Male Twins (male + twin)

Distribution by Scientific Domains


Selected Abstracts


Polymicrogyria in monozygous twins and an elder sibling

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 7 2003
Po-Cheng Hung MD
Monozygous twin births have been associated with brain lesions such as hydranencephaly, multicystic encephalomalacia, and porencephaly. Prenatal circulatory injury has been considered to be the cause. Polymicrogyria is rare but has been reported in autopsied cases. The sibship in this case report, comprising monozygotic male twins and their elder sister from the same non-consanguineous parents, all had global developmental delay. Brain MRI showed polymicrogyria. We suggest that, apart from circulatory compromise, genetic etiology must be implicated as the cause of polymicrogyria. [source]


Modeling the genetic and environmental association between peer group deviance and cannabis use in male twins

ADDICTION, Issue 3 2009
Nathan A. Gillespie
ABSTRACT Background Peer group deviance (PGD) is linked strongly to liability to drug use, including cannabis. Our aim was to model the genetic and environmental association, including direction of causation, between PGD and cannabis use (CU). Method Results were based on 1736 to 1765 adult males from the Mid-Atlantic Twin Registry with complete CU and PGD data measured retrospectively at three time-intervals between 15 and 25 years using a life-history calendar. Results At all ages, multivariate modeling showed that familial aggregation in PGD was explained by a combination of additive genetic and shared environmental effects. Moreover, the significant PGD,CU association was best explained by a CU,PGD causal model in which large portions of the additive genetic (50,78%) and shared environmental variance (25,73%) in PGD were explained by CU. Conclusions Until recently PGD was assumed to be an environmental, upstream risk factor for CU. Our data are not consistent with this hypothesis. Rather, they suggest that the liability to affiliate with deviant peers is explained more clearly by a combination of genetic and environmental factors that are indexed by CU which sits as a ,risk indicator' in the causal pathway between genetic and environmental risks and the expression of PGD. This is consistent with a process of social selection by which the genetic and environmental risks in CU largely drive the propensity to affiliate with deviant peers. [source]


Religiousness, Antisocial Behavior, and Altruism: Genetic and Environmental Mediation

JOURNAL OF PERSONALITY, Issue 2 2007
Laura B. Koenig
ABSTRACT Although religiousness is considered a protective factor against antisocial behaviors and a positive influence on prosocial behaviors, it remains unclear whether these associations are primarily genetically or environmentally mediated. In order to investigate this question, religiousness, antisocial behavior, and altruistic behavior were assessed by self-report in a sample of adult male twins (165 MZ and 100 DZ full pairs, mean age of 33 years). Religiousness, both retrospective and current, was shown to be modestly negatively correlated with antisocial behavior and modestly positively correlated with altruistic behavior. Joint biometric analyses of religiousness and antisocial behavior or altruistic behavior were completed. The relationship between religiousness and antisocial behavior was due to both genetic and shared environmental effects. Altruistic behavior also shared most all of its genetic influence, but only half of its shared environmental influence, with religiousness. [source]


Alcohol Dependence and Reproductive Onset: Findings in Two Australian Twin Cohorts

ALCOHOLISM, Issue 11 2008
Mary Waldron
Background:, Although early alcohol use is a strong predictor of future alcohol problems and adolescent drinking is associated with risky sexual behavior predictive of early childbearing, reproductive dysfunctions associated with delayed childbearing have been reported in adult drinkers. We examine the relationship between lifetime history of alcohol dependence (AD) and timing of first childbirth across reproductive development. Methods:, Data were drawn from two cohorts of Australian twins born between 1893 and 1964 (3634 female and 1880 male twins) and between 1964 and 1971 (3381 female and 2748 male twins). Survival analyses were conducted using Cox proportional hazards regression models predicting age at first childbirth from AD, with sociodemographic characteristics, regular smoking, history of psychopathology, and family and childhood risks included as control variables in adjusted models. Results:, Results suggest alcoholic women in both cohorts show overall delayed reproduction, with little effect of AD on timing of first reproduction in men. Effects of AD are particularly strong for women in the older cohort, where AD is associated with 73% decreased likelihood of first childbirth after age 29 [hazard ratio (HR) = 0.27, 95% CI: 0.10,0.75]. In adjusted models, effects reduce only slightly (HR = 0.29, 95% CI: 0.11,0.80). For women in the young cohort, AD is associated with delayed reproduction after age 24, with 40% decreased likelihood of first childbirth (HR = 0.60, 95% CI: 0.48,0.75). AD remains predictive in adjusted models, but without age interaction (HR = 0.72, 95% CI: 0.62,0.85). Conclusions:, Findings of delayed reproductive onset in alcoholic women are consistent with alcohol-related reproductive dysfunctions, although underlying mechanisms remain largely unknown. To better understand AD differences in reproductive onset, continued research on both biological and psychosocial risks is needed. [source]


Pulmonary interstitial glycogenosis in identical twins

PEDIATRIC PULMONOLOGY, Issue 4 2005
W. Onland MD
Abstract We present the clinical, radiological, and pathological findings of open lung biopsies from monozygotic prematurely born male twins with respiratory distress at ages 6 and 8 weeks postnatally. Radiological examination showed a reticular nodular interstititial pattern on chest radiography. High-resolution computed tomography (HRCT) revealed ground-glass opacification and thickened interstitial septae in both infants. Lung biopsies showed a similar histology. There was diffuse interstitial thickening of the alveolar septa by mesenchymal cells, without prominent hyperplasia of type 2 pneumocytes, and without airspace exudates. Sections were periodic acid-Schiff (PAS)-positive within the cytoplasm of interstitial cells, indicating the presence of glycogen. Thus the diagnosis of pulmonary interstitial glycogenosis was made. Both infants were treated with glucocorticoids and had a favorable outcome. We speculate that pulmonary interstitial glycogenosis could be a histopathological form of chronic lung disease (CLD) of infancy. Pediatr Pulmonol. © 2005 Wiley-Liss, Inc. [source]


Stability, consistency, and heritability of electrodermal response lability in middle-aged male twins

PSYCHOPHYSIOLOGY, Issue 4 2004
Andrew Crider
Abstract We examined individual differences in nonspecific electrodermal response (EDR) lability in terms of retest stability, cross-situational consistency, and heritability in a sample of 345 adult monozygotic and dizygotic twin pairs. We also examined the phenotypic and genetic relationships between EDR lability and speed of habituation of the specific EDR to a nonsignal stimulus. Individual variation in EDR lability showed substantial retest stability and cross-situational consistency and also predicted resistance to specific EDR habituation. Structural equation modeling showed that the covariation among EDR lability measures and resistance to specific EDR habituation operated through a single latent phenotype, which was influenced in approximately equal measure by genetic and unique environmental factors. We discuss these findings in terms of an information processing account of individual differences in phasic EDR activation. [source]


Genetic and environmental influences on the transmission of parental depression to children's depression and conduct disturbance: an extended Children of Twins study

THE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 6 2010
Judy L. Silberg
Background:, Despite the increased risk of depression and conduct problems in children of depressed parents, the mechanism by which parental depression affects their children's behavioral and emotional functioning is not well understood. The present study was undertaken to determine whether parental depression represents a genuine environmental risk factor in children's psychopathology, or whether children's depression/conduct can be explained as a secondary consequence of the genetic liability transmitted from parents to their offspring. Methods:, Children of Twins (COT) data collected on 2,674 adult female and male twins, their spouses, and 2,940 of their children were used to address whether genetic and/or family environmental factors best account for the association between depression in parents and depression and conduct problems in their children. Data collected on juvenile twins from the Virginia Twin Study of Adolescent Behavioral Development (VTSABD) were also included to estimate child-specific genetic and environmental influences apart from those effects arising from the transmission of the parental depression itself. The fit of alternative Children of Twin models were evaluated using the statistical program Mx. Results:, The most compelling model for the association between parental and juvenile depression was a model of direct environmental risk. Both family environmental and genetic factors accounted for the association between parental depression and child conduct disturbance. Conclusions:, These findings illustrate how a genetically mediated behavior such as parental depression can have both an environmental and genetic impact on children's behavior. We find developmentally specific genetic factors underlying risk to juvenile and adult depression. A shared genetic liability influences both parental depression and juvenile conduct disturbance, implicating child conduct disturbance (CD) as an early indicator of genetic risk for depression in adulthood. In summary, our analyses demonstrate differences in the impact of parental depression on different forms of child psychopathology, and at various stages of development. [source]