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The literature on personality trait development has mainly focused on influences of life experiences in one single life domain (e.g., work or family) separate from one another and has primarily examined personality development in early life stages. Thus, less attention has been devoted to influences from interplays across different life domains and personality development in middle and late adulthood. Synthesizing the literature on personality science and organizational research, we built a theoretical model and investigated what, how, and why the interplay between two central life domains-work and family-may be related to personality trait development of people at their middle and late life stages, and more important, change-related reciprocal relationships between personality traits and work-family experiences. Generally, convergent findings with data from two longitudinal studies (National Survey of Midlife in the United States, maximum N = 3,192, three waves; and Health and Retirement Study, maximum N = 1,133, three waves except anxiety) revealed that work-to-family conflict, family-to-work conflict, work-to-family facilitation, and family-to-work facilitation mostly had lagged effects on changes of Conscientiousness, Extraversion, and Neuroticism, and the influences were generally channeled through changes of anxiety. Personality traits also had lagged influences on changes of work-family experiences, with some influences deteriorating over time. Change-related reciprocal relationships were recorded mainly between Neuroticism and Extraversion with work-family experiences. Some selection effects were larger than socialization effects. Our research contributes to the personality and the work-family literature and represents a useful example of cross-fertilization of research in different areas of psychology to advance personality research. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Low serum albumin level is linked to the emergence of many cardiovascular diseases, including AF. In this study, we aim to characterize the nature and magnitude of the prospective association between serum albumin and incident AF in the Atherosclerosis Risk in Communities (ARIC) Study and investigate any causal relevance to the association between them. ARIC Study is a population-based, prospective, cohort study of cardiovascular risk factors in four US communities, initially consisting of 15,792 participants, aged 45-64 years, recruited between 1987 and 1989 (visit 1). The final sample size was 12,833 in this study. Baseline (visit 1) characteristics were compared between groups using one-way ANOVA test, Chi square test, or Kruskal-Wallis test as appropriate. We used multivariable Cox' hazard regression models to assess the association between albumin and incident AF. Two-sample Mendelian randomization (MR) based on publicly available summary-level data from genome-wide association studies was used to estimate the causal influence of the serum albumin and incident AF. During a median follow-up of 25.1 years, 2259 (17.6%) participants developed incident AF. After multiple adjustment, serum albumin was inversely associated with incidence of AF [HR = 0.90, 95% CI 0.86-0.94, per SD (0.27 g/dL) increase; HR = 0.80, 95% CI 0.71-0.91, Q4 vs. Q1]. In MR analysis, we detected no evidence for a causal relation between serum albumin level and AF in inverse-variance weighted (IVW) method (odds ratio: 0.996, 95% CI 0.980-1.012, per 1 g/dL increase of albumin; P = 0.620) without evidence of heterogeneity between estimates from individual SNPs (P heterogeneity  = 0.981 [MR-Egger] and P heterogeneity  = 0.860 [IVW]) nor pleiotropy effect (P pleiotropy  = 0.193). The serum albumin level is independently inverse associated with incident AF in a linear pattern. However, MR analyses did not support a causal role of serum albumin in the etiology of AF.

Obesity is a growing health problem in the U.S. As a complex trait, obesity involves multiple genes and gene-gene and gene-environment interactions that contribute to its pathogenesis. Here we report significant linkage from a scan of a large sample segregating extreme obesity and normal weight. We have used 382 microsatellite markers in 1,297 individuals from 260 European-American families. We conducted nonparametric linkage (NPL) analyses for dichotomous BMI (using BMI >/=27, >/=30, >/=35, and >/=40 kg/m(2)) using Genehunter. We also analyzed quantitative traits (BMI, percentage of fat, and waist circumference) by the family regression method using Merlin_regress. We found evidence for linkage on chromosome 12 (125 cM, D12S2070, logarithm of odds [LOD] 3.79, P = 0.00001 for percentage of fat; LOD 2.98, P = 0.0001 for BMI; and LOD 2.86, P = 0.00014 for waist circumference) by family regression analyses. Adding three additional markers to the intervals flanking the chromosome 12 peak yielded an LOD score of 4.08 (P = 0.00001) for percentage of fat at 116 cM and LOD scores of 3.57 (P = 0.00003) and 3.05 (P = 0.00009) for BMI and waist circumference, respectively, at 125 cM. We also obtained other suggestive linkages on chromosomes 2, 3, 7, 8, 9, 12, 13, and 21. Our results suggest multiple loci that could influence obesity, particularly a locus in chromosome region 12q23-24.

Several groups have completed autosomal genome scans for human obesity, but only two have examined the X chromosome. A French group reported linkage of BMI to Xp and Xq markers, and a Finnish group reported linkage of BMI to Xq. We scanned the X chromosome in two cohorts, 190 European-American families (940 members) and 43 African-American families (208 members). We examined five correlated obesity phenotypes, BMI, body fat percentage, hip and waist circumferences, and plasma leptin concentration. We also examined leptin resistance (leptin/BMI) and fat patterning (waist-to-hip ratio [WHR]). Variables were adjusted for age within generation, race, and sex. We genotyped 20 markers with average spacing of 10 cM and no interval >22 cM and conducted nonparametric analyses. Suggestive linkage was found for WHR only. Linkage was supported in both family sets, and support was especially strong for females. Z scores for analyses of female phenotypes were 2.69, 1.73, and 2.37 (P = 0.0036, 0.0418, and 0.0089) for African-Americans, European-Americans, and the combined sample, respectively. The peaks were 51-73 cM from the p terminus, 14-34 cM distal of the French report in Xp22. Our results suggest that a quantitative trait locus influencing fat distribution in women may lie in chromosome region Xp21-22; however, the linked interval is large and differs substantially from that of the French and Finnish groups. Given the positive but divergent results, it would be worthwhile for others to examine the X chromosome.

Aims/hypothesis: Obesity is a complex trait influenced by multiple genes. We evaluated linkage in three regions of human chromosome 10 previously linked to obesity-related phenotypes., Methods: We conducted non-parametric linkage analysis of obesity-related phenotypes in cohorts of 170 European-American and 43 African-American families having extremely obese and normal weight subjects., Results: We found support for linkage of an obesity phenotype (BMI > or = 27 kg/m2) in both cohorts, as well as in a combined analysis (European-American cohort, Z = 1.90, p = 0.03; African-American cohort, Z = 2.25, p = 0.014; combined cohort, Z = 2.55, p = 0.005)., Conclusion/interpretation: These results confirm previous reports of linkage in French and German families. The consistency of results across these four cohorts supports the localization of a quantitative trait locus influencing obesity to human chromosome region 10p12.