Polygenic prediction of educational attainment within and between families from genome-wide association analyses in 3 million individuals

We conduct a genome-wide association study (GWAS) of educational attainment (EA) in a sample of ~3 million individuals and identify 3,952 approximately uncorrelated genome-wide-significant single-nucleotide polymorphisms (SNPs). A genome-wide polygenic predictor, or polygenic index (PGI), explains 12–16% of EA variance and contributes to risk prediction for ten diseases. Direct effects (i.e., controlling for parental PGIs) explain roughly half the PGI’s magnitude of association with EA and other phenotypes. The correlation between mate-pair PGIs is far too large to be consistent with phenotypic assortment alone, implying additional assortment on PGI-associated factors. In an additional GWAS of dominance deviations from the additive model, we identify no genome-wide-significant SNPs, and a separate X-chromosome additive GWAS identifies 57

Polygenic prediction of educational attainment within and between families from genome-wide association analyses in 3 million individuals

Publisher Copyright: © 2022, The Author(s).We conduct a genome-wide association study (GWAS) of educational attainment (EA) in a sample of ~3 million individuals and identify 3,952 approximately uncorrelated genome-wide-significant single-nucleotide polymorphisms (SNPs). A genome-wide polygenic predictor, or polygenic index (PGI), explains 12–16% of EA variance and contributes to risk prediction for ten diseases. Direct effects (i.e., controlling for parental PGIs) explain roughly half the PGI’s magnitude of association with EA and other phenotypes. The correlation between mate-pair PGIs is far too large to be consistent with phenotypic assortment alone, implying additional assortment on PGI-associated factors. In an additional GWAS of dominance deviations from the additive model, we identify no genome-wide-significant SNPs, and a separate X-chromosome additive GWAS identifies 57.Peer reviewe

Within-sibship genome-wide association analyses decrease bias in estimates of direct genetic effects

Estimates from genome-wide association studies (GWAS) of unrelated individuals capture effects of inherited variation (direct effects), demography (population stratification, assortative mating) and relatives (indirect genetic effects). Family-based GWAS designs can control for demographic and indirect genetic effects, but large-scale family datasets have been lacking. We combined data from 178,086 siblings from 19 cohorts to generate population (between-family) and within-sibship (within-family) GWAS estimates for 25 phenotypes. Within-sibship GWAS estimates were smaller than population estimates for height, educational attainment, age at first birth, number of children, cognitive ability, depressive symptoms and smoking. Some differences were observed in downstream SNP heritability, genetic correlations and Mendelian randomization analyses. For example, the within-sibship genetic correlation between educational attainment and body mass index attenuated towards zero. In contrast, analyses of most molecular phenotypes (for example, low-density lipoprotein-cholesterol) were generally consistent. We also found within-sibship evidence of polygenic adaptation on taller height. Here, we illustrate the importance of family-based GWAS data for phenotypes influenced by demographic and indirect genetic effects

Polygenic prediction of educational attainment within and between families from genome-wide association analyses in 3 million individuals

We conduct a genome-wide association study (GWAS) of educational attainment (EA) in a sample of ~3 million individuals and identify 3,952 approximately uncorrelated genome-wide-significant single-nucleotide polymorphisms (SNPs). A genome-wide polygenic predictor, or polygenic index (PGI), explains 12-16% of EA variance and contributes to risk prediction for ten diseases. Direct effects (i.e., controlling for parental PGIs) explain roughly half the PGI's magnitude of association with EA and other phenotypes. The correlation between mate-pair PGIs is far too large to be consistent with phenotypic assortment alone, implying additional assortment on PGI-associated factors. In an additional GWAS of dominance deviations from the additive model, we identify no genome-wide-significant SNPs, and a separate X-chromosome additive GWAS identifies 57

Essays on the collective action dilemma of vaccination

Vaccines famously possess positive externalities that make them susceptible to the collective action dilemma: when I get vaccinated, I protect not only myself, but also those who I might otherwise have infected. Thus, some people will have an incentive to free ride on the immunity of others. In a population of rational agents, the critical level of vaccination uptake required for herd immunity will therefore be difficult to attain in the long run, which poses difficulties for disease eradication. In this doctoral dissertation, I explore different implications of the collective action dilemma of vaccination, and different ways of ameliorating it. First: given that coercion or force could solve the dilemma, and democracies may be less likely to engage in policies that violate the physical integrity of citizens, democracies may also be at a disadvantage compared to non-democracies when securing herd immunity. In essay I, I show that this is, empirically, indeed the case. Barring the use of extensive coercion therefore necessitates other solutions. In essay II, I highlight the exception to individual rationality found in other-regarding motivations such as altruism. Our moral psychology has likely evolved to take other's welfare into account, but the extent of our prosocial motivations vary: a wider form of altruism that encompasses not just family or friends, but strangers, is likely to give way to a more narrow form when humans pair-bond and have children. This dynamic is shown to apply to the sentiments underlying vaccination behavior as well: appeals to the welfare of society of getting vaccinated have positive effects on vaccination propensity, but this effect disappears in people with families and children. On this demographic, appeals to the welfare of close loved ones instead appears to have large effects. In essay III, I investigate whether the prosocial motivations underlying vaccination behavior are liable to be affected by motivation crowding - that is, whether they are crowded out when introducing economic incentives to get vaccinated. I find that on average, economic incentives do not have adverse effects, but for a small minority of highly prosocially motivated people, they might

Moral Enhancement Should Target Self-Interest and Cognitive Capacity

Current suggestions for capacities that should be targeted for moral enhancement has centered on traits like empathy, fairness or aggression. The literature, however, lacks a proper model for understanding the interplay and complexity of moral capacities, which limits the practicability of proposed interventions. In this paper, I integrate some existing knowledge on the nature of human moral behavior and present a formal model of prosocial motivation. The model provides two important results regarding the most friction-free route to moral enhancement. First, we should consider decreasing self-interested motivation rather than increasing prosociality directly. Second, this should be complemented with cognitive enhancement. These suggestions are tested against existing and emerging evidence on cognitive capacity, mindfulness meditation and the effects of psychedelic drugs and are found to have sufficient grounding for further theoretical and empirical exploration. Furthermore, moral effects of the latter two are hypothesized to result from a diminished sense of self with subsequent reductions in self-interest

Är Leviathan giftig? : Autonomi och repression som förklaringar till regimskillnader i förväntad livslängd

Det senaste decenniet har en rad studier publicerats som undersöker hur ett lands mest fundamentala politiska organisationssätt, regimtypen, påverkar befolkningens hälsa. Resultaten pekar entydigt på att invånare i demokratier lever längre och friskare liv än invånare i icke-demokratier. Flera förklaringar till detta har förts fram, bland annat att demokratier omfördelar mer och är bättre på att investera i hälsofrämjande resurser, och att diktaturers tendens att kontrollera media går ut över förmågan att sprida hälsofrämjande information. När dessa mekanismer kontrolleras för visar det sig dock att demokrati har en stor kvarvarande samvariation med exempelvis medellivslängden, vilket talar för att andra mekanismer också är inblandade.I denna uppsats undersöks två ytterligare mekanismer som berör de eventuella psykosocialt medierade hälsoeffekter som regimtypen kan ha, nämligen via politisk repression, och de negativa effekter på kronisk stress detta kan tänkas ha, samt autonomi, vilket ansluter till en omfattande tidigare socialepidemiologisk litteratur. I uppsatsen används en ekologisk tvärsnittsdesign och landnivådata, huvudsakligen från Världsbanken och Freedom House, analyseras med enkel multipel OLS-regression. Resultaten visar att all kvarvarande samvariation fångas upp av faktorn autonomi, medan politisk repression inte får något stöd som medierande faktor. Detta kan tyda på att den känsla av personlig autonomi som demokratier kan tillgodose är en minst lika viktig faktor att ta i beaktande som fördelning av resurser och tillgång till information.During the last decade a number of studies have been published that investigate how the most fundamental aspect of political organization, the regime type, affects population health. The results unanimously show that citizens of democracies live longer and healthier lives than citizens of non-democracies. Many explanations for this have been suggested, among these are that democracies redistribute more and invest more in salutogenic resources, and that the tendency of dictatorships to control the media negatively affects the ability to spread information crucial to public health. When these mechanisms are controlled for, however, it turns out that democracy has a large residual correlation with for example life expectancy, which suggests that other mechanisms are also involved.In this paper two new mechanisms regarding the possible psychosocially mediated health effects of the regime type are investigated, namely political repression, and the possible negative effects this might have on the levels of chronic stress, and autonomy, which connects to a large previous literature in social epidemiology. In the paper an ecological cross-country design is used and country-level data, provided mainly by the World Bank and Freedom House, is analyzed with a simple multiple OLS-regression model. The results show that that all residual correlation is captured by autonomy, while there is no evidence for political repression as a mediating factor. This could suggest that the feeling of personal autonomy that democracies can fulfill is an equally important factor to take into account as distribution of resources and access to information

Extraversion Probably Does Not Cause Political Participation. Evidence from Two Genetically Informed Designs

A substantial literature in political psychology has emphasized the importance of personality traits for understanding differences in political participation. One such trait is extraversion. However, the causal status of this relationship is complicated by a number of issues, not least genetic confounding stemming from the heritability of both personality traits and political participation. This study confirms the well-established naive relationship between extraversion and participation, but goes on with (a) a discordant MZ twin design and (b) a new approach using measured genetic variation, or a polygenic index, in the given trait (extraversion) to assess the causal nature of this relationship. First, utilizing variation in extraversion and participation within identical twin pairs shows that twins with higher extraversion do not participate more. Second, random variation within fraternal twin pairs in a polygenic index of extraversion does predict trait extraversion, but does not predict political participation. In summary, previously identified associations between extraversion and political participation are not likely to be causal, but instead reflect common underlying familial factors

Uncovering the source of patrimonial voting

The boom in wealth inequality seen in recent decades has generated a steep rise in scholarly interest in both the drivers and the consequences of the wealth gap. In political science, a pertinent questionregards the political behavior across the wealth spectrum. A common argument is that the wealthy practice patrimonial voting, i.e. voting for right-wing parties to maximize returns on their assets. While thispattern is descriptively well documented, it is less certain to what extent this reflects an actual causal relationship between wealth and political preferences. In this study, we provide new evidence by exploitingwealth variation within identical twin pairs. Our findings suggest that while more wealth is descriptivelyconnected to more support for right-wing parties, the causal impact of wealth on policy preferences islikely highly overstated. For several relevant policy areas these effects may not exist at all. Furthermore,the bias in naive observational estimates seems to be mainly driven by environmental familial confoundersshared within twin pairs, rather than genetic confounding