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"Gilgamesh, Scientism, and the Search for Immortality" by Khushali Vyas

Updated: Oct 26, 2023

Gilgamesh, Scientism, and the Search for Immortality

Khushali Vyas, Cedar Crest College

Abstract: The idea of immortality has widely been misinterpreted from a historical and scientific view. From a historical standpoint, one of the first stories ever recovered, the Epic of Gilgamesh, has often been misinterpreted as a story emphasizing human desire for immortality, however, this analysis misses the main message of the story. Furthermore, popular culture largely focuses on either the immortality aspect of the story or other themes of the story, often missing how the literary work reveals meaning to us. This misinterpretation of Gilgamesh’s quest for immortality is also present in the scientific realm in the form of scientism. Scientism, an aspect of popular culture that ascribes miraculous powers to science, falsely believes that science can one day make humans immortal. It misinterprets scientists’ quest for lengthening human lifespan and reducing the impact of disease on humans. Scientism enthusiasts fail to see that science itself indicates that immortality can never exist. An examination of the mechanisms behind aging, reversal of immunosenescene, tissue rejuvenation and stem cells, telomerase activation, and nanotechnology, science has only shown us that immortality is a work of fiction. While popular culture attempts to make immortality a reality, the Epic of Gilgamesh and science reveal the meaning of the human quest for immortality.



The question of immortality is timeless. It was even present in the oldest surviving story with origins in 3,000 B.C. (Sadigh, 2010). The Sumerian work the Epic of Gilgamesh details the journey of the tyrant king Gilgamesh of Uruk attempting to attain immortality (Harvard Museum of the Ancient Near East 2017). As Gilgamesh committed many atrocious acts against the people of Uruk, the townspeople complained to the gods to help. The gods then created a wild man, Enkidu, who was strong enough to challenge Gilgamesh. Enkidu meets Gilgamesh and, after a brief battle, they become the best of friends. Gilgamesh then convinces Enkidu to accompany him in a battle against Huwawa, who they subsequently kill. The gods become angry with the killing of Huwawa, and thus make Enkidu so sick that he dies. Gilgamesh becomes very upset with the death of Enkidu, and his refusal to accept the inevitability of death motivates him to go on a quest for immortality. Many consider this tale to be about just a quest for immortality; however, this quest is where Gilgamesh discovers the inevitable nature of individual human mortality, leading him to reflect on the meaning of his own life. While people may reduce this to a story of the past, we can still witness humanity’s desire for immortality in our world today. In the present day, the desire for human immortality is clearly seen through the concept of scientism, which gives science the power to do anything, even make humans immortal. Scientism supporters gain this optimism through seeing the research done by scientists exploring how to extend the human lifespan; however, carefully uncovering the research can reveal to one the unlikely possibility of human immortality. Scientism presents a distorted view of science that perpetuates humanity’s desire for immortality while scientific research, revealing the complexity of the human body, has shown immortality to be far from our reach.

Immortality in Science

As a subject rooted in factual evidence, science would likely have no place for a concept such as human immortality. Although scientists realize the implausible nature of human immortality, misinterpretation of science in a concept known as scientism highlights humanity’s greed for immortality. Popular culture’s misinterpretation of science is rooted in periods of history like the Enlightenment. The Enlightenment from the 17th to the early 19th century saw the concept of science and reason overpowering faith (White, 2018). This concept was emphasized by French philosophers, who even claimed that science could be a substitute for religion (Burnett, 2012). In the 19th century, the idea of positivism rose, which believed that all human knowledge would come from science and if not, then this knowledge is a myth. In the 20th century, positivism was altered into logical positivism. In this new form of positivism, logic, mathematics, and anything that can be tested experimentally was meaningful and everything outside this realm, such as religion, was not a true concept. These positivisms giving utmost importance to science were precursors to the modern concept of scientism. Scientism gives science the highest and only power to advance knowledge, dismissing other fields. It focuses highly on humans and gives exaggerated powers to science, introducing the idea that science will be able to make anything possible, even human immortality. This is a foolish goal that science does not support. Although science has continuously worked to lengthen the life span of humans, immortality of the human body is believed to be impossible and thought of as fiction. Science, in contrast to scientism, works to explore and expand our understanding of the world (Burnett, 2012). Therefore, in the world of science there is no room for the concept of human immortality.

In the scientific realm, immortality is often explored at the cellular level. As Hayflick (1989) states in “Antecedents of Cell Aging Research,” one of the first reports of cellular immortality began with an experiment by Alexis Carrel. In this experiment, Carrel extracted chick heart cells and grew them in culture, outside the whole living organism for an indefinite period. This discovery of cellular immortality intrigued scientists and has led them to believe that the mortality of cells is due to the cells being part of a living organism (in vivo) and not because of processes within each individual cell. People believed that if they were able to create the right conditions for cellular immortality in vivo, they could make humans live forever. Establishing these right conditions for cellular immortality in vivo has been referred to as the search for the “fountain of youth,” in reference to a real-life search by Ponce de Leon, a Spanish explorer who sought an actual “fountain of youth” in the early 1500s. The concept of immortal cells was reinforced in the 1950s when cultures of HeLa cells, cervical cancer cells, were shown to infinitely divide (Hayflick, 1989). In fact, HeLa cells, isolated from the cancer cells of Henrietta Lacks in the 1950s, are still used in research labs today for biomedical research (Lyapun, 2019). In 1961, Hayflick and Moorhead introduced the concept of aging at a cellular level by showing the finite number of divisions (known as the “Hayflick limit”) in normal human fibroblasts, thus disproving all cells are immortal in culture (Hayflick, 1989). While Hayflick and Moorhead recognized that some cells were able to divide indefinitely, they also note that these immortal cells could produce a tumor in a living organism. They discussed that normal cells with finite replication could become immortal if they acquired cancer cell-like properties. The cells in our bodies are mortal unless they become cancerous, causing damage in the body, and ultimately leading to death of the organism. Thus, we reach this paradox of cellular immortality in the body becoming the reason for human mortality.

Apart from cancer cells, bacteria and stem cells are other cell types that are thought to be immortal. Bacteria are thought to be immortal because they can replicate until external factors outside the cell lead to its death. However, internal mechanisms of bacteria have been found to contribute to its aging (MG Gomez, 2010). Bacteria divide through binary fission in which one cell replicates it contents and splits into two cells. Also, bacteria undergo replicative aging during these divisions. When a bacterium replicates its material and divides into two, the center of division incorporates a newly synthesized cell wall while the ends of the cell are the old poles. Therefore, the daughter cell that gets the old pole has a decreased replicative capacity and increased damage which contributes to the daughter cell’s aging (Steiner, 2021). This shows that bacteria are not immortal because they go through the process of aging.

Stem cells are another cell type that are also considered to be immortal. Stem cells are cells that have a self-renewal ability and can turn into multiple cell types; a process known as differentiation (Keith 2004). Stem cells found in adult tissue usually have a limited replicative ability; however, stem cells found in the embryo, known as embryonic stem cells (ESCs), have the ability to replicate indefinitely (Miura, Mattson & Rao 2004). ESCs turn into the multiple different cell types that are needed for mammalian life (Keith, 2004). A comparison between stem cells and cancer cells illustrates an important difference between the two, focused on the stem cell’s ability to differentiate. Once a stem cell turns into another cell type with finite ability to replicate, it loses its ability to self-renew (Miura, Mattson & Rao, 2004). A balance is made between the self-renewing stem cells and differentiating cells that have a finite number of divisions, limiting the potential of stem cells to turn into cancerous cells (Clarke & Fuller, 2006). In addition, there are multiple genes whose protein products prevent unlimited stem cell expansion, blocking the formation of a tumor (Clarke & Fuller, 2006). When this regulation of stem cell renewal and differentiation becomes abnormal, cancerous stem cells can result (Clarke & Fuller, 2006). This concept of immortal cells comes with risks as this abnormal renewal of cells, or cell immortality, is the hallmark of cancerous cells.

Now that we have discussed immortality on a cellular level, we can expand out to immortality on a human level. As previously discussed, immortality at the cellular level results in development of cancerous cells. If cellular immortality cannot be obtained, human immortality becomes impossible to perceive and only exists in the scientism realm. Recently, we see scientism disguised as concepts like transhumanism in which people believe that advanced biotechnological advancements can enhance the human species and may be able to reverse the aging process (Ostberg, 2022). Transhumanists believe that brain chips or computerized systems will be able to extend human consciousness leading to human immortality. While scientists around the world may be discovering the mechanisms of aging (Mc Auley et al., 2017), stimulating tissue rejuvenation (de Keizer, 2017), and using genetic engineering to lengthen human life (Noonan, 2016), they never suggest that human immortality is possible. The complexity of multicellular organisms shows us that while humans may be able to extend their lifespan, human immortality is highly unlikely to occur.

Lengthening Lifespan in Science

Research into the extension of the human lifespan can be seen most clearly in the biological sciences where scientists attempt to better understand living organisms. The study of genes, cells, plants, animals, bacteria, and disease all work together to explain how we can improve the quality of human life and therefore extend the lifespan of humans. Medications and therapies that prevent disease are in turn extending the human lifespan. Research into the mechanisms of aging, reversing immunosenescence (decline of immune system function with increasing age), tissue rejuvenation and stem cell, and telomerase (the enzyme that functions in extending telomeres) activation may show the potential for lifespan extension, but they also illustrate the unlikely nature of immortality.

Molecular Mechanisms of Aging

In order to find solutions for extending the human lifespan, scientists have focused on determining the molecular mechanisms of aging in order to better understand how processes including DNA damage, telomere shortening, protein degradation/dysfunction, mitochondrial damage and reactive oxygen species (ROS), longevity genes, and cytokine signaling contribute to disease and death (Mc Auley et al., 2017).

DNA damage contributes to aging as DNA encodes the proteins essential for cellular processes that in turn are essential for human life. When DNA damage is recognized in the cell, the cell activates DNA damage response mechanisms that can repair the damage before cell division occurs and the damage is passed on to the newly divided cell (Yousefzadeh et al., 2021). If the damage is unable to be corrected, the cell can activate mechanisms leading to cell death, so that damage does not accumulate, which can increase its potential to become a cancerous cell. Therefore, mutations in these DNA repair mechanisms that prevent them from functioning correctly are especially harmful. It is through diseases which we see harmful mutations in the DNA repair mechanisms that the correlation of DNA damaging and aging is clearly seen. For example, in the case of the disease Ataxia telangiectasia, a mutation in the ATM gene which functions in DNA damage response, leads to aging associated symptoms such as premature bone marrow exhaustion, diabetes, and neurodegeneration (Yousefzadeh et al., 2021). Furthermore, in the disease state of Cockayne syndrome, mutations in genes that affect DNA repair, cause ataxia (loss of muscle control), cataracts, muscle atrophy (decrease in muscle size), and neurodegeneration, which are all symptoms of aging (Yousefzadeh et al., 2021). DNA damage plays an important role in aging since if DNA damage response mechanisms do not function correctly, it can lead to aging associated diseases.

DNA encodes the proteins needed to carry out cellular processes, so if DNA damage contributes to aging, it comes as no surprise that protein dysfunction/degradation can also contribute to aging associated diseases. Protein dysfunction also affects aging since protein function is important to carry out normal cellular processes that are essentially important for life. If proteins are altered, in addition to decreased functions of the protein, altered proteins can become toxic through their accumulation in the cell (Goto et al., 2001). For example, in the case of the aging associated disease, Alzheimer’s, there is accumulation of an altered form of -amyloid resulting in problems with brain function.

Mitochondrial damage is another factor that contributes to aging. The mitochondria are components of the cell that supply the cell with energy and have their own mitochondrial genome separate from the nuclear genome (Singh, 2006). When mitochondria and their genome become damaged, they will be unable to perform their functions effectively which can affect cellular processes (Mc Auley et al., 2017). Damaged mitochondria also release reactive oxygen species (ROS) causing more DNA damage in the cell contributing to aging associated diseases. Accumulating mutations in the mitochondrial DNA itself can lead to mitochondrial dysfunction and are associated with aging (Singh, 2006). In a study referenced by (Singh, 2006), when mitochondrial DNA was removed from cells grown in culture, it quickly led to cell senescence in which the cells were unable to divide. This shows that researchers have been studying the importance of the damage to mitochondria and its DNA contributing the aging.

Researchers have also studied genes that encode proteins that have been associated with longevity. It has been studied that FOXO proteins have been shown to play a role in cellular signaling pathways that affect longevity (de Keizer, 2017). FOXO proteins also play a role in longevity in nematodes, flies, and mammals, as they mediate antioxidant response and DNA damage repair and activate genes involved in pro-survival functions. Antioxidant response is important as it helps reduce amount of reactive oxygen species therefore reducing DNA damage. As we saw earlier, DNA damage repair is important since mutations in DNA damage response can contribute to aging associated diseases. In addition to FOXO proteins, another group of proteins, sirtuins, play a role in cell response to stress and cell metabolism, which can also contribute to longevity (Grabowska, Sikora & Bielak-Zmijewska, 2017). This shows there are many complex molecular mechanisms that contribute to aging, and manipulation of these mechanisms may be able to help slow the processes of aging.

Lifestyle Mechanisms of Aging

In addition to the many molecular mechanisms that play a role in aging, researchers also study lifestyle changes that can increase an individual’s lifespan. For example, improved antioxidant activity helps reduce reactive oxygen species which decreases damage of DNA and proteins which in turn can lead to a longer lifespan (Bartke et al., 2004). Furthermore, reduced body temperature and metabolic rate may also contribute to antioxidant activity promoting longevity. In addition, a positive correlation exists when comparing concentration of antioxidants and lifespan of organism (Cutler, 1991). As a result, lifestyle changes, such as eating antioxidant-rich foods, are often advertised to help lengthen lifespan. There has also been evidence suggesting that antioxidants in fruits and vegetables can prevent diseases such as cardiovascular disease, cancer, and neurological diseases (Wootton-Beard & Ryan, 2011). By preventing disease, antioxidants are in turn able to lengthen human lifespan.

Calorie restricted diets are also lifestyle changes that have been associated with contributing to lifespan increase. In one study, individuals on a calorie-restricted diet had a lower body temperature and this lower body temperature, and not changes in body composition, contributed to an anti-aging effect (Soare et al., 2011). It has also been seen that a calorie-restricted diet increased levels of most sirtuins, which shows that sirtuins could potentially play a role in the anti-aging effect (Watroba & Szukiewicz, 2016). From these studies examining the anti-aging mechanisms, we are able to witness scientists’ quest to extend human lifespan. In addition, the complexity of all the different factors that influence the aging process shows that science is still far from defeating mortality.

Reversing Immunosenescence

One of the mechanisms of aging of the human body is the aging of the immune system, also known as immunosenescence. A working immune system is needed for the human body to defend against pathogens it encounters in the environment everyday (Aw, Silva & Palmer, 2007). However, as the human body ages, there is increased risk of infections, cancers, and autoimmune diseases due to a declining immune system function. In addition, immunosenescence results in abnormal pro-inflammatory cytokine release, increasing inflammation in the body, which can damage tissue and increase rate of disease and death (Mc Auley et al., 2017).

There are also different methods to counter immunosenescence, such as manipulating the microbiome inside the human body (Capri et al., 2006). In one study, peripheral blood mononuclear cells from healthy donors were taken out and incubated with DNA from different strains of bacteria (Lammers et al., 2003). Cytokine production was then measured since it is known that cytokines such as IL-10 can control inflammation and help with immune function. From this study, it was seen that DNA from a species of Bifidobacterium bacteria increased production of anti-inflammatory cytokines such as IL-10. Another example would be to use genetic engineering methods to deliver anti-inflammatory cytokines, components of the immune system that help reduce inflammation and promote healing. By promoting the number of anti-inflammatory cytokines in the body, it may be able stop or reverse the effects of senescent cells releasing pro-inflammatory cytokines that cause inflammation in the body causing damage to tissues. Another method involves the generation of T-cells in culture and their subsequent transplantation into the body, creating an immune system that only consists of young immune cells. In another review, they discuss the possibility of targeting different immune regulation signaling pathways to counter immunosenescence (Fulop et al., 2017). For example, inhibition of mTOR, a protein that plays a role in regulation of immune cells, helped improve immune response of elderly patients to the influenza vaccine. Improving immune function could in turn have benefits to increase lifespan, and so by studying immunosenescene, scientists’ once again display their curiosity in the possibility of human longevity. However, the immune system is not the only aging system in our bodies. The ability to reverse immunosenescene will not give scientists the power to significantly lengthen human lifespan; therefore, they will not be able to make human immortality possible.

Tissue Rejuvenations and Stem Cells

Scientists are studying stem cells and tissue rejuvenation as a potential therapy to reverse aging and prevent disease. In order for us to understand tissue rejuvenation, it becomes important to first understand cell senescence. Senescence of a cell refers to the inability of the cell to divide (de Keizer, 2017). Senescent cells are able to secrete proteins that can disturb the function of other nearby cells. As a result, senescent cells can play a role in aging and disease. In order to further examine the effect of senescent cells on aging, a group of researchers cleared senescent cells in mice (Baker et al., 2011). To do this, they used a marker that is specifically expressed in senescent cells to detect senescent cells in the mice. They then designed a method for the elimination of cells positive for the senescent marker with drug treatment. Their results concluded that drug-induced removal of senescent cells increased the lifespan in mice. Further analysis in this study was done by suggesting tissue rejuvenation upon clearance of senescent cells (de Keizer, 2017).

In addition to clearing senescent cells, tissue rejuvenation also becomes important as senescent cells release proteins that negatively influence stem cell differentiation blocking the potential for renewal of damaged cells (de Keizer, 2017). Therefore, improving stem cell function through tissue rejuvenation after removal of senescent cells may potentially play a role in the aging process. For this tissue rejuvenation stimulation, targeting FOXO protein signaling may be beneficial (de Keizer, 2017). While tissue rejuvenation after senescent cell clearance may not lead to human immortality, it can increase the period of time an individual lives without disease (de Keizer, 2017). By preventing disease for a longer time, an individual has a better chance to live longer.

Stem cell research has also been used in the field of organ transplantation where a population of stem cells are taken from a patient, differentiated into cells of a specific organ, and then placed back into the body the patient (Ratajczak et al., 2014). This procedure would be done to replace damaged organs, such as the brain, heart, or liver. By replacing damaged organs that are essential for life, we are in turn able to expand the lifespan of humans, but the possibility of human immortality is still far from reality. Although scientists, and society, continue to chase after the concept of living longer, if not immortal lives, scientific research shows scientists and society that the complexity of our human bodies is a major obstacle when it comes to making human life immortal.

Telomerase Activation

Another target of longevity research is the study of telomeres and telomerase. Telomeres are DNA-protein structures located at the end of a chromosome that shorten every time the cell divides because of a phenomenon referred to as the End Replication Problem (Ungar et al., 2009). In DNA replication, the ends of the chromosome fail to replicate due to complications that arise from their linear nature, the directionality of replication, and the removal of RNA primers that were used in the initiation of the process. Once the telomeres become too short, the DNA is unable to be replicated without losing important genomic DNA; thus, the cell is unable to divide and enters a state of senescence or cell death. This is part of what contributes to the finite number of cell divisions known as the Hayflick limit.

To counteract the shortening of telomeres in cells, such as skin cells, that must continue to actively divide in the body, our cells have an enzyme known as telomerase that is able to lengthen the telomere sequence. Since many studies have shown that shorter telomeres can result in multiple aging-associated diseases and overall death (Boccardi & Paolisso, 2014), researchers have hypothesized that reactivation of telomerase could reverse cell senescence or death, which can contribute to increasing human lifespan (Boccardi & Paolisso, 2014). However, as mentioned in our discussion regarding the Hayflick limit, cellular immortality often coincides with the acquisition of cancer-like properties. One of these cancer-like properties includes uncontrolled telomerase activation, again connecting the search for cellular immortality with a reason for our mortality.

Research into ways to activate telomerase in cells while not increasing cancer risk in these cells has been conducted. For example, researchers examined the effect of telomerase-based gene therapy in one and two-year-old mice (Bernardes de Jesus et al., 2012). In the experiment, they expressed part of the telomerase enzyme that functions in telomere length regulation, known as TERT, in the mice using a viral vector. Their results showed that the TERT expression had beneficial effects on the health of the mice and reduced ageing associated diseases such as osteoporosis and insulin sensitivity. Furthermore, the median lifespan of the mice increased by 24% for the one-year-old mice and 13% for the two-year-old mice without increasing cancer incidence as compared to the control group not expressed with TERT. While this study suggests potential for human immortality, this therapy has not been tested on humans, and so any off-target effects are unknown. Furthermore, as discussed previously, there are so many other factors that contribute to aging and just focusing on telomerase activation may not be enough to extend human lifespan to a significant extent. While scientism uses this research to boost optimism regarding the possibility of immortality, science itself has shown that human immortality is highly unlikely.


Scientism often misinterprets scientists’ quest to lengthen human lifespan, which includes research into mechanisms of aging, reversing immunosenescene, tissue rejuvenation and stem cell research, and telomerase reactivation. While these research areas can lengthen human lifespan or delay the onset of aging associated diseases, it is highly unlikely that they will make humans immortal. This was most clearly seen when we explored the concept of cellular immortality, as immortal cells inherit cancer-like properties, leading to this idea of the consequence of cellular immortality being the reason for human mortality. Furthermore, though we are able to help our organs function more effectively, and therefore increase our lifespan, the intriguing complexity of our bodies make human immortality far from possible.

Similar to how scientific research is able to challenge the ideas presented by scientism, in the Epic of Gilgamesh, Gilgamesh’s journey to dive deeper into his quest for immortality, reveals to him the pointless nature of his desires. In one version of the story, when Gilgamesh searches for immortality, he first meets Siduri, a tavern-keeper, who tells him that mortality is inevitable for humans and that he should focus on making the best of his life instead of searching for immortality (Abusch, 2001). In another version, Gilgamesh finds a plant of rejuvenation that can restore one’s youth, however he loses this plant to a snake on his way back to Uruk (Harvard Museum of the Ancient Near East, 2017). Society often sees the end of the Epic of Gilgamesh when Gilgamesh loses the plant of rejuvenation. The minds of the audience may become frustrated with Gilgamesh’s foolishness to leave the plant out in the open while he went to bathe in the river. However, that is not the end. As Gilgamesh travels back to Uruk after losing the plant of rejuvenation, he is forever changed from his quest to find immortality. From the violent king he once was, he becomes a good king and devotes his life to serving his people. After finding that immortality is impossible, he decides to make the most out of his mortal life. Gilgamesh may not have made this transformation if he were to become immortal, and the realization of death gave him his meaning of life. From the perspective of literature, it is revealed that our lives are made meaningful knowing there is an end to it. Just as fascinating, from the scientific perspective, is to see that the human body’s complexity, a characteristic that separates the human race from all the other species in the world, is one of the major reasons that human immortality cannot exist. Science and literature, two subjects often thought of as poles apart, may take different paths to make sense of human immortality, but both conclude the futile nature of the search for immortality.


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