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Although research shows a strong positive association between perceived stress and loneliness, the genetic and environmental etiology underlying their association remains unknown. People with a genetic predisposition to perceived stress, for example, may be more prone to feeling lonely and vice versa. Conversely, unique factors in people's lives may explain differences in perceived stress levels that, in turn, affect feelings of loneliness. We tested whether genetic factors, environmental factors, or both account for the association between perceived stress and loneliness. Participants were 3,066 individual twins (n Female  = 2,154, 70.3%) from the Washington State Twin Registry who completed a survey during April-May, 2020. Structural equation modeling was used to analyze the item-level perceived stress and loneliness measures. The correlation between latent perceived stress and latent loneliness was .68. Genetic and nonshared environmental variance components underlying perceived stress accounted for 3.71% and 23.26% of the total variance in loneliness, respectively. The genetic correlation between loneliness and perceived stress was .45 and did not differ significantly between men and women. The nonshared environmental correlation was .54 and also did not differ between men and women. Findings suggest that holding constant the strong genetic association between perceived stress and loneliness, unique life experiences underlying people's perceived stress account for individual differences in loneliness., (© 2024. The Author(s).)

Owing to high rates of prenatal complications, twins are, on average, substantially smaller than population norms on physical measurements including height, weight, and head circumference at birth. By early childhood, twins are physically average. This study is the first to explore the process of catch-up growth by fitting asymptotic growth models to age-standardized height, weight, and head circumference measurements in a community sample of twins (n = 1281, 52.3% female) followed at up to 17 time points from birth to 15 years. Catch-up growth was rapid over the first year and plateaued around the population mean by early childhood. Shared environmental factors accounted for the majority of individual differences in initial physical size (57.7-65.5%), whereas additive genetic factors accounted for the majority of individual differences in the upper asymptotes of height, weight, and head circumference (73.4-92.6%). Both additive genetic and shared environmental factors were associated with variance in how quickly twins caught up. Gestational age and family SES emerged as important environmental correlates of physical catch-up growth., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: A large literature demonstrates associations between socioeconomic status (SES) and health, including physiological health and well-being. Moreover, gender differences are often observed among measures of both SES and health. However, relationships between SES and health are sometimes questioned given the lack of true experiments, and the potential biological and SES mechanisms explaining gender differences in health are rarely examined simultaneously., Purpose: To use a national sample of twins to investigate lifetime socioeconomic adversity and a measure of physiological dysregulation separately by sex., Methods: Using the twin sample in the second wave of the Midlife in the United States survey (MIDUS II), biometric regression analysis was conducted to determine whether the established SES-physiological health association is observed among twins both before and after adjusting for potential familial-level confounds (additive genetic and shared environmental influences that may underly the SES-health link), and whether this association differs among men and women., Results: Although individuals with less socioeconomic adversity over the lifespan exhibited less physiological dysregulation among this sample of twins, this association only persisted among male twins after adjusting for familial influences., Conclusions: Findings from the present study suggest that, particularly for men, links between socioeconomic adversity and health are not spurious or better explained by additive genetic or early shared environmental influences. Furthermore, gender-specific role demands may create differential associations between SES and health., (© Society of Behavioral Medicine 2021. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Objectives: To examine whether neighborhood income and neighborhood safety concerns influence multisystem physiological risk after adjusting for genetic and environmental selection effects that may have biased previous tests of this association., Methods: We used structural equation modeling with a genetically informed sample of 686 male and female twin pairs in the Midlife in the United States Study II (2004)., Results: Controlling for additive genetic and shared environmental processes that may have biased neighborhood-health links in previous examinations, higher neighborhood safety concerns were associated with less physiological risk among women but not men., Discussion: Our findings suggest a possible causal role of neighborhood features for a measure of physiological risk that is associated with the development of disease. Efforts to increase neighborhood safety, perhaps through increased street lighting or neighborhood watch programs, may improve community-level health., (© The Author(s) 2018. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Openness to experience has been found to be a correlate of successful aging outcomes yet also has been found to decline from middle age onward. We hypothesized that decline in openness would be associated with death. Using longitudinal data from the Swedish Adoption/Twin Study of Aging (SATSA), the analytic sample encompassed 1954 individuals, approximately two-thirds of whom were deceased. We tested whether openness declines across late adulthood and, central to our hypothesis, whether the decline correlated with age at death. Multivariate modeling adjusted for age at study entry, sex, education, as well as the time-varying effects of physical illness, depressive symptoms, and cognitive ability. Correlations between change in neuroticism and extraversion and death were modeled for comparison. A follow-up cotwin control analysis adjusted for genetic and environmental familial confounders. Significant mean-level change was identified in all personality traits, but only for openness was change correlated with age at death, in support of our hypothesis. The findings were not explained by health factors or cognition. Cotwin control analyses indicated that the twin who died earlier showed a greater drop in openness prior to death, compared with their cotwin measured at the same time points. There was no cotwin finding for neuroticism or extraversion. We suggest that declines in openness may reflect a change in goal orientation due to the experience of a shortened time horizon, leading to an optimized selection of experiences as people approach the end of life. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Gene-environment correlation (rGE) exists both within and between families. Between families, accumulating rGE has been used to explain dramatic changes in phenotypic means over time. The Dickens and Flynn model of increases in cognitive ability over generational time, for example, suggests that small changes in phenotype can lead to subsequent reallocation of environmental resources. This process sets up a reciprocal feedback loop between phenotype and environment, producing accumulating rGE that can cause large changes in the mean of ability, even though ability remains highly heritable in cross-sectional data. We report simulations suggesting that similar processes may operate within twin and sibling pairs. Especially in dizygotic twins and siblings, small differences in phenotype can become associated with reallocations of environmental resources within families. We show that phenotype-environment effects can account for age-related increases in rGE, rapid differentiation of siblings raised together, and widely reported increases in the heritability of behavior during childhood and adolescence.

Behavior genetic methods are useful for examining mechanisms underlying the interaction between genetic and family environmental factors of internalizing problem behavior (INT). Previous twin studies, however, have shown little consistency in interaction patterns, depending on type and operationalization of measured environments. The aim of the current study was to explore different gene-by-environment interaction patterns among different family-level environmental risk factors and resources known to correlate with INT. Using an empirical-based approach, we combined various indicators of the family environment to derive four dimensions: "positive parenting," "negative parenting," "lack of parental resources," and "socioeconomic status." We then used a genetically informed design of twins raised in the same family to test whether interaction patterns followed a diathesis stress or vantage sensitivity model formulation. The sample consisted of 2,089 twin pairs and their families from two twin birth cohorts (ages 11 and 17) participating in Wave 1 of the German TwinLife study of social inequalities. In line with a vantage sensitivity pattern of interaction and with the bioecological model of development (Bronfenbrenner & Ceci, 1994), evidence for a general mechanism of gene-environment interaction with increasing nonshared environmental variance for more adverse and less propitious family conditions was found. In preadolescence, parenting behavior had a greater moderating influence on INT compared to general family conditions like socioeconomic status. Interventions for INT that directly involve parents, thus, may be more important in preadolescent populations whereas individual interventions for adolescents may be more successful if they are adapted to different levels of socioeconomic status.

Twins regularly score nearly a standard deviation below the population mean on standardized measures of cognitive development in infancy but recover to the population mean by early childhood, making rapid gains through the toddler years. To date, only polynomial growth models have been fit to model cognitive recovery across childhood, limiting the applicability of the growth parameters to later developmental periods. We fit a nonlinear asymptotic Gompertz growth model to prospective cognitive scores from 1,153 individual twins from 578 families (47.9% male, 91.5% White, 61.6% monozygotic) measured at 16 time points between 3 months and 15 years. Twins displayed a lower asymptote of 86.47 (0.90 SD below the population mean) and gained on average 17.01 points, achieving an upper asymptote of 103.48. Growth was observed to be most rapid at 3.26 years, highlighting the importance of the toddler years in cognitive development. Biometric analyses revealed that shared environmental factors accounted for the majority of the variance in initial cognitive ability as well as asymptotic growth in cognitive ability. Gestational age and family socioeconomic status (SES) were robust predictors of cognitive growth. Results from the present study provide insight into the growth processes underlying the recovery of cognitive ability to the population mean for children evincing slight delays in their initial cognitive ability. In particular, findings highlight prenatal factors and family economic resources as important aspects of the environment in the recovery of cognitive ability.

We examined whether attained socioeconomic status (SES) moderated genetic and environmental sources of individual differences in cognitive performance using pooled data from 9 adult twin studies. Prior work concerning SES moderation of cognitive performance has focused on rearing SES. The current adult sample of 12,196 individuals (aged 27-98 years) allowed for the examination of common sources of individual differences between attained SES and cognitive performance (signaling potential gene-environment correlation mechanisms, rGE), as well as sources of individual differences unique to cognitive performance (signaling potential gene-environment interaction mechanisms, G × E). Attained SES moderated sources of individual differences in 4 cognitive domains, assessed via performance on 5 cognitive tests ranging 2,149 to 8,722 participants. Attained SES moderated common sources of influences for 3 domains and influences unique to cognition in all 4 domains. The net effect was that genetic influences on the common pathway tended to be relatively more important at the upper end of attained SES indicating possible active rGE, whereas, genetic influences for the unique pathway were proportionally stable or less important at the upper end of attained SES. As a noted exception, at the upper end of attained SES, genetic influences unique to perceptual speed were amplified and genetic influences on the common pathway were dampened. Accounting for rearing SES did not alter attained SES moderation effects on cognitive performance, suggesting mechanisms germane to adulthood. Our findings suggest the importance of gene--environment mechanisms through which attained SES moderates sources of individual differences in cognitive performance.

This study tested phenotypic and biometric associations between physical and cognitive catch‐up growth in a community sample of twins (n = 1285, 51.8% female, 89.3% White). Height and weight were measured at up to 17 time points between birth and 15 years, and cognitive ability was assessed at up to 16 time points between 3 months and 15 years. Weight and length at birth were positively associated with cognitive abilities in infancy and adolescence (r's =.16–.51). More rapid weight catch‐up growth was associated with slower, steadier cognitive catch‐up growth. Shared and nonshared environmental factors accounted for positive associations between physical size at birth and cognitive outcomes. Findings highlight the role of prenatal environmental experiences in physical and cognitive co‐development. [ABSTRACT FROM AUTHOR]

Twins regularly score nearly a standard deviation below the population mean on standardized measures of cognitive development in infancy but recover to the population mean by early childhood, making rapid gains through the toddler years. To date, only polynomial growth models have been fit to model cognitive recovery across childhood, limiting the applicability of the growth parameters to later developmental periods. We fit a nonlinear asymptotic Gompertz growth model to prospective cognitive scores from 1,153 individual twins from 578 families (47.9% male, 91.5% White, 61.6% monozygotic) measured at 16 time points between 3 months and 15 years. Twins displayed a lower asymptote of 86.47 (.90 SD below the population mean) and gained on average 17.01 points, achieving an upper asymptote of 103.48. Growth was observed to be most rapid at 3.26 years, highlighting the importance of the toddler years in cognitive development. Biometric analyses revealed that shared environmental factors accounted for the majority of the variance in initial cognitive ability as well as asymptotic growth in cognitive ability. Gestational age and family socioeconomic status (SES) were robust predictors of cognitive growth. Results from the present study provide insight into the growth processes underlying the recovery of cognitive ability to the population mean for children evincing slight delays in their initial cognitive ability. In particular, findings highlight prenatal factors and family economic resources as important aspects of the environment in the recovery of cognitive ability. [ABSTRACT FROM AUTHOR]

The Louisville Twin Study (LTS) began in 1958 and became a premier longitudinal twin study of cognitive development. The LTS continuously collected data from twins through 2000 after which the study closed indefinitely due to lack of funding. Now that the majority of the sample is age 40 or older (61.36%, N = 1770), the LTS childhood data can be linked to midlife cognitive functioning, among other physical, biological, social, and psychiatric outcomes. We report results from two pilot studies in anticipation of beginning the midlife phase of the LTS. The first pilot study was a participant tracking study, in which we showed that approximately 90% of the Louisville families randomly sampled (N = 203) for the study could be found. The second pilot study consisted of 40 in-person interviews in which twins completed cognitive, memory, biometric, and functional ability measures. The main purpose of the second study was to correlate midlife measures of cognitive functioning to a measure of biological age, which is an alternative index to chronological age that quantifies age as a function of the breakdown of structural and functional physiological systems, and then to relate both of these measures to twins' cognitive developmental trajectories. Midlife IQ was uncorrelated with biological age (−.01) while better scores on episodic memory more strongly correlated with lower biological age (−.19 to −.31). As expected, midlife IQ positively correlated with IQ measures collected throughout childhood and adolescence. Additionally, positive linear rates of change in FSIQ scores in childhood significantly correlated with biological age (−.68), physical functioning (.71), and functional ability (−.55), suggesting that cognitive development predicts lower biological age, better physical functioning, and better functional ability. In sum, the Louisville twins can be relocated to investigate whether and how early and midlife cognitive and physical health factors contribute to cognitive aging. [ABSTRACT FROM AUTHOR]

ABSTRACT Objective Prior twin studies provide support for a single 'common factor' that contributes genetic and environmental risk to a range of disordered eating symptoms. However, the common factor may be indexed less well by binge eating (BE) than other symptoms of eating disorders [i.e., body dissatisfaction (BD) and weight preoccupation (WP)]. We sought to explore the presence of a common factor and test whether loadings differed across three key symptoms (i.e., BE, BD, WP). Method Disordered eating was assessed via self-report in 631 female twin pairs from the Michigan State University Twin Registry. Results We detected a common disordered eating factor that was influenced primarily by additive genetic and nonshared environmental influences. However, we observed different loadings on this common factor by symptom type, as factor loadings for BD and WP were stronger than that for BE. Moreover, the residual environmental and/or genetic variances (i.e., those that are independent of the common factor) were larger in BE than those of BD or WP. Discussion Although all three symptoms share a common set of genetic and environmental influences, risk for BE may involve additional genetic, biological, and environmental factors that are not shared with other symptoms of eating pathology. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2017; 50:157-161) [ABSTRACT FROM AUTHOR]