Shared Environmental Factors Research Articles

Genetic and environmental variation in educational attainment: an individual-based analysis of 28 twin cohorts

We investigated the heritability of educational attainment and how it differed between birth cohorts and cultural–geographic regions. A classical twin design was applied to pooled data from 28 cohorts representing 16 countries and including 193,518 twins with information on educational attainment at 25 years of age or older. Genetic factors explained the major part of individual differences in educational attainment (heritability: a2 = 0.43; 0.41–0.44), but also environmental variation shared by co-twins was substantial (c2 = 0.31; 0.30–0.33). The proportions of educational variation explained by genetic and shared environmental factors did not differ between Europe, North America and Australia, and East Asia. When restricted to twins 30 years or older to confirm finalized education, the heritability was higher in the older cohorts born in 1900–1949 (a2 = 0.44; 0.41–0.46) than in the later cohorts born in 1950–1989 (a2 = 0.38; 0.36–0.40), with a corresponding lower influence of common environmental factors (c2 = 0.31; 0.29–0.33 and c2 = 0.34; 0.32–0.36, respectively). In conclusion, both genetic and environmental factors shared by co-twins have an important influence on individual differences in educational attainment. The effect of genetic factors on educational attainment has decreased from the cohorts born before to those born after the 1950s.

Association of subclinical psychosis with suicidal ideation: A twin study

Subclinical psychosis, including schizotypal indicators and psychotic experiences, predicts future suicidal ideation. This relationship may reflect unmeasured confounding from environmental factors, genetic factors, or both. We used a genetically-informative twin design to understand if the association between subclinical psychosis and suicidal ideation is independent of shared genetic and environmental factors. We analysed cross-sectional associations of age-22 self-reported subclinical psychosis (positive, negative, and disorganised features) with suicidal ideation in twins participating in the FinnTwin12 study (maximum n = 1213). Then, we analysed the reverse association of age-14 suicidal ideation with age-22 subclinical psychosis. Associations were studied first among individuals and then within monozygotic (MZ) and dizygotic (DZ) pairs. Individual-level analyses showed that all subclinical psychosis factors were associated with suicidal ideation. In within-pair analyses, estimates of associations were lower for MZ pairs than DZ pairs, except for the negative schizotypy–suicidal ideation association where estimates were consistent across individual-level and within-pair analyses. Findings provide evidence that the association between negative features and suicide ideation is not explained by familial factors and may be causal, though the possibility of confounding by individual-specific environmental factors and reverse causation cannot be ruled out. The relationships of positive and disorganised subclinical psychosis features with suicidal ideation cannot be explained by confounding due to environmental factors shared between siblings, but their associations may be due to shared genetic factors.

Nasopharyngeal Epstein-Barr virus DNA loads in high-risk nasopharyngeal carcinoma families: Familial aggregation and host heritability.

Nasopharyngeal carcinoma (NPC), the most common head and neck cancer, is characterized by distinct geographic distribution and familial aggregation. Multiple risk factors, including host genetics, environmental factor, and EBV infection, have been linked to the development of NPC, particularly in the familial clustering cases. However, the cause of NPC endemicity remains enigmatic due possibly to the complicated interplay between these risk factors. Recently, positive Epstein‐Barr virus (EBV) DNA loads at nasopharyngeal (NP) cavity has been found to reflect NPC development and applied in NPC screening. To examine whether the increased NP EBV loads could aggregate in the families and be affected by host genetics and environmental factor, EBV loads were obtained by 510 NP brushing samples from eligible unaffected individuals, who have two or more relatives affected with NPC, in 116 high‐risk NPC families. The correlation of relative pairs was estimated using S.A.G.E. (version 6.4, 2016), and host heritability of NP EBV loads was calculated with variance component models using SOLAR (version 8.4.2, 2019). In result, significant correlations of EBV loads were observed between parent‐offspring pairs and sibling‐sibling pairs (P < .001), but not in distant kin relationship pairs. Interestingly, after excluding the shared environmental factor within families, host genetics contributes significantly to NP EBV loads with a heritability of 56.41% (P = 1.00 × 10−7), and its effect was slightly elevated (68.86%, P = 3.40 × 10−6) in families with more NPC cases (≥3). These findings indicate that additional host‐genetic variants involved in the EBV local NP mucosal behavior may be especially important for the development of NPC.

Cohort profile: the AUstralian Twin BACK pain and physical activity study (AUTBACK study)

PurposeDespite the growing evidence that physical activity and familial factors play a role in low back pain (LBP), there is a lack of robust longitudinal studies that (1) investigate the...

Association of parental substance misuse with offspring substance misuse and criminality: a genetically informed register-based study.

Genetically informed studies have provided mixed findings as to what extent parental substance misuse is associated with offspring substance misuse and antisocial behavior due to shared environmental and genetic factors. We linked data from nationwide registries for a cohort of 2 476 198 offspring born in Sweden 1958-1995 and their parents. Substance misuse was defined as International Classification of Diseases diagnoses of alcohol/drug use disorders or alcohol/drug-related criminal convictions. Quantitative genetic offspring-of-siblings analyses in offspring of monozygotic and dizygotic twin, full-sibling, and half-sibling parents were conducted. Both maternal and paternal substance misuse were robustly associated with offspring substance misuse [maternal adjusted hazard ratio (aHR) = 1.83 (95% confidence interval (CI) 1.80-1.87); paternal aHR = 1.96 (1.94-1.98)] and criminal convictions [maternal aHR = 1.56 (1.54-1.58); paternal aHR = 1.66 (1.64-1.67)]. Additive genetic effects explained 42% (95% CI 25-56%) and 46% (36-55%) of the variance in maternal and paternal substance misuse, respectively, and between 36 and 44% of the variance in substance misuse and criminality in offspring. The associations between parental substance misuse and offspring outcomes were mostly due to additive genetic effects, which explained 54-85% of the parent-offspring covariance. However, both nuclear and extended family environmental factors also contributed to the associations, especially with offspring substance misuse. Our findings from a large offspring-of-siblings study indicate that shared genetic influences mostly explain the associations between parental substance misuse and both offspring substance misuse and criminality, but we also found evidence for the contribution of environmental factors shared by members of nuclear and extended families.

Pre-Term Delivery and Risk of Ischemic Heart Disease in Women

BackgroundWomen who deliver pre-term have been reported to have increased future risks of cardiometabolic disorders. However, their long-term risks of ischemic heart disease (IHD) and whether such risks are due to shared familial factors are unclear. A better understanding of these risks may help improve long-term clinical follow-up and interventions to prevent IHD in women. ObjectivesThe purpose of this study was to determine the long-term risks of IHD in women by pregnancy duration. MethodsA national cohort study was conducted of all 2,189,190 women with a singleton delivery in Sweden from 1973 to 2015, who were followed up for IHD through the end of 2015. Cox regression was used to compute adjusted hazard ratios (aHRs) for IHD associated with pregnancy duration, and cosibling analyses assessed the influence of shared familial (genetic and/or environmental) factors. ResultsIn 47.5 million person-years of follow-up, 49,955 (2.3%) women were diagnosed with IHD. In the 10 years following delivery, the aHR for IHD associated with pre-term delivery (<37 weeks) was 2.47 (95% confidence interval [CI]: 2.16 to 2.82), and further stratified was 4.04 (95% CI: 2.69 to 6.08) for extremely pre-term (22 to 27 weeks), 2.62 (95% CI: 2.09 to 3.29) for very pre-term (28 to 33 weeks), 2.30 (95% CI: 1.97 to 2.70) for late pre-term (34 to 36 weeks), and 1.47 (95% CI: 1.30 to 1.65) for early-term (37 to 38 weeks), compared with full-term (39 to 41 weeks). These risks declined but remained significantly elevated after additional follow-up (pre-term vs. full-term, 10 to 19 years: aHR: 1.86; 95% CI: 1.73 to 1.99; 20 to 29 years: aHR: 1.52; 95% CI: 1.45 to 1.59; 30 to 43 years: aHR: 1.38; 95% CI: 1.32 to 1.45). These findings did not appear attributable to shared genetic or environmental factors within families. Additional pre-term deliveries were associated with further increases in risk. ConclusionsIn this large national cohort, pre-term delivery was a strong independent risk factor for IHD. This association waned over time but remained substantially elevated up to 40 years later. Pre-term delivery should be recognized as a risk factor for IHD in women across the life course.

1653-P: Association between Genetic Admixture Estimates for Five Ancestral Populations and Diabetes-Related Traits in Pacific Islanders

Ecological studies have shown different risks for diabetes (DM) among many ethnic groups, but whether they are due to genetic or non-genetic factors is hard to dissect. We conducted a community-based study aimed at identifying risk factors for DM and related traits in Pacific Islanders from Guam and Saipan. We analyzed the genetic structure of our sample and estimated individual-level admixture using genome-wide SNP data (49,300 variants). We found that genetic ancestry largely derived from 5 populations, representing Marianas Islanders (MI) (mean % heritage, or μ=43%), East Asians (EA, μ=22%), Micronesians (MC, μ=19%), Europeans (EU, μ=13%), and Melanesians (ML, μ=3%). We then tested the association of ancestry estimates with DM, fasting glucose and fasting insulin levels in study participants (n=1,853). Covariates included age, sex and end-stage kidney disease. For fasting insulin, only nondiabetic subjects were used in analyses. All 3 traits were associated with genetic ancestry (p&amp;lt;e-4). EA was associated with lowest DM risk and lowest mean levels of glucose and insulin, while DM risk and fasting glucose were highest in MI. DM risk (measured as odds ratio [OR]) for MI vs. EA was 6.9 (95% CI=3.3-14.7). Mean difference (β) in fasting glucose and insulin for MI vs. EA was 0.83 and 0.76 s.d. units, respectively. MI had higher DM risk compared to MC (OR=1.79, p=0.022), but similar risk to EU and ML. MI had higher mean glucose vs. MC (β=0.23 s.d. units, p=0.014). However, MI had comparable insulin levels to EU and MC, but lower than ML (β=-1.37 s.d. units, p=0.0046). In summary, there were large and statistically significant differences in DM-related traits among Pacific Islanders with different genetic ancestral backgrounds. Although genetic ancestry estimates may still be confounded by shared environmental factors, the present findings suggest that admixture mapping may be a potentially powerful approach for identifying unique DM loci in Pacific Islanders. Disclosure W. Hsueh: None. P. Kumar: None. S. Safabakhsh: None. L. Jones: None. J. Curran: None. W.C. Knowler: None. R.G. Nelson: None. R.L. Hanson: None.

Effects of parental sensitivity in different contexts on children’s hot and cool effortful control.

To thrive as an individual and within society, children need to develop the ability to control their behavior. Using a twin design, we estimated the relative influence of genetic, shared, and unique environmental factors on hot and cool effortful control (EC). Furthermore, we investigated whether parental sensitivity in a play, task, or discipline context when the children were on average 3.78 years old, was differentially related to children's hot and cool EC 1 year later (Mage 4.77 years). We included 476 children from 238 twin pairs (48% boys, 58% monozygotic) and their primary parent. Hot EC (delay of gratification) was measured with the marshmallow test and cool EC (response inhibition) was measured with a stop-signal task. The behavioral genetics analyses showed that individual differences in hot and cool EC were mostly explained by unique environmental factors, whereas their association was mostly explained by shared environmental factors. Controlling for sensitivity in the other contexts, task sensitivity contributed to the prediction of cool EC, and sensitive discipline contributed to both cool and hot EC. Play sensitivity did not contribute to the prediction of hot or cool EC over and above parental sensitivity in the other contexts. Our study contributes to a better understanding of the unique and shared antecedents of hot and cool EC, suggesting parental sensitive discipline as a focus for preventive interventions targeting both hot and cool EC. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Common etiological architecture underlying reward responsiveness, externally driven eating behaviors, and BMI in childhood: findings from the Gemini twin cohort.

BackgroundStudies have reported that impulsivity predicts childhood BMI and that the association is mediated by eating behaviors. One aspect of impulsivity – potentially crucial in the obesity context – is reward responsiveness, which may predispose to responsiveness to palatable food cues. The behavioral susceptibility theory hypothesizes that genetic susceptibility to obesity operates partly via genetically determined differences in appetite regulation. Reward responsiveness may therefore be one of the neuro-endophenotypes that mediates genetic susceptibility to obesity.ObjectiveTo test whether reward responsiveness, eating behaviors and child BMI share common genetic architecture.MethodsWe examined reward responsiveness, eating behaviors and BMI in five-year-old children from Gemini, a UK birth cohort of 2,402 twin pairs born in 2007. All measures were collected by parent report. Reward responsiveness was derived from the Behavioral Approach System. Compulsion to eat and eating for pleasure was measured with the ‘food responsiveness’ scale of the Child Eating Behavior Questionnaire. Wanting to eat in response to environmental food cues was measured with the ‘external eating’ scale of the Dutch Eating Behavior Questionnaire. Maximum-likelihood structural equation modelling was used to establish underlying common genetic and environmental influences.ResultsThere were significant positive phenotypic correlations between all traits except for reward responsiveness and BMI. Genetic factors explained the majority of the association between food responsiveness and external eating (74%, 95%CI: 61, 87), whereas common shared environmental factors explained the majority of the associations between reward responsiveness with both food responsiveness (55%, 95%CI: 20, 90) and external eating (70%, 95%CI: 39, 100).ConclusionsOur study demonstrates the importance of common environmental factors in the shared etiology between reward responsiveness and childhood eating behaviors. However, the common etiology underlying both reward responsiveness and BMI is unclear, as there was no phenotypic correlation between reward responsiveness and BMI at this age. Further longitudinal research needs to detangle this complex relationship throughout development.

Association between personality profile and subclinical atherosclerosis: The role of genes and environment

BackgroundThe mechanism underlying the association between personality profile and subclinical atherosclerosis is poorly understood. This study explores the association between personality, carotid atherosclerosis and arterial stiffness, and the contribution of genes and environment to this association. MethodsEarly atherosclerotic traits, including carotid intima-media thickness (CCA-IMT), aortic pulse wave velocity (PWVao) and heart rate, were assessed in 318 adult twins, who also completed a Big Five personality questionnaire. Using the co-twin control approach, the association between intra-pair differences in clinical and personality scores was assessed in dizygotic (DZ) and monozygotic (MZ) twins separately. ResultsAn association between CCA-IMT and extroverted personality, as well as between PWVao and openness to experience was detected. The inverse association between CCA-IMT and extraversion was persistent in DZ and disappeared in MZ twins, suggesting genetic confounding. In contrast, the association between PWVao and openness to experience was of the same magnitude in DZ and MZ twins, thus surviving the adjustment for genetic and shared environmental factors. ConclusionsThis study highlights that the association between some psychological factors and cardiovascular traits may be partly explained by genetic factors. This result may provide support for the feasibility of prevention programs based on assessing familiarity for personality disorders to detect genetic risk for subclinical cardiovascular disease.

Effects of immunization with heat-killed Mycobacterium vaccae on autism spectrum disorder-like behavior and epileptogenesis in a rat model of comorbid autism and epilepsy

Autism spectrum disorders (ASDs) and epilepsy are often comorbid. The basis for this co-occurrence remains unknown; however, inflammatory stressors during development are a shared risk factor. To explore this association, we tested the effect of repeated immunizations using a heat-killed preparation of the stress-protective immunoregulatory microbe Mycobacterium vaccae NCTC 11,659 (M. vaccae) on the behavioral and epileptogenic consequences of the combined stress-terbutaline (ST) rat model of ASD-like behavior/epilepsy. Repeated immunization of the dam with M. vaccae during pregnancy, followed by immunization of the pups after terbutaline injections, prevented the expression of ASD-like behavior but did not appear to protect against, and may have even enhanced, the spontaneous epileptogenic effects of ST. Maternal M. vaccae injections transferred an anti-inflammatory immunophenotype to offspring, and repeated injections across development prevented ST-induced increases in microglial density at early developmental time points in a region-specific manner. Despite epidemiological comorbidity between ASD/epileptic conditions and shared environmental risk factors, our results suggest that the expression of ASD-like behaviors, but perhaps not epileptogenesis, is sensitive to early anti-inflammatory intervention. These data provide support for the exploration of immunoregulatory strategies to prevent the negative neurodevelopmental behavioral effects of stressors during early critical periods.

Modeling Etiology of Smoking During Pregnancy in Swedish Twins, Full-, and Half-Siblings, Reared Together and Apart.

Using Swedish nationwide registry data, we investigated the contribution of genetic and environmental risk factors to the etiology of smoking status across stages of pregnancy with increasing degrees of social and psychological pressure to reduce or quit smoking, by twin and sibling modeling. Smoking status was available before, and during early and late pregnancy from the Medical Birth Register. Twin, full-, and half-sibling pairs, both reared together and apart, born between 1960 and 1990 were obtained from national twin and genealogical registers. Genetic structural equation modeling in OpenMx was applied to the population-based data to estimate shared genetic and/or environmental covariance across stages of pregnancy, accounting for maternal birth cohort and age at pregnancy. Analyses of paired data on 258 749 individuals suggested that risk factors for smoking status changed across stages of pregnancy. Results predicted substantial heritability (60-70%) and moderate contributions of shared environmental factors (10-15%) for smoking status. Whilst the same shared environmental factors were amplified from before pregnancy to late pregnancy, new primarily unique environmental factors explained ~10% of the variance during early pregnancy which was carried forward to late pregnancy. Using registry data on women across pregnancy, we replicated that smoking status is highly heritable. Furthermore, we found support for increased impact of shared environmental factors during pregnancy of factors already present prior to pregnancy, and an independent set of mostly new unique environmental factors that may be triggered by increased social pressure to reduce or quit smoking during pregnancy. As new factors partially explain smoking status during pregnancy and the effects of familial factors increase across pregnancy, efforts to prevent or reduce smoking during pregnancy should receive continued attention, with a focus on both the individual and the family unit.

How Heritable are Parental Sensitivity and Limit-Setting? A Longitudinal Child-Based Twin Study on Observed Parenting.

We examined the relative contribution of genetic, shared environmental and non‐shared environmental factors to the covariance between parental sensitivity and limit‐setting observed twice in a longitudinal study using a child‐based twin design. Parental sensitivity and parental limit‐setting were observed in 236 parents with each of their same‐sex toddler twin children (M age = 3.8 years; 58% monozygotic). Bivariate behavioral genetic models indicated substantial effects of similar shared environmental factors on parental sensitivity and limit‐setting and on the overlap within sensitivity and limit‐setting across 1 year. Moderate child‐driven genetic effects were found for parental limit‐setting in year 1 and across 1 year. Genetic child factors contributing to explaining the variance in limit‐setting over time were the same, whereas shared environmental factors showed some overlap.

Does listening to music increase your ability to discriminate musical sounds?

Music listening plays an important role in the daily lives of many. It remains unclear what explains variation in how much time people spend listening to music and whether music listening improves musical auditory discrimination skills. In 10,780 Swedish twin individuals, data were available on hours of music listening, musical engagement and musical auditory discrimination. Genetic and shared environmental factors together explain half of the variation in music listening in both sexes. Hours of music listening was positively associated with musical auditory discrimination in both sexes and this effect was independent of whether individuals played a musical instrument. However, the effect disappeared when applying a co-twin control analysis to control for genetic and shared environmental confounding. These findings suggest that music listening may not causally improve musical auditory discrimination skills, but rather that the association is likely due to shared familial factors.

Familial Aggregation and Heritability of Aldosteronism with Cardiovascular Events

To date, the effect of positive family history as a risk factor of primary aldosteronism (PA) is largely unknown. Studies have failed to distinguish the heritability of PA as well as the associations between positive family history of PA and clinical outcomes. We quantified the prevalence, the extent of familial aggregation, the heritability of PA among family members of patients with PA, and the association between positive PA family history and major cardiovascular events (MACE). Using the Taiwan National Health Insurance Database, 30 245 077 National Health Insurance beneficiaries (both alive and those deceased between January 1, 1999, and December 31, 2015) were identified. We identified 7902 PA patients. Forty-four had PA (0.3%) among 10 234 individuals with affected parents, 2298 with affected offspring, 1924 with affected siblings, and 22 with affected twins. A positive family history was associated with the adjusted relative risk (RR) (95% confidence interval [CI]) of 11.60 (7.63-17.63) for PA in people with an affected first-degree relative. In subgroup analysis, the risk for PA across all relationships (parent, siblings, offspring, and spouse) showed highly significant differences to PA without family history. The accountability for phenotypic variance of PA was 51.0% for genetic factors, 24.9% for shared environmental factors, and 24.1% for nonshared environmental factors. PA patients with an affected first-degree relative were associated with an increased risk for composite major cardiovascular events (RR 1.31; 95% CI 1.24-1.40, P < .001) compared with PA patients without family history. Familial clustering of PA exists among a population-based study, supporting a genetic susceptibility leading to PA. There is increased coaggregation of MACE in first-degree relatives of PA patients. Our findings suggest a strong genetic component in the susceptibility of PA, involving different kinships.

Systemic manifestations of inflammatory bowel diseases

The article is devoted to the current data regarding the pathogenesis, classification and frequency of extraintestinal manifestations (EIMs) in inflammatory bowel diseases. We discuss two distinct theories of EIMs pathogenesis. First, EIMs arise from an extension of antigen-specific immune responses from the intestine to non-intestinal sites. Second, EIMs are independent inflammatory events initiated or perpetuated by the presence of IBD or by shared genetic or environmental risk factors in the host. These mechanisms are not mutually exclusive and may contribute to varying degrees in different EIMs. Early diagnosis of EIMs contributes to prevention disability and enhancement of quality of life of IBD patients. It is concluded that treatment of extraintestinal manifestations should be carried out taking into account the course of the IBD and the multidisciplinary approach, which requires close cooperation of doctors of various specialties. Assessment of prognostic markers and predictors for EIM in IBD will be part of a future investigation.

A221 CROHN’S DISEASE POLYGENIC RISK SCORE IS ASSOCIATED WITH FECAL CALPROTECTIN CONCENTRATION IN ASYMPTOMATIC FIRST-DEGREE RELATIVES OF CROHN’S DISEASE PATIENTS

Abstract Background Fecal calprotectin concentration (FC), a measure of gut inflammation is reported to be significantly higher in healthy first-degree relatives (FDR) of Crohn’s disease (CD) patients compared to healthy controls. In contrast, FC in spouses of CD patients was not significantly different from controls, suggesting that a genetic predisposition rather than a shared environmental factor affects FC. Aims We investigated the genetic association with FC in healthy FDRs of CD patients. Notably, these subjects are known to be enriched with CD risk alleles. Methods We investigated 1455 healthy Caucasian FDRs of CD patients from the GEM Project. Subjects were genotyped by HumanCoreEXOME chip and ImmunoChip platforms and then imputed by the Haplotype Reference Consortium v1.1 panel (Michigan Imputation Server). SNPs with a minor allele frequency&amp;lt;5% were removed. FC was measured using BUHLMANN ELISA kit. Heritability was estimated using a pedigree based SOLAR program and a SNP-based GCTA software. Genome wide association of FC was tested using the GEE framework that accounts for family clusters, age, sex, first 3 genetic principal components and multiplex family status (≥2 FDRs diagnosed with CD). In addition, CD-polygenic risk scores were derived based on summary statistics and imputed SNPs from a recent GWAS by pruning and thresholding (P+T) and LDPred algorithm (PMID:31002795). Results Among 1455 subjects, 45.2% were male, median age was 19 years (IQR 13–26), 8.8% were from multiplex families, and median FC was 52 mg/kg (IQR 31–87; 20.8% had FC&amp;gt;100). We estimated the heritability of FC to be 27% (27.1%, standard error=9%, p&amp;lt;0.001 by pedigree approach; 27.9%, SE=12%, p&amp;lt;0.001 by SNP approach). An untargeted GWAS failed to show any significant association with FC (i.e. p&amp;lt;5x10-8). The lowest p value was obtained for rs224631 (p=5x10-7). Strikingly, an increase in CD polygenic risk scores was significantly associated with an increase of FC (p=5.2x10-5 with P+T method). Conclusions We demonstrate that FC concentration is a heritable trait in unaffected FDRs of CD patients. Although the association between genetic variants with FC did not reach GWAS significance, CD-polygenic risk score, which incorporates small effect size CD-associated SNPs, was significantly associated with FC concentrationin this cohort. Our results suggest that FC concentration is influenced genetically with contributions from CD-associated SNPs in unaffected FDRs of CD probands. It remains to be determined if the genetic influence to FC concentration is dependent/independent with the future development of CD. Submitted on behalf of The CCC-GEM Project research team Funding Agencies CCCHelmsley Charitable Trust/ Mount Sinai Hospital Fellowship Award

Alternative polygenic associations

Human Genetics To predict traits and/or disease from genomic information, we must understand the genetics of the associations between genotype and phenotype. Polygenic risk scores are increasingly used to make predictions of phenotype on the basis of all the loci that correlate with a specific trait identified in genome-wide association studies (GWASs). However, population-level genetics and variable environmental effects can affect GWAS results. To determine the extent of any skewed GWAS results, Mostafavi et al. examined the accuracy of GWASs in a relatively homogeneous population: individuals of European-British descent within the UK Biobank. They found that sex, age, and socioeconomic status can affect GWAS signals. The authors suggest that using data from families within GWASs should help pull out direct and indirect effects, such as shared environmental factors and assortative mating to increase the accuracy of polygenic risk score prediction. eLife 9 , e48376 (2020).

The Roadmap From Allergic Rhinitis to Asthma

Upper and lower airways display some common characteristic described as a holistic model. Because rhinitis may proceed asthma, it is imperative to understand the mechanisms and risk factors responsible for the progression from rhinitis to asthma. Subclinical lower airway abnormalities have been observed in patients with rhinitis without asthma. Recent evidence indicates that these patients may have an increased risk of developing asthma. Environmental and genetic factors can contribute to enhance this possibility. The treatments of rhinitis have also been shown to be beneficial to the lower airway, and therefore potentially modify the natural evolution of the atopic march. Lower airway disease is a good predictor for the roadmap from rhinitis to asthma. The shared genetic link and environmental factors could be essential for this progression. Albeit treatment of rhinitis has a beneficial effect on lower airway defects, their role to prevent the progression to asthma remains yet to be confirmed.

Sources of Stability in Social and Economic Ideological Orientations: Cohort, Context, and Construct Effects

Abstract Existing research shows that ideological orientations are stable after young adulthood. Extending research on the sources of ideological stability, we examine social and economic ideology over a 3- to 4-year period in two twin panels (one Danish and one American). We find evidence for the importance of genetic influences and individual life experiences on the stability of social ideology in both contexts; shared environmental factors play an important role in the younger, Danish sample only. For economic ideology, genetic factors contribute to stability in the American sample only. Our findings show that the role of genetic and environmental factors in the stability of ideological orientations varies by type of ideology, national context, and, possibly, age cohort.