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Social changes, such as the expansion of legal forms of gambling, can influence not only the prevalence of gambling, but can also shape the relative importance of genetic and environmental contributions to individual differences in the propensity to gamble. In the present study, I examined differences in the prevalence and in the relative contribution of genetic and environmental factors to gambling involvement in the United States in 1962 versus 2002. The data came from two sources: (1) a survey of 839 17-year-old same-sex twin pairs from the National Merit Scholarship Qualifying Test twin study, and (2) an interview of 477 18- to 26-year-old same-sex twin pairs from Wave III of the National Longitudinal Study of Adolescent to Adult Health. Similar measures of gambling participation were included in the two studies. Evidence for a genotype-by-time interaction was evaluated by testing whether the contribution of genetic influences was greater in the more recently born cohort of twins. Despite the major changes in the gambling landscape over the intervening 40 years, there was no evidence for such an interaction. The contribution of genetic factors and environmental factors did not significantly differ and there was no evidence for genetic influences at either time point. Instead, the variation in the propensity to gamble was explained nearly equally by common and unique environmental factors. Explanations for this surprising finding are discussed.

AbstractProfessor Nicholas G. Martin, from QIMR Berghofer Medical Research Institute in Brisbane, Australia, is a world leader in the effort to understand the genetic architecture underlying disordered gambling. This article pays tribute to Nick and his almost two decades of gambling research, highlighting his many strengths, ranging from the use of ingenious recruitment approaches, twin study methods, genomewide association studies, to facilitating international collaborations.

AbstractThe aim of this study was to estimate the rates of recovery, treatment-seeking, and natural recovery from pathological gambling (PG) in men and women in a community-based national survey, and to examine the role of gambling problem recognition in recovery from PG. Participants were 4,764 individuals from a community-based Australian national twin registry (104 with a lifetime history of PG) who were administered a structured psychiatric telephone interview. Women were more likely than men to recover from (56% versus 36%; odds ratio = 2.3) and to seek treatment for PG (32% versus 13%; odds ratio = 3.2). Most individuals who recovered from PG did so without treatment (82%), but this was higher among men than among women (92% versus 57%; odds ratio = 5.3). This is the first study to document sex differences in treatment-seeking and recovery from PG. These findings highlight the value in continuing to develop self-help and brief treatments for PG that will appeal to those who are unlikely to seek formal help.

AbstractDisordered gambling (DG) is a rare but serious condition that results in considerable financial and interpersonal harms. Twin studies indicate that DG is heritable but are silent with respect to specific genes or pathways involved. Existing genomewide association studies (GWAS) of DG have been substantially underpowered. Larger GWAS of other psychiatric disorders now permit calculation of polygenic risk scores (PRSs) that reflect the aggregated effects of common genetic variants contributing risk for the target condition. The current study investigated whether gambling and DG are associated with PRSs for four psychiatric conditions found to be comorbid with DG in epidemiologic surveys: major depressive disorder (MDD), attention-deficit hyperactivity disorder (ADHD), bipolar disorder (BD) and schizophrenia (SCZ). Genotype data and survey responses were analyzed from the Wave IV assessment (conducted in 2008) of the National Longitudinal Study of Adolescent to Adult Health, a representative sample of adolescents recruited in 1994–1995 and followed into adulthood. Among participants classified as having European ancestry based on genetic analysis (N= 5215), 78.4% reported ever having gambled, and 1.3% reported lifetime DG. Polygenic risk for BD was associated with decreased odds of lifetime gambling,OR= 0.93 [0.87, 0.99],p= .045, pseudo-R2(%) = .12. The SCZ PRS was associated with increased odds of DG,OR= 1.54 [1.07, 2.21],p= .02, pseudo-R2(%) = .85. Polygenic risk scores for MDD and ADHD were not related to either gambling outcome. Investigating features common to both SCZ and DG might generate valuable clues about the genetically influenced liabilities to DG.

AbstractImpulsivity is a personality trait characterized by acting suddenly in an unplanned manner in order to satisfy a desire without consideration for the consequences of such behavior. There are several psychiatric disorders that include the term impulsivity as a criterion and, therefore, it has been suggested that impulsivity may be an important phenotype that may link a number of different behavioral disorders, including substance abuse. This study's aims were to determine if a significant association could be detected between the (AAT)n triplet repeat polymorphism as well as 5 single nucleotide polymorphisms (SNPs) in or near theCNR1receptor gene and impulsivity in Southwest California 'Mission' Indians (SWC). Impulsivity was assessed using a scale derived from the Maudsley personality inventory, and blood samples were collected for DNA analyses from 251 individuals recruited from local Indian reservations. The estimated heritability (h2) for the impulsivity phenotype was 0.20 + 0.12 (p< .004). Impulsivity was significantly associated with the 6-repeat allele of the triplet repeat polymorphism (AATn/A6;p< .0001), as well as four SNPs in or near theCNR1receptor gene: rs1535255 (p= .001), rs2023239 (p= .004), rs1049353 (p< .001) and rs806368 (p< .0006). These studies provide data to suggest that theCNR1receptor gene may be significantly associated with impulsivity in SWC Indians.

AbstractThis study employs multiple regression models based on DeFries and Fulker (1985), and a large sample of twins, to assess heritability in attitudes towards economic risk, and the extent to which this heritability differs between males and females. Consistent with Cesarini et al. (2009), it is found that attitudes towards risk are moderately heritable, with about 20 percent of the variation in these attitudes across individuals being linked to genetic differences. This value is less than one-half the estimates reported by Zyphur et al. (2009) and Zhong et al. (2009). While females are more risk averse than males, there is no evidence that heritability in attitudes towards risk differs between males and females. Even though heritability is shown to be important to economic risk-taking, the analyses suggest that multivariate studies of the determinants of attitudes towards risk which to not take heritability into consideration still provide reliable estimates of the partial effects of other key variables, such as gender and educational attainment.

AbstractThe purpose of this study was to examine potential biases in family history reports of problem gambling and gambling frequency. Same-sex twin pairs discordant for a history of problem (n= 230 pairs) and pathological gambling (n= 48 pairs) and for three indexes of gambling frequency (ever gambling, monthly gambling, and weekly gambling;n= 44–517 pairs) were identified from a large Australian national twin study. The problem gambling affected twin was significantly more likely to endorse paternal problem gambling than the problem gambling unaffected cotwin (OR = 5.5), and similar findings were obtained for family history reports of gambling frequency (OR = 2.0–2.8). These results could not be explained by differences between the discordant pairs in whether they had spent time gambling with the parents; there was no association between a history of problem, monthly or weekly gambling and having gambled with the parents among discordant twin pairs. The results of this study suggest that relying solely on family history assessments of disordered gambling and gambling involvement can lead to incorrect estimates of the strength of the family history effect.

Disordered gambling (DG) will soon be included along with the substance use disorders in a revised diagnostic category of the Diagnostic and Statistical Manual of Mental Disorders DSM-5 called 'Substance Use and Addictive Disorders'. This was premised in part on the common etiologies of DG and the substance use disorders. Using data from the national community-based Australian Twin Registry, we used biometric model fitting to examine the extent to which the genetic liabilities for DG and alcohol use disorder (AUD) were shared, and whether this differed for men and women. The effect of using categorical versus dimensional DG and AUD phenotypes was explored, as was the effect of using diagnoses based on the DSM-IV and the proposed DSM-5 diagnostic criteria. The genetic correlations between DG and AUD ranged from 0.29 to 0.44. There was a significantly larger genetic correlation between DG and AUD among men than women when using dimensional phenotypes. Overall, about one-half to two-thirds of the association between DG and AUD was due to a shared genetic vulnerability. This study represents one of the few empirical demonstrations of an overlap in the genetic risk for DG and another substance-related addictive disorder. More research is needed on the genetic overlap between DG and other substance use disorders, as well as the genetic overlap between DG and other (non-substance-related) psychiatric disorders.

AbstractProblem (P) and pathological gambling (PG) symptoms wax and wane. Past symptoms are a risk for future symptoms even after controlling for familial influences. To address the genetic architecture of lifetime PG and current PG symptoms, we tested for common and unique genetic factors to lifetime PG symptoms at baseline and past year PG symptoms at 10-year follow-up. Diagnostic and Statistical Manual of Mental Disorders (3rd ed., Rev.; DSM-III-R; American Psychiatric Association, 1987) lifetime criteria of one or more PG symptoms were derived in 1992 and past year PG symptoms in 2002 from 1675 individual twins from the Vietnam Era Twin Registry. Cholesky decomposition models were fit to baseline and past year PG symptoms. Under the best fitting model we observed that 49% of the risk for one or more baseline PG symptoms in 1992 was due to a genetic factor and 51% of the risk was due to a unique environmental factor. All of the genetic variance (57.5%) in risk to past year PG symptoms in 2002 was common with baseline PG symptoms. Unique environment accounted for the remaining variance in past year PG symptoms with 13% common to baseline and 30% specific to past year PG symptoms. The genetic contributions to lifetime and past year gambling symptoms 10 years later are similar. There is no evidence for genetic contributions unique to past year PG symptoms. However, most of the unique environmental influences to past year PG are not shared with lifetime PG. This may reflect the changed social–cultural environment between 1992 and 2002, characterized by increasing access to legalized gambling.

AbstractTwo major challenges to conducting a community-based twin study of pathological gambling (PG) disorder are that: (a) it is relatively rare, and (b) individuals with the disorder in the community may be difficult to locate and recruit. We describe a new study of 4,764 individuals recruited from the Australian Twin Registry in which we attempt to effectively deal with the first challenge and examine the impact of the second challenge. The lifetime prevalence of DSM-IV PG in this Australian twin sample was 2.2%, which is 400–500% higher than has been obtained in prevalence surveys conducted in the United States. A number of predictors of non-participation were identified, including a lifetime PG disorder diagnosis, but these did not have a large net effect on the estimated number of individuals with PG or related characteristics in the twin sample. Results of biometric modeling suggested that the effect of genetic, shared family environmental, and nonshared environmental influences on the propensity to engage in 11 different specific forms of gambling (e.g., playing the lottery, betting on horse or dog races, playing electronic gaming machines) were generally moderate, low, and moderate, respectively, with mean parameter estimates obtained of 43%, 10%, and 46%. An intriguing comparison with results from a 1963 US adolescent twin study conducted by Loehlin and Nichols (1976) suggests that: (a) propensity genes for gambling involvement may be more likely to be expressed in the heavy-gambling Australian culture, or that (b) the family environment has a transient effect on the gambling behavior of young people.

AbstractGenes associated with educational attainment may be related to or interact with adolescent alcohol, tobacco and cannabis use. Potential gene–environment interplay between educational attainment polygenic scores (EA-PGS) and adolescent alcohol, tobacco, and cannabis use was evaluated with a series of regression models fitted to data from a sample of 1871 adult Australian twins. All models controlled for age, age2, cohort, sex and genetic ancestry as fixed effects, and a genetic relatedness matrix was included as a random effect. Although there was no evidence that adolescent alcohol, tobacco or cannabis use interacted with EA-PGS to influence educational attainment, there was a significant, positive gene–environment correlation with adolescent alcohol use at all PGS thresholds (ps <.02). Higher EA-PGS were associated with an increased likelihood of using alcohol as an adolescent (ΔR2 ranged from 0.5% to 1.1%). The positive gene–environment correlation suggests a complex relationship between educational attainment and alcohol use that is due to common genetic factors.

Background: Previous studies have found that child attention-deficit/hyperactivity disorder (ADHD) is associated with more parental marital problems. However, the reasons for this association are unclear. The association might be due to genetic or environmental confounds that contribute to both marital problems and ADHD. Method: Data were drawn from the Australian Twin Registry, including 1,296 individual twins, their spouses, and offspring. We studied adult twins who were discordant for offspring ADHD. Using a discordant twin pairs design, we examined the extent to which genetic and environmental confounds, as well as measured parental and offspring characteristics, explain the ADHD–marital problems association. Results: Offspring ADHD predicted parental divorce and marital conflict. The associations were also robust when comparing differentially exposed identical twins to control for unmeasured genetic and environmental factors, when controlling for measured maternal and paternal psychopathology, when restricting the sample based on timing of parental divorce and ADHD onset, and when controlling for other forms of offspring psychopathology. Each of these controls rules out alternative explanations for the association. Conclusion: The results of the current study converge with those of prior research in suggesting that factors directly associated with offspring ADHD increase parental marital problems.