Genetic and Environmental Influences on Stressful Life Events and their Associations with Executive Functions in Young Adulthood: A Longitudinal Twin Analysis.
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ABSTRACT:
SUBMITTER: Morrison CL
PROVIDER: S-EPMC7855628 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Research on executive functions (EFs) has revealed that individual differences in general EF abilities are highly correlated across the first few decades of life, especially at the level of genetic influences. Our work has also provided evidence for substantial heritability of this Common EF factor in midlife, but it remains unclear whether individual differences in Common EFs continue to show strong stability in middle age. We examined data from 1,464 middle-aged twins from the Vietnam Era Twin Study of Aging, most of whom completed 7 neuropsychological measures of EFs at 2 points in middle age (Mages = 56 and 62). Confirmatory factor analysis indicated that individual differences in Common EF, a latent factor explaining variation in seven neuropsychological EF tasks, were highly correlated across this 6-year period (r = .97), and that the same genetic and environmental influences were operating across this interval (genetic and shared environmental correlations = 1.0, nonshared environment correlation = .95). Similar phenotypic and genetic stability was observed for a Working Memory (WM)-Specific latent factor, which explained additional variance in working memory span tasks not captured by Common EF (r = .98, genetic correlation = 1.0, nonshared environmental correlation = .88). There was a large mean-level performance decline in Common EF (d = -.60) but not WM-Specific (d = -.03). These results suggest that there is substantial decline in Common EF abilities across middle age but that individual differences are almost perfectly stable. (PsycINFO Database Record
| S-EPMC5905725 | biostudies-literature
Project description:Depression is associated with deficits in executive functions (EFs)-cognitive control abilities that regulate goal-directed thoughts and actions-but the etiology of these associations is unclear. We examined the relations between depressive symptoms and multiple EF latent variables in a population-based sample of 439 twin pairs assessed at mean ages 12, 17, and 23 years. Greater depressive symptoms negatively related to a Common EF factor capturing shared variance across response inhibition, working memory updating, and mental set shifting tasks, and also negatively related to an Updating-Specific factor, but not a Shifting-Specific factor. Cross-lagged panel models suggested that the Common EF correlations reflected within-wave associations rather than prospective effects, whereas the Updating-Specific correlations reflected associations of earlier depression levels with later Updating-Specific ability. Twin models were consistent with a model in which Common EF and Updating-Specific abilities relate to depression through correlated genetic risk, with no significant environmental correlations.
| S-EPMC6150459 | biostudies-literature
Project description:Executive functions (EFs) and intelligence (IQ) are phenotypically correlated. In twin studies, latent variables for EFs and IQ display moderate to high heritability estimates; however, they show variable genetic correlations in twin studies spanning childhood to middle age. We analyzed data from over 11,000 children (9- to 10-year-olds, including 749 twin pairs) in the Adolescent Brain Cognitive Development (ABCD) Study to examine the phenotypic and genetic relations between EFs and IQ in childhood. We identified two EF factors-Common EF and Updating-Specific-which were both related to IQ (rs = 0.64-0.81). Common EF and IQ were heritable (53%-67%), and their genetic correlation (rG = 0.86) was not significantly different than 1. These results suggest that EFs and IQ are phenotypically but not genetically separable in middle childhood, meaning that this phenotypic separability may be influenced by environmental factors.
| S-EPMC8639807 | biostudies-literature
Project description:Child maltreatment has consistently been found to be associated with attention deficit/hyperactivity disorder (ADHD). However, the robustness of this association and the direction of the link between maltreatment and ADHD remain unclear. We used data from the Environmental Risk (E-Risk) Longitudinal Twin Study, a cohort of 2232 British twins, to investigate the associations between exposure to abuse/neglect and ADHD in childhood and in young adulthood, and to test their robustness and specificity. We also aimed to test longitudinal associations between abuse/neglect and ADHD from childhood to young adulthood, controlling for confounders. Results indicated strong associations between abuse/neglect and ADHD in childhood and also in young adulthood. In childhood, the association was concentrated among children with comorbid conduct disorder. Longitudinal analyses showed that childhood ADHD predicted abuse/neglect in later years. This association was again concentrated among individuals with comorbid conduct disorder. Abuse/neglect in childhood was not associated with later ADHD in young adulthood after adjusting for childhood ADHD. Our study does not provide support of a causal link between child abuse/neglect and adult ADHD but highlights the possibility of a long-term effect of disruptive behaviors on the risk for experiencing abuse/neglect. These findings emphasize the need for clinicians treating people with ADHD, especially those with comorbid conduct disorder, to be aware of their increased risk for experiencing abuse/neglect. Interventions aimed at reducing risks of abuse/neglect should also focus on the environment of individuals with disruptive behaviors.
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Project description:BackgroundBlood pressure (BP) and cholesterol are major modifiable risk factors for cardiovascular disease (CVD), but effects of exposures during young adulthood on later life CVD risk have not been well quantified.ObjectiveThe authors sought to evaluate the independent associations between young adult exposures to risk factors and later life CVD risk, accounting for later life exposures.MethodsThe authors pooled data from 6 U.S. cohorts with observations spanning the life course from young adulthood to later life, and imputed risk factor trajectories for low-density lipoprotein (LDL) and high-density lipoprotein cholesterols, systolic and diastolic BP starting from age 18 years for every participant. Time-weighted average exposures to each risk factor during young (age 18 to 39 years) and later adulthood (age ≥40 years) were calculated and linked to subsequent risks of coronary heart disease (CHD), heart failure (HF), or stroke.ResultsA total of 36,030 participants were included. During a median follow-up of 17 years, there were 4,570 CHD, 5,119 HF, and 2,862 stroke events. When young and later adult risk factors were considered jointly in the model, young adult LDL ≥100 mg/dl (compared with <100 mg/dl) was associated with a 64% increased risk for CHD, independent of later adult exposures. Similarly, young adult SBP ≥130 mm Hg (compared with <120 mm Hg) was associated with a 37% increased risk for HF, and young adult DBP ≥80 mm Hg (compared with <80 mm Hg) was associated with a 21% increased risk.ConclusionsCumulative young adult exposures to elevated systolic BP, diastolic BP and LDL were associated with increased CVD risks in later life, independent of later adult exposures.
| S-EPMC6764095 | biostudies-literature
Project description:Height variation is known to be determined by both genetic and environmental factors, but a systematic description of how their influences differ by sex, age and global regions is lacking. We conducted an individual-based pooled analysis of 45 twin cohorts from 20 countries, including 180,520 paired measurements at ages 1-19 years. The proportion of height variation explained by shared environmental factors was greatest in early childhood, but these effects remained present until early adulthood. Accordingly, the relative genetic contribution increased with age and was greatest in adolescence (up to 0.83 in boys and 0.76 in girls). Comparing geographic-cultural regions (Europe, North-America and Australia, and East-Asia), genetic variance was greatest in North-America and Australia and lowest in East-Asia, but the relative proportion of genetic variation was roughly similar across these regions. Our findings provide further insights into height variation during childhood and adolescence in populations representing different ethnicities and exposed to different environments.
| S-EPMC4917845 | biostudies-literature
Project description:BackgroundPrevious studies have found that stressful life events (SLEs) are associated with an increased risk of adult depression. However, many studies are observational in nature and limited by methodological issues, such as potential confounding by genetic factors. Genetically informative research, such as the co-twin control design, can strengthen causal inference in observational studies. Discrete-time survival analysis has several benefits and multilevel survival analysis can incorporate frailty terms (random effects) to estimate the components of the biometric model. In the current study, we investigated associations between SLEs and depression risk in a population-based twin sample (N = 2299).MethodsA co-twin control design was used to investigate the influence of the occurrence of SLEs on depression risk. The co-twin control design involves comparing patterns of associations in the full sample and within dizygotic (DZ) and monozygotic twins (MZ). Associations were modelled using discrete-time survival analysis with biometric frailty terms. Data from two time points were used in the analyses. Mean age at Wave 1 was 28 years and mean age at Wave 2 was 38 years.ResultsSLE occurrence was associated with increased depression risk. Co-twin control analyses indicated that this association was at least in part due to the causal influence of SLE exposure on depression risk for event occurrence across all SLEs and for violent SLEs. A minor proportion of the total genetic risk of depression reflected genetic effects related to SLEs.ConclusionsThe results support previous research in implicating SLEs as important risk factors with probable causal influence on depression risk.
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Project description:Co-twin comparisons address familial confounding by controlling for genetic and environmental influences that twin siblings share. We applied the co-twin comparison design to investigate associations of adolescent factors with alcohol dependence (AD) symptoms. Participants were 1286 individuals (581 complete twin pairs; 42% monozygotic; and 54% female) from the FinnTwin12 study. Predictors included adolescent academic achievement, substance use, externalizing problems, internalizing problems, executive functioning, peer environment, physical health, relationship with parents, alcohol expectancies, life events, and pubertal development. The outcome was lifetime AD clinical criterion count, as measured in young adulthood. We examined associations of each adolescent domain with AD symptoms in individual-level and co-twin comparison analyses. In individual-level analyses, adolescents with higher levels of substance use, teacher-reported externalizing problems at age 12, externalizing problems at age 14, self- and co-twin-reported internalizing problems, peer deviance, and perceived difficulty of life events reported more symptoms of AD in young adulthood (ps < .044). Conversely, individuals with higher academic achievement, social adjustment, self-rated health, and parent-child relationship quality met fewer AD clinical criteria (ps < .024). Associations between adolescent substance use, teacher-reported externalizing problems, co-twin-reported internalizing problems, peer deviance, self-rated health, and AD symptoms were of a similar magnitude in co-twin comparisons. We replicated many well-known adolescent correlates of later alcohol problems, including academic achievement, substance use, externalizing and internalizing problems, self-rated health, and features of the peer environment and parent-child relationship. Furthermore, we demonstrate the utility of co-twin comparisons for understanding pathways to AD. Effect sizes corresponding to the associations between adolescent substance use, teacher-reported externalizing problems, co-twin-reported internalizing problems, peer deviance, and self-rated health were not significantly attenuated (p value threshold = .05) after controlling for genetic and environmental influences that twin siblings share, highlighting these factors as candidates for further research.
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Project description:Poor executive functions (EFs) have been linked to substance use and abuse across multiple substances. However, it is unclear whether these associations are stronger for some EFs over others and/or some stages of substance use over others (e.g., ever using substances vs. dependence). It is also unknown whether such patterns change from adolescence to early adulthood, a transition that is characterized by changes to both EFs and substance use behaviors. In this longitudinal study of approximately 850 twins, we examined the relations between multiple EF abilities (including a common EF factor predicting 9 EF tasks) and measures of general substance use and dependence/abuse in late adolescence (mean age 17 years) and early adulthood (mean age 23 years). At the phenotypic level, common EF in adolescence was negatively related to the number of substances ever used and to last 6-month frequency of use, but not to dependence/abuse vulnerability (i.e., the number of dependence and abuse symptoms endorsed per substance that had been repeatedly used). However, in the same participants in early adulthood, common EF was only weakly related to the number of substances used, and not related to concurrent frequency of use nor dependence/abuse vulnerability. Twin analyses revealed that these associations were primarily genetic in origin, and that the genetic correlations were relatively stable over time. These results suggest that low common EF is a genetic risk factor for increased polysubstance use in late adolescence, but that non-EF factors play a larger role in the progression to substance dependence/abuse. (PsycINFO Database Record
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Project description:Disentangling the genetic and environmental influences of gambling is important for explaining the roots of individual differences in gambling behavior and providing guidance for precaution and intervention, but we are unaware of any comprehensive and systematic quantitative meta-analysis. We systematically identified 18 twin studies on gambling in the meta-analysis. The correlation coefficients within monozygotic (MZ) and dizygotic (DZ) twins, along with the corresponding sample size, were used to calculate the proportion of the total variance accounted for by additive genes (A), dominant genes (D), the shared environment (C), and the non-shared environment plus measurement error (E). We further assessed the moderating effects of gambling assessment (symptom oriented assessment vs. behavior oriented assessment), age, and sex. The whole sample analyses showed moderate additive genetic (a2 = 0.50) and non-shared environmental influences (e2 = 0.50) on gambling. The magnitude of the genetic influence (a2) was higher for disordered gambling assessed with symptom oriented assessment (53%) than for general gambling assessed with behavior oriented assessment (41%). Additionally, the magnitude of the genetic influence (a2) was higher for adults (53%) than adolescents (42%). Genetic influence (a2) was greater for male (47%) gambling than female (28%) gambling. Shared environment had noticeable effects on female gambling (c2 = 14%) but zero effect on male gambling. In conclusion, gambling behavior was moderately heritable and moderately influenced by non-shared environmental factors. Gambling assessment, age, and sex significantly moderated the magnitude of genetic and environmental influences on gambling. Note that the number of studies might serve as a limitation.
| S-EPMC5723410 | biostudies-literature