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The aim of this study is to quantify the genetic and environmental variation in biological parameters of the adolescent growth in stature in both sexes, using structural equation models. Standing height was measured in 99 twin pairs from the Leuven Longitudinal Twin Study. Subjects were seen at semi-annual intervals between 10 and 16 years and at 18 years. Preece-Baines model I was fitted to the individual data and biologically meaningful parameters were derived. Path models were fitted to these parameters and a gender heterogeneity analysis was performed. A model including additive genetic and specific environmental factors (AE-model), allowing for a difference in total variance or in genetic/environmental variance components in males and females best explains most of the growth characteristics. For the timing and velocity of the adolescent growth spurt, no gender heterogeneity was observed, and the genetic (0.89 to 0.93) and specific environmental (0.07 to 0.11) contributions were equal in both sexes. For stature at take-off, stature at peak height velocity and for adult stature, gender heterogeneity was observed and different models appeared to result in the best fit for boys and girls. For height at PHV and adult stature, the significant contribution of a common environmental (0.39 to 0.56) factor in boys was noteworthy. For percentage of adult stature and distances between relevant time points of the growth curve, a non-scalar effect was observed, indicating that different genes affect these characteristics in boys and girls. It is concluded that most characteristics of the growth spurt in stature are under strong genetic control. Gender heterogeneity is present for stature and for a number of derived growth characteristics. [ABSTRACT FROM AUTHOR]

Although the transmission of religiousness has been assumed to be purely cultural, behavior genetic studies have demonstrated that genetic factors play a role in the individual differences in some religious traits. This article reviews the extant behavior genetic literature and presents new analyses from the "Virginia 30,000" on the causes of variation in religious affiliation, attitudes, and practices, and relates these to personality as construed by Eysenck. Results indicate that religious affiliation is primarily a culturally transmitted phenomenon, whereas religious attitudes and practices are moderately influenced by genetic factors. Further, Eysenck's personality traits do not mediate genetic influences on religiousness, but significant negative genetic correlations are found between church attendance and liberal sexual attitudes. Implications and possibilities for future studies are discussed. [ABSTRACT FROM AUTHOR]

Background: The Adolescent Brain Cognitive Development ™ Study (ABCD Study®) is an open-science, multi-site, prospective, longitudinal study following over 11,800 9- and 10-year-old youth into early adulthood. The ABCD Study aims to prospectively examine the impact of substance use (SU) on neurocognitive and health outcomes. Although SU initiation typically occurs during teen years, relatively little is known about patterns of SU in children younger than 12., Methods: This study aims to report the detailed ABCD Study® SU patterns at baseline (n = 11,875) in order to inform the greater scientific community about cohort's early SU. Along with a detailed description of SU, we ran mixed effects regression models to examine the association between early caffeine and alcohol sipping with demographic factors, externalizing symptoms and parental history of alcohol and substance use disorders (AUD/SUD)., Primary Results: At baseline, the majority of youth had used caffeine (67.6 %) and 22.5 % reported sipping alcohol (22.5 %). There was little to no reported use of other drug categories (0.2 % full alcohol drink, 0.7 % used nicotine, <0.1 % used any other drug of abuse). Analyses revealed that total caffeine use and early alcohol sipping were associated with demographic variables (p's<.05), externalizing symptoms (caffeine p = 0002; sipping p = .0003), and parental history of AUD (sipping p = .03)., Conclusions: ABCD Study participants aged 9-10 years old reported caffeine use and alcohol sipping experimentation, but very rare other SU. Variables linked with early childhood alcohol sipping and caffeine use should be examined as contributing factors in future longitudinal analyses examining escalating trajectories of SU in the ABCD Study cohort., (Copyright © 2021 Elsevier B.V. All rights reserved.)

The phenotypic and genetic interrelationships underlying ADHD symptomatology assessed by various instruments were examined on a sample of 735 male and 819 female same-sex twin pairs, aged 8 to 16 years, participating in the first phase of the Virginia Twin Study of Adolescent Behavioral Development (VTSABD). Multivariate analyses were applied to parental and teacher ratings from an investigator-based interview, the CAPA, and three questionnaires (the CBCL and the Rutter Parent and Teacher Scales). Results from patterns of intercorrelations and factor analyses of maternal measures suggested that at the phenotypic level, these assessed the same underlying behavioural construct, which differed from other emotional and behavioural constructs. However, genetic analyses showed that in addition to a common factor underlying the expression of ADHD as assessed across the range of measures, additional genetic factors were identified that were method- and rater-specific. The findings suggest that although the investigator-based interview and the behavioural checklists tap similar aspects of ADHD behaviour, there is additional rater-specific variance.

In this report we characterize associations between parental psychiatric disorders and children's psychiatric symptoms and disorders using a population-based sample of 850 twin families. Juvenile twins are aged 8-17 years and are personally interviewed about their current history of DSM-III-R conduct, depression, oppositional-defiant, overanxious, and separation anxiety disorders using the CAPA-C. Mothers and fathers of twins are personally interviewed about their lifetime history of DSM-III-R alcoholism, antisocial personality disorder, generalized anxiety disorder, major depression, panic disorder/agoraphobia, social phobia, and simple phobia using a modified version of the SCID and the DIS. Generalized least squares and logistic regression are used to identify the juvenile symptoms and disorders that are significantly associated with parental psychiatric histories. The specificity of these associations is subsequently explored in a subset of families with maternal plus parental psychiatric histories with a prevalence > 1%. Parental depression that is not comorbid or associated with a different spousal disorder is associated with a significantly elevated level of depression and overanxious disorder symptoms and a significantly increased risk for overanxious disorder. Risks are higher for both symptomatic domains in association with maternal than paternal depression, and highest in association with maternal plus paternal depression. Risks for otherjuvenile symptoms and disorders index the comorbid and spousal histories with which parental depression is commonly associated. Paternal alcoholism that is not comorbid or associated with a maternal disorder is not significantly associated with current psychiatric symptoms or disorders in offspring. Risks for oppositional-defiant or conduct symptoms/disorders in the offspring of alcoholic parents index parental comorbidity and/or other spousal histories.

Background: The role of genetics in the etiology of peanut allergy is unknown. For complex genetic traits, twin studies can provide information on the relative contribution of genetic factors to a disease, as the relative confounding effects of environmental factors are markedly decreased., Objective: This study was performed to search for evidence that genetic factors influence peanut allergy by comparing the concordance rate for this allergy among monozygotic and dizygotic twins., Methods: Twin pairs with at least one member with peanut allergy were ascertained through the Food Allergy Network by advertisements in the organization's newsletters and Web site. Individuals with peanut allergy or parental surrogates were interviewed by telephone. A full atopic history was obtained, and peanut allergy and zygosity were determined using previously validated questionnaires. Heritability of peanut allergy was determined using univariate genetic model fitting by maximum likelihood with the Mx statistical modeling software package., Results: Seventy-five twin pairs were recruited. Seventeen pairs were excluded because of unconvincing peanut allergy histories (9 pairs, including 4 of uncertain zygosity) or because one twin had reportedly never ingested peanut (8 pairs). The median age of the 58 remaining twin pairs was 5 years (range 1 to 58 years). Seventy individuals had peanut allergy. In addition to convincing histories of peanut allergy, 52 (74%) had been tested (skin prick testing with or without radioallergosorbent assay) and all had positive reactions to peanut. Twenty-nine of the 70 had experienced >1 reaction to peanut; 29 of 70 had multisystem reactions. Among the monozygotic pairs (n = 14), 9 were concordant for peanut allergy (pairwise concordance, 64.3%) and among dizygotic pairs (n = 44), 3 were concordant for peanut allergy (pairwise concordance, 6.8%; chi(2) = 21.38, P <.0001). Heritability of peanut allergy was estimated at 81. 6% (95% confidence interval 41.6% to 99.7%) with model fitting using a population prevalence of peanut allergy of 0.4%., Conclusions: The significantly higher concordance rate of peanut allergy among monozygotic twins suggests strongly that there is a significant genetic influence on peanut allergy.

This study explores the use of an individual's genetic (IGFS) and environmental factor score (IEFS), constructed using genetic model fitting of a multivariate strength phenotype. Maximal isometric and dynamic strength measures, one maximal repetition load (1RM) and muscle cross-sectional area (MCSA) were measured in 25 monozygotic and 16 dizygotic twin pairs. The use of IGFS and IEFS in predicting the sensitivity to environmental stress was evaluated by the association of the scores with strength training gains after a 10-week high resistance strength training programme. Results show a high contribution of genetic factors to the covariation between maximal strength and muscle cross-sectional area (84-97%) at pre-training evaluation. Individual factor scores explained the largest part of the variation in IRM and other strength measures at pre-training and post-training evaluation respectively. Genes that are switched on due to training stress (gene-environment interaction) could explain the decrease in explained variation over time. A negative correlation was found between IGFS and strength training gains (-0.24 to -0.51, P < 0.05); individuals with a high IGFS tend to gain less strength than individuals with low IGFS. Individual environmental factor scores have lower differential power. The predictive value of the IGFS has potential utility in identifying an individual's susceptibility to environmental stress in a variety of multifactorial characteristics, eg diseases and impairments, and for selection of sib pairs for QTL analyses.

We examine the hypothesis that environmental transmission is a significant factor in individual differences for Neuroticism among 45,850 members of extended twin kinships from Australia (N = 20,945) and the United States (N = 24,905). To this large data set we fitted a model estimating genetic and environmental components of variance and gene-environmental covariance to examine the causes of individual differences in Neuroticism. For the combined sample we reject models including environmental transmission, shared environment, and a special twin environment in favor of more parsimonious genetic models. The best-fitting model involved only modest assortative mating, nonshared environment, and both additive and nonadditive genetic components. We conclude, first, that there is no evidence for environmental transmission as a contribution to individual differences in Neuroticism in these replicated samples, drawn from different continents, and, second, that a simple genetic structure underlies familial resemblance for the personality trait of Neuroticism. It is interesting that, despite the opportunity provided by the elaborate design and extensive power of our study, the picture revealed for the causes of individual differences in Neuroticism is little more complex than that found from earlier, simpler designs applied to smaller samples. However, this simplicity could not have been confirmed without using a highly informative design and a very large sample.

Data on frequency of church attendance have been obtained from separate cohorts of twins and their families from the USA and Australia (29,063 and 20,714 individuals from 5670 and 5615 families, respectively). The United States sample displayed considerably higher frequency of attendance at church services. Sources of family resemblance for this trait also differed between the Australian and US data, but both indicated significant additive genetic and shared environment effects on church attendance, with minor contributions from twin environment, assortative mating and parent-offspring environmental transmission. Principal differences between the populations were in greater maternal environmental effects in the US sample, as opposed to paternal effects in the Australian sample, and smaller shared environment effects observed for both women and men in the US cohort.

Religious attendance has been shown to correlate negatively with alcohol use. We investigated whether this relationship is driven by genetic or environmental factors. Data on frequency of church attendance and frequency of alcohol use were obtained from twins and their families in the Virginia 30,000 study. A comprehensive bivariate model of family resemblance was fitted to the data using Mx. This model is described in detail. Results indicate that genetic factors primarily account for the relationship between alcohol and church attendance in males, whilst shared environmental factors, including cultural transmission and genotype-environment covariance, are stronger determinants of this association in females.

An analysis of the cellular and humoral immune responses after bacille Calmette-Guerin (BCG) vaccination and during tuberculosis treatment favors the hypothesis of an immune defence developed in four overlapping successive stages. The initial immune response is innate. The following two intermingle innate and specific responses against low molecular weight oligopeptidic and nonpeptidic antigens, as muramyldipeptide and trehalose dimycolate, and large molecular weight nonpeptidic antigens such as lipoarabinomannan. The ultimate specific response is directed against protein antigens as Antigen 60. BCG and primary tuberculosis (TB) infections induce cellular and humoral immune responses essentially against oligopeptidic and small and large molecular weight nonpeptidic antigens. Immune responses against non-peptidic substances contribute to the immunoprotection of the infected person who develops a primary infection. Some infected people allow the expression of the immunosuppressive activity of the pathogen. This results in the synthesis of interleukin-10 (IL-10), which suppresses the formation of interferon-gamma (INF-gamma) and IL-2, and of IL-6, which suppresses T-cell responses. These patients have a skewed immune response against non-peptidic antigens and present with symptoms. They will not recover unless responses directed against proteinic antigens occur, which restore INF-gamma and IL-2 production. The formation of immumoglobulin-G (IgG)-type antibodies and of a cellular immunity against mycobacterial peptidic antigens is essential for a good protection against a post-primary infection.

Research has consistently shown that religiousness is associated with lower levels of alcohol and drug use, but little is known about the nature of adolescent religiousness or the mechanisms through which it influences problem behavior in this age group. This paper presents preliminary results from the Mid-Atlantic School Age Twin Study, a prospective, population-based study of 6-18-year-old twins and their mothers. Factor analysis of a scale developed to characterize adolescent religiousness, the Religious Attitudes and Practices Inventory (RAPI), revealed three factors: theism, religious/spiritual practices, and peer religiousness. Twin correlations and univariate behavior-genetic models for these factors and a measure of belief that drug use is sinful reveal in 357 twin pairs that common environmental factors significantly influence these traits, but a minor influence of genetic factors could not be discounted. Correlations between the multiple factors of adolescent religiousness and substance use, comorbid problem behavior, mood disorders, and selected risk factors for substance involvement are also presented. Structural equation modeling illustrates that specific religious beliefs about the sinfulness of drugs and level of peer religiousness mediate the relationship between theistic beliefs and religious/spiritual practices on substance use. Limitations and future analyses are discussed.

We present a novel, simple and straightforward method to obtain mouse bone marrow-derived dendritic cells (DC) from C57Bl/6 CD4/CD8(-/-) double knock-out mice. This new method, involving culture of bone marrow cells in medium supplemented with Interleukin 4 and Granulocyte-Macrophage Colony-Stimulating Factor, does not involve negative immunodepletion of CD4+ and CD8+ populations, or extensive prior manipulations of the starting population. The resulting, loosely adherent cell population, exhibited the morphological characteristics and typical surface markers of DCs, and were endowed with the functional activities characteristic of bone marrow-derived DCs of wild-type mice. Interestingly, LCMV GP33-41 peptide-loaded CD4/CD8(-/-) DCs were efficiently lysed by peptide-specific activated CTLs in vitro. Furthermore, these peptide-loaded CD4/CD8(-/-) DCs induced a peptide-specific CTL response upon immunization of wild-type C57Bl/6 mice.

Univariate and multivariate analyses of the genetic and environmental contributions to variance in adipose tissue and adipose tissue distribution were carried out in early adolescents. Stature, weight, body mass index (BMI), and five subcutaneous skinfolds were measured at half-yearly intervals in 105 MZ and DZ twin pairs from 10 to 14 years. The most parsimonious model, which provided an adequate explanation for variation in the BMI, five skinfolds, and the T/E ratio, included additive genetic and specific environmental factors. Multivariate analyses of the genetic architecture of subcutaneous fat indicated a general skinfold genetic factor, an extremity skinfold genetic factor, and skinfold specific genetic factors. This implies that all skinfolds are under control of the same set of genes, that a different set of genes partly controls extremity skinfolds, and that other genes have a small skinfold specific impact. Environmental contributions included a general skinfold environmental factor and skinfold specific environmental factors. BMI is under control of the same set of genes as skinfolds and shows high genetic correlations with trunk skinfolds, which implies that nearly the same genes may influence trunk skinfolds and the BMI. All models were fairly consistent across the age range.

Purpose: This study focuses on the quantification of genetic and environmental factors in arm strength after high-resistance strength training., Methods: Male monozygotic (MZ, N = 25) and dizygotic (DZ, N = 16) twins (22.4 +/- 3.7 yr) participated in a 10-wk resistance training program for the elbow flexors. The evidence for genotype*training interaction, or association of interindividual differences in training effects with the genotype, was tested by a two-way ANOVA in the MZ twins and using a bivariate model-fitting approach on pre- and post-training phenotypes in MZ and DZ twins. One repetition maximum (1RM), isometric strength, and concentric and eccentric moments in 110 degree arm flexion at velocities of 30 degrees x s(-1), 60 degrees x s(-1), and 12 degrees x s(-1) were evaluated as well as arm muscle cross-sectional area (MCSA)., Results: Results indicated significant positive training effects for all measures except for maximal eccentric moments. Evidence for genotype*training interaction was found for 1RM and isometric strength, with MZ intra-pair correlations of 0.46 and 0.30, respectively. Bivariate model-fitting indicated that about 20% of the variation in post-training 1RM, isometric strength, and concentric moment at 120 degrees x s(-1) was explained by training-specific genetic factors that were independent from genetic factors that explained variation in the pretraining phenotype (30-77%)., Conclusions: Genetic correlations between measures of pre- and post-training strength were indicative for high pleiotropic gene action and minor activation of training-specific genes during training.

The magnitude of genetic and environmental factors and the influence of contrast effects on attention-deficit hyperactivity disorder (ADHD) symptomatology were examined on a sample of 900 twin pairs, aged 7-13, participating in the Virginia Twin Study of Adolescent Behavioral Development (VTSABD). In addition, the genetic and environmental correlations between ADHD and oppositional-defiant disorder/conduct disorder (ODD/CD) symptomatology were estimated. A series of structural models was applied to maternal ratings from a telephone survey, designed to screen for the three dimensions of ADHD symptomatology (hyperactivity, impulsivity, and inattention) and ODD/CD symptomatology. Model-fitting results suggested that ADHD symptomatology is highly heritable and influenced mostly by additive genetic, specific environmental, and contrast effects. However, this analysis could not exclude with statistical significance additional effects from dominance. The results of the best-fitting bivariate model suggested that the genetic correlation between the two traits is 50% and replicated previous findings of a common genetic factor influencing the comorbidity of ADHD and ODD/CD symptomatologies.

Little is known about the contribution of genetic and environmental factors to risk for juvenile psychopathology. The Virginia Twin Study of Adolescent Behavioral Development allows these contributions to be estimated. A population-based, unselected sample of 1412 Caucasian twin pairs aged 8-16 years was ascertained through Virginia schools. Assessment of the children involved semi-structured face-to-face interviews with both twins and both parents using the Child and Adolescent Psychiatric Assessment (CAPA). Self-report questionnaires were also completed by parents, children, and teachers. Measures assessed DSM-III-R symptoms of Attention Deficit Hyperactivity Disorder (ADHD). Conduct Disorder, Oppositional Defiant Disorder, Overanxious Disorder, Separation Anxiety, and Depressive Disorder. Factorially derived questionnaire scales were also extracted. Scores were normalized and standardized by age and sex. Maximum likelihood methods were used to estimate contributions of additive and nonadditive genetic effects, the shared and unique environment, and sibling imitation or contrast effects. Estimates were tested for heterogeneity over sexes. Generally, monozygotic (MZ) twins correlated more highly than dizygotic (DZ) twins, parental ratings more than child ratings, and questionnaire scales more highly than interviews. DZ correlations were very low for measures of ADHD and DZ variances were greater than MZ variances for these variables. Correlations sometimes differed between sexes but those for boy-girl pairs were usually similar to those for like-sex pairs. Most of the measures showed small to moderate additive genetic effects and moderate to large effects of the unique individual environment. Measures of ADHD and related constructs showed marked sibling contrast effects. Some measures of oppositional behavior and conduct disorder showed shared environmental effects. There were marked sex differences in the genetic contribution to separation anxiety, otherwise similar genetic effects appear to be expressed in boys and girls. Effects of rater biases on the genetic analysis are considered. The study supports a widespread influence of genetic factors on risk to adolescent psychopathology and suggests that the contribution of different types of social influence may vary consistently across domains of measurement.

Background: The Virginia Twin Study of Adolescent Behavioral Development is a cohort-longitudinal epidemiological study that uses the genetic twin design to study the development and maintenance of child psychiatric disorders. We determined the rates of DSM-III-R disorders, disorders with impairment, and age, sex, and comorbidity effects., Methods: Families of 2762 white twins aged 8 to 16 years participated. Twins and their parents were asked systematically about risk factors and current psychiatric symptoms by means of investigator-based psychiatric interviews and questionnaires. The DSM-III-R diagnoses were made for major depressive disorder, separation anxiety, overanxious disorder, simple phobia, social phobia, agoraphobia, oppositional defiant disorder, conduct disorder, and attention deficit hyperactivity disorder., Results: The 3-month point prevalence for any DSM-III-R disorders was 413 per 1000, and that for disorders with associated impairment was 142 per 1000. Emotional disorders with impairment occurred in 89 per 1000, with girls being more commonly affected; behavioral disorders had a prevalence of 71 per 1000, with boys being more frequently affected. The proportion with disorder who also had functional impairment varied across disorders; anxiety and phobic disorders were particularly likely not to be accompanied by impairment. Rates of emotional and behavioral disorders increased over the age range. There was extensive comorbidity among disorders., Conclusions: The prevalence rates and patterns of findings from this study of twins are consistent with those of other epidemiological studies, supporting previous findings of few differences in rates of psychiatric disorder between twins and singletons. The importance of including measures of functional impairment is evident by its effect on rates of disorder and patterns of comorbidity.

We review the literature on the familial resemblance of body mass index (BMI) and other adiposity measures and find strikingly convergent results for a variety of relationships. Results from twin studies suggest that genetic factors explain 50 to 90% of the variance in BMI. Family studies generally report estimates of parent-offspring and sibling correlations in agreement with heritabilities of 20 to 80%. Data from adoption studies are consistent with genetic factors accounting for 20 to 60% of the variation in BMI. Based on data from more than 25,000 twin pairs and 50,000 biological and adoptive family members, the weighted mean correlations are .74 for MZ twins, .32 for DZ twins, .25 for siblings, .19 for parent-offspring pairs, .06 for adoptive relatives, and .12 for spouses. Advantages and disadvantages of twin, family, and adoption studies are reviewed. Data from the Virginia 30,000, including twins and their parents, siblings, spouses, and children, were analyzed using a structural equation model (Stealth) which estimates additive and dominance genetic variance, cultural transmission, assortative mating, nonparental shared environment, and special twin and MZ twin environmental variance. Genetic factors explained 67% of the variance in males and females, of which half is due to dominance. A small proportion of the genetic variance was attributed to the consequences of assortative mating. The remainder of the variance is accounted for by unique environmental factors, of which 7% is correlated across twins. No evidence was found for a special MZ twin environment, thereby supporting the equal environment assumption. These results are consistent with other studies in suggesting that genetic factors play a significant role in the causes of individual differences in relative body weight and human adiposity.

The maximal isometric moment at five different elbow joint angles was measured in 25 monozygotic and 16 dizygotic male adult twin pairs (22.4 +/- 3.7 yr). Genetic model fitting was used to quantify the genetic and environmental contributions to individual differences in isometric strength. Additive genetic factors explained 66-78% of the variance in maximal torque at 170-140-110 and 80 degrees flexion (extension = 180 degrees). At 50 degrees flexion, common and subject-specific environmental factors contributed equally to the variation. The contribution of unique environmental factors concurs with the level of variability in muscle activation and (dis)-comfort of torque production in the specific angle. The relative contribution of lever arm and force-length relationship in torque varies according to the angle. Because these factors might be genetic, this variability is reflected in the genetic contribution at the extreme angles of 170 and 50 degrees. Multivariate analyses suggested a general set of genes that control muscle area and isometric strength, together with a more specific strength factor. Genetic correlations were high (0.82-0.99). Genes responsible for arm-segment lengths did not contribute to muscle area nor to isometric strength.

This study focuses on the quantification of genetic and environmental sources of variation in physical fitness components in 105 10-yr-old twin pairs and their parents. Nine motor tests and six skinfold measures were administered. Motor tests can be divided into those that are performance-related: static strength, explosive strength, running speed, speed of limb movement, and balance; and those that are health-related: trunk strength, functional strength, maximum oxygen uptake, and flexibility. The significance and contribution of genetic and environmental factors to variation in physical fitness were tested with model fitting. Performance-related fitness characteristics were moderately to highly heritable. The heritability estimates were slightly higher for health-related fitness characteristics. For most variables a simple model including genetic and specific environmental factors fitted the observed phenotypic variance well. Common environmental factors explained a significant part of the variation in speed components and flexibility. Assortative mating was significant and positive for speed components, balance, trunk strength, and cardiorespiratory fitness, but negative for adiposity. Static strength, explosive strength, functional strength, and cardiorespiratory fitness showed evidence for reduced genetic transmission or dominance. The hypothesis that performance-related fitness characteristics are more determined by genetic factors than health-related fitness was not supported. At this prepubertal age, genetic factors have the predominant effect on fitness.