Improving estimation in genetic models using prior information

Statistical models used to investigate research questions in behavioral genetics often require large amounts of data. This paper introduces some key concepts of Bayesian analysis and illustrates how these methods can aid model estimation when the data does not provide enough information to reliably answer research questions. The use of informative prior distributions is discussed as a method of incorporating information from other sources than the data at hand. The procedure is illustrated with an ACE model decomposition of the variance of antisocial personality disorder. The data originates from the Norwegian Twin Registry, and includes adult twins assessed with the Structured Interview for DSM Personality (SIDP-IV). Inclusion of prior information lead to a shift with respect to conclusions about the presence of shared environmental effects compared to a traditional analysis. Small and medium sized studies should consider use of prior information to aid estimation of population parameters

Agrárpiaci Jelentések Gabona és ipari növények

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Maternal prenatal depressive symptoms and risk for early-life psychopathology in offspring: results from a genetically-informative, population-based sample

Background: Maternal prenatal depression is a known risk factor for early-life psychopathology among offspring; however, potential risk transmission mechanisms need to be distinguished. We aimed to test the relative importance of passive genetic transmission, direct exposure, and indirect exposure in the association between maternal prenatal depressive symptoms and early-life internalising and externalising psychopathology in offspring. Methods: We used structural equation modelling of phenotypic data and genetically informative relationships from the families of participants in the Norwegian Mother and Child Birth Cohort Study (MoBa). The analytic subsample of MoBa used in the current study comprises 22 195 mothers and 35 299 children. We used mothers' self-reported depressive symptoms during pregnancy, as captured by the Symptom Checklist, and their reports of symptoms of psychopathology in their offspring during the first few years of life (measured at 18, 36, and 60 months using the Child Behavior Checklist). Findings: Maternal prenatal depressive symptoms were found to be associated with early-life psychopathology primarily via intergenerationally shared genetic factors, which explained 41% (95% CI 36–46) of variance in children's internalising problems and 37% (30–44) of variance in children's externalising problems. For internalising problems, phenotypic transmission also contributed significantly, accounting for 14% (95% CI 5–19) of the association, but this contribution was found to be explained by exposure to concurrent maternal depressive symptoms, rather than by direct exposure in utero. Interpretation: Associations between maternal prenatal depressive symptoms and offspring behavioural outcomes in early childhood are likely to be at least partially explained by shared genes. This genetic confounding should be considered when attempting to quantify risks posed by in-utero exposure to maternal depressive symptoms. Funding: UK Economic and Social Research Council, Norwegian Research Council, Norwegian Ministries of Health and Care Services, and Education & Research, Wellcome Trust, Royal Society, and National Institute for Health Research

On the importance of parenting in externalizing disorders: an evaluation of indirect genetic effects in families

Background: Theoretical models of the development of childhood externalizing disorders emphasize the role of parents. Empirical studies have not been able to identify specific aspects of parental behaviors explaining a considerable proportion of the observed individual differences in externalizing problems. The problem is complicated by the contribution of genetic factors to externalizing problems, as parents provide both genes and environments to their children. We studied the joint contributions of direct genetic effects of children and the indirect genetic effects of parents through the environment on externalizing problems. Methods: The study used genome-wide single nucleotide polymorphism data from 9,675 parent–offspring trios participating in the Norwegian Mother Father and child cohort study. Based on genomic relatedness matrices, we estimated the contribution of direct genetic effects and indirect maternal and paternal genetic effects on ADHD, conduct and disruptive behaviors at 8 years of age. Results: Models including indirect parental genetic effects were preferred for the ADHD symptoms of inattention and hyperactivity, and conduct problems, but not oppositional defiant behaviors. Direct genetic effects accounted for 11% to 24% of the variance, whereas indirect parental genetic effects accounted for 0% to 16% in ADHD symptoms and conduct problems. The correlation between direct and indirect genetic effects, or gene–environment correlations, decreased the variance with 16% and 13% for conduct and inattention problems, and increased the variance with 6% for hyperactivity problems. Conclusions: This study provides empirical support to the notion that parents have a significant role in the development of childhood externalizing behaviors. The parental contribution to decrease in variation of inattention and conduct problems by gene–environment correlations would limit the number of children reaching clinical ranges in symptoms. Not accounting for indirect parental genetic effects can lead to both positive and negative bias when identifying genetic variants for childhood externalizing behaviors.publishedVersio

Modeling assortative mating and genetic similarities between partners, siblings, and in-laws

Assortative mating on heritable traits can have implications for the genetic resemblance between siblings and in-laws in succeeding generations. We studied polygenic scores and phenotypic data from pairs of partners (n = 26,681), siblings (n = 2,170), siblings-in-law (n = 3,905), and co-siblings-in-law (n = 1,763) in the Norwegian Mother, Father and Child Cohort Study. Using structural equation models, we estimated associations between measurement error-free latent genetic and phenotypic variables. We found evidence of genetic similarity between partners for educational attainment (rg = 0.37), height (rg = 0.13), and depression (rg = 0.08). Common genetic variants associated with educational attainment correlated between siblings above 0.50 (rg = 0.68) and between siblings-in-law (rg = 0.25) and co-siblings-in-law (rg = 0.09). Indirect assortment on secondary traits accounted for partner similarity in education and depression, but not in height. Comparisons between the genetic similarities of partners and siblings indicated that genetic variances were in intergenerational equilibrium. This study shows genetic similarities between extended family members and that assortative mating has taken place for several generations.publishedVersio

Familial confounding or measurement error? How to interpret findings from sibling control studies.

Epidemiological researchers often examine associations between risk factors and health outcomes in non-experimental designs. Observed associations may be causal or confounded by unmeasured factors. Sibling and co-twin control studies account for familial confounding by comparing exposure levels among siblings (or twins). If the exposure-outcome association is causal, the siblings should also differ regarding the outcome. However, such studies may sometimes introduce more bias than they alleviate. Measurement error in the exposure may bias results and lead to erroneous conclusions that truly causal exposure-outcome associations are confounded by familial factors. The current study used Monte Carlo simulations to examine bias due to measurement error in sibling control models when the observed exposure-outcome association is truly causal. The results showed that decreasing exposure reliability and increasing sibling-correlations in the exposure led to deflated exposure-outcome associations and inflated associations between the family mean of the exposure and the outcome. The risk of falsely concluding that causal associations were confounded was high in many situations. For example, when exposure reliability was 0.7 and the observed sibling-correlation was r = 0.4, about 30–90% of the samples (n = 2,000) provided results supporting a false conclusion of confounding, depending on how p-values were interpreted as evidence for a family effect on the outcome. The current results have practical importance for epidemiological researchers conducting or reviewing sibling and co-twin control studies and may improve our understanding of observed associations between risk factors and health outcomes. We have developed an app (SibSim) providing simulations of many situations not presented in this paper

Le politiche per l'agricoltura biologica in Emilia-Romagna

Analisi degli effetti delle misure di carattere politico sullo sviluppo dell'agricoltura biologica in Emilia-Romagna: descrizione della struttura del PSR; analisi degli elementi caratterizzanti la situazione dell'agricoltura biologica in Emilia-Romagna; analisi dei punti di forza e di debolezza del comparto biologico regionale, attraverso la realizzazione di un caso di studio

An Anatomy of Intergenerational Transmission: Learning from the educational attainments of Norwegian twins and their parents

Research on the intergenerational correlation of educational attainment (ICE) has long attempted to identify the impact of family background, specifically parent’s education. However, previous research has largely ignored genetic inheritance. We address this shortcoming by adopting a Multiple-Children-of-Twin design and decompose the ICE into its environmental and genetic transmission mechanisms. This decomposition reveals to what extent the impact of parents’ education operates through the rearing context and/or genetic factors. We use a register-based dataset from Norway, a context with egalitarian access to education. Our results show that the direct impact of parents’ education is negligible once genetic factors are accounted for. While genetic factors represent the main driver of the ICE, the genetic variants that mattered for educational attainment in the parent generation overlap only partially with those that mattered for their offspring’s attainment. Together, our findings complement common sociological narratives on how parent’s education affects offspring’s education by emphasizing the role of genetic transmission. Furthermore, our study challenges current research practices in genetics that overlook the importance of parallel changes in social structures and gene-expression over generations