Stable Genetic Effects on Symptoms of Alcohol Abuse and Dependence from Adolescence into Early Adulthood

Relatively little is known about how genetic influences on alcohol abuse and dependence (AAD) change with age. We examined the change in influence of genetic and environmental factors which explain symptoms of AAD from adolescence into early adulthood. Symptoms of AAD were assessed using the four AAD screening questions of the CAGE inventory. Data were obtained up to six times by self-report questionnaires for 8,398 twins from the Netherlands Twin Register aged between 15 and 32 years. Longitudinal genetic simplex modeling was performed with Mx. Results showed that shared environmental influences were present for age 15–17 (57%) and age 18–20 (18%). Unique environmental influences gained importance over time, contributing 15% of the variance at age 15–17 and 48% at age 30–32. At younger ages, unique environmental influences were largely age-specific, while at later ages, age-specific influences became less important. Genetic influences on AAD symptoms over age could be accounted for by one factor, with the relative influence of this factor differing across ages. Genetic influences increased from 28% at age 15–17 to 58% at age 21–23 and remained high in magnitude thereafter. These results are in line with a developmentally stable hypothesis that predicts that a single set of genetic risk factors acts on symptoms of AAD from adolescence into young adulthood.     

Genetic and Environmental Causes of Variation in Trait Resilience in Young People

The aim of this multi-informant twin study was to determine the relative role of genetic and environmental factors in explaining variation in trait resilience in adolescents. Participants were consenting families (N = 2,638 twins in 1,394 families), from seven national cohorts (age 12–18 years, both sexes) of monozygotic and dizygotic twins reared together. Questionnaire data on the adolescents’ Ego-resilience (ER89) was collected from mothers, fathers and twins, and analysed by means of multivariate genetic modelling. Variance in trait resilience was best represented in an ADE common pathways model with sex limitation. Variance in the latent psychometric resilience factor was largely explained by additive genetic factors (77% in boys, 70% in girls), with the remaining variance (23 and 30%) attributable to non-shared environmental factors. Additive genetic sources explained more than 50% of the informant specific variation in mothers and fathers scores. In twins, additive and non-additive genetic factors together explained 40% and non-shared environmental factor the remaining 60% of variation. In the mothers’ scores, the additive genetic effect was larger for boys than for girls. The non-additive genetic factor found in the twins’ self ratings was larger in boys than in girls. The remaining sex differences in the specific factors were small. Trait resilience is largely genetically determined. Estimates based on several informants rather than single informants approaches are recommended.     

Depressive Symptoms and Alcohol Use are Genetically and Environmentally Correlated Across Adolescence

Depressive symptoms and alcohol use are frequently positively associated during adolescence. This study aimed to assess the heritability of each phenotype across adolescence; to assess potential shared liabilities; to examine changes in the nature of shared liabilities across adolescence; and to investigate potential causal relationships between depressive symptoms and alcohol use. We studied a longitudinally assessed sample of adolescent Finnish twins (N = 1,282) to test hypotheses about genetic and environmental influences on these phenotypes within and across ages, using data from assessments at ages 12, 14, and 17.5 years. The heritability of depressive symptoms is consistent across adolescence (~40–50%), with contributions from common and unique environmental factors. The heritability of alcohol use varies across time (a² = .25–.44), and age 14 alcohol use is heavily influenced by shared environmental factors. Genetic attenuation and innovation were observed across waves. Modest to moderate genetic (r_A = .26–.59) and environmental (r_C = .30–.63) correlations between phenotypes exist at all ages, but decrease over time. Tests for causal relationships between traits differed across ages and sexes. Intrapair MZ difference tests provided evidence for reciprocal causation in girls at ages 14 and 17.5. Formal causal models suggested significant causal relationships between the variables in both boys and girls. The association between depressive symptoms and alcohol use during adolescence is likely due to a combination of shared genetic and environmental influences and causal influences. These influences are also temporally dynamic, complicating efforts to understand factors contributing to the relationship between these outcomes.     

Thought Problems from Adolescence to Adulthood: Measurement Invariance and Longitudinal Heritability

This study investigates the longitudinal heritability in Thought Problems (TP) as measured with ten items from the Adult Self Report (ASR). There were ~9,000 twins, ~2,000 siblings and ~3,000 additional family members who participated in the study and who are registered at the Netherlands Twin Register. First an exploratory factor analysis was conducted to examine the underlying factor structure of the TP-scale. Then the TP-scale was tested for measurement invariance (MI) across age and sex. Next, genetic and environmental influences were modeled on the longitudinal development of TP across three age groups (12–18, 19–27 and 28–59 year olds) based on the twin and sibling relationships in the data. An exploratory factor analysis yielded a one-factor solution, and MI analyses indicated that the same TP-construct is assessed across age and sex. Two additive genetic components influenced TP across age: the first influencing TP throughout all age groups, while the second arises during young adulthood and stays significant throughout adulthood. The additive genetic components explained 37% of the variation across all age groups. The remaining variance (63%) was explained by unique environmental influences. The longitudinal phenotypic correlation between these age groups was entirely explained by the additive genetic components. We conclude that the TP-scale measures a single underlying construct across sex and different ages. These symptoms are significantly influenced by additive genetic factors from adolescence to late adulthood.     

The Genetic and Environmental Etiology of Antisocial Behavior from Childhood to Emerging Adulthood

Previous research suggests that both genetic and environmental influences are important for antisocial behavior across the life span, even though the prevalence and incidence of antisocial behavior varies considerably across ages. However, little is known of how genetic and environmental effects influence the development of antisocial behavior. A total of 2,600 male and female twins from the population-based Swedish Twin Registry were included in the present study. Antisocial behavior was measured on four occasions, when twins were 8–9, 13–14, 16–17, and 19–20 years old. Longitudinal analyses of the data were conducted using structural equation modeling. The stability of antisocial behavior over time was explained by a common latent persistent antisocial behavior factor. A common genetic influence accounted for 67% of the total variance in this latent factor, the shared environment explained 26%, and the remaining 7% was due to the non-shared environment. Significant age-specific shared environmental factors were found at ages 13–14 years, suggesting that common experiences (e.g., peers) are important for antisocial behavior at this age. Results from this study show that genetic as well as shared environmental influences are important in antisocial behavior that persists from childhood to emerging adulthood.     

Heritability and Longitudinal Stability of Schizotypal Traits During Adolescence

The study investigated the genetic and environmental etiology of schizotypal personality traits in a non-selected sample of adolescent twins, measured on two occasions between the ages of 11 and 16 years old. The 22-item Schizotypal Personality Questionnaire- Child version (SPQ-C) was found to be factorially similar to the adult version of this instrument, with three underlying factors (Cognitive-Perceptual, Interpersonal-Affective, and Disorganization). Each factor was heritable at age 11–13 years (h ² = 42–53%) and 14–16 years old (h ² = 38–57%). Additive genetic and unique environmental influences for these three dimensions of schizotypal personality acted in part through a single common latent factor, with additional genetic effects specific to both Interpersonal-Affective and Disorganization subscales at each occasion. The longitudinal correlation between the latent schizotypy factor was r = 0.58, and genetic influences explained most of the stability in this latent factor over time (81%). These longitudinal data demonstrate significant genetic variance in schizotypal traits, with moderate stability between early to middle adolescence. In addition to common influences between the two assessments, there were new genetic and non-shared environmental effects that played a role at the later assessment, indicating significant change in schizotypal traits and their etiologies throughout adolescence.     

Endophenotypes in a Dynamically Connected Brain

We examined the longitudinal genetic architecture of three parameters of functional brain connectivity. One parameter described overall connectivity (synchronization likelihood, SL). The two others were derived from graph theory and described local (clustering coefficient, CC) and global (average path length, L) aspects of connectivity. We measured resting state EEG in 1,438 subjects from four age groups of about 16, 18, 25 and 50 years. Developmental curves for SL and L indicate that connectivity is more random at adolescence and old age, and more structured in middle-aged adulthood. Individual variation in SL and L were moderately to highly heritable at each age (SL: 40–82%; L: 29–63%). Genetic factors underlying these phenotypes overlapped. CC was also heritable (25–49%) but showed no systematic overlap with SL and L. SL, CC, and L in the alpha band showed high phenotypic and genetic stability from 16 to 25 years. Heritability for parameters in the beta band was lower, and less stable across ages, but genetic stability was high. We conclude that the connectivity parameters SL, CC, and L in the alpha band show the hallmarks of a good endophenotype for behavior and developmental disorders.     

Genes and Developmental Stabiltiy of Aggressive Behavior Problems at Home and School in a Community Sample of Twins Aged 7–12

Though behavioral genetic studies of aggression have implicated heritable and environmental factors, there is limited understanding of how these factors influence aggression across different settings and over time. Ratings for 732 twins were collected from parents and teachers during middle childhood and early adolescence. Total aggression scores on the Child Behavioral Checklist (CBCL) and Teacher Report Form (TRF) were examined at each age, across both settings, and developmentally. In this sample, aggressive behavior was moderately to largely heritable at each age within the home (.76–.84) and school (.42–.61). Across each age, ratings by parents and teachers were moderately correlated (.19–.36). Genetic and environmental effects that were limited to a particular setting were important etiological factors for aggressive behavior consistently within each setting, while only genetic factors influenced levels of aggression across both settings. Stability during these ages was due to genetic effects common to each age and the persistence of child-specific environmental experiences within each setting. These results suggest that genetic and environmental influences on children’s aggressive behavior are largely setting specific. Levels of aggression seen consistently across both settings are due to genetic influences. Developmentally stable levels of aggressive behavior result from genetic influences common to all ages and individual environmental influences whose effects persist across ages.Edited by Danielle Posthuma     

Fractal dynamics of polarized bioelectrodes

This study is concerned with mathematical modelling of the fundamental relationship which exists between the current density and the overpotential across the metalsolution interface in the linear range using methods of system theory enhanced by ‘fractal’ concepts. A primer for both 1/f-type scaling and ‘anomalous’ relaxation/dispersion concepts is provided, followed by a brief review of the research history pertinent to the metal electrode polarization dynamics. Next, the ‘fractal relaxation systems’ approach is introduced to characterize, systems which attenuate with a fractional power-low dependence on frequency through a ‘scaling exponent’. The ‘singularity structure’ which is a scaling, rational system function is proposed to expand fractal systems in terms of basic subsystems individually representing elementary exponential relaxations and collectively exhibiting scaling properties. We stress that the ‘singularity structure’ carries scaling information identical to the conventional ‘distribution of relaxation times’ function. ‘Structure scale’ and ‘view scale’ concepts are presented in the due course to streamline the analysis of scaling phenomena in general and the polarization impedance in particular. System theory-wise, the notable result is that the fractional power function attenuation, or equivalently, the logarithmic nature of the distribution function translates into the ‘self-similar’ pattern replication of the system singularities in the s-plane. The singularity arrangement is governed by a recursive rule solely based on the knowledge of the fractional power factor or the scaling exponent.     

Genetic Regulation of Pre-Pubertal Development of Body Mass Index: A Longitudinal Study of Japanese Twin Boys and Girls

We analyzed the genetic architecture of prepubertal development of relative weight to height in 216 monozygotic and 159 dizygotic complete Japanese twin pairs (52% girls). Ponderal index at birth (kg/m³) and body mass index (BMI, kg/m²) from 1 to 11 years of age were used. Additive genetic factors explained the major proportion (52–74%) of the variation of BMI from 1 to 11 years of age. Environmental factors common to both co-twins also showed some effect (7–28%), but at most ages this was not statistically significant. Strong genetic tracking was found for BMI from 1 to 11 years of age, but there was also evidence for a persistent effect of common environmental factors. Our results suggest that the genetic architecture of BMI development in the Japanese population is generally similar to that found in previous twin studies in Caucasian populations.     

Genetic and Environmental Transmission of Body Mass Index Fluctuation

This study sought to determine the relationship between body mass index (BMI) fluctuation and cardiovascular disease phenotypes, diabetes, and depression and the role of genetic and environmental factors in individual differences in BMI fluctuation using the extended twin-family model (ETFM). This study included 14,763 twins and their relatives. Health and Lifestyle Questionnaires were obtained from 28,492 individuals from the Virginia 30,000 dataset including twins, parents, siblings, spouses, and children of twins. Self-report cardiovascular disease, diabetes, and depression data were available. From self-reported height and weight, BMI fluctuation was calculated as the difference between highest and lowest BMI after age 18, for individuals 18–80 years. Logistic regression analyses were used to determine the relationship between BMI fluctuation and disease status. The ETFM was used to estimate the significance and contribution of genetic and environmental factors, cultural transmission, and assortative mating components to BMI fluctuation, while controlling for age. We tested sex differences in additive and dominant genetic effects, parental, non-parental, twin, and unique environmental effects. BMI fluctuation was highly associated with disease status, independent of BMI. Genetic effects accounted for ~34 % of variance in BMI fluctuation in males and ~43 % of variance in females. The majority of the variance was accounted for by environmental factors, about a third of which were shared among twins. Assortative mating, and cultural transmission accounted for only a small proportion of variance in this phenotype. Since there are substantial health risks associated with BMI fluctuation and environmental components of BMI fluctuation account for over 60 % of variance in males and over 50 % of variance in females, environmental risk factors may be appropriate targets to reduce BMI fluctuation.     

Genetic and Environmental Factors Influencing BMI Development from Adolescence to Young Adulthood

BMI increases progressively from adolescence to young adulthood. The aims of the present study were firstly, to investigate the extent to which genetic and environmental influences account for differences in BMI trajectories during this period, and secondly to examine whether boys and girls show divergences in these influences, as their BMI normally start differing across adolescence. The study sample consisted of 4,915 monozygotic and like- and unlike-sex dizygotic twins, born between 1975 and 1979. Data on BMI was gathered when twins were on average 16.1, 17.1, 18.6 and 24.4 years old. Genetic and environmental influences on the BMI trajectories were modeled using a latent growth curve approach. The results showed that the heritability of BMI decreased slightly after the adolescence period, from ≈80 to 70%. BMI transition from adolescence to young adulthood was best described by a quadratic trajectory that was highly accounted (61.7–86.5%) for by additive genetic influences. Genetic influences on BMI level showed a low correlation with those on the trend in BMI with age indicating that different sets of genes underlie the change of BMI during this period. Importantly, the analyses also evidenced that different genetic and environmental influences may underlie boys and girls evolution. In conclusion, our results suggested specific genetic influences accounting for the BMI rate-of-change from adolescence to young adulthood. This indicates that the specific genes behind BMI level may not be the same as the genes affecting BMI change which should be taken into account in further efforts to identify these genes.     

Effect of cold water immersion on 100-m sprint performance in well-trained swimmers

The aim of the present study was to examine the effect of cold water immersion (CWI) on sprint swimming performance in simulated competition conditions. Ten well-trained swimmers (5 males, 5 females; 19.0 ± 3.9 years) performed two 100-m swimming sprints (S1 and S2) interspersed with a 30-min passive recovery period, during which athletes were randomly assigned to 5 min of CWI (14°C) or an out-of-water control condition (CON 28°C). During tests, sprint times, heart rate (HR), pre- and post-race parasympathetic activity via HR variability (natural logarithm of the square root of the mean of the sum of the squares of differences between adjacent normal R–R intervals; Ln rMSSD) and blood lactate accumulation ([La]_ac) and clearance ([La]_cle) were recorded. Rates of perceived recovery (RPR) and exertion (RPE) were evaluated before and after each sprint. CWI was associated with a ‘likely’ decrease in swimming performance [1.8% (90% CI 0.2, 3.5)], as well as ‘likely’ lower peak HR [−1.9% (−3.6, −0.2)]. CWI was also associated with a ‘likely’ smaller decrease in Ln rMSSD after the first sprint [−16.7% (−30.9, −4.1)]. RPR was ‘likely’ better [+27.2% (−3.7, 68.0)] following CWI. ‘unclear’ effects were observed for [La]_ac [+24.7% (−13.4, 79.5)], [La]_cle [−7.6% (−24.2, 12.7)] or RPE [+2.0% (−12.3, 18.5)]. Following CWI, changes in sprint times were ‘largely’ correlated with changes in peak HR (r = 0.80). Despite a subjective perception of improved recovery following CWI, this recovery intervention resulted in slower swimming times in well-trained athletes swimming in simulated competition conditions.     

A Twin Study of the Genetics of High Cognitive Ability Selected from 11,000 Twin Pairs in Six Studies from Four Countries

Although much genetic research has addressed normal variation in intelligence, little is known about the etiology of high cognitive abilities. Using data from 11,000 twin pairs (age range = 6–71 years) from the genetics of high cognitive abilities consortium, we investigated the genetic and environmental etiologies of high general cognitive ability (g). Age-appropriate psychometric cognitive tests were administered to the twins and used to create g scores standardized within each study. Liability-threshold model fitting was used to estimate genetic and environmental parameters for the top 15% of the distribution of g. Genetic influence for high g was substantial (0.50, with a 95% confidence interval of 0.41–0.60). Shared environmental influences were moderate (0.28, 0.19–0.37). We conclude that genetic variation contributes substantially to high g in Australia, the Netherlands, the United Kingdom and the United States. Edited by Dick Rose.     

Genetic and Environmental Factors Affecting Self-Rated Health from Age 16–25: A Longitudinal Study of Finnish Twins

We analyzed genetic and environmental determinants of self-rated health and its change from adolescence to early adulthood. Questionnaires were mailed to Finnish twins born 1975–1979 at ages 16, 17, and, on average, 25 years of age (N = 2465 complete twin pairs). The data were analyzed using quantitative genetic methods for twin data by the Mx statistical package. Heritability of self-rated health was greatest at age 16 (63%, 95% confidence intervals (CI) 56–67%, men and women together) and declined steadily to age 25 (33%, 95% CI 25–41%). The residual variation was due to unshared environments. Health ratings at different ages were modestly correlated (r = 0.33–0.61). These correlations were mainly due to genetic factors, but unshared environment also contributed to them. An important challenge for further research is to identify environmental influences contributing to self-rated health independently of, or in interaction with, genetic factors. Edited by Peter McGuffin and John Hewitt     

Finger interaction during maximal radial and ulnar deviation efforts: experimental data and linear neural network modeling

The purpose of this study was to characterize finger interactions during radial/ulnar deviation, including interactions with flexion movements. Subjects performed single-finger and multi-finger maximal voluntary contraction (MVC), and maximal forces and various indices of interaction among the fingers were quantified. MVCs in radial/ulnar deviation were 50–80% as strong as in flexion. Along with the ‘master’ fingers (i.e., those explicitly instructed to produce force), substantial force production was also observed in ‘slave’ fingers (i.e., those not explicitly instructed to produce force), a phenomenon termed: force ‘enslaving’. In addition, a drop in MVC during multi-finger tasks as compared to single finger tasks (force ‘deficit’) was also observed. A previously unreported phenomenon that we term: ‘preferred direction enslaving’ was also apparent; both master and slave fingers produced force in the instructed direction with a non-zero perpendicular component. Due to the architectural separation of the involved muscles, preferred direction enslaving provides strong evidence that enslaving results from neural rather than biomechanical factors. A final new phenomenon: ‘negative deficit’, or force ‘facilitation’ was observed in 46.4% of the trials in 21 out of 23 subjects during multi-finger lateral efforts and was further demonstrative of extensive interconnection among neurons serving hand muscles. The data were modeled with high accuracy (∼4% mean square error) using a linear neural network with motor ‘commands’ as inputs and finger forces as outputs. The proposed network, equivalent to linear regression, can be used to determine the extent to which finger forces are influenced by peripheral constraints during functional prehensile activities.     

Internalizing Behavior in Adolescent Girls Affects Parental Emotional Overinvolvement: A Cross-lagged Twin Study

The aim of this study was to examine the direction and the etiology of the association between different parenting styles (parental emotional overinvolvement [EOI] and parental criticism) and internalizing behavior from adolescence to early adulthood. A longitudinal genetically informative cross-lagged design was applied to a population-based sample of Swedish twins contacted at age 16–17 (n = 2369) and at age 19–20 (n = 1705). Sex-limitation modelling revealed different effects for boys and girls. For girls, genetic influences on internalizing problems at age 16–17 independently explained 2.7% of the heritability in parental EOI at age 19–20. These results suggest that emotionally overinvolved and self-sacrificing parental behavior stems in part from daughters (but not sons) genetic predisposition for internalizing behavior. These findings highlight the importance of genetically influenced child-driven effects underlying the parenting-internalizing association, and clarify that the role of such effects may differ depending on sex, type of parenting and developmental period.     

Adaptation changes the spatial frequency tuning of adult cat visual cortex neurons

The modular layout of striate cortex is arguably a hallmark of all cortical organization. Neurons of a given module or domain respond optimally to very few specific properties, such as orientation or direction. However, it is possible, under appropriate conditions, to compel a neuron to respond preferentially to a different optimal property. In anesthetized cats, prepared for electrophysiological recordings in the visual cortex, we applied a spatial frequency (SF) that differs (by 0.25–3.0 octaves) from the optimal one for 7–13 min without interruption. This application shifted the tuning curve of the cell mainly in the direction of the imposed SF. Indeed, results indicate an attractive push occurring more frequently (50%) than a repulsive (30%) shift in cortical cells. The increase of responsivity is band-limited and is around the imposed SF, while flanked responses remained unmodified in all conditions. We hypothesize that the observed reversible plasticity is obtained by a modulation of the balance between the strengths of the respective synaptic inputs. These changes in preferred original optimal spatial frequencies may allow a dynamic reaction of cortex to a new environment and particularly to ‘‘zoom’’ cellular activity toward persistent stimuli in spite of the tuning inherited from genetic programming of response properties and environmental conditions during critical periods in new born animals.     

Pleiotropic Effects of DCDC2 and DYX1C1 Genes on Language and Mathematics Traits in Nuclear Families of Developmental Dyslexia

Converging evidence indicates that developmental problems in oral language and mathematics can predate or co-occur with developmental dyslexia (DD). Substantial genetic correlations have been found between language, mathematics and reading traits, independent of the method of sampling. We tested for association of variants of two DD susceptibility genes, DCDC2 and DYX1C1, in nuclear families ascertained through a proband with DD using concurrent measurements of language and mathematics in both probands and siblings by the Quantitative Transmission Disequilibrium Test. Evidence for significant associations was found between DCDC2 and ‘Numerical Facts’ (p value = 0.02, with 85 informative families, genetic effect = 0.57) and between ‘Mental Calculation’ and DYX1C1 markers -3GA (p value = 0.05, with 40 informative families, genetic effect = −0.67) and 1249GT (p value = 0.02, with 49 informative families, genetic effect = −0.65). No statistically significant associations were found between DCDC2 or DYX1C1 and language phenotypes. Both DCDC2 and DYX1C1 DD susceptibility genes appear to have a pleiotropic role on mathematics but not language phenotypes.     

Genetic and environmental influences on growth from late childhood to adulthood: a longitudinal study of two Finnish twin cohorts

Objectives: Human growth is a complex process that remains insufficiently understood. We aimed to analyze genetic and environmental influences on growth from late childhood to early adulthood. Methods: Two cohorts of monozygotic and dizygotic (same sex and opposite sex) Finnish twin pairs were studied longitudinally using self‐reported height at 11–12, 14, and 17 years and adult age (FinnTwin12) and at 16, 17, and 18years and adult age (FinnTwin16). Univariate and multivariate variance component models for twin data were used. Results: From childhood to adulthood, genetic differences explained 72–81% of the variation of height in boys and 65–86% in girls. Environmental factors common to co‐twins explained 5–23% of the variation of height, with the residual variation explained by environmental factors unique to each twin individual. Common environmental factors affecting height were highly correlated between the analyzed ages (0.72–0.99 and 0.91–1.00 for boys and girls, respectively). Genetic (0.58–0.99 and 0.70–0.99, respectively) and unique environmental factors (0.32–0.78 and 0.54–0.82, respectively) affecting height at different ages were more weakly, but still substantially, correlated. Conclusions: The genetic contribution to height is strong during adolescence. The high genetic correlations detected across the ages encourage further efforts to identify genes affecting growth. Common and unique environmental factors affecting height during adolescence are also important, and further studies are necessary to identify their nature and test whether they interact with genetic factors. Am. J. Hum. Biol., 2011. © 2011Wiley‐Liss, Inc.