ABSTRACT
Genome-wide association studies of human personality have been carried out, but transcription of the whole genome has not been studied in relation to personality in humans. We collected genome-wide expression profiles of adults to characterize the regulation of expression and function in genes related to human personality. We devised an innovative multi-omic approach to network analysis to identify the key control elements and interactions in multi-modular networks. We identified sets of transcribed genes that were co-expressed in specific brain regions with genes known to be associated with personality. Then we identified the minimum networks for the co-localized genes using bioinformatic resources. Subjects were 459 adults from the Young Finns Study who completed the Temperament and Character Inventory and provided peripheral blood for genomic and transcriptomic analysis. We identified an extrinsic network of 45 regulatory genes from seed genes in brain regions involved in self-regulation of emotional reactivity to extracellular stimuli (e.g., self-regulation of anxiety) and an intrinsic network of 43 regulatory genes from seed genes in brain regions involved in self-regulation of interpretations of meaning (e.g., production of concepts and language). We discovered that interactions between the two networks were coordinated by a control hub of 3 miRNAs and 3 protein-coding genes shared by both. Interactions of the control hub with proteins and ncRNAs identified more than 100 genes that overlap directly with known personality-related genes and more than another 4000 genes that interact indirectly. We conclude that the six-gene hub is the crux of an integrative network that orchestrates information-transfer throughout a multi-modular system of over 4000 genes enriched in liquid-liquid-phase-separation (LLPS)-related RNAs, diverse transcription factors, and hominid-specific miRNAs and lncRNAs. Gene expression networks associated with human personality regulate neuronal plasticity, epigenesis, and adaptive functioning by the interactions of salience and meaning in self-awareness.
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BACKGROUND: A great number of case-control and population-based studies have shown that depression patients differ from healthy controls in their temperament traits. We investigated whether polygenic risk for depression predicts trajectories of temperament traits from early adulthood to middle age. METHODS: Participants came from the population-based Young Finns Study (n = 2212). The calculation for Polygenic risk for depression (PRS) was based on the most recent genome-wide association study. Temperament traits of Harm Avoidance, Novelty Seeking, Reward Dependence, and Persistence were assessed with the Temperament and Character Inventory in 1997, 2001, 2007, and 2012 (participants being 24-50-year-olds). As covariates, we used depressive symptoms as assessed by a modified version of the Beck Depression Inventory, psychosocial family environment from parent-filled questionnaires, and socioeconomic factors from adulthood. RESULTS: High PRS predicted higher Persistence from early adulthood to middle age (p = 0.003) when controlling for depressive symptoms, psychosocial family environment, and socioeconomic factors. PRS did not predict trajectories of Novelty Seeking (p = 0.063-0.416 in different models) or Reward Dependence (p = 0.531-0.736). The results remained unaffected when participants with diagnosed affective disorders were excluded. Additionally, we found an interaction between PRS and depressive symptoms when predicting the Harm Avoidance subscale Anticipatory Worry, indicating that the association of Anticipatory Worry with depressive symptoms is stronger in individuals with higher (vs. lower) PRS. LIMITATIONS: There was some attrition due to the long follow-up. CONCLUSIONS: High polygenic risk for major depression may predict differences in temperament trajectories among those who have not developed any severe affective disorders.
Subject(s)
Depressive Disorder, Major , Temperament , Middle Aged , Humans , Adult , Depression/epidemiology , Depression/genetics , Depression/diagnosis , Genome-Wide Association Study , Depressive Disorder, Major/psychology , Character , Personality InventoryABSTRACT
Schizophrenia is often regarded as a disorder of premature aging. We investigated (a) whether polygenic risk for schizophrenia (PRSsch ) relates to pace of epigenetic aging and (b) whether personal dispositions toward active and emotionally close relationships protect against accelerated epigenetic aging in individuals with high PRSsch . The sample came from the population-based Young Finns Study (n = 1348). Epigenetic aging was measured with DNA methylation aging algorithms such as AgeAccelHannum , EEAAHannum , IEAAHannum , IEAAHorvath , AgeAccelHorvath , AgeAccelPheno , AgeAccelGrim , and DunedinPACE. A PRSsch was calculated using summary statistics from the most comprehensive genome-wide association study of schizophrenia to date. Social dispositions were assessed in terms of extraversion, sociability, reward dependence, cooperativeness, and attachment security. We found that PRSsch did not have a statistically significant effect on any studied indicator of epigenetic aging. Instead, PRSsch had a significant interaction with reward dependence (p = 0.001-0.004), cooperation (p = 0.009-0.020), extraversion (p = 0.019-0.041), sociability (p = 0.003-0.016), and attachment security (p = 0.007-0.014) in predicting AgeAccelHannum , EEAAHannum , or IEAAHannum . Specifically, participants with high PRSsch appeared to display accelerated epigenetic aging at higher (vs. lower) levels of extraversion, sociability, attachment security, reward dependence, and cooperativeness. A rather opposite pattern was evident for those with low PRSsch . No such interactions were evident when predicting the other indicators of epigenetic aging. In conclusion, against our hypothesis, frequent social interactions may relate to accelerated epigenetic aging in individuals at risk for psychosis. We speculate that this may be explained by social-cognitive impairments (perceiving social situations as overwhelming or excessively arousing) or ending up in less supportive or deviant social groups.
Subject(s)
Schizophrenia , Humans , Schizophrenia/genetics , Genome-Wide Association Study , Finland , Epigenesis, Genetic/genetics , Aging/genetics , DNA Methylation/geneticsABSTRACT
BACKGROUND: We investigated (a) whether polygenic risk for schizophrenia predicts different trajectories of social development among those who have not developed psychoses and (b) whether possible associations are PRSSCZ-specific or evident also for any polygenic risk for mental disorders, e.g. for major depression. METHODS: Participants came from the population-based Young Finns Study (n = 2377). We calculated a polygenic risk score for schizophrenia (PRSSCZ) and for major depression (PRSDEP). Diagnoses of psychotic disorders were derived from the hospital care register. Social development from adolescence to middle age was measured by (a) perceived social support from friends, family, and a close other, (b) perceived sociability, and (c) family structure (partnership status, number of children, age of first-time parenthood). RESULTS: Among those without manifest psychoses, high PRSSCZ predicted lower experienced support from friends (B = -0.04, p = 0.009-0.035) and family (B = -0.04, p = 0.009-0.035) especially after early adulthood, and also lower perceived sociability (B = -0.05, p = 0.010-0.026). PRSSCZ was not related to family structure. PRSDEP did not predict any domain of social development. CONCLUSIONS: Individuals at high PRSSCZ (not converted to psychosis) seem to experience a lower preference to be with others over being alone. Individuals with high (v. low) PRSSCZ seem to have a similar family structure in terms of partnership status or number of children but, nevertheless, they experience less support from their family. Among those not converted to psychosis in a typical age period, high PRSSCZ may predict a 'later risk phase' and reduced functional resilience when approaching middle age.
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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.
Subject(s)
Psychotic Disorders , Humans , Child , Cohort Studies , Follow-Up Studies , Psychotic Disorders/epidemiology , Parents , Mood DisordersABSTRACT
We investigated whether individuals, who have a high polygenic loading for schizophrenia and major depression (PGL) but have not developed the respective disorders, are still susceptible to experience milder forms of ill-being in terms of job strain or exhaustion. We used the population-based Young Finns Study data (n = 928). PGL was assessed with a cumulative score of the polygenic risk scores for schizophrenia and depression. Participants (24-49-year-olds) evaluated their exhaustion levels and perceived job characteristics over a 10-year follow-up (2001, 2007, 2011). Participants with diagnosed psychotic or affective disorders were excluded. We found that high PGL did not predict less favorable perceptions of job environment (job strain, demands, control, satisfaction, social support at work) but high PGL predicted a higher trajectory of exhaustion in early adulthood and middle age. Additionally, high (vs. low) PGL predicted a stronger increase in exhaustion at increased levels of job strain. These findings remained after controlling for sex, socioeconomic factors, health behaviors, and cognitive performance. In conclusion, individuals with high PGL may have an elevated liability to experience exhaustion especially in early adulthood and middle age (despite they perceive their job environment similarly than others), and especially and at high levels of job strain.
Subject(s)
Burnout, Professional , Occupational Stress , Middle Aged , Humans , Adult , Burnout, Professional/psychology , Occupational Stress/psychology , Socioeconomic Factors , Personal Satisfaction , Finland/epidemiology , Job Satisfaction , Surveys and QuestionnairesABSTRACT
Individuals with grandiose narcissism exhibit enhanced antagonism and a defensive pattern of discordance between their emotional and physiological reactions to self-threatening evaluations. Although theoretical perspectives link narcissistic defensiveness to negative emotions, empirical evidence linking grandiose narcissism to emotional reactivity remains mixed. The current study used self-reported affect, electrocardiography, and facial electromyography (fEMG) to examine whether people scoring high in grandiose narcissism show amplified physiological and self-reported emotional reactivity to negative social evaluation. Following two challenging cognitive tasks, participants received negative and neutral feedback in a face-to-face evaluation situation. Receiving negative feedback decreased self-reported positive affect and dominance, slowed heart rate, and amplified fEMG activity related to frowning and eye constriction. Although self-reported emotional reactions were unrelated to grandiose narcissism, fEMG activity associated with negative affect was significantly enhanced by grandiose narcissism. In conclusion, individuals with higher levels of grandiose narcissism may not be willing to report overt emotional reactivity to self-threatening feedback, but physiological responses "beneath their thin skin" reveal amplified threat-related facial muscle activity suggestive of a negative emotional state.
Subject(s)
Narcissus , Humans , Facial Muscles , Emotions , Mood Disorders , NarcissismABSTRACT
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.
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Background: We investigated whether stress-related exhaustion (chronic or short-term, and co-occurring with depression or not) is related to cognitive performance and whether polygenic cognitive potential modifies these associations. Methods: The participants were from the Young Finns Study (N = 541-1273). Stress-related exhaustion was assessed using the Maastricht Questionnaire, depressive symptoms with the Beck Depression Inventory, and cognitive performance with subtests of the Cambridge Neuropsychological Test Automated Battery, measuring visuospatial learning, reaction time, sustained attention, and executive function. Cognitive performance and depression were assessed in 2011, and exhaustion in 2001, 2007, and 2011. A polygenic score for cognitive potential was calculated based on a GWAS on intelligence. Results: High stress-related exhaustion, especially chronic, was associated with slower reaction time. Only clinical levels of depression were related to slower reaction time. Polygenic cognitive potential did not modify these associations. There were no differences in cognitive performance between individuals with co-occurring exhaustion and depression vs. those with only either condition. Conclusion: Stress-related exhaustion, especially if chronic, seems to relate to slower reactions. Co-occurring exhaustion and depression may not have additive effects on cognitive performance. High polygenic cognitive potential may not protect from or predispose to harmful effects of exhaustion or depression on reaction time. Supplementary Information: The online version contains supplementary material available at 10.1007/s10608-023-10354-z.
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OBJECTIVE: An adverse psychosocial environment in childhood may harm cognitive development, but the associations for adulthood cognitive function remain obscure. We tested the hypothesis that adverse childhood psychosocial factors associate with poor cognitive function in midlife by leveraging the prospective data from the Young Finns Study. METHOD: At the age of 3-18 years, the participants' psychosocial factors (socioeconomic and emotional environment, parental health behaviors, stressful events, child's self-regulatory behavior, and social adjustment) were collected. In addition to the separate psychosocial factors, a score indicating their clustering was created. Cognitive function was measured at the age of 34-49 years with a computerized test addressing learning and memory (N = 1,011), working memory (N = 1,091), sustained attention and information processing (N = 1,071), and reaction and movement time (N = 999). RESULTS: We observed an inverse association between the accumulation of unfavorable childhood psychosocial factors and poorer learning and memory in midlife (age, sex, education, adulthood smoking, alcohol drinking, and physical activity adjusted ß = -0.032, SE = 0.01, p = .009). This association corresponded approximately to the effect of 7 months aging. Specifically, poor self-regulatory behavior (ß = -0.074, SE = 0.03, p = .032) and social adjustment in childhood (ß = -0.111, SE = 0.03, p = .001) associated with poorer learning ability and memory 30 years later. No associations were found for other cognitive domains. CONCLUSIONS: The findings suggest an association of childhood psychosocial factors with midlife learning ability and memory. If these links are causal, the results highlight the importance of a child's self-regulation and social adjustment as plausible determinants for adulthood cognitive health. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
Subject(s)
Cognition , Smoking , Child , Humans , Adult , Child, Preschool , Adolescent , Middle Aged , Finland/epidemiology , Prospective Studies , Risk FactorsABSTRACT
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.
Subject(s)
Cognition , Genome-Wide Association Study , Adult , Child , Educational Status , Humans , Neuropsychological Tests , Prospective StudiesABSTRACT
Substantial genetic correlations have been reported across psychiatric disorders and numerous cross-disorder genetic variants have been detected. To identify the genetic variants underlying general psychopathology in childhood, we performed a genome-wide association study using a total psychiatric problem score. We analyzed 6,844,199 common SNPs in 38,418 school-aged children from 20 population-based cohorts participating in the EAGLE consortium. The SNP heritability of total psychiatric problems was 5.4% (SE = 0.01) and two loci reached genome-wide significance: rs10767094 and rs202005905. We also observed an association of SBF2, a gene associated with neuroticism in previous GWAS, with total psychiatric problems. The genetic effects underlying the total score were shared with common psychiatric disorders only (attention-deficit/hyperactivity disorder, anxiety, depression, insomnia) (rG > 0.49), but not with autism or the less common adult disorders (schizophrenia, bipolar disorder, or eating disorders) (rG < 0.01). Importantly, the total psychiatric problem score also showed at least a moderate genetic correlation with intelligence, educational attainment, wellbeing, smoking, and body fat (rG > 0.29). The results suggest that many common genetic variants are associated with childhood psychiatric symptoms and related phenotypes in general instead of with specific symptoms. Further research is needed to establish causality and pleiotropic mechanisms between related traits.
Subject(s)
Attention Deficit Disorder with Hyperactivity , Bipolar Disorder , Attention Deficit Disorder with Hyperactivity/genetics , Attention Deficit Disorder with Hyperactivity/psychology , Bipolar Disorder/genetics , Genetic Predisposition to Disease , Genome-Wide Association Study/methods , Humans , Polymorphism, Single NucleotideABSTRACT
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.
Subject(s)
Psychotic Disorders , Schizophrenia , Middle Aged , Humans , Adult , Child , Young Adult , Schizophrenia/genetics , Schizophrenia/diagnosis , Genome-Wide Association Study , Multifactorial Inheritance/genetics , Psychotic Disorders/diagnosis , Risk Factors , Genetic Predisposition to Disease/geneticsABSTRACT
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.
Subject(s)
Cognition , Temperament , Adult , Character , Humans , Intelligence/genetics , Middle Aged , Multifactorial InheritanceABSTRACT
Introduction: This meta-analysis investigated (1) whether ethnic minority and majority members have a neural inter-group bias toward each other, and (2) whether various ethnic groups (i.e., White, Black, and Asian) are processed in the brain differently by the other respective ethnicities. Methods: A systematic coordinate-based meta-analysis of functional magnetic resonance imaging (fMRI) studies was conducted using Web of Science, PubMed, and PsycINFO (altogether 50 datasets, n = 1211, 50.1% female). Results: We found that ethnic minority members did not show any signs of neural inter-group bias (e.g., no majority-group derogation). Ethnic majority members, in turn, expressed biased responses toward minority (vs. majority) members in frontal, parietal, temporal, and occipital regions that are known to be involved in e.g., facial processing, attention, and perspective-taking. We also found differences in neural response patterns toward different ethnic groups (White, Black, and Asian); broadest biases in neural response patterns were evident toward Black individuals (in non-Black individuals). Heterogeneity was mostly minor or low. Discussion: Overall, the findings increase understanding of neural processes involved in ethnicity perception and cognition as well as ethnic prejudices and discrimination. This meta-analysis provides explanations for previous behavioral reports on ethnic discrimination toward minority groups.
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We investigated (a) whether psychosocial factors (experienced stress, anticipatory worry, social detachment, sleeping disturbances, alcohol use) predict the course of paranoid ideation between the ages of 24 to 50 years and (b) whether the predictive relationships are more likely to proceed from the psychosocial factors to paranoid ideation, or vice versa. The participants (N = 1534-1553) came from the population-based Young Finns study. Paranoid ideation and psychosocial factors were assessed by reliable self-report questionnaires in 2001, 2007, and 2011/2012. The data were analyzed using growth curve and structural equation models. High experienced stress, anticipatory worry, social detachment, frequent sleeping disturbances, and frequent alcohol use predicted more paranoid ideation. More risk factors predicted increasing paranoid ideation. There were bidirectional predictive relationships of paranoid ideation with experienced stress, anticipatory worry, social detachment, and sleeping disturbances. The link between alcohol use and paranoid ideation was only correlative. In conclusion, paranoid ideation increases by reciprocal interactions with stress, worry, social detachment, and sleeping disturbances. The findings support the threat-anticipation model of paranoid ideation, providing important implications for treatment of paranoia.
Subject(s)
Anxiety , Paranoid Disorders , Adult , Anxiety/psychology , Humans , Middle Aged , Paranoid Disorders/etiology , Paranoid Disorders/psychology , Risk Factors , Self Report , Surveys and Questionnaires , Young AdultABSTRACT
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.
ABSTRACT
In-group favoritism and prejudices relate to discriminatory behaviors but, despite decades of research, understanding of their neural correlates has been limited. A systematic coordinate-based meta-analysis of functional magnetic resonance imaging (fMRI) studies (altogether 87 original datasets, n = 2328) was conducted to investigate neural inter-group biases, i.e., responses toward in-group vs. out-group in different contexts. We found inter-group biases in some previously identified brain regions (e.g., the medial prefrontal cortex, insula) but also in many previously non-identified brain regions (e.g., the cerebellum, precentral gyrus). Sub-group analyses indicated that neural correlates of inter-group biases may be mostly context-specific. Regarding different types of group memberships, inter-group bias toward trivial groups was evident only in the cingulate cortex, while inter-group biases toward "real" groups (ethnic, national, or political groups) involved broader sets of brain regions. Additionally, there were heightened neural threat responses toward out-groups' faces and stronger neural empathic responses toward in-groups' suffering. We did not obtain significant publication bias. Overall, the findings provide novel implications for theory and prejudice-reduction interventions.
Subject(s)
Brain Mapping , Brain , Bias , Brain/diagnostic imaging , Brain/physiology , Humans , Magnetic Resonance Imaging/methods , PrejudiceABSTRACT
Dispositional compassion has been shown to predict higher well-being and to be associated with lower perceived stress and higher social support. Thus, compassion may be a potential individual factor protecting from job strain. The current study examines (i) whether dispositional compassion predicts job strain and effort-reward imbalance (ERI) or does the predictive relationship run from job strain and ERI to dispositional compassion and (ii) the effect of dispositional compassion on the developmental trajectory of job strain and ERI over a 11-year follow-up. We used data from the Young Finns study (n=723) between 2001 and 2012. The direction of the predictive relationships was analyzed with cross-lagged panel models. Compassion's effect on the trajectories of job strain, ERI, and their components was examined with multilevel models. First, the cross-lagged panel models demonstrated there was no evidence for the predictive pathways between compassion and job strain or its components. However, the predictive pathways from high dispositional compassion to low ERI and high rewards had better fit to the data than the predictive pathways in the opposite direction. In addition, multilevel models showed that high compassion predicted various job characteristics from early adulthood to middle age (lower job strain and higher job control as well as lower ERI and higher reward). Compassion did not predict job demand/effort. The findings were obtained independently of age, gender, and socioeconomic factors in childhood and adulthood. These findings indicate that compassion may be beneficial in work context. Further, compassion might be useful in the management or prevention of some aspects of strain. Our study provides new insight about the role of compassion in work life.
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BACKGROUND: Temperament is associated with circulating inflammatory biomarkers, such as C-reactive protein (CRP), which has been associated with various health conditions, including depression. This study aims to investigate whether genetic disposition for increased circulating CRP concentration may influence temperament over the life-course. METHODS: Using a longitudinal cohort that began in 1980-the Cardiovascular Risk in Young Finns Study (YFS)-we included 920 participants (59.8% female) aged 3-12 years old at baseline (childhood), and the same participants again at ages 30-39 years old (adulthood) in this study. We used both ordinary least-squares regression (OLS linear regression) and instrumental variable (IV) regression to assess associations between CRP concentration and temperament dimensions (negative emotionality, activity, and sociability). To represent genetically determined risk for increase in circulating CRP concentration, we calculated a weighted genetic risk score (GRS) which reflects risk for increased circulating CRP concentration. RESULTS: In OLS linear regression analyses, we found that increased circulating CRP concentration in childhood was associated with slightly higher scores for sociability in childhood (19% increase, CI â= â7-32%) and adulthood (13% increase, CI â= â2-27%), and lower activity scores in adulthood (15% decrease, CI â= â3-25%). For all IV regressions, there were no apparent associations between GRS and temperament in either childhood or adulthood (all p>0.3). The Durbin-Wu-Hausman test for endogeneity produced p-values (all>0.05) that suggest there is no evidence for disagreement between the OLS and IV estimates. CONCLUSIONS: We found no clear evidence for an association of GRS for elevated CRP with childhood or adulthood emotionality, activity, or sociability, although circulating CRP was associated with some of these traits.