Human lifespan is the maximum length of time the human organism can live and changes little with chronological period or environment or across geographical boundaries. Gerontologically, the human lifespan has long been considered to be about 120 years (Bromley 1974, 25; Hayflick 1998), with recent additional scientific support that this limit is “fixed and subject to natural constraints” (Dong, Milholland, and Vijg 2016). Interestingly, this span is consistent with the traditional Hebrew blessing “Ad me’ah ve-essrim shana” (may you live for 120 years) and has biblical support from Genesis 6:1–4, where the 120-year limit is to be interpreted not as God’s wrathful castigation against sin but as the divine parent-like maintenance of boundaries and protection within those boundaries (Westermann 1984, 367–76). Thus, a degree of consistency can be found between biology’s outlook on lifespan as a natural limit and theology’s outlook as a divinely appointed limit.

Life expectancy, on the other hand, is the length of time a human can expect to live and is highly variable across time, environment, and geography. Extrinsic factors negatively modulate the aging process and can cause an end to life before 120 years (Baltes and Smith 2003). Observations of improved health-span and longer life expectancy in some settings are indications of life expectancy’s plasticity, and of how those extrinsic factors can themselves be modulated to influence life expectancy. Figure 1 distinguishes life expectancy from lifespan, highlighting some extrinsic factors.

With that important distinction comes questions of aging. The causal link between aging and natural physical death is well accepted: aging precipitates natural physical death (World Health Organization 2022). But the nuance between aging that leads to lifespan and aging that leads to life expectancy is critical. It is here that molecular biology offers explanations that also have theological relevance. This article focuses on molecular biological processes that are intrinsic to the human body, proposing that those processes are causally connected to aging that determines lifespan. It is this aging that this article terms “human biological aging,” or HBA. Aging that determines life expectancy is the topic of subsequent investigation.

The study of aging in populations considers a myriad of extrinsic factors that require epidemiological tools for analysis. Changes in the aging of a population may not necessarily apply to every individual in that population, so there will be limits to how these inform the nature of the aging process. This article focuses on the determinants of aging in the human organism rather than the aging of populations.

Is age-associated disease an integral part of the aging process (such that they cannot be separated even by definition), or can aging be a process independent of age-related diseases? This question has plied the minds of some of the finest researchers in this field, Robin Holliday and Leonard Hayflick, who offer opposing answers in the Journals of Gerontology: A, Biological Science (Holliday 2004; Hayflick 2004) and elsewhere (Hayflick 2000).

Hayflick, who argues for a clear demarcation between biological aging and age-related diseases, has the more convincing argument for his following reasons: (a) the pervasive occurrence of aging across virtually all species; (b) aging’s occurrence even within species removed from the wild and protected from disease; (c) that not all features of aging apply to disease; and (d) medicine’s improvement of the treatment of age-related diseases—to the point of sometimes overcoming them—yet aging is not thereby prevented (though health-span and life expectancy may improve). To those substantial arguments I add the following: (e) the claim that all human aging necessarily and by definition includes age-associated disease is refuted by one or more examples to the contrary, such as the documentation of natural death without obvious pathology in both nonhuman and human organisms. A notable study is that of Isaio Shimokawa et al., where rats (an organism valued for its human-like physiology) were fed certain diets. At necropsy, 25 percent of rats that died at old age did not show signs of pathology that could cause death (Shimokawa et al. 1993). For humans, one such example is that of Jeanne Calment, who died aged 122 years with no illness recorded on her death record (Robine and Allard 2003). Moreover, old-age death without disease is accepted in gerontological literature (Cavanaugh and Blanchard-Fields 2011, 16). And (f), a demarcation between aging and disease is evidenced in the current and disturbing trend worldwide of ten different cancers that traditionally have been associated with later aging now markedly increasing in incidence in the thirty- to fifty-year-old age bracket (Mauri et al. 2024). Overall, this article accounts for these considerations as a reasonable argument for the position that aging and age-related diseases are distinct.

Collectively, then, these distinctions add nuance to a perspective on aging—distinctions that are necessary as further on the article provides molecular biological evidence to show that HBA leading to lifespan can be theologically considered a good of creation.

Since the seminal papers of Leonard Hayflick and P. S. Moorhead in the 1960s (Hayflick and Moorhead 1961; Hayflick 1965), the gradual erosion or shortening of proliferative cells’ chromosomal telomeric repeats as a function not of time but of the number of cell cycles has been confirmed in humans and across species, in vivo and in vitro, and from thousands of publications. It is well understood that this is significant for cell and tissue aging: cells have limited lifespans determined by the length of telomeres at the ends of chromosomes. Once a critical telomere erosion point is reached, cells undergo death or a nonfunctional state termed senescence. After a certain number of cell divisions, tissues comprised of proliferative cell populations eventually decline into reduced function or dysfunction, a process that partly but definitely contributes to organismal aging, diagrammed in Figure 2.

Intuitively, one may evaluate telomere “erosion” as a random process, but it is not. The family of enzymes responsible for copying chromosomes, DNA polymerases, have extraordinary copying fidelity—by the enzyme’s proofreading ability, an error rate of one mismatch per three thousand million nucleotides (Korona, LeCompte, and Pursell 2010; Thomas et al. 1991). That copying accuracy is a function of the gene sequences encoding the polymerases and determining the enzymes’ tertiary structures and catalytic sites. Thus, DNA polymerase accuracy is genetically programmed.

However, due to “inherent properties” (Chan and Blackburn 2004) in the way this copying machinery works, as proposed famously by James Watson and Francis Crick in 1953 (Watson and Crick 1953) and confirmed, this DNA polymerase family cannot copy the chromosomal ends completely. Known as the end replication problem, the critical consequence is that with every cell division, progressive shortening of the telomere’s building blocks occurs. The more division, the more the loss of telomeric repeats. This would be inevitable in all normal somatic dividing cells. The point to emphasize here is that, like polymerase accuracy, telomere erosion is also genetically programmed.

Through normal cell division, telomere erosion to the critical threshold length leads to either replicative cell senescence or cell death (apoptosis). When either of these events dominate over cell population renewal, then tissue renewal and homeostasis are disrupted, and a tissue’s regenerative capacity deteriorates. Both telomere-induced cell senescence and apoptosis are nonrandom and highly coordinated, with the key intermediate step being the initiation of the DNA damage response pathway (DDR). As an overview, a scheme showing the flow of action from telomere erosion to cell senescence or death and organismal aging is shown in Figure 3 (Itahana, Dimri, and Campisi 2001; Multani and Chang 2007).

Within Figure 3’s overview, the DDR is central. Fabrizio d’Adda di Fagagna, Soo-Hwang Teo, and Stephen P. Jackson (2004) consider the DDR “an integrated and highly coordinated set of events” akin to a classical signal transduction pathway, described in categories of stimulus, sensors, transduction and amplification, and output. This pathway’s purposeful coordination is outlined in Figure 4, simplified because the coordination of the DDR involves over twenty proteins (see Figure 2 in d’Adda di Fagagna [2008]).

Telomere erosion to the critical threshold, recognized as DNA damage, can also induce apoptosis, the major form of programmed cell death (Rich, Allen, and Wyllie 2000). Figure 5 summarizes this.

Apoptosis amounts to a series of coordinated molecular events and is far from random, purposeless, or accidental. It is, even in itself, a functional system.

Elizabeth Blackburn’s laboratory found that telomeric sequences are added to the ends of Tetrahymena chromosomes (Blackburn et al. 1983). This led to the discovery of a unique enzyme complex named telomerase, which, coupled with an RNA component, synthesizes telomeric building blocks and preserves telomere length (Greider and Blackburn 1985). Humans, as with many other organisms, possess a gene that encodes a similar telomerase (Morin 1989).

In humans, however, telomerase is active in germline cells but inactive in most somatic cell types (Kim et al. 1994; Wright et al. 1996). Either the genes, though present, are switched off and the telomerase complex is not expressed, or telomerase expression is at low levels. It is this absence or reduction of telomerase in most somatic human cells that comprises the other key component, along with DNA polymerase’s inherent end replication problem, that prevents the preservation of telomere length as cell populations divide.

Absence or reduction of telomerase is not an accidental, uncontrolled, or random process. Rather, it is genetically programmed, predominantly during embryogenesis. Significant changes occur in the expression of telomerase in the somatic cells of the developing embryo, fetus, and newborn. The existence of a program would point to a purposeful role for telomerase non-expression and therefore telomere erosion in postnatal human beings.

Regarding early-stage embryonic development, from work with murine, bovine, and human cells, telomerase expression is elevated and telomere elongation occurs at the morula to blastocyst transition (reviewed in Ozturk, Sozen, and Demir 2013). Yet, a remarkable reversal of telomerase expression eventuates during longer-term human gestation. Woodring Wright et al. (1996) found that at sixteen weeks of gestation, activity is found in a broad range of tissues yet becomes undetectable in the same tissues only a few months after birth. Further work (Ulaner and Giudice 1997; Ulaner et al. 1998) delineated the consistent dependency of telomerase levels on gestational and post-gestational age in different tissues.

Thus, over the longer term of gestation, a cessation of telomerase activity in somatic tissues is the normal phenomenon. In light of the sheer precision of embryogenesis and the replicability of telomerase expression across the embryogenesis of species and different organisms, there is little if no support for a random, uncontrolled cessation of telomerase expression. Rather, the reasonable conclusion is that telomerase non-expression in postnatal organisms is a genetically controlled developmental program, contributing to telomere erosion in postnatal somatic tissues.

Evidence presented so far has focused on intracellular systems of organismal aging. However, the recent work of Guo Zhang et al. (2013) focused on the systemic control pathways in an organism, in particular the hypothalamus of the central nervous system, showing this control center to have a programmatic role in the aging process and in lifespan determination.

In initial experiments, male and female mice (like rats, a classic humanlike physiological model) of a set middle age were engineered to have either artificially lower or higher levels of hypothalamic NF-kB, a key transcriptional regulator. Compared with control mice, mice with artificially inhibited NF-kB lived longer and showed better cognitive function and muscle endurance, thicker muscle fibers, thicker skin, and more bone mass. Elevated NF-kB levels produced the opposite effects. From these experiments, Zhang et al. were able to conclude that both the protein that switches on NF-kB activation (IKK-β) and NK-kB itself form a “driving force” in aging by the hypothalamus.

Following this, middle–old aged mice were genetically engineered to have a nonfunctional IKK-β gene in hypothalamic microglial cells. This prevented the age-associated increase in microglial cell numbers in the hypothalamus; moreover, TNF-α production in both microglia and in neurons was not induced as age progressed. From these results, the researchers formed a hypothesis: that removing IKK-β from hypothalamic microglia will slow the systemic aging process. When tested, indeed this was the case. Thus, modulating the levels of IKK-β and of NF-kB in the hypothalamus causally affected aging in the whole mouse.

But what might brain IKK-β and NF-kB be acting on at the molecular level to effect systemic aging? The release of hypothalamic Gonadotropin-releasing hormone (GnRH) for the stimulation of sex hormone production gives GnRH its fundamental role in sexual development and reproduction. But in this work, Zhang et al. (2013, 215) “revealed a direct link between IKK-β and NF-kB activation and GnRH decline” that drives sex-independent systemic aging. Importantly, GnRH-related age changes occurred in the brain and beyond in the periphery.

Stages in the mechanistic pathway are outlined in Figure 6.

Zhang et al. (2013, 215) concluded this important work by stating: “Our findings provide a proof of principle to the hypothesis that ageing is a life event that is programmed by the hypothalamus.”

Further explorations of a mechanism for the systemic control of aging have come from subsequent work on neural stem cells of the mediobasal hypothalamic region, an area “crucial for the neuroendocrine regulation of the physiological homeostasis of the whole body” (Zhang et al. 2017, 52). Here, Yalin Zhang et al. (2017, 2018) showed that, within normal physiology, hypothalamic adult neural stem cells secrete exosomal miRNAs into cerebrospinal fluid to control aging speed. Subsequent work has drawn attention to what molecular events occur upstream to control the release of exosomal miRNAs by htNSCs. Work by Yu-Zhong Xiao et al. (2020) showed that depletion of a long noncoding RNA, Hnscr, is sufficient to drive the senescence of htNSCs and aging-like phenotypes in mice. “Mechanistically, Hnscr binds to Y-box protein 1 (YB-1) to prevent its degradation and thus the attenuation of transcription of the senescence marker gene p16^INK4A” (Xiao et al. 2020). In exploring the functional processes affected by Hnscr deficiency, the most significantly altered biological processes included signal pathways involved in cell senescence and apoptosis, inflammatory responses, glucose metabolism, and protein degradation.

Overall, this work forms a highly significant contribution to understanding aging as a programmed life event.

Considering these molecular processes in isolation from one another hides a remarkable fact worth developing: on multiple biological strata—on the levels of molecule, process and pathway, organelle, organ, and organism of the whole human—the aging process is indivisible from life, health, and growth processes.

At the molecule level, DDR proteins, for example ATM and ATR, are not only essential for the DNA damage response triggered by telomere erosion but are also critical factors in telomere maintenance and homeostasis; in other words, they play roles in genome integrity (part of cell health) and cell demise, and which role is channeled depends on how critically short the telomeres are (Shiloh 2003, 2014). Transcription factor p53 is another example. Known as the “the guardian of the genome,” it acts on many levels to regulate genome integrity and cell safety, survival, and health (Vousden and Lane 2007; Park et al. 2016), with studies also showing its involvement in the more organismal-level functions of development, metabolism, and reproduction (Rufini et al. 2013). But p53 also acts to remove damaged cells by participating in the DNA damage response and activating the processes of senescence and of apoptosis (Lane 1992; Sahin and Depinho 2010; Royds and Iacopetta 2006; Multani and Chang 2007). This strong link (Yu and Zhang 2003; Villunger et al. 2003; Chen, Hales, and Ozanne 2007) shows p53 to be both a center of action (Yee and Vousden 2005) and a center of control (Laptenko and Prives 2006; Braithwaite, Del Sal, and Lu 2006). Connected with p53’s role in activating senescence and apoptosis, evidence supports the claim that p53 regulates organismal aging (Tyner et al. 2002; Rufini et al. 2013). Importantly, as with ATM and ATR, p53 fundamentally contributes to both cell life/health and cell demise.

At molecular pathway and process levels, apoptosis, the major form of programmed cell death, directly contributes to mammalian embryogenesis and normal and healthy postnatal growth and occurs even in mature organismal tissues in both vertebrates and invertebrates (Staley, Blaschke, and Chun 1997). John Kerr, A. H. Wyllie, and A. R. Currie (1972) consider apoptosis to have a “complementary but opposite role to mitosis [cell division] in the regulation of animal cell populations”; apoptosis occurs in order for normal growth to occur (Judah, Ahmed, and McLean 1965; Kerr 1971).

At the organelle level within cells, mitochondria use respiratory oxygen to generate the universal energy molecule of living cells, ATP, in a process termed oxidative phosphorylation, or cellular respiration (Newmeyer and Ferguson-Miller 2003). ATP synthesis requires the activity of a series of protein complexes embedded in the mitochondrion’s inner membrane that form the electron transport chain. The protein cytochrome c is a critical component of these complexes and therefore intimately involved in the life process of cellular respiration.

Yet, mitochondria and cytochrome c are also essential to the intrinsic apoptosis pathway. Mitochondrial cytochrome c forms part of the apoptosome, which initiates the “executioner” pathway of apoptosis. Thus, mitochondria and their molecules, cytochrome c, drive cell life; they also drive cell death (Ozoren and El-Deiry 2002; Khosravi-Far and Esposti 2004).

At the organ level, the mammalian brain’s hypothalamus is essential for life, health, and growth processes, being a master regulator for reproduction and sexual development in both males, and females energy metabolism, body temperature, and circadian rhythms. But as we have seen, Zhang et al.’s (2013) work broke new ground by showing this control center to have a programmatic role in the aging process and in lifespan control.

At the organism level, the creation of a living human body during embryogenesis involves the activation and coordination of aging–death processes: the genetic program of cessation of telomerase expression in somatic cells, and apoptosis.

The indivisibility between life–health–growth processes and aging processes across multiple biological strata is shown in Figure 7.

As noted, Christian theology has polarized responses as to whether aging is of God or an effect of sin. Is human aging “good” in the biblical creation sense? I am concerned here with the seminal creation data of Genesis 1:1–2:3 and its explicit, prominent, and repetitive “approval” formula that proclaims creation’s categories as “good” and the whole as “very good.” With attention to this and other scriptures, and to the exegetical parameters of literary and historical context, authorial intent, textual boundaries, style, and structure, “creational good” is defined as being (a) willed and accomplished by God the master craftsman, (b) reflecting the goodness and character of God, (c) having harmony and complementarity, (d) forming part of the relational good of creation, and (e) being fit for purpose (Hooker 2021, 50–60).

Several of these descriptors reflect the ancient Hebrew understanding of a functional ontology for creation rather than the modern Western material ontology. John Walton (2009, 26–28, 36–45) brings this out well: to the ancient Hebrews, a “good” created entity existed “by virtue of it having a function in an ordered system.” Here, Walton echoes the Hebrew conception of an ordered system as “society and culture,” yet the concept of an ordered, functional system cannot exclude other discoverable ordered systems such as those in biological systems discussed here.

Considering the molecular biology of aging in light of the aforementioned, the answer is yes, there is support for a biblical “goodness” in aging’s molecular processes. We observe genetic control, purpose, direction, orchestration and complex organization, intracellular and intercellular communication, sensors, and the transduction of information, all of which argue for functional systematization.

Yet, some may challenge this. In witnessing inbuilt molecular mechanisms of aging, could we be witnessing the changes in the human body that are the very marks of the effect of humanity’s fall? Has science discovered theology’s concept of a cosmic fall? If this is so, then the “post-fall” changes to every relevant gene in every cell of every human—forming part of the normal genetic code—make every human being, including post-fall Adam, fundamentally and physically unlike pre-fall Adam and would have major implications (some may say devastating implications) for our understanding of imago Dei.

The more appropriate response has the stronger argument: the inseparability of coordinated molecular processes of life and those of aging–death leads us down an altogether different path. Aging’s coordinated molecular phenomena exist on five strata of physical existence: at the levels of molecule, process and pathway, organelle, organ, and organism. One may be inclined to say “remove apoptosis, remove cytochrome c and p53 and mitochondria and the hypothalamus —all those entities known to cause death and aging —and we will have a more ‘vigorous’ human being.” But this cannot be ventured because these very entities are essential to life, health, and growth; without these entities, there would be no living human organism. Thus, science confronts theology with the probability that aging is exquisitely and intricately built into life.

Altogether, the evidence and implications of that evidence build a reasonable argument for evaluating HBA (a) as an intrinsic biological life process and physiological program that determines lifespan, (b) not as a random process nor one determined exclusively by external factors, and (c) as an assertion, with Hayflick, that “aging is not a disease” but rather that it is good in the biblical creation sense.

Beyond an alignment of the molecular data with the concept of human aging as good in the biblical creation sense, it is appropriate to gauge how theology may interact in a deeper way. William Desmond’s three modalities of wonder—curiosity, perplexity, and astonishment—provide a framework for interaction (Tyson 2023). With Desmond, science is often scientistic in its self-belief. Here, finding answers is driven by curiosity. This seems harmless enough, but it is a drive that believes all is determinate, that science can find “a determinate solution to a determinate problem,” driving as on a hamster wheel a “ceaseless accumulation of determinate cognitions” (Desmond 2023, 20, 24).

Scientistic self-belief leaves out the other modalities of perplexity and astonishment, and to Desmond (2023, 25), this is a mistake. Penetratingly, Desmond proposes that in its contraction down to mere curiosity, science expands its concept of knowing to an “idolatrous knowing” where the “too-muchness” in the “given being” is dismissed. Without science retaining astonishment and perplexity in its enterprise, the determinate vanquishes both the indeterminate and “overdeteminate,” idolatrously becoming a project of “self-determination.” There is much to appreciate here in Desmond’s assessment.

With Paul Tyson (2023, 11), knowledge in science is to be subordinated to worship. Theology has a role here: to speak reverence, to preserve astonishment. Notably, Desmond (2023, 25) selects the word “astonishment” because it stresses “the emphatic beyond expectation.” Astonishment involves the unexpected. The unexpected calls us to stop, step off the ceaseless hamster wheel fueled by curiosity, take a seat to reflect, and adopt an attitude of humility.

Within this framework, then, HBA as a divine creative good warrants reflection. Inbuilt aging processes, and their intricacy, evoke astonishment. The aging process is inseparably intertwined with human biological life. This indivisibility is, quite reasonably, astounding, perhaps even perplexing. There is room for reverence here.

A considered humility is also appropriate. First, perhaps surprisingly, the various orchestrated intrinsic molecular processes move humans toward biological instability. Humans seek life, health, and growth, yet this article argues that humans cannot achieve these fine goals without also aging. Second, the observed is further witness to how humans share biological solidarity with other creatures. Just as many animals age and die through intrinsic coordinated processes, so do humans, as exemplified by the programmed cell death process of apoptosis that occurs in a vast range of organisms from insects to mammals (Staley, Blaschke, and Chun 1997) and in modified form even in plants (Wang et al. 1996; Dickman et al. 2017). Moreover, unlike humans, some species of metazoa negligibly age. Aside from the obvious problems this creates for Christian theology’s cosmic fall theory, we must ask: How can humanity, the “pinnacle of creation,” age and die faster than a lobster? The fact is that within the broad range of aging rates in the animal kingdom, humans fall somewhere—without fanfare—in the middle, which rather dilutes the perspective of an innate biological superiority of humans over other lifeforms and steers us away from potential idolatrous anthropocentrism.

Within Desmond’s framework is a valuable assessment of the effect science’s contraction of wonder to mere curiosity has on the nature of gaining new knowledge. He notes: “[T]here are ways of questioning that lack reverence for the thing questioned” (Desmond 2023, 37). The “idolatrous knowing” of the scientific enterprise is observed in how science perceives the knowledge of human aging and what questions it asks of aging. To ask such questions as “How can we understand aging to master it, to stop or reverse it, perceiving it as defect or disease?” may well lack that reverence, belonging to that “impious” category of question.

These perceptions are found among prominent scientists in the aging field. David Gems summarizes the 2010 meeting of the Royal Society of London for Improving Natural Knowledge in his 2011 paper, writing for the nineteen scientists of that meeting. Here he promotes aging as a disease (Gems 2011): “The evolutionary theory provides the bleak insight that aging serves no purpose in terms of fitness, but instead is a lethal genetic disease that afflicts all human beings.” Likewise, David Sinclair, in Lifespan: Why We Age and Why We Don’t Have To, promotes the perspective that aging is a disease and that therefore aging and death are to be overcome (Sinclair 2019, xvii, xiv, xxi, 67, 81, 83). More generally, scientific efforts have been underway for some decades to reverse aging (Fossel 2015, 187–202).

Contrary to these perspectives, on the basis of the scientific data presented here and its alignment with aging as one of the goods of creation, it is appropriate to seriously question both transhumanist goals of age reversal and cybernetic immortality, and the evaluation of human biological aging as a disease.

The inseparability of aging processes and life, health, and growth processes adds clarity to interpretations of the consequences of humanity’s fall. Relevant here is Christian theology’s cosmic fall theory, which claims that the disobedience of the first humans not only effected a break in humanity’s relationship with God but also directly brought about an intrinsic physical change in all creation, leading to (among other effects) dissolution and degeneration, including aging.

As John Bimson (2006) has noted, this doctrine has a history almost as long as Christianity itself. The theory continues and develops through the centuries with such influential and prolific thinkers as the post-Nicene John Chrysostom (349–407AD; Chrysostom 1979, 444), John Calvin (1540; Calvin 1965, 119, 174; 1960a, 173–74), and several influential contemporary biblical theologians (Cassuto 1961, 163–69; Barth 1968, 29, 308–9; Mathews 2002, 249ff.; Murray 1968, 302–4; Godet 1977, 314; Beker 1980, 149, 232; Bruce 1985, 170; Ziesler 1989, 219–21; Fitzmyer 1993, 505, 507, 509; Moo 1991, 554; 1996, 517; Kruse 2012, 347–48; Merrill 2016). Calvin, for example, speaks of the world’s “degeneration,” “corruption,” and “wretched defilement,” Barth of the “present misery” of every “particle of the world,” Frederic Louis Godet of the “sombre hue” of nature, and Joseph A. Fitzmyer of creation’s present “lack of beauty, vitality, and strength.” Thus, this theory is highly influential and still a force to be reckoned with in traditional Christian theology.

Biblical commentators mentioned here as well as Augustine, Aquinas, Pannenberg, Rahner, and Zizioulas noted earlier—all effectively championing aging as an effect of the fall—may well find the molecular data astonishingly, perhaps perplexedly, unexpected because that data, from a theological standpoint, disputes the concept of HBA as an effect of sin.

As noted earlier, the accepted relationship is that aging precipitates natural physical death. Yet, the traditional position within much of Western theology forges a strong causal link between humanity’s fall and human physical death: sin leads to natural physical death. Louis Berkhof (1996, 258–61, 669–70) goes so far as to say, “The position of the Church has always been that death in the full sense of the word, including physical death, is not only the consequence but the penalty of sin.” Is human natural physical death the consequence of humanity’s fall or, in stark contrast, a part of God’s good creation? This is a fundamental yet problematic and troubling question; Barth (1958a, 593) calls its resolution “extraordinarily difficult.”

A few contemporary examples within theology illustrate the challenge. In his interpretations of Paul the apocalypticist, J. Christiaan Beker supports physical death and a cosmic fall as consequences of humanity’s fall but at the same time highlights an important problem: in Pauline theology, in Christ, sin has been overcome, but death remains. “Paul’s apocalyptic thinking connects death so closely with sin that cosmic death is the inevitable result of sin.” Yet, Beker goes on: “Death executes its reign over the created order like an infectious disease even after its ally, sin, has been defeated by Christ. The relation of suffering and finitude to sin and death remains unclear. There seems to be a residue of death in the created order that is not directly related to sin” (Zizioulas 2008, 101). This article argues that natural physical death—as the precipitant of aging—is more reasonably explained thus: (a) while agreeing with Beker that natural death is “not directly related to sin”; yet, (b) contra Beker, there is no need to conceptualize physical death as a problematic “residue;” rather, natural physical death, as the precipitant of a creationally good aging, actually resides within God’s good creation (Beker 1980, 215, 222).

In another example, Zizioulas draws a strong line between, on the one hand, unlimited life and God, and on the other hand, finitude, dissolution, and physical death. It could be construed from statements as such as “Biology sees death as a process that begins at birth, and links aging to reproduction. The mystery of life and phenomenon of death are bound together for life bears death within itself” (Zizioulas 2008, 98) that aging is claimed as a normal and good part of creation. This would be an incorrect assessment, however, for Zizioulas (2008, 98–101) goes on to claim that aging, dissolution, and physical death are direct consequences of the fall: “This counterfeit life . . . which carries death within it, is the outcome of the fall. It is a poor, evil and intolerable form of life. The Christian view is that death is never good, it is always an outrage.” The work of this article is contra Zizioulas: from the biology of the natural human being, one cannot separate molecular processes of aging from those of life. Against Zizioulas (2008, 101), who says that “related to God, creation would have life without limit,” limit is inseparably intertwined with this good creation.

These examples briefly highlight the struggle to get the link right between natural physical death and the fall. But on a more constructive note, one should probe whether support for the central claim of this article can be found in alternative avenues of investigation. In fact, support comes from exegesis of the Eden story (Genesis 2:4b–3:24), to which we now briefly turn.

Two foci are significant in the construction of further support1: the meaning of YHWH’s warning of the death sentence in Genesis 2:16–17 and the Yahwist source’s transformation of ancient Near Eastern (ANE) motifs for life, death, and the tree of life. Adhering to the principle that literary structure communicates meaning, Jerome Walsh’s synchronic exegesis reveals the Eden story to be a play of seven scenes. The strong chiastic structure of this text is built from both form (Walsh 1977) and antiparallel themes (Hooker 2021, 324–50). The play presents aetiology symbolically (symbolism here is an artful means of expressing realities; that is, the fall is historical). The chiasm places the death threat of 2:17 in scene one, with the eating of the forbidden fruit forming the central scene four. There is wide agreement that, in Nils Lund’s words, “identical ideas are distributed across the passage at the extremes and centre” (Lund 1942, emphasis added; Blomberg 1989; Thomson 1995); thus, scenes one and seven with the central scene four. Significant for our discussions, the chiasm informs the meaning of death in scene one’s death threat as follows: death is tied explicitly to the eating in scene one and implicitly (via scene one’s threat) to the eating in the central scene four. Yet, it must be asked: Is there an antiparallel thematic counterpart in scene seven for the theme of death in scene one? Affirmatively, “the sentence of death threatened” in scene one has its counterpart as “the sentence of death realized” in scene seven. Scene seven’s fulfillment of the death threatened in scene one is the expulsion from Eden, complemented by its out-workings predicted in scene six, a concept that excludes physical death. The exclusion of physical death from the death threat, then, argues for a demarcation between natural physical death and sin’s consequence, and for a creationally “good” pre-fall human mortality.

Semantic, literary, and historical considerations augment such a conclusion (Hooker 2021, 340–47). Of particular note is the impact from narrative tension. As a classic case of prolepsis, scene four’s 2:16–17 is extremely important for the movement of the narrative. The reader is guided to ask, and awaits answers to, two questions: “Will humans eat the fruit?” and “What will happen when they eat the fruit?” The answer to the first question comes at scene four; however, where is the answer to the second question? On the basis of proleptic fulfillment of narrative tension, it is problematic to contend that the death in 2:16–17 is physical death. Then there is no fulfillment in the Eden story, and one must wait several hundred years for Adam’s unremarkable, anticlimactic death—not in the Yahwist but in the Priestly account. It makes much more literary sense to interpret death’s threatened sentence as fulfilled at scene one’s mirrored scene one, yielding a resolution internal to the story.

The perspective that the Eden story is polemic against ANE concepts of life and death adds to these considerations. The Eden story takes several themes from ANE myths and refutes or transforms them. In particular, negating what is virtually a maxim among ANE tales that eternal life is the prerogative only of the gods, in the Eden story, it is YHWH’s intention for humanity to be gifted life from the tree of life. Humanity dwells in the heavenly abode with God, and with uninhibited access to this tree, of which, in the strong case made by Herman Obbink (1928), Adam and Eve freely eat before the fall. However, within the sanctuary symbolism of the narrative, elaborated by Gordon Wenham (1994), “life” is transformed from the everlasting physical immortality of ANE tales to definitively one of life with God in the sanctuary, a life of intimate friendship. Bearing this transformation of “life” in mind, it is reasonable to venture that the Eden story has also transformed the typical ANE concept of “death” as physical death into a spiritual death. Death’s meaning is the very component of the story that is deliberately held over in tension, awaiting explanation in scene seven and supplying an atypical answer to the question, “What does death, the penalty for sin, look like?”

Moving very briefly to a psychosocial perspective, contemporary Western society individualizes, atomizes, and fragments human life. Life is defined as stages: young, middle, and old are the obvious. But our fragmentation goes much further; even prenatal life has fetal stages that serve to validate when or when not to abort. This defined fragmentation shapes our behavior toward others. Aged care medicine is not immune to this, as physician Karen Hitchcock (2015, 132–33) observes: “Medicine takes the ill and chops them up as if a person is a walking textbook of distinct chapters: lung, heart, liver, brain . . . cigarettes smoked, alcohol consumed, blood sugar level.” She goes on to rightly criticize the prejudiced fragmentation of hospital care into care for the young above care for the old; ageism asserts itself in the lesser priority given to the sick elderly because “they have had their turn.”

However, if aging is intertwined with life processes, then the stage of life we call elderly cannot be—must not be—separated from other stages of life we may popularly think of as “good.” Thus, we would speak of the whole person through the whole of his or her time, a perspective that has the potential to transform aged care medicine. Simone de Beauvoir (1996) echoes this thought of continuity when she says, “What should a society be, so that in his last years a man might still be a man? The answer is simply: he would always have to have been treated as a man” (quoted in Hitchcock 2015, 131). The creational goodness of human aging provides the foundation upon which de Beauvoir’s answer of continuity can rest.

The work of this article informs pastoral theology’s response to the models of human limitation, such as medical models of disability, D. Creamer’s “limits” model of disability, and societal models of normalcy. The inseparability of aging processes from life processes, and the positioning of aging as a good of creation, helps correct what Michael Mawson (2023), I think rightly, sees as society’s and even medicine’s “misguided” perception of aging as a “problem” and shifts it back into the category of “normal” human life.