scholarly journals Gambling, disordered gambling and their association with major depression and substance use: a web-based cohort and twin-sibling study

2011 ◽  
Vol 42 (3) ◽  
pp. 497-508 ◽  
Author(s):  
C. Blanco ◽  
J. Myers ◽  
K. S. Kendler

BackgroundRelatively little is known about the environmental and genetic contributions to gambling frequency and disordered gambling (DG), the full continuum of gambling-related problems that includes pathological gambling (PG).MethodA web-based sample (n=43 799 including both members of 609 twin and 303 sibling pairs) completed assessments of number of lifetime gambling episodes, DSM-IV criteria for PG, alcohol, nicotine and caffeine intake, and nicotine dependence (ND) and DSM-III-R criteria for lifetime major depression (MD). Twin modeling was performed using Mx.ResultsIn the entire cohort, symptoms of DG indexed a single dimension of liability. Symptoms of DG were weakly related to caffeine intake and moderately related to MD, consumption of cigarettes and alcohol, and ND. In twin and sibling pairs, familial resemblance for number of times gambled resulted from both familial–environmental (c2=42%) and genetic factors (a2=32%). For symptoms of DG, resemblance resulted solely from genetic factors (a2=83%). Bivariate analyses indicated a low genetic correlation between symptoms of DG and MD (ra=+0.14) whereas genetic correlations with DG symptoms were substantially higher with use of alcohol, caffeine and nicotine, and ND (ranging from +0.29 to +0.80). The results were invariant across genders.ConclusionsWhereas gambling participation is determined by shared environmental and genetic factors, DG constitutes a single latent dimension that is largely genetically determined and more closely related to externalizing than internalizing behaviors. Because these findings are invariant across genders, they suggest that the etiological factors of DG are likely to be similar in men and women.

2020 ◽  
Vol 31 (1) ◽  
pp. 77-88
Author(s):  
Suyu Zhong ◽  
Long Wei ◽  
Chenxi Zhao ◽  
Liyuan Yang ◽  
Zengru Di ◽  
...  

Abstract To understand the origins of interhemispheric differences and commonalities/coupling in human brain wiring, it is crucial to determine how homologous interregional connectivities of the left and right hemispheres are genetically determined and related. To address this, in the present study, we analyzed human twin and pedigree samples with high-quality diffusion magnetic resonance imaging tractography and estimated the heritability and genetic correlation of homologous left and right white matter (WM) connections. The results showed that the heritability of WM connectivity was similar and coupled between the 2 hemispheres and that the degree of overlap in genetic factors underlying homologous WM connectivity (i.e., interhemispheric genetic correlation) varied substantially across the human brain: from complete overlap to complete nonoverlap. Particularly, the heritability was significantly stronger and the chance of interhemispheric complete overlap in genetic factors was higher in subcortical WM connections than in cortical WM connections. In addition, the heritability and interhemispheric genetic correlations were stronger for long-range connections than for short-range connections. These findings highlight the determinants of the genetics underlying WM connectivity and its interhemispheric relationships, and provide insight into genetic basis of WM connectivity asymmetries in both healthy and disease states.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yusuke Takahashi ◽  
Anqing Zheng ◽  
Shinji Yamagata ◽  
Juko Ando

AbstractUsing a genetically informative design (about 2000 twin pairs), we investigated the phenotypic and genetic and environmental architecture of a broad construct of conscientiousness (including conscientiousness per se, effortful control, self-control, and grit). These four different measures were substantially correlated; the coefficients ranged from 0.74 (0.72–0.76) to 0.79 (0.76–0.80). Univariate genetic analyses revealed that individual differences in conscientiousness measures were moderately attributable to additive genetic factors, to an extent ranging from 62 (58–65) to 64% (61–67%); we obtained no evidence that shared environmental influences were observed. Multivariate genetic analyses showed that for the four measures used to assess conscientiousness, genetic correlations were stronger than the corresponding non-shared environmental correlations, and that a latent common factor accounted for over 84% of the genetic variance. Our findings suggest that individual differences in the four measures of conscientiousness are not distinguishable at both the phenotypic and behavioural genetic levels, and that the overlap was substantially attributable to genetic factors.


Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 171
Author(s):  
Federica Arienti ◽  
Giulia Lazzeri ◽  
Maria Vizziello ◽  
Edoardo Monfrini ◽  
Nereo Bresolin ◽  
...  

Corticobasal syndrome (CBS) is an atypical parkinsonian presentation characterized by heterogeneous clinical features and different underlying neuropathology. Most CBS cases are sporadic; nevertheless, reports of families and isolated individuals with genetically determined CBS have been reported. In this systematic review, we analyze the demographical, clinical, radiological, and anatomopathological features of genetically confirmed cases of CBS. A systematic search was performed using the PubMed, EMBASE, and Cochrane Library databases, included all publications in English from 1 January 1999 through 1 August 2020. We found forty publications with fifty-eight eligible cases. A second search for publications dealing with genetic risk factors for CBS led to the review of eight additional articles. GRN was the most common gene involved in CBS, representing 28 out of 58 cases, followed by MAPT, C9ORF72, and PRNP. A set of symptoms was shown to be significantly more common in GRN-CBS patients, including visuospatial impairment, behavioral changes, aphasia, and language alterations. In addition, specific demographical, clinical, biochemical, and radiological features may suggest mutations in other genes. We suggest a diagnostic algorithm to help in identifying potential genetic cases of CBS in order to improve the diagnostic accuracy and to better understand the still poorly defined underlying pathogenetic process.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jessica Tyrrell ◽  
Jie Zheng ◽  
Robin Beaumont ◽  
Kathryn Hinton ◽  
Tom G. Richardson ◽  
...  

AbstractLarge studies such as UK Biobank are increasingly used for GWAS and Mendelian randomization (MR) studies. However, selection into and dropout from studies may bias genetic and phenotypic associations. We examine genetic factors affecting participation in four optional components in up to 451,306 UK Biobank participants. We used GWAS to identify genetic variants associated with participation, MR to estimate effects of phenotypes on participation, and genetic correlations to compare participation bias across different studies. 32 variants were associated with participation in one of the optional components (P < 6 × 10−9), including loci with links to intelligence and Alzheimer’s disease. Genetic correlations demonstrated that participation bias was common across studies. MR showed that longer educational duration, older menarche and taller stature increased participation, whilst higher levels of adiposity, dyslipidaemia, neuroticism, Alzheimer’s and schizophrenia reduced participation. Our effect estimates can be used for sensitivity analysis to account for selective participation biases in genetic or non-genetic analyses.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Said ◽  
Y.J Van De Vegte ◽  
N Verweij ◽  
P Van Der Harst

Abstract Background Caffeine is the most widely consumed psychostimulant and is associated with lower risk of coronary artery disease (CAD) and type 2 diabetes (T2D). However, whether these associations are causal remains unknown. Objectives This study aimed to identify genetic variants associated with caffeine intake, and to investigate possible causal links between genetically determined caffeine intake and CAD or T2D. Additionally, we aimed to replicate previous observational findings between caffeine intake and CAD or T2D. Methods Genome wide associated studies (GWAS) were performed on caffeine intake from coffee, tea or both in 407,072 UK Biobank participants. Identified variants were used in a two-sample Mendelian randomization (MR) approach to investigate evidence for causal links between caffeine intake and CAD in CARDIoGRAMplusC4D (60,801 cases; 123,504 controls) or T2D in DIAGRAM (26,676 cases; 132,532 controls). Observational associations were tested within UK Biobank using Cox regression analyses. Results Moderate observational caffeine intakes from coffee or tea were associated with lower risks of CAD or T2D compared to no or high intake, with the lowest risks at intakes of 120–180 mg/day from coffee for CAD (HR=0.77 [95% CI: 0.73–0.82; P&lt;1e-16]), and 300–360 mg/day for T2D (HR=0.76 [95% CI: 0.67–0.86]; P=1.57e-5). GWAS identified 51 novel genetic loci associated with caffeine intake, enriched for central nervous system genes. In contrast to observational analyses, MR analyses in CARDIoGRAMplusC4D and DIAGRAM yielded no evidence for causal links between caffeine intake and the development of CAD or T2D. Conclusions MR analyses indicate caffeine intake might not protect against CAD or T2D, despite protective associations in observational analyses. Manhattan_plot_CaffeineIntake Funding Acknowledgement Type of funding source: None


1996 ◽  
Vol 168 (S30) ◽  
pp. 68-75 ◽  
Author(s):  
Kenneth S. Kendler

In both clinical and epidemiological samples, major depression (MD) and generalised anxiety disorder (GAD) display substantial comorbidity. In a prior analysis of lifetime MD and GAD in female twins, the same genetic factors were shown to influence the liability to MD and to GAD. A follow-up interview in the same twin cohort examined one-year prevalence for MD and GAD (diagnosed using a one-month minimum duration of illness). Bivariate twin models were fitted using the program Mx. High levels of comorbidity were observed between MD and GAD. The best-fitting twin models, when GAD was diagnosed with or without a diagnostic hierarchy, found a genetic correlation of unity between the two disorders. The correlation in environmental risk factors was +0.70 when GAD was diagnosed non-hierarchically, but zero when hierarchical diagnoses were used. Our findings provide further support for the hypothesis that in women, MD and GAD are the result of the same genetic factors. Environmental risk factors that predispose to ‘pure’ GAD episodes may be relatively distinct from those that increase risk for MD.


2000 ◽  
Vol 24 (3) ◽  
pp. 373-381 ◽  
Author(s):  
Hilary Towers ◽  
Erica Spotts ◽  
Jenae M. Neiderhiser ◽  
Robert Plomin ◽  
E. Mavis Hetherington ◽  
...  

The knowledge we have of childhood and adolescent behaviour is, to some extent, a function of the unique perspective of the rater. Although many behavioural genetics studies have used parent and child self-reports in their assessments of child and adolescent adjustment, few have included teacher ratings of behaviour. It is possible that genetic and environmental contributions to teacher reports are different from those using parent and self-reports. The present study examined genetic and environmental influences on six subscales of the Child Behavior Checklist Teacher Report Form (CBC-TRF) using a normative sample of adolescents. The sample consisted of 373 same-sex twin and sibling pairs of varying degrees of genetic relatedness participating in the Nonshared Environment in Adolescent project (NEAD). For all of the CBC subscales, except attention problems and social problems, nonshared environmental influence was the most important source of variance. Additive genetic factors were of moderate importance for externalising behaviours, whereas nonadditive genetic factors contributed to the anxious/depressed, attention problems, withdrawn, and social problems subscales. For none of the constructs was shared environment a significant influence. Three alternative models testing for contrast effects, differences in twin and nontwin siblings, and differences in nondivorced and stepfamilies were examined. In most cases, the best-fitting model was a model that did not include any of these effects, suggesting that these factors do not critically affect the basic model. However, some of the patterns of correlations and parameter estimates were unusual and may warrant future investigation.


2005 ◽  
Vol 133 (11-12) ◽  
pp. 532-534 ◽  
Author(s):  
Sanja Milenkovic ◽  
Goran Belojevic ◽  
Radojka Kocijancic

Lateralisation associates the extremities and senses of one side of the body, which are connected by afferent and efferent pathways, with the primary motor and sensory areas of the hemisphere on the opposite side. Dominant laterality denotes the appearance of a dominant extremity or sense in the performance of complex psychomotor activities. Laterality is manifested both as right-handedness or left-handedness, which are functionally equivalent and symmetrical in the performance of activities. Right-handedness is significantly more common than left-handedness. Genetic theory is most widely accepted in explaining the onset of lateralisation. According to this theory, the models of brain organisation asymmetry (anatomical, functional, and biochemical) are strongly, genetically determined. However, the inability to clearly demonstrate the association between genetic factors and left-handedness has led researchers to investigate the effects of the environment on left-handedness. Of particular interest are the intrauterine environment and the factors influencing foetal development, of which hormones and ultrasound exposure are the most significant. It has been estimated that an extra five cases of nonright-handed lateralisation can be expected in every 100 males who were exposed to ultrasound in utero compared to those who were not. Socio-cultural pressure on left-handed individuals was much more severe in the past, which is confirmed by scientific findings that left-handedness is present in 13% of individuals in their twenties, while in less than 1% of individuals in their eighties.


2019 ◽  
Author(s):  
Jessica K. Abbott ◽  
Oscar Rios-Cardenas ◽  
Molly Morris

AbstractAlternative reproductive tactics occur when individuals of the same sex have a suite of morphological and/or behavioural traits that allow them to pursue different reproductive strategies. A common pattern is e.g. the existence of “courter” and “sneaker” tactics within males. We have previously argued that alternative reproductive tactics should be subject to genetic conflict over the phenotypic expression of traits, similar to sexual antagonism. In this process, which we called intra-locus tactical conflict, genetically determined tactics experience conflicting selection on a shared phenotypic trait, such as body size, but a positive genetic correlation between tactics in body size prevents either tactic from reaching its optimum. Recently, other authors have attempted to extend this idea to developmentally plastic alternative reproductive tactics, with mixed results. However, it is not clear whether we should expect intra-locus tactical conflict in developmentally plastic tactics or not. We have therefore run a series of simulation models investigating under what conditions we should expect to see positive estimates of the inter-tactical genetic correlation, since a positive genetic correlation is a prerequisite for the existence of intra-locus tactical conflict. We found that for autosomal, X-linked, and Y-linked genetically-determined tactics, estimated inter-tactical genetic correlations were generally high. However, for developmentally plastic tactics, the genetic correlation depends on the properties of the switching threshold between tactics. If it is fixed, then estimated genetic correlations are positive, but if there is genetic variation in the switch-point, then any sign and magnitude of estimated genetic correlation is possible, even for highly heritable traits where the true underlying correlation is perfect. This means that caution should be used when investigating genetic constraints in plastic phenotypes.


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