Disparities in the pace of biological aging among midlife adults of the same chronological age have implications for future frailty risk and policy.
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ABSTRACT:
SUBMITTER: Elliott ML
PROVIDER: S-EPMC8009092 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The ability to control one's own emotions, thoughts, and behaviors in early life predicts a range of positive outcomes in later life, including longevity. Does it also predict how well people age? We studied the association between self-control and midlife aging in a population-representative cohort of children followed from birth to age 45 y, the Dunedin Study. We measured children's self-control across their first decade of life using a multi-occasion/multi-informant strategy. We measured their pace of aging and aging preparedness in midlife using measures derived from biological and physiological assessments, structural brain-imaging scans, observer ratings, self-reports, informant reports, and administrative records. As adults, children with better self-control aged more slowly in their bodies and showed fewer signs of aging in their brains. By midlife, these children were also better equipped to manage a range of later-life health, financial, and social demands. Associations with children's self-control could be separated from their social class origins and intelligence, indicating that self-control might be an active ingredient in healthy aging. Children also shifted naturally in their level of self-control across adult life, suggesting the possibility that self-control may be a malleable target for intervention. Furthermore, individuals' self-control in adulthood was associated with their aging outcomes after accounting for their self-control in childhood, indicating that midlife might offer another window of opportunity to promote healthy aging.
| S-EPMC7826388 | biostudies-literature
Project description:ObjectivesChildhood caries is associated with poorer self-rated general health in adulthood, but it remains unclear whether that holds for physical health and aging. The aim of this study was to identify whether age-5 caries is associated with (a) biomarkers for poor physical health, and (b) the pace of aging (PoA) by age 45 years.MethodsParticipants are members of the Dunedin Multidisciplinary Health and Development Study birth cohort. At age 45, 94.1% (n = 938) of those still alive took part. Data on age-5 caries experience and age-45 health biomarkers were collected. The PoA captures age-related decline across the cardiovascular, metabolic, renal, immune, dental and pulmonary systems from age 26 to 45 years. We used (a) generalized estimating equations to examine associations between age-5 caries and poor physical health by age 45 years, and (b) ordinary least squares regression to examine whether age-5 caries was associated with the PoA. Analyses adjusted for sex, perinatal health, childhood SES and childhood IQ.ResultsHigh caries experience at age-5 was associated with higher risk for some metabolic abnormalities, including BMI ≥30, high waist circumference, and high serum leptin. Those with high caries experience at age-5 were aging at a faster rate by age 45 years than those who had been caries-free.ConclusionsOral health is essential for wellbeing. Poor oral health can be an early signal of a trajectory towards poor health in adulthood. Management for both conditions should be better-integrated; and integrated population-level prevention strategies should be foundational to any health system.
| S-EPMC10919959 | biostudies-literature
Project description:ContextUnderstanding the menopause association with body weight is important because excess weight increases risk for stroke, incident cardiovascular disease, cardiovascular mortality, and all-cause mortality among the middle-aged.ObjectiveThe objective of this study was to examine chronological age and ovarian age and consider how these could influence body size and composition in midlife women.Design and settingThe Study of Women's Health Across the Nation is a longitudinal, community-based study. This report uses data from the Michigan Study of Women's Health Across the Nation site.ParticipantsParticipants were 543 premenopausal or early perimenopausal African-American and Caucasian women aged 42-52 yr at baseline examination.Main outcome measuresWaist circumference, fat mass and skeletal muscle mass, from bioelectrical impedance, were assessed in seven annual serial measures. Annual FSH values were assayed by ELISA. The final menstrual period was defined retrospectively after 12 months of amenorrhea.ResultsThere was an absolute cumulative 6-yr increase in fat mass of 3.4 kg and a 6-yr decrease in skeletal muscle mass of approximately 0.23 kg. There was an absolute cumulative 6-yr increase of approximately 5.7 cm in waist circumference. The (log)FSH change was positively correlated with (log)(fat mass) change. Waist circumference increased over the time period, but 1 yr after final menstrual period, the rate of increase slowed. Fat mass continued to increase with no change in rate.ConclusionsBoth time (chronological aging) and ovarian aging contributed to substantial changes in body composition (fat and skeletal muscle mass) and waist circumference. These changes have important ramifications for establishing a metabolic environment that can be healthy or unhealthy.
| S-EPMC2714766 | biostudies-literature
Project description:Epigenetic alterations are a hallmark of aging and age-related diseases. Computational models using DNA methylation data can create "epigenetic clocks" which are proposed to reflect "biological" aging. Thus, it is important to understand the relationship between predictive clock sites and aging biology. To do this, we examined over 450,000 methylation sites from 9,699 samples. We found ~20% of the measured genomic cytosines can be used to make many different epigenetic clocks whose age prediction performance surpasses that of telomere length. Of these predictive sites, the average methylation change over a lifetime was small (~1.5%) and these sites were under-represented in canonical regions of epigenetic regulation. There was only a weak association between "accelerated" epigenetic aging and disease. We also compare tissue-specific and pan-tissue clock performance. This is critical to applying clocks both to new sample sets in basic research, as well as understanding if clinically available tissues will be feasible samples to evaluate "epigenetic aging" in unavailable tissues (e.g., brain). Despite the reproducible and accurate age predictions from DNA methylation data, these findings suggest they may have limited utility as currently designed in understanding the molecular biology of aging and may not be suitable as surrogate endpoints in studies of anti-aging interventions. Purpose-built clocks for specific tissues age ranges or phenotypes may perform better for their specific purpose. However, if purpose-built clocks are necessary for meaningful predictions, then the utility of clocks and their application in the field needs to be considered in that context.
| S-EPMC8590098 | biostudies-literature
Project description:IntroductionWe tested the hypothesis that healthy diet protects against dementia because it slows the pace of biological aging.MethodsWe analyzed Framingham Offspring Cohort data (≥60y). We measured healthy diet using the Dietary Guideline for Americans (DGA, 3 visits 1991-2008), pace of aging using the DunedinPACE epigenetic clock (2005-2008), and incident dementia and mortality using records (compiled 2005-2018).ResultsOf n=1,525 included participants (mean age 69.7, 54% female), n=129 developed dementia and n=432 died over follow-up. Greater DGA adherence was associated with slower DunedinPACE and reduced risks for dementia and mortality. Slower DunedinPACE was associated with reduced risks for dementia and mortality. Slower DunedinPACE accounted for 15% of the DGA association with dementia and 39% of the DGA association with mortality.DiscussionFindings suggest that slower pace of aging mediates part of the relationship of healthy diet with reduced dementia risk. Monitoring pace of aging may inform dementia prevention.
| S-EPMC10312831 | biostudies-literature
Project description:Aging is the main risk factor for cardiovascular diseases. In humans, cardiac aging remains poorly characterized. Most studies are based on chronological age (CA) and disregard biological age (BA), the actual physiological age (result of the aging rate on the organ structure and function), thus yielding potentially imperfect outcomes. Deciphering the molecular basis of ventricular aging, especially by BA, could lead to major progresses in cardiac research. We aim to describe the transcriptome dynamics of the aging left ventricle (LV) in humans according to both CA and BA and characterize the contribution of microRNAs, key transcriptional regulators. BA is measured using two CA-associated transcriptional markers: CDKN2A expression, a cell senescence marker, and apparent age (AppAge), a highly complex transcriptional index. Bioinformatics analysis of 132 LV samples shows that CDKN2A expression and AppAge represent transcriptomic changes better than CA. Both BA markers are biologically validated in relation to an aging phenotype associated with heart dysfunction, the amount of cardiac fibrosis. BA-based analyses uncover depleted cardiac-specific processes, among other relevant functions, that are undetected by CA. Twenty BA-related microRNAs are identified, and two of them highly heart-enriched that are present in plasma. We describe a microRNA-gene regulatory network related to cardiac processes that are partially validated in vitro and in LV samples from living donors. We prove the higher sensitivity of BA over CA to explain transcriptomic changes in the aging myocardium and report novel molecular insights into human LV biological aging. Our results can find application in future therapeutic and biomarker research.
| S-EPMC8282276 | biostudies-literature
Project description:Objective: Treatment of glioblastoma in elderly patients is particularly challenging due to their general condition and comorbidities. Treatment decisions are often based on chronological age. Frailty screening tests promise an assessment tool to stratify geriatric patients and identify those at risk for an unfavorable outcome. This study aims to evaluate the impact of age and frailty on the surgical outcome and overall survival in geriatric patients with glioblastoma. Methods: Data acquisition was conducted as a single-center retrospective analysis. From January 1st 2015, and December 31st 2019, 104 glioblastoma patients over 70 years of age were included in our study. Demographic data, tumor size, Karnofsky Performance Score (KPS), and Eastern Cooperative Oncology Group Performance Status (ECOG), as well as treatment modalities, were assessed. The Geriatric 8 health status screening tool (G8) and Groningen Frailty Index (GFI) were compiled pre-and postoperatively. Results: The mean patient age was 76.86 ± 4.11 years. Forty-nine (47%) patients were female, 55 (53%) male. Sixty-seven patients underwent microsurgical tumor resection, 37 received tumor biopsy alone. Mean G8 on admission was 12.4 ± 2.0, mean GFI 5.0 ± 2.5. In our cohort, frailty was independent of patient age, tumor size, or localization. Frailty, defined by G8 and GFI, is associated with shorter overall survival (G8: p = 0.0035; GFI: p = 0.0136) and higher numbers of surgical complications (G8: p = 0.0326; GFI: p = 0.0388). Frailer patients are more likely to receive best supportive care (p = 0.004). Nevertheless, frailty did not affect adjuvant treatment decision-making toward either single-use of chemo- or radiation therapy, stratified treatment, or concomitant therapy. The surgical decision on the extent of resection was not based on pre-operative frailty. Conclusion: In our study, frailty is a predictor of poorer surgical outcomes, post-operative complications, and impaired overall survival independent of chronological age. Frailty screening tests offer an additional assessment tool to stratify geriatric patients with glioblastoma and identify those at risk for a detrimental outcome and thus should be implemented in therapeutic decision making.
| S-EPMC8669893 | biostudies-literature
Project description:BackgroundIndividuals who are socioeconomically disadvantaged are at increased risk for aging-related diseases and perform less well on tests of cognitive function. The weathering hypothesis proposes that these disparities in physical and cognitive health arise from an acceleration of biological processes of aging. Theories of how life adversity is biologically embedded identify epigenetic alterations, including DNA methylation (DNAm), as a mechanistic interface between the environment and health. Consistent with the weathering hypothesis and theories of biological embedding, recently developed DNAm algorithms have revealed profiles reflective of more advanced aging and lower cognitive function among socioeconomically-at-risk groups. These DNAm algorithms were developed using blood-DNA, but social and behavioral science research commonly collect saliva or cheek-swab DNA. This discrepancy is a potential barrier to research to elucidate mechanisms through which socioeconomic disadvantage affects aging and cognition. We therefore tested if social gradients observed in blood DNAm measures could be reproduced using buccal-cell DNA obtained from cheek swabs.ResultsWe analyzed three DNAm measures of biological aging and one DNAm measure of cognitive performance, all of which showed socioeconomic gradients in previous studies: the PhenoAge and GrimAge DNAm clocks, DunedinPACE, and Epigenetic-g. We first computed blood-buccal cross-tissue correlations in n = 21 adults (GEO111165). Cross-tissue correlations were low-to-moderate (r = .25 to r = .48). We next conducted analyses of socioeconomic gradients using buccal DNAm data from SOEP-G (n = 1128, 57% female; age mean = 42 yrs, SD = 21.56, range 0-72). Associations of socioeconomic status with DNAm measures of aging were in the expected direction, but were smaller as compared to reports from blood DNAm datasets (r = - .08 to r = - .13).ConclusionsOur findings are consistent with the hypothesis that socioeconomic disadvantage is associated with DNAm indicators of worse physical health. However, relatively low cross-tissue correlations and attenuated effect sizes for socioeconomic gradients in buccal DNAm compared with reports from analysis of blood DNAm suggest that in order to take full advantage of buccal DNA samples, DNAm algorithms customized to buccal DNAm are needed.
| S-EPMC10148429 | biostudies-literature
Project description:Discrimination is a social determinant of health and health disparities for which the biological mechanisms remain poorly understood. This study investigated the hypothesis that discrimination contributes to poor health outcomes by accelerating biological processes of aging. We analyzed survey and blood DNA methylation data from the Midlife in the United States (MIDUS) study (N = 1967). We used linear regression analysis to test associations of everyday, major, and workplace discrimination with biological aging measured by the DunedinPACE, PhenoAge, and GrimAge2 epigenetic clocks. MIDUS participants who reported more discrimination tended to exhibit a faster pace of aging and older biological age as compared to peers who reported less discrimination. Effect-sizes for associations tended to be larger for the DunedinPACE pace-of-aging clock (effect-size range r = 0.1-0.2) as compared with the PhenoAge and GrimAge2 biological-age clocks (effect-sizes r < 0.1) and for experiences of everyday and major discrimination as compared with workplace discrimination. Smoking status and body-mass index accounted for roughly half of observed association between discrimination and biological aging. Reports of discrimination were more strongly associated with accelerated biological aging among White as compared with Black participants, although Black participants reported more discrimination overall and tended to exhibit older biological age and faster biological aging. Findings support the hypothesis that experiences of interpersonal discrimination contribute to accelerated biological aging and suggest that structural and individual-level interventions to reduce discrimination and promote adaptive coping have potential to support healthy aging and build health equity.
| S-EPMC11315217 | biostudies-literature
Project description:BackgroundAdvanced age is the most important risk factor for atrial fibrillation (AF); however, the mechanism remains unknown. Telomeres, regions of DNA that shorten with cell division, are considered reliable markers of biological aging. We sought to examine the association between leukocyte telomere length (LTL) and incident AF in a large population-based cohort using direct LTL measurements and genetic data. To further explore our findings, we compared atrial cell telomere length and LTL in cardiac surgery patients.Methods and resultsMean LTL and the TERT rs2736100 single nucleotide polymorphism were assessed as predictors of incident AF in the Cardiovascular Health Study (CHS). Among the surgical patients, within subject comparison of atrial cell telomere length versus LTL was assessed. Among 1639 CHS participants, we observed no relationship between mean LTL and incident AF before and after adjustment for potential confounders (adjusted hazard ratio, 1.09; 95% confidence interval: 0.92-1.29; P=0.299); chronologic age remained strongly associated with AF in the same model. No association was observed between the TERT rs2736100 single nucleotide polymorphism and incident AF (adjusted hazard ratio: 0.95; 95% confidence interval: 0.88-1.04; P=0.265). In 35 cardiac surgery patients (26 with AF), atrial cell telomere length was longer than LTL (1.19 ± 0.20 versus 1.02 ± 0.25 [T/S ratio], P<0.001), a finding that remained consistent within the AF subgroup.ConclusionsOur study revealed no evidence of an association between LTL and incident AF and no evidence of relative atrial cell telomere shortening in AF. Chronological aging independent of biological markers of aging is the primary risk factor for AF.
| S-EPMC4294941 | biostudies-literature