Encyclopedia of Evolutionary Psychological Science

Living Edition
| Editors: Todd K. Shackelford, Viviana A. Weekes-Shackelford


  • Douglas E. CrewsEmail author
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-16999-6_2356-1



Senescence is a multifactorial, deleterious, progressive, and cumulative alteration of cells and somatic structures that occurs in an age-related, but not age-determined, fashion, thereby decreasing individual probabilities of survival and reproduction with increasing age.

Senescence is a soma-wide process of functional losses secondary to decreased replicative capacity in dividing cells and accumulated exposures to stressors and related damage in both dividing and nondividing cells as their time of survival increases. Senescent biology progresses as age-related declines in cellular, tissue, and organ fidelity and function lead to decreased reproductive potential, physiological and psychological dysregulation, and increased probability of death.


Currently, across multiple populations, average life spans exceed 80 years (e.g., Italy, Japan, Sweden, women in the USA), and the verified maximum human life span has exceeded 121 years (France). Many factors have contributed to achieving these demographic landmarks. Primary among these have been social and political changes leading to improved public health, hygiene, and population nutrition. These, along with advancements in biotechnology, improved the understanding of the biological and social basis of disease, and applications of evidence-based medicine have contributed to large portions of many populations surviving past their 65th year. In Europe, improvements in average life span began during the nineteenth century as their current economies and social systems emerged and developed. Over the twentieth century, similar demographic trends have affected most of the world’s populations (The World Bank 2013). In 1930, the average age at death was 60 years (men 58, women 61 years) in the USA, and only 50% of men and 57% of women survived to age 65 (Bell and Miller 2002). Across nations worldwide, age 65 years is a common criterion for retirement and social security programs, which provides a standard age for internal and cross-national comparisons and health evaluations. Eighty years later, life expectancy was 75 years among men and 80 years among women, with 80% and 88%, respectively, surviving to their 65th year (Bell and Miller 2002). Elsewhere average life spans are lower. In Kuwait life span averages 70 years and in Madagascar 64 years, with only 3% and 2%, respectively, surviving to age 65 years. Average life spans exceeding 70 years with maxima of 13 decades are a new frontier for humankind. Just 40 kya (kiloyears ago), few individuals appeared to have survived past their 40th year (see Caspari and Lee 2004).

Today, those aged 65+ years are an increasing proportion of most national populations. During the 1920s, less than 5% of the US population was aged 65+ years; in 1950–1960, they exceeded 8% of the total; today they make up 14% (see Bell and Miller 2002; The World Bank 2013). Exceeding the USA, Japan’s population includes 24% who are over 65 years and Sweden 21%, while Poland ties the USA at about 14%. Over the nineteenth and twentieth centuries, continued development of built environments, new agriculture methods, advances in medical treatment, and improved diets have reduced multiple stressors that limited human growth, development, and life span in previous environmental settings. These changes allowed today’s elders (persons aged 65+ years) to escape many external hazards while receiving better nutritional and energetic intakes and medical care during their growth, development, and reproductive adulthood than did their ancestors.

Today, in high-income industrialized settings, over 80% of people survive to age 65, and 1 of every 4 persons who do so may expect to survive into their 90th year. Such long lives do not characterize our closest primate relatives, gorillas and chimpanzees. Even when housed in well-maintained zoological settings with healthcare, immunizations, balanced nutrition, and free from predation and most parasites, the oldest documented age for a gorilla is 60 years (Colo was born December 1956 at the Columbus Zoo and Aquarium and died there in 2017). Among humans, average life spans of women commonly exceed their reproductive spans by decades. Broad differences in the timing and pattern of life history events between humans and other large-bodied apes throughout life, particularly during the latter decades of life, did not arise solely due to long-term sociocultural developments. More likely, new patterns of sexuality, gestation, somatic growth and development, neurological and physiological systems, psychological structures, and sociality arose as humans and their immediate ancestors (hominins) exploited and adapted to prevailing conditions of the late Pliocene, through the Pleistocene and Holocene. Humankind’s ancestors exploited and adapted to niches significantly different from those exploited by competing hominins and other species. Among these divergent adaptations were upper limbs freed from weight-bearing and bipedalism. These were followed, several million years later, by a long-term trend toward brain expansion, suggesting not only increasing dependence on cognition and evolution of integrated physiological and psychological systems but also evolution of the theory of mind and intentionality (see Dunbar 1998). This evolutionary trend toward dependence on cognition required evolving hominins to allocate additional time and energy to neocortical tissues during their growth and development. This shift in resource allocation also initiated a trend toward secondarily altricial offspring, i.e., neurologically and physically immature at birth compared to other large-bodied apes. Eventually, evolutionary trends in hominin growth and development would require over a decade and a half of relatively high and constant parental investment before they were reproductively mature and socially capable of birthing or siring their own offspring (see Crews 2003; Crews and Bogin 2010).

By decreasing the rate of development and maturation from conception to reproductive adulthood, slow-maturating secondarily altricial offspring reshaped the hominin and human life history pattern compared to other large-bodied apes (see Crews 2003; Crews and Bogin 2010). As this life history pattern evolved over the last 2-plus million years, hominins showed an increasing life span potential (illustrated in Carey and Judge 2000, Fig. 8, p. B207). This long-term evolutionary trend, in conjunction with the development of language, sociocultural systems, built environments, and agriculture, produced the 80+ year average and 120+ year maximum life spans observed today. This contribution explores the evolutionary bases for extended human life spans and their concomitants, senescence and aging. The first focus is on the evolutionary basis of senescent biology being an indirect consequence of surviving and reproducing in a stressful world since the beginning of life. At its most basic, senescence reflects a compromise between countervailing evolutionary pressures to survive and maintain the soma while also being reproductively successful. The model followed here is that stressor-related damage to cells, tissues, organs, and somatic systems along with their internal fragility produces the senescent phenotype (see also Kim and Jazwinski 2015). This is not a review of the biology of senescence, which would fill an encyclopedia of its own. Rather, it is an evolutionary perspective on how humans came to survive a century and more.

Evolution and Stressors

To survive and reproduce, early life (likely RNA-based replicators) responded to Earth’s challenges by evolving multiple stressor-limiting adaptations (e.g., DNA, membranes, cells, multicellularity, mobility). To maintain fidelity and reproduction of its hereditary material, life evolved many forms, none of which escapes environmental and internal stressors. All life-forms evolved their current phenotypes and life history patterns, periods of growth, development, somatic maintenance, and reproductive effort as adaptations to stressors their ancestors experienced. As adaptive responses accumulated, new phenotypes emerged, including offspring who required extended time to grow, develop, and mature. As these increasingly complex phenotypes evolved, early phases of human life history were altered. Among these were, “secondarily altricial offspring” birthed at an earlier stage of development than other apes, extended periods of growth and development including addition of childhood and adolescence phases, and parental provisioning over 1.5-plus decades. To accommodate these evolutionary adaptations, later life history phases necessarily were delayed, and achievable life spans extended (see Carey and Judge 2000; Crews 2003; Crews and Bogin 2010). Across species, longevity (length of life) increased as successive generations evolved increasingly efficient adaptive responses to life’s stressors. As more complex stress-limiting adaptations evolved (e.g., digestive and nervous systems, neurological integration, skeletons, cognitive processing), they required longer periods of growth and development to fully mature. Among humans, these processes extended the premature stage of life leading to our current altricial offspring and delaying commencement of reproductive effort. Evolution of altricial offspring extended the time needed for parental investment and, apparently, also slowed the pace of human cellular senescence. By extending growth and development and delaying the onset of reproductive effort, this suite of adaptations altered human life history, slowed phenotypic aging, and extended human survival.

Although all organisms show deleterious cellular and somatic alterations with increasing survival, senescence is not viewed as an outcome of positive natural selection for cellular dysfunction, organismal frailty, decrepitude, or death in most organisms (see Williams 1957; Kirkwood and Austad 2000; Crews 2003; Arking 2006; Crews and Bogin 2010; Crews and Ice 2012). Rather, biological dysfunction likely developed as a by-product of natural selection for improved defenses against stressors limiting survival and reproductive success (see Williams 1957; Kirkwood and Austad 2000; Arking 2006). Senescence is an inherent by-product of life’s fragility. As structural, somatic, physiological, psychological, and behavioral responses to senescent-promoting stressors improved, species’ life span potential increased apace. These evolved responses to ancient and more recent stressors continue to mold human phenotypes, senescent biology, and life history. Senescence results from progressive, deleterious, cumulative, and age-related, but not age-determined, alterations associated with decreasing probabilities of reproduction and survival (Arking 2006; Crews and Ice 2012). Biological senescence is an ancient and universal cellular process associated with the loss of cellular integrity that proceeds at a biological, not a chronological, pace (Arking 2006). In dividing cells, senescence is paced by cycles of DNA replication and mitosis. Aging, or organismal senescence, is paced by losses of terminally differentiated (nondividing) cells, physiological function, strength, agility, and endurance and increased somatic, physiological, and psychological dysregulation, frailty, morbidity, and mortality.

An introduction to life’s evolution is necessary to review the evolutionary basis of senescence. Among life’s earliest ancestors, individual existence likely was short and replication rapid. Eventually, these short-lived ancestors of life evolved adaptive responses to environmental stressors they encountered (see Hoeppner et al. 2012). One major adaptation was DNA to replace error-prone RNA as a hereditary molecule. More stable than RNA, DNA was a major evolutionary leap. As early replicators evolved internal processes and structures to protect themselves and their hereditary molecules (e.g., membranes, organelles, multicellularity), they increased their survival time (longevity). Eventually, these accumulated adaptive responses led to integrated vascular and neurophysiological systems, skin and skeletons, brains, and complex minds. The latter eventually provided humankind the ability to conceptualize and engage in intentional niche construction and build environments in which to better survive and reproduce. All extinct and existing species evolved as their progenitors responded adaptively to experienced environmental stressors. As biotic evolution continued, organisms capable of slowing their own demise lived sufficiently long to experience senescent biology as a by-product of their evolutionary success. Eventually an array of life-forms evolved, some that today survive only hours before reproducing and perishing, others that live a few days, and still others showing 100+ year life spans. Such differences in longevity and senescence are evolved products of life’s continuing struggle to halt damage from stressors while surviving and reproducing in stressful environments.

Stressors and Senescent Biology

Although specifics differ, damage to life from environmental challenges continues today. For many ancient stressors (e.g., UV radiation, nonenzymatic glycation, reactive oxygen species, mutagens), life continues to evolve protective responses. Still, damage to nuclear DNA (nDNA) and mitochondrial DNA (mtDNA), long-lived proteins and cells, and housekeeping systems increases with age. Many environmental stressors challenging human survival have declined or been altered in modern settings, for example, mega predators (e.g., leopards, tigers, bears) and infectious and parasitic organisms (e.g., bacteria, viruses, worms). At the same time, new stressors have emerged, exposures to pollution, human and animal wastes, built environments, artificial lighting, noise, and sociocultural stressors related to living in groups with high population density. Although all life-forms evolved because of their ancestors’ adaptive responses, they still are not able to halt all related damage and losses. As a result, senescent processes are common to all biotic life, and different phenotypes and divergent LH patterns have evolved as populations and species followed their unique adaptive paths to survive and reproduce.

Multiple life history commonalities exist across species, including, for instance, a period of growth and development that culminates in a mature reproductive adult, who eventually succumbs to life’s stressors. Commonly, this adult stage coincides with a period of maximum reproductive potential and effort when somatic and physiological function, psychological balance, and somatic resilience are at their maxima. Whether species’ survival potential is days or decades, during immature life all organisms must possess sufficient resources, response systems, and/or social support to delay current stressors sufficiently long to mature and engage in reproductive effort. As survival time increases, progressive and cumulative damage to cells and tissues disrupts organismal function producing deleterious changes throughout the system; concurrently, organ and somatic damage secondary to external and internal stressors accumulate. Among multicellular life-forms, some long-lived (nondividing) cells senesce and lose their integrity, while others die as damage to their DNA, proteins, organelles, and membranes accumulates, leading to systemic physiological and psychological dysregulation. Similarly, as dividing cells sustain damage over time, their replication time increases, and, eventually, they cease proliferating.

Stress-Limiting Systems

The multiple stress responses cells eventually evolved (e.g., multicellularity, organs and organ systems, defensive and repair systems, and psychological structures) constitute sets of overlapping survival and senescence-delaying mechanisms. Many previously evolved defensive adaptations likely have been lost as species went extinct. Other successful adaptations have been conserved and remain observable today as anti-stressor/anti-senescence responses, mechanisms, structures, and modules across species. Such features include the skin, fur, shells, tree bark, slime, vision, neurological structures, theory of mind, introspection, behavioral flexibility, verbal communication, and social systems. These anti-stressor adaptations continue to aid species survival and reproduction. Our cells, organs, and internal structures, whether skeletal, muscular, cardiovascular, neural, or psychological, evolved as adaptations to preserve life and reproduce in ecological settings where resources were scarce, stressors were immediate, life was short, built environments were nonexistent, and hominins were not a dominant species. In today’s physically secure and nutritionally adequate settings, humans grow and develop sufficient organ and somatic capacity to exceed that necessary to survive and reproduce (see Crews 2003; Crews and Bogin 2010). Some organs (e.g., kidneys, liver, heart, bone) significantly exceed their minimal capacity to sustain life through the period of reproductive effort, including fledging of offspring. Among these, humans have an innate ability to use available energy in excess of what is needed for growth, development, and reproductive effort to build cellular, organ, somatic, and structural reserve capacity. In many of today’s environmental settings, humans are able to accumulate energetic, somatic, physiological, and psychological capacities exceeding what they need to survive and reproduce. This accumulated reserve capacity helps support somatic function during later decades of human post-reproductive life (see Crews 2003; Crews and Bogin 2010).

Human Evolution and Variation

Aspects of modern biology and senescence separating humans from other modern apes are based upon adaptive responses and peculiarities hominins evolved as their phylogenetic branch led to modern humans through the Pleistocene (approximately the past 2.6 million years, ending with commencement of the Holocene about 12,000 years ago). Humankind’s current somatic, physiological, and psychological capacities coevolved as hominins responded to environments that stretched their adaptive limits, somatic reserves, and mental capacities to survive and reproduce in stressful environments (see Dunbar 1998; Crews 2003; Crews and Bogin 2010). Settings wherein, the hominin adaptive repertoire likely provided sufficient capacity for growth, development, survival, and reproductive effort, but little for late-life survival. In built environments of the twenty-first century, phenotypes based on this adaptive repertoire are able to exceed somatic and energetic capacities required to complete their growth, development, reproduction, and fledge offspring. In high-income settings today, this trend toward building reserve capacity continues into reproductive adulthood, providing a physiological reserve to support average life spans far exceeding those of our hominin ancestors. Today, a similar trend is observed among cats and dogs humans have domesticated as pets within built environments.

As living systems evolved, they faced not only old and new external challenges but also internal stressors generated by the processes evolved to defend themselves against external stressors. While responding to life’s stressors over their 160 million years of existence, mammals evolved finely tuned and highly interactive neuroendocrine, immune, physiological, and psychological networks to modulate their internal milieu, behaviors, and external environment. Still, over their life spans, terminally differentiated and dividing cells; the tissues, organs, and physiological and psychological systems they form; and somas they comprise lose their functional capabilities as maintenance, defense, and structural systems fail. Because the genomes of well-adapted organisms change slowly, some somatic structures, physiological and psychological capacities that evolved during earlier phases of hominin evolution, to then stressful environments, may not be ideal adaptations in current environmental and sociocultural settings. The Pleistocene is conceived by some as humankind’s environment of evolutionary adaptedness, a time when our current biology and physiological and psychological systems evolved (see Foley 1995). Rapid improvements in life spans across not only high-income, industrialized, and wealthy nations but most populations have occurred in recent centuries, prima facie evidence that environmental and social stressors during earlier phases of evolution significantly constrained human somatic maintenance and life span. A doubling of life expectancy in the USA from the eighteenth to twentieth centuries, along with a current life expectancy 30% higher than in 1900, additionally attests to the severity of environmental and sociocultural influences affecting human survival as recently as a century ago.

Assessing Senescence

Gerontologists and geriatricians have proposed a variety of overlapping definitions for senescence and aging (reviewed in Crews 2003; Crews and Ice 2012). However, they have not agreed upon any specific quantitative measure for assessing the senescent phenotype that predicts mortality more accurately than age alone. Because senescence is a multifactorial outcome of innumerable interacting traits, no simple scale for assessing an individual’s senescent phenotype is available. Rather, combinations of multiple physiological and somatic biomarkers currently are the best estimators of senescent dysregulation. Alterations in DNA expression patterns, mRNA and protein profiles, losses of mitochondria, and instability across the genome, including telomeres and epigenetic markers, pace cellular senescence (see Arking 2006; López-Otín et al. 2013). At the organismal level, following growth and development, humans generally experience a period of health and somatic maintenance during their period of maximum reproductive effort. This commonly is followed by a period of somatic decline, physical and mental losses, and increasing frailty and chronic diseases, described as somatic aging.

Theoretically, aggregate biomarker indices integrate and reflect aspects of systems biology shared across all populations by tapping into individual variability secondary to genetic, familial, local, historical, cultural, and ecological backgrounds and current circumstances. These indices are proposed to assess clinical, and even subclinical, aspects of somatic, physiological, and psychological dysfunction. The main phenotypic assessments in current use to determine senescent losses are activities of daily living (ADLs; see Katz et al. 1963) and its secondary derivative, independent activities of daily living (IADLs). Others include biological age (see Levine and Crimmins 2014); metabolic syndrome (Camus 1966); the Framingham index (Wilson et al. 1998); allostatic load, a measure of physiological dysregulation (McEwen 2003); and frailty, a measure of somatic dysfunction (Walston 2005). Theoretically, when based on groupings of age-related biomarkers of functional and physical loses, stress response, and physiological dysregulation, these indices should assess current morbidity and predict future morbidity and mortality risks, cognitive and physical declines, and life span across populations. All are known to assess to at least some degree somatic and physiological losses over the life span. Two of the most recently proposed indices, allostatic load and frailty, are reviewed here.

Physiological Dysregulation and Senescence

Stressor exposures are a constant of life. Throughout growth and development and during adult life, exposures to persistent non-life-threatening stressors (e.g., hypoxia, cold, toxins) may improve somatic function and limit negative response in that specific setting, a process of adaptability known as hormesis. Still, following a lifetime of stressors and stress responses (allostasis), our inability to halt all related damage leads to physiological dysregulation and increases risks for noncommunicable diseases and mortality (see Sterling and Eyer 1988; McEwen 1998, 2003; McEwen and Seeman 1999; Edes and Crews 2017). Jointly stressors and responses produce senescence (see Crews 2003; Kim and Jazwinski 2015), a multifactorial phenotype uniquely expressed by each individual.

By combining soma-wide sensory neurons, neurotransmitters, and hormones to modulate human physiology, the mammalian hypothalamic-pituitary-adrenal axis (HPA) regulates human allostasis (stress response) (see Sterling and Eyer 1988; McEwen 2003). Allostasis occurs in response to observable, quantifiable stressors (e.g., heat, hypoxia) and stressful situations (e.g., predator avoidance, antagonistic interactions, lack of food or water), along with individual mental states, including anticipated, perceived, and not quantifiable stressors, even when these do not occur. Allostasis alters hormonal and physiological set points (e.g., cortisol, epinephrine, blood pressure, glycemia, body temperature) in response to cognitive dissonance (Sterling and Eyer 1988; McEwen 1998, 2003) as external or internal stressors alter one’s mindscape from moment to moment (discussed by Peters et al. 2017). Following allostasis, system components reset to their current optima. As a dynamic neurophysiological response to stressors, allostasis evolved to promote current survival by limiting systemic perturbations secondary to external and internal stressors (see Sterling and Eyer 1988; McEwen 1998; Peters et al. 2017). Over time, stressor exposures may overwhelm response systems, attenuating, over-activating, or halting allostasis, thereby promoting progressive physiological dysregulation, a hallmark of senescence (see Crews 2003; Austad 1997; Rose 1994; Arking 2010).

Allostatic load indices combine neuroendocrine and physiological biomarkers of stress response to assess cumulative somatic dysregulation theoretically attributed to stressors (see Sterling and Eyer 1988; McEwen 1998; Edes and Crews 2017). When stressful events occur, they induce cognitive dissonance (Peters et al. 2017). When this signal reaches the hypothalamus, it promotes the release of corticotrophin-releasing hormone (CRH) to the anterior pituitary, stimulating the release of adrenocorticotrophic hormone (ACTH) to the circulation. ACTH activates the sympathetic-adrenal system to release cortisol, adrenaline, and noradrenaline, promoting behavioral and psychological (e.g., aggression, agitation, attentiveness, fear, fight-or-flight) and physiological responses (e.g., increased blood pressure and heart rate, reduced visceral blood flow) (see Sterling and Eyer 1988; McEwen 1998; Peters et al. 2017; Edes and Crews 2017). Excessive, constant, and lifelong allostatic responses tend to damage cells and organs, alter systemic regulation, and lead to progressive physiological dysregulation and increased allostatic load. This system can neither sustain its function indefinitely nor halt all stressor-related damage (Sterling and Eyer 1988).

Frailty, a Clinical Syndrome of Functional Losses

Since humans first recorded their aliments, they have remarked on losses of physiological function and physical abilities with increasing age (frailty). Frailty is a clinical phenotype of declining somatic function secondary to physical losses, including sarcopenia (loss or death of muscle cells) and osteoporosis (reduced bone matrix leading to fragility). Loss of function and the physical changes associated with frailty include unintended weight loss; declining strength, endurance, and walking speed; and reduced physical activity. Frailty indices are based upon tabulations of accumulated somatic deficits and losses that correlate significantly with age and tend to increase exponentially during the later years of human life (see Studenski et al. 2004; Walston 2005; Kim and Jazwinski 2015). Illustrating the likely genetic basis of frailty, offspring of short-lived parents show more rapid increases in frailty than do children of long-lived parents (Kim and Jazwinski 2015).

As a clinical phenotype, frailty increases with age and predicts future morbidity and mortality across samples (Walston 2005). Frailty differs from allostatic load in that it measures current functional abilities, not physiology. Losses of functionality lead to reduced physical activity, less activity-related energy expenditure, poorer nutrition, weight loss, muscle weakness, and exhaustion. Various combinations of biomarkers, from as few as 5 to over 100, have been amalgamated into frailty indices (see Studenski et al. 2004; Walston 2005). Across multiple samples, frailty indices predict future losses of mobility, inabilities to complete ADLs/IADLs, more frequent falls and injuries, and higher morbidity and mortality, particularly among those aged over 65 years (Walston 2005, 2005; Studenski et al. 2004). Increased frailty and allostatic load over the life span are not solely a consequence of senescent biology; illness, trauma, accidents, social support, and psychological factors also contribute.

Senescence: An Evolutionary Trade-Off

Once growth and development are complete and reproductive effort commences, with increasing survival time, an evolutionary trade-off between somatic maintenance-survival and reproductive effort reduces investments in the former to support the latter. With increasing age postmaturity, cellular senescence and somatic wear and tear promote physiological dysregulation and reduce resilience leaving organisms more vulnerable to stressors. Given the variety of processes involved, human senescent phenotypes are as heterogeneous and similar as are fingerprints, facial features, and disease risks. Senescence is a change in systemic biology, not a process unique to a specific organ, physiological system, or psychological construct. Among most life-forms, alterations reflecting changes in systemic allocations of somatic resources from growth, development, and maintenance to investments in reproductive effort follow attainment of reproductive maturity. Switches in resource allocation usually are not as obvious among humans and nonhuman primates as they may be among other species. Still, age-related alterations in phenotypes and underlying genetic and molecular regulators are fundamental to species life histories. An interesting example is a senescent-promoting genetic switch observed in nematodes, C. elegans. Following gamete production, germline stem cells produce a molecule halting production of heat-shock proteins, thereby limiting stress response and promoting somatic decline within 8 h of maturity (see Labbadia and Morimoto 2015). When this gene is blocked, heat-shock proteins remain active, stress resistance is maintained, and life is extended (Labbadia and Morimoto 2015). Likely, many early life-forms evolved gene-based single-locus switches and responses over their evolution. Some likely went extinct, while others likely have been passed on in evolutionarily modified forms.

Ancient adaptations, more recently evolved genetic propensities, and variable environmental settings continue to interact, modulating senescent biology across organisms. Among modern humans, growth, development, and reproductive and post-reproductive adulthood occur in environmental, ecological, and sociocultural settings differing significantly from conditions proposed for the “environment of evolutionary adaptedness.” In modern environments, humans experience variable stressor exposures and show broad variation in age-associated physical and psychological decrements and average life spans. Differences in familial disease risks and longevity attest to influences of shared genes and environments on life span. Across human samples, few specific SNPs, alleles, or haplotypes have shown consistent associations with life span, although distributions of multiple SNPs, candidate alleles, and haplotypes differ between younger and older cohorts within populations. Variants enriched among older cohorts in one population usually are not in others. Variability in genomic associations with longevity across populations suggests that strong gene-environment along with gene-environment-sociocultural interactions influence late-life survival. They also illustrate the need to apply evolutionary, systems biology, and social-ecological approaches and models to aid understanding of variability in human senescence and longevity.

As age increases, somatic and behavioral stress points that prime the soma for higher allostatic load, frailty, morbidity, and mortality reveal evolutionary compromises in basic physiological, immune, neural, and psychological functions. These stress points reflect evolutionary trade-offs related to competing needs for somatic growth, development, maintenance, defense, and reproductive effort (see Ellison 2014). Age-related processes of physiological dysregulation, fragility, and frailty simply reflect the inability of living systems to optimize their physiology, protect themselves from all internal and environmental insults, and show long-term reproductive success via evolutionary mechanisms. Given multiple trade-offs and evolutionary constraints (inertia) on the metabolism and structure of organisms, the individual cells of which they are compose likely are as optimized as possible for maintaining their function and reproducing their somas (see Vijg 2007). This applies equally to neurons and the cells composing our neurological structures, the brain, amygdala, hypothalamus, pituitary, and endocrine system. Similarly, continuing selective processes over hominid, hominin, and human evolution likely have optimized human neurological structures, along with their systemic connectivity, including the hypothalamus-pituitary-adrenal axis and the human mind. Theoretically, human neurological structures and the theory of mind they maintain also are adapted and optimized to receive and process selected sensory information, assess its survival and reproductive consequences, and produce as optimal a response as is currently possible.

Internal metabolism is another evolutionary stable trade-off, one between providing energy for cellular respiration and function while also generating reactive oxygen species (ROS) that damage DNA, membranes, and other cellular organelles, leading to cellular dysfunction, senescence, and death. Across the spectrum of life, organismal biology depends on evolutionary compromises (see Ellison 2014). At the DNA level, alleles conferring a net survival advantage during early life and reproductive ages, while also promoting detrimental phenotypes at later ages, are evolutionary advantaged because of their early life effects (see Williams 1957). Due to early benefits, alleles showing such antagonistic pleiotropy increase in population gene pools despite their late-life ill effects. Williams (1957) articulated two associated hypotheses about evolution and senescence. First, later-life ill effects of alleles showing antagonistic pleiotropy will accumulate at ages just beyond those required to maintain their selective advantages. Second, as the late-acting detrimental effects of alleles exhibiting antagonistic pleiotropy reduce the relative reproductive success of their carriers, selection will push any associated ill effects to later ages. Observed in experimental settings with worms and fruit flies, antagonistic pleiotropy is a fitness trade-off that also affects humans. Proposed examples include testosterone levels in men, apolipoprotein variants across populations, reactive oxygen species (ROS) created during oxidative phosphorylation, and multiple late-life penetrant chronic and genetic conditions. Cellular senescence and somatic aging reflect multiple long-term evolutionary trade-offs across the spectrum of life. For most species, senescence follows periods of growth, development, and reproductive adulthood and effort associated with a relatively well-maintained soma. In humans, following about two decades of life to attain maximum somatic and reproductive function and 30+ additional years of reproductive effort, output, and parental investment, the soma shows a LH trade-off, increasing internal and external signs of dysfunction and physiological dysregulation.

Stressors and Life Span

In general, the evolved physiological and psychological propensities and systems of humans are the same across all people and populations. However, variable genes, along with their combinations, and developmental processes influence individual response, reactivity, resistance, and resilience to stressors. Stressor exposures of parents, grandparents, and more remote ancestors that marked their DNA or personalities (e.g., epigenetic markers, historical trauma) also may contribute to individual stressor responses. Variation in life span also is affected by developmental processes and differential exposures to early life stressors and life events. As each individual lives postmaturity, their unique genetic endowment, developmental processes, stressor exposures, and related responses during life produce variability in their somatic function and dysregulation as their age increases.

Those experiencing greater adversity (e.g., undernutrition, malnutrition, infections, trauma, psychosocial, physical abuse) during early life, whether prenatal or postnatal, expend a larger proportion of their total lifetime energetic and physiological capacity resisting current stressors leaving little opportunity to accumulate reserve capacity (see Crews 2003; Crews and Bogin 2010). Conversely, those whose social and physical environments limit their exposures to early life stressors experience more opportunities to build reserve capacity, thereby promoting resilience and resistance to stressors and longer lives. Unfortunately, as age increases, defense and maintenance costs increase and reserve capacity declines as it is expended to meet current needs. Total daily energy expenditure (TDEE) is an ideal example of a physiological trade-off and decline with age. TDEE has three components, resting metabolic rate (RMR ~ 60–70%), activity energy expenditure (AEE ~ 20–30%), and diet-induced thermogenesis (DIT ~ 10%) (see Kim and Jazwinski 2015, Fig. 4). On average, all three components decrease with age among older adults. In the Louisiana Healthy Aging Study among participants aged 60+ years, RMR was higher at older ages but remained inversely associated with age (Kim and Jazwinski 2015). In one interpretation, as age increases and health declines, additional energy is required to maintain the soma, leaving less available for physical activity. Supporting this interpretation, in the Louisiana study, TDEE remained stable over the age span examined, suggesting physical activity decreased and additional energy for survival (RMR) was derived from AEE (Kim and Jazwinski 2015).

At all ages, but particularly among the aged, reduced physical activity sets the stage for sarcopenia and bone loss, components of the frailty syndrome. Decreased physical activity begins a cycle of bone and muscle loss, reduced activity, and increasing frailty. Disrupted growth during early life is associated with poor somatic and neurological development, impaired physiological and psychological function, increased risk for chronic conditions, more rapid progress of allostatic load and frailty during adulthood, and early senescence (Crews 2003; Walston 2005; Crews and Ice 2012). Physiological and psychological processes by which early life insults, trauma, and mental abuse influence adult and late-life physical and mental morbidity and mortality are open questions. Long-term research across the biological and psychological sciences, including evolutionary psychology and biological anthropology, will be necessary to identify and untangle them.

Physiological Losses

After completion of reproduction, multiple age-correlated vulnerabilities appear in all life-forms. Over the human life span, physiological and psychological stress responses decline, and stress-related physiological dysregulation increases. Although all show age-related physiological losses, these vary between individuals and families and across local and regional settings. Within individuals, functional and physical losses do not pace chronological age; rather they occur at variable rates. Bone biology, biomechanical stability, and skeletal function provide a specific example. Many species evolved bony skeletons and structures for support and mobility, to encase their fragile organs, and to promote their long-term survival and reproductive success. Over its long evolutionary history, bone has been optimized to perform these functions. Among humans, bone and muscle loss, impaired mobility, and subsequent frailty are differentially distributed by age and sex and differ across samples of the same age and sex across settings and nationalities (Walston 2005; Kim and Jazwinski 2015). Variation occurs because genetic interactions and propensities, developmental insults/benefits, hormonal variability, lifestyles, environmental stressor exposures, and individual patterns of genetic endowment and wear and tear influence muscle and bone biology and structure. The aging skeleton clearly illustrates cellular senescence and losses. Mobility is a major adaptation supporting organismal health and survival across species. Human mobility is dependent on more than a functioning skeleton to support the body with muscles and tendons to move it. Mobility also is dependent on physiological and psychological mechanisms that allow cognitive processing and produce the abilities to walk with a steady gait while moving with balance and agility. Impairment of these components increases with use, as do risks for accidents, injuries, and fractures. Concurrently, as age increases, injuries take longer to heal and may lead to additional gait and mobility problems, producing a cycle of functional losses and increased frailty. Sarcopenia, osteoporosis, and loss of strength with age correlate with psychosocial stress, allostatic load, frailty, and the onset and progression of noncommunicable diseases. As in past populations, wear and tear occurs on the joints of modern people, along with injury- and osteoporosis-related lesions and fractures, impairing mobility and leading to frailty. Even with available medical remedies and interventions, among Medicare-eligible beneficiaries ages 65+ years in the USA in 1999–2005, 25% had osteoporosis, while 42% of women and 10% of men who received benefits for 6–7 years had osteoporosis (Cheng et al. 2009).

Male-Female Mortality Differentials

Across all current sociocultural setting, women outlive men. However, over their longer life spans, women experience higher risks not only for osteoporosis but also other illnesses (e.g., urinary tract infections, depression, arthritis), morbidity (e.g., stroke, fatal heart attack), and disability than do same-aged men. Still, across all age groups, men die more frequently and earlier in life than do women. Longer life spans among women reflect evolved differences from men in their patterns of growth, development, reproductive effort, and reproductive output that have differentially patterned their LH schedules and, thus, their senescent biology. Observed differences in disability, morbidity, and mortality, among men and women, represent a morbidity-mortality paradox. A tendency for females to outlive males is observed across diverse species from insects and birds to primates (see Oksuzyan et al. 2008). Data suggest that among humans, patterns of frailty and disability reflect physiological and psychological processes differing from those that increase risks for morbidity, disease, and death. This further suggests frailty may not directly predict mortality. Over their shorter lives, males generally show higher risks for congenital, chronic, and genetic conditions, more frequently engage in competition with conspecifics, engage in more risky behaviors, are more susceptible to environmental stressors, and expend greater proportions of their time and available energy on growth, development, and somatic maintenance and repair earlier in life than do women.


Multiple stressors challenge human somatic integrity over their finite life spans, underlying senescent biology and somatic aging. Our major response system to life’s constant external and internal stressors is allostasis, a cognitively based, neurophysiological, and systemic response. Allostasis evolved to modulate, delay, and halt adverse physiological outcomes arising from stressor exposures. Human cells and the somas they build did not evolve to be immortal, nor did single-celled organisms. Immortal individual organisms are an evolutionary impossibility, but long life is not. As previously stated, biological life cannot optimize somatic growth, maintenance, reproduction, and reproductive effort via evolutionary processes. Eventually, all life succumbs to stressor exposures that promote cellular senescence and somatic aging. Across long-lived animal species, survival depends on genetic propensities that slow molecular damage and cellular loses while maintaining somatic integrity. Animals, not able to promote their own resilience and maintain their systemic biology via genetic, physiological, psychological, and allostatic processes, show more rapid senescence; sarcopenia; bone loss; fraying of their tendons, ligaments, and supporting structures; cardiovascular and metabolic dysfunction; physiological dysregulation; allostatic load; frailty; and mortality.

During the late Pliocene, through the Pleistocene and Holocene, and into the Anthropocene, humans have experienced continually changing ecological settings and social/cultural systems. Adaptive responses to earlier unconstructed environments, from alleles to genotypes and epigenetic marks, may not be as “fit” (in the Darwinian sense) in current ecological and sociocultural settings including newly emerged and emerging stressors. Current human life history, including growth, development, adulthood, reproductive effort, and senescence, along with our stressor responses is based on 160MY of mammalian, 65+MY of primate, and 7+MY of evolution among bipedal hominins to modern humans. Multiple adaptations and physiological functions that enhanced survival and reproductive success of our ancestors during these earlier periods remain beneficial today. Other adaptations likely limit organismal survival and later-life reproductive effort. Given the premise that no organism is immortal, senescence and aging result from two major processes, exposures to environmental and internal stressors and the quality of their genome-based somatic resilience to stressors. Somatic structures, physiological allostasis, and psychological constructs evolved, and even sociocultural systems developed, in response to life’s pervasive stressors. Concurrently, systemic biological interactions across cells and tissues evolved to repair damage sustained from stressors, while psychological modules, constructs, and processes evolved to promote behaviors that enhance organismal resilience and slow, delay, or halt stressors.

Evolutionarily, a key component of success among humans has been their adaptive flexibility. Over hominin evolution, multiple genetically programed phenotypes and behaviors adaptive among our ancestral species likely became less able to track rapidly changing ecological settings, particularly as the pace of sociocultural developments increased exponentially. Adaptive flexibility allowed humans to rapidly alter their behaviors as they experienced new challenges and environments. Most species show genetically programed responses to their common environmental stressors. Likely, humankind’s earlier ancestors did also. Today, some human behavioral responses likely are highly evolved gene-based propensities for responding to current informational inputs, acting like switches for turning on allostasis, e. g., jumping away from a snake, or detecting falsehoods. Among humans much of this genetic programming appears to have been overlain and to variable degrees replaced by flexible responses to environmental input at a variety of phenotypic levels. This flexibility includes fetal programming, developmentally variable responses to experienced environments, and individual and genomic epigenetic modulation of DNA expression. Physiological systems and psychological mechanisms attuned to environmental inputs during growth and development provide greater opportunity for phenotypic flexibility and rapid responses to changing environments than does the slower process of genetic change, perhaps even at so fine a level as generation-to-generation. Changing selective pressures over hominin evolution produced a trend toward secondarily altricial offspring with slower cellular senescence and promoted humankind to evolve a slower LH pattern than other apes. One based on a growth strategy of developmental responses to experienced environments over an extended period of maturation, rather than specific genetic adaptations to relatively constant environmental pressures. Today, genetic structures underlying human physiological and psychological responses to stressors continue to evolve, and life span continues to increase across human populations as developmental processes during growth occur in ever more secure constructed environments. At the same time, elders now survive sufficiently long to invest not only in their offspring but also their grand-offspring and kindred’s survival and reproduction, thereby enhancing selective pressures to extend human life.



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Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  1. 1.Anthropology and Public Health, Department of AnthropologyOhio State UniversityColumbusUSA

Section editors and affiliations

  • Curtis S. Dunkel
    • 1
  1. 1.Department of PsychologyWestern Illinois UniversityMacombUSA