Additive Genetic Influences Research Articles

Overlap of heritable influences between cannabis use disorder, frequency of use and opportunity to use cannabis: trivariate twin modelling and implications for genetic design.

The genetic component of Cannabis Use Disorder may overlap with influences acting more generally on early stages of cannabis use. This paper aims to determine the extent to which genetic influences on the development of cannabis abuse/dependence are correlated with those acting on the opportunity to use cannabis and frequency of use. A cross-sectional study of 3303 Australian twins, measuring age of onset of cannabis use opportunity, lifetime frequency of cannabis use, and lifetime DSM-IV cannabis abuse/dependence. A trivariate Cholesky decomposition estimated additive genetic (A), shared environment (C) and unique environment (E) contributions to the opportunity to use cannabis, the frequency of cannabis use, cannabis abuse/dependence, and the extent of overlap between genetic and environmental factors associated with each phenotype. Variance components estimates were A = 0.64 [95% confidence interval (CI) 0.58-0.70] and E = 0.36 (95% CI 0.29-0.42) for age of opportunity to use cannabis, A = 0.74 (95% CI 0.66-0.80) and E = 0.26 (95% CI 0.20-0.34) for cannabis use frequency, and A = 0.78 (95% CI 0.65-0.88) and E = 0.22 (95% CI 0.12-0.35) for cannabis abuse/dependence. Opportunity shares 45% of genetic influences with the frequency of use, and only 17% of additive genetic influences are unique to abuse/dependence from those acting on opportunity and frequency. There are significant genetic contributions to lifetime cannabis abuse/dependence, but a large proportion of this overlaps with influences acting on opportunity and frequency of use. Individuals without drug use opportunity are uninformative, and studies of drug use disorders must incorporate individual exposure to accurately identify aetiology.

Genetic and Environmental Influences on Gambling: A Meta-Analysis of Twin Studies.

Disentangling the genetic and environmental influences of gambling is important for explaining the roots of individual differences in gambling behavior and providing guidance for precaution and intervention, but we are unaware of any comprehensive and systematic quantitative meta-analysis. We systematically identified 18 twin studies on gambling in the meta-analysis. The correlation coefficients within monozygotic (MZ) and dizygotic (DZ) twins, along with the corresponding sample size, were used to calculate the proportion of the total variance accounted for by additive genes (A), dominant genes (D), the shared environment (C), and the non-shared environment plus measurement error (E). We further assessed the moderating effects of gambling assessment (symptom oriented assessment vs. behavior oriented assessment), age, and sex. The whole sample analyses showed moderate additive genetic (a2 = 0.50) and non-shared environmental influences (e2 = 0.50) on gambling. The magnitude of the genetic influence (a2) was higher for disordered gambling assessed with symptom oriented assessment (53%) than for general gambling assessed with behavior oriented assessment (41%). Additionally, the magnitude of the genetic influence (a2) was higher for adults (53%) than adolescents (42%). Genetic influence (a2) was greater for male (47%) gambling than female (28%) gambling. Shared environment had noticeable effects on female gambling (c2 = 14%) but zero effect on male gambling. In conclusion, gambling behavior was moderately heritable and moderately influenced by non-shared environmental factors. Gambling assessment, age, and sex significantly moderated the magnitude of genetic and environmental influences on gambling. Note that the number of studies might serve as a limitation.

Approximate number sense shares etiological overlap with mathematics and general cognitive ability

Approximate number sense (ANS), the ability to rapidly and accurately compare quantities presented non-symbolically, has been proposed as a precursor to mathematics skills. Earlier work reported low heritability of approximate number sense, which was interpreted as evidence that approximate number sense acts as a fitness trait. However, viewing ANS as a fitness trait is discordant with findings suggesting that individual differences in approximate number sense acuity correlate with mathematical performance, a trait with moderate genetic effects. Importantly, the shared etiology of approximate number sense, mathematics, and general cognitive ability has remained unexamined. Thus, the etiology of approximate number sense and its overlap with math and general cognitive ability was assessed in the current study with two independent twin samples (N=451 pairs). Results suggested that ANS acuity had moderate but significant additive genetic influences. ANS also had overlap with generalist genetic mechanisms accounting for variance and covariance in mathematics and general cognitive ability. Furthermore, ANS may have genetic factors unique to covariance with mathematics beyond overlap with general cognitive ability. Evidence across both samples was consistent with the proposal that the etiology of approximate number sense functions similar to that of mathematics and general cognitive skills.

Genetic and environmental influences on emotion regulation: A twin study of cognitive reappraisal and expressive suppression.

Previous studies have established that personality traits related to emotionality are moderately heritable. However, the relative heritability of the strategies people use to regulate emotions is unknown. The present study compared the magnitude of additive genetic, shared environmental, and nonshared environmental influences on 2 commonly used emotion regulation strategies: cognitive reappraisal and expressive suppression. In 743 twin pairs (1,486 twins), we replicated previous estimates of heritability of neuroticism (a2 = .41). Furthermore, cognitive reappraisal was significantly less heritable and more influenced by nonshared environment (a2 = .20; e2 = .80) than either neuroticism or suppression (a2 = .35; e2 = .65), another emotion regulation strategy. Finally, Cholesky decomposition modeling suggested that while there were common genetic and environmental influences on neuroticism, reappraisal and suppression, there were also significant nonshared environmental influences common between reappraisal and adaptive emotional functioning after controlling for neuroticism and suppression. These findings highlight that different aspects of emotional processing, even the use of different emotion regulation strategies, are differentially heritable. The importance of the nonshared environmental influences specific to reappraisal and adaptive emotional functioning speaks to the potential impact of social context, social partners, and psychosocial interventions on reappraisal habits. (PsycINFO Database Record

Genetics of serum carotenoid concentrations and their correlation with obesity-related traits in Mexican American children

Background: Dietary intake of phytonutrients present in fruits and vegetables, such as carotenoids, is associated with a lower risk of obesity and related traits, but the impact of genetic variation on these associations is poorly understood, especially in children.Objective: We estimated common genetic influences on serum carotenoid concentrations and obesity-related traits in Mexican American (MA) children.Design: Obesity-related data were obtained from 670 nondiabetic MA children, aged 6-17 y. Serum α- and β-carotenoid concentrations were measured in ∼570 (α-carotene in 565 and β-carotene in 572) of these children with the use of an ultraperformance liquid chromatography-photodiode array. We determined heritabilities for both carotenoids and examined their genetic relation with 10 obesity-related traits [body mass index (BMI), waist circumference (WC), high-density lipoprotein (HDL) cholesterol, triglycerides, fat mass (FM), systolic and diastolic blood pressure, fasting insulin and glucose, and homeostasis model assessment of insulin resistance] by using family data and a variance components approach. For these analyses, carotenoid values were inverse normalized, and all traits were adjusted for significant covariate effects of age and sex.Results: Carotenoid concentrations were highly heritable and significant [α-carotene: heritability (h2) = 0.81, P = 6.7 × 10-11; β-carotene: h2 = 0.90, P = 3.5 × 10-15]. After adjusting for multiple comparisons, we found significant (P ≤ 0.05) negative phenotypic correlations between carotenoid concentrations and the following traits: BMI, WC, FM, and triglycerides (range: α-carotene = -0.19 to -0.12; β-carotene = -0.24 to -0.13) and positive correlations with HDL cholesterol (α-carotene = 0.17; β-carotene = 0.24). However, when the phenotypic correlations were partitioned into genetic and environmental correlations, we found marginally significant (P = 0.051) genetic correlations only between β-carotene and BMI (-0.27), WC (-0.30), and HDL cholesterol (0.31) after accounting for multiple comparisons. None of the environmental correlations were significant.Conclusions: The findings from this study suggest that the serum carotenoid concentrations were under strong additive genetic influences based on variance components analyses, and that the common genetic factors may influence β-carotene and obesity and lipid traits in MA children.

Perceived Family Cohesion Moderates Environmental Influences on Prosocial Behavior in Nigerian Adolescent Twins.

Research shows that perceived family cohesion is positively related to prosocial behavior in adolescents. In this study, we investigated heritability of prosocial behavior (PB) and perceived family cohesion (FC) among Nigerian twins attending public schools in Lagos State, Nigeria (mean age = 14.7 years, SD = 1.7 years), and explored the issue of whether children's perception of cohesive family environment moderated genetic and environmental influences on (PB). The PB scale of the Strengths and Difficulties Questionnaire and the FC scale of the Family Adaptability and Cohesion Evaluation Scale III were completed by 2,376 twins (241 monozygotic (MZ) male, 354 MZ female, 440 dizygotic (DZ) male, 553 DZ female, and 788 opposite-sex DZ twins). A general sex-limitation and the bivariate genotype by environment interaction (G×E) models were applied to the data. The general sex-limitation model showed no significant sex differences, indicating that additive genetic and non-shared environmental influences were, 38% (95% CI = 31, 46) and 62% (95% CI = 54, 69) for PB and 33% (95% CI = 24, 40) and 67% (95% CI = 60, 76) for FC in both sexes. These estimates were similar to those found in Western and Asian twin studies to date. The correlation between PB and FC was 0.36. The best-fitting bivariate G×E model indicated that FC significantly moderated non-shared environmental influence unique to PB (E×E interaction). Specifically, non-shared environmental contributions to PB were highest when FC was lowest, and decreased as the levels of FC increased. However, genetic variances in PB were stable across all levels of FC. These findings suggest that FC reduces individual differences in PB by changing non-shared environmental experiences rather than genetic factors in PB.

An examination of the etiologic overlap between the genetic and environmental influences on insomnia and common psychopathology.

Insomnia is comorbid with internalizing and externalizing psychiatric disorders. However, the extent to which the etiologic influences on insomnia and common psychopathology overlap is unclear. There are limited genetically informed studies of insomnia and internalizing disorders and few studies of overlap exist with externalizing disorders. We utilized twin data from the Virginia Adult Twin Studies of Psychiatric and Substance Use Disorders (total n = 7,500). Insomnia, internalizing disorders (major depressive disorder [MDD], generalized anxiety disorder [GAD]), and alcohol abuse or dependence (AAD) were assessed at two time points, while antisocial personality disorder (ASPD) was assessed once. Cholesky decompositions were performed in OpenMx and longitudinal measurement models were run on available phenotypes to reduce measurement error. The latent additive genetic influences on insomnia overlapped significantly (56% for females, 74% for males) with MDD and were shared completely (100%) with GAD. There was significant overlap of latent unique environmental influences, with overlap ranging from 38 to 100% across disorders. In contrast, there was less genetic overlap between insomnia and externalizing disorders, with 18% of insomnia's heritability shared with AAD and 23% with ASPD. Latent unique environmental overlap between insomnia and both externalizing disorders was negligible. The evidence for substantial genetic overlap between insomnia and stable aspects of both internalizing disorders suggests that there may be few insomnia-specific genes and investigation into unique environmental factors is important for understanding insomnia development. The modest overlap between insomnia and externalizing disorders indicates that these disorders are genetically related, but largely etiologically distinct.

Genetic parameters for fatty acids in intramuscular fat from feedlot-finished Nelore carcasses

The aim of the present study was to estimate covariance components and genetic parameters for beef fatty acid (FA) composition of intramuscular fat in the longissimus thoracis muscle in Nelore bulls finished in feedlot. Twenty-two FAs were selected. The heritability estimates for individual FAs ranged from 0.01 to 0.35. The heritability estimates for myristic (0.25 ± 0.09), palmitic (0.18 ± 0.07), oleic (0.28 ± 0.09), linoleic (0.16 ± 0.06) and α-linolenic (0.35 ± 0.10) FAs were moderate. Stearic, elaidic, palmitoleic, vaccenic, conjugated linoleic acid, docosahexanoic, eicosatrienoic and arachidonic FAs had heritability estimates below 0.15. The genetic-correlation estimates between the individual saturated FAs (SFAs) were low and negative between myristic and stearic FAs (–0.22 ± 0.84), moderate between palmitic and myristic FAs (0.58 ± 0.56) and negative between palmitic and stearic FAs (–0.69 ± 0.45). The genetic correlations between the individual long-chain polyunsaturated FAs (PUFAs) were positive and moderate (>0.30). However, the genetic-correlation estimates between long-chain PUFAs and α-linolenic acid were low (<0.30), except for the correlation between arachidonic and α-linolenic acids. The genetic correlation estimates of the sums of SFAs with monounsaturated fatty acids and omega 6 FAs were low (0.25 ± 0.59 and –0.02 ± 0.51 respectively), high with PUFAs and omega 9 FAs (–0.85 ± 0.15 and 0.86 ± 0.17 respectively) and moderate with omega 3FAs (–0.67 ± 0.26). The present study demonstrated the existence of genetic variation and, hence, the possibility to increase the proportion of healthy and favourable beef FAs through selection. The results obtained in the study have provided knowledge to elucidate the additive genetic influence on FA composition of intramuscular fat. In addition, genetic-relationship estimates of intramuscular FA profile help seek strategies for genetic selection or genetic-based diet management to enhance the FA profile in Zebu cattle.

Not all risks are created equal: A twin study and meta-analyses of risk taking across seven domains.

Humans routinely deal with both traditional and novel risks. Different kinds of risks have been a driving force for both evolutionary adaptations and personal development. This study explored the genetic and environmental influences on human risk taking in different task domains. Our approach was threefold. First, we integrated several scales of domain-specific risk-taking propensity and developed a synthetic scale, including both evolutionarily typical and modern risks in the following 7 domains: cooperation/competition, safety, reproduction, natural/physical risk, moral risk, financial risk, and gambling. Second, we conducted a twin study using the scale to estimate the contributions of genes and environment to risk taking in each of these 7 domains. Third, we conducted a series of meta-analyses of extant twin studies across the 7 risk domains. The results showed that individual differences in risk-taking propensity and its consistency across domains were mainly regulated by additive genetic influences and individually unique environmental experiences. The heritability estimates from the meta-analyses ranged from 29% in financial risk taking to 55% in safety. Supporting the notion of risk-domain specificity, both the behavioral and genetic correlations among the 7 domains were generally low. Among the relatively few correlations between pairs of risk domains, our analysis revealed a common genetic factor that regulates moral, financial, and natural/physical risk taking. This is the first effort to separate genetic and environmental influences on risk taking across multiple domains in a single study and integrate the findings of extant twin studies via a series of meta-analyses conducted in different task domains. (PsycINFO Database Record

Genetic and environmental associations between body dissatisfaction, weight preoccupation, and binge eating: Evidence for a common factor with differential loadings across symptom type.

Prior twin studies provide support for a single "common factor" that contributes genetic and environmental risk to a range of disordered eating symptoms. However, the common factor may be indexed less well by binge eating (BE) than other symptoms of eating disorders [i.e., body dissatisfaction (BD) and weight preoccupation (WP)]. We sought to explore the presence of a common factor and test whether loadings differed across three key symptoms (i.e., BE, BD, WP). Disordered eating was assessed via self-report in 631 female twin pairs from the Michigan State University Twin Registry. We detected a common disordered eating factor that was influenced primarily by additive genetic and nonshared environmental influences. However, we observed different loadings on this common factor by symptom type, as factor loadings for BD and WP were stronger than that for BE. Moreover, the residual environmental and/or genetic variances (i.e., those that are independent of the common factor) were larger in BE than those of BD or WP. Although all three symptoms share a common set of genetic and environmental influences, risk for BE may involve additional genetic, biological, and environmental factors that are not shared with other symptoms of eating pathology. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2017; 50:157-161).

Genetic and environmental influences on the associations between change in kidney function and changes in cardiometabolic factors in Koreans.

This study aimed to evaluate genetic and environmental relations between change in estimated glomerular filtration rate (eGFR) and changes in cardiometabolic factors. In 1772 Korean adults without diabetes and chronic kidney disease at baseline, changes in eGFR using the Chronic Kidney Disease Epidemiology Collaboration equation, blood pressure (BP), fasting serum glucose (FSG), insulin, homeostasis model assessment of insulin resistance index (HOMA-IR), hemoglobin A1c, triglycerides, high and low density lipoprotein cholesterol (HDL and LDL), uric acid, white blood cell (WBC) count, and body mass index (BMI) were calculated as follows: (value at follow-up-value at baseline)×100/[value at baseline×follow-up interval (years)]. eGFR change was associated with 10% changes in FSG (Odds ratio, OR=1.36), uric acid (OR=2.49), HDL (OR=0.69), LDL (OR=1.26), and WBC (OR=1.15) after adjusting for age, sex, intra-familial and twin correlations, smoking, alcohol use, and physical activity at baseline, and BMI change using a generalized estimating equation. In bivariate variance-component analysis, eGFR change had additive genetic correlations ([Formula: see text]) with changes in insulin (-0.26), HOMA-IR (-0.24), diastolic BP (-0.15), uric acid (-0.45), triglycerides (-0.30), WBC (-0.46), and HDL (0.41), and environmental correlations ([Formula: see text]) with changes in FSG (-0.11), uric acid (-0.32), LDL (-0.14), and WBC (0.10). In co-twin control analyses in 319 monozygotic twin pairs, the ORs for having a greater eGFR decline with a 1% increase in diastolic BP, uric acid, and LDL were 1.04, 1.09, and 1.03, respectively after adjusting for change in BMI and health behaviors at baseline. In these Korean twins and families, additive genetic influences and environmental effects play significant roles in the associations between eGFR change and changes in cardiometabolic factors.

Evidence of Shared Genome-Wide Additive Genetic Effects on Interpersonal Trauma Exposure and Generalized Vulnerability to Drug Dependence in a Population of Substance Users.

Exposure to traumatic experiences is associated with an increased risk for drug dependence and poorer response to substance abuse treatment (Claus & Kindleberger, 2002; Jaycox, Ebener, Damesek, & Becker, 2004). Despite this evidence, the reasons for the observed associations of trauma and the general tendency to be dependent upon drugs of abuse remain unclear. Data (N = 2,596) from the Study of Addiction: Genetics and Environment were used to analyze (a) the degree to which commonly occurring single nucleotide polymorphisms (SNPs; minor allele frequency > 1%) in the human genome explains exposure to interpersonal traumatic experiences, and (b) the extent to which additive genetic effects on trauma are shared with additive genetic effects on drug dependence. Our results suggested moderate additive genetic influences on interpersonal trauma, h(2) SNP-Interpersonal = .47, 95% confidence interval (CI) [.10, .85], that are partially shared with additive genetic effects on generalized vulnerability to drug dependence, h(2) SNP-DD = .36, 95% CI [.11, .61]; rG-SNP = .49, 95% CI [.02, .96]. Although the design/technique does not exclude the possibility that substance abuse causally increases risk for traumatic experiences (or vice versa), these findings raise the possibility that commonly occurring SNPs influence both the general tendency towards drug dependence and interpersonal trauma.

A Longitudinal Adoption Study of Substance Use Behavior in Adolescence.

Although cross-sectional twin studies have assessed the genetic and environmental etiologies of substance use during adolescence and early adulthood, comparisons of results across different samples, measures, and cohorts are problematic. While several longitudinal twin studies have investigated these issues, few corroborating adoption studies have been conducted. The current study is the first to estimate the magnitude of genetic, shared environmental, and non-shared environmental influences on substance use (cigarettes, alcohol, and marijuana) from ages 14 to 18 years, using a prospective longitudinal adoption design. Adoptive and control sibling correlations provided substantial evidence for early genetic effects on cigarette, alcohol, and marijuana use/no use. Shared environmental effects were relatively modest, except for alcohol use, which showed increases in late adolescence (age 17 to 18 years). Sibling similarity for quantity/frequency of use also support additive genetic influences across adolescence, with some shared environmental influences for all three substances. To test the stability of these influences across time, a series of independent pathway models were run to explore common and age-specific influences. For all substances, there were minimal age-specific additive genetic and shared environmental influences on quantity/frequency of use. Further, there was a trend toward increasing genetic influences on cigarette and alcohol use across ages. Genetic influences on marijuana were important early, but did not contribute substantially at age 17 and 18 years. Overall, the findings indicate that genetic influences make important contributions to the frequency/quantity of substance use in adolescence, and suggest that new genetic influences may emerge in late adolescence for cigarette and alcohol use.

Genetic influences on heart rate variability

Heart rate variability (HRV) is the variation of cardiac inter-beat intervals over time resulting largely from the interplay between the sympathetic and parasympathetic branches of the autonomic nervous system. Individual differences in HRV are associated with emotion regulation, personality, psychopathology, cardiovascular health, and mortality. Previous studies have shown significant heritability of HRV measures. Here we extend genetic research on HRV by investigating sex differences in genetic underpinnings of HRV, the degree of genetic overlap among different measurement domains of HRV, and phenotypic and genetic relationships between HRV and the resting heart rate (HR). We performed electrocardiogram (ECG) recordings in a large population-representative sample of young adult twins (n=1060 individuals) and computed HRV measures from three domains: time, frequency, and nonlinear dynamics. Genetic and environmental influences on HRV measures were estimated using linear structural equation modeling of twin data. The results showed that variability of HRV and HR measures can be accounted for by additive genetic and non-shared environmental influences (AE model), with no evidence for significant shared environmental effects. Heritability estimates ranged from 47 to 64%, with little difference across HRV measurement domains. Genetic influences did not differ between genders for most variables except the square root of the mean squared differences between successive R-R intervals (RMSSD, higher heritability in males) and the ratio of low to high frequency power (LF/HF, distinct genetic factors operating in males and females). The results indicate high phenotypic and especially genetic correlations between HRV measures from different domains, suggesting that >90% of genetic influences are shared across measures. Finally, about 40% of genetic variance in HRV was shared with HR. In conclusion, both HR and HRV measures are highly heritable traits in the general population of young adults, with high degree of genetic overlap across different measurement domains.

Genome-wide single nucleotide polymorphism heritability of nicotine dependence as a multidimensional phenotype.

Heritability estimates from twin studies of the multi-faceted phenotype of nicotine dependence (ND) range from moderate to high (31-60%), but vary substantially based on the specific ND-related construct examined. The current study estimated the aggregate role of common genetic variants on key ND constructs. Genomic-relationship-matrix restricted maximum likelihood (GREML) was used to decompose phenotypic variance across multiple ND indices using 796 125 polymorphisms from 2346 unrelated 'lifetime ever smokers' of European ancestry. Measures included DSM-IV ND and Fagerström Test for Nicotine Dependence (FTND) summary measures and constituent constructs (e.g. withdrawal severity, tolerance, heaviness of smoking and time spent smoking). Exploratory and confirmatory factor models were used to describe the covariance structure across ND measures; resulting factor(s) were the subject(s) of GREML analyses. Factor models indicated highly correlated DSM-IV and FTND factors for ND (0.545, 95% confidence interval 0.50-0.60) that could be represented as a higher-order factor (NIC DEP). Additive genetic influence on NIC DEP was 33% (s.e. = 0.14, p = 0.009). Post-hoc analyses indicated moderate genetic effects on the DSM-IV (34%, s.e. = 0.14, p = 0.008) and FTND (26%, s.e. = 0.14, p = 0.032) factors, both of which were influenced by the same genetic effects (r G-SNP = 1.00, s.e. = 0.09, p < 0.00001). Overall, common single nucleotide polymorphisms accounted for a large proportion of the genetic influences on ND-related phenotypes that have been observed in twin studies. Genetic contributions across distinct ND scales were largely influenced by shared genetic factors.

Antisocial peer affiliation and externalizing disorders: Evidence for Gene × Environment × Development interaction.

Gene × Environment interaction contributes to externalizing disorders in childhood and adolescence, but little is known about whether such effects are long lasting or present in adulthood. We examined gene-environment interplay in the concurrent and prospective associations between antisocial peer affiliation and externalizing disorders (antisocial behavior and substance use disorders) at ages 17, 20, 24, and 29. The sample included 1,382 same-sex twin pairs participating in the Minnesota Twin Family Study. We detected a Gene × Environment interaction at age 17, such that additive genetic influences on antisocial behavior and substance use disorders were greater in the context of greater antisocial peer affiliation. This Gene × Environment interaction was not present for antisocial behavior symptoms after age 17, but it was for substance use disorder symptoms through age 29 (though effect sizes were largest at age 17). The results suggest adolescence is a critical period for the development of externalizing disorders wherein exposure to greater environmental adversity is associated with a greater expression of genetic risk. This form of Gene × Environment interaction may persist through young adulthood for substance use disorders, but it appears to be limited to adolescence for antisocial behavior.

Genetics factors in pathogenesis and clinical genetics of binge eating disorder

Genetic studies have shown that binge eating disorder (ВЕD) aggregates in families, heritability was estimated as about 60% and additive genetic influences on BED up to 50%. Using a genetic approach has proved useful for verifying the diagnostic categories of BED using DSM-IV criteria and supporting the validity of considering this pathology as a separate nosological category. The results confirmed the genetic and pathogenic originality of BED as a separate psychopathological phenomenon, but not a subtype of obesity. It seems fruitful to considerate BED as a disease with hereditary predisposition with significant genetic influence and a complex psychopathological syndrome, including not only eating disorders, but also depressive and addictive component. A possible mechanism of pathogenesis of BED may be the interaction of the neuroendocrine and neurotransmitters systems including the active involvement of the reward system in response to a variety of chronic stress influences with the important modulatory role of specific personality traits. The high level of genetic influence on the certain clinical manifestations of BED confirms the ability to identify the subphenotypes of BED on genetic basis involving clinical criteria. It can not only contribute to further genetic studies, taking into account more homogeneous samples, but also help in finding differentiated therapeutic approaches.

Childhood attention-deficit/hyperactivity disorder symptoms and the development of adolescent alcohol problems: A prospective, population-based study of Swedish twins.

Children with attention-deficit/hyperactivity disorder (ADHD) are at increased risk of problematic alcohol and other substance use in adolescence. This study used data from an ongoing, prospective, population-based twin study of Swedish children and adolescents to evaluate the extent to which the association between ADHD symptoms and alcohol problems reflects a unique source of genetic or environmental risk related to ADHD versus a broader predisposition to youth externalizing behavior. We used all available data from same-sex monozygotic (MZ) and dizygotic (DZ) twins on ADHD symptoms in childhood (age 9/12; N = 15,549) and alcohol problems in late adolescence (age 18; N = 2,564). Consistent with prior longitudinal studies, the phenotypic association between hyperactive/impulsive ADHD symptoms and alcohol problems was small in magnitude, whereas the association for inattentive symptoms was even weaker. Additive genetic influences explained 99.8% of the association between hyperactive/impulsive symptoms and alcohol problems. Furthermore, we found that the genetic risk specifically associated with hyperactive/impulsive symptoms was attenuated when estimated in the context of externalizing behavior liability during childhood, of which ADHD symptoms were specific expressions. In sensitivity analyses exploring hyperactivity in mid-adolescence, we found a similar pattern of genetic associations. These results are consistent with previous findings of genetically driven overlap in the etiology of ADHD and problematic alcohol use. At least some of this co-occurrence may result from a general predisposition to externalizing behaviors in youth. © 2015 Wiley Periodicals, Inc.

Crossability In Interspecific Hybrid Between Eucalyptus Pellita and E. Urophylla

A controlled crossing experiment using a factorial mating design, involving female parents of E. pellita and male parents of E. urophyla that randomly sampled from the breeding population of both species, was conducted to assess the degree of genetic control on interspecific crossability for hybrid between E. pellita and E. urophylla. As measures of crossability, number of seeds per capsule and percentage of germinated seed were determined for each individual cross. The effect of female, male and female × male was significant on number of seed per capsule and percentage of germination. There was a slight tendency that the family produced more viable seed might produce less viable seed. Additive and dominance genetic varians were estimated as measures of the genetic control. The dominance variance had the major contribution to the genetic control of seed production and seed germination. Female source of variation has the major contribution to the additive genetic influence. Therefore, to maximize the production of viable seed, parent trees with desired traits should be selected on specific cross basis.

Factor structure and aetiological architecture of the BRIEF: A twin study.

Executive function is a broad construct that encompasses various processes involved in goal-directed behaviour in non-routine situations (Banich, 2009). The present study uses a sample of 560 5- to 16-year-old twin pairs (M=11.14, SD=2.53): 219 monozygotic twin pairs (114 female; 105 male) and 341 dizygotic twin pairs (136 female, 107 male; 98 opposite sex) to extend prior literature by providing information about the factor structure and the genetic and environmental architecture of the Behavior Rating Inventory of Executive Function (BRIEF; Gioia etal., 2000, Child Neuropsychol., 6, 235; Gioia etal., 2000, Behavior rating inventory of executive function, Lutz, FL: Psychological Assessment Resources), a multifaceted rating scale of everyday executive functions. Phenotypic results revealed a 9-scale, 3-factor model best represents the BRIEF structure within the current sample. Results of the genetically sensitive analyses indicated the presence of rater bias/contrast effects for the Initiate, Working Memory, and Task-Monitor scales. Additive genetic and non-shared environmental influences were present for the Initiate, Plan/Organize, Organization of Materials, Shift, and Monitor and Self-Monitor scales. Influences on Emotional Control were solely environmental. Interestingly, the aetiological architecture observed was similar to that of performance-based measures of executive function. This observed similarity provided additional evidence for the usefulness of the BRIEF as a measure of 'everyday' executive function.