Suchergebnisse

"Idén med boken kom av att låta föra samman essäer kring frågor som på olika sätt berör Sverige från synvinklar som inte är direkt gängse. Både in- och utrikespolitiskt har den förda politiken länge splittrat och försvagat landet utan att någon riktigt förmått (eller vågat) staka ut en annan färdriktning. Det gör Haveriet till en unik bok i Sverige. Ett slags nutidsdokument över rådande samhällsutveckling. Möjligen säger det något om vårt lands tillstånd när kända debattörer och författare väljer att gå samman och skapa en bok som speglar samhällsutvecklingen och föreslår lösningar på en rad olika samhällsproblem."--Provided by the publisher

Recent studies have shown that trusting attitudes and behavior are biologically influenced. Focusing on the classic trust game, it has been demonstrated that oxytocin increases trust and that humans are endowed with genetic variation that influences their behavior in the game. Moreover, several studies have shown that a large share of the variation in survey responses to trust items is accounted for by an additive genetic component. Against this backdrop, this article makes two important contributions. First, utilizing a unique sample of more than 2,000 complete Swedish twin pairs, we provide further evidence of the heritability of social trust. Our estimates of the additive genetic component in social trust were consistent across the sexes – .33 for males and .39 for females – and are similar to the results reported in earlier studies. Secondly, we show that social trust is phenotypically related to three psychological traits – extraversion, personal control, and intelligence – and that genetic factors account for most of these correlations. Jointly, these psychological factors share around 30% of the genetic influence on social trust both for males and females. Future studies should further explore the possible causal pathways between genes and trust using panel data on both psychological traits and social trust.

AbstractThe Swedish Twin Registry functions as research infrastructure containing information on 216,258 twins born between 1886 and 2015, of whom 86,199 pairs have zygosity determined by DNA, an intrapair similarity algorithm, or being of opposite sex. In essence, practically all twins alive and currently 9 years or older have been invited for participation and donation of DNA on which genomewide single nucleotide polymorphisms array genotyping has been performed. Content, management and alternatives for future improvements are discussed.

According to the theory of evolved sex differences in jealousy, the challenge for women to ensure paternal investment increased their jealousy response to emotional infidelity, whereas paternal uncertainty exerted selective pressures that shaped men to become more distressed by sexual infidelity. Several studies have investigated whether the effect of these sexually dimorphic selection pressures can be detected in contemporary human populations, with conflicting results. To date, no genetically informed studies of sex differences in jealousy have been conducted. We used data from the Screening Across the Lifespan of Twins Younger (SALTY) sample, containing information concerning self-rated jealousy from 3,197 complete twin pairs collected by the Swedish Twin Registry. Intra-class correlations and structural equation models were used to assess the genetic influence on jealousy and to investigate sex differences at genetic level. We saw a highly significant sex effect on the relationship between infidelity types, indicating that men, relative to women, reported greater jealousy in response to sexual infidelity than in response to emotional infidelity. The twin models revealed significant heritabilities for both sexual (32%) and emotional (26%) jealousy. The heritabilities were of a similar magnitude in both sexes, and no qualitative sex differences could be detected. We show for the first time that variance in jealousy is to some extent explained by genetic factors. Even though our results from the mean value analyses are in line with the theory of evolved sex differences in jealousy, we could not identify any sex differences on a genetic level.

One of the clearest results in previous studies on social trust is the robust positive relationship with educational attainment. The most common interpretation is that education has a causal effect on social trust. The theoretical argument and empirical results in this article suggest a different interpretation. We argue that common preadult factors such as cognitive abilities and personality traits rooted in genes and early‐life family environment may confound the relationship between educational attainment and social trust. We provide new evidence on this question by utilizing the quasi‐experiment of twinning. By looking at the relationship between education and social trust within monozygotic (MZ) twin pairs, we are able to avoid potential confounders rooted in genetic factors and common environmental influences because the monozygotic twins share both. The results suggest that when controlling for such familial factors the estimated effects of education on social trust are close to zero and far from reaching statistical significance. Further analyses show that the relationship between education and social trust largely is driven by common genetic factors.

Recent research demonstrates that a wide range of political attitudes, beliefs, and behaviors canbe explained in part by genetic variation. However, these studies have not yet identied themechanisms that generate such a relationship. Some scholars have speculated that psychologicaltraits mediate the relationship between genes and political participation, but so far there havebeen no empirical tests. Here we focus on the role of three psychological traits that are believed toinuence political participation: cognitive ability, personal control, and extraversion. Utilizinga unique sample of more than 2,000 Swedish twin pairs, we show that a common genetic factorcan explain most of the relationship between these psychological traits and acts of politicalparticipation as well as predispositions related to participation. While our analysis is not adenitive test, our results suggest an upper bound for a proposed mediation relationship betweengenes, psychological traits, and political participation. ; Nature, nurture, and political attitudes and behavior

Asthma is a common childhood disease and several risk factors have been identified; however, the impact of genes and environment is not fully understood. The aim of the Swedish Twin study On Prediction and Prevention of Asthma (STOPPA) is to identify environmental (birth characteristics and early life) and genetic (including epigenetic) factors as determinants for asthmatic disease. Based on the Child and Adolescent Twin Study in Sweden (CATSS) (parental interview at 9 or 12 years, N ~23,900) and an asthma and/or wheezing algorithm, we identified a sample of monozygotic (MZ) and dizygotic (DZ) same-sexed twin pairs. The twin pairs were classified as asthma concordant (ACC), asthma discordant (ADC) and healthy concordant (HCC). A sample of 9- to 14-year-old twins and their parents were invited to participate in a clinical examination. Background characteristics were collected in questionnaires and obtained from the National Health Registers. A clinical examination was performed to test lung function and capacity (spirometry with reversibility test and exhaled nitric oxide) and collect blood (serology and DNA), urine (metabolites), feces (microbiota), and saliva (cortisol). In total, 376 twin pairs (752 individual twins) completed the study, response rate 52%. All participating twins answered the questionnaire and >90% participated in lung function testing, blood-, and saliva sampling. This article describes the design, recruitment, data collection, measures, and background characteristics, as well as ongoing and planned analyses in STOPPA. Potential gains of the study include the identification of biomarkers, the emergence of candidates for drug development, and new leads for prevention of asthma and allergic disease.

Recent research demonstrates that a wide range of political attitudes, beliefs, and behaviors can be explained in part by genetic variation. However, these studies have not yet identified the mechanisms that generate such a relationship. Some scholars have speculated that psychological traits mediate the relationship between genes and political participation, but so far there have been no empirical tests. Here we focus on the role of three psychological traits that are believed to influence political participation: cognitive ability, personal control, and extraversion. Utilizing a unique sample of more than 2,000 Swedish twin pairs, we show that a common genetic factor can explain most of the relationship between these psychological traits and acts of political participation, as well as predispositions related to participation. While our analysis is not a definitive test, our results suggest an upper bound for a proposed mediation relationship between genes, psychological traits, and political participation.

Recent research has demonstrated that genetic differences explain a sizeable fraction of the variance in political orientations but little is known about the pathways through which genes might affect political preferences. In this paper we use a uniquely assembled dataset of almost 1,000 Swedish male twin pairs containing detailed information on cognitive ability and political attitudes in order to further examine the genetic and environmental causes of political orientations. Our study makes three distinct contributions to our understanding of the etiology of political orientations: (i) we report heritability estimates across different dimensions of political ideology; (ii) we show that cognitive ability and political orientations are related; and (iii) we provide evidence consistent with the hypothesis that cognitive ability mediates part of the genetic influence on political orientations. These findings provide important clues about the nature of the complex pathways from molecular genetic variation to political orientations. ; NAture, nurture and political orientations

AbstractIn twin studies of cardiovascular disease biomarkers the dizygotic correlations are often estimated to be less than half of monozygotic correlations indicating a potential influence of nonadditive genetic factors. Using a large and homogenous sample, we estimated the additive and dominance genetic influences on levels of high density lipoprotein, low density lipoprotein, apolipoprotein A-I, apolipoprotein B, total cholesterol, triglycerides, glucose, hemoglobin Alc and c-reactive protein, all of which are biomarkers associated with cardiovascular disease. The blood biomarkers were measured on 12,000 Swedish twins born between 1911 and 1958. The large sample allowed us to obtain heritability estimates with considerable precision and provided adequate statistical power for estimation of dominance genetic components. Our study showed complete absence of the shared environment component for the investigated traits. Dominant genetic component was shown to be significant for low density lipoprotein (0.18), glucose (0.31), Hemoglobin Alc (0.55), and c-reactive protein (0.27). To our knowledge, this is the first statistically significant evidence for dominance genetic variance found for low density lipoprotein, glucose, hemoglobin Alc, and c-reactive protein in a population based twin sample. The study highlights the importance of acknowledging nonadditive genes underlying the risk of developing cardiovascular diseases.

Recent research has demonstrated that genetic differences explain a sizeable fraction of the variance in political orientations, but little is known about the pathways through which genes might affect political preferences. In this article, we use a uniquely assembled dataset of almost 1,000 Swedish male twin pairs containing detailed information on cognitive ability and political attitudes in order to further examine the genetic and environmental causes of political orientations. Our study makes three distinct contributions to our understanding of the etiology of political orientations: (1) we report heritability estimates across different dimensions of political ideology; (2) we show that cognitive ability and political orientations are related; and (3) we provide evidence consistent with the hypothesis that cognitive ability mediates part of the genetic influence on political orientations. These findings provide important clues about the nature of the complex pathways from molecular genetic variation to political orientations.

Monozygotic (MZ) twins stem from the same single fertilized egg and therefore share all theirinheritedgenetic variation. This is one of the unequivocal facts on which genetic epidemiology and twin studies are based. To what extent this also implies that MZ twins share genotypes in adult tissues is not precisely established, but a common pragmatic assumption is that MZ twins are 100% genetically identical also in adult tissues. During the past decade, this view has been challenged by several reports, with observations of differences in post-zygotic copy number variations (CNVs) between members of the same MZ pair. In this study, we performed a systematic search for differences of CNVs within 38 adult MZ pairs who had been misclassified as dizygotic (DZ) twins by questionnaire-based assessment. Initial scoring by PennCNV suggested a total of 967 CNV discordances. The within-pair correlation in number of CNVs detected was strongly dependent on confidence score filtering and reached a plateau ofr= 0.8 when restricting to CNVs detected with confidence score larger than 50. The top-ranked discordances were subsequently selected for validation by quantitative polymerase chain reaction (qPCR), from which one single ~120kb deletion inNRXN1on chromosome 2 (bp 51017111–51136802) was validated. Despite involving an exon, no sign of cognitive/mental consequences was apparent in the affected twin pair, potentially reflecting limited or lack of expression of the transcripts containing this exon in nerve/brain.