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Results for “Biological age”

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At least 19 recordsLinked to original sources
PubMed2026

Early life sugar rationing and ageing related diseases, biological ageing and mortality.

Early-life nutrition may influence lifelong ageing, yet human evidence is scarce. Using Britain's postwar sugar rationing as a natural experiment, we examine its long-term effects in 64,809 United Kingdom Biobank participants. Exposure to sugar rationing during the first 1,000 days of life is associated with a 9% lower incidence of hallmark-related disease, with a hazard ratio of 0.91 and a 95% confidence interval of 0.88-0.94, and a 19% lower risk of all-cause mortality, with a hazard ratio of 0.81 and a 95% confidence interval of 0.69-0.93. Mediation analysis indicates that the survival association is statistically mediated, by approximately 60%, through differences in incident hallmark-related disease. Rationed individuals show 1.0-1.2-year younger biological ages across multiple clocks and lower organ ages, particularly in the lung, heart, and liver. Proteomic profiling identifies 47 altered proteins, with enrichment of adenosine monophosphate-activated protein kinase and longevity pathways and suppression of mechanistic target of rapamycin signaling. These findings are consistent with international recommendations to limit free or added sugars from the World Health Organization, United States Dietary Guidelines, and American Heart Association, and may inform policy discussions related to sugar taxation and infant food and marketing policies under the United Nations 2030 Agenda.

Humans↗
PubMed1992

[Research on aging: biological perspectives].

Aging is a part of the continuous process from conception to death and is strongly modulated by environmental factors throughout the lifespan. Variability in functional capacity between different organs and between individuals therefore increases with aging. This review will discuss two tissues of importance for the fitness of the aging human being: connective tissue and bone. Connective tissues become stiffer with age, which can be mitigated by physical exercise. The physical-chemical stability of collagen is a precise measure for the functional age of the organism. While in the aged, the healing (formation of connective tissue scar) of uncomplicated incisional wounds is slightly impaired, the healing of ischemic wounds is endangered. The clinical observation that "simple" wounds also heal less well in the aged might be due to the presence of diseases with ischemia and other pathologies. During normal aging bone loses mass, structural continuity, and strength. When pronounced, these changes cause osteopenia and osteoporotic fractures. The age-adjusted incidence of osteoporotic fractures is increasing on account of changes in our lifestyle. Preventive efforts, with increased physical activity as the main feature, must be implemented to alter this trend. Our knowledge of the mechanisms of aging is not yet sufficient to formulate a policy containing preventive measures enabling man to achieve his maximum biological lifespan with good physical health and a high quality of life. Multidisciplinary efforts by biologists, clinicians and epidemiologists are warranted to achieve this goal.

Aged↗
PubMed2026

Sex-specific biological aging clocks across organs and omics.

Sex differentially shapes aging, neurodevelopment and neurodegenerative diseases such as Alzheimer's disease (AD). However, most biological aging clocks (artificial intelligence-predicted age minus chronological age) were trained on sex-pooled samples and implicitly assume sex invariance.Here we developed 38 sex-specific biological aging clocks across 15 organ systems. We first demonstrate the importance of sex-stratified training for constructing sex-specific healthy normative references and then reveal marked divergence between female and male clocks. Key genetic parameters and Mendelian randomization results indicate that organ-specific aging liability and its relationships to cardiometabolic, endocrine and mental traits are configured differently in females and males. Proteomic analyses identify distinct, organ-resolved synaptic, immune, vascular and metabolic networks that differentially track female and male biological aging. In longitudinal survival analyses, sex-specific clocks predict whole-body systemic diseases and all-cause mortality in a sex-dependent and organ-dependent manner. Further analyses reveal sex-dependent associations between the brain aging clock and cognitive decline trajectory during a preclinical AD clinical trial. Sex-stratified clocks may offer distinct value by defining biological age against sex-appropriate normative references and revealing sex-dependent genetic, molecular and clinical signatures that pooled models may obscure. Meanwhile, sex-pooled and sex-interaction approaches remain valuable, as human aging and disease also share fundamental biological similarities between females and males. Together, these findings reveal sex-specific biological aging signatures in aging, AD and systemic health, highlighting the need for explicitly sex-stratified modeling approaches.

Journal Article↗
PubMed1975

Current theories of biological aging.

Several lines of evidence have led to the notion that biological aging occurs as a result of changes in the information-containing molecules either at the genetic or epigenetic level. The error theory, the redundant message theory, the codon restriction theory, and the transcriptional event theory represent the major current conceptualizations of biological aging as held by most gerontologists. The finding that cultured normal human and animal cells undergo a finite number of population doublings in vitro has provided new insights into age changes at the cellular level. The number of mitotic events that cultured normal animal cells can undergo appears to be inversely related to the age of the donor. A direct proportionality exists, however, between the mean maximum life-span of a species and the number of population doublings that their cultured embryonic cells will undergo. The several biochemical decrements known to occur prior to the cessation of mitotic activity in vitro are thought to herald those manifestations of senescence seen in the whole animal. Yet to be explained is how those cell classes such as the germ plasm and continuously propagable cancer cells escape from the inevitability of biological aging.

Aging↗
PubMed1976

[Assessment of the biological age in the animal-experiment (author's transl)].

Experimental investigations of internal and external factors presumably influencing the aging process require an objective assessment of the biological age or vitality respectively by means of as many age parameters as possible. Using the rat, a valuable test animal in experimental gerontology, whose life expectancy of about 40 month allows longitudinal studies, a standard test programm for the estimation of the biological age has been developed. The age parameters used originate from investigations of 1. the tail tendon collagen, 2. the skin, 3. the aorta, 4. the ECG, 5. the lipofuscin content of brain and heart, 6. the tissue respiration of various organs, 7, the motor activity and 8. learning and memory. Using the above-mentioned age parameters a statistical measure for the biological age will be calculated by means of multivariate analysis and will allow the comparison of differeent age-and experimental-groups.

Aging↗
PubMed1979

[Degree of sexual maturation as an index of biological age].

Attempt was made to establish some characteristics of sexual maturation, depending upon chronologic and biologic age. A total of 1277 girls from 8 to 17 years of age in the city of Sofia are included in the study. There were no cases of precocious of considerably delayed pubertal development. Essential differences were found in the body dimensions, in connection with the increase in the degree of sexual maturation in one and the same chronologic age. The importance of biologic age for the individual approach to teen-agers girls and boys is emphasized.

Adolescent↗
PubMed1976

[Methodological problems in the determination of biological age].

It is reported on a new method of the establishment of the biological age. The test battery designed comprises 12 parameters, from which a so-called biological index can be calculated which on its part serves as basis for the establishment of biological age. The realisability of the methods is demonstrated by examinations carried out on 340 healthy persons. The method developed for the geriatric practice is regarded as supplementation of the general medical examination and for the clarification of certain, above all gerontologically orientated questions.

Aging↗
PubMed2026

Accelerated Biological Aging Increases the Risk of Head and Neck Cancer: Insights From Genetic Instruments of Epigenetic Clocks.

Epigenetic clocks are robust biomarkers of biological aging and have been associated with cancer susceptibility. However, the relationship between genetically predicted epigenetic age acceleration and head and neck cancer risk remains unclear. Using a large case-control study of 2189 head and neck squamous cell carcinoma (HNSCC) cases and 2189 age- and sex-matched controls, we investigated the associations between polygenic scores (PGSs) for multiple epigenetic clocks and HNSCC risk, and evaluated their potential causal roles using two-sample Mendelian randomization (MR). Genome-wide association study (GWAS)-identified single nucleotide polymorphisms (SNPs) associated with four epigenetic clocks (HannumAge, HorvathAge, GrimAge, and PhenoAge) were used to construct clock-specific PGSs. Logistic regression models were applied to assess associations between PGSs and HNSCC risk, while MR analyses, including inverse-variance weighted (IVW), weighted median, and MR-Egger methods, were used to infer potential causal relationships. Among the 48 epigenetic clock-associated SNPs, 12 showed nominal associations with HNSCC risk, and one variant (rs2275558 in PBX1) remained significant after Bonferroni correction (OR = 0.67, 95% CI: 0.60-0.76). PGSs for all four epigenetic clocks were higher in cases than in controls. In logistic regression analyses, each standard deviation increase in HannumAge PGS was associated with a 25% higher risk of HNSCC (OR = 1.25, 95% CI: 1.10-1.41), whereas HorvathAge, GrimAge, and PhenoAge PGSs showed weaker positive associations (ORs ranging from 1.06 to 1.10). Individuals in the highest PGS quartile for all four epigenetic clocks exhibiting 14%-25% higher risk than those in the lower three quartiles. MR analyses supported potential causal effects of genetically predicted HannumAge (IVW OR = 1.24 per SD increase, 95% CI: 1.09-1.42) and GrimAge (IVW OR = 1.23 per SD increase, 95% CI: 0.98-1.56) on HNSCC risk, with consistent estimates in weighted median analyses. Our results highlight biological aging as a potential etiologic mechanism for HNSCC and suggest that epigenetic clock-related genetic profiles may improve HNSCC risk stratification.

Humans↗
PubMed2026

An open benchmark and language models for AI in aging biology.

Over the past two decades, human aging has been characterized across DNA methylation, transcriptomic, proteomic, and clinical modalities, yet no benchmark evaluates whether AI systems can interpret these heterogeneous data types in the context of aging biology. We introduce LongevityBench, an open suite of 17 tasks spanning five biodata domains, and use it to assess 18 frontier AI systems from six developer teams. Despite recent advances in AI, no single model dominates all tasks, with omics-based age prediction being the hardest task regardless of scale. To test whether these gaps can be closed without frontier-scale resources, we fine-tuned a family of five multitask Longevity-LLMs on domain-specific aging data. The compact (0.6B-9B parameters) Longevity-LLMs matched or exceeded far larger frontier systems on LongevityBench, showing that general-purpose language models can be adapted to structured-omics tasks. We publicly release the benchmark, models, and Longevity Claw, an agentic research interface for aging researchers.

Aging↗
PubMed2026

Investigation of the Causal Association Between Biological Aging Indicators and Vascular Disease Through Two-Sample Mendelian Randomization Analysis.

ObjectiveThis study used two-sample Mendelian Randomization to investigate the causal link between multiple biological aging indicators and vascular disease.MethodsSummary genetic data was obtained from genome-wide association studies (GWAS) focusing on aging-related exposures and various vascular disease outcomes. The exposures included granulocyte proportions, PAI-1 (plasminogen activator inhibitor-1), telomere lengths, and the Frailty Index. The primary analysis employed the Inverse Variance Weighted (IVW) method to estimate causal relationships, supported by MR-Egger, weighted median, and weighted mode methods. Sensitivity analyses, including Cochran's Q test, MR-Egger regression, leave-one-out test, and the MR Pleiotropy Residual Sum and Outlier (MR-PRESSO) test, were conducted to evaluate heterogeneity and pleiotropy.ResultsThe analysis revealed distinct pathways after sensitivity adjustments. A higher genetically predicted Frailty Index was associated with an increased risk of abdominal aortic aneurysm (OR=2.5935, 95% CI: 1.3936-4.8268, P=0.0026, false discovery rate (FDR)=0.0475), atherosclerosis excluding cerebral and coronary sclerosis (OR=2.0262, 95% CI:1.5179-2.705, P=1.66×10-6, FDR=1×10-4), and arterial thromboembolic events (OR = 4.0306, 95% CI: 1.7133-9.4818, P = 0.0014, FDR = 0.0337). Conversely, longer telomere length demonstrated a strong, specific protective effect against abdominal aortic aneurysm (OR=0.5008, 95% CI:0.4111-0.6100, P=6.42×10-12, FDR=9.25×10-10), indicating that shorter telomere length is associated with an increased risk of AAA. Furthermore, a lower granulocyte proportion was causally linked to an increased risk of thoracic aortic aneurysm (OR=0.0181, 95% CI: 0.0014-0.2376, P=0.0023, FDR=0.0465).ConclusionThis study identifies three genetic pathways linking biological aging to vascular disease, offering new molecular targets for its prevention and treatment.

Humans↗
PubMed1975

Biological age, health, and health-risk indicators among 25-57-year-old men in two parts of Finland.

Biological age, health, and health-risk indicators were examined among 460 systematically chosen men, aged 25-57 years, in two parts of Finland. Morbidity rates and the prevalence of some health-risk indicators were higher and the standard of living lower in North Karelia than in South-West Finland. The index of biological age (IBA) did not show significant differences between the districts and did not correlate with health-risk indicators. People working in physically hard occupations (industrial and mining workers) were found to have more diseases and had higher IBA values than had workers in lighter occupations. The results suggest that both ageing and morbidity are regulated by occupational status and social conditions connected with it.

Adult↗
PubMed1976

Concerning the estimation of biological age.

The conditions which must be satisfied by an index of biological age are discussed, and a high correlation with chronological age is shown to be neither a necessary nor a sufficient condition to be satisfied by any such index.

Adult↗
PubMed1975

Biological age and habitual physical activity in relation to physical fitness in 12- and 13-year-old schoolboys.

PURPOSE: The purpose of this study was to investigate the relationship between biological age, habitual physical activity and anthropometrical and physiological characteristics in 12- and 13-year-old schoolboys (n = 70). METHODS: At the beginning and the end of the school year 1971/2 biological age was determined by measuring skeletal age from left hand X-ray photographs. Habitual physical activity was determined by questionnaire interview and pedometers. RESULTS: All anthropometrical characteristics showed significant correlations (P less than 0.05) with skeletal age except for bicipital and tricipital skinfolds. Out of 9 physical fitness tests handgrip was the only test that showed a significant correlation (0.52) with skeletal age. Pedometer scores gave significant negative correlations (P less than 0.05) with anthropometrical characteristics except for tricipital skinfold. The fitness tests bent arm hang, 12 min run walk, sit and reach and W-170 showed significant correlations (P less than 0.05) with pedometer scores.

Activities of Daily Living↗
PubMed2025

Genome-wide methylation biomarkers and biological aging in patients with bipolar disorder characterized for lithium response.

BACKGROUND: Epigenetic mechanisms might play a role in modulating susceptibility to bipolar disorder (BD) and response to lithium, the mainstay treatment for BD. Additionally, individuals with BD experience accelerated biological aging. METHODS: We compared blood DNA methylation profiles measured with EPIC v.2.0 arrays between patients with BD (33 lithium responders and 31 nonresponders) and nonpsychiatric controls (n = 32), as well as based on long-term lithium response. In addition, we compared cellular aging between these groups using epigenetic age, pace of aging, and, for the first time, transcriptional age acceleration based on bulk RNA sequencing in 93 patients and 56 controls. RESULTS: We identified 191 differentially methylated positions (DMPs) and 8 differentially methylated regions between patients with BD and controls, located in genes enriched for "Postsynaptic Density" (odds ratio = 6.81, p = 0.001). No DMP was significantly associated with lithium response after multiple testing correction. Patients showed a significantly higher biological age acceleration than controls based on two epigenetic clocks (GrimAge, Mann-Whitney U = 551, p = 0.0009; GrimAge2: U = 477, p = 9.0E-05) and pace of aging (DunedinPACE, t = 3.01, p = 0.003), but not on transcriptional age. While we observed no significant difference in epigenetic aging based on lithium response, lithium responders showed lower epigenetic acceleration using all clocks, with a trend observed using the PhenoAge clock (t = 1.97, p = 0.053). CONCLUSIONS: Our findings point to methylation patterns characterizing BD and support the hypothesis of accelerated cellular aging in BD.

Humans↗
PubMed2026

Genetic and epigenetic underpinnings of biological aging: a multi-omics study integrating Mendelian randomization, spatial transcriptomics, and drug target discovery.

Inflammaging represents a hallmark of biological aging, yet the causal inflammatory mediators driving multi-dimensional epigenetic aging and their effector genes remain poorly characterized at the genetic level. We developed a four-tier analytical framework integrating causal screening, multi-omics effector gene mapping, spatial transcriptomics, and drug target evaluation. Two-sample Mendelian randomization (MR) of 91 circulating inflammatory proteins against six aging phenotypes identified IL-12B, IFNG, and IL-2 as the most robust pro-aging mediators with consistent effects across independent outcomes. Using multi-omics summary-based MR (SMR) as the core analytical engine, we integrated four-layer whole-blood molecular QTL resources eQTL (eQTLGen, n = 31,684), sQTL (GTEx, n = 755), pQTL (INTERVAL + SCALLOP, n = 34,232), and mQTL (McRae et al., n = 1,980) - with GWAS summary statistics for four epigenetic age acceleration measures. At a stringent threshold (P_SMR < 1&#xd7;10&#x207b;&#xb9;&#xb2;), seven high-confidence effector genes were identified: NHLRC1, TPMT, SELP, and RIPPLY3 for IEAA; ZNF373A and PLDN for HannumAA; and EDARADD for PhenoAA. The chromosome 6p21 NHLRC1-TPMT locus, overwhelmingly driven by methylation QTL signals (-log&#x2081;&#x2080;P = 26.06), emerged as the dominant genetic node of epigenetic aging. Spatial projection via gsMap onto a mouse E16.5 embryo atlas (121,767 cells) revealed preferential enrichment in smooth muscle and lung, with EDARADD showing marked specificity in mucosal epithelium. Cross-database drug target mining classified TPMT and SELP as repurposable known targets and NHLRC1 as a high-priority novel druggable candidate. This study provides multi-omics convergent causal evidence for inflammation-driven epigenetic aging and delivers genetically anchored targets for precision anti-aging intervention.

Aging↗
PubMed1975

Assessment of biological age by multiple regression analysis.

In order to generate a reference value of aging, estimation of chronological age of healthy subjects was made by multiple regression analysis. It was shown that the estimated ages of hypertensive subjects by the formula used were significantly higher than their chronological ages. It was further observed that parameters representing various ability of movements might yield an alternative regression formula and that the accuracy in age estimation was improved with application of a second-order regression formula.

Accommodation, Ocular↗