Childhood family environment predicting psychotic disorders over a 37-year follow-up - A general population cohort study.

BACKGROUND: Childhood adverse effects and traumatic experiences increase the risk for several psychiatric disorders. We now investigated whether prospectively assessed childhood family environment per se contributes to increased risk for psychotic disorders in adulthood, and whether these family patterns are also relevant in the development of affective disorders. METHODS: We used the Young Finns Data (n = 3502). Childhood family environment was assessed in 1980/1983 with previously constructed risk scores: (1) disadvantageous emotional family atmosphere (parenting practices, parents' life satisfaction, parents' mental disorder, parents' alcohol intoxication), (2) adverse socioeconomic environment (overcrowded apartment, home income, parent's employment, occupational status, educational level), and (3) stress-prone life events (home movement, school change, parental divorce, death, or hospitalization, and child's hospitalization). Psychiatric diagnoses (ICD-10 classification) over the lifespan were collected up to 2017 from the national registry of hospital care. Non-affective psychotic disorder and affective disorder groups were formed. RESULTS: Frequent stress-prone life events predicted higher likelihood of non-affective psychotic disorders (OR = 2.401, p = 0.001). Adverse socioeconomic environment or emotional family atmosphere did not predict psychotic disorders. Only disadvantageous emotional family atmosphere predicted modestly higher likelihood of affective disorders (OR = 1.583, p = 0.013). CONCLUSIONS: Our results suggest that childhood family environment and atmosphere patterns as such contribute to the risk for developing adulthood mental disorders with relative disorder specificity. The results emphasize the importance of both individual and public health preventive initiatives, including family support interventions.

Does social disadvantage persist over generations due to an uneven distribution of mental health diagnoses? A longitudinal investigation of Finnish register data.

Social disadvantages persist over generations, while the mechanisms behind the intergenerational transmission are not well understood. To fill this gap, first, we examine to what degree being diagnosed with a mental health disorder in adolescence mediate the transmission of social disadvantage. Second, we investigate whether the role of mental health varies for different outcomes. Third, we examine differences between disorder groups and gender. We exploited register data on the full Finnish population including information on mental health diagnoses (MHD) based on ICD-10 classification recorded in public specialized health care. As socioeconomic outcomes, we used offspring's (N = 511,835) records for low educational attainment, unemployment, and social assistance dependency in early adulthood. In addition to linear probability models, the g-computation method was used to simulate the degree to which reducing mental health inequalities in adolescence could narrow the differences between children of different family backgrounds. Our results show that adolescents with MHD had a higher likelihood of experiencing social disadvantage as young adults even after accounting for parental socioeconomic status and alternative health pathways. The counterfactual analysis indicated that the proportion mediated by unevenly distributed MHD was with 7.5% highest for social assistance followed by 4.2% for education and 3.2% for unemployment. The effect of mental health was modified by gender yet direction and strength varied across methods and externalizing behaviors mattered more for the intergenerational persistence than internalizing behaviors. Hypothetically reducing MHD to the level of families with high socioeconomic status might indeed lower part of the intergenerational transmission of social assistance dependency but to lesser degree of unemployment and low educational attainment. We demonstrate the need of support and services for those with MHD, especially among socially disadvantaged groups. However, social disadvantage should not be overly medicalized as family background has an important independent effect on offspring's socioeconimic outcomes.

The relationship of trait-like compassion with epigenetic aging: The population-based prospective Young Finns Study.

Introduction: Helping others within and beyond the family has been related to living a healthy and long life. Compassion is a prosocial personality trait characterized by concern for another person who is suffering and the motivation to help. The current study examines whether epigenetic aging is a potential biological mechanism that explains the link between prosociality and longevity. Methods: We used data from the Young Finns Study that follows six birth-cohorts from age 3-18 to 19-49. Trait-like compassion for others was measured with the Temperament and Character Inventory in the years 1997 and 2001. Epigenetic age acceleration and telomere length were measured with five DNA methylation (DNAm) indicators (DNAmAgeHorvath, IEAA_Hannum, EEAA_Hannum, DNAmPhenoAge, and DNAmTL) based on blood drawn in 2011. We controlled for sex, socioeconomic status in childhood and adulthood, and body-mass index. Results and discussion: An association between higher compassion in 1997 and a less accelerated DNAmPhenoAge, which builds on previous work on phenotypic aging, approached statistical significance in a sex-adjusted model (n = 1,030; b = -0.34; p = 0.050). Compassion in 1997 predicted less accelerated epigenetic aging over and above the control variables (n = 843; b = -0.47; p = 0.016). There was no relationship between compassion in 2001 (n = 1108/910) and any of the other four studied epigenetic aging indicators. High compassion for others might indeed influence whether an individual's biological age is lower than their chronological age. The conducted robustness checks partially support this conclusion, yet cannot rule out that there might be a broader prosocial trait behind the findings. The observed associations are interesting but should be interpreted as weak requiring replication.

Does social intolerance vary according to cognitive styles, genetic cognitive capacity, or education?

BACKGROUND: Low education, low cognitive abilities, and certain cognitive styles are suggested to predispose to social intolerance and prejudices. Evidence is, however, restricted by comparatively small samples, neglect of confounding variables and genetic factors, and a narrow focus on a single sort of prejudice. We investigated the relationships of education, polygenic cognitive potential, cognitive performance, and cognitive styles with social intolerance in adulthood over a 15-year follow-up. METHODS: We used data from the prospective population-based Young Finns Study (n = 960-1679). Social intolerance was evaluated with the Social Intolerance Scale in 1997, 2001, and 2011; cognitive performance with the Cambridge Neuropsychological Test Automated Battery in 2011; cognitive styles in 1997; and socioeconomic factors in 1980 (childhood) and 2011 (adulthood); and polygenic cognitive potential was calculated based on genome-wide association studies. RESULTS: We found that nonrational thinking, polygenic cognitive potential, cognitive performance, or socioeconomic factors were not related to social intolerance. Regarding cognitive styles, low flexibility (B = -0.759, p < .001), high perseverance (B = 1.245, p < .001), and low persistence (B = -0.329, p < .001) predicted higher social intolerance consistently in the analyses. DISCUSSION: When developing prejudice-reduction interventions, it should be considered that educational level or cognitive performance may not be crucial for development of social intolerance. Adopting certain cognitive styles may play more important roles in development of social intolerance.

Magical thinking in individuals with high polygenic risk for schizophrenia but no non-affective psychoses-a general population study.

A strong genetic background for psychoses is well-established. Most individuals with a high genetic risk for schizophrenia, however, do not develop the disorder. We investigated whether individuals, who have a high genetic risk for schizophrenia but no non-affective psychotic disorders, are predisposed to develop milder forms of deviant thinking in terms of magical thinking. Participants came from the population-based Young Finns Study (n = 1292). The polygenic risk score for schizophrenia (PRS) was calculated on the basis of the most recent genome-wide association study (GWAS). Psychiatric diagnoses over the lifespan were collected up to 2017 from the registry of hospital care. Magical thinking was evaluated with the Spiritual Acceptance Scale (e.g., beliefs in telepathy, miracles, mystical events, or sixth sense) of the Temperament and Character Inventory in 1997, 2001, and 2012 (participants were 20-50-year-olds). We found that, among those who did not develop non-affective psychotic disorders, high PRS predicted higher magical thinking in adulthood (p = 0.001). Further, PRS predicted different developmental courses: a low PRS predicted a steady decrease in magical thinking from age 20 to 50 years, while in individuals with high PRS the decrease in magical thinking ceased in middle age so that their level of magical thinking remained higher than expected for that age. These findings remained when controlling for sex, childhood family environment, and adulthood socioeconomic factors. In conclusion, if high PRS does not lead to a non-affective psychotic disorder, it predicts milder forms of deviant thinking such as elevated magical thinking in adulthood, especially in middle age. The finding enhances our understanding of different outcomes of high genetic psychosis risk.

The relationship between temperament, polygenic score for intelligence and cognition: A population-based study of middle-aged adults.

We investigated whether temperament modifies an association between polygenic intelligence potential and cognitive test performance in midlife. The participants (n = 1647, born between 1962 and 1977) were derived from the Young Finns Study. Temperament was assessed with Temperament and Character Inventory over a 15-year follow-up (1997, 2001, 2007, 2012). Polygenic intelligence potential was assessed with a polygenic score for intelligence. Cognitive performance (visual memory, reaction time, sustained attention, spatial working memory) was assessed with CANTAB in midlife. The PGSI was significantly associated with the overall cognitive performance and performance in visual memory, sustained attention and working memory tests but not reaction time test. Temperament did not correlate with polygenic score for intelligence and did not modify an association between the polygenic score and cognitive performance, either. High persistence was associated with higher visual memory (B = 0.092; FDR-adj. p = 0.007) and low harm avoidance with higher overall cognitive performance, specifically better reaction time (B = -0.102; FDR-adj; p = 0.007). The subscales of harm avoidance had different associations with cognitive performance: higher "anticipatory worry," higher "fatigability," and lower "shyness with strangers" were associated with lower cognitive performance, while the role of "fear of uncertainty" was subtest-related. In conclusion, temperament does not help or hinder one from realizing their genetic potential for intelligence. The overall modest relationships between temperament and cognitive performance advise caution if utilizing temperament-related information e.g. in working-life recruitments. Cognitive abilities may be influenced by temperament variables, such as the drive for achievement and anxiety about test performance, but they involve distinct systems of learning and memory.

Compassion protects against vital exhaustion and negative emotionality.

We investigated (i) the predictive relationships of compassion with negative emotionality (a marker of susceptibility to stress) and vital exhaustion (a marker of chronic stress response) and (ii) the effect of compassion on the developmental courses of negative emotionality and vital exhaustion over a follow-up from early adulthood to middle age. We used the prospective Young Finns data (n = 1031-1495, aged 20-50). Compassion was evaluated in 1997, 2001, and 2012; and vital exhaustion and negative emotionality in 2001, 2007, and 2012. The predictive paths from compassion to vital exhaustion and negative emotionality were stronger than vice versa: high compassion predicted lower vital exhaustion and lower negative emotionality. The effect of high compassion on lower vital exhaustion and lower negative emotionality was evident from early adulthood to middle age. Overall, high compassion appears to protect against dimensions of stress from early adulthood to middle age, whereas this study found no evidence that dimensions of stress could reduce disposition to feel compassion for others' distress over a long-term follow-up. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s11031-021-09878-2.

Genetic differential susceptibility to the parent-child relationship quality and the life span development of compassion.

The development of compassion for others might be influenced by the social experiences made during childhood and has a genetic component. No research has yet investigated whether the parent-child relationship quality interacts with genetic variation in the oxytocin and dopamine systems in predicting compassion over the life span. In the prospective Young Finns Study (N = 2099, 43.9% men), we examined the interaction between mother-reported emotional warmth and intolerance toward their child assessed in 1980 (age of participants, 3-18 years) and two established genetic risk scores for oxytocin levels and dopamine signaling activity. Dispositional compassion for others was measured with the Temperament and Character Inventory 1997, 2001, and 2012 (age of participants, 20-50 years). We found a gene-environment interaction (p = .031) that remained marginally significant after adjustment for multiple testing. In line with the differential susceptibility hypothesis, only participants who carry alleles associated with low dopamine signaling activity had higher levels of compassion when growing up with emotionally warm parents, whereas they had lower levels of compassion when their parents were emotionally cold. Children's genetic variability in the dopamine system might result in plasticity to early environmental influences that have a long-lasting effect on the development of compassion. However, our findings need replication.

Functional Polymorphisms in Oxytocin and Dopamine Pathway Genes and the Development of Dispositional Compassion Over Time: The Young Finns Study.

Background: We define compassion as an enduring disposition that centers upon empathetic concern for another person's suffering and the motivation to act to alleviate it. The contribution of specific candidate genes to the development of dispositional compassion for others is currently unknown. We examine candidate genes in the oxytocin and dopamine signaling pathways. Methods: In a 32-year follow-up of the Young Finns Study (N = 2,130, 44.0% men), we examined with multiple indicators latent growth curve modeling the molecular genetic underpinnings of dispositional compassion for others across the life span. We selected five single nucleotide polymorphisms (SNPs) whose functions are known in humans: rs2268498 (OXTR), rs3796863 (CD38) (related to lower oxytocin levels), rs1800497 (ANKK1/DRD2), rs4680 (COMT), and rs1611115 (DBH) (related to higher dopamine levels). Compassion was measured with Cloninger's Temperament and Character Inventory on three repeated observations spanning 15 years (1997-2012). Differences between gender were tested. Results: We did not find an effect of the five SNPs in oxytocin and dopamine pathway genes on the initial levels of dispositional compassion for others. Individuals who carry one or two copies of the T-allele of DBH rs1611115, however, tend to increase faster in compassion over time than those homozygotes for the C-allele, b = 0.063 (SE = 0.027; p = 0.018). This effect was largely driven by male participants, 0.206 (SE = 0.046; p < 0.001), and was not significant in female participants when analyzed separately. Conclusions: Men who are known to have, on average, lower compassion than women seem to reduce this difference over time if they carry the T-allele of DBH rs1611115. The direction of the association indicates that dopamine signaling activity rather than overall dopamine levels might drive the development of compassion.

The relationship of socioeconomic status in childhood and adulthood with compassion: A study with a prospective 32-year follow-up.

The objective of this study was to investigate (i) whether childhood family SES predicts offspring's compassion between ages 20-50 years and (ii) whether adulthood SES predicts compassion or vice versa. We used the prospective population-based Young Finns data (N = 637-2300). Childhood family SES was evaluated in 1980; participants' adulthood SES in 2001 and 2011; and compassion for others in 1997, 2001, and 2012. Compassion for others was evaluated with the Compassion scale of the Temperament and Character Inventory. The results showed that high childhood family SES (a composite score of educational level, occupational status, unemployment status, and level of income) predicted offspring's higher compassion between ages 30-40 years but not in early adulthood or middle age. These results were obtained independently of a variety of potential confounders (disruptive behavior in childhood; parental mental disorder; frequency of parental alcohol use and alcohol intoxication). Moreover, high compassion for others in adulthood (a composite score of educational level, occupational status, and unemployment status) predicted higher adulthood SES later in their life (after a 10-year follow-up), but not vice versa. In conclusion, favorable socioeconomic environment in childhood appears to have a positive effect on offspring's compassion in their middle adulthood. This effect may attenuate by middle age. High compassion for others seems to promote the achievement of higher SES in adulthood.

Risky emotional family environment in childhood and depression-related cytokines in adulthood: The protective role of compassion.

BACKGROUND: Previously, compassion has been found to protect against depressive symptoms, while emotional adversities in childhood are suggested to increase inflammatory responses. The current study investigated (a) whether emotional family environment in childhood predicts levels of such cytokines in adulthood that are previously found to be elevated in depression (interleukin [IL]-2, IL-6, IL-1b, monocyte chemoattractant protein-1, interferon-gamma [IFN-γ], and tumor necrosis factor alpha [TNF-α]) and (b) whether these associations are modified by compassion in adulthood. METHODS: The participants (N = 1,198-1,523) came from the prospective population-based Young Finns data. Emotional family environment and parental socioeconomic factors were evaluated in 1980; participants' compassion in 2001; and participants' cytokine levels and adulthood covariates in 2007. RESULTS: Risky emotional family environment in childhood predicted higher levels of IL-2, IL-6, IFN-γ, and TNF-α in adulthood. Additionally, there were significant interaction effects between compassion and emotional risk in childhood, when predicting IL-2, IL-6, and TNF-α. Specifically, individuals who grew up in a risky emotional family environment had on average higher levels of IL-2, IL-6, and TNF-α in adulthood when combined with low compassion. CONCLUSIONS: In individuals coming from risky emotional family environments, high compassion for others may protect against elevated levels of cytokines previously linked with depression.

Alcohol-related mortality and all-cause mortality following bereavement in two successive generations.

BACKGROUND AND AIM: Bereavement affects the health of the bereaved both emotionally and physically. Bereavement resulting from alcohol-related death of the previous generation (parents-first generation) may increase the risk of alcohol abuse and consequently alcohol-related mortality as well as all-cause mortality in the next generation (offspring-second generation). Furthermore, these associations can be bi-directional. However, there is no conclusive evidence of these effects, and studies exploring these intergenerational effects are rare. This study investigates these associations. METHODS: A longitudinal data were constructed by linking participants from the Adolescent Health and Lifestyle Surveys (AHLS) from 1979 to 1997 with census and registry-based data from Statistics Finland containing the socioeconomic status of the survey participants and their parents (N = 78610) to investigate these associations. Multivariate Cox proportional hazards models were used to calculate hazard ratios with 95% confidence intervals to determine the effect of bereavement with alcohol-related mortality and all-cause mortality. RESULTS: The findings suggest that bereavement following the death of an offspring increases the risk of both alcohol-related and all-cause mortality among both parents. The magnitude of the risk of mortality following the death of an offspring is higher for mothers than for fathers. There were no clear associations of a parent's death with an offspring's alcohol-related or all-cause mortality. However, generally, a father's death seems to be protective of the risk of mortality among the offspring while a mother's alcohol-related death slightly increased the risk of alcohol-related mortality among their offspring. CONCLUSIONS: These findings emphasise the role of bereavement, particularly resulting from the death of an offspring, on alcohol-related and all-cause mortality and therefore inequalities in mortality. Furthermore, the findings highlighting the need for alcohol abuse intervention and emotional support for bereaved persons following the death of an offspring.

Bidirectional Relationship of Sleep with Emotional and Behavioral Difficulties: A Five-year Follow-up of Finnish Adolescents.

The long-term effects of sleep on adolescent psychosocial well-being are mostly unknown, although insufficient sleep has been associated with emotional and behavioral difficulties in cross-sectional studies. With a five-year follow-up of Finnish adolescents (Time 1: n = 8834; Mean age = 13 years, 51.1% female, Time 2: n = 5315, Mean age = 15 years, 51.6% female, Time 3: n = 3712; Mean age = 17 years; 50.2% female), the purpose of this longitudinal study was to investigate the relations between self-reported sleep duration, sleep problems, and emotional and behavioral difficulties during adolescence. Emotional and behavioral difficulties were assessed using The Strengths and Difficulties Questionnaire (SDQ) measuring emotional symptoms, conduct problems, hyperactivity, peer problems and total difficulties. Sleep duration was calculated by counting the hours between self-reported bedtime and wake-up time. Sleep problems were assessed with a single question about the general sleep problems. According to the cross-lagged models for sleep and emotional and behavioral difficulties, the findings of this study indicate a developmental process during adolescence where, firstly, short sleep duration is a stronger predictor for current and prospective emotional and behavioral difficulties than vice versa. Secondly, increased emotional and behavioral difficulties expose adolescents to current and later sleep problems more strongly than reverse. Thus, the results show that short sleep duration predisposed to emotional and behavioral difficulties across adolescence, which then led to more prospective sleep problems. These findings suggest a developmental process where sleep and emotional and behavioral difficulties are intertwined in shaping adolescents' health.

Late start of upper secondary education and health-compromising behaviours among Finnish adolescents-a follow-up study.

BACKGROUND: The Finnish government has emphasized the need to expedite educational transitions. We study if a late start of upper secondary education is related to health-related selection, namely health-compromising behaviours in adolescence. METHODS: A large cohort of adolescents from the seventh (12-13 years) and ninth (15-16 years) grades answered online classroom surveys (total n = 10 873). They were followed to the start of upper secondary education, obtained from the Joint Application Registry. We compared those who continued studies directly from the ninth grade with later starters. We measured late bedtime, breakfast not every school day, tooth brushing less than twice-a-day, monthly alcohol consumption, weekly smoking, daily energy drinks, physical activity <6 days/week and excessive screen time. Multilevel logistic regressions and latent class analyses were conducted. RESULTS: In gender and school adjusted models in the seventh grade, all behaviours except physical activity predicted the late start. The strongest predictor was smoking, OR = 2.96 (CI = 2.25-3.89). In the ninth grade, smoking, breakfast, tooth brushing and energy drinks, OR = 1.80, (CI = 1.36-2.39, strongest), were predictive. After controlling for sociodemographic background and academic achievement, associations for alcohol and screen time became non-significant in the seventh grade. In the ninth grade, only screen time remained significant, OR = 1.33 (CI = 1.04-1.71). Health-compromising behaviours formed clusters. Belonging to the unhealthy cluster predicted the late start in both grades, in adjusted models only in the seventh grade. CONCLUSIONS: Students with health-compromising behaviours are less likely to start upper secondary education directly after the compulsory education. This may increase the risk for fragmentary educational trajectories and work careers.

Health and educational aspirations in adolescence: a longitudinal study in Finland.

BACKGROUND: The health selection hypothesis suggests that poor health leads to low educational attainment during the life course. Adolescence is an important period as poor health might prevent students from making the best educational choices. We test if health in adolescence is associated with educational aspirations and whether these associations persist over and above sociodemographic background and academic achievement. METHODS: Using classroom surveys, a cohort of students (n = 5.614) from the Helsinki Metropolitan Region was followed from the 7th (12-13 years,) up to the 9th grade (15-16 years) when the choice between the academic and the vocational track is made in Finland. Health factors (Strengths and Difficulties Questionnaire (SDQ), self-rated health, daily health complaints, and long-term illness and medicine prescribed) and sociodemographic background were self-reported by the students. Students' educational aspirations (applying for academic versus vocational track, or both) and their academic achievement were obtained from the Joint Application Registry held by the Finnish National Agency for Education. We conducted multilevel multinomial logistic regression analyses, taking into account that students are clustered within schools. RESULTS: All studied health factors were associated with adolescents' educational aspirations. For the SDQ, daily health complaints, and self-rated health these associations persisted over and above sociodemographic background and academic achievement. Students with better health in adolescence were more likely to apply for the academic track, and those who were less healthy were more likely to apply for the vocational track. The health in the group of those students who had applied for both educational tracks was in between. Inconsistent results were observed for long-term illness. We also found robust associations between educational aspirations and worsening health from grade 7 to grade 9. CONCLUSIONS: Our findings show that selection by health factors to different educational trajectories takes place at early teenage much before adolescents choose their educational track, thus supporting the health selection hypothesis in the creation of socioeconomic health inequalities. Our findings also show the importance of adolescence in this process. More studies are needed to reveal which measures would be effective in helping students with poor health to achieve their full educational potential.

The role of oxytocinergic genes in the intergenerational transmission of parent-child relationship qualities.

Parenting qualities are known to transmit across generations, but less is known about genetic processes that may modify how strongly parenting quality carries across generations. We examined in prospective data whether oxytocinergic genes of offspring moderate the intergenerational transmission of warm and accepting parent-child relationship qualities. The sample comprised 1167 Finnish parents (G2, 62% female) and their mothers (G1). At the study baseline, G1 mothers (Mage = 38) reported parent-child relationship qualities towards G2 children (age range 3-18). After 28-34 years, G2 offspring reported parent-child relationship qualities towards their own children using the same questionnaire. A cumulative genetic score was computed for G2 by summing up previously identified four alleles associated with non-optimal parenting or social impairments across OXTR (rs1042778, rs2254298, rs53576) and CD38 (rs3796863) genes. Results indicated no interaction effects of G2 cumulative genetic score on the transmission of parent-child relationship qualities. Among single polymorphisms in OXTR, the interaction effects of rs53576 and rs1042778 were found. G1 maternal emotional warmth was associated with higher G2 emotional warmth among G2 participants with the OXTR rs53576 AA/AG genotype, but not among those with the GG genotype. G1 maternal acceptance was associated with higher G2 acceptance among those G2 participants with the OXTR rs1042778 GG/GT genotype, but not among those with the TT genotype. Oxytocinergic genes may influence sensitivity to quality of parent-child relationship, although this needs replication in future studies.

Physical Activity, Sleep, and Symptoms of Depression in Adults-Testing for Mediation.

PURPOSE: Physical activity, sleep problems, and symptoms of depression contribute to overall well-being. The factors are reciprocally associated, but the nature of these associations remains unclear. The present study examined whether sleep problems mediated the association between physical activity and depressive symptoms. METHODS: The eligible population (n = 3596) consisted of adults from the ongoing, population-based Cardiovascular Risk in Young Finns Study started in 1980. Participants' leisure-time physical activity was assessed with physical activity index (2007) and sleep problems with Jenkins' Sleep Questionnaire in 2007 and 2011. Depressive symptoms were measured using modified Beck Depression Inventory in 2007 and 2012, from which the items reflecting sleep problems were excluded. Mediation analyses, through which the associations between the variables were examined, were adjusted for sex and a set of health-related covariates assessed in 2007 and 2011. RESULTS: Physical activity was associated with decreased levels of sleep problems and depressive symptoms (P < 0.05). The association between physical activity and depressive symptoms (b = -0.10, P < 0.01) was partly mediated by sleep problems (proportion mediated = 0.36, P < 0.01). The adjustment for depressive symptoms at baseline attenuated the mediation effect (proportion mediated = 0.30, P > 0.05). CONCLUSIONS: Physical activity's favorable contribution to depressive symptoms was mediated partly by sleep, but the mediation effect disappeared after adjusting for the previous depressive symptoms in adulthood.

Parent-child-relationship quality predicts offspring dispositional compassion in adulthood: A prospective follow-up study over three decades.

Compassion is known to predict prosocial behavior and moral judgments related to harm. Despite the centrality of compassion to social life, factors predicting adulthood compassion are largely unknown. We examined whether qualities of parent-child-relationship, namely, emotional warmth and acceptance, predict offspring compassion decades later in adulthood. We used data from the prospective population-based Young Finns Study. Our sample included 2,761 participants (55.5% women). Parent-child-relationship qualities were reported by each participant's parents at baseline in 1980 (T0) when participants were between 3 and 18 years old. Compassion was self-reported 3 times: in 1997 (T1), 2001 (T2), and 2012 (T3) with the Temperament and Character Inventory (Cloninger, Przybeck, Svrakic, & Wetzel, 1994). By using age at the assessment as a time-variant variable, we applied multilevel modeling for repeated measurements to examine developmental trajectories of compassion from the ages of 20 (the age of the youngest cohort at T1) to 50 (the age of the oldest cohort at T3). On average, compassion increased in a curvilinear pattern with age. Higher acceptance (p = .013) and higher emotional warmth (p < .001) were related to higher compassion in adulthood. After adjusting for childhood confounds (i.e., participant gender, birth cohort, externalizing behavior, parental socioeconomic status, and parental mental health problems), only emotional warmth (p < .001) remained a significant predictor of compassion. Quality of the parent-child-relationship has long-term effects on offspring compassion. An emotionally warm and close relationship, in particular, may contribute to higher offspring compassion in adulthood. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

Gene-environment correlations in parental emotional warmth and intolerance: genome-wide analysis over two generations of the Young Finns Study.

BACKGROUND: Genomic analysis of the child might offer new potential to illuminate human parenting. We examined whether offspring (G2) genome-wide genotype variation (SNPs) is associated with their mother's (G1) emotional warmth and intolerance, indicating a gene-environment correlation. If this association is stronger than between G2's genes and their emotional warmth and intolerance toward their own children, then this would indicate the presence of an evocative gene-environment correlation. To further understand how G1 mother's parenting has been evoked by genetically influenced characteristics of the child (G2), we examined whether child (G2) temperament partially accounted for the association between offspring genes and parental responses. METHODS: Participants were from the Young Finns Study. G1 mothers (N = 2,349; mean age 39 years) self-reported the emotional warmth and intolerance toward G2 in 1980 when the participants were from 3 to 18 years old. G2 participants answered the same parenting scales in 2007/2012 (N = 1,378; mean age = 38 years in 2007; 59% female) when their children were on average 11 years old. Offspring temperament traits were self-reported in 1992 (G2 age range 15-30 years). Estimation of the phenotypic variance explained by the SNPs of G2 was done by genome-wide complex trait analysis with restricted maximum likelihood (GCTA-GREML). RESULTS: Results showed that the SNPs of a child (G2) explained 22.6% of the phenotypic variance of maternal intolerance (G1; p-value = .039). G2 temperament trait negative emotionality explained only 2.4% points of this association. G2 genes did not explain G1 emotional warmth or G2's own emotional warmth and intolerance. However, further analyses of a combined measure of both G1 parenting scales found genetic effects. Parent or child gender did not moderate the observed associations. CONCLUSIONS: Presented genome-wide evidence is pointing to the important role a child plays in affecting and shaping his/her family environment, though the underlying mechanisms remain unclear.

Oxytocin receptor gene (OXTR) variant rs1042778 moderates the influence of family environment on changes in perceived social support over time.

BACKGROUND: Lack of social support is an established risk factor across health outcomes, making it important to examine its family environmental and genetic determinants. METHODS: In a 27-year follow-up of the Young Finns Study (N = 2341), we examined with a latent growth curve model whether genes involved in the oxytocin signaling pathway-namely, oxytocin receptor gene (OXTR) variants rs1042778, rs2254298, and rs53576-moderate the effect of early-life social experiences on perceived social support across the life span. Mothers reported the emotional warmth and acceptance towards their children at baseline when the participants were from 3 to 18 years old (1980). Perceived family support and support from friends and peripheral sources were assessed in five follow-ups 18 years apart (1989-2007). RESULTS: Maternal emotional warmth and acceptance predicted the initial level of perceived social support across subscales, while the rate of change in family support was affected by the family environment only if participants carried the T-allele of OXTR rs1042778. This gene-environment interaction was not found for the rate of change in support from friends and peripheral sources and we also did not find associations between latent growth in perceived social support and OXTR variants rs53576 and rs2254298. LIMITATIONS: Selective attrition in perceived social support, maternal emotional warmth and acceptance, gender, and SES. Family environment was assessed by a non-standardized measure. CONCLUSIONS: OXTR rs1042778 polymorphism seems to contribute to changes in perceived family support in that way that some individuals (T-allele carriers) 'recover', to some extent, from the effects of early-life social experiences, whereas others (G/G genotype carriers) do not.