The Ethics of “Curing” Aging

The Ethics of “Curing” Aging
May 5, 2022 No Comments Global Bioethics Katie Tan

Defying Death: Cellular Reprogramming to “Cure” Aging

By Katie Tan

What if we could live forever? What would be the consequences of eliminating aging from society? Would we still be human? All of these questions are important when determining the ethicality of pursuing anti-aging technology, which is closer to the future than people may think. Cellular reprogramming has the potential to reverse symptoms of aging, and therefore will affect all humans, making it a global bioethical dilemma. This paper will examine whether pursuing this technology sacrifices the integrity of the medical field, if doctors have a responsibility to reduce suffering due to aging, and the negative consequences that might come from a population without aging. 

Table of Contents


Cell reprogramming is the process of turning specialized (somatic) cells into induced pluripotent stem cells (iPSC). This process was developed by scientist Shinya Yamanaka in 2006. The introduction of four specific genes (oct4, sox2, klf4, and c-myc), known as Yamanaka factors, can create iPSC. As cells age, epigenetic markers evolve and change the expression of genes in cells. The epigenetic model of aging includes changes in DNA methylation, histone modification, and chromatin remodeling; the decrease in DNA methylation, increase in active histones, and chromatin remodeling lead to the hallmarks of aging. Cellular reprogramming can rejuvenate cells which could promote life extension by preventing aging in humans. This raises ethical concerns around integrity and responsibility while also requiring the evaluation of consequences of prolonged human lifespan on society. This paper will attempt to answer the question, is it ethical to extend human lifespans by “curing” aging.


This paper will focus on cell reprogramming and its possible cure for aging, as well as its role in the slippery slope to immortality. Currently, iPSC has been used as a way to cure symptoms of aging and extend life such as disease modeling, drug discovery, and cell therapy development. Disease modeling is the study of causes of diseases, and requires experimentation on primary cells, which can be hard to access from certain organs such as the brain and heart. iPSC presents a solution as, “human diseases (particularly those with defined genetic causes) could in principle be modeled using iPSCs derived from easily accessible cell types, such as skin fibroblasts and blood cells from diverse patients.” iPSC have also been used in target-based and phenotypic screening. The ability to repeat disease phenotypes has led to the finding of potential drugs for certain diseases. Finally, iPSC have been proven to work in cell therapy, “In 2014, the first clinical study using human iPSC products was initiated by transplanting RPE [retinal pigment epithelium] sheets derived from the patient’s own iPSCs. The therapy has resulted in positive results, stopping macular degeneration and improving the vision of the patient” (Shi et al., 2016). So far, scientists have not reached the stage of being able to prevent death, but humans are heading in that direction.

I will be looking at this issue through the values of integrity and responsibility and with a lens of consequentialism, specifically, looking at the consequences of extending life. Within the value of integrity, I will be assessing the arguments that life extension falls in line with the pattern of progress in science/medicine, the usefulness that curing aging will have in treating diseases in the future, and how the universal nature of aging and eventual death counters the ethics of pursuing life extension. In the responsibility section, I plan to look at whether anti-aging treatments have the potential to improve quality of life (specifically, mental and physical health), and if so, whether doctors have a responsibility to extend life. I will also research the consequences of curing aging such as unequal access, increased ageism, and overpopulation.

Defining Aging

One definition states that aging is characterized by “the progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death” (Lópes-Otín et al.). However, there are multiple different ways to think about aging besides defining it. Some methods of assessing aging are through chronological age, biological age, the hallmarks of aging, and measuring age through epigenetics. 

Chronological and biological age are two ways to measure a person’s age, where “chronological age refers to the actual amount of time a person has existed, biological age refers to epigenetic alterations…” (Räsänan). Chronological age increases at the same rate for everybody, while biological age is dependent on different factors such as environment, genes, diet, exercise, etc. To calculate biological age, scientists take a sample of cells and look at specific sites along the genome and see what proportion of the cells are marked with DNA methylation (“What Is Your Biological Age? And Why Does It Matter?”). Experiments with iPSC have proven that it is possible to reverse biological age through targeting epigenetic changes. 

The Hallmarks of Aging

Scientists have identified nine key hallmarks of aging which can be broken into three categories: primary causes (genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis), antagonistic hallmarks (deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence), and systemic hallmarks (altered intercellular communication, and stem cell exhaustion).

Genomic instability is the result of the accumulation of genetic damage. Telomere attrition is when the telomeres (the caps on the end of chromosomes) shorten as cells divide. Eventually, they become too short, which means the cell cannot divide anymore (cellular senescence). Loss of proteostasis means that proteins are no longer folded correctly, leading to many age-related diseases such as Alzheimer’s. “Nutrient signalling encompasses various cell signalling pathways that are regulated by nutrient availability. Changing nutrient levels activates signalling cascades that modulate fundamental cellular processes including metabolism, proliferation, secretion, and autophagy” (“Nutrient signalling,” The mitochondria are responsible for aerobic respiration and allow energy production; mitochondrial dysfunction means that over time, energy production becomes less efficient. Cellular senescence is when cells stop dividing. Intracellular communication causes cells to not work properly, which can then lead to age-related diseases. Finally, stem cell exhaustion is the loss of stem cells in the body. Because stem cells are used for the regeneration of tissue, losing them means the body cannot repair itself anymore (“What Are the Hallmarks of Aging?” 03:15–05:21). Epigenetic changes, although only of the primary causes of aging, are most useful when assessing aging because most of the hallmarks of aging (such as telomere shortening, cellular senescence, stem cell exhaustion, and mitochondrial dysfunction) can be regulated through epigenetics. 


Epigenetics seeks to understand how behaviors and the environment cause changes that affect how genes work. Epigenetics involves changing the expression of genes by either activating or deactivating specific genes. Genes become expressed when they are read and transcribed into RNA, then RNA is translated into proteins by ribosomes; epigenetic changes (caused by lifestyle factors) can interfere with the transcription of genes. These changes occur because chemical tags attach to the DNA or protein; the combination of all the chemical tags is known as the epigenome. It is important to note that epigenetic changes are normal. As babies develop, certain genes are expressed or silenced which is the cause for cell specialization (“What Is Epigenetics? – Carlos Guerrero-Bosagna” 03:15–05:21). Aspects such as radiation exposure, diet, and exercise can cause changes to the epigenome and signs of aging. 

Christoph Bock, Wikimedia Commons

Epigenetic alterations include three changes: DNA methylation, histone modification, chromatin remodeling. DNA methylation is the transfer of a methyl group onto the C5 position of the cytosine (Moore et al.). The location of this transfer “blocks the proteins that attach to DNA to ‘read’ the gene (CDC . What this means is that the genes are silenced, or in other words, not expressed. 

The core histones play structural roles in chromatin assembly and compaction by forming the nucleosome (Mariño-Ramírez et al.); “…replicative aging is accompanied by loss of approximately half of the core histone proteins” (Pal and Tyler). In addition, depending on whether genes are wrapped or not around histones contributes to the silencing or expression of those genes: “When DNA is wrapped tightly around histones, it cannot be accessed by proteins that ‘read’ the gene. Some genes are wrapped around histones and are turned ‘off’ while some genes are not wrapped around histones and are turned ‘on’ ” (CDC) . 

Finally, the decay of heterochromatin occurs during aging in all eukaryotes. The decay of these heterochromatin results in the loss of transcriptional silencing (Pal and Tyler). The ways these changes present in older versus younger cells will be addressed later. I have chosen to focus on the epigenetic alterations of aging because, again,  these three alterations are the root causes of many of the hallmarks of aging. 

The epigenetic model of aging places evaluates biological age, as it looks at the correlation between aging and changes to cells. Measuring aging at a cellular level places aging on a more scientific, objective playing field. Furthermore, evaluating aging through cells separates the field of aging from death. Separating aging from death has the potential to destigmatize the aging process, and can encourage solutions for it. The one issue with using a more scientific lens, and encouraging solutions to aging, is that it’s assumed that aging is a disease, and that it should be treated. This problem is the reason I will address whether I believe aging can be considered a disease and how that affects the ethics of curing aging to extend human life. Finally, I will answer whether iPSC can reverse epigenetic alterations, if that reversal could be the key to life extension, and the ethical implications of life extension.

Cellular Reprogramming Background

Induced Pluripotent cells, known as iPSC, can convert any mitotic cell (a cell that divides) to a stem cell with master genes known as Yamanaka factors. Before iPSC were discovered, rejuvenation was a topic that was being researched. It started with Dolly, the first mammalian cloning in 1996. Scientists have concluded that the cytoplasm of mature oocytes contains molecules able to turn a somatic nucleus into an embryonic one. In oocyte cytoplasm, people believed there had to be reprogramming factors that would turn the somatic nucleus into an embryonic one. Ten years later, in 2006, scientists Shinya Yamanaka and Kazutoshi Takahashi reprogrammed mice fibroblast cells to behave like embryonic stem cells. The new cells generated were called iPSC. Takahashi and Yamanaka were able to create iPSC by injecting four master genes (oct4, sox2, klf4, and c-myc) into adult mouse fibroblasts (connective tissue). When these four genes, known as Yamanaka factors, were injected into the cell, it was able to reprogram them to behave like embryonic cells (Goya).

Changing a cell to the pluripotency stage means that the cell can specialize into different cell types. The difference between somatic cells and pluripotent stem cells (PSC) are that somatic cells are specialized while PSC are not. As humans develop, PSC specializes in becoming different types of cells (i.e skin cells, blood cells, etc.). These somatic cells eventually make up the different organs and tissues in our bodies. Before the development of iPSC, PSC were usually harvested from embryos in blastocyst stages, but this often resulted in the death of the embryo. iPSC became a solution to this problem as it was able to change a somatic cell to a PSC using skin cells and the Yamanaka factors. When somatic cells change into iPSC, DNA packaging, as well as the level of expression of certain genes changes (NIE Singapore 03:15- 05:21). 

How Reprogramming Cells to iPSC Reverses Epigenetic Alterations

Reprogramming cells back to the pluripotency stage can change aged cells back to the embryonic stage. In the process, the epigenetics marks found in the aged cells will also revert to the state they were in during the embryonic stage. The stages of cell aging can be divided into four categories: A0, A1,  A2, A3. A0 is the embryonic stage, A1 stage is the “young” stage (when the cell begins to age), A2 stage (also known as the aged stage), and A3 is the senescent stage (cellular senescence means that cells stop dividing). Reprogramming cells (using Yamanaka factors) change epigenetic markers and can revert A2 cells back to A0 cells (Kane and Sinclair). By changing the stages of aging in cells, the epigenetic markers of the cells also change. 

In younger cells there are tightly packaged heterochromatin, repressive histone marks, Hp1 protein binding, and increase in DNA methylation. Chromatin is the material that chromosomes are made of and they can be separated into two types, euchromatin and heterochromatin. Euchromatin is open and transcriptionally active, while heterochromatin is tightly closed chromatin and transcriptionally silent. The tightly packaged heterochromatin, repressive histone marks, and Hp1 protein binding all contribute to the silencing of genes. Again, the expression of genes as we get older causes aging, meaning that the silencing of genes in younger cells is the reason why symptoms of aging don’t appear when we are younger (Kane and Sinclair).

Some common characteristics of older cells are reduced heterochromatin, a decrease in repressive histone marks (an increase in active marks), and overall hypomethylation. The connection between DNA methylation and aging is still being researched. However, there is evidence that as we get older, DNA methylation decreases, “a centenarian’s methylome displays reduced DNA methylation levels as well as a decreased pair-wise correlation in the methylation status of neighboring CpG sites relative to the methylome of a newborn” (Salameh et al., 2020). Another study showed that in cultured human embryonic lung fibroblasts, global hypomethylation occurs during both stress-induced and replicative senescence.

Epigenetic alterations associated with aging can be fixed with cell reprogramming. Most of the hallmarks of aging are due to epigenetic alterations. For example, Telomere shortening, cellular senescence, stem cell exhaustion, and mitochondrial dysfunction are regulated through epigenetics. Converting aged cells to iPSC can prevent these hallmarks of aging. Recent studies have produced promising results for the use of iPSC in “curing” aging. One successful experiment was done by Australian biologist David Sinclair. Sinclair is the co-director of the Paul F. Glenn Center for Biology of Aging Research at Harvard Medical School. His study was able to successfully create axon growth and vision in previously blind mice using iPSC. These traits are characteristics of embryonic stem cells, proving that iPSC can change aging biomarkers in cells and cure symptoms of aging. 

David Sinclair’s Study

David Sinclair’s study noted that iPSC could cause an A2 cell to revert its embryonic state. The experiment targeted neurons called retinal ganglion cells. They chose to do this because the difference between younger and aged cells is more pronounced in this specific cell type; an embryonic or newborn mouse can regenerate the optic nerve if it gets severed, but that ability vanishes with time. Sinclair and other scientists were able to damage the optic nerve in mice and inject a harmless virus into the eye carrying the genes for the 3 reprogramming factors. The injection was able to prevent some damaged cells from dying, and some axons began to grow (just like embryonic/newborn mice can regenerate). Looking at a cellular level, parts of the genome were able to reverse the aging epigenetic marks found in these ganglion cells. Sinclair and his team did a similar experiment with glaucoma (vision loss, blind mice). After the treatment of the reprogramming factors, the mice were able to gain about half of their vision back (Servick). In summary, iPSC have the ability to cure biological aging, meaning that aging is being targeted at the cellular level. When cells revert to their embryonic state, epigenetic changes associated with aging are reverted as well. As epigenetic changes are ameliorated, traits that were previously expressed become silenced, as they were in their younger stage. While human tests have not been conducted, there have been successful cases with animals.

Ethical Values: Integrity and Responsibility


When assessing the use of iPSC in curing aging, two values that come to mind are integrity and responsibility — the integrity of the scientific and medical field, as well as the responsibilities of society. A key point that will be addressed is whether or not age can be considered a disease, and the use of consequentialism will be important in determining the ethicality of “curing” aging if it can be considered a “disease.”  

Integrity can be defined as the quality of being honest and having strong moral principles. An ethical question that arises from anti-aging technology is whether humans have a moral obligation to extend life as long as possible. Two perspectives in favor of the ability to cure aging are the obligation to make advancements in science and the potential to reduce the burden of age-related diseases. Some arguments against this technology are that aging cannot be classified as a disease and that this technology will further stigmatize the aging process. 

Medical progress has allowed humans to live longer lives, and because of that, society has been able to progress rapidly. I believe that humans have a moral responsibility to progress society by extending life (by researching cures for aging). Before thinking about the ethics of curing aging and possibly extending life, it is important to note the difference between lifespan and life expectancy. Lifespan is a measure of the actual length of an individual’s life while life expectancy is the average lifespan of an entire population.“The human lifespan of about 122 years is the maximum that a human has been proven to live. It has remained fixed for the last 100,000 years based on extrapolations made from the remarkable consistency in the relationship of the brain-weight/body-weight ratio to lifespan in primates” (Hayflick 20-26).  As technology advances, lifespans and life expectancy will probably continue to increase, although we won’t be “living longer now than ever before.” Scientists hope that the cure for aging, found in iPSC, will increase both lifespans and life expectancies.  

Excluding child mortality (which is the share of children who die before their 5th birthday), life expectancies have been increasing since the 19th century:

“In 1841 a five-year-old could expect to live 55 years. Today a five-year-old can expect to live 82 years. An increase of 27 years. The same is true for any higher age cut-off. A 50-year-old could once expect to live up to the age of 71. Today, a 50-year-old can expect to live up to 83. A gain of 13 years.”


By 1950, in Europe, North America, Oceania, Japan, and parts of South America, life expectancy for newborns was already over 60 years (but there was a great divide between life expectancies in all other parts of the world). In 2019, the global average life expectancy is around 72 years (Roser et al.). A key reason why life expectancy has increased is because of the advances in medicine and science, specifically the development of new treatments and procedures (Inventions). We can use medical technologies such as insulin and antibiotics to demonstrate this point; insulin was developed in 1922 and has saved 15 million lives (to date) and antibiotics, developed in 1928 have saved 200 million lives (to date). Both of these advancements have contributed to increased lifespans and life expectancies since their development by improving the quantity and quality of treatments for certain diseases. If scientists had not researched, and eventually discovered new advances in medicine, people would be dying more often. Illnesses which are seen as non-fatal today would still be fatal. The quality of life would lessen as people would be falling ill and dying more frequently. Because certain treatments have been researched, fewer lives have been lost than if scientific progress had not been made. 

The constant development of new advancements in the medical field with the goal of saving lives has set a precedent to keep extending human lifespans. From this standpoint, anti-aging technology can be seen as ethical because it would lead to longer-living, healthier people. There is a moral obligation to pursue anti-aging technologies because it will result in increased lifespans. The medical community’s obligation to preserve life means that pursuing anti-aging technologies (with the potential to allow humans to live longer and healthier) demonstrates strong moral principles, and therefore holds up the integrity of the medical community.  

Another argument in favor of anti-aging is that it is a more efficient method to cure age-related diseases, which could prevent the loss of lives that result from aging. Aubrey de Grey is a biomedical gerontologist who founded SENS Research Foundation. His company is a non-profit that works to develop, promote, and ensure widespread access to therapies that cure and prevent the diseases and disabilities of aging. “Drawing upon science’s moral obligation, de Grey articulates the importance of adopting a different approach to aging. His take on science’s moral mandate is unambiguous: ‘we risk being responsible for the deaths of over 100,000 people every day that [Engineered Negligible Senescence] is not developed.’ ” (Mykytyn 20). In addition to preventing loss of life that results from aging, de Grey and his company focus on treating age-related ill health, which leads to the idea that doctors have an obligation to reduce the burden of age-related diseases.

One organization working towards these goals is the National Institute on Aging or NIA. According to its mission statement, “NIA was established in 1974 to improve the health and well-being of older adults through research. It conducts and supports genetic, biological, behavioral, social, and economical research on aging and the challenges and needs of older adults. NIA is at the forefront of scientific discovery about the nature of healthy aging to extend the healthy, active years of life.” One of its goals is to develop effective interventions to maintain health, well-being, and function, and prevent or reduce the burden of age-related diseases, disorders, and disabilities. 

According to the CDC, 17% of adults aged 65 and older have been diagnosed with coronary heart disease; 13% of Americans aged 50 and older suffer from osteoporosis; the incidence rate for cancer increases as people age from less than .025% (aged less than 20) to greater than 1% (aged 60 and above) (Age and Cancer Risk). While diseases such as cardiovascular disease, osteoporosis, and cancer are not necessarily due to old aging, as humans get older, we become more prone to these illnesses. Instead of treating these diseases as they arise, it could be more beneficial and more cost-efficient to take measures to prevent the onset of these diseases. 

While countless lives have been saved as a product of medical advancement, finding a solution for aging differs from the medical advancements mentioned because aging, and eventual death, cannot be treated as a disease to be fixed because aging is a universal process. It is not very clear what conditions count as a disease; however, an article from Britannica defines disease as, “any harmful deviation from the normal structure or functional state of an organism, generally associated with certain signs and symptoms and differing in nature from physical injury” (Burrows). This definition is broad, and it allows aging to be included because as humans age, the natural state of the body alters and deteriorates. 

One reason why it is unethical to “cure” aging is that aging cannot be considered a disease. Aging differs from other diseases because it is an inevitable and universal process that no living being is exempt from. Leonard Hayflick provides six reasons why the aging process cannot be pathologized :

(1) They occur in every animal that reaches a fixed size in adulthood.

(2) They cross virtually every species barrier. 

(3) They occur in all animals that reach a fixed size in adulthood and occur only after sexual maturation.

(4) They occur in animals removed from the wild and protected by humans even when that species has not been known to have experienced aging during any of its previous thousands or millions of years of existence. 

(5)  They increase vulnerability to death in 100 percent of the animals in which the changes occur. 

(6) They occur in both animate and inanimate objects. 

(Hayflick 20-26)

The medical technologies mentioned, such as insulin or antibiotics, are used to treat diseases that aren’t universal or inevitable. As Hayflick describes, aging applies to everything in our world, alive or not. Whether it’s aging in humans and other species or the breaking down of inanimate objects, things deteriorate. In living things, this process of deterioration will always increase vulnerability to death. It is a natural process for things to live and to eventually deteriorate and die, so removing aging from society would decrease the value of life, possibly making us less “human”. Because aging in and of itself is normal, the worsening of some physical and mental symptoms accompanied by aging should also be considered normal, and should not be the reason aging is reversed. Regarding physical and mental symptoms, I believe medicine the way it is practiced now—treating one disease at a time—is more ethical than treating aging as a disease. The possible consequences of trying to reverse aging (and maybe even death) are that it’s going to provide a “solution” to the problem of aging when aging shouldn’t be viewed as a problem to be solved.

It is important also to consider the possible consequences of curing aging. If aging is continually seen as a disease that can be treated, death will continue to be seen as a failure in society, but particularly, in the medical community. This notion that death is a failure implies that there is somehow an alternative option. It puts a negative connotation on aging and death, even when it’s a normal part of life. Yes, diseases can be treated, but death from “natural causes” cannot be prevented (right now). In his book Being Mortal, Atul Gawande discusses how people process death differently:

“Dying and death confront every new doctor and nurse. The first time, some cry. Some shut down. Some hardly notice.”

(Gawande 7)

He then goes on to talk about how he would have “recurring nightmares in which I’d find my patients’ corpses in my house—in my own bed.” He attributes these nightmares to a sense of failure.  Trying to combat aging and eventual death could lead to a greater sense of failure for those in the medical community who witness death frequently. 

When looking at impacts on the elderly community, researching cures for aging sends the message that something is wrong with aging and that the elderly are not respected. While pursuing anti-aging technology may demonstrate that the elderly are valued—by trying to improve quality of life by relieving elderly of age-related diseases—it shows a lack of respect and dignity for the elderly in their current state.  

Because aging is so fundamental to being alive, I believe that trying to reverse it for the sake of pursuing medical progress would not be morally acceptable (and therefore would be violating the value of integrity). Having strong moral principles includes knowing where boundaries are, and while treating aging as a disease might be able to target age-related diseases more efficiently, it pushes a boundary that is fundamental to being alive. Aging is a key aspect of being alive because, again, it applies to every living being, not just humans. When all life goes through a process (such as aging) it shows how basic and foundational it is to live, and therefore that line cannot be crossed without sacrificing integrity.    


If iPSC can cure aging, the principle of beneficence says that doctors have a responsibility to maintain the health of patients and prevent disease, sickness, and suffering. A question that arises is whether extending life spans by curing aging prevents suffering.

Anti-aging treatments could greatly improve quality of life by improving physical health. This would mean that people would live longer and healthier. David Gems is a British geneticist and biogerontologist. He is a Professor of Biology of Aging at University College London and is also deputy director of the Institute of Healthy Aging. According to Gems: “[decelerated aging] would greatly reduce the frequency of aging-related illness at any given age. This could achieve an amelioration of human suffering on a very large scale, perhaps comparable in magnitude only to that resulting from the development of antibiotics. This would be a triumph of human endeavor” (Gems). If anti-aging treatments were able to prevent the onset of these diseases, it could prevent physical suffering for people with these diseases, as well as reduce the financial burdens that come with old age, particularly the cost of healthcare. 

Curing aging could  improve the mental health of older people by releasing the burden of age-related diseases, “thus, decelerated aging presents a dilemma. Either one must pursue it and reduce suffering but risk extending lifespan to a degree that is socially and existentially problematic; or one must abjure it thereby avoiding the troubles that life extension may cause, but permitting avoidable suffering on a great scale” (Gems). Along with physical symptoms, older people suffer emotionally. A 2018 article from the Guardian stated: “According to the charity Age UK, half a million people over the age of 60 usually spend each day in complete solitude, and nearly half a million more tend not to see or speak to anyone for at least five days in any given week” (Harris). Two factors affecting the mental health of the elderly are participation in meaningful activities and relationships. Improving the symptoms of aging could provide a way for older people who are limited, physically, by their old age to become more active. 

As previously stated, common age-related diseases include cardiovascular disease, osteoporosis, and cancer. With the onset of these diseases comes an increase in the financial burden to treat these illnesses. According to one paper:

“We use data from the Medicare Current Beneficiary Survey (MCBS) to document the medical spending of Americans aged 65 and older. We find that medical expenses more than double between ages 70 and 90 and that they are very concentrated: the top 10 percent of all spenders are responsible for 52 percent of medical spending in a given year.”

(Nardi et al. 728)

The doubling of expenses is proof that aging has not only created physical and mental tolls but also contributes to the financial burdens of the elderly. Money is needed to treat illnesses, and as a result, is key to releasing the physical and mental suffering that signs of aging cause. If doctors have a responsibility to benefit the patients, and anti-aging technology has the potential to reduce physical, mental, and financial burdens, then doctors/scientists should support the creation of anti-aging technologies. 

Possible Consequences of Anti-aging Technology

Unequal Access

An important consideration is whether everyone will have access to this technology. In regenerative medicine, iPSC can be used to repair damaged tissue. Producing generations of these cells is an expensive process, costing thousands of dollars. Currently, with many billionaires investing in anti-aging research, it looks like only the wealthiest in society will be able to use this technology. An article from the Guardian states that the anti-aging industry will increase from 200 billion to 420 billion by 2030. Currently, big names such as Larry Page, Sergey Brin, Peter Thiel, and Jeff Bezos have all been funding companies looking for a cure for aging/life extension (Harris). The potential consequence of the wealthy having access is that it puts a price tag on life because only those who have enough money will be able to live longer and healthier. If this happens, then it will create bigger divides between classes. The length of life people get to live will be dependent on socioeconomic status. 

Increased Ageism

Ageism is also another consideration and is already prevalent in the health care system. Some examples are, dismissing a treatable pathology because of old age, treating the natural effects of aging as a disease, and adults with multi-chronic illnesses are excluded from clinical trials to keep them focused on the general population (“Why Ageism in Health Care Is a Growing Concern”). Ageism, as defined by Dr. Robert N, Butler is the systemic stereotyping and discrimination against people because they are old. If life extension technology became readily available, it would slowly decrease the amount of elderly in our community, making them more ostracized from the “general public.” This is just one example of current ageist practices, and how life extension treatment could worsen ageist practices as well as attitudes inside and outside of the healthcare system.  


Finally, an important consideration is the overpopulation of people. As stated before, overall life expectancy in humans is rising. Between 2015 and 2030, the number of people over 60 years old is expected to increase by 56%. In the U.S, the number of Americans over the age of 65 is expected to double (from 50 million to nearly 100 million). This trend does not just apply to the United States, and problems related to the number of elderly people have occurred. During the 2008 financial crisis, European countries had to increase the retirement age, limit the number of benefits, and reduce resources put towards healthcare and social care (Haseltine). 

Because population growth has been decreasing since 1950, it might seem as if anti-aging treatments to extend life would be good. If the treatment were to be manufactured, it would likely be sold at a high price, with not many people being able to afford it. As technology increases though, the price of manufacturing, and eventual selling price, might lower making overpopulation a more relevant concern. The problem with longer living populations is that an increased number of people are going to cause many environmental issues and scarce resources. An increase in people requires more space needed for living as well as more food produced. This would require clearing of land and destroying habitats. If the goal is to grow enough food to sustain everybody, more greenhouse gasses will be released. The numerous negative environmental impacts of a longer-living population make pursuing the cure for aging an irresponsible move. 

Is Society on a Slippery Slope To Immortality?

Through the infusion of Yamanaka factors, cells revert from A2 (aged) cells to A0 (embryonic) cells. This change also results in the reverting of epigenetic marks of the cells, ameliorating signs of aging and extending human lifespans. Currently, this technology can extend lifespans, but not indefinitely. iPSC cannot prevent death in humans. With upholding scientific progress in mind, a question that arises is whether there is a difference ethically, between advancements with the ability to extend life versus preventing death. As mentioned previously, comparing human lifespans from the 19th century to the present day, there has been a 27-year increase, mainly attributed to advancements in medicine and science. In fact, the medical field, in some way, extends human life beyond the current boundaries. For example, a modern ICU ventilator can work in place of your lungs to pump oxygen-rich blood throughout the body. So, if a person had trouble breathing (whether sick or needing to be sedated for a procedure) there would be no solution (Kacmarek). This is just one example of how medical technologies have pushed the boundaries of lifespans. It also demonstrates how certain vital organs are becoming less vital in maintaining life. If cellular reprogramming via iPSC ultimately extends human life, then there is no difference between the technology and other advancements made in past centuries. 

Current Technology – Anti-aging Pills

While there may have been successful experiments done on mice, there is still a long way to go before successful human trials and the distribution of iPSC technology. Currently, products such as anti-aging pills are being produced and have been proven to extend the lifespan of mice by 24 percent. Dr. Rajagopal Viswanath Sekhar is an associate professor of medicine-endocrinology at Baylor College of Medicine, who along with his colleagues, discovered that using a supplement called GlyNAC was able to increase the lifespans of the mice. GlyNAC can  extend life by correcting the glutathione deficiency of animals (Hawkins). Glutathione (GSH) has many anti-aging properties that are being researched. So far, scientists know that it plays a role in protecting cells against oxidative stress-induced cellular damage and detoxifying xenobiotics (chemical substances that are foreign to animals) and drug metabolism (Homma and Fujii). 

Anti-aging pills are more likely to impact humans/human lifespans in the near future. While scientists develop these pills, as well as iPSC technology, the progress made in the field of anti-aging technology is limitless and unknown. Along the way, discoveries may be made around preventing death. If iPSC has the potential to avoid death, the ethical stance I have supported may change, because there is a difference between preventing death and extending life. 

Extending Life Versus Preventing Death

Life on Earth ends after we die for all living beings. As Leonard Hayflick argued, death is an essential aspect of human life because it is a universal event that occurs across all living beings. The universal nature of this process makes it unethical to try to prevent death. However, the hope for iPSC and cellular reprogramming is to allow humans to live longer and healthier lives; the purpose is not to prevent death yet. The ability to live longer and healthier is not different in end goals from the medical field. New scientific inventions are constantly pushing the boundaries of how long people are living. Ventilators are just one example, but take organ donation as an example. The ability to keep on living despite organ failure has extended the lifespans of many people who would have passed away had the technology not been invented.  Although iPSC and continued research in anti-aging might one day lead to being able to prevent death, it cannot be factored into the ethicality of the technology because nobody knows the future. 


iPSC has the potential to “cure” aging through cellular reprogramming. Being able to cure aging means that humans have longer, healthier lives. While we may not be preventing death yet, extending human lives beyond their regular amount of time has the potential to redefine what it means to be human. During the research process and presentations, a question that seems to be repeated is, “What defines being human?” At first, I believed that lifespan was a key factor, yet the field of medicine is always striving to extend human lifespans. And it is evident from the data that scientific advancements have contributed greatly to the increase in longevity in humans. Two considerations related to the idea of humanity and how it contributes to the ethicality of anti-aging technology are: what gives meaning to life, and future uses of this technology.

Perhaps the most important question is whether life extension is something that people want—Would it make people happier? Does it change the meaningfulness of life? According to an article by Lisa Bortolotti, an argument is that “…a significantly extended life would no longer be distinctly human: the brevity of life is regarded as an essential feature of humanity, and the value of what is human partly depends on the certainty and proximity of death.” “Haidit (2006) argues that happiness does not lie in the satisfaction of one’s desires, but in the pursuit of one’s goals” (Bortolotti 46). This raises more questions about whether humans have a responsibility to merely extend life or to improve the quality and happiness of life. If it is the latter, then life extension would not be worth pursuing as it does not improve the quality of life.  

Another argument comes from philosophers such as Bernard Williams, who say that happiness comes from categorical desires, which are exhaustible (Some examples are a job, a car, a house, etc.). Because these desires are finite, Williams argues that humans would be bored or pursue desires that they are not passionate about, therefore, living a longer life would decrease the quality of life. (Pereira) While it is true that some desires are categorical, I agree with the counterarguments to Williams that not all desires are categorical (i.e the pursuit of knowledge and building relationships) and that happiness comes from pursuing goals. The ability to continually fulfill desires and goals means that people could continually be happy, meaning that extending life would not lead to a decreased quality of life. 

Cellular Reprogramming and Eugenics

Because iPSC can target certain cells, and revert them back to a younger stage, they have the potential to fix specific diseases and parts of the body. The scientist mentioned previously (David Sinclair) conducted another experiment that tested cellular reprogramming on blind mice. After the treatment of the Yamanaka Factors, the mice were able to gain half their vision back. iPSC not only has the potential to increase the length of life, but it can also cure certain diseases. The ability to target specific illnesses or disabilities could lead to a slippery slope and potential eugenics. Human traits that people do not like, regardless of how old they are, could be changed or “treated.” Although anti-aging technology can reduce physical and mental suffering, it also has the potential to be used to fix traits that seem undesirable. 

Connected to this point is the effect that anti-aging technology has on the elderly population. By pursuing this advancement, it sends the message to older individuals that aging should be something that is cured or treated, it makes it seem like something unnatural even when that is not the case. This leads to the broader theme of dignity, both for the elderly, and anyone who might be potentially affected by this development. The possibility of eugenics reemerging as a result of iPSC to “cure” aging also means that the dignity of those possible people needs to be taken into account as well. 

Eugenics, as defined by the Oxford English Dictionary, is the study of the arrangement of human reproduction in order to increase the proportion of characteristics regarded as desirable (or to reduce the proportion regarded as undesirable) within a population or the species as a whole. Within society, there is a stigma against aging. Ads are constantly being aired of products that claim to make you look younger, and these products are specifically related to the beauty industry. These ads send a message that physical signs of aging are not desired under societal beauty norms. The ability to act on the ads that are promoting ways to gain a more youthful appearance means that anti-aging technologies could eventually spiral into another eugenics movement. In the future, cellular reprogramming could start to eliminate undesired physical traits, not just certain conditions related to aging. Those who have access to the technology would have the ability to create the “ideal” versions of themselves, also exacerbating the problems of unequal access. This is because, with unequal access to cellular reprogramming technology, lifespans as well as the ability to change your physical appearance will be dependent on how much money a person has. 

Consequentialism – Weighing the Pros and Cons

When balancing the potential benefits with the potential consequences of anti-aging technology, I don’t believe pursuing anti-aging technology is ethically permissible. The potential benefits of combating aging would be reducing physical and mental suffering for the elderly as well as the ability to live for a longer amount of time. What is at stake is the possibility of having unequal access to a longer lifespan (purely based on financial means), a possible increase in discrimination against the elderly population, as well as worsening environmental issues. Because there are currently methods, such as medications, that can reduce physical suffering (and are more equally accessible to everyone) I don’t believe that the possibility of reducing physical suffering (via cellular reprogramming) outweighs the negative consequences mentioned above, In summary, the environmental impacts, unequal access, loss of dignity for the elderly, and treating aging as a disease make  anti-aging technology unethical to pursue. When considering human happiness, I do not believe that living longer will necessarily bring the most joy because it’s about the experiences that you have during your life that contribute to happiness and the overall human experience. While in theory, you might be able to form new experiences the longer you live, nobody can know the future. There is no certainty that people will continue to have good and bad experiences, and therefore, it cannot be used as a justification for pursuing anti-aging technology. Naturally, this paper does not address everything. If I were to continue this research, I would try to include the ethical analysis of using iPSC in parts of the world where the average lifespan is lower than in other developed countries. I think it would also be interesting to address the argument of older people becoming an increased burden to their families and the younger population. 

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