Concurrent and enduring associations between married partners' shared beliefs and markers of aging.
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ABSTRACT:
SUBMITTER: Mejia ST
PROVIDER: S-EPMC8389359 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Purpose of the studyIndividual beliefs are known to be predictive of health. This study examines the co-construction of couple norms and links couples' shared beliefs about aging to future individuals' and couples' functional limitations.Design and methodsData from the 2008 and 2014 waves of the Health and Retirement Study (1,231 couples; age range = 51-90) were analyzed using latent variables that estimated shared and individual variance in beliefs about aging in 2008 and functional limitations at follow-up in 2014. Spouses' individual processes of physical activity and disease burden were modeled to contribute to couples' shared beliefs about aging and subsequent functional limitations. Models progressively controlled for indicators of partner selection, couples' shared health experiences, and similarities and differences in age.ResultsCouples' beliefs about aging predicted future functional limitations. The effect magnitude decreased but remained significant in all models. Physical activity predicted couples' future functional limitations but was largely explained by shared health experiences and similarities and differences in age for wives and husbands, respectively. Disease burden contributed to couples' shared beliefs about aging. Husbands' contributions were explained by partner selection, but wives' contributions remained significant in all models. The effect of couples' shared beliefs on change in couples' functional limitations was explained by couples' shared health experiences.ImplicationsBeliefs about aging and health occur within the context of close relationships and shared experiences. Knowledge of couples' beliefs and health is necessary to support their individual and collective efforts to age successfully together.
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Project description:Life span is a complex and multifactorial trait, which is shaped by genetic, epigenetic, environmental, and stochastic factors. The possibility that highly hypervariable short tandem repeats (STRs) associated with longevity has been largely explored by comparing the genotypic pools of long lived and younger individuals, but results so far have been contradictory. In view of these contradictory findings, the present study aims to investigate whether HUMTHO1 and HUMCSF1PO STRs, previously associated with longevity, exert a role as a modulator of life expectancy, as well as to assess the extent to which other autosomal STR markers are associated with human longevity in population from northern Spain. To that end, 21 autosomal microsatellite markers have been studied in 304 nonagenarian individuals (more than 90 years old) and 516 younger controls of European descent. Our results do not confirm the association found in previous studies between longevity and THO1 and CSF1PO loci. However, significant association between longevity and autosomal STR markers D12S391, D22S1045, and DS441 was observed. Even more, when we compared allelic frequency distribution of the 21 STR markers between cases and controls, we found that 6 out of the 21 STRs studied showed different allelic frequencies, thus suggesting that the genomic portrait of the human longevity is far complex and probably shaped by a high number of genomic loci.
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Project description:Alcohol use behaviors are highly heterogeneous, posing significant challenges to etiologic research of alcohol use disorder (AUD). Magnetic resonance imaging (MRI) provides intermediate endophenotypes in characterizing problem alcohol use and assessing the genetic architecture of addictive behavior. We used connectivity features derived from resting state functional MRI to subtype alcohol misuse (AM) behavior. With a machine learning pipeline of feature selection, dimension reduction, clustering, and classification we identified three AM biotypes-mild, comorbid, and moderate AM biotypes (MIA, COA, and MOA)-from a Human Connectome Project (HCP) discovery sample (194 drinkers). The three groups and controls (397 non-drinkers) demonstrated significant differences in alcohol use frequency during the heaviest 12-month drinking period (MOA > MIA; COA > non-drinkers) and were distinguished by connectivity features involving the frontal, parietal, subcortical and default mode networks. Further, COA relative to MIA, MOA and controls endorsed significantly higher scores in antisocial personality. A genetic association study identified that an alcohol use and antisocial behavior related variant rs16930842 from LINC01414 was significantly associated with COA. Using a replication HCP sample (28 drinkers and 46 non-drinkers), we found that subtyping helped in classifying AM from controls (area under the curve or AUC = 0.70, P < 0.005) in comparison to classifiers without subtyping (AUC = 0.60, not significant) and successfully reproduced the genetic association. Together, the results suggest functional connectivities as important features in classifying AM subgroups and the utility of reducing the heterogeneity in connectivity features among AM subgroups in advancing the research of etiological neural markers of AUD.
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Project description:Partners resemble each other in health behaviors and outcomes such as alcohol use, smoking, physical activity, and obesity. While this is consistent with social contagion theory suggesting partner influence, it is notoriously difficult to establish causality because of assortative mating and contextual confounding. We offer a novel approach to studying social contagion in health in long-term partnerships by combining genetic data of both partners in married/cohabiting couples with longitudinal data on their health behaviors and outcomes. We examine the influence of the partner's genetic predisposition for three health outcomes and behaviors (BMI, smoking, and drinking) among married/cohabiting couples. We use longitudinal data from the Health and Retirement Study and the English Longitudinal Study of Ageing with data on health outcomes and genotypes for both partners. Results show that changes over time in BMI, smoking, and drinking depend on the partner's genetic predispositions to these traits. These findings underline the importance of people's social surroundings for their health and highlight the potential of targeting health interventions at couples.
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Project description:BackgroundChildhood maltreatment is one of the strongest predictors of adulthood depression and alterations to circulating levels of inflammatory markers is one putative mechanism mediating risk or resilience.AimsTo determine the effects of childhood maltreatment on circulating levels of 41 inflammatory markers in healthy individuals and those with a major depressive disorder (MDD) diagnosis.MethodWe investigated the association of childhood maltreatment with levels of 41 inflammatory markers in two groups, 164 patients with MDD and 301 controls, using multiplex electrochemiluminescence methods applied to blood serum.ResultsChildhood maltreatment was not associated with altered inflammatory markers in either group after multiple testing correction. Body mass index (BMI) exerted strong effects on interleukin-6 and C-reactive protein levels in those with MDD.ConclusionsChildhood maltreatment did not exert effects on inflammatory marker levels in either the participants with MDD or the control group in our study. Our results instead highlight the more pertinent influence of BMI.Declaration of interestD.A.C. and H.W. work for Eli Lilly Inc. R.N. has received speaker fees from Sunovion, Jansen and Lundbeck. G.B. has received consultancy fees and funding from Eli Lilly. R.H.M.-W. has received consultancy fees or has a financial relationship with AstraZeneca, Bristol-Myers Squibb, Cyberonics, Eli Lilly, Ferrer, Janssen-Cilag, Lundbeck, MyTomorrows, Otsuka, Pfizer, Pulse, Roche, Servier, SPIMACO and Sunovian. I.M.A. has received consultancy fees or has a financial relationship with Alkermes, Lundbeck, Lundbeck/Otsuka, and Servier. S.W. has sat on an advisory board for Sunovion, Allergan and has received speaker fees from Astra Zeneca. A.H.Y. has received honoraria for speaking from Astra Zeneca, Lundbeck, Eli Lilly, Sunovion; honoraria for consulting from Allergan, Livanova and Lundbeck, Sunovion, Janssen; and research grant support from Janssen. A.J.C. has received honoraria for speaking from Astra Zeneca, honoraria for consulting with Allergan, Livanova and Lundbeck and research grant support from Lundbeck.
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Project description:BackgroundAnticoagulation control with vitamin-K antagonists (VKAs) in patients with atrial fibrillation (AF) or venous thromboembolism (VTE) can be measured using time in therapeutic range (TTR), where TTR >65% is considered good and low TTR may be associated with low adherence.MethodsThis cross-sectional observational study compared illness beliefs, treatment beliefs, and treatment satisfaction of patients with TTR >75% and TTR <50% using validated tools to determine their association with TTR. Adults requiring chronic VKA therapy were recruited from 2 hospital anticoagulation clinics in London, UK.Results311 patients with TTR >75% and 214 with TTR <50% were recruited. TTR >75% patients had been taking warfarin on average over 2 years longer than TTR <50% patients (P < .001). Statistically significant differences in beliefs were found in all subscales other than in treatment control, general harm, and general overuse. Cluster analysis determined there were 4 distinct clusters of beliefs among patients. Multivariate binary logistic regression found VTE patients were least likely to have poor TTR (OR = 0.49; 95% CI 0.29, 0.77). Patients in the "cautious of therapy and fearful of illness" cluster were most likely to have low TTR (OR = 4.75; 95% CI 2.75, 8.77).ConclusionIllness perceptions, medication beliefs and treatment satisfaction were associated with INR control. VTE patients and those who were accepting of both illness and treatment were most likely to have optimal INR control.
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Project description:The stem cell differentiation paradigm is based on the progression of cells through generations of daughter cells that eventually become restricted and committed to one lineage resulting in fully differentiated cells. Herein, we report on the differentiation of adult human mesenchymal stem cells (hMSCs) towards adipogenic and osteogenic lineages using established protocols. Lineage specific geneswere evaluated by quantitative real-time PCR relative to two reference genes. The expression of osteoblast-associated genes (alkaline phosphatase, osteopontin, and osteocalcin)was detected in hMSCs that underwent adipogenesis. When normalized, the expression of adipocyte marker genes (adiponectin, fatty acid binding protein P4, and leptin) increasedin a time-dependent manner during adipogenic induction. Adiponectin and leptin were also detected in osteoblast-induced cells. Lipid vacuoles that represent the adipocyte phenotype were only present in the adipogenic induction group. Conforming to the heterogeneous nature of hMSCs and the known plasticity between osteogenic and adipogenic lineages, these data indicatea marker overlap between MSC-derived adipocytes and osteoblasts. Weproposea careful consideration of experimental conditions such as investigated timepoints, selected housekeeping genesand the evidence indicating lack of differentiation into other lineageswhen evaluating hMSC differentiation.
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Project description:Background: Lung cancer and oesophageal cancer are prevalent malignancies with rising incidence and mortality worldwide. While some environmental and behavioural risk factors for these cancers are established, the contribution of genetic factors to their pathogenesis remains incompletely defined. This study aimed to interrogate the intricate genetic relationship between lung cancer and oesophageal cancer and their potential comorbidity. Methods: We utilised linkage disequilibrium score regression (LDSC) to analyse the genetic correlation between oesophageal carcinoma and lung carcinoma. We then employed several approaches, including pleiotropic analysis under the composite null hypothesis (PLACO), multi-marker analysis of genomic annotation (MAGMA), cis-expression quantitative trait loci (eQTL) analysis, and a pan-cancer assessment to identify pleiotropic loci and genes. Finally, we performed bidirectional Mendelian randomisation (MR) to evaluate the causal relationship between these malignancies. Results: LDSC revealed a significant genetic correlation between oesophageal carcinoma and lung carcinoma. Further analysis identified shared gene loci including PGBD1, ZNF323, and WNK1 using PLACO. MAGMA identified enriched pathways and 9 pleiotropic genes including HIST1H1B, HIST1H4L, and HIST1H2BL. eQTL analysis integrating oesophageal, lung, and blood tissues revealed 26 shared genes including TERT, NKAPL, RAD52, BTN3A2, GABBR1, CLPTM1L, and TRIM27. A pan-cancer exploration of the identified genes was undertaken. MR analysis showed no evidence for a bidirectional causal relationship between oesophageal carcinoma and lung carcinoma. Conclusions: This study provides salient insights into the intricate genetic links between lung carcinoma and oesophageal carcinoma. Utilising multiple approaches for genetic correlation, locus and gene analysis, and causal assessment, we identify shared genetic susceptibilities and regulatory mechanisms. These findings reveal new leads and targets to further elucidate the genetic basis of lung and oesophageal carcinoma, aiding development of preventive and therapeutic strategies.
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Project description:Neuroinflammation caused by COVID-19 negatively impacts brain metabolism and function, while pre-existing brain pathology may contribute to individuals' vulnerability to the adverse consequences of COVID-19. We used summary statistics from genome-wide association studies (GWAS) to perform Mendelian randomization (MR) analyses, thus assessing potential associations between multiple sclerosis (MS) and two COVID-19 outcomes (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2] infection and COVID-19 hospitalization). Genome-wide risk genes were compared between the GWAS datasets on hospitalized COVID-19 and MS. Literature-based analysis was conducted to construct molecular pathways connecting MS and COVID-19. We found that genetic liability to MS confers a causal effect on hospitalized COVID-19 (odd ratio [OR]: 1.09, 95% confidence interval: 1.03-1.16) but not on SARS-CoV-2 infection (1.03, 1.00-1.05). Genetic liability to hospitalized COVID-19 confers a causal effect on MS (1.15, 1.02-1.30). Hospitalized COVID-19 and MS share five risk genes within two loci, including TNFAIP8, HSD17B4, CDC37, PDE4A, and KEAP1. Pathway analysis identified a panel of immunity-related genes that may mediate the links between MS and COVID-19. Our study suggests that MS was associated with a 9% increased risk for COVID-19 hospitalization, while hospitalized COVID-19 was associated with a 15% increased risk for MS. Immunity-related pathways may underlie the link between MS on COVID-19.
| S-EPMC9880714 | biostudies-literature
Project description:Background Individuals of the same chronological age may exhibit diverse susceptibilities to death. However, few studies have investigated the associations between blood pressure and the accelerated aging. Methods and Results A cross-sectional study was conducted in 288 adults aged ≥50 years. We assessed the DNA methylation-based measures of biological age using CpG sites on the Illumina HumanMethylationEPIC BeadChip. Epigenetic age acceleration metrics were derived by regressing residuals (ΔAge) and ratios (aging rate) of DNA methylation age on chronological age. Dose-response relationships between blood pressure and epigenetic age acceleration were quantified using multiple linear regression and restricted cubic regression models. We found that each 10-mm Hg increase in systolic blood pressure was associated with 0.608 (95% CI, 0.231-0.984) years increase in ΔAge and 0.007 (95% CI, 0.002-0.012) increase in aging rate; meanwhile, for pulse pressure, the increase was 1.12 (95% CI, 0.625-1.61) years for ΔAge and 0.013 (95% CI, 0.007-0.020) for aging rate. Subgroup analysis showed that the significant associations of systolic blood pressure and pulse pressure with epigenetic age acceleration appeared to be limited to women, although interactions between blood pressure and sex were not significant (P values for interaction >0.05). The combination of women and hypertension was associated with a much higher increase in ΔAge (β [95% CI], 4.05 [1.07-7.02]) and aging rate (β [95% CI], 0.047 [0.008-0.087]), compared with male participants without hypertension. Conclusions Our findings suggested that high systolic blood pressure and pulse pressure were associated with the epigenetic age acceleration, providing important clues for relationships between blood pressure and epigenetic aging.
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