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Background Wellbeing is relatively stable over the life span. However, individuals differ in this stability and change. One explanation for these differences could be the influence of different genetic or environmental factors on wellbeing over time. Methods To investigate causes of stability and change of wellbeing across the lifespan, we used cohort-sequential data on wellbeing from twins and their siblings of the Netherlands Twin Register (NTR) (total N = 46.885, 56% females). We organized wellbeing data in multiple age groups, from childhood (age 5), to adolescence, up to old age (age 61+). Applying a longitudinal genetic simplex model, we investigated the phenotypic stability of wellbeing and continuity and change in genetic and environmental influences. Results Wellbeing peaked in childhood, decreased during adolescence, and stabilized during adulthood. In childhood and adolescence, around 40% of the individual differences was explained by genetic effects. The heritability decreased toward old adulthood (35–24%) and the contribution of unique environmental effects increased to 76%. Environmental innovation was found at every age, whereas genetic innovation was only observed during adolescence (10–18 years). In childhood and adulthood, the absence of genetic innovation indicates a stable underlying set of genes influencing wellbeing during these life phases. Conclusion These findings provide insights into the stability and change of wellbeing and the genetic and environmental influences across the lifespan. Genetic effects were mostly stable, except in adolescence, whereas the environmental innovation at every age suggests that changing environmental factors are a source of changes in individual differences in wellbeing over time. [ABSTRACT FROM AUTHOR]

In the current study, common and unique genetic and environmental influences on personality and a broad range of well-being measures were investigated. Data on the Big Five, life satisfaction, quality of life, self-rated health, loneliness, and depression from 14,253 twins and their siblings (age M: 31.82, SD: 14.41, range 16–97) from the Netherlands Twin Register were used in multivariate extended twin models. The best-fitting theoretical model indicated that genetic variance in personality and well-being traits can be decomposed into effects due to one general, common factor (Mdn: 60%, range 15%–89%), due to personality-specific (Mdn: 2%, range 0%–78%) and well-being-specific (Mdn: 12%, range 4%–35%) factors, and trait-specific effects (Mdn: 18%, range 0%–65%). Significant amounts of non-additive genetic influences on the traits' (co)variances were found, while no evidence was found for quantitative or qualitative sex differences. Taken together, our study paints a fine-grained, complex picture of common and unique genetic and environmental effects on personality and well-being. Implications for the interpretation of shared variance, inflated phenotypic correlations between traits and future gene finding studies are discussed. [ABSTRACT FROM AUTHOR]

Background: Extensive research has focused on the potential benefits of education on various mental and physical health outcomes. However, whether the associations reflect a causal effect is harder to establish., Methods: To examine associations between educational duration and specific aspects of well-being, anxiety and mood disorders, and cardiovascular health in a sample of European Ancestry UK Biobank participants born in England and Wales, we apply four different causal inference methods (a natural policy experiment leveraging the minimum school-leaving age, a sibling-control design, Mendelian randomization [MR], and within-family MR), and assess if the methods converge on the same conclusion., Results: A comparison of results across the four methods reveals that associations between educational duration and these outcomes appears predominantly to be the result of confounding or bias rather than a true causal effect of education on well-being and health outcomes. Although we do consistently find no associations between educational duration and happiness, family satisfaction, work satisfaction, meaning in life, anxiety, and bipolar disorder, we do not find consistent significant associations across all methods for the other phenotypes (health satisfaction, depression, financial satisfaction, friendship satisfaction, neuroticism, and cardiovascular outcomes)., Conclusions: We discuss inconsistencies in results across methods considering their respective limitations and biases, and additionally discuss the generalizability of our findings in light of the sample and phenotype limitations. Overall, this study strengthens the idea that triangulation across different methods is necessary to enhance our understanding of the causal consequences of educational duration.

In the current study, we investigated the influence of using skewed sum scores on estimated gene-by-environment interaction effects (GxE) for life satisfaction and happiness with perceived social support. To this end, we analyzed item-level data from a large adult twin sample (Ns between 3610 and 11,305) of the Netherlands Twin Register. Item response theory (IRT) models were incorporated in unmeasured (univariate) GxE models, and measured GxE models (with social support as moderator). We found that skewness introduced spurious GxE effects, with the largest effect for the most skewed variable (social support). Finally, in the IRT model for life satisfaction, but not for happiness, heritability estimates decreased with higher social support, while this was not observed when analyzing sum scores. Together, our results indicate that IRT can be used to address psychometric issues related to the use of sum scores, especially in the context of GxE, for complex traits like well-being., (© 2023. The Author(s).)

Rationale: The coronavirus disease 2019 (COVID-19) pandemic and consequent lockdown measures have had a large impact on people's lives. Recent evidence suggests that self-rated health (SRH) scores remained relatively stable or increased during the pandemic., Objective: For the current project, we examine potential changes in the variance decomposition of SRH before and during the COVID-19 pandemic in the Netherlands., Methods: We analyse data from the Netherlands Twin Register to examine pre-pandemic SRH scores (N = 16,127), pandemic SRH scores (N = 17,451), and SRH difference scores (N = 7464). Additionally, we perform bivariate genetic analyses to estimate genetic and environmental variance components in pre-pandemic and pandemic SRH, and estimate the genetic correlation to assess potential gene-environment interaction., Results: The majority of the sample (66.7%) reported the same SRH before and during the pandemic, while 10.8% reported a decrease, and 22.5% an increase. Individuals who reported good/excellent SRH before the pandemic were most likely to report unchanged SRH during the pandemic, and individuals with bad/mediocre/reasonable SRH more often reported increased SRH. The bivariate longitudinal genetic model reveals no significant change in variance decomposition of SRH from before to during the pandemic, with a heritability estimate of 45% (CI 36%-52%). We found that the genetic correlation could be constrained to 1, and a moderate unique environmental correlation (r E  = 0.49, CI = 0.37 to 0.60)., Conclusions: We theorize that the increases in SRH are explained by uninfected individuals evaluating their health more positively than under normal circumstances (partly through social comparison with infected individuals), rather than actual improvements. As the same genes are expressed under different environmental exposures, these results imply no evidence for gene-environment interaction. While different environmental factors might influence SRH at the two time-points, the influence of environmental factors does not become relatively more important during the pandemic., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)