular disease, diabetes, cancer, neurodegenerative processes, and other conditions. This has led to the development of a distinct field of research—geroscience. [41]

The main hypothesis of geroscience is that if we can safely target the fundamental mechanisms of aging, it will theoretically be possible to delay several conditions at once, rather than combat each age-related disease separately, preserving human functional capacity for longer. In animals, the fundamental variability of lifespan and healthy lifespan has already been convincingly demonstrated through genetic, nutritional, and pharmacological interventions. In humans, such translation is considerably less proven. [42]

The World Health Organization therefore defines healthy aging not as the complete absence of all diagnoses, but as the preservation of functional ability that allows a person to do what is important to them. A person with well-controlled hypertension or osteoarthritis can have a high level of independence and quality of life, whereas the absence of a formal diagnosis does not guarantee good physical or cognitive function. [43]

Is it possible to slow down aging today?

The most reliably proven interventions today are aimed primarily not at "age reprogramming," but at maintaining health and functional reserve. Regular physical activity improves physical function, maintains muscle and bone health, and is associated with a lower risk of cardiovascular disease, type 2 diabetes, and a number of other adverse outcomes. The National Institute on Aging emphasizes the benefits of aerobic, strength, and balance training in older age. [44]

The importance of physical activity particularly well illustrates the difference between aging and the consequences of aging. Exercise doesn't literally make a person's DNA younger or reset telomeres, but it can maintain muscle strength, insulin sensitivity, cardiovascular function, mobility, and the ability to independently cope with everyday tasks. Therefore, a person is able to age functionally significantly more successfully, even as the calendar continues to tick. [45]

Healthy sleep, quitting smoking, managing blood pressure and chronic diseases, eating a balanced diet, and maintaining physical activity have a much more robust evidence base for maintaining health than most commercial "anti-aging" supplements. While this may sound less glamorous than the promise of cellular rejuvenation, it is precisely these measures that have proven practical value today. [46]

What about calorie restriction?

Calorie restriction without nutrient deprivation significantly extends lifespan in a number of model organisms, so this approach has been studied in gerontology for decades. In the human CALERIE study, more than 200 healthy, non-obese individuals were followed for two years; the dietary restriction group was able to reduce energy intake by an average of approximately 12%, although the target was 25%. [47]

In a subsequent analysis, participants in the calorie restriction group showed a slight change in one measure of epigenetic aging, DunedinPACE. However, other epigenetic clocks, including PhenoAge and GrimAge, showed no significant changes in biological age. The authors themselves emphasized that definitive proof of slowing human aging must come from long-term studies measuring real-world outcomes—disease, functional status, and mortality—and not just changes in molecular patterns. [48]

Therefore, CALERIE cannot be interpreted as evidence that people should voluntarily restrict their calorie intake by a certain percentage to prolong life. Particularly in the elderly, excessive calorie restriction may conflict with the need to maintain muscle mass and adequate nutrient intake. Experimental gerontology and standard nutritional recommendations are not the same thing.

Metformin, rapamycin and the “anti-aging pill”

Rapamycin is one of the most impressive examples of a drug capable of extending lifespan in several model organisms, including mammals. It interferes with the mechanistic target of rapamycin (MTRA) signaling pathway, which is associated with growth, metabolism, and cellular responses to nutrients. However, clinical experience with inhibitors of this pathway in humans is primarily limited to transplantation and oncology, where serious side effects are possible. Studies of the use of such drugs specifically against aging processes do not yet allow them to be recommended for life extension in healthy individuals. [49]

Metformin is also being actively studied due to its metabolic effects and observational data on age-associated diseases. However, the drug has been proven primarily as a treatment for specific metabolic conditions, not as a drug that healthy individuals should take to slow aging. Geroscience research is ongoing, but data from diabetology or mouse experiments cannot be generalized to prophylactic use in healthy individuals. [50]

The National Institute on Aging has explicitly warned that neither rapamycin, nor metformin, nor nicotinamide adenine dinucleotide-acting compounds, nor other investigational agents have yet been shown to extend human lifespan or healthy life span in a manner that would allow them to be used as standard "anti-aging" therapies.[51]

Is it possible not just to slow down, but to reverse aging?

This is one of the fastest-growing areas of research. Partial epigenetic reprogramming—an attempt to temporarily activate some of the factors capable of reverting an adult cell to a younger state without completely erasing its specialized identity—is of particular interest. Animal studies have demonstrated capabilities that until recently seemed impossible. But the safety of such interventions is critical: too much reprogramming could potentially disrupt cell identity or increase other risks. [52]

In February 2026, a major transition from preclinical science to human use occurred: the US Food and Drug Administration approved the start of a phase I study of ER-100, a therapy that uses three reprogramming factors—OCT4, SOX2, and KLF4. However, the trial is intended for patients with eye disease and primarily aims to assess safety. It is not a proof-of-concept for human rejuvenation or a test for life extension in healthy individuals. [53]

Therefore, the assertion that "science can already reverse human age" is premature as of September 2026. It is far more accurate to say that researchers have learned to alter some age-associated processes in cells and animals and are beginning to test certain methods in humans. There remains a vast scientific gap between molecular cellular rejuvenation and the safe extension of healthy human life.

Why does one person age noticeably faster than another?

Calendar age adds a year to each person's age uniformly, but biological changes occur unevenly. Even people of similar ages can experience significant differences in muscle strength, vascular health, cognitive function, metabolism, and recovery from illness. The World Health Organization emphasizes that the range of functional capabilities in old age is extremely wide, and chronological age alone is a poor predictor of a specific individual's condition. [54]

Heredity plays a role, but it is not the only "blueprint for aging." Over the course of life, genetics interacts with nutrition, physical activity, infections, diseases, environmental pollution, stress, medications, and social conditions. The NIA now views biological, behavioral, and social factors of aging as interacting across the lifespan, rather than as independent categories. [55]

Therefore, two people with the same passport age can have very different physiological resilience. This doesn't mean it's correct to declare one of them "18 years younger" based on a single commercial test. However, differences in functional status have real medical significance: walking speed, strength, endurance, cognitive function, and the ability to recover from exercise directly determine independence and quality of life.

What we don't yet know about aging

Even the current system of 12 features is not a definitive causality map. The problem is that a change can simultaneously be a cause, a consequence, and an amplifier of other age-related processes. For example, inflammation can damage tissue, but itself arises in response to damage; senescent cells alter the environment, but their appearance can be a consequence of DNA damage; epigenetic changes can influence cell function, but some of them may simply reflect processes occurring within the cell. [56]

This is why modern gerontology is gradually shifting from the question "what changes with age?" to the more complex question "which of these changes actually drives aging, and what happens if we intervene specifically?" Measuring correlation is significantly easier than proving causation. This is especially important for biomarkers and commercial tests: a marker may be a good predictor of age, but that doesn't mean that changing it rejuvenates the body. [57]

This is one of the major scientific challenges of the coming decades. Researchers already know how to alter the lifespan of laboratory organisms and influence individual signs of aging. Now it's necessary to determine which interventions safely improve real human outcomes—not just molecular clock numbers, but lifespan free from serious illness and loss of independence. [58]

What is often misunderstood

"Free radicals cause aging." Reactive oxygen species are involved in damage and cellular signaling, but modern science does not consider them the sole cause of aging. The classical free radical theory has proven too simple to explain the accumulated experimental data. [59]

"Telomeres are everything." Telomere shortening is indeed one of the hallmarks of aging, but individual telomere length is not an accurate predictor of remaining lifespan. [60]

"If cells are constantly renewed, a person should be rejuvenated." New cells appear within an already altered tissue environment, and the regenerative systems themselves are also subject to age-related changes. [61]

"The biological clock already accurately measures true age." It is useful in research, but different clocks measure different signals and are not yet a reliable individual diagnostic tool for choosing treatment. [62]

"There are already drugs proven to stop human aging." Rapamycin, metformin, senolytics, cellular reprogramming, and other approaches are being actively researched, but there is no proven therapy that safely reverses systemic aging in healthy individuals. [63]

Key points from experts

Tony Wyss-Coray, Ph.D. - DH Chen, Distinguished Professor of Neurology and Neurological Sciences, Stanford University, Director of the Knight Initiative for Brain Resilience. A Nature Medicine 2026 review, co-authored with Eric Topol, highlights the biological clock as a promising way to study the aging of individual organs and evaluate future interventions, but also emphasizes the need to critically understand which biological process a particular algorithm reflects. This is especially important against the backdrop of the commercialization of "biological age" tests. [64]

João Pedro de Magalhães, Ph.D., is a professor of molecular biogerontology at the University of Birmingham. In his work on the causality of aging, he draws attention to the fundamental distinction between the changes observed during aging and the changes that actually cause it. He also notes the diminishing role of classical free-radical theory and the need to test causality using human genetics and experimental models, rather than automatically assuming that any age-related biomarker is a mechanism of aging. [65]

Frequently Asked Questions

At what age does a person begin to age?

There is no single age. Development and age-related changes partially overlap, and different tissues and biological processes have their own trajectories. Therefore, numbers like 25, 30, or 40 years cannot be considered a universal starting point for aging. [66]

Is it true that aging accelerates sharply at 44 and 60 years of age?

Such a conclusion cannot yet be drawn. A 2024 study reported similar molecular peaks, but in July 2026, Nature Aging posted an editorial notice raising questions about the reliability of the corresponding analysis. [67]

Is it possible to find out your true biological age?

There is currently no single, universally accepted clinical test. Epigenetic, proteomic, and other clocks are used in research, but the results of different methods can vary and should not yet, on their own, guide medical decisions for a particular individual. [68]

If you lengthen your telomeres, can you stop aging?

There is no such evidence. Telomere shortening is only one of twelve recognized hallmarks of aging, and artificially maintaining the ability of cells to divide indefinitely creates additional biological problems, including tumor control. [69]

Why aren't children of old parents born "old"?

During the formation of germ cells and the early development of the next generation, a massive biological restructuring occurs. The offspring does not simply receive a copy of the accumulated age of the parents' somatic tissues. This is a good example of how aging represents a state of the body and its regulatory systems, not simply a number of years recorded in the DNA sequence.

Can you stop aging with exercise?

No, exercise doesn't stop the passage of biological time. But regular physical activity helps maintain muscle strength, mobility, cardiovascular and metabolic health, and can thus significantly improve the trajectory of healthy aging. [70]

Do antioxidants help prevent aging?

There is no compelling evidence to support the use of antioxidants as a universal method for slowing aging. Our current understanding of the process is significantly more complex than the classical free radical theory. [71]

Is it possible to rejuvenate an old cell?

Experimentally, some cell characteristics can indeed be shifted to a more youthful state. Partial epigenetic reprogramming has already reached phase I clinical trials for eye disease, but its safety and clinical efficacy in humans are still being tested. [72]

Does this mean that humans will soon be able to live 150-200 years?

Current data do not support such a conclusion. The ability to influence individual aging mechanisms is not equivalent to proof of a radical increase in maximum human lifespan.

Will aging ever become a curable disease?

For now, it's more accurate to view aging as a complex biological process and a major risk factor for multiple age-associated diseases, rather than as a single disease with a single cause and a single cure. Geroscience is exploring the possibility of intervening in common mechanisms to simultaneously delay multiple diseases and functional loss. [73]

Main

We age because evolution has created an extremely efficient, but not infinitely perfect, system for maintaining the body. Throughout life, the genome, epigenetic regulation, protein control, mitochondria, autophagy, stem cells, immunity, intercellular communication, and the microbiome gradually change. No single process alone explains all of aging; it is far more accurate to view them as an interconnected network. [74]

However, the biological trajectory is not entirely predetermined. Animal experiments demonstrate fundamental variability in the rate of aging, and in humans, physical activity, disease prevention, and other well-studied factors can significantly influence the duration of healthy and independent life. However, there is still a very clear line of evidence between "improving health in old age" and "reversing human aging." [75]

It is particularly interesting that in 2026, partial cellular reprogramming research will enter the clinical phase for the first time. This is an important scientific milestone, but not proof of the existence of a technology for human rejuvenation. The most fundamental question remains open: which of the many age-related changes are the true root causes, and which merely reflect or amplify the process. The answer to this question will likely determine how far medicine can move from healthy aging to directly influencing its biological rate. [76]