Search

Objectives This paper models cognitive aging, across mid and late life, and estimates birth cohort and sex differences in both initial levels and aging trajectories over time in a sample with multiple cohorts and a wide span of ages. Methods The data used in this study came from the first 9 waves of the English Longitudinal Study of Ageing, spanning 2002–2019. There were n = 76,014 observations (proportion male 45%). Dependent measures were verbal fluency, immediate recall, delayed recall, and orientation. Data were modeled using a Bayesian logistic growth curve model. Results Cognitive aging was substantial in 3 of the 4 variables examined. For verbal fluency and immediate recall, males and females could expect to lose about 30% of their initial ability between the ages of 52 and 89. Delayed recall showed a steeper decline, with males losing 40% and females losing 50% of their delayed recall ability between ages 52 and 89 (although females had a higher initial level of delayed recall). Orientation alone was not particularly affected by aging, with less than a 10% change for either males or females. Furthermore, we found cohort effects for initial ability level, with particularly steep increases for cohorts born between approximately 1930 and 1950. Discussion These cohort effects generally favored later-born cohorts. Implications and future directions are discussed. [ABSTRACT FROM AUTHOR]

Using a large longitudinal sample of adults from the Midlife in the United States (MIDUS) study, the present study extended a recently developed hierarchical model to determine how best to model the accumulation of stressors, and to determine whether the rate of change in stressors or traditional composite scores of stressors are stronger predictors of health outcomes. We used factor analysis to estimate a stress-factor score and then, to operationalize the accumulation of stressors we examined five approaches to aggregating information about repeated exposures to multiple stressors. The predictive validity of these approaches was then assessed in relation to different health outcomes. The prediction of chronic conditions, body mass index, difficulty with activities of daily living, executive function, and episodic memory later in life was strongest when the accumulation of stressors was modeled using total area under the curve (AUC) of estimated factor scores, compared to composite scores that have traditionally been used in studies of cumulative stress, as well as linear rates of change. Like endogenous, biological markers of stress reactivity, AUC for individual trajectories of self-reported stressors shows promise as a data reduction technique to model the accumulation of stressors in longitudinal studies. Overall, our results indicate that considering different quantitative models is critical to understanding the sequelae and predictive power of psychosocial stressors from midlife to late adulthood. • Five approaches to creating composite scores of cumulative stress were examined. • The strength of these approaches to predict different health outcomes was tested. • Area under the curve with respect to ground outperformed alternative approaches. • The effects of cumulative stress varied across age groups and health outcomes. [ABSTRACT FROM AUTHOR]

Symptoms of anxiety and depression are commonly comorbid and partially share a genetic etiology. Mean levels of anxiety and depression increase over the transition to adolescence, particularly in girls, suggesting a possible role of pubertal development in the activation of underlying genetic risks. The current study examined how genetic and environmental influences on anxiety and depression differed by chronological age and pubertal status. We analyzed composite scores from child self-reports and parent informant-reports of internalizing symptomology in a racially and socioeconomically diverse sample of 1,913 individual twins from 1,006 pairs (ages 8-20 years) from the Texas Twin Project. Biometric models tested age and pubertal status as moderators of genetic and environmental influences shared between and specific to anxiety and depression to determine whether etiology of internalizing symptomology differs across development as a function of age or puberty. Genetic influences did not increase as a function of age or puberty, but instead shared environmental effects decreased with age. In an exploratory model that considered the moderators simultaneously, developmental differences in etiology were reflected in genetic and environmental effects unique to depression. Results suggest that genetic variance in internalizing problems is relatively constant during adolescence, with environmental influences more varied across development. [ABSTRACT FROM AUTHOR]

Background: Antisocial behavior (ASB) can be meaningfully divided into nonaggressive rule-breaking versus aggressive dimensions, which differ in developmental course and etiology. Previous research has found that genetic influences on rule-breaking, but not aggression, increase from late childhood to mid-adolescence. This study tested the extent to which the developmental increase in genetic influence on rule-breaking was associated with pubertal development compared to chronological age. Method: Child and adolescent twins (n = 1,031), ranging in age from 8 to 20 years (M age = 13.5 years), were recruited from public schools as part of the Texas Twin Project. Participants reported on their pubertal development using the Pubertal Development Scale and on their involvement in ASB on items from the Child Behavior Checklist. Measurement invariance of ASB subtypes across age groups (≤12 years vs. >12 years old) was tested using confirmatory factor analyses. Quantitative genetic modeling was used to test whether the genetic and environmental influences on aggression and rule-breaking were moderated by age, pubertal status, or both. Results: Quantitative genetic modeling indicated that genetic influences specific to rule-breaking increased as a function of pubertal development controlling for age (a gene × puberty interaction), but did not vary as a function of age controlling for pubertal status. There were no developmental differences in the genetic etiology of aggression. Family-level environmental influences common to aggression and rule-breaking decreased with age, further contributing to the differentiation between these subtypes of ASB from childhood to adolescence. Conclusions: Future research should discriminate between alternative possible mechanisms underlying gene 9 puberty interactions on rule-breaking forms of antisocial behavior, including possible effects of pubertal hormones on gene expression. [ABSTRACT FROM AUTHOR]