Sexual Development in Adolescence: An Examination of Genetic and Environmental Influences.
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ABSTRACT:
SUBMITTER: Clark DA
PROVIDER: S-EPMC7253320 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectiveResearch on sources of variation in adolescent's gonadal hormone levels is limited. We sought to decompose individual differences in adolescent testosterone, estradiol, and pubertal status, into genetic and environmental components.DesignA sample of male and female adolescent twins from the greater Austin and Houston areas provided salivary samples, with a subset of participants providing longitudinal data at 2 waves.ParticipantsThe sample included 902 adolescent twins, 49% female, aged 13-20 years (M = 15.91) from the Texas Twin Project. Thirty-seven per cent of twin pairs were monozygotic; 30% were same-sex dizygotic (DZ) pairs; and 33% were opposite-sex DZ pairs.MeasurementsSaliva samples were assayed for testosterone and estradiol using chemiluminescence immunoassays. Pubertal status was assessed using self-report. Biometric decompositions were performed using multivariate quantitative genetic models.ResultsGenetic factors contributed substantially to variation in testosterone in males and females in the follicular phase of their menstrual cycle (h2 = 60% and 51%, respectively). Estradiol was also genetically influenced in both sexes, but was predominately influenced by nonshared environmental factors. The correlation between testosterone and estradiol was mediated by a combination of genetic and environmental influences for males and females. Genetic and environmental influences on hormonal concentrations were only weakly correlated with self-reported pubertal status, particularly for females.ConclusionsBetween-person variability in adolescent gonadal hormones and their interrelationship reflects both genetic and environmental processes, with both testosterone and estradiol containing sizeable heritable components.
| S-EPMC5771835 | biostudies-literature
Project description:Sleep disturbances regularly co-occur with clinical psychotic disorders and dimensions of psychotic-like experiences (PLEs). One possible explanation for this, which has yet to be tested, is that similar genetic or environmental influences underlie sleep disturbances and vulnerability to PLEs. We conducted a twin study to test this possibility in relation to sleep disturbances and six specific PLEs in adolescence in the general population. Approximately 5,000 16-year-old twin pairs completed the Pittsburgh Sleep Quality Index and Insomnia Severity Index. PLEs were assessed using the Specific PLEs Questionnaire, comprising five self-report subscales (Paranoia, Hallucinations, Cognitive Disorganization, Grandiosity, and Anhedonia) and one parent-report subscale (Negative Symptoms). The associations between these measures were tested using structural equation twin model fitting. Paranoia, Hallucinations, and Cognitive Disorganization displayed moderate and significant correlations with both sleep measures (0.32-.42), while Negative Symptoms, Anhedonia, and Grandiosity showed lower correlations (0.01-0.17). Genetic and environmental influences significantly overlapped across PLEs (Paranoia, Hallucinations, Cognitive Disorganization) and both types of sleep disturbance (mean genetic and nonshared environmental correlations = 0.54 and 0.24, respectively). These estimates reduced, yet remained significant, after controlling for negative affect. The association between PLEs with sleep disturbances in adolescence is partly due to genetic and environmental influences that are common to them both. These findings indicate that the known neurobiology of sleep disturbance may provide clues regarding the causes of PLEs in adolescence.
| S-EPMC4532318 | biostudies-other
Project description:Rumination is an established cognitive vulnerability for depression. Despite substantial work on the environmental origins of rumination, the heritability of rumination has not been examined and it is not known whether rumination accounts for some of the genetic vulnerability associated with depression. 756 adolescent twins ages 12-14 years completed the Response Styles Questionnaire and multiple measures of depressive symptoms. Brooding correlated positively and distraction correlated negatively with concurrent depressive symptoms. Estimated heritabilites were 54% for depression, 21% for brooding, 37% for reflection, and 30% for distraction. Bivariate genetic analyses suggested that (1) individual differences in distraction share both genetic and environmental sources of variation with depression; and (2) although the heritable influences on brooding are small, these heritable influences account for the majority of the relationship between brooding and depression (h2 = .62).
| S-EPMC3742117 | biostudies-literature
Project description:In this report, we present the first regional quantitative analysis of age-related differences in the heritability of cortical thickness using anatomic MRI with a large pediatric sample of twins, twin siblings, and singletons (n = 600, mean age 11.1 years, range 5-19). Regions of primary sensory and motor cortex, which develop earlier, both phylogenetically and ontologically, show relatively greater genetic effects earlier in childhood. Later developing regions within the dorsal prefrontal cortex and temporal lobes conversely show increasingly prominent genetic effects with maturation. The observation that regions associated with complex cognitive processes such as language, tool use, and executive function are more heritable in adolescents than children is consistent with previous studies showing that IQ becomes increasingly heritable with maturity(Plomin et al. 1997: Psychol Sci 8:442-447). These results suggest that both the specific cortical region and the age of the population should be taken into account when using cortical thickness as an intermediate phenotype to link genes, environment, and behavior.
| S-EPMC6870600 | biostudies-literature
Project description:This multiwave longitudinal study tested two quantitative genetic developmental models to examine genetic and environmental influences on exposure to negative dependent and independent life events. Participants (N = 457 twin pairs) completed measures of life events annually from ages 9 to 16. The same genetic factors influenced exposure to dependent events across time and increased in magnitude during the transition to adolescence. Independent events were less genetically influenced than dependent events in boys, but not girls. Shared environmental influences decreased in magnitude as youth transitioned into adolescence. Nonshared environmental influences were mostly age specific and contributed significantly to both types of events at all ages. Results provide theoretical implications for developmental risk pathways to stress exposure and stress-related psychopathology.
| S-EPMC3659182 | biostudies-literature
Project description:Few studies have investigated potential gender differences in the genetic and environmental influences on the prospective associations between parent-child conflict and later depression, a notable gap given substantial gender differences in rates of depression and suggestive evidence of differences in the etiology of depression among females and males. To fill this gap, we evaluated whether the prospective relationship between parent-child conflict and major depressive disorder symptoms varied as a function of parent-child gender composition. A combined twin and adoption sample was used (53% female; 85% European ancestry), containing 1,627 adolescent sibling pairs (789 monozygotic twin pairs, 594 dizygotic/full-biological pairs, 244 genetically unrelated pairs) with assessments at two time points in adolescence (approximate ages 15 and 18). Prospective associations between parent-child conflict and subsequent adolescent depression were explained predominately through common genetic influences for mother-daughter and mother-son pairs but less so for father-daughter and father-son pairs. Results support the notion that processes of gene-environment correlation involved in the prospective associations between parent-child conflict, and later adolescent depression appear to be less relevant to father-child relationships in comparison to mother-child relationships. Notably, results did not show that parent-child conflict was more relevant to the etiology of major depressive disorder (MDD) for girls than boys; gender differences in depression do not appear to be due to differences in the associations between parent-child conflict and child depression.
| S-EPMC5065391 | biostudies-literature
Project description:The current review summarizes recent advances in the origin of brown adipocytes in rodents and humans.This review describes recent insights into induction of the brown adipocyte phenotype (BAP) in white fat (WAT) revealed by murine studies during the early postnatal period and reversible temperature transitions. The origin of adipocytes and identity of progenitors as indicated by lineage tracing experiments are reviewed.We describe a genetic model for brown adipocyte development that involves the appearance of brown adipocytes in WAT at 21 days of age and a mechanism of post-weaning involution relevant for acquisition of the BAP in fully functional WAT in mice. Under normal physiological conditions, the BAP is dormant with the potential to be stimulated by changes in the external environment. Current evidence for the acquisition of brown adipocytes by interconversion of mature adipocytes versus de novo recruitment of progenitors suggests that mechanisms for acquisition of the BAP in WAT in mice are depot-specific and controlled by allelic variation.Although the BAP is highly variable among mice, there is no information on genetic variability in the expression of brown adipocytes in humans. Thus, deeper understanding of genetic mechanisms underlying development of functional brown adipocytes is crucial.
| S-EPMC4744992 | biostudies-other
Project description:BackgroundPsychotic experiences (PEs) such as paranoia and hallucinations, and negative symptoms (NS) such as anhedonia and flat affect are common in adolescence. Psychotic experiences and negative symptoms (PENS) increase risk for later psychiatric outcomes, particularly when they persist. The extent to which genetic and environmental influences contribute to the stability of PENS in mid-to-late adolescence is unknown.MethodsUsing the Specific Psychotic Experiences Questionnaire (SPEQ) twice across ~9 months in adolescence, N = 1,448 twin pairs [M = 16.32 (0.68)] reported experiences of paranoia, hallucinations, cognitive disorganization, grandiosity and anhedonia, and their parents reported on a range of NS. Individuals were split into low-scoring, decreasing, increasing and persistent groups for each subscale. Frequencies and mean differences in distress, depression traits and emotional problems were investigated across groups. Longitudinal structural equation modelling was used to estimate the aetiological components underlying the stability of PENS.ResultsPhenotypic stability was moderate for all PENS (r = .59-.69). Persistent PENS across 9 months were associated with greater levels of distress (V = 0.15-0.46, for PEs only), depression traits (d = 0.47-1.67, except grandiosity) and emotional problems (d = 0.47-1.47, except grandiosity and anhedonia) at baseline compared to groups with transitory or low levels of PENS. At both ages PENS were heritable and influenced by shared and nonshared environment. Genetic influences contributed 38%-62% and shared environment contributed 13%-33% to the stability of PENS. Nonshared environment contributed 34%-41% (12% for parent-rated NS). There was strong overlap of genetic and shared environmental influences across time, and lower overlap for nonshared environment. Imperfect stability of PENS was at least partly due to nonshared environmental influences.ConclusionsWhen adolescent PENS persist over time, they are often characterized by more distress, and higher levels of other psychopathology. Both genetic and environmental effects influence stability of PENS.
| S-EPMC6619355 | biostudies-literature
Project description:Conduct problems in children and adolescents can predict antisocial personality disorder and related problems, such as crime and conviction. We sought an explanation for such predictions by performing a genetic longitudinal analysis. We estimated the effects of genetic, shared environmental, and unique environmental factors on variation in conduct problems measured at childhood and adolescence and antisocial personality problems measured at adulthood and on the covariation across ages. We also tested whether these estimates differed by sex. Longitudinal data were collected in the Netherlands Twin Register over a period of 27 years. Age appropriate and comparable measures of conduct and antisocial personality problems, assessed with the Achenbach System of Empirically Based Assessment, were available for 9783 9-10-year-old, 6839 13-18-year-old, and 7909 19-65-year-old twin pairs, respectively; 5114 twins have two or more assessments. At all ages, men scored higher than women. There were no sex differences in the estimates of the genetic and environmental influences. During childhood, genetic and environmental factors shared by children in families explained 43 and 44% of the variance of conduct problems, with the remaining variance due to unique environment. During adolescence and adulthood, genetic and unique environmental factors equally explained the variation. Longitudinal correlations across age varied between 0.20 and 0.38 and were mainly due to stable genetic factors. We conclude that shared environment is mainly of importance during childhood, while genetic factors contribute to variation in conduct and antisocial personality problems at all ages, and also underlie its stability over age.
| S-EPMC6133103 | biostudies-literature
Project description:BackgroundThis study examined the genetic and environmental influences underlying baseline level and developmental course of callous-unemotional (CU) traits across childhood and adolescence.MethodsThe data on 8,958 twin pairs (3,108 MZ twin pairs and 5,850 DZ twin pairs) from the Twins Early Development Study were analysed. CU traits were assessed at ages 7, 9, 12 and 16 by mothers and analysed using a biometric latent growth model.ResultsIndividual differences in the baseline level of CU traits were highly heritable (76.5%), while the heritability of the developmental course of CU traits was moderate (43.6%). The genetic influences on baseline level and developmental course of CU traits were mostly nonoverlapping. Nonshared environment made a modest contribution to the baseline level of CU traits (21.7%). Nonshared environmental influences on the developmental course of CU traits were moderate (43.2%), with nearly half of them being the same as those influencing the baseline level and just over half being specific. Shared environmental effects did not contribute to systematic change across childhood and adolescence but were rather age-specific.ConclusionsOur findings demonstrate that rather than only being conceptualized as factors of stability, genes also play a dynamic role in explaining systematic change in CU traits. Genetic effects for the initial risk and subsequent development of CU traits are not the same. In addition to genetic factors, nonshared environmental influences play an important role in explaining why some children will increase or maintain their CU traits over time, whereas other will desist. New genetic and environmental influences with age suggest that repeated, age-tailored interventions may be required throughout development to make a lasting difference in the presentation of CU traits and associated outcomes.
| S-EPMC8432158 | biostudies-literature