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.

UNASSIGNED: Family members resemble each other in their propensity for aggression. In twin studies, approximately 50% of the variance in aggression can be explained by genetic influences. However, if there are genotype-environment correlation mechanisms, such as environmental manifestations of parental and sibling genotypes, genetic influences may partly reflect environmental influences. In this study, we investigated the importance of indirect polygenic score (PGS) effects on aggression.
UNASSIGNED: We modeled the effect of PGSs based on 3 genome-wide association studies: early-life aggression, educational attainment, and attention-deficit/hyperactivity disorder (ADHD). The associations with aggression were tested in a within- and between-family design (37,796 measures from 7740 individuals, ages 3-86 years [mean = 14.20 years, SE = 12.03], from 3107 families, 55% female) and in a transmitted/nontransmitted PGS design (42,649 measures from 6653 individuals, ages 3-61 years [mean = 11.81 years, SE = 8.68], from 3024 families, 55% female). All participants are enrolled in the Netherlands Twin Register.
UNASSIGNED: We found no evidence for contributions of indirect PGS effects on aggression in either a within- and between-family design or a transmitted/nontransmitted PGS design. Results indicate significant direct effects on aggression for the PGSs based on early-life aggression, educational attainment, and ADHD, although explained variance was low (within- and between-family: early-life aggression R2 = 0.3%, early-life ADHD R2 = 0.6%, educational attainment R2 = 0.7%; transmitted/nontransmitted PGSs: early-life aggression R2 = 0.2%, early-life ADHD R2 = 0.9%, educational attainment R2 = 0.5%).
UNASSIGNED: PGSs included in the current study had a direct (but no indirect) effect on aggression, consistent with results of previous twin and family studies. Further research involving other PGSs for aggression and related phenotypes is needed to determine whether this conclusion generalizes to overall genetic influences on aggression.

Higher BMI in childhood is associated with emotional and behavioural problems, but these associations may not be causal. Results of previous genetic studies imply causal effects but may reflect influence of demography and the family environment.
This study used data on 40,949 8-year-old children and their parents from the Norwegian Mother, Father and Child Cohort Study (MoBa) and Medical Birth Registry of Norway (MBRN). We investigated the impact of BMI on symptoms of depression, anxiety, and attention-deficit hyperactivity disorder (ADHD) at age 8. We applied within-family Mendelian randomization, which accounts for familial effects by controlling for parental genotype.
Within-family Mendelian randomization estimates using genetic variants associated with BMI in adults suggested that a child\'s own BMI increased their depressive symptoms (per 5 kg/m2 increase in BMI, beta = 0.26 S.D., CI = -0.01,0.52, p=0.06) and ADHD symptoms (beta = 0.38 S.D., CI = 0.09,0.63, p=0.009). These estimates also suggested maternal BMI, or related factors, may independently affect a child\'s depressive symptoms (per 5 kg/m2 increase in maternal BMI, beta = 0.11 S.D., CI:0.02,0.09, p=0.01). However, within-family Mendelian randomization using genetic variants associated with retrospectively-reported childhood body size did not support an impact of BMI on these outcomes. There was little evidence from any estimate that the parents\' BMI affected the child\'s ADHD symptoms, or that the child\'s or parents\' BMI affected the child\'s anxiety symptoms.
We found inconsistent evidence that a child\'s BMI affected their depressive and ADHD symptoms, and little evidence that a child\'s BMI affected their anxiety symptoms. There was limited evidence of an influence of parents\' BMI. Genetic studies in samples of unrelated individuals, or using genetic variants associated with adult BMI, may have overestimated the causal effects of a child\'s own BMI.
This research was funded by the Health Foundation. It is part of the HARVEST collaboration, supported by the Research Council of Norway. Individual co-author funding: the European Research Council, the South-Eastern Norway Regional Health Authority, the Research Council of Norway, Helse Vest, the Novo Nordisk Foundation, the University of Bergen, the South-Eastern Norway Regional Health Authority, the Trond Mohn Foundation, the Western Norway Regional Health Authority, the Norwegian Diabetes Association, the UK Medical Research Council. The Medical Research Council (MRC) and the University of Bristol support the MRC Integrative Epidemiology Unit.
Some studies show that children with obesity are more likely to receive a diagnosis of depression, anxiety, or attention-deficit hyperactivity disorder (ADHD). But this does not necessarily mean obesity causes these conditions. Depression, anxiety, or ADHD could cause obesity. A child\'s environment, including family income or their parents\' mental health, could also affect a child\'s weight and mental health. Understanding the nature of these relationships could help scientists develop better interventions for both obesity and mental health conditions. Genetic studies may help scientists better understand the role of the environment in these conditions, but it\'s important to consider both the child\'s and their parents’ genetics in these analyses. This is because parents and children share not only genes, but also environmental conditions. For example, families that carry genetic variants associated with higher body weight might also have lower incomes, if parents have been affected by biases against heavier people in society and the workplace. Children in these families could have worse mental health because of effects of their parent’s weight, rather than their own weight. Looking at both child and adult genetics can help disentangle these processes. Hughes et al. show that a child\'s own body mass index, a ratio of weight and height, is not strongly associated with the child’s mental health symptoms. They analysed genetic, weight, and health survey data from about 41,000 8-year-old children and their parents. The results suggest that a child\'s own BMI does not have a large effect on their anxiety symptoms. There was also no clear evidence that a child\'s BMI affected their symptoms of depression or ADHD. These results contradict previous studies, which did not account for parental genetics. Hughes et al. suggest that, at least for eight-year-olds, factors linked with adult weight and which differ between families may be more critical to a child\'s mental health than a child’s own weight. For older children and adolescents, this may not be the case, and the individual’s own weight may be more important. As a result, policies designed to reduce obesity in mid-childhood are unlikely to greatly improve the mental health of children. On the other hand, policies targeting the environmental or societal factors contributing to higher body weights, bias against people with higher weights, and poor child mental health directly may be more beneficial.

This study using PROSPER data (N = 977, age 11.5 to age 15) investigated the longitudinal within-family associations between parent-reported parental monitoring and adolescent aggression. Importantly, this study is the first one to examine parent gender and adolescent gender differences on these within-family associations. Results differed between mothers and fathers. There was a negative, bidirectional within-family association between maternal monitoring and adolescent aggression, such that more maternal monitoring than usual was associated with fewer adolescent aggressive behavior problems than usual within the same family, and vice versa. In contrast, during mid-adolescence, a positive, bidirectional within-family association between paternal monitoring and adolescent males\' aggression was found, such that more paternal monitoring than usual was related to more adolescent males\' aggression than usual within the same family, and vice versa. Practical implications on intervention strategies are discussed.

While transactional models suggest that parent and child mental health reciprocally influence one another over development, research has largely focused on parent-to-child effects. Additionally, it is not known whether observed associations hold when appropriate statistical tools are used to operationalise within-family dynamics.
We investigated within-family mental health dynamics using autoregressive latent trajectory models with structured residuals, stratified by child gender. Parental psychological distress was assessed using the Kessler (K6) scale, and children\'s internalising and externalising problems were assessed using the Strengths and Difficulties Questionnaire. Both measures were administered at the age 3, 5, 7, 11, 14 and 17 waves of the Millennium Cohort Study (N = 10,746, ~50% female).
Maternal psychological distress was positively associated with subsequent internalising and externalising problems for girls but only with internalising problems for boys. Paternal psychological distress was associated with boys\' later internalising and externalising problems during early adolescence. Among boys, internalising problems were associated with later maternal psychological distress, while externalising problems were associated with later paternal psychological distress. Among girls, internalising problems were associated with subsequent paternal psychological distress, while externalising problems were associated with later maternal psychological distress. Finally, maternal and paternal psychological distress showed negative bidirectional associations in early childhood but positive associations in middle childhood and early adolescence.
Findings support a transactional model of family mental health, with both child-to-parent and parent-to-child effects playing a role in the development of mental health difficulties. Mental health intervention efforts should, therefore, target the whole family system.

BACKGROUND: Adolescence is a period when adolescents seek autonomy and parent-adolescent conflict appears inevitable. Even though some research found that parental psychological control triggered parent-adolescent conflict, studies clarifying the directionality of effects at the within-family level are scarce. This study investigated the longitudinal relations between parental psychological control and parent-adolescent conflict using a traditional cross-lagged panel model (CLPM) and the random-intercept CLPM (RI-CLPM) framework.
METHODS: Data from 2473 Chinese adolescents (Mage Time1 = 13.20 years, standard deviation = 0.52 years; 51.4% male) were collected via a cross-sectional survey across three time points. Adolescents reported on parental psychological control, parent-adolescent conflict, and demographic characteristics at each time point. CLPM and RI-CLPM were utilized.
RESULTS: The results from the CLPM analyses suggested a reciprocal effects model. However, the results from the RI-CLPM framework supported a conflict-driven model at the within-family level, wherein if parent-adolescent conflict increased, subsequent parental psychological control would increase as a result. The reverse pattern was not observed.
CONCLUSIONS: These findings indicate the maladaptive processes of parent-adolescent conflict that shape parental psychologically controlling behaviors in Chinese families at the within-family level. Practical implications, including how to assist Chinese parents to address parent-adolescent conflict and to reduce psychological control, are discussed.

Indirect genetic effects from relatives may result in misleading quantifications of heritability, but can also be of interest in their own right. In this paper we propose Trio-GCTA, a model for separating direct and indirect genetic effects when genome-wide single nucleotide polymorphism data have been collected from parent-offspring trios. The model is applicable to phenotypes obtained from any of the family members. We discuss appropriate parameter interpretations and apply the method to three exemplar phenotypes: offspring birth weight, maternal relationship satisfaction, and paternal body-mass index, using real data from the Norwegian Mother, Father and Child Cohort Study (MoBa).

Adolescence is often a period of onset for internalizing and externalizing problems. At the same time, adolescent maturation and increasing autonomy from parents push for changes in family functioning. Even though theoretically expected links among the changes in family functioning and adolescent internalizing and externalizing problems exist, studies examining this link on the within-family level are lacking. This longitudinal, pre-registered, and open-science study, examined the within-family dynamic longitudinal associations among family functioning, and internalizing and externalizing problems. Greek adolescents (N = 480, Mage = 15.73, 47.9% girls, at Wave 1) completed self-report questionnaires, three times in 12 months. Random-Intercept Cross-Lagged Panel Models (RI-CLPM) were applied; such models explicitly disentangle between-family differences from within-family processes, thereby offering a more stringent examination of within-family hypotheses. Results showed that family functioning was not significantly associated with internalizing or externalizing problems, on the within-family level. Also, alternative standard Cross-Lagged Panel Models (CLPM) were applied; such models have been recently criticized for failing to explicitly disentangle between-family variance from within-family variance, but they have been the standard approach to investigating questions of temporal ordering. Results from these analyses offered evidence that adolescents with higher internalizing and externalizing problems compared to their peers, tended to be those who later experienced worse family functioning, but not vice versa. Implications for theory and practice are discussed.

Understanding the factors that predict adolescent delinquency is a key topic in parenting research. An open question is whether prior results indicating relative differences between families reflect the dynamic processes occurring within families. Therefore, this study investigated concurrent and lagged associations among parental behavioral control, parental solicitation, adolescent disclosure, and adolescent delinquency by separating between-family and within-family effects in three-wave annual data (N = 1515; Mage = 13.01 years at T1; 50.6% girls). At the within-family level, parental behavioral control negatively predicted adolescent delinquency. Adolescent disclosure and delinquency, and adolescent disclosure and parental solicitation, reciprocally predicted each other. Parental solicitation negatively predicted parental behavioral control. The findings indicate a prominent role of adolescent disclosure in within-family processes concerning parental-adolescent communication and adolescent delinquency.