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1.
Edwards AC Sihvola E Korhonen T Pulkkinen L Moilanen I Kaprio J Rose RJ Dick DM 《Behavior genetics》2011,41(4):476-487
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 (rA = .26–.59) and environmental (rC = .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. 相似文献
2.
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. 相似文献
3.
Sarah E. Garcia Erin C. Tully Nicholas Tarantino Susan South William G. Iacono Matt McGue 《Journal of affective disorders》2013
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. 相似文献4.
Ortega-Alonso A Pietiläinen KH Silventoinen K Saarni SE Kaprio J 《Behavior genetics》2012,42(1):73-85
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. 相似文献
5.
Thought Problems from Adolescence to Adulthood: Measurement Invariance and Longitudinal Heritability
Abdellaoui A de Moor MH Geels LM van Beek JH Willemsen G Boomsma DI 《Behavior genetics》2012,42(1):19-29
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. 相似文献
6.
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 相似文献
7.
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 相似文献
8.
This longitudinal study used a representative community sample of same-sex twins (485 monozygotic pairs, 271 dizygotic pairs) to study longitudinal changes in genetic and environmental influences on nicotine dependence (NicD) symptoms and major depressive disorder (MDD) symptoms and the longitudinal relationships between NicD and MDD symptoms at three relatively discrete ages spanning middle adolescence to early adulthood (ages 15, 18, and 21). Clinical interviews were used to assess NicD and MDD symptoms lifetime at age 15 and during the previous 3 years at the two subsequent assessments. Biometric models revealed similar patterns of findings for NicD and MDD. Heritability increased with age, particularly between ages 15 and 18. Shared environmental influences were small, and the proportion of variance attributed to shared environmental influences decreased with age. Nonshared environmental influences were moderate to large in magnitude and were entirely age specific. Both NicD and MDD symptoms showed considerable stability from age 15 to 21, and at each age those with one disorder showed elevated rates of the other. However, a cross-lagged model revealed no longitudinal predictive relationships between MDD symptoms and NicD symptoms after accounting for stability of symptoms within disorders. In summary, the transition between middle and late adolescence is a critical period for developmental shifts in the magnitudes of genetic and environmental influences on both MDD and NicD symptoms. Despite similarities in the development of genetic and environmental influences for the two phenotypes, the association between NicD and MDD reflects concurrent covariation rather than one phenotype being an antecedent influence on the subsequent development of the other. 相似文献
9.
10.
Jelenkovic A Ortega-Alonso A Rose RJ Kaprio J Rebato E Silventoinen K 《American journal of human biology》2011,23(6):764-773
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. 相似文献
11.
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. 相似文献
12.
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. 相似文献
13.
Malone SM Taylor J Marmorstein NR McGue M Iacono WG 《Development and psychopathology》2004,16(4):943-966
Genetic and environmental influences on symptoms of adult antisocial behavior (AAB) and alcohol dependence at ages 17, 20, and 24 were examined cross-sectionally and longitudinally in 188 monozygotic and 101 dizygotic male twin pairs. A moderate genetic influence on both AAB and alcohol dependence was found at each age, with a substantial proportion of this influence common to the two disorders, suggesting they share susceptibility genes. Biometrical models showed that continuity effects accounted for most of the stable variance in symptoms of both AAB and alcohol dependence, indicating that genetic and environmental effects associated with each of these disorders were similar at each age. Significant cross-lag effects (effects of alcohol dependence contributing to variance in AAB and vice versa) were observed at ages 20 and 24 for both disorders. The largest and theoretically most interesting of these effects indicated that one sixth of the genetic influence on AAB at age 20 was due to genetic effects associated with alcohol dependence at age 17. Thus, alcohol dependence symptoms at age 17 in particular had an effect on antisocial behavior symptoms at age 20, suggesting that alcohol involvement in adolescence may ensnare otherwise desisting youth in persistent antisocial behavior. 相似文献
14.
Assessing gene-environment interactions on anxiety symptom subtypes across childhood and adolescence 总被引:2,自引:0,他引:2
Consistent evidence shows both genetic and stress-related risks on child and adolescent anxiety, yet few studies have considered the degree to which genetic effects are moderated by stress (gene-environment interaction). We used longitudinal data from both a child and adolescent sample of twins to examine three novel issues on the presence of gene-environment interaction on anxiety symptoms. First, we assessed moderation of genetic risks on anxiety symptoms by negative life events in each age group. Second, by distinguishing between "stable" and "age-specific" genetic factors, we explored the continuity of gene-environment interaction across time and/or its emergence at specific ages. Third, we compared the presence of gene-environment interaction across different symptom types (general, panic, social, and separation). Genetic effects on separation anxiety symptoms in childhood (mean age = 8 years, 6 months) and panic anxiety symptoms in adolescence (mean age = 15 years) increased across independent negative life events. Shared environmental effects on separation anxiety symptoms and non shared environmental effects on general anxiety symptoms in adolescence were also moderated by negative life events. We interpret these preliminary findings tentatively in the context of gene-environment interaction on anxiety in general, and on early separation and later panic anxiety in particular. 相似文献
15.
Hoekstra RA Bartels M Hudziak JJ Van Beijsterveldt TC Boomsma DI 《Behavior genetics》2008,38(5):447-461
We examined the contribution of genetic and environmental influences on the stability of withdrawn behavior (WB) in childhood
using a longitudinal multiple rater twin design. Maternal and paternal ratings on the withdrawn subscale of the Child Behavior
Checklist (CBCL) were obtained from 14,889 families when the twins were 3, 7, 10 and 12 years old. A longitudinal psychometric
model was fitted to the data and the fit of transmission and common factor models were evaluated for each variance component.
WB showed considerable stability throughout childhood, with correlation coefficients ranging from about .30 for the 9-year
time interval to .65 for shorter time intervals. Individual differences in WB as observed by the mother and the father were
found to be largely influenced by genetic effects at all four time points, in both boys (50–66%) and girls (38–64%). Shared
environmental influences explained a small to modest proportion (0–24%) of the variance at all ages and were slightly more
pronounced in girls. Non-shared environmental influences were of moderate importance to the variance and slightly increased
with age, from 22–28% at age 3 to 35–41% at age 12 years. The stability of WB was largely explained by genetic effects, accounting
for 74% of stability in boys and 65% in girls. Shared environmental effects explained 7% (boys) and 17% (girls) of the behavioral
stability. Most shared environmental effects were common to both raters, suggesting little influence of rater bias in the
assessment of WB. The shared environmental effects common to both raters were best described by a common factor model, indicating
that these effects are stable and persistent throughout childhood. Non-shared environmental effects accounted for the remaining
covariance over time.
Edited by Hermine Maes. 相似文献
16.
D. J. A. Smit M. Boersma C. E. M. van Beijsterveldt D. Posthuma C. J. Stam E. J. C. de Geus 《Behavior genetics》2010,40(2):167-177
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. 相似文献
17.
The way people cope with stressors of day to day living has an important influence on health. The aim of the present study was to explore whether genetic and environmental variations in stress-coping differ over time during adulthood. The brief COPE was mailed to a large sample of the UK female twins (N = 4,736) having a wide range of age (20–87 years). Factor analyses of the items of the brief COPE yielded three coping scales: ‘Problem-Solving’, ‘Support Seeking’, and ‘Avoidance’. Monozygotic and dizygotic twin correlations tended to become lower with age for all three scales, suggesting that unique environmental factors may become more important with age during adulthood. Model-fitting results showed that relative influences of unique environmental factors increased from 60 % at age 20 years to 74% at age 87 years for ‘Problem-Solving’ and 56 % at age 20 years to 76% at age 87 years for ‘Avoidance’. During the same age period, genetic factors decreased from 40 to 26 % for ‘Problem-Solving’ and from 44 to 24 % for ‘Avoidance’. For ‘Seeking Support’, the magnitude of genetic and unique environmental factors was not significantly different across the adulthood. For all three scales, shared environmental effects were negligible. Overall, our findings implicate that the effects of environment that stem from idiosyncratic experience of stressful life events accumulate and become increasingly important in adulthood. 相似文献
18.
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. 相似文献
19.
Tanya M. M. Button Michael C. Stallings Soo Hyun Rhee Robin P. Corley John K. Hewitt 《Behavior genetics》2011,41(2):201-210
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. 相似文献
20.
Measures of intelligence were collected in 209 twin pairs at 5, 7, 10, and 12 years of age, as part of a longitudinal project on intelligence, brain function, and behavioral problems. Intelligence was measured at 5, 7, and 10 years of age with the RAKIT, a well-known Dutch intelligence test, consisting of 6 subscales. At 12 years of age, the complete WISC-R was administered (12 subscales). Both intelligence tests resulted in a measure of full-scale IQ (FSIQ). Participation rate is around 93% at age 12. Correlation coefficients over time are high: (r(5–7) = .65; r(5–10) = .65; r(5–12) = .64; r(7–10) = .72; r(7–12) = .69 and r(10–12) = .78). Genetic analyses show significant heritabilities at all ages, with the expected increase of genetic influences and decrease of shared environmental influences over the years. Genetic influences seem to be the main driving force behind continuity in general cognitive ability, represented by a common factor influencing FSIQ at all ages. Shared environmental influences are responsible for stability as well as change in the development of cognitive abilities, represented by a common factor influencing FSIQ at all ages and age-specific influences, respectively. 相似文献