Fact-checked by Grok 2 weeks ago

Gerontology

Gerontology is the multidisciplinary study of aging processes and older adults, examining biological, psychological, social, and cultural dimensions across the lifespan.^[1]^[2] The field, derived from the Greek term for "old man," integrates insights from biology, sociology, psychology, and public policy to understand physical changes, cognitive function, social roles, and societal impacts of population aging.^[3] Coined in 1903, gerontology has evolved alongside increases in human longevity driven by medical and public health advances, shifting focus from mere survival to quality of life in later years.^[4]^[5] Key aspects include research on cellular senescence, chronic disease management, and interventions to mitigate frailty, alongside social analyses of retirement, family dynamics, and elder care systems.^[6] Gerontologists apply empirical findings to enhance well-being through education, policy advocacy, and practice, such as developing age-friendly environments and addressing multimorbidity.^[1] Notable achievements encompass elucidating mechanisms like telomere attrition and inflammation in age-related decline, informing targeted therapies, though the field cautions against unsubstantiated anti-aging claims that conflate extension of lifespan with reversal of entropy-driven deterioration.^[7] Controversies persist over paradigms like "successful aging," criticized for overlooking structural inequalities and emphasizing individual responsibility over systemic factors, and the pseudoscientific fringes of anti-aging medicine, which gerontology distinguishes from rigorous senescence research.^[8]^[9] As global populations gray—projected to see those over 65 outnumber children by 2050—gerontology underscores causal realities of aging as a progressive, multifactorial process amenable to mitigation but not elimination.^[4]

Definition and Scope

Core Concepts and Multidisciplinary Approach

Gerontology encompasses the empirical investigation of aging as a multifaceted process spanning biological, psychological, social, and environmental domains, grounded in observable data and causal mechanisms rather than normative assumptions. It examines how aging unfolds across the human lifespan, including physiological changes, cognitive trajectories, interpersonal dynamics, and societal influences, with a focus on population-level patterns derived from longitudinal studies and controlled experiments.^[2]^[1] Central to gerontology is the delineation from geriatrics, the latter being a medical subspecialty dedicated to diagnosing and treating diseases prevalent in older adults, such as frailty, dementia, and multimorbidity, often through clinical interventions. Gerontology, by contrast, prioritizes the analysis of normative aging—non-pathological declines in function and adaptations—without conflating it with disease management, thereby avoiding overmedicalization of age-related variations. This distinction underscores gerontology's broader scope, integrating evidence from cellular senescence to cohort-specific behaviors to inform preventive strategies over curative ones.^[10]^[11] The field's multidisciplinary framework synthesizes contributions from biology (e.g., genetic and metabolic pathways), psychology (e.g., resilience and decision-making shifts), sociology (e.g., family structures and inequality effects), and economics (e.g., resource allocation in aging societies) to dissect aging's root causes. Core metrics include lifespan, the duration from birth to death, and healthspan, the subset of years free from significant disability or chronic impairment; globally, the healthspan-lifespan gap averages 9.6 years across 183 countries, with projections indicating further widening absent targeted interventions, as lifespan extensions via reduced mortality have not proportionally compressed morbidity.^[1]^[12]^[13] This lag highlights causal disconnects, such as inflammation accumulation outpacing organ repair, informing gerontology's emphasis on verifiable outcomes over unsubstantiated longevity claims.^[13]

Historical Development

Early Foundations (19th-early 20th Century)

In the late 19th century, August Weismann advanced an evolutionary framework for understanding aging through his germ plasm theory, articulated in his 1892 essay and expanded in Das Keimplasma (1892). Weismann posited that hereditary material resides exclusively in the immortal germ plasm of reproductive cells, isolated from the mortal soma, which undergoes progressive deterioration without influencing inheritance. This separation explained aging as a non-adaptive outcome of natural selection prioritizing reproductive success over post-reproductive somatic maintenance, as selective pressures diminish after reproduction, allowing deleterious mutations to accumulate in somatic tissues.^[14]^[15] Early 20th-century biological inquiries shifted toward cellular mechanisms, with Élie Metchnikoff, Nobel laureate for phagocytosis in 1908, conceptualizing aging as a disease-like process driven by impaired cellular immunity. In works such as The Nature of Man (1903), Metchnikoff argued that aging stems from the accumulation of cellular waste and toxins, which phagocytes fail to adequately clear, leading to chronic inflammation and tissue degeneration; he advocated interventions like probiotics and antioxidants to enhance phagocytic function and extend vitality.^[16]^[17] His empirical observations on invertebrate longevity and human pathology laid groundwork for viewing senescence as potentially modifiable rather than inevitable. Foundational experiments on dietary modulation emerged in the 1910s–1920s, building on nutritional studies that inadvertently revealed longevity effects. Researchers like Thomas Osborne and Lafayette Mendel observed in rats that underfeeding, without malnutrition, retarded growth but extended lifespan beyond ad libitum-fed controls, suggesting caloric intake influences aging trajectories. These precursors culminated in Clive McCay's systematic 1935 trials, where rats restricted to 40–60% of normal calories from weaning achieved up to 50% lifespan extension, establishing caloric restriction as a replicable modulator of senescence in mammals.^[18]^[19]

Mid-20th Century Institutionalization

The Gerontological Society of America was founded in 1945 as the premier interdisciplinary organization dedicated to fostering scientific research on aging processes and their implications.^[20] This establishment occurred amid post-World War II demographic transitions in developed nations, where advances in public health and medicine extended average life expectancy—rising from approximately 47 years in the U.S. in 1900 to 68 years by 1950—resulting in a growing proportion of individuals over age 65, from 4% to about 8% of the population.^[21] These shifts, driven by reduced infant and mid-life mortality rather than birth rate changes, created empirical imperatives for systematic investigation into age-related physiological declines, independent of expanding welfare systems.^[22] A hallmark of this era's institutionalization was the pivot toward longitudinal, data-intensive studies to delineate normative aging from pathology. The Baltimore Longitudinal Study of Aging, launched in 1958 by the National Institutes of Health's Gerontology Branch, exemplifies this approach: it recruited over 3,000 healthy male volunteers initially (expanding later) for biennial assessments of organ function, body composition, and biomarkers, yielding datasets on trajectories like gradual renal function decline uncorrelated with overt disease.^[23] This methodology supplanted earlier cross-sectional or anecdotal methods, enabling causal inferences about intrinsic aging mechanisms through repeated measures on the same individuals.^[24] Parallel theoretical advancements grounded gerontology in evolutionary biology. In 1957, evolutionary biologist George C. Williams articulated the antagonistic pleiotropy hypothesis in a seminal paper, arguing that genes conferring reproductive advantages early in life—such as enhanced growth or fertility—often impose fitness costs later, as natural selection exerts weaker pressure post-reproduction; this explains why senescence evolves despite its apparent maladaptiveness.^[25] Williams supported this with evidence from pleiotropic effects observed in model organisms, positing trade-offs like early vitality at the expense of late-life frailty, a framework that integrated aging into Darwinian principles without invoking programmed decay.^[26] Culminating these efforts, the U.S. National Institute on Aging was created in 1974 under Public Law 93-296 as a dedicated NIH component, tasked with funding biomedical and behavioral research on aging while disseminating findings to address the health needs of an expanding older demographic, then comprising 10% of the U.S. population.^[27] This federal institutionalization reflected accumulated evidence from prior decades, prioritizing empirical validation over speculative interventions and establishing gerontology as a federally backed scientific enterprise.^[28]

Late 20th to 21st Century Advances

In 2023, researchers expanded the hallmarks of aging framework to twelve primary mechanisms, adding disabled macroautophagy, chronic inflammation, and dysbiosis to the original nine, with cross-species data from model organisms and humans affirming their contributions to age-related decline through disrupted cellular homeostasis and microbial imbalance.^[29]01377-0.pdf) This update emphasized empirical validation over prior theoretical categorizations, highlighting causal links observed in diverse taxa where interventions targeting these hallmarks extended healthspan in preclinical settings but required cautious extrapolation to human longevity.^[30] Senolytic therapies, designed to selectively eliminate senescent cells implicated in tissue dysfunction, progressed into human trials by the mid-2020s, yet results indicated limited efficacy against core aging phenotypes. A 2025 National Institute on Aging-funded clinical study of dasatinib and quercetin in postmenopausal women demonstrated only subtle enhancements in bone mineral density and markers of bone turnover, failing to produce robust reversal of frailty or multimorbidity.^[31] Similarly, intermittent dosing regimens showed feasibility and safety but marginal functional benefits in cognition and mobility among at-risk older adults, underscoring translational gaps from rodent models where lifespan extensions were more pronounced.^[32] Epidemiological data from high-income nations reveal decelerating life expectancy gains post-1990, with annual increases dropping from over 0.2 years in the mid-20th century to near zero by the 2020s, attributed to diminishing returns on public health interventions and entrenched biological limits.^[33] Projections for cohorts born after 2000 forecast maximal lifespans stabilizing below 90 years on average, as human trials of caloric restriction mimetics and other interventions have not altered record maximums near 122 years, challenging optimistic narratives from short-lived animal proxies.^[34] Critiques emphasize overreliance on such models, which inflate intervention effects due to compressed lifespans and artificial disease acceleration, while human cohort studies confirm stasis in extreme longevity despite biomedical advances.^[35]^[36]

Biological Mechanisms of Aging

Hallmarks of Aging

The hallmarks of aging constitute a conceptual framework identifying the principal molecular and cellular mechanisms underlying the progressive decline in organismal function, as proposed by López-Otín et al. in 2013 and expanded in 2023 to encompass twelve interconnected processes.^[29] These hallmarks are categorized into primary (initiators of cellular damage), antagonistic (adaptive responses that become maladaptive), and integrative (manifestations driving systemic pathophysiology).01377-0) Primary hallmarks include genomic instability, arising from unrepaired DNA damage accumulation at rates exceeding repair capacity (e.g., 10^4-10^5 oxidative lesions per human cell daily), telomere attrition (shortening by 20-40 base pairs per cell division in humans), epigenetic alterations (e.g., global DNA methylation loss of 0.2-0.5% per decade), and loss of proteostasis (impaired protein folding and degradation, leading to aggregates in 20-30% of aged neuronal proteomes).^[37]^[38] Antagonistic hallmarks emerge as compensatory mechanisms to primary damage but exacerbate aging when dysregulated: deregulated nutrient sensing (e.g., hyperactivated mTOR signaling reducing autophagy by 50% in aged tissues), mitochondrial dysfunction (ROS production increasing 2-3 fold with age), cellular senescence (senescent cell burden rising from <1% to 10-15% in aged mouse livers), stem cell exhaustion (regenerative capacity declining by 70-90% in hematopoietic stems by middle age), disabled macroautophagy (flux reduced by 40-60% in aged rodents), and altered intercellular communication (e.g., elevated SASP factors promoting paracrine damage).^[39] Integrative hallmarks culminate in organismal dysfunction: chronic inflammation ("inflammaging," with IL-6 levels doubling every decade post-30) and dysbiosis (gut microbiota diversity dropping 25-50% with age, correlating with barrier permeability increases).^[40] Causal evidence from model organisms underscores these as root drivers rather than mere correlates; in Caenorhabditis elegans and mice, engineered DNA damage accumulation (e.g., via polymerase defects) shortens lifespan by 20-50% independently of caloric intake, while proteostasis enhancers (e.g., HSP90 modulation) extend it by 15-30% via reduced aggregates, indicating intrinsic molecular erosion over extrinsic lifestyle dominance.^[41]^[38] Quantitative links to diseases reveal inevitability: genomic instability correlates with 70-80% of cancers via mutation loads rising exponentially (e.g., 10-100 somatic mutations per year post-60), telomere attrition with 2-3 fold cardiovascular risk elevation, and chronic inflammation with 1.5-2 fold odds for Alzheimer's and diabetes, as meta-analyses of longitudinal cohorts (e.g., Framingham) show hallmark indices predicting multimorbidity with R² >0.4 after age adjustment.^[42]^[43] This framework highlights aging's mechanistic universality across species, with hallmark convergence amplifying frailty despite partial modifiability.^[44]

Cellular and Molecular Processes

Mitochondrial dysfunction manifests as a core cellular process in aging, characterized by reduced oxidative phosphorylation efficiency, accumulation of mtDNA mutations, and elevated reactive oxygen species (ROS) production, which collectively impair ATP synthesis and exacerbate macromolecular damage. Empirical evidence from human and model organism studies demonstrates a progressive decline in mitochondrial respiratory capacity with age, correlating with bioenergetic deficits in post-mitotic tissues like muscle and brain. This dysfunction links causally to organismal decline through a feedback loop where impaired mitophagy fails to clear damaged organelles, amplifying oxidative stress and energy shortages that propagate to adjacent cellular compartments.^[45]^[46] Deregulated nutrient-sensing pathways, notably hyperactivity in the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1), drive aging by skewing cellular resource allocation toward growth and biosynthesis rather than repair and autophagy. In aged cells, persistent mTORC1 activation—often triggered by chronic nutrient excess—suppresses autophagic flux and proteostasis, fostering protein aggregation and metabolic inflexibility. Caloric restriction experiments in rodents and nonhuman primates reveal that mTORC1 inhibition restores autophagic activity and delays age-related pathologies, underscoring the pathway's causal role in metabolic failure without invoking adaptive purpose.^[47]^[48] Stem cell exhaustion emerges as a molecular amplifier of tissue-level decline, wherein repeated divisions and environmental insults deplete self-renewal capacity through telomere attrition, epigenetic drift, and accumulated DNA damage, curtailing differentiation potential. Human studies, including analyses of bone marrow and muscle biopsies from individuals over 70 years, show diminished hematopoietic and satellite stem cell proliferation rates compared to younger cohorts, with functional deficits evidenced by reduced colony-forming units and impaired engraftment. This exhaustion causally hinders homeostatic renewal, as quiescent stem cells fail to mobilize effectively, leading to chronic repair deficits independent of extrinsic factors like inflammation.^[49]^[50] Altered intercellular communication, primarily via the senescence-associated secretory phenotype (SASP), propagates molecular dysfunction across tissues by secreting proinflammatory cytokines (e.g., IL-6, IL-8) and matrix-degrading enzymes from senescent cells, fostering a paracrine environment that accelerates neighbor cell senescence and extracellular matrix stiffening. Quantitative proteomics of aged human fibroblasts confirms SASP enrichment with age, correlating with disrupted signaling in pathways like NF-κB, which sustains a low-grade inflammatory state detrimental to cellular integrity. This process reflects a breakdown in signaling fidelity rather than coordinated adaptation, as SASP components empirically correlate with frailty markers in longitudinal cohorts.^[51]^[52] From an evolutionary standpoint, these cellular processes align with aging as a non-adaptive byproduct of selection pressures prioritizing reproductive fitness over indefinite somatic maintenance, where post-reproductive decline arises from pleiotropic genes beneficial early in life but deleterious later due to incomplete repair mechanisms against entropy-driven degradation. Antagonistic pleiotropy models, supported by genomic analyses across species, predict that mutations enhancing early fecundity at the cost of late-life robustness persist, explaining the universality of molecular decay without teleological intent. This framework debunks programmed aging narratives, emphasizing instead the causal primacy of unrepaired molecular lesions accumulating beyond selection's reach.^[53]^[54]

Demographic and Epidemiological Patterns

Global Trends in Population Aging

The global proportion of older individuals has risen steadily, driven primarily by sustained declines in fertility rates below replacement levels in most countries and reductions in mortality from infectious diseases and chronic conditions due to medical and public health advancements. Between 1950 and 2024, the share of the world population aged 65 and older nearly doubled from 5.5% to 10.3%, with fertility rates falling to levels where over three-quarters of countries are projected to have rates insufficient to sustain population size by 2050.^[55]^[56] This shift reflects a demographic transition where post-World War II cohorts enter older ages while younger cohorts shrink, amplifying aging even in regions with prior high growth.^[57] Projections indicate acceleration, with the number of people aged 60 and older expected to reach 1.4 billion by 2030, comprising one in six globally, up from 1.1 billion in 2023.^[58] Growth is anticipated to be most rapid in low- and middle-income countries, where current shares of older populations remain lower but institutional capacities for support are often limited. Meanwhile, global life expectancy at birth stood at 73.3 years in 2024, reflecting gains of about 8.4 years since 1995, yet recent analyses show deceleration in improvements, with cohort-specific advances now at 37-58% of historical paces in high-income settings.^[59]^[60] Empirical evidence underscores that while average life expectancy has extended, the maximum human lifespan remains constrained around 115-122 years, as evidenced by verified supercentenarian records and actuarial models showing no upward trend beyond biological limits observed since the early 20th century.^[61] Healthspan extensions have lagged, with the gap between lifespan and years lived in good health widening; for instance, U.S. data indicate an increase from 10.9 years in 2000 to higher disparities by 2024, as morbidity from noncommunicable diseases persists or expands rather than compresses into terminal phases.^[62] This pattern holds globally, where longevity gains from interventions like vaccinations and sanitation have not proportionally reduced disability duration.^[63]

Variations by Gender, Geography, and Socioeconomics

Women exhibit a global life expectancy advantage of approximately 5 years over men, with female life expectancy at birth averaging 76 years compared to 71 for males as of recent estimates.^[64] This gap arises primarily from biological factors, such as estrogen's protective effects against cardiovascular disease and women's genetic advantages including two X chromosomes that enhance immune responses and DNA repair, alongside behavioral differences where men engage more frequently in high-risk activities like smoking, excessive alcohol consumption, and occupational hazards leading to higher rates of accidents and violence.^[65] ^[66] ^[67] Geographic variations in longevity reflect disparities between high-income nations and developing regions, with Japan achieving a life expectancy of about 85 years in 2023, far exceeding averages in low-income countries where figures often fall below 70 years due to persistent infectious diseases and malnutrition.^[68] These differences stem largely from improvements in nutrition and sanitation in affluent areas, which historically reduced mortality from waterborne illnesses and nutrient deficiencies, enabling better physiological resilience to aging-related declines rather than solely from policy frameworks.^[69] Socioeconomic status correlates with longevity gradients, where individuals in the highest income or education quintiles experience life expectancies 10-15 years longer than those in the lowest, as evidenced by U.S. studies showing substantial differentials by occupation and housing tenure.^[70] These gaps are driven by lifestyle factors tied to socioeconomic position, including access to nutrient-dense diets, physical activity levels, and avoidance of obesogenic environments, compounded by heritable traits influencing metabolic health and stress responses that favor those with advantageous genetics often concentrated in higher strata.^[71] ^[72]

Key Subfields

Biogerontology

Biogerontology examines the biological mechanisms underlying aging at the cellular and molecular levels, focusing on processes such as senescence, genomic instability, and metabolic dysregulation that drive age-related decline. This subfield emphasizes empirical observations from controlled laboratory experiments, including the identification of conserved pathways like insulin/IGF-1 signaling, which modulate lifespan in invertebrates but show constrained translational potential to vertebrates due to differences in physiology and environmental interactions.^[73] Research prioritizes quantifiable endpoints, such as replicative exhaustion in cell cultures, over speculative extensions of healthspan, acknowledging that aging arises from accumulated damage rather than programmable design. Studies in model organisms, particularly Caenorhabditis elegans, have elucidated genetic interventions affecting longevity; for instance, mutations in the daf-2 gene, encoding an insulin/IGF-1 receptor homolog, extend mean lifespan by over twofold in fertile adults under standard conditions, primarily through enhanced stress resistance and reduced reproductive output.^[74] However, such findings reveal applicability limits for humans, as daf-2 effects diminish under variable nutrient or temperature stresses mimicking natural environments, and mammalian orthologs yield smaller extensions (e.g., 20-30% in mice) without proportionally scaling to radical human lifespan gains.^[75] Complementary work on telomere maintenance highlights progressive shortening as a senescence trigger, with telomerase activation preserving length in proliferative cells but risking oncogenesis if dysregulated, as evidenced by elevated tumor incidence in individuals with congenitally long telomeres.^[76]^[77] Efforts to clear senescent cells via senolytics, such as dasatinib plus quercetin, have yielded modest clinical outcomes; a 2025 phase 2 trial in postmenopausal women reported subtle improvements in bone metabolism markers but no significant fracture risk reduction, while a pilot study in older adults with frailty showed feasibility and minor gains in mobility without robust cognitive enhancements.^[31]00056-8/fulltext) These results underscore empirical ceilings, exemplified by the Hayflick limit—human diploid fibroblasts undergo approximately 40-60 divisions before irreversible senescence, as demonstrated in 1961 serial passaging experiments—imposing thermodynamic and replicative constraints that preclude indefinite postponement of organismal decay despite targeted interventions.^[78] Skepticism persists regarding claims of dramatic extension, given inconsistent cross-species efficacy and the absence of evidence overriding fundamental entropy in biological systems. Social gerontology examines the interplay between aging individuals and societal structures, including roles, networks, and institutions, while psychological gerontology focuses on mental processes such as cognition, emotion, and adaptation. Early theories include disengagement theory, which posits a mutual withdrawal between older adults and society as natural and beneficial for preparation for death, activity theory, which advocates maintaining high levels of social engagement to sustain well-being akin to midlife, and continuity theory, which emphasizes preserving familiar patterns and preferences across the lifespan for psychological stability.^[79] ^[80] Empirical reviews indicate limited support for universal disengagement, as many older adults remain engaged, yet critiques of activity theory highlight its oversight of physical limitations, socioeconomic barriers, and individual variability, favoring continuity's realistic adaptation over mandates for perpetual activity that may impose undue pressure.^[80] ^[81] Psychological changes in aging often involve gradual declines in fluid cognitive abilities, such as processing speed and working memory, driven primarily by biological accumulations like neurodegeneration rather than social factors alone. Dementia prevalence rises sharply with extreme age, affecting approximately 13-33% of individuals aged 85 and older, with rates doubling roughly every five years until that threshold, underscoring age as the predominant risk factor rooted in cellular and vascular pathologies.^[82] ^[83] Although observational studies associate social isolation with accelerated cognitive decline, causal mechanisms remain unclear, potentially involving reverse causation where early biological impairments precede withdrawal, rather than isolation independently driving pathology.^[84] ^[85] Family dynamics in later life reveal tensions between support expectations and practical burdens, challenging notions of seamless multigenerational harmony. Empirical data show that caregivers, often adult children, experience heightened emotional and physical strain from providing care, with family conflicts and role ambiguities exacerbating burden independently of care recipients' impairment levels.^[86] In extended family structures, intergenerational obligations can amplify resentment and resource competition, as evidenced by higher reported caregiving stress compared to nuclear setups, prioritizing individual agency in negotiating support over idealized collective duties.^[87] This underscores the need for adaptive strategies that respect personal boundaries amid demographic shifts straining traditional kin networks.

Environmental and Policy Gerontology

Environmental gerontology examines how physical surroundings, including urban planning and housing design, influence older adults' health, independence, and quality of life, while policy gerontology analyzes governmental and economic frameworks shaping aging outcomes, often highlighting the superiority of market-driven approaches over expansive state programs in promoting efficiency and autonomy. Empirical studies demonstrate that features of the built environment, such as walkable neighborhoods with high street connectivity and mixed land uses, causally increase mobility among the elderly by facilitating more frequent out-of-home activities and reducing isolation. For instance, dense, accessible urban designs correlate with higher levels of physical engagement and lower risks of sedentary behavior, as evidenced by longitudinal analyses controlling for individual confounders like health status. Conversely, car-dependent suburbs or poorly lit pedestrian paths exacerbate mobility limitations, contributing to higher fall risks and dependency on informal caregiving networks.^[88]^[89]^[90] Aging-in-place initiatives, which enable seniors to remain in familiar homes with modifications rather than relocating to institutions, reflect growing preferences and cost advantages, with 75% of U.S. adults aged 50 and older expressing a desire to stay in their current residences as of late 2024. Home-based care proves more economical than institutional alternatives, as average annual nursing home costs exceed $100,000 per resident while aging-in-place adaptations like bathroom grab bars or ramps average $9,500, often yielding long-term savings through reduced hospitalization rates. Employment data from 2024 further underscore this shift, with home and community-based care sectors employing 4.3 million workers—surpassing institutional facilities—and demonstrating scalability via private innovations in assistive technologies. Market incentives, such as tax credits for home modifications, outperform rigid government mandates by spurring competitive adaptations tailored to individual needs, avoiding the inefficiencies of one-size-fits-all public subsidies.^[91]^[92]^[93] Policy critiques emphasize the fiscal unsustainability of entitlement expansions amid demographic pressures, as U.S. Social Security's combined trust funds face depletion by 2035 under 2025 projections, requiring either a 3.82% payroll tax hike or equivalent benefit cuts to restore solvency over 75 years. Such strains arise from pay-as-you-go structures ill-suited to shrinking worker-to-retiree ratios, projected to drop below 2.8 by 2035, rendering further benefit growth counterproductive without corresponding revenue reforms. Advocates for personal savings mechanisms, including privatized retirement accounts, argue these foster individual accountability and higher returns via market investments, contrasting with public programs' historical underperformance adjusted for inflation and administrative overhead. Empirical modeling supports shifting toward incentive-based policies, like expanded health savings accounts, which could generate $3 in economic returns per $1 invested in preventive aging measures by enhancing self-reliance over dependency on strained entitlements.^[94]^[95]^[96]

Interventions and Longevity Strategies

Lifestyle and Behavioral Factors

Regular engagement in resistance training has been shown in meta-analyses of randomized controlled trials to enhance muscle strength, reduce all-cause mortality risk by approximately 21%, and improve physical functioning in older adults, contributing to extended healthspan through preservation of sarcopenic tissue and metabolic efficiency.^[97]^[98] Adherence to protocols involving 2-3 weekly sessions of progressive overload, using free weights or machines for at least 8-12 weeks, yields measurable gains in lower extremity hypertrophy and functional capacity, independent of baseline fitness levels.^[99]^[100] These outcomes underscore the causal role of mechanical loading in countering age-related frailty, with dose-response effects observed in strength adaptations.^[101] Dietary patterns emphasizing whole foods, such as the Mediterranean diet rich in olive oil, fruits, vegetables, and lean proteins, correlate with reduced all-cause mortality risk by 23% in cohort studies and randomized trials tracking longevity outcomes.^[102]^[103] This regimen supports telomere maintenance and cardiovascular health via anti-inflammatory mechanisms, with meta-analyses confirming lower incidence of chronic diseases that accelerate aging.^[104] Empirical data from interventions demonstrate causal benefits in glycemic control, blood pressure reduction, and weight management, extending healthspan by mitigating oxidative stress without reliance on caloric restriction alone.^[105] Smoking cessation exhibits a dose-response reversal of cardiovascular aging markers, including arterial stiffness and subclinical inflammation, with quitters showing risk profiles approaching never-smokers within 5 years for heavy prior users (≥20 pack-years).^[106]^[107] Randomized and longitudinal evidence links pack-year accumulation to elevated biomarkers like augmentation index and thromboxane levels, while abstinence rapidly attenuates these via endothelial repair.^[108] Similarly, reducing alcohol intake from heavy to mild-moderate levels (≤1-2 drinks daily) lowers major adverse cardiovascular events by 23%, countering dose-dependent acceleration of hypertension, cardiomyopathy, and vascular stiffening.^[109]^[110] Excessive consumption (>20g/day ethanol) promotes frailty and telomere attrition, whereas strict abstinence or minimal intake preserves organ reserve in aging populations.^[111] Adequate sleep duration (7-9 hours nightly) maintains telomere length, with short sleep (<6 hours) empirically associated with accelerated shortening akin to 5-10 years of chronological aging in cross-sectional and prospective studies.^[112] Observational data from large cohorts reveal causal links via disrupted circadian repair processes, though randomized interventions remain limited; consistent patterns hold across populations controlling for confounders like BMI.^[113] Chronic stress exposure, measured via perceived stress scales, correlates with telomere attrition in meta-analyses, with high-stress individuals exhibiting 0.05-unit shortening over a decade independent of demographics.^[114]^[115] Behavioral mitigation through mindfulness or routine disrupts this via reduced cortisol-mediated oxidative damage, prioritizing self-directed habits over pharmacological proxies for sustained telomeric integrity.^[116]

Pharmacological and Biotechnological Approaches

Pharmacological interventions targeting the hallmarks of aging, such as cellular senescence, have centered on senolytics, which selectively induce apoptosis in senescent cells to mitigate their secretory phenotype and associated tissue dysfunction.^[117] The combination of dasatinib, a tyrosine kinase inhibitor, and quercetin, a flavonoid, has been tested in early human trials, demonstrating reduced senescent cell burden in adipose tissue among patients with diabetic kidney disease following intermittent dosing.^[118] A 2025 pilot study in older adults reported modest improvements in physical function and cognition after dasatinib-quercetin administration, though effects were subtle and not uniformly replicated across biomarkers of aging.^[119] Similarly, a phase 1 trial for Alzheimer's disease indicated safety and preliminary reductions in tau and amyloid markers, but larger studies are needed to confirm efficacy against age-related decline.^[120] Metformin, an antidiabetic biguanide, is under investigation for repurposing as a geroprotector due to its effects on nutrient sensing pathways like AMPK activation and mTOR inhibition, potentially addressing multiple aging hallmarks including mitochondrial dysfunction and inflammation.^[121] Observational data link metformin use to lower incidence of age-related diseases, but randomized trials yield mixed results; for instance, the 2025 MET-PREVENT trial found no enhancements in grip strength, walking speed, or muscle mass after four months of treatment in nondiabetic older adults.^[122] The Targeting Aging with Metformin (TAME) trial, a planned six-year study enrolling 3,000 individuals aged 65-79, aims to assess delays in age-related disease onset as a proxy for aging intervention, though as of 2025 it remains in preparatory stages amid funding and regulatory challenges.^[123]^[124] Biotechnological strategies, including gene editing, target genetic drivers of aging in preclinical models. CRISPR-Cas9 and base editing have corrected the LMNA mutation in progeria, a premature aging syndrome, restoring nuclear integrity and extending lifespan in mouse models, with 2024-2025 reviews highlighting potential for broader senescent cell reprogramming.^[125]^[126] High-throughput CRISPR screens in neural stem cells identified regulators of age-related quiescence, suggesting therapeutic knockouts could enhance regenerative capacity, yet human translation faces scalability issues like off-target edits and delivery inefficiencies in vivo.^[127] Stem cell rejuvenation approaches leverage mesenchymal or induced pluripotent stem cells to counteract hematopoietic and tissue-specific stem cell exhaustion. Preclinical studies demonstrate that transplanting young or epigenetically reprogrammed stem cells ameliorates frailty and restores organ function in aged rodents, with partial cellular rejuvenation via Yamanaka factors showing promise in reversing epigenetic clocks.^[128]^[129] Early clinical trials, including autologous stem cell infusions for frailty, report safety but inconsistent efficacy in healthspan metrics as of 2025, constrained by regulatory approvals, tumorigenicity risks, and ethical concerns over sourcing and equity.^[130]^[131]

Empirical Evidence and Skeptical Perspectives

Empirical studies on longevity interventions, such as pharmacological agents like rapamycin, reveal significant challenges in translating preclinical success to human outcomes. In mouse models, rapamycin administration has extended median lifespan by up to 60% when initiated in middle age, with transient treatment showing sustained benefits.^[132] However, human applications, primarily in transplant patients at immunosuppressive doses, are associated with adverse effects including hyperglycemia, hyperlipidemia, insulin resistance, and elevated risk of infections and new-onset diabetes, often outweighing potential anti-aging gains.^[133] ^[134] Low-dose intermittent regimens in recent trials, such as the 2025 PEARL study, report modest immune enhancements and tolerability over one year but lack robust evidence for lifespan extension, with inconsistent results across small cohorts underscoring translation gaps from rodents to humans.^[135] ^[136] The concept of morbidity compression—postponing disability to later life stages without expanding total unhealthy years—remains debated, with evidence indicating delays in onset but persistent or expanding periods of decline. Theoretical models suggest interventions that steepen survival curves (reducing late-life deaths) could compress morbidity by aligning disability onset closer to death.^[137] Yet, population-level data from 2020-2024 analyses show mixed results; for instance, while some chronic conditions exhibit compressed timelines, overall healthy life expectancy has not uniformly expanded, and years lived with disability have increased in certain demographics, challenging full realization of the hypothesis.^[138] ^[139] Skeptics argue that aging's multifactorial nature resists simple postponement, as delayed morbidity often shifts rather than eliminates frailty, with epidemiological trends revealing expansion in pain-related disabilities despite longevity gains.^[139] Economic analyses highlight resource constraints in pursuing marginal longevity benefits, questioning societal returns on investment. While models project trillions in value from even modest life expectancy increases (e.g., $38 trillion for one year), real-world interventions yield high development and implementation costs relative to incremental healthspan gains, often failing to offset broader healthcare burdens.^[140] For example, biomarker-driven therapies and clinical trials incur substantial expenses, yet historical failures in anti-aging ventures—such as inconsistent epigenetic clocks and unproven supplements—demonstrate low ROI when side effects and scalability issues dominate.^[141] Critics emphasize causal realism: interventions like caloric restriction mimetics show preclinical promise but falter in humans due to adherence barriers and negligible net benefits, diverting resources from proven public health measures.^[136] This underscores a need for rigorous cost-benefit scrutiny, as hype around unverified therapies risks inefficient allocation amid rising aged-care demands.

Societal Impacts and Challenges

Healthcare Systems and Caregiving

Aging populations impose significant strains on healthcare infrastructure, particularly through the escalating prevalence of dementia, which demands intensive resource allocation for diagnosis, management, and long-term support. According to National Institute on Aging projections, approximately 7.1 million Americans currently exhibit Alzheimer's symptoms, with estimates indicating this figure could rise to over 13.9 million in the coming decades, driven by demographic shifts. New dementia cases are forecasted to double by 2060, reaching about 1 million annually in the United States, exacerbating pressures on medical facilities already challenged by workforce shortages and coordination complexities.^[142]^[143] Caregiving demands further compound these inefficiencies, as family and professional caregivers face high burnout rates amid fragmented care delivery. Surveys indicate that 70% of dementia caregivers experience substantial stress from coordinating services across multiple providers, contributing to emotional exhaustion and reduced care quality. Roughly one in five caregivers risks burnout, characterized by chronic fatigue and diminished capacity, which perpetuates system-wide deficits in sustained support for frail elderly patients. These challenges highlight causal links between inadequate interdisciplinary protocols and diminished caregiver resilience, underscoring the need for streamlined interventions to mitigate turnover and service gaps.^[144]^[145] Efforts to address polypharmacy represent a targeted approach to enhancing efficiency in geriatric care, particularly through deprescribing protocols that curb medication-related harms in frail individuals. UpToDate guidelines updated in September 2025 emphasize deprescribing to alleviate overall drug burdens and lower risks of adverse events like falls and delirium, which are prevalent in multimorbid elderly populations. Clinical evidence supports the safety of discontinuing antihypertensives in frail older adults via shared decision-making, reducing unnecessary exposures without compromising essential outcomes. Such practices counter incentives favoring pharmaceutical escalation over holistic assessment, yet implementation lags due to provider habits and regulatory structures prioritizing volume over precision.^[146] Patient dissatisfaction reflects broader systemic misalignments, with 82% of older adults reporting frustration with healthcare delivery in 2024 surveys, often tied to fragmented access and overtreatment patterns. This discontent stems from incentives that reward procedural interventions over preventive or de-escalatory strategies, fostering inefficiencies like redundant testing and sustained polypharmacy despite evident risks. Empirical data from geriatric assessments reveal that these dynamics erode trust and adherence, perpetuating cycles of avoidable hospitalizations and strained resources. Reorienting toward evidence-based deprescribing and integrated caregiving models could alleviate these deficits, though entrenched reimbursement models pose barriers to widespread adoption.^[147]^[148]

Economic Burdens and Resource Allocation

Aging populations impose substantial fiscal strains on public budgets through escalating entitlement expenditures, particularly for pensions, healthcare, and long-term care. In the United States, the Medicare Hospital Insurance (HI) Trust Fund, which finances Part A services, faces depletion projected for 2036 under intermediate assumptions in the 2024 Trustees Report, after which incoming revenues would cover only 89% of scheduled benefits without legislative action. This projection reflects demographic pressures from the retirement of baby boomers, with program costs rising from 3.6% of GDP in 2023 to 5.8% by 2035. Similarly, OECD analyses indicate that population aging will elevate public spending on age-related programs by 2-5% of GDP across member countries by mid-century, driven by higher per capita outlays for older individuals who consume disproportionate shares of health and pension resources.^[149]^[150]^[151] These fiscal dynamics exacerbate intergenerational inequities, as shrinking cohorts of working-age individuals shoulder increased tax burdens to sustain benefits for larger retiree populations. Empirical models show that in advanced economies, the old-age dependency ratio—defined as persons aged 65+ per 100 working-age adults (20-64)—stood at 33 in 2024 and is forecasted to nearly double to around 50-60 by 2050 in many OECD nations, inverting traditional support structures where two workers previously supported one retiree. This shift correlates with productivity losses, as labor force participation declines and fiscal transfers from younger to older generations intensify, potentially crowding out investments in education and infrastructure that benefit future cohorts. Studies quantify this inequity through lifetime net fiscal impacts, revealing that post-1965 birth cohorts in the U.S. and Europe may receive 20-30% less in net benefits relative to contributions compared to earlier generations, due to parametric reforms or implicit debt accumulation.^[152]^[153]^[154] Market-oriented solutions, including expanded private insurance mechanisms and technological innovations, offer pathways to alleviate these burdens by reducing reliance on strained public systems. Private long-term care insurance and defined-contribution pensions can mitigate entitlement shortfalls by incentivizing personal savings and risk pooling, as evidenced by lower public outlays in systems with strong private supplementation, such as parts of the U.S. and Singapore. In caregiving, AI-driven tools—such as remote monitoring robots and predictive analytics—promise cost efficiencies; pilot deployments have demonstrated 20-40% reductions in human labor hours for routine tasks like fall detection and medication adherence, potentially offsetting labor shortages in elder care sectors projected to require millions more workers by 2050. Critics of expansive public entitlements argue that such state-heavy models foster moral hazard and inefficiency, advocating privatization to align incentives with productivity gains from healthier aging, though scalability depends on addressing digital divides among the elderly.^[155]^[153]

Controversies and Debates

Theoretical Disputes on Aging Processes

Theories of aging are broadly divided into programmed and damage-based (or stochastic) categories. Programmed theories posit that aging follows a genetically regulated timetable, involving mechanisms such as telomere attrition, epigenetic alterations, and hormonal changes that actively enforce decline after reproductive maturity.^[156] In contrast, damage-based theories attribute aging to the progressive accumulation of unrepaired molecular and cellular lesions, including oxidative damage from reactive oxygen species (ROS), mitochondrial mutations, and protein cross-linking, which stochastically impair function over time.^[156] Empirical evidence, such as elevated ROS-induced lipid peroxidation and DNA adducts in aging tissues, supports the primacy of damage accumulation, as interventions reducing oxidative stress (e.g., antioxidants in model organisms) extend lifespan without altering purported genetic clocks.^[157]^[158] From an evolutionary standpoint, the disposable soma theory integrates damage accumulation with causal realism, explaining aging as an emergent outcome of natural selection prioritizing reproductive fitness over somatic maintenance. Proposed by Kirkwood in 1977 and refined subsequently, it argues that finite resources compel organisms to allocate energy toward growth and reproduction rather than indefinite repair, leading to tolerated damage post-reproduction; this is evidenced by trade-offs observed in caloric restriction studies, where reduced fecundity correlates with enhanced longevity via bolstered maintenance.^[159] Critics of programmed theories note their inconsistency with evolutionary data, as no adaptive mechanism enforces post-reproductive decline in species without extrinsic mortality pressures, whereas damage models align with observed genomic instability and proteostasis loss across taxa.^[160] Psychosocial models, such as Rowe and Kahn's 1997 framework of successful aging—defined by low disease probability, high cognitive/physical function, and social engagement—have faced critiques for overlooking biological determinism, with a 2016 systematic review documenting widespread dissatisfaction among researchers for its emphasis on modifiable behaviors while ignoring inexorable molecular deterioration.^[161] Disputes persist on the feasibility of negating aging via damage repair. Proponents like Aubrey de Grey advocate SENS (Strategies for Engineered Negligible Senescence), a 2002 framework targeting seven damage categories—cell loss, senescent cells, mitochondrial mutations, death-resistant cells, extracellular aggregates, intracellular aggregates, and nuclear mutations—through periodic biotechnological interventions to restore youthful physiology without addressing root evolutionary trade-offs.^[162] Optimists cite preclinical successes, such as senolytic drugs clearing senescent cells to alleviate age-related pathologies in mice, as validating incremental progress toward comprehensive rejuvenation.^[163] Skeptics counter that SENS underestimates systemic complexity, including pleiotropic effects and emergent interactions among damage types, rendering negligible senescence improbable without unforeseen synergies; for instance, 2005 debates highlighted risks of incomplete repair accelerating secondary damages, with no empirical trajectory toward human escape velocity despite decades of advocacy.^[164]^[163] These views underscore a divide between engineering-focused optimism and biologically grounded caution, informed by the field's reliance on model organisms where interventions yield modest, non-translatable extensions.

Ethical Dilemmas in Extension and End-of-Life Care

Ethical dilemmas in gerontology arise from tensions between prolonging life and preserving quality, particularly when interventions divert resources from younger populations or exacerbate inequalities. Empirical analyses indicate that end-of-life healthcare expenditures in the United States consume a disproportionate share of total costs, with Medicare data showing that up to 25% of lifetime benefits are spent in the final year of life, raising questions about intergenerational equity as funds are reallocated from preventive care for youth to terminal extensions for the elderly.^[165] This resource diversion is evidenced by cost-benefit studies revealing that aggressive longevity pursuits, such as biotechnological trials, often prioritize high-income participants, with socioeconomic status strongly correlating to extended lifespan outcomes in midlife cohorts.^[166] Access to longevity extension technologies highlights equity concerns, as market segmentation patterns demonstrate that benefits accrue disproportionately to affluent demographics capable of affording experimental therapies. A 2025 analysis of longevity market dynamics found that socioeconomic factors segment participation, with wealthier individuals gaining preferential access to trials and interventions, potentially widening existing longevity gaps where higher socioeconomic status already predicts up to several additional years of life expectancy.^[167] Critics argue this elite bias undermines utilitarian justifications for research funding, as public investments in gerontology may yield private gains for a select few while neglecting broader societal needs, though proponents counter that trickle-down innovations could eventually democratize benefits despite initial disparities.^[168] In end-of-life care, debates over patient autonomy versus societal safeguards intensify around euthanasia and assisted dying. In the Netherlands, where euthanasia has been legal since 2002, annual cases rose from approximately 1,882 in 2003 to over 8,000 by 2022, comprising about 5% of all deaths, with expansions to include non-terminal conditions like psychiatric disorders and dementia prompting slippery slope concerns.^[169] Empirical reviews present mixed evidence: while some studies find no uncontrolled shift to non-voluntary euthanasia, others document a progression from terminal illness to broader criteria, with psychiatric cases increasing from 0.4% of total euthanasias in 2010 to around 2% by 2023, raising causal risks of coercion or diminished safeguards for vulnerable elderly populations.^[170] Advocates emphasize enhanced dignity through autonomy, citing high patient satisfaction in reported outcomes, yet first-principles scrutiny highlights potential for expanded normalization eroding protections against undue influence from family or providers.^[171]^[172] Over-treatment in gerontology manifests as futile interventions that extend physiological existence at the expense of suffering and resources. Peer-reviewed data from hospital admissions identify futile care—defined as treatments offering no reasonable benefit—in 12.1% of end-of-life cases among the elderly, often involving mechanical ventilation or aggressive chemotherapy that prolongs dying without improving quality of life.^[173] Cost-benefit evaluations confirm these practices inflate expenditures, with U.S. studies estimating billions annually in non-beneficial care for injured elderly patients, where burdens like pain and dependency outweigh marginal survival gains, supporting arguments for reallocating resources to palliative alternatives that prioritize comfort over prolongation.^[174] Such evidence underscores ethical imperatives to integrate patient preferences and prognostic realism, mitigating iatrogenic harm while addressing systemic incentives in fee-for-service models that favor intervention over restraint.^[175]

Debunking Myths and Addressing Biases

A prevalent misconception in popular and some academic discourse posits that human aging is predominantly or entirely driven by environmental and lifestyle factors, implying high malleability through behavioral interventions alone. Twin studies, however, demonstrate that genetic factors account for approximately 25% of variation in human lifespan, with heritability estimates ranging from 20% to 30% across multiple cohorts born in the late 19th and early 20th centuries.^[176] ^[177] For instance, analyses of Danish twin pairs born between 1870 and 1900 yielded heritability figures of 0.26 for males and 0.23 for females, underscoring a substantial inherited component independent of shared environment.^[178] This genetic influence increases with age, as shared environmental effects diminish, highlighting that while modifiable factors like diet and exercise contribute, they do not override underlying biological determinism.^[179] Another bias in gerontology involves an overemphasis on ageism and social discrimination as primary explanations for observed declines in older adults' competence and health, often downplaying intrinsic physiological deterioration. Empirical reviews find no consistent evidence that perceived ageism accelerates biological aging markers, such as telomere length or epigenetic clocks, suggesting that claims of discrimination as a causal driver lack robust causal support.^[180] Biological primacy is evident in universal patterns of senescence, including sarcopenia, reduced cognitive processing speed, and increased frailty, which correlate more strongly with chronological age than with reported discriminatory experiences.^[181] This selective focus may stem from institutional preferences in academia and media for sociocultural narratives over mechanistic biology, potentially inflating ageism's role while understating senescence as a programmed process. Competence declines, for example, manifest in slower reaction times and memory retrieval averaging 20-30% reductions by age 70, attributable to neural atrophy rather than external bias alone.^[182] Pseudoscientific claims promising reversal of aging through unverified supplements or therapies further mislead public understanding, often evading rigorous validation. The U.S. Food and Drug Administration has repeatedly warned against products like human growth hormone marketed for anti-aging, deeming such uses illegal and unsupported by evidence, as they pose risks without proven extension of healthy lifespan.^[183] Similarly, dietary supplements claiming to combat cellular aging lack FDA approval for these purposes and frequently rely on anecdotal rather than controlled trial data, with government reports highlighting potential physical harm and economic exploitation targeting seniors.^[184] Rigorous gerontological research prioritizes interventions backed by longitudinal trials, dismissing hype around "miracle" compounds until efficacy is demonstrated beyond placebo effects.

References

[1]
About GSA - Gerontological Society of America
Gerontology is the study of aging processes and individuals across the life course. It includes: The study of physical, mental, and social changes in people as ...Board of Directors · Donations · Past Visiting Scholars
[2]
What is Gerontology?
Gerontology is the study of the biological, psychological and sociological aspects of human development and the intricacies of aging across the lifespan.Missing: sources | Show results with:sources
[3]
Gerontology - an overview | ScienceDirect Topics
Gerontology refers to the study of aging, research, and scholarship in all its aspects. The word is derived from the Greek word for an old man, geront or ...
[4]
What Is Gerontology? - College of Public Health UGA
Definition of Gerontology. Gerontology is the study of aging and older adults. The science of gerontology has evolved as longevity has improved.
[5]
Gerontology competencies: Construction, consensus and contribution
Sep 27, 2019 · The term “gerontology” was coined in 1903 and is defined as the study of social, cultural, psychological, cognitive, and biological aspects ...
[6]
Gerontology in Public Health: A Scoping Review of Current ... - NIH
Jul 31, 2024 · Gerontology, the study of the aging process and the issues that affect older adults examines various aspects of aging, including biological, ...
[7]
Are “Anti-Aging Medicine” and “Successful Aging” Two Sides of the ...
Sep 10, 2013 · This article analyzes data from interviews with anti-aging practitioners to evaluate how their descriptions of the work they do, their definitions of aging, ...Missing: achievements | Show results with:achievements
[8]
Critical Perspectives on Successful Aging: Does It “Appeal More ...
Apr 18, 2014 · A key contribution of critical gerontology is its reflexive attitude toward the major concepts by which problems of aging are addressed.Missing: achievements | Show results with:achievements
[9]
[PDF] Are "Anti-Aging Medicine" and "Successful Aging" Two
Gerontologists have vehemently distanced themselves from A4M, which has, since its incep- tion, been embroiled with lawsuits with one another over the founders' ...
[10]
Gerontology vs. Geriatrics: The High Demand in Health Care
Sep 6, 2023 · While geriatrics deals with the care of the elderly and their needs, gerontology is the study of aging and its impacts on the population.
[11]
What Is a Gerontologist? - Cleveland Clinic
Jan 29, 2024 · Gerontologist. A gerontologist studies all aspects of the aging process and works to support the needs and wants of older adults.Missing: key | Show results with:key
[12]
What is Gerontology? The Study of Aging | SNHU
May 3, 2024 · Gerontology is the study of the physical aspects of aging, as well as the mental, social and societal implications of aging.What Do Gerontologists Do? · Emerging Opportunities For... · Starting A Career In...
[13]
Global Healthspan-Lifespan Gaps Among 183 World Health ...
Dec 11, 2024 · Globally, the mean healthspan-lifespan gap was 9.6 years, and women exhibited a mean 2.4-year larger gap than men, associated with a ...
[14]
Evolution of ageing since Darwin - PubMed
In the late 19th century, the evolutionary approach to the problem of ageing was initiated by August Weismann, who argued that natural selection was more ...Missing: foundations demographic
[15]
The Germ-Plasm: a Theory of Heredity (1893), by August Weismann
Jan 26, 2015 · In The Germ-Plasm, Weismann proposed a theory of heredity based on the concept of the germ plasm, a substance in the germ cell that carries ...Missing: aging | Show results with:aging
[16]
Centenary of the death of Elie Metchnikoff - ScienceDirect.com
Elie Metchnikoff passed away on July 15th, 1916. He is considered to be the father of phagocytes, cellular innate immunity, probiotics, and gerontology.
[17]
Elie Metchnikoff, the Man and the Myth - PMC - NIH
Feb 3, 2016 · Elie Metchnikoff, the father of innate immunity and discoverer of the significance of phagocytosis in development, homeostasis and disease.
[18]
Honoring Clive McCay and 75 Years of Calorie Restriction Research
Mean lifespan had reached only 53 y of age in 1935. The 1920s and 1930s were still plagued by high infant mortality, childhood diseases that killed millions of ...
[19]
Caloric restriction and its mimetics - PMC - NIH
(7). In the early 1900s, they reported that the restriction of food intake of rats retarded their growth, but prolonged their lifespan.
[20]
The Gerontological Society of America | GSA Journals
The Gerontological Society of America (GSA) was founded in 1945 to promote the scientific study of aging, to encourage exchanges among researchers and ...
[21]
[PDF] World Population Ageing 2017 - UN.org.
during the post-World War II baby boom, mean that the older population is itself ageing. The proportion of the world's older persons who are aged 80 years or ...
[22]
Demographic Trends - Aging and the Macroeconomy - NCBI - NIH
Population aging is largely caused by two demographic trends. Most obviously, people today are living longer than before.
[23]
About the Baltimore Longitudinal Study of Aging
Jul 27, 2018 · It began in 1958, when gerontology—the study of aging—was still very much in its infancy. Today, the BLSA is world-renowned, having generated ...
[24]
The Baltimore Longitudinal Study of Aging - National Institute on Aging
The BLSA began in 1958. Read about its history and timeline. arrows pointing forward · BLSA Research Advances.
[25]
PLEIOTROPY, NATURAL SELECTION, AND THE EVOLUTION OF ...
PLEIOTROPY, NATURAL SELECTION, AND THE EVOLUTION OF SENESCENCE ; First published: December 1957 ; Citations · 2,332 ; Contribution number 92 from the Department of ...
[26]
Is antagonistic pleiotropy ubiquitous in aging biology? - PMC - NIH
When George Williams first proposed his theory of antagonistic pleiotropy in 1957, he concocted a hypothetical example of a gene that hastened the calcification ...
[27]
National Institute on Aging (NIA) - NIH
Jan 21, 2025 · NIA was established in 1974 to improve the health and well-being of older adults through research. It conducts and supports genetic, biological, ...
[28]
National Institute on Aging's 50th anniversary: Advancing aging ...
Mar 6, 2024 · The National Institute on Aging (NIA), part of the National Institutes of Health (NIH), was founded in 1974 to support and conduct research ...
[29]
Hallmarks of aging: An expanding universe - PubMed
Jan 19, 2023 · We propose the following twelve hallmarks of aging: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled ...
[30]
The hallmarks of aging as a conceptual framework for health and ...
In this regard, three new hallmarks were finally added to the previous nine determinants of aging: disabled macroautophagy, chronic inflammation and dysbiosis ...
[31]
Senolytic therapy shows subtle impact on age-related bone health in ...
Feb 27, 2025 · An NIA-funded clinical trial investigating whether senolytics could improve bone health in older women had just subtle results.
[32]
A pilot study of senolytics to improve cognition and mobility in older ...
This study suggests that intermittent DQ treatment is feasible and safe; data hint at potential functional benefits in older adults at risk of Alzheimer's ...
[33]
We May Never See Average Lifespans Hit 100 - SciTechDaily
Oct 9, 2025 · Life expectancy in wealthy nations has plateaued after rapid 20th-century gains, according to new research in PNAS. The study forecasts that ...
[34]
New research reveals longevity gains slowing, life expectancy of ...
Aug 25, 2025 · ... life expectancy gains made by high-income countries in the first half of the 20th century have slowed significantly, and that none of the …Missing: 2020s | Show results with:2020s
[35]
Pitfalls of animal model systems in ageing research - ScienceDirect
Pitfalls include overly optimistic reports, difficulty separating disease from aging, and models susceptible to diseases that shorten lifespan. Numerous ...
[36]
Animal models of aging research: implications for human ... - PubMed
Animal models are useful for studying aging because almost all organisms age, and understanding aging may help develop treatments for age-related diseases.
[37]
DNA damage—how and why we age? - PMC - PubMed Central
Jan 29, 2021 · Here, we review evidence that DNA damage plays a causal role in aging. We also provide evidence that genotoxic stress is linked to other ...
[38]
The central role of DNA damage in the ageing process - PMC
Jan 17, 2023 · We synthesize accumulating evidence that DNA damage affects most if not all aspects of the ageing phenotype making it a most likely unifying cause of ageing.
[39]
Hallmarks of aging: An expanding universe - ScienceDirect.com
Jan 19, 2023 · These hallmarks are grouped into three categories: primary, antagonistic, and integrative. The interdependence of aging hallmarks means that ...
[40]
Aging Hallmarks and Progression and Age-Related Diseases
Dec 14, 2023 · The major cellular and molecular hallmarks of aging have been identified, and their relationships to age-related diseases and malfunctions have been explored.<|separator|>
[41]
DNA damage—how and why we age? - eLife
Jan 29, 2021 · Here, we review evidence that DNA damage plays a causal role in aging. We also provide evidence that genotoxic stress is linked to other ...
[42]
Aging Hallmarks and Progression and Age-Related Diseases - NIH
The major cellular and molecular hallmarks of aging have been identified, and their relationships to age-related diseases and malfunctions have been explored.
[43]
Aging and aging-related diseases: from molecular mechanisms to ...
Dec 16, 2022 · Thus far, a number of molecular mechanisms that regulate aging have been discovered, such as telomere dysfunction, loss of proteostasis, ...
[44]
Hallmarks of aging: A user's guide for comparative biologists
Here, we review each of the twelve hallmarks of aging defined by Lopez-Otin in 2023 with respect to the availability of data from diverse species.
[45]
Mitochondrial and metabolic dysfunction in ageing and age-related ...
Feb 10, 2022 · Mitochondrial dysfunction during ageing predisposes the elderly to age-related metabolic diseases. Diseases associated with metabolic ...
[46]
Mitochondrial dysfunction and its association with age-related ...
Any defect or deficit in mitochondrial number and function might be responsible for cellular damage. Mitochondrial dysfunction has been reported to be ...
[47]
Calorie restriction and rapamycin distinctly mitigate aging ... - Nature
Aug 10, 2024 · Calorie restriction (CR) and treatment with rapamycin (RM), an inhibitor of the mTORC1 growth-promoting signaling pathway, are known to slow aging and promote ...
[48]
Hyperactive mTORC1/4EBP1 signaling dysregulates proteostasis ...
These results show that a hyperactive mTORC1/4EBP1 axis accelerates cardiac aging, potentially by dysregulating proteostasis.
[49]
Stem cell aging: mechanisms, regulators and therapeutic opportunities
Aging tissues experience a progressive decline in homeostatic and regenerative capacities, which has been attributed to degenerative changes in tissue-specific ...Missing: biopsies | Show results with:biopsies
[50]
Why We Age: Stem Cell Exhaustion | Lifespan Research Institute
Jan 7, 2025 · Stem cell exhaustion is now recognized as a hallmark of aging. It impairs tissue maintenance and increases disease susceptibility, including anemia, ...Missing: biopsies | Show results with:biopsies<|separator|>
[51]
The Hallmarks of Aging - PMC - NIH
These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial ...Missing: classification | Show results with:classification
[52]
Classical and Nonclassical Intercellular Communication in ...
Here, we review the different means of intercellular communication including soluble factors in the context of senescence, ageing, and age-related diseases.Cellular Senescence: A... · Emerging Classical Sasps · Concluding Remarks And...
[53]
The Evolution of Aging | Learn Science at Scitable - Nature
Aging evolves because natural selection becomes inefficient at maintaining function (and fitness) at old age.Missing: foundations | Show results with:foundations
[54]
On the Programmed/Non-Programmed Nature of Ageing within the ...
Sep 27, 2011 · The evolutionary theory of ageing is generally portrayed as rejecting the notion that ageing has an adaptive basis, i.e. that an age-related ...
[55]
Ageing | United Nations Population Fund
Jun 19, 2024 · The world is ageing rapidly. Between 1974 and 2024, the worldwide share of people aged 65 almost doubled – increasing from 5.5 per cent to 10.3 per cent.<|separator|>
[56]
The Lancet: Dramatic declines in global fertility rates set to transform ...
Mar 20, 2024 · By 2050, over three-quarters of countries will not have high enough fertility rates to sustain population size over time.
[57]
[PDF] World Population Ageing 2023 - UN.org.
The decline of fertility during the demographic transition initiates a period in which a country's working-age population increases as a share of the total.<|separator|>
[58]
Ageing: Global population - World Health Organization (WHO)
Feb 21, 2025 · Globally, life expectancy at birth reached 73.3 years in 2024, an increase of 8.4 years since 1995. The number of people aged 60 and older ...Missing: Prospects | Show results with:Prospects
[59]
Ageing | United Nations
By the late 2070s, the global population aged 65 and older is projected to reach 2.2 billion, surpassing the number of children under age 18. By the mid-2030s, ...
[60]
Cohort mortality forecasts indicate signs of deceleration in ... - PNAS
Aug 25, 2025 · Forecasted cohort life expectancy improvements range from 37% to 52% of the best-practice pace, and 44% to 58% of the median. Table 1. Open in ...<|separator|>
[61]
Implausibility of radical life extension in humans in the twenty-first ...
Oct 7, 2024 · Survival to the age of 122.45 years—the maximum lifespan observed for humans as determined by the documented survival of Jeanne Calment, who ...
[62]
Healthspan-lifespan gap differs in magnitude and disease ... - NIH
Sep 1, 2025 · By the year 2100, the median healthspan-lifespan gap is predicted to rise globally by 22% (Fig. 5b), ranging from 7.3 to 18.8 years ( ...
[63]
Healthspan-lifespan gap differs in magnitude and disease ... - Nature
Sep 1, 2025 · Life expectancy, gross domestic product, and noncommunicable disease burden most consistently correlate with the healthspan-lifespan gap.
[64]
Why do women live longer than men? - Our World in Data
Nov 27, 2023 · Women tend to live longer than men. In 2021, this difference amounted to a 5-year gap in global life expectancy: the average life expectancy was 73.8 years for ...
[65]
Gender gap in health expectancy - PMC - PubMed Central - NIH
The paradox is likely to be due to multiple causes that include biological, behavioral, and social differences between the sexes.
[66]
Explaining the Life Expectancy Gap Between Men and Women
Mar 13, 2024 · Men and women have genetic, physiological and hormonal differences. These disparities make up the biological factors that affect a person's life ...
[67]
Gender Gap in Life Expectancy and Its Socio-Economic Implications
Oct 1, 2024 · These include higher consumption of alcohol, tobacco, and fats among men as well as a generally riskier behavior. The gender gap in life ...
[68]
Life Expectancy by Country and in the World (2025) - Worldometer
The world's life expectancy is 73.5. Hong Kong has the highest at 85.77, while the US is at 79.61.
[69]
Determinants of life expectancy in most polluted countries - NIH
Many socioeconomic, nutritional, lifestyle, genetic and environmental factors can influence a nation's health and longevity. Environmental degradation is one of ...
[70]
Marked Disparities in Life Expectancy by Education, Poverty Level ...
Adults with lower education, higher poverty levels, in manual occupations, and with rental housing had substantially lower life expectancy.
[71]
The growing life-expectancy gap between rich and poor | Brookings
Researchers have long known that the rich live longer than the poor. Evidence now suggests that the life expectancy gap is increasing.
[72]
Understanding the Rise in Life Expectancy Inequality
Mar 19, 2024 · As can be seen in figure 3, for males, the gap in life expectancy between the rich and poor increased in total by approximately 1.4 years.
[73]
Biogerontology: research status, challenges and opportunities - PMC
Biogerontology is the study of the biological basis of ageing and age-related diseases. The phenomenon and the process of ageing are well understood in ...
[74]
A C. elegans mutant that lives twice as long as wild type - PubMed
We have found that mutations in the gene daf-2 can cause fertile, active, adult Caenorhabditis elegans hermaphrodites to live more than twice as long as wild ...
[75]
Mutation of daf‐2 extends lifespan via tissue‐specific effectors ... - NIH
Feb 20, 2021 · We have described how daf‐2(rf) increases lifespan by causing p Age and, in some contexts, by reducing P frequency. Both Daf‐c and Age ...
[76]
Telomere dysfunction in ageing and age-related diseases - Nature
Feb 14, 2022 · Telomere shortening and damage are recognized causes of cellular senescence and ageing. Several human conditions associated with normal ageing are precipitated ...
[77]
Long Telomeres, the Endcaps on DNA, Not the Fountain of Youth ...
May 4, 2023 · People with long telomeres tend to develop a range of benign and cancerous tumors, as well as the age-related blood condition clonal hematopoiesis.Missing: maintenance | Show results with:maintenance
[78]
The serial cultivation of human diploid cell strains - ScienceDirect.com
December 1961, Pages 585-621. Experimental Cell Research. The serial cultivation of human diploid cell strains☆. Author links open overlay panelL. Hayflick,Missing: original | Show results with:original
[79]
(PDF) Social Gerontology Theory - ResearchGate
This paper presents a review of social theories of aging including early theories based on role, disengagement, activity, and continuity.
[80]
https://oxfordre.com/psychology/display/10.1093/acrefore/9780190236557.001.0001/acrefore-9780190236557-e-335
[81]
Theoretical Challenges and Social Inequalities in Active Ageing - PMC
Aug 30, 2021 · This study aims to make a critical-theoretical and empirical assessment of the active ageing concept, challenging the active ageing discourse from two ...
[82]
2024 Alzheimer's disease facts and figures
Apr 30, 2024 · Five percent of people age 65 to 74, 13.2% of people age 75 to 84, and 33.4% of people age 85 or older have Alzheimer's dementia (see ...
[83]
[PDF] National Health Statistics Reports - CDC
Jun 13, 2024 · The percentage of adults with a dementia diagnosis increased with age, from 1.7% in those ages 65–74 to 13.1% in those age. 85 and older, and ...
[84]
Are social isolation and loneliness associated with cognitive decline ...
Feb 23, 2023 · The results showed that both social isolation and loneliness were associated with poor cognition in ageing, with depression as a possible mediator.
[85]
How Isolation Affects Brain Disease - American Brain Foundation
Apr 22, 2025 · The link between social isolation and dementia risk is complex, and the precise mechanisms for these effects are not yet fully understood.
[86]
Influence of family dynamics on burden among family caregivers in ...
Jul 22, 2016 · Our findings indicate that family dynamics strongly influences burden experienced by caregiving family members, regardless of the care receiver's degree of ...
[87]
(PDF) Intergenerational relationships and caregiving burden among ...
Aug 12, 2022 · ... In our study, it was found that caregivers living in extended families had higher caregiving burden than those living in single and nuclear ...Missing: evidence | Show results with:evidence
[88]
A tale of two aging nations: How do urban designs impact older ...
Our results suggest that dense and accessible neighborhood designs can enhance older people's mobility with more out-of-home activities.
[89]
How Design of Places Promotes or Inhibits Mobility of Older Adults
We identified several influences of the built environment that appear to affect certain aspects of mobility in older adults (in particular, walking for ...
[90]
The Impact of Built Environment Factors on Elderly People's Mobility ...
May 19, 2022 · Existing research has confirmed that the built environment can greatly influence elderly people's travel behavior [12,28,39]. However, most ...
[91]
New AARP Report: Majority of Adults 50-plus Want to Age in Place ...
Dec 10, 2024 · A strong majority of adults aged 50 and older (75%) wish to remain in their current homes as they age, and 73% hope to stay in their communities.Missing: institutional | Show results with:institutional
[92]
https://carex.com/blogs/resources/aging-in-place-statistics
[93]
Economic trends: home and community-based care versus ...
The two industries that provide care in home and community-based settings together accounted for 4.3 million jobs in July 2024, considerably higher than the 3. ...
[94]
Analysis of the 2025 Social Security Trustees' Report
Jun 18, 2025 · Social Security's 75-year solvency gap increased relative to last year's projections, from 3.50 percent of payroll to 3.82 percent of payroll.Missing: critiques expansion personal
[95]
Social Security's Financial Outlook: The 2025 Update in Perspective
Jul 8, 2025 · The 2025 Trustees Report shows a modest increase in Social Security's 75-year deficit, while the depletion date for the retirement trust ...Missing: expansion savings
[96]
The economic benefits of healthy aging interventions | McKinsey
Sep 4, 2025 · Investing $1 annually in healthy aging interventions can yield $3 in economic and healthcare benefits in the United States—and potentially ...
[97]
Increasing the health span: unique role for exercise
Another systematic review and meta-analysis indicated that self-reported engagement in resistance exercise was associated with a 21% lower risk of all-cause ...
[98]
Resistance training and health in adults: an overview of systematic ...
RT was associated with a reduction in all-cause mortality and cardiovascular disease incidence, and an improvement in physical functioning.<|separator|>
[99]
Lower extremity muscle hypertrophy in response to resistance ...
RT promotes muscle hypertrophy in older adults at both whole-muscle and fiber levels, with training duration potentially influencing the response.
[100]
Machine-Based Resistance Training Improves Functional Capacity ...
The aim of this systematic review and meta-analysis was to explore the impact of machine-based RT on strength and functional capacity in older adults.
[101]
Dose–Response Relationships of Resistance Training in Healthy ...
Sep 29, 2015 · The aims of this systematic review and meta-analysis were to determine the general effects of RT on measures of muscle strength and morphology
[102]
Mediterranean Diet Adherence and Risk of All-Cause Mortality in ...
May 31, 2024 · In this cohort study, higher adherence to the Mediterranean diet was associated with 23% lower risk of all-cause mortality.
[103]
Mediterranean diet and life expectancy; beyond olive oil, fruits ... - NIH
Two large randomized trials support the benefits of the Mediterranean dietary pattern to increase life expectancy, reduce the risk of major chronic disease,
[104]
Mediterranean Diet and Telomere Length: A Systematic Review and ...
The aim of this meta-analysis was to determine the associations between MedDiet adherence and TL maintenance. MEDLINE-PubMed and Cochrane databases were ...
[105]
The effects of Mediterranean diet on cardiovascular risk factors ...
Apr 19, 2024 · The meta-analysis presented evidence supporting the beneficial effects of the Mediterranean diet on blood pressure, glycemic control, and weight loss.
[106]
Dose-Response Association between Smoking Cessation and ...
Conclusions. A dose-response association between smoking cessation and AIx was revealed, which implies the possibility of a reversible effect of smoking ...Missing: markers | Show results with:markers
[107]
Smoking Cessation and Incident Cardiovascular Disease | Cardiology
Nov 1, 2024 · In this cohort study, smoking and CVD risk exhibited a dose-dependent association, with light ex-smokers having a CVD risk similar to that of never-smokers.Missing: aging markers
[108]
Cardiovascular risk of smoking and benefits of smoking cessation
Heavy smokers (≥20 pack-years) who quit smoking showed a lower risk of CVD within 5 years compared to current heavy smokers and this reduction was significant ( ...
[109]
Reduced Alcohol Consumption and Major Adverse Cardiovascular ...
Mar 28, 2024 · Lowering alcohol intake to mild to moderate level was associated with a 23% reduction in the risk of major adverse cardiovascular events compared with ...
[110]
Chronic alcohol consumption accelerates cardiovascular aging and ...
Mar 20, 2025 · Excessive alcohol consumption exacerbates these risks by promoting hypertension, stroke, arrhythmias, coronary artery disease, cardiomyopathy, ...
[111]
Alcohol and Cardiovascular Health: The Dose Makes the Poison ...
Excessive alcohol consumption, in a dose-dependent fashion, commonly causes both reversible hypertension and atrial fibrillation and accounts for one-third of ...
[112]
The association between sleep quality and telomere length
Short sleep duration, sleep apnoea, and insomnia are significantly associated with shorter telomeres, a biological marker of cellular aging.
[113]
The association between sleep quality and telomere attrition
Psychosocial stressors accelerate telomere attrition, a biomarker of cell aging, whereas good sleep is hypothesized to be a mitigating factor.
[114]
https://pmc.ncbi.nlm.nih.gov/articles/PMC5590630
[115]
Stress and telomere shortening: Insights from cellular mechanisms
Short telomeres confer risk of degenerative diseases. Chronic psychological stress can lead to disease through many pathways, and research from in vitro ...
[116]
How chronic stress is harming our DNA
Oct 1, 2014 · A number of studies have linked stress with shorter telomeres, a chromosome component that's been associated with cellular aging and risk for heart disease, ...Missing: empirical | Show results with:empirical
[117]
Targeting Cellular Senescence for Healthy Aging: Advances in ...
Sep 19, 2025 · While preclinical studies have demonstrated promising results for both senolytic and senomorphic therapies, translating these findings into ...
[118]
The senolytic cocktail, dasatinib and quercetin, impacts the ...
Jan 20, 2025 · The first human studies showed a reduced senescent cell burden in the adipose tissue of patients suffering from diabetic kidney disease [9] and ...
[119]
A pilot study of senolytics to improve cognition and mobility in older ...
Feb 25, 2025 · This single-arm study evaluates the feasibility, safety, and preliminary effects of two senolytic agents, Dasatinib and Quercetin (DQ), ...
[120]
Results of a Phase 1 Trial of Senolytics for Alzheimer's - Lifespan.io
May 19, 2025 · Dasatinib and quercetin are very well-known to reduce cellular senescence, and they have been reported to reduce both tau [1] and amyloid beta ...
[121]
Metformin's Mechanisms in Attenuating Hallmarks of Aging and Age ...
Metformin exerts antiaging effects by intervening in nutrient sensing, DNA damage, the accumulation of ROS, telomere attrition, inflammation, cellular ...
[122]
Emerging uncertainty on the anti-aging potential of metformin
In the most recent MET-PREVENT trial, metformin for 4 months did not improve grip strength, walking speed, physical performance, muscle mass, quality of life, ...
[123]
TAME - Targeting Aging with Metformin
The Targeting Aging with Metformin (TAME) Trial is a series of nationwide, six-year clinical trials at 14 leading research institutions across the country.
[124]
Nir Barzilai: “Positive Evidence for Metformin is Mounting” - Lifespan.io
Aug 12, 2025 · To summarize, you're still bullish on metformin. This brings us to the TAME trial, which was designed to answer questions about delaying aging ...
[125]
Gene Editing: PRF I The Progeria Research Foundation
Aug 8, 2025 · Base editing therapy uses CRISPR technology to target and correct a specific DNA base (or “letter”) in the genetic code. Because Progeria is ...
[126]
A Disease That Makes Children Age Rapidly Gets Closer to a Cure
Jul 24, 2024 · A cure for an ultrarare disease, progeria, could be on the horizon. The disease speeds up aging in children and dramatically shortens their lives.Missing: models | Show results with:models
[127]
CRISPR–Cas9 screens reveal regulators of ageing in neural stem ...
Oct 2, 2024 · Here we develop in vitro and in vivo high-throughput CRISPR–Cas9 screening platforms to systematically uncover gene knockouts that boost NSC activation in old ...
[128]
Cell-based regenerative and rejuvenation strategies for treating ...
Apr 6, 2025 · These strategies aim to mitigate the effects of cellular senescence by (1) rejuvenating existing cells to restore youthful function, (2) ...
[129]
Recent progress in stem cell and immune cell-based interventions ...
This review systematically examines current understanding of aging mechanisms, recent advancements in stem cell/immune cell technologies, and their clinical ...
[130]
Recent clinical trials with stem cells to slow or reverse normal aging ...
Apr 6, 2023 · Aging is associated with a decline in the regenerative potential of stem cells. In recent years, several clinical trials have been launched ...
[131]
Rejuvenated Autologous Adult Stem Cells: Emerging Front Runners ...
This review delves into our current biological insights into cellular rejuvenation and provides an overview of both pre-clinical and clinical experiences with ...
[132]
Transient rapamycin treatment can increase lifespan and ...
Aug 23, 2016 · Here we show that 3 months of rapamycin treatment is sufficient to increase life expectancy by up to 60% and improve measures of healthspan in middle-aged mice.Transient Rapamycin... · Rapamycin Changes The... · Article And Author...Missing: trials | Show results with:trials
[133]
About-face on the metabolic side effects of rapamycin - PMC - NIH
Feb 14, 2015 · Primary amongst these are metabolic defects that include hyperglycemia, hyperlipidemia, insulin resistance and increased incidence of new-onset type 2 diabetes.Missing: trials | Show results with:trials
[134]
Rapamycin in aging and disease: maximizing efficacy while ...
Jul 19, 2016 · Patients taking rapamycins to prevent organ transplant rejection have presented with adverse effects including stomatitis, thrombocytopenia, ...
[135]
Rapamycin for longevity: the pros, the cons, and future perspectives
Jun 19, 2025 · The recently published PEARL trial demonstrated that low-dose intermittent rapamycin was well tolerated over 1 year and resulted in modest ...
[136]
What is the clinical evidence to support off-label rapamycin therapy ...
Aug 7, 2025 · Thus, while promising, this study does not constitute firm evidence that rapamycin can extend healthspan or lifespan in humans. Trials of ...
[137]
Compression of morbidity by interventions that steepen the survival ...
Apr 8, 2025 · Longevity research aims to extend the healthspan while minimizing the duration of disability and morbidity, known as the sickspan.
[138]
Mixed evidence for the compression of morbidity hypothesis for ...
Dec 18, 2020 · The aim of this study was to conduct a systematic review of the literature to synthesize existing evidence on the effect of smoking status on ...Abstract · Introduction · Methods · Discussion
[139]
Are We Adding Pain-Free Years to Life? A Test of Compression ...
Jun 15, 2024 · This study uses health expectancy methods and tests an expansion versus compression of morbidity with respect to pain.
[140]
The economic value of targeting aging | Nature Aging
Jul 5, 2021 · We show that a slowdown in aging that increases life expectancy by 1 year is worth US$38 trillion, and by 10 years, US$367 trillion.
[141]
Are 'Biological Age' Tests Dangerously Misleading? - StudyFinds
Jun 10, 2025 · Results. The attempt to build an aging clock based on truly random methylation drift largely failed, showing only a 0.38 correlation with age.
[142]
2025 NIH Alzheimer's Disease and Related Dementias Research ...
Sep 8, 2025 · An estimated 7.1 million Americans are currently living with symptoms of Alzheimer's, and it is predicted that more than 13.9 million will be ...Missing: projections | Show results with:projections
[143]
01/17/2025: Study: Dementia cases to double in U.S. by 2060 | News
Jan 17, 2025 · New cases of dementia will double by 2060, when 1 million US adults are projected to develop the condition each year, according to a new study published this ...
[144]
The 2024 Facts & Figures report also shows the latest national & state
Mar 20, 2024 · 70% of dementia caregivers report that coordinating care is stressful. 60% of health care workers surveyed believe the U.S. health care system ...
[145]
Prevalence of depression, anxiety, burden, burnout, and stress in ...
Moreover, approximately one in five caregivers is estimated to be at risk of experiencing burnout, a syndrome characterised by emotional exhaustion, ...
[146]
Deprescribing - UpToDate
Sep 10, 2025 · Common goals for deprescribing include reducing overall medication burden, reducing the risk of specific geriatric syndromes such as falls and ...
[147]
Survey Finds that 82% of Older Adults are Dissatisfied with Health ...
Survey Finds that 82% of Older Adults are Dissatisfied with Health Care System. Sep 18, 2024. A survey released by Age Wave and The John A. Hartford ...Missing: elderly | Show results with:elderly
[148]
Healthcare on the brink: navigating the challenges of an aging ...
Apr 6, 2024 · This paper aims to spark dialogue and collaboration among healthcare stakeholders and inspire action to meet the needs of the aging population.<|separator|>
[149]
FAQs on Medicare Financing and Trust Fund Solvency - KFF
May 29, 2024 · In the 2024 Medicare Trustees report, the trustees project that reserves in the Part A trust fund will be depleted in 2036, 12 years from now.
[150]
[PDF] 2023 Medicare Trustees Report - CMS
Mar 31, 2023 · This is the 2023 annual report of the Boards of Trustees for the Federal Hospital Insurance and Federal Supplementary Medical Insurance Trust ...
[151]
Population ageing and government revenue - OECD
Population ageing is expected to result in significantly higher government spending in many OECD countries in the coming decades. This paper sheds light on ...
[152]
Old-age dependency ratio - OECD
Old-age dependency ratio is the number of individuals aged 65 or older per 100 people of working age, defined as those aged between 20 to 64 years old.<|separator|>
[153]
Confronting the consequences of a new demographic reality
Jan 15, 2025 · Falling fertility rates shift the demographic balance toward youth scarcity and more older people, who are dependent on a shrinking working-age population.
[154]
https://www.oecd.org/content/dam/oecd/en/publications/reports/2025/10/ageing-populations-their-fiscal-implications-and-policy-responses_be4bd619/6aec03b3-en.pdf
[155]
Artificial Intelligence (AI) and Robotics in Elderly Healthcare
Aug 3, 2023 · This review article examines the applications of AI and robotics in elderly care, focusing on their role in promoting independence, monitoring health, helping, ...
[156]
Modern Biological Theories of Aging - PMC - NIH
Modern biological theories of aging in humans fall into two main categories: programmed and damage or error theories. The programmed theories imply that aging ...
[157]
The oxidative damage theory of aging - ScienceDirect.com
The proposal suggests that aging is caused by accumulation of free radical mediated oxidative damage to various biological molecules in tissue cells. The ...
[158]
The oxidative stress theory of aging: embattled or invincible ... - NIH
The second theory is based upon the hypothesis that accumulation of oxidative damage is responsible for the progressive functional deterioration with ...
[159]
The disposable soma theory of aging in reverse | Cell Research
Nov 5, 2013 · These ideas were formalized by Thomas Kirkwood in the disposable soma theory of aging. For the last several decades the aging research community ...
[160]
Evolutionary and mechanistic theories of aging - PubMed
We describe the development of the general evolutionary theory, along with the mutation accumulation, antagonistic pleiotropy, and disposable soma versions of ...
[161]
Successful Aging and Its Discontents: A Systematic Review of the ...
The purpose of this study was to analyze the range of critiques of successful aging models and the suggestions for improvement as expressed in the social ...
[162]
Strategies for Engineered Negligible Senescence
About 10 years ago, Aubrey de Grey proposed the SENS approach with the goal of curing aging (de Grey et al., 2002a; de Grey, 2003; de Grey and Rae, 2008).
[163]
Resistance to debate on how to postpone ageing is delaying ... - NIH
Conversely, perhaps the SENS approach is the more promising, and if so it will eventually attract the funding necessary to realize it. That funding will not be ...
[164]
Wake-Up Call | Science | AAAS
A software engineer is the last person you'd expect to see dissecting the biology of aging. But Aubrey de Grey's radical views have stirred up debate.
[165]
The Cost of End-of-Life Care | Circulation - AHA Journals
Mar 1, 2009 · Care near the end of life consumes a disproportionate share of costs and is a logical target for efforts to promote value in health care.Disease Severity And... · Comparing Hospitals · Aha/acc Standards For...
[166]
Association of Wealth With Longevity in US Adults at Midlife
Jul 23, 2021 · In contrast to most previous studies that examined associations between socioeconomic position and longevity using between-person analytic ...
[167]
(PDF) Predicting Longevity Market Dynamics: Who Benefits from Life ...
Jul 4, 2025 · Abstract. This paper examines market segmentation patterns in longevity technologies and analyzes benefit distribution across demographic and ...<|separator|>
[168]
Wealth Redistribution to Extend Longevity in the US - JAMA Network
Jan 29, 2024 · In this study, we explore the association between wealth inequality and longevity in the US and model the potential increases in longevity ...Missing: trials | Show results with:trials
[169]
Incidence and Prevalence of Reported Euthanasia Cases in ... - NIH
Apr 23, 2025 · The empirical slippery slope from voluntary to non-voluntary euthanasia. ... Euthanasia in Belgium and the Netherlands: on a slippery slope?
[170]
Trends in Euthanasia Among Patients with Psychiatric Disorders ...
Jan 10, 2025 · Empirical evidence demonstrates no dramatic increase in euthanasia for non-terminal conditions between 2003 and 2023: psychiatric disorders and ...<|separator|>
[171]
Assisted Dying and the Slippery Slope Argument - JAMA Network
Apr 23, 2025 · A lack of empirical evidence for the slippery slope argument demonstrated by the report of Wels and Hamarat3 confirms extended evidence from ...
[172]
The Empirical Slippery Slope from Voluntary to Non ... - Sage Journals
(“The Netherlands has moved from assisted suicide to euthanasia, from euthanasia for the terminally ill to euthanasia for the chronically ill, from euthanasia ...Missing: statistics outcomes
[173]
Incidence, duration and cost of futile treatment in end-of-life hospital ...
The incidence rate of futile treatment in end-of-life admissions was 12.1% across the three study hospitals (range 6.0%–19.6%).
[174]
Is Futile Care in the Injured Elderly an Important Target for Cost ...
This study proposes a definition of futile care and quantifies its cost in injured elders. This was a retrospective study of Medicare patients with an ICD-9 ...Missing: suffering peer-
[175]
A systematic review defining non-beneficial and inappropriate end ...
Nov 9, 2022 · “Inappropriate” end-of-life care was defined by accounting for patient preferences, protecting their wishes and even those of the family and ...
[176]
The quest for genetic determinants of human longevity: challenges ...
Twin studies have consistently found that for cohorts born around 100 years ago, approximately 25% of the variation in lifespan is caused by genetic differences ...
[177]
A meta-analysis of genome-wide association studies identifies ...
Aug 14, 2019 · Based on twin studies, the heritability of human lifespan has been estimated to be ~25%, although this estimate differs among studies. On ...
[178]
a population-based study of 2872 Danish twin pairs born 1870-1900
The heritability of longevity was estimated to be 0.26 for males and 0.23 for females. The small sex-difference was caused by a greater impact of non-shared ...
[179]
The effect of genetic factors for longevity: a comparison of identical ...
Conclusions: Over the total age range examined, a maximum of around one third of the variance in longevity is attributable to genetic factors, and almost all ...
[180]
No Consistent Evidence that Ageism Is Linked to Biological Aging ...
Jan 10, 2025 · We found no consistent evidence linking ageism to biological aging status. Further research should investigate why.Missing: decline | Show results with:decline
[181]
No Consistent Evidence that Ageism Is Linked to Biological Aging ...
Aug 6, 2025 · While discrimination has often been shown to negatively impact health, whether ageism might accelerate biological aging itself is unclear.
[182]
Historical demography and longevity genetics: Back to the future
Historical demographic data containing deep genealogical information may help in estimating the best definition and heritability for longevity.Missing: foundations | Show results with:foundations
[183]
The Legal Issues: Anti-Aging Quackery: Human Growth Hormone ...
Federal law states that distributing or administering human growth hormone for anti-aging or age-related problems is illegal.Missing: unverified | Show results with:unverified<|separator|>
[184]
"Anti-Aging" Products Pose Potential for Physical and Economic Harm
Health Products for Seniors: "Anti-Aging" Products Pose Potential for Physical and Economic Harm (07-SEP-01, GAO-01-1129). Dietary supplements marketed as ...Missing: unverified | Show results with:unverified