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.     

Stable Genes and Changing Environments: Body Mass Index Across Adolescence and Young Adulthood

The transition between adolescence and young adulthood is a developmentally sensitive time where children are at an increased risk for becoming overweight and developing obesity. Twin studies have reported that body mass index [BMI] is highly heritable, however, it remains unclear whether the genetic influences are sex-limited and whether non-additive genetic influences contribute to body mass index [BMI] during these ages. In the current report, we examined self-reported data on BMI in same [n = 2,744] and opposite-sex [n = 1,178] siblings participating in the National Longitudinal Study on Adolescent Health [Add Health]. To investigate whether the same or different genes contributed to BMI for both sexes, we fit quantitative sex-limited genetic models to three waves of data collection. At each of the three Waves of assessment, models that included additive genetic, individual-specific environment, and no sex-limited genetic influences fit the data most parsimoniously. Heritable effects on BMI at each of the three Waves were large for both sexes and ranged between .75 and .86. While genetic contributions across the ages were highly correlated, longitudinal analyses indicated that the relevant individual-specific environmental influences on BMI in adolescence and young adulthood change sizably. These results underscore the importance of understanding early genetic influences on BMI and highlight the role environmental experiences have at later ages when new genetic influences appear to make a small contribution to individual variation in BMI.     

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.     

Genetic and Environmental Correlations Between Body Mass Index and Waist Circumference in China: The Qingdao Adolescent Twin Study

We aimed to analyze how genetic and environmental factors account for variations in body mass index (BMI), waist circumference (WC) and their mutual correlation in Chinese children. We measured BMI and WC in 588 pairs of twins (53 % monozygotic twins) aged 8–17 years and applied structural equation modeling to the data. For the younger children (8–12 years of age), heritability estimates of BMI were 0.56 for boys and 0.69 for girls; for the older children (13–17 years of age), the corresponding figures were 0.64 and 0.71, respectively. We observed moderate heritability estimates in WC: the corresponding figures were 0.24 and 0.56 for the younger children, and 0.27 and 0.33 for the older children, respectively. The heterogeneity test for genetic variance of BMI and WC was statistically significant between the two age groups for both sexes (p < 0.001). The proportions of BMI and WC variations due to shared and non-shared environmental factors remained stable during childhood in both sexes. Bivariate genetic analyses showed that genetic correlations between BMI and WC were strong for the younger children (r_g = 0.75 for boys, r_g = 0.98 for girls) and the older children (r_g = 1.0 for both boys and girls). Both sexes showed moderate non-shared environmental correlations in the two age groups, whereas shared environmental correlations––except among male younger children––were not statistically significant. Genetic factors play an important role in variations in BMI and WC during childhood. Common genetic and non-shared environmental factors explained most of the association between BMI and WC for both boys and girls.     

The Etiology of Stability and Change in Religious Values and Religious Attendance

Studies have demonstrated little to no heritability for adolescent religiosity but moderate genetic, shared environmental, and nonshared environmental influences on adult religiosity. Only one longitudinal study of religiosity in female twins has been conducted (Koenig et al., Dev Psychol 44:532?C543, 2008), and reported that persistence from mid to late adolescence is due to shared environmental factors, but persistence from late adolescence to early adulthood was due to genetic and shared environmental factors. We examined the etiology of stability and change in religious values and religious attendance in males and females during adolescence and early adulthood. The heritability of both religious values and religious attendance increased from adolescence to early adulthood, although the increase was greater for religious attendance. Both genetic and shared environmental influences contributed to the stability of religious values and religious attendance across adolescence and young adulthood. Change in religious values was due to both genetic and nonshared environmental influences specific to early adulthood, whereas change in religious attendance was due in similar proportions to genetic, shared environmental, and non-shared environmental influences.     

Changes in genetic and environmental influences on trait anxiety from middle adolescence to early adulthood

Background

Middle adolescence to early adulthood is an important developmental period for the emergence of anxiety. Genetically-influenced stable traits are thought to underlie internalizing psychopathology throughout development, but no studies have examined changes in genetic and environmental influences on trait anxiety during this period.

Method

A longitudinal twin study design was used to study same-sex twin pairs (485 monozygotic pairs, 271 dizygotic pairs) at three ages, 14, 18, and 21 years, to examine developmental shifts in genetic and environmental effects on trait anxiety.

Results

The heritability of trait anxiety increased with age, particularly between ages 14 and 18, no significant new genetic influences emerged after age 14, and the genetic influences were highly correlated across the three ages, supporting developmentally stable genetic risk factors. The environmental effects shared by members of a family decreased in influence across adolescence, while the influence of environmental effects unique to each individual twin remained relatively stable over the course of development and were largely age-specific.

Limitations

The twin study design does not inform about specific genes and environmental risk factors.

Conclusions

Genetic influences increased in importance from middle to late adolescence but common genetic factors influenced trait anxiety across the three ages. Shared environmental influences decreased in importance and demonstrated negligible influence by late adolescence/early adulthood. Nonshared environmental effects were almost entirely age-specific. These findings support the importance of developmentally-sensitive interventions that target shared environmental factors prior to middle adolescence and shifting non-shared environmental risks at each age.     

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.     

Genetic and environmental factors affecting self-esteem from age 14 to 17: a longitudinal study of Finnish twins

BACKGROUND: We analysed genetic and environmental influences on self-esteem and its stability in adolescence. METHOD: Finnish twins born in 1983-1987 were assessed by questionnaire at ages 14 (n = 4132 twin individuals) and 17 years (n = 3841 twin individuals). Self-esteem was measured using the Rosenberg global self-esteem scale and analyzed using quantitative genetic methods for twin data in the Mx statistical package. RESULTS: The heritability of self-esteem was 0.62 [95% confidence interval (CI) 0.56-0.68] in 14-year-old boys and 0.40 (95% CI 0.26-0.54) in 14-year-old girls, while the corresponding estimates at age 17 were 0.48 (95% CI 0.39-0.56) and 0.29 (95% CI 0.11-0.45). Rosenberg self-esteem scores at ages 14 and 17 were modestly correlated (r = 0.44 in boys, r = 0.46 in girls). In boys, the correlation was mainly (82%) due to genetic factors, with residual co-variation due to unique environment. In girls, genetic (31%) and common environmental (61%) factors largely explained the correlation. CONCLUSIONS: In adolescence, self-esteem seems to be differently regulated in boys versus girls. A key challenge for future research is to identify environmental influences contributing to self-esteem during adolescence and determine how these factors interact with genetic influences.     

Genetic etiology of stability of attention problems in young adulthood.

Variation in attention problems in children and adolescents from non-clinical samples is highly heritable. It is unknown how attention problems develop later in life and whether the heritability in the general adult population is the same as in children and adolescents. We assessed the heritability and stability of individual differences in attention problems in the general young adult population and explored to what extent the stability can be attributed to genetic or environmental factors. On one or more occasions, young adult twins (age range, 18-30 years, N = 4,245) from the Netherlands Twin Registry filled out the attention problems (AP) subscale of the Young Adult Self-Report [Achenbach, 1997]: in 1991, N = 1,755 (of which 842 complete pairs), in 1995, N = 2,428 (1156 complete pairs) and in 1997, N = 2,344 (958 pairs). There was only a slight decrease in the average level of attention problems during young adulthood. The heritability at each occasion was around 40%. The correlation of attention problems across a period of 6 years was 0.42, and 77% of this correlation could be ascribed to genetic influences. Thus, individual differences in attention problems in young adulthood are heritable, and stability in individual differences over time can largely be ascribed to genetic influences. Genetic correlations across time were high, suggesting that the genes that influence variability in attention problems in late adolescence are largely the same as those that influence variability in early adulthood.     

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.     

Sex differences in the genetic and environmental influences on the development of antisocial behavior

The present study uses a population-based sample of 6.806 adult twins from same-sex and opposite-sex twin pairs to examine sex differences in the underlying genetic and environmental architecture of the development of antisocial behavior (AB). Retrospective reports of AB during three different developmental periods were obtained: prior to age 15 years (childhood), age 15-17 years (adolescent), and age 18 years and older (adult). Structural equation modeling analyses revealed that there was no evidence for sex-specific genetic or sex-specific shared family environmental influences on the development of AB; that is, the types of genetic and environmental influence were similar for males and females. For both sexes, a model that allowed for genetic influences on adolescent and adult AB that were not shared with childhood AB fit better than a model with a single genetic factor. In contrast, shared environmental influences on adolescent and adult AB overlapped entirely with shared environmental influences on childhood AB. Genetic factors played a larger role in variation in childhood AB among females, whereas shared environmental factors played a larger role among males. However, heritability of AB increased from childhood to adolescence and adulthood for both sexes, and the magnitude of genetic and environmental influences on adolescent and adult AB was approximately equal across sex. We speculate that sex differences in timing of puberty may account for the earlier presence of genetic effects among females.     

The influence of five monoamine genes on trajectories of depressive symptoms across adolescence and young adulthood

The influence of five monoamine candidate genes on depressive symptom trajectories in adolescence and young adulthood were examined in the Add Health genetic sample. Results indicated that, for all respondents, carriers of the dopamine receptor D4 5-repeat allele were characterized by distinct depressive symptom trajectories across adolescence and early adulthood. Similarly, for males, individuals with the monoamine oxidase A 3.5-repeat allele exhibited unique depressive symptom trajectories. Specifically, the trajectories of those with the dopamine receptor D4 5-repeat allele were characterized by rising levels in the transition to adulthood, while their peers were experiencing a normative drop in depressive symptom frequency. Conversely, males with the monoamine oxidase A 3.5-repeat allele were shown to experience increased distress in late adolescence. An empirical method for examining a wide array of allelic combinations was employed, and false discovery rate methods were used to control the risk of false positives due to multiple testing. Special attention was given to thoroughly interrogate the robustness of the putative genetic effects. These results demonstrate the value of combining dynamic developmental perspectives with statistical genetic methods to optimize the search for genetic influences on psychopathology across the life course.     

Contributions of Genes and Environments to Stability and Change in Externalizing and Internalizing Problems During Elementary and Middle School

We examined longitudinally collected behavioral reports by teachers on a unique twin sample at the ages of 7, 8, 9, 10, 11, and 12 years. As twin and adoption studies implicate the role of genetic influence on behavioral problems found to be stable in epidemiological samples, the current study employs a developmental behavior genetic model to examine the extent to which genetic and environmental contributions to problem behaviors are stable and/or change during development. In this sample of 410 monozygotic (MZ) and 354 dizygotic (DZ) twins, MZ twins were rated as more similar than DZ twins on average. In general, boys were more frequently rated as displaying externalizing behaviors than were girls across each of the six observations, while girls’ internalizing problems were found not to be significantly different from boys’. For both sexes, stability in externalizing problem behaviors was due to a single common genetic factor whose effects acted pleiotropically at each age in the presence of unique environmental influences that were transmitted from age-to-age. Change was largely due to uncorrelated age-specific non-shared environmental and additive genetic effects. Contributions to stability for internalizing problems were due to age-to-age transmission of earlier expressed genetic effects. Change for girls and boys internalizing problems were largely due to environmental experiences unique to siblings along with uncorrelated age-specific genetic effects. These results further inform the notion that individual environments are important factors in the etiology of problem behaviors, but suggest that heritable contributions to phenotypic stability are largely the same across middle childhood and early adolescence. Clinical implications of these findings are discussed.     

Similarities in Drinking Behavior of Twin’s Friends: Moderation of Heritability of Alcohol Use

Previous research has indicated that friends’ drinking may influence alcohol use in adolescents and young adults. We explored whether similarities in the drinking behavior of friends of twins influence the genetic architecture of alcohol use in adolescence and young adulthood. Survey data from The Netherlands Twin Register were available for 1,526 twin pairs aged 16–25 years. We categorized the twin pairs as concordant (both report similar alcohol use in their friends) or discordant for the alcohol use of their friends. Genetic moderator models were tested by carrying out multi-group analyzes in Mplus. Findings showed a significant moderation effect. Genetic factors were more and common environment less important in the explanation of variation in alcohol use in twins discordant for alcohol use of friends than in twins concordant for alcohol use of friends. Edited by Michael Lyons.     

Co-occurrence of Aggressive Behavior and Rule-Breaking Behavior at Age 12: Multi-Rater Analyses

Aggressive Behavior (AGG) and Rule-Breaking Behavior (RB) are two of the eight CBCL syndromes. The phenotypic correlation between AGG and RB ranges from .48 to .76, and varies depending on the rater and the sex of the child. Prevalence of AGG and RB (i.e., T 67) is in the range of 6%–7% in both boys and girls. Fifty percent to 60% of the children who are deviant on AGG are also deviant on RB and vice versa. Why so many children show problem behavior in the clinical range for both syndromes is unclear. This co-occurrence could be due to genetic factors influencing both traits, to environmental factors influencing both traits, or to both. The purpose of this study is to use a genetically informative sample to estimate genetic and environmental influences on AGG and RB and to investigate the etiology of the co-occurrence of both behaviors. We do this using multiple informants to take into account underlying sources of parental agreement and disagreement in ratings of their offspring. To this end, mother and father ratings of AGG and RB were collected by using the Child Behavior Checklist in a large sample of 12-year-old twins. Parental agreement is represented by an interparent correlation in the range of .53–.76, depending on phenotype (AGG or RB) and sex of the child. Genetic influences account for 79% and 69% of the individual differences in RB and AGG behavior (defined as AGG and RB on which both parents do agree) in boys. In girls 56% and 72% of the variance in RB and AGG are accounted for by genetic factors. Shared environmental influences are significant for RB in girls only, explaining 23% of the total variance. Eighty percent of the covariance between AGG and RB, similarly assessed by both parents, can be explained by genetic influences. So, co-occurrence in AGG and RB is mainly caused by a common set of genes. Parental disagreement seems to be a combination of so-called rater bias and of parental specific views.     

Heritability of somatotype components from early adolescence into young adulthood: a multivariate analysis on a longitudinal twin study

BACKGROUND: Several studies with different designs have attempted to estimate the heritability of somatotype components. However they often ignore the covariation between the three components as well as possible sex and age effects. Shared environmental factors are not always controlled for. AIM: This study explores the pattern of genetic and environmental determination of the variation in Heath-Carter somatotype components from early adolescence into young adulthood. SUBJECTS AND METHODS: Data from the Leuven Longitudinal Twin Study, a longitudinal sample of Belgian same-aged twins followed from 10 to 18 years (n = 105 pairs, equally divided over five zygosity groups), is entered into a multivariate path analysis. Thus the covariation between the somatotype components is taken into account, gender heterogeneity can be tested, common environmental influences can be distinguished from genetic effects and age effects are controlled for. RESULTS: Heritability estimates from 10 to 18 years range from 0.21 to 0.88, 0.46 to 0.76 and 0.16 to 0.73 for endomorphy, mesomorphy and ectomorphy in boys. In girls, heritability estimates range from 0.76 to 0.89, 0.36 to 0.57 and 0.57 to 0.76 for the respective somatotype components. Sex differences are significant from 14 years onwards. More than half of the variance in all somatotype components for both sexes at all time points is explained by factors the three components have in common. CONCLUSIONS: The finding of substantial genetic influence on the variability of somatotype components is further supported. The need to consider somatotype as a whole is stressed as well as the need for sex- and perhaps age-specific analyses. Further multivariate analyses are needed to confirm the present findings.     

Heritability of somatotype components from early adolescence into young adulthood: a multivariate analysis on a longitudinal twin study

Background : Several studies with different designs have attempted to estimate the heritability of somatotype components. However they often ignore the covariation between the three components as well as possible sex and age effects. Shared environmental factors are not always controlled for. Aim : This study explores the pattern of genetic and environmental determination of the variation in Heath-Carter somatotype components from early adolescence into young adulthood. Subjects and methods : Data from the Leuven Longitudinal Twin Study, a longitudinal sample of Belgian same-aged twins followed from 10 to 18 years ( n = 105 pairs, equally divided over five zygosity groups), is entered into a multivariate path analysis. Thus the covariation between the somatotype components is taken into account, gender heterogeneity can be tested, common environmental influences can be distinguished from genetic effects and age effects are controlled for. Results : Heritability estimates from 10 to 18 years range from 0.21 to 0.88, 0.46 to 0.76 and 0.16 to 0.73 for endomorphy, mesomorphy and ectomorphy in boys. In girls, heritability estimates range from 0.76 to 0.89, 0.36 to 0.57 and 0.57 to 0.76 for the respective somatotype components. Sex differences are significant from 14 years onwards. More than half of the variance in all somatotype components for both sexes at all time points is explained by factors the three components have in common. Conclusions : The finding of substantial genetic influence on the variability of somatotype components is further supported. The need to consider somatotype as a whole is stressed as well as the need for sex- and perhaps age-specific analyses. Further multivariate analyses are needed to confirm the present findings.     

Genetic and Environmental Influences on Separation Anxiety Disorder Symptoms and Their Moderation by Age and Sex

We estimated genetic and environmental influences on mother-rated DSM-III-R separation anxiety disorder (SAD) symptoms in 2043 3 to 18-year-old male and female twin pairs and their siblings (348 pairs) recruited from the Australian NH&MRC Twin Registry. Using DeFries and Fulker's (1985) multiple regression analysis, we found that genetic and shared environmental influences both contributed appreciably to variation in SAD symptoms (h ² = .47, SE = .07; c ² = .21, SE = .05) and were significantly moderated by both sex and age. Genetic influences were greater for girls than boys (h ² = .50 and .14, respectively), whereas shared environmental influences were greater for boys than girls (c ² = .51 and .21, respectively). Genetic influences increased with age, whereas shared environmental influences decreased with age. Shared environmental influences were greater in magnitude for twins than for nontwin siblings (c ² = .28 versus .13, respectively). Implications of these findings for theories of the cause of separation anxiety are discussed.     

Does adolescent depression predict obesity in black and white young adult women?

BACKGROUND: To examine whether adolescent depressive symptoms predict young adult body mass index (BMI) and obesity in black and white women. METHOD: Participants included 1554 black and white adolescent girls from the National Heart, Lung, and Blood Institute Growth and Health Study (NGHS) who completed the Center for Epidemiological Studies--Depression Scale (CES-D) at ages 16 and 18 years. RESULTS: Regression analyses showed that depressive symptoms at both ages 16 and 18 were associated with increased risk of obesity (BMI > or = 30) and elevated BMI in young adulthood (age 21) in both black and white girls. Black girls exhibited a significantly greater likelihood of obesity and higher BMI (i.e. a main effect of race), but the race x CES-D interaction was not significant in any analysis. CONCLUSIONS: Depressive symptoms in adolescence appear to be predictive of obesity and elevated BMI in early adulthood for both black and white girls, even when taking prior BMI into account, indicating that depressive symptoms confer risk for obesity above and beyond the known tracking of body weight. Obesity prevention studies might consider assessing depressive symptoms in adolescence in order to more fully capture important risk variables.     

Correlates of Positive Parenting Behaviors

The present study examined the influence of maternal and child characteristics on parenting behaviors in a genetically informative study. The participants were 976 twins and their mothers from the Colorado Longitudinal Twin Study and the Twin Infant Project. Indicators of positive parenting were coded during parent–child interactions when twins were 7–36 months old. Child cognitive abilities and affection were independent correlates of positive parenting. There were significant gender differences in the magnitude of genetic and environmental influences on positive parenting, with shared environmental influences on parenting of girls and additive genetic influences on parenting of boys. Girls received significantly more positive parenting than boys. Differences in etiology of positive parenting may be explained by developmental gender differences in child cognitive abilities and affection, such that girls may have more rewarding interactions with parents, evoking more positive parenting.