How not to respond to populism

Although the nature and definition of populism are a source of considerable disagreement, there seems to be a minimal consensus by now that populism poses a number of threats to liberal democracy, and that public authorities should therefore act in defence of the latter. In searching for appropriate responses, however, most scholars draw from strategies for combatting anti-democratic or extremist parties, without considering the important differences between populist parties and these other political actors. We argue that the two central types of democratic defence—the ‘intolerant’ militant democratic defence and the ‘tolerant’ defence—do not offer satisfying responses to populist parties precisely because they were conceived and developed as responses to different phenomena. For public authorities to successfully address populism, responses need to contain its most egregious characteristics, yet salvage its productive side

Nativism, civic nationalism and the malleability of voter attitudes

Nativism is one of the defining phenomena of the contemporary era. Yet, we know little about how malleable citizen attitudes associated with nativism and nationalism are to priming effects when media frames which deal with key issues such as immigration are introduced. In this article, we present the findings from a survey experiment fielded to a nationally representative sample of voters in Australia in May 2019. In it, we explore whether the attitudes of voters for different political parties can be primed by introducing two contrasting media frames to measure these effects. We find positive and negative frames have no effect on the attitudes of voters for Australia’s populist radical right party, but that the former has an effect on centre-right voters in Australia. Such findings have important implications for our understanding of political communication and the malleability of political attitudes

The Democracy in Europe Movement (DiEM25) and the limitations of transnational populism

Can you create an electorally successful left populist movement beyond the nation state? Benjamin Moffitt, Benjamin De Cleen, Panos Panayotu and Yannis Stavrakakis examine the transnational populist European movement DiEM25, which stood in several countries in the recent European Parliament elections, and considers its prospects in establishing an electorally competitive movement at the transnational level

Association between genetic and socioenvironmental risk for schizophrenia during upbringing in a UK longitudinal cohort

BACKGROUND: Associations of socioenvironmental features like urbanicity and neighborhood deprivation with psychosis are well-established. An enduring question, however, is whether these associations are causal. Genetic confounding could occur due to downward mobility of individuals at high genetic risk for psychiatric problems into disadvantaged environments. METHODS: We examined correlations of five indices of genetic risk [polygenic risk scores (PRS) for schizophrenia and depression, maternal psychotic symptoms, family psychiatric history, and zygosity-based latent genetic risk] with multiple area-, neighborhood-, and family-level risks during upbringing. Data were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally-representative cohort of 2232 British twins born in 1994–1995 and followed to age 18 (93% retention). Socioenvironmental risks included urbanicity, air pollution, neighborhood deprivation, neighborhood crime, neighborhood disorder, social cohesion, residential mobility, family poverty, and a cumulative environmental risk scale. At age 18, participants were privately interviewed about psychotic experiences. RESULTS: Higher genetic risk on all indices was associated with riskier environments during upbringing. For example, participants with higher schizophrenia PRS (OR = 1.19, 95% CI = 1.06–1.33), depression PRS (OR = 1.20, 95% CI = 1.08–1.34), family history (OR = 1.25, 95% CI = 1.11–1.40), and latent genetic risk (OR = 1.21, 95% CI = 1.07–1.38) had accumulated more socioenvironmental risks for schizophrenia by age 18. However, associations between socioenvironmental risks and psychotic experiences mostly remained significant after covariate adjustment for genetic risk. CONCLUSION: Genetic risk is correlated with socioenvironmental risk for schizophrenia during upbringing, but the associations between socioenvironmental risk and adolescent psychotic experiences appear, at present, to exist above and beyond this gene-environment correlation

Mother's and children's ADHD genetic risk, household chaos and children's ADHD symptoms:A gene–environment correlation study

BACKGROUND: Chaotic home environments may contribute to children's attention‐deficit hyperactivity disorder (ADHD) symptoms. However, ADHD genetic risk may also influence household chaos. This study investigated whether children in chaotic households had more ADHD symptoms, if mothers and children with higher ADHD genetic risk lived in more chaotic households, and the joint association of genetic risk and household chaos on the longitudinal course of ADHD symptoms across childhood. METHODS: Participants were mothers and children from the Environmental Risk (E‐Risk) Longitudinal Twin Study, a UK population‐representative birth cohort of 2,232 twins. Children's ADHD symptoms were assessed at ages 5, 7, 10 and 12 years. Household chaos was rated by research workers at ages 7, 10 and 12, and by mother's and twin's self‐report at age 12. Genome‐wide ADHD polygenic risk scores (PRS) were calculated for mothers (n = 880) and twins (n = 1,999); of these, n = 871 mothers and n = 1,925 children had information on children's ADHD and household chaos. RESULTS: Children in more chaotic households had higher ADHD symptoms. Mothers and children with higher ADHD PRS lived in more chaotic households. Children's ADHD PRS was associated with household chaos over and above mother's PRS, suggesting evocative gene–environment correlation. Children in more chaotic households had higher baseline ADHD symptoms and a slower rate of decline in symptoms. However, sensitivity analyses estimated that gene–environment correlation accounted for a large proportion of the association of household chaos on ADHD symptoms. CONCLUSIONS: Children's ADHD genetic risk was independently associated with higher levels of household chaos, emphasising the active role of children in shaping their home environment. Our findings suggest that household chaos partly reflects children's genetic risk for ADHD, calling into question whether household chaos directly influences children's core ADHD symptoms. Our findings highlight the importance of considering parent and child genetic risk in relation to apparent environmental exposures

Polygenic risk and the course of Attention-Deficit/Hyperactivity Disorder from childhood to young adulthood:Findings from a nationally representative cohort

OBJECTIVE: To understand whether genetic risk for attention-deficit/hyperactivity disorder (ADHD) is associated with the course of the disorder across childhood and into young adulthood. METHOD: Participants were from the Environmental Risk (E-Risk) Longitudinal Twin Study, a population-based birth cohort of 2,232 twins. ADHD was assessed at ages 5, 7, 10, and 12 with mother- and teacher-reports and at age 18 with self-report. Polygenic risk scores (PRSs) were created using a genome-wide association study of ADHD case status. Associations with PRS were examined at multiple points in childhood and longitudinally from early childhood to adolescence. We investigated ADHD PRS and course to young adulthood, as reflected by ADHD remission, persistence, and late onset. RESULTS: Participants with higher ADHD PRSs had increased risk for meeting ADHD diagnostic criteria (odds ratios ranging from 1.17 at age 10 to 1.54 at age 12) and for elevated symptoms at ages 5, 7, 10, and 12. Higher PRS was longitudinally associated with more hyperactivity/impulsivity (incidence rate ratio = 1.18) and inattention (incidence rate ratio = 1.14) from age 5 to age 12. In young adulthood, participants with persistent ADHD exhibited the highest PRS (mean PRS = 0.37), followed by participants with remission (mean PRS = 0.21); both groups had higher PRS than controls (mean PRS = −0.03), but did not significantly differ from one another. Participants with late-onset ADHD did not show elevated PRS for ADHD, depression, alcohol dependence, or marijuana use disorder. CONCLUSION: Genetic risk scores derived from case-control genome-wide association studies may have relevance not only for incidence of mental health disorders, but also for understanding the longitudinal course of mental health disorders