Aging, Senescence, and Human Variation

Crews, Douglas E.; Ice, Gillian H.

doi:10.1002/9781118108062.ch13

Cited by 9 publications

(14 citation statements)

References 169 publications

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“…Baker (1984) articulated a human adaptability process whereby cycles of social, cultural, developmental, or genetic adjustments that alleviate stressors often generate new stressors requiring new adjustments. Biological anthropologists continue to explore how human stressors and related behavioral, social, environmental, metabolic, neuroendocrine, genetic, and cultural factors jointly modulate physiological stress responses and phenotypes in humans (Crews, 2003(Crews, , 2007Crews & Ice, 2012;Danese & McEwen, 2012;Ice & James, 2007;Juster, McEwen, & Lupien, 2010;Kusano et al, 2016;Leahy & Crews, 2012;Leonard & Crawford, 2002;McDade, 2002McDade, , 2007McDade & Nyberg, 2010;McEwen, 2008McEwen, , 2012Schulkin, 2004).…”

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confidence: 99%

Allostatic load and biological anthropology

Edes

Crews

2017

American J Phys Anthropol

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Multiple stressors affect developing and adult organisms, thereby partly structuring their phenotypes. Determining how stressors influence health, well-being, and longevity in human and nonhuman primate populations are major foci within biological anthropology. Although much effort has been devoted to examining responses to multiple environmental and sociocultural stressors, no holistic metric to measure stress-related physiological dysfunction has been widely applied within biological anthropology. Researchers from disciplines outside anthropology are using allostatic load indices (ALIs) to estimate such dysregulation and examine life-long outcomes of stressor exposures, including morbidity and mortality. Following allostasis theory, allostatic load represents accumulated physiological and somatic damage secondary to stressors and senescent processes experienced over the lifespan. ALIs estimate this wear-and-tear using a composite of biomarkers representing neuroendocrine, cardiovascular, metabolic, and immune systems. Across samples, ALIs are associated significantly with multiple individual characteristics (e.g., age, sex, education, DNA variation) of interest within biological anthropology. They also predict future outcomes, including aspects of life history variation (e.g., survival, lifespan), mental and physical health, morbidity and mortality, and likely health disparities between groups, by stressor exposures, ethnicity, occupations, and degree of departure from local indigenous life ways and integration into external and commodified ones. ALIs also may be applied to similar stress-related research areas among nonhuman primates. Given the reports from multiple research endeavors, here we propose ALIs may be useful for assessing stressors, stress responses, and stress-related dysfunction, current and long-term cognitive function, health and well-being, and risk of early mortality across many research programs within biological anthropology. K E Y W O R D Saging, allostasis, frailty, growth and development, nonhuman primates, senescence, stress | I N T R O D U C T I O NTraditional research foci within biological anthropology include variations in stress, morbidity, and mortality (for reviews, see Ice & James, 2007;Little, 2010). Despite this long-term focus, the field continues to pursue a reliable, relatively easy to apply metric for assessing lifetime stress and stress-related outcomes. We suggest incorporating the theory of allostasis and methods for assessing allostatic load within anthropological theory and methodology to aid in closing this gap. As a theory, allostasis was developed to explain how mammalian physiological responses to stressors in their environments evolved to maximize the probability of survival while limiting somatic damage (Korte, Koolhaas, Wingfield, & McEwen, 2005;McEwen & Stellar, 1993;McEwen & Wingfield, 2003;Sterling, 2004Sterling, , 2012Sterling & Eyer, 1988). Unfortunately, such beneficial defensive responses come at a cost and, over time, repeated allostatic activi...

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confidence: 99%

Allostatic load and biological anthropology

Edes

Crews

2017

American J Phys Anthropol

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“…It is incorrect to assume that chronic diseases are only a manifestation of modern Western lifestyles in humans, since whatever genes are responsible for them have likely been with the genus Homo since its inception [1]. In fact, allelic variants that can cause chronic disorders in humans are probably evolutionarily older than the appearance of the primates, and may be at least as ancient as the common ancestor of rodents and humans, as artificial selection in rats and mice have created strains that develop genetically based chronic conditions such as spontaneous hypertension, obesity and various cancers that parallel similar conditions in humans [1].…”

Section: The Persistence Of Chronic Disease In Human Evolutionmentioning

confidence: 99%

“…In fact, allelic variants that can cause chronic disorders in humans are probably evolutionarily older than the appearance of the primates, and may be at least as ancient as the common ancestor of rodents and humans, as artificial selection in rats and mice have created strains that develop genetically based chronic conditions such as spontaneous hypertension, obesity and various cancers that parallel similar conditions in humans [1].…”

Section: The Persistence Of Chronic Disease In Human Evolutionmentioning

confidence: 99%

“…These theories focus on two main principles: 1) genotypic adaptations that are rendered maladaptive when there is a substantial environmental change, such as dietary change (thrifty genotype) and 2) tradeoffs within the genome that evolved as a compromise but which ensure survival and reproductive success (antagonistic pleiotrophy) [1]. Some tradeoffs involve natural selection for alleles that are beneficial early in life (prior to and during the reproductive phase of life) but which have detrimental consequences later in life (after reproduction is complete).…”

Section: The Persistence Of Chronic Disease In Human Evolutionmentioning

confidence: 99%

“…Epidemiologically, the incidence and prevalence of these disorders are far greater now than at any time in our evolutionary past. One reason for this increase is the fact that these conditions generally manifest their symptoms in people over 40 years of age, a segment of human populations that has grown disproportionately in modern, industrialized societies where survivorship has increased to six decades and longer for both men and women, particularly over the past century [1]. Determining why genetic variants that lead to or cause chronic conditions such as hypertension, arteriosclerosis, or non-insulin dependent diabetes mellitus perpetuate in human populations continues to be a significant challenge for biomedical science.…”

Section: Introductionmentioning

confidence: 99%

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Human Evolution and Chronic Diseases: Genes, Allostasis, and Cut-Points

James¹

2014

Anthropol

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Aging/senescence

Crews

2018

The International Encyclopedia of Biological Anthropology

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With increasing age, cellular senescence and physiological dysregulation proceed, reducing somatic resilience, increasing frailty, and leading to increased physical disability, morbidity, and mortality. By promoting variability in somatic outcomes, developmental processes and environmental and ecological settings set the stage for senescent biology and variable lifespans. Early life adversity forces organisms to expend more physiological capacity resisting stressors, while environments limiting stressor exposures promote greater physiological reserve and resilience. At reproductive maturity, somatic resources are reallocated toward reproductive effort. Individual and familial patterns of morbidity and longevity attest to genetic influences on lifespan, but few specific alleles and haplotypes are associated with human lifespan. Stressor exposures are a major contributor to age‐related losses of functional abilities (frailty) and physiological dysfunction (allostatic load). Reduced physical activity at older ages promotes osteopenia and sarcopenia, twin biomarkers of frailty, and frailty indices reflect age‐related senescent losses. Age‐related physiological dysregulation and frailty are inherent to living systems as life cannot simultaneously optimize all physiological functions, protect their somas from all environmental insults, and still be reproductively successful.

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Aging, Senescence, and Human Variation

Cited by 9 publications

References 169 publications

Allostatic load and biological anthropology

Allostatic load and biological anthropology

Human Evolution and Chronic Diseases: Genes, Allostasis, and Cut-Points

Aging/senescence

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