scholarly journals Extended Twin Study of Alcohol Use in Virginia and Australia

2018 ◽  
Vol 21 (3) ◽  
pp. 163-178 ◽  
Author(s):  
Brad Verhulst ◽  
Michael C. Neale ◽  
Lindon J. Eaves ◽  
Sarah E. Medland ◽  
Andrew C. Heath ◽  
...  

Drinking alcohol is a normal behavior in many societies, and prior studies have demonstrated it has both genetic and environmental sources of variation. Using two very large samples of twins and their first-degree relatives (Australia ≈ 20,000 individuals from 8,019 families; Virginia ≈ 23,000 from 6,042 families), we examine whether there are differences: (1) in the genetic and environmental factors that influence four interrelated drinking behaviors (quantity, frequency, age of initiation, and number of drinks in the last week), (2) between the twin-only design and the extended twin design, and (3) the Australian and Virginia samples. We find that while drinking behaviors are interrelated, there are substantial differences in the genetic and environmental architectures across phenotypes. Specifically, drinking quantity, frequency, and number of drinks in the past week have large broad genetic variance components, and smaller but significant environmental variance components, while age of onset is driven exclusively by environmental factors. Further, the twin-only design and the extended twin design come to similar conclusions regarding broad-sense heritability and environmental transmission, but the extended twin models provide a more nuanced perspective. Finally, we find a high level of similarity between the Australian and Virginian samples, especially for the genetic factors. The observed differences, when present, tend to be at the environmental level. Implications for the extended twin model and future directions are discussed.

2005 ◽  
Vol 36 (1) ◽  
pp. 109-118 ◽  
Author(s):  
JULIA D. GRANT ◽  
JEFFREY F. SCHERRER ◽  
MICHAEL T. LYNSKEY ◽  
MICHAEL J. LYONS ◽  
SETH A. EISEN ◽  
...  

Background. Early alcohol use is associated with abuse and dependence of licit and illicit substances later in life. The role of genetic and environmental factors in this association is not conclusive.Method. In 1992, data on substance use, abuse/dependence and psychiatric disorders were collected from 8169 male twin members of the Vietnam Era Twin Registry. The interview obtained age of onset of regular drinking (one drink/month for 6 or more months). Regression analyses of twin pairs discordant for early alcohol use tested whether the association between early drinking (before age 17) and adult substance use and abuse/dependence remained after controlling for genetic factors, family environment and covariates. Twin models tested for common genetic and/or environmental influences on early drinking and adult alcohol dependence and ever use and abuse/dependence on marijuana and other drugs.Results. Co-twin analyses suggested the association between early regular alcohol use and adult alcohol dependence, marijuana and other drug use, and marijuana and other drug abuse/dependence could not be entirely explained by common genetic and shared family environmental factors. Genetic contributions to early regular drinking were significantly correlated with those on use of marijuana (rA=0·59), use of other drugs (rA=0·64), alcohol dependence (rA=0·54) and abuse/dependence of marijuana and other drugs (rA=0·63 and 0·66). Small but significant unique environmental correlations (rE range 0·11–0·22) indicated that familial factors could not entirely explain the association between early alcohol use and later substance use, abuse and dependence.Conclusions. Early regular drinking is associated with later alcohol dependence and use, abuse/dependence on drugs. The association is not entirely explained by genetic or shared family environmental factors. This suggests unique environmental factors contribute to transitions from early regular alcohol drinking to use, abuse and dependence on alcohol and other substances.


2013 ◽  
Vol 21 (3) ◽  
pp. 368-389 ◽  
Author(s):  
Brad Verhulst ◽  
Peter K. Hatemi

In this article, we respond to Shultziner's critique that argues that identical twins are more alike not because of genetic similarity, but because they select into more similar environments and respond to stimuli in comparable ways, and that these effects bias twin model estimates to such an extent that they are invalid. The essay further argues that the theory and methods that undergird twin models, as well as the empirical studies which rely upon them, are unaware of these potential biases. We correct this and other misunderstandings in the essay and find that gene-environment (GE) interplay is a well-articulated concept in behavior genetics and political science, operationalized as gene-environment correlation and gene-environment interaction. Both are incorporated into interpretations of the classical twin design (CTD) and estimated in numerous empirical studies through extensions of the CTD. We then conduct simulations to quantify the influence of GE interplay on estimates from the CTD. Due to the criticism's mischaracterization of the CTD and GE interplay, combined with the absence of any empirical evidence to counter what is presented in the extant literature and this article, we conclude that the critique does not enhance our understanding of the processes that drive political traits, genetic or otherwise.


2020 ◽  
Author(s):  
Zenab Tamimy ◽  
Sofieke T. Kevenaar ◽  
Jouke Jan Hottenga ◽  
Michael D. Hunter ◽  
Eveline L. de Zeeuw ◽  
...  

AbstractThe classical twin model can be reparametrized as an equivalent multilevel model. The multilevel parameterization has underexplored advantages, such as the possibility to include higher-level clustering variables in which lower levels are nested. When this higher-level clustering is not modeled, its variance is captured by the common environmental variance component. In this paper we illustrate the application of a 3-level multilevel model to twin data by analyzing the regional clustering of 7-year-old children’s height in the Netherlands. Our findings show that 1.8%, of the phenotypic variance in children’s height is attributable to regional clustering, which is 7% of the variance explained by between-family or common environmental components. Since regional clustering may represent ancestry, we also investigate the effect of region after correcting for genetic principal components, in a subsample of participants with genome-wide SNP data. After correction, region did no longer explain variation in height. Our results suggest that the phenotypic variance explained by region actually represent ancestry effects on height.


2011 ◽  
Vol 41 (9) ◽  
pp. 1987-1995 ◽  
Author(s):  
N. Czajkowski ◽  
K. S. Kendler ◽  
K. Tambs ◽  
E. Røysamb ◽  
T. Reichborn-Kjennerud

BackgroundTo explore the genetic and environmental factors underlying the co-occurrence of lifetime diagnoses of DSM-IV phobia.MethodFemale twins (n=1430) from the population-based Norwegian Institute of Public Health Twin Panel were assessed at personal interview for DSM-IV lifetime specific phobia, social phobia and agoraphobia. Comorbidity between the phobias were assessed by odds ratios (ORs) and polychoric correlations and multivariate twin models were fitted in Mx.ResultsPhenotypic correlations of lifetime phobia diagnoses ranged from 0.55 (agoraphobia and social phobia, OR 10.95) to 0.06 (animal phobia and social phobia, OR 1.21). In the best fitting twin model, which did not include shared environmental factors, heritability estimates for the phobias ranged from 0.43 to 0.63. Comorbidity between the phobias was accounted for by two common liability factors. The first loaded principally on animal phobia and did not influence the complex phobias (agoraphobia and social phobia). The second liability factor strongly influenced the complex phobias, but also loaded weak to moderate on all the other phobias. Blood phobia was mainly influenced by a specific genetic factor, which accounted for 51% of the total and 81% of the genetic variance.ConclusionsPhobias are highly co-morbid and heritable. Our results suggest that the co-morbidity between phobias is best explained by two distinct liability factors rather than a single factor, as has been assumed in most previous multivariate twin analyses. One of these factors was specific to the simple phobias, while the other was more general. Blood phobia was mainly influenced by disorder specific genetic factors.


2021 ◽  
Author(s):  
Z. Tamimy ◽  
S. T. Kevenaar ◽  
J. J. Hottenga ◽  
M. D. Hunter ◽  
E. L. de Zeeuw ◽  
...  

AbstractThe classical twin model can be reparametrized as an equivalent multilevel model. The multilevel parameterization has underexplored advantages, such as the possibility to include higher-level clustering variables in which lower levels are nested. When this higher-level clustering is not modeled, its variance is captured by the common environmental variance component. In this paper we illustrate the application of a 3-level multilevel model to twin data by analyzing the regional clustering of 7-year-old children’s height in the Netherlands. Our findings show that 1.8%, of the phenotypic variance in children’s height is attributable to regional clustering, which is 7% of the variance explained by between-family or common environmental components. Since regional clustering may represent ancestry, we also investigate the effect of region after correcting for genetic principal components, in a subsample of participants with genome-wide SNP data. After correction, region no longer explained variation in height. Our results suggest that the phenotypic variance explained by region might represent ancestry effects on height.


Genetics ◽  
2016 ◽  
Vol 202 (4) ◽  
pp. 1313-1328 ◽  
Author(s):  
Liang He ◽  
Mikko J. Sillanpää ◽  
Karri Silventoinen ◽  
Jaakko Kaprio ◽  
Janne Pitkäniemi

1989 ◽  
Vol 48 (2) ◽  
pp. 283-291 ◽  
Author(s):  
Susan Brotherstone ◽  
W. G. Hill ◽  
R. Thompson

ABSTRACTWith a view to incorporating identifiable environmental factors such as month of calving as random effects in models for dairy sire and cow breeding value estimation, an analysis was undertaken of environmental components of variance for fat yield in lactations 1 to 5 of pedigree British Friesian-Holstein cattle. Records of fat yield and of log fat yield on daughters of widely used sires were first corrected for age and month of calving and for sire in each lactation on a national basis. Variance components for herd-year, herd-year × lactation, herd-year × month of calving, herd-year × month of calving × lactation and error were then estimated for pairs of lactations.The results were most consistent for log fat yield, where heterogeneity of variance was less. Correlations were, approximately, 0·45 and 0·42 for records in the same herd-year and lactation for lactation 1 or a later lactation, respectively, and approximately 0·40 for records in the same herd-year and different lactations. Within herd-year and lactation, correlations of records in the same month were approximately 0·10 for lactation 1 and 0·08 for later lactations, and for different lactations the correlations were 0·06 if lactation 1 was included and 0·08 otherwise. Thus, the effects appear to be similar for later lactations, which can be pooled, but effects for month and month × lactation 1 v. later should be fitted.


2021 ◽  
Author(s):  
Lianne P. de Vries ◽  
Toos C. E. M. van Beijsterveldt ◽  
Hermine Maes ◽  
Lucía Colodro-Conde ◽  
Meike Bartels

AbstractThe distinction between genetic influences on the covariance (or bivariate heritability) and genetic correlations in bivariate twin models is often not well-understood or only one is reported while the results show distinctive information about the relation between traits. We applied bivariate twin models in a large sample of adolescent twins, to disentangle the association between well-being (WB) and four complex traits (optimism, anxious-depressed symptoms (AD), aggressive behaviour (AGG), and educational achievement (EA)). Optimism and AD showed respectively a strong positive and negative phenotypic correlation with WB, the negative correlation of WB and AGG is lower and the correlation with EA is nearly zero. All four traits showed a large genetic contribution to the covariance with well-being. The genetic correlations of well-being with optimism and AD are strong and smaller for AGG and EA. We used the results of the models to explain what information is retrieved based on the bivariate heritability versus the genetic correlations and the (clinical) implications.


2003 ◽  
Vol 15 (4) ◽  
pp. 337-349 ◽  
Author(s):  
Silvia Mejía ◽  
Margarita Giraldo ◽  
David Pineda ◽  
Alfredo Ardila ◽  
Francisco Lopera

Objective: The purpose of this research was to identify environmental and personal factors that could be related to the variability in the age of onset of familial Alzheimer's disease (FAD) (36–62 years). Methods: A sample was taken of 49 subjects with FAD and with the mutation E280A in the presenilin-1 gene on chromosome 14; the sample was divided into two subgroups: 27 individuals with age of onset of the disease between 36 and 46 years (early onset) and 22 individuals whose disease began between 47 and 62 years (late onset). Information on environmental and personal factors was collected by means of a questionnaire answered by the patients if their clinical condition allowed it, or by their relatives; such information was organized in a categorical way. Comparisons between the two groups for each categorical variable were done by means of the chi-square test. Noncollinear variables that showed statistical significance were included as independent variables in a logistic regression analysis to predict their association with early onset of the disease. Results: Only 5 of the 140 studied variables were different between the two groups in univariate analysis: education, surgical history, type of stressful event, depression, and affective losses. The logistic regression model was constituted by education, depression, and affective losses. High-level education had approximately 15 times more probability of association with an early onset of the disease; both the history of affective losses and depressive symptoms had 4 times more probability of a similar association. Conclusions: The association of high-level education and early onset of the disease could be related to an earlier detection of symptoms, in turn determined by greater intellectual and environmental demands. The occurrence of depression and affective losses has been considered a prodromic manifestation of the disease. Our findings are evidence of high clinical heterogeneity even in a genetically homogeneous group.


2021 ◽  
pp. 1-10
Author(s):  
Mark J. Taylor ◽  
Angelica Ronald ◽  
Joanna Martin ◽  
Sebastian Lundström ◽  
Georgina M. Hosang ◽  
...  

Abstract Background There is evidence that autism spectrum disorders (ASDs) co-occur with bipolar disorder (BD) relatively frequently. Individuals with BD often report symptoms of mania and hypomania during adolescence, prior to the age of onset for BD. It is unknown whether these symptoms are associated with ASDs. We examined whether diagnoses of ASDs and autistic traits were associated with hypomania in a large, population-based Swedish twin sample. Methods Parental structured interviews assessed autistic traits, and were used to assign screening diagnoses of ASDs, when twins were aged 9 or 12 (N = 13 533 pairs). Parents then completed questionnaires assessing hypomania when the twins were aged 15 and 18 (N = 3852 pairs at age 15, and 3013 pairs at age 18). After investigating the phenotypic associations between these measures, we used the classical twin design to test whether genetic and environmental influences on autistic traits influence variation in adolescent hypomania. Results Autistic traits and ASD diagnoses in childhood were associated with elevated scores on the measures of adolescent hypomania. Twin analyses indicated that 6–9% of the variance in hypomania was explained by genetic influences that were shared with autistic traits in childhood. When repeating these analyses for specific autistic trait domains, we found a stronger association between social interaction difficulties and hypomania than for other autistic trait domains. Conclusions These results indicate a genetic link between autistic traits and hypomania in adolescence. This adds to the growing evidence base of genetic factors associated with ASDs showing links with psychiatric outcomes across childhood and into adulthood.


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