This study uses behavior genetic (BG) methodology to investigate Freud’s theory of depression as aggression directed toward the self (1930) and the extent to which genetically and environmentally influenced aggressive tendencies contribute to depressive symptoms. Data from the Twin and Offspring Study in Sweden (TOSS) is used to demonstrate how, in estimating shared and unique environmental influences, BG methods can inform psychoanalytic theory and practice, particularly because of their shared emphasis on the importance of individual experience in development. The TOSS sample consists of 909 pairs of adult twins, their partners, and one adolescent child per couple. The Center for Epidemiologic Studies Depression Scale (Radloff 1977) was used to measure depressive symptoms and the Karolinska Scales of Personality (Schalling and Edman 1993) to measure internally directed aggression. Genetic analyses indicated that for both men and women, their unique experiences as well as genetic factors contributed equally to the association between internally directed aggression and depressive symptoms. These findings support Freud’s theory that constitutionally based differences in aggression, along with individual experiences, contribute to a person’s depressive symptoms. Establishing that an individual’s unique, not shared, experiences and perceptions contribute to depressive symptoms and internally directed aggression reinforces the use of patient-specific treatment approaches implemented in psychoanalytic psychotherapy or psychoanalysis.
A recent meta-analysis (Burt, 2009) indicated that shared environmental influences (C) do not contribute to Attention-Deficit/Hyperactivity Disorder (ADHD). Unfortunately, the meta-analysis relied almost exclusively on classical twin studies. Although useful in many ways, some of the assumptions of the classical twin model (e.g., dominant genetic and shared environmental influences do not simultaneously influence the phenotype) can artifactually decrease estimates of C. There is thus a need to confirm that dominant genetic influences are not suppressing estimates of C on ADHD. The current study sought to do just this via the use of a nuclear twin family model, which allows researchers to simultaneously model and estimate dominant genetic and shared environmental influences. We examined two independent samples of child twins: 312 pairs from the Michigan State University Twin Registry (MSUTR) and 854 pairs from the PrEschool Twin Study in Sweden (PETSS). Shared environmental influences were found to be statistically indistinguishable from zero and accounted for less than 5% of the variance. We conclude that the presence of dominant genetic influences does not account for the absence of C on ADHD.
ADHD; nuclear twin family model; shared environment; genetic influences
Children born to older fathers are at higher risk to develop severe psychopathology (e.g., schizophrenia and bipolar disorder), possibly due to increased de novo mutations during spermatogenesis with older paternal age. Since severe psychopathology is correlated with antisocial behavior, we examined possible associations between advancing paternal age and offspring violent offending.
Interlinked Swedish national registers provided information on fathers’ age at childbirth and violent criminal convictions in all offspring born 1958–1979 (n=2,359,921). We used ever committing a violent crime and number of violent crimes as indices of violent offending. The data included information on multiple levels; we compared differentially exposed siblings in within-family analyses to rigorously test causal influences.
In the entire population, advancing paternal age predicted offspring violent crime according to both indices. Congruent with a causal effect, this association remained for rates of violent crime in within-family analyses. However, in within-analyses, we found no association with ever committing a violent crime, suggesting that factors shared by siblings (genes and environment) confounded this association. Life-course-persistent criminality has been proposed to have a partly biological etiology; our results agree with a stronger biological effect (i.e., de novo mutations) on persistent violent offending.
Paternal age; Violent criminality; De novo mutations; Sibling comparison
Advancing paternal age has been linked to autism.
To further expand knowledge about the relation between paternal age and autism by studying the effect of grandfathers’ age on childhood autism.
Population-based multigenerational case-control study.
Nationwide Multi-Generation and Patient registers in Sweden.
We conducted a study of individuals born in Sweden since 1932. Parental age at birth was obtained for over 90% of the cohort. Grandparental age at the time of birth of the parent was obtained for a smaller subset (5,936 cases and 30,923 controls).
Main Outcome Measures
International Classification of Diseases (ICD) diagnosis of childhood autism in the Patient Registry.
There was a statistically significant monotonic association between advancing grandpaternal age at the time of birth of the parent and risk of autism in grandchildren. Men who had a daughter when they were 50 or older were 1.79 times (95% confidence interval: 1.35-2.37, p<0.001) more likely to have a grandchild with autism, and men who had a son when they were 50 or older were 1.67 times (95% confidence interval: 1.35-2.37, p<0.001) more likely to have a grandchild with autism, compared to men who had children when they were 20-24, after controlling for birth year, sex, age of the spouse, family history of psychiatric disorders, highest family education and residential county. There was also a statistically significant monotonic association between advancing paternal age and risk of autism in the offspring. Sensitivity analyses indicated that these findings were not the result of bias due to missing data on grandparental age.
Advanced grandparental age was associated with increased risk of autism, suggesting that risk for autism could develop over generations. The results are consistent with mutations and/or epigenetic alterations associated with advancing paternal age.
Exome sequencing is emerging as a popular approach to study the effect of rare coding variants on complex phenotypes. The promise of exome sequencing is grounded in theoretical population genetics and in empirical successes of candidate gene sequencing studies. Many projects aimed at common diseases are underway, and their results are eagerly anticipated. In this Perspective, using exome sequencing data from 438 individuals, we discuss several aspects of exome sequencing studies that we view as particularly important. We review processing and quality control of raw sequence data, evaluate the statistical properties of exome sequencing studies, discuss rare variant burden tests to detect association to phenotypes, and demonstrate the importance of accounting for population stratification in the analysis of rare variants. We conclude that enthusiasm for exome sequencing studies of complex traits should be combined with the caution that thousands of samples may be required to reach sufficient statistical power.
Hoarding Disorder (HD) is often assumed to be an ‘old age’ problem, but many individuals diagnosed with HD retrospectively report first experiencing symptoms in childhood or adolescence. We examined the prevalence, comorbidity and etiology of hoarding symptoms in adolescence.
To determine the presence of clinically significant hoarding symptoms, a population-based sample of 15-year old twins (N = 3,974) completed the Hoarding Rating Scale-Self Report. Co-occurring Obsessive Compulsive Disorder (OCD), Autism Spectrum Disorders (ASD) and Attention Deficit Hyperactivity Disorder (ADHD) were estimated from parental report. Model-fitting analyses divided hoarding symptom scores into additive genetic, shared, and non-shared environmental effects.
The prevalence of clinically significant hoarding symptoms was 2% (95% CI 1.6–2.5%), with a significantly higher prevalence in girls than boys. Exclusion of the clutter criterion (as adolescents do not have control over their environment) increased the prevalence rate to 3.7% (95% CI 3.1–4.3%). Excessive acquisition was reported by 30–40% among those with clinically significant hoarding symptoms. The prevalence of co-occurring OCD (2.9%), ASD (2.9%) and ADHD (10.0%) was comparable in hoarding and non-hoarding teenagers. Model-fitting analyses suggested that, in boys, additive genetic (32%; 95% CI 13–44%) and non-shared environmental effects accounted for most of the variance. In contrast, among girls, shared and non-shared environmental effects explained most of the variance, while additive genetic factors played a negligible role.
Hoarding symptoms are relatively prevalent in adolescents, particularly in girls, and cause distress and/or impairment. Hoarding was rarely associated with other common neurodevelopmental disorders, supporting its DSM-5 status as an independent diagnosis. The relative importance of genetic and shared environmental factors for hoarding differed across sexes. The findings are suggestive of dynamic developmental genetic and environmental effects operating from adolescence onto adulthood.
We examined the association among current self-reported sleep problems, lifetime binge eating, and current obesity in women from the Swedish Twin study of Adults: Genes and Environment study
Logistic regression analyses were used to evaluate these associations in 3,790 women aged 20-47 years.
Binge eating was reported by 244 (6.4%) women and was positively associated with not getting enough sleep (p < .015), sleeping poorly (p < .001), problems falling asleep (p < .001), feeling sleepy during work or free time (p < .001), and disturbed sleep (p < .001). These same sleep variables, as well as napping and being a night person, were also significantly associated with obesity. The associations between binge eating and sleep remained after accounting for obesity.
This investigation offers empirical support for an independent association between sleep problems and binge eating, which is likely due to complex psychological, biological, neuroendocrine, and metabolic factors.
Maternal smoking during pregnancy (SDP) has been extensively studied as a risk factor for adverse offspring outcomes and is known to co-occur with other familial risk factors. Accounting for general familial risk factors has attenuated associations between SDP and adverse offspring outcomes, and identifying these confounds will be critical to elucidating the relationship between SDP and its psychological correlates.
The current study aimed to disentangle the relationship between maternal SDP and co-occurring risk factors (maternal criminal activity, drug problems, teen pregnancy, educational attainment, and cohabitation at childbirth) using a population-based sample of full- (n=206,313) and half-sister pairs (n=19,363) from Sweden. Logistic regression models estimated the strength of association between SDP and co-occurring risk factors. Bivariate behavioral genetic models estimated the degree to which associations between SDP and co-occurring risk factors are attributable to genetic and environmental factors.
Maternal SDP was associated with an increase in all co-occurring risk factors. Of the variance associated with SDP, 45% was attributed to genetic factors and 53% was attributed to unshared environmental factors. In bivariate models, genetic factors accounted for 21% (non- drug-, non-violence-related crimes) to 35% (drug-related crimes) of the covariance between SDP and co-occurring risk factors. Unshared environmental factors accounted for the remaining covariance.
The genetic factors that influence a woman’s criminal behavior, substance abuse, and her offspring’s rearing environment also influence SDP. Therefore, the intergenerational transmission of genes conferring risk for antisocial behavior and substance misuse may influence the associations between maternal SDP and adverse offspring outcomes.
smoking; pregnancy; antisocial; criminal; drug; behavior genetic
The Presidential Address of the European Association of Developmental Psychology this year concerned how genes and environments interplay to shape loneliness and other developmental psychological relevant outcomes. This is a very welcome. However, when developmental psychology now is ready to integrate recent genetic and neuroscience knowledge and methods, I think it would be very wise to not uncritical go through the mistakes that have be done in other disciplines and instead learn from their hard lessons. I discuss some problems (genes versus environments, identifying gene for a phenotype, environments cause of developmental outcomes, and gene X environment interaction and epigenetics) and some suggestions for solutions which can be used to avoid throwing in the bathwater with the baby.
This study examined the contributions of personality to the emotional and behavior dynamics of families. Analyses assessed the degrees to which personality accounts for associations between marital quality and parenting, and mediates genetic contributions to these relationships. Participants included 318 male and 544 female same-sex twin pairs from the Twin and Offspring Study in Sweden. All twins completed self-report measures of marital quality and personality (anxiousness, aggression, sociability). Composite measures of parent negativity and warmth were derived from the twins' and their adolescent children's ratings of the twins' disciplinary styles and the emotional tone of the parent-child relationship. Observational ratings of marital quality and parenting were also obtained for a subset of twins. Analyses indicated that personality characteristics explain 33% to 42% of the covariance between reported marital quality and parenting, and 26% to 28% of the covariance between observed marital quality and parenting. For both sets of analyses personality accounted for more than half of the genetic contributions to covariance between marital quality and parenting. Results indicate that personality significantly contributes to associations between marital quality and parenting, and that personality is an important path through which genetic factors contribute to family relationships.
Marriage; Parenting; Personality; Twins
Previous studies indicate that maternal anxiety is associated with asthma in the adolescent child, but mechanisms are unclear.
To investigate the association between maternal anxiety and maternal, self- and register-based report of asthma in the adolescent child, and whether the association remains after control of familial confounding (shared environmental and genetic factors).
From the Twin and Offspring Study of Sweden, 1691 mothers (1058 twins) and their adolescent child were included. The association between maternal self-reported anxiety (Beck Anxiety Inventory (BAI) and Karolinska Scales of Personality (KSP) somatic or psychic anxiety) and asthma based on subjective (maternal or child report) or objective (register-based diagnosis and medication) measures were analysed using logistic regression. The children-of-twins design was used to explore whether genes or environment contribute to the association.
Maternal BAI anxiety (OR 2.02, CI 1.15–3.55) was significantly associated with adolescent asthma reported by the mother. Maternal KSP somatic anxiety (OR 1.74, CI 1.04–2.91) and psychic anxiety (OR 1.74, CI 1.05–2.86) was significantly associated with breathlessness reported by the adolescent child. In contrast, maternal anxiety was not associated with increased risk for the register-based outcomes of asthma diagnosis or medication. The results remained also after adjusting for covariates and the children-of-twins analyses which indicate that the association was due to familial confounding.
We found some associations between maternal anxiety and subjectively reported offspring asthma or breathlessness which may be due to familial effects. A likely candidate for explaining this familial confounding is heritable personality traits associated with both anxiety and subjective measures of asthma.
Teenage childbirth is a risk factor for poor offspring outcomes, particularly offspring antisocial behaviour. It is not clear if maternal age at first birth (MAFB) is causally associated with offspring antisocial behavior or if this association is due to selection factors that influence both the likelihood that a young woman gives birth early and that her offspring engage in antisocial behavior. The current study addresses the limitations of previous research by using longitudinal data from Swedish national registries and children-of-siblings and children-of-twins comparisons to identify the extent to which the association between MAFB and offspring criminal convictions is consistent with a causal influence and confounded by genetic or environmental factors that make cousins similar. We found offspring born to mothers who began childbearing earlier were more likely to be convicted of a crime than offspring born to mothers who delayed childbearing. The results from comparisons of differentially exposed cousins, especially born to discordant MZ twin sisters, provide support for a causal association between MAFB and offspring criminal convictions. The analyses also found little evidence for genetic confounding due to passive gene-environment correlation. Future studies are needed to replicate these findings and to identify environmental risk factors that mediate this causal association.
Teenage childbirth; teenage motherhood; criminal behavior; antisocial behavior
Although perinatal factors are associated with the development of several psychiatric disorders, it is unknown whether these factors are linked with personality disorder. Cases of personality disorder were drawn from a national registry of all forensic psychiatric evaluations (n=150). Two control groups were used: 1. A sample of forensic evaluations without any psychiatric disorder (n=97) allowing for a nested case-control investigation; 2: A population-based sample matched by age and gender with no history of psychiatric hospitalization (n=1498). Prematurity (<37 weeks of completed gestation) was significantly associated with a diagnosis of personality disorder, both in the nested and the population-based case-control comparisons with adjusted odds ratios (OR) for this risk factors ranging from 2 to 4. Asphyxia (adjusted OR=2.4, 95% CI: 1.4-4.1) and complicated delivery (adjusted OR=1.5, 1.0-2.1) were associated with personality disorder in the population-based study, and the former remained significant in multivariate models. Overall, perinatal complications were found to be associated with a later diagnosis of personality disorder in this selected sample. As with other psychiatric disorders where such associations have been demonstrated, changes during the perinatal period may lead to abnormal brain development and function.
Perinatal risk factors; personality disorder; asphyxia; borderline personality disorder; antisocial personality disorder; nested case-control study
We examined whether the risk for psychiatric morbidity requiring inpatient care was higher in offspring who experienced parental suicide compared to offspring who experienced parental fatal accidents, and if the association varied by the deceased parent’s gender.
Subjects and Methods
Children and adolescents (age 0-17 years) who experienced maternal (n=5,600) or paternal suicide (n=17,847) during 1973-2003 in Sweden were identified using national, longitudinal population-based registries. Cox regression modeling was used to compare psychiatric hospitalization risks among offspring of suicide decedents with propensity-matched offspring of accident decedents.
Offspring of maternal suicide decedents had increased risk of hospitalization for suicide attempt after controlling for psychiatric hospitalization in decedents and surviving parents, compared to offspring of maternal accidental decedents. Offspring of paternal suicide decedents had similar risk of hospitalization for suicide attempt compared to offspring of accident decedents but had increased risk of hospitalization for depressive and anxiety disorders. The magnitude of risks for offspring hospitalization for suicide attempt was greater for those who experienced maternal versus paternal suicide, as compared to their respective controls (interaction p=0.05) [AHR (95%CI) = 1.80 (1.19-2.74) in offspring of maternal decedents vs. 1.14 (0.96-1.35) in offspring of paternal decedents].
Maternal suicide is associated with increased risk of hospitalization for suicide attempt in offspring, beyond the risk associated with maternal accidental death. However, paternal suicide is not associated with hospitalization for suicide attempt. Future studies should examine factors that might differ between offspring who experience maternal versus paternal suicide, including genetic or early environmental determinants.
suicide; attempted; mental disorders; parent-child relations; death; parents; mothers; fathers
Advanced paternal age has been linked with neurodevelopmental disorders such as schizophrenia. If age-related de novo mutations in the male germ line underlie this association, it would be expected that grandpaternal as well as paternal age may influence the risk of schizophrenia. The aim of the current study was to explore the links between both paternal and grandpaternal age with respect to the risk of schizophrenia in a large, national register-based sample.
The study was based on Swedish Multi-Generation and Hospital Discharge Registers. Parents’ ages at offspring birth were compared between 20,582 affected and 100,176 non-affected individuals. Grandparents’ ages at the birth of the parent were compared between 2,511 affected and 15,619 non-affected individuals. The risk of schizophrenia was examined when the predictor variable (parent or grandparent age) was examined in age strata with logistic regression. Planned sensitivity analyses included exploring the variables of interest in males and females separately.
After adjusting for maternal age, birth year and sex of the proband, we confirmed that the offspring of older fathers have an increased risk of schizophrenia (e.g. compared to paternal age 20–24 years, those with fathers > 55 years had a two-fold increased risk). With respect to grandparent age, older maternal (but not paternal) grandfather age was associated with an increased risk of schizophrenia. Compared to maternal grandfather age 20–24 years, those with maternal grandfathers >55 years had a significantly increased risk of schizohrpenia (Adjusted Odds ratio and 95% Confidence intervals; 2.79, 1.71 – 4.56). The pattern of findings were essentially unchanged when we examine male and female probands separately.
This is the first the study to show an association between grandpaternal age and risk of schizophrenia. The selective effect of advanced maternal grandfather age suggests that the biological mechanisms involving the X chromosome may differentially contribute to the association between paternal age and risk of schizophrenia.
schizophrenia; paternal age; grandparental age; mutation
Offspring to patients with schizophrenia exhibit poorer school performance compared to offspring of non-schizophrenic parents. We aimed to elucidate the mechanisms behind this association.
We linked longitudinal national population registers in Sweden and compared school performance among offspring to schizophrenic parents to offspring of non-schizophrenic parents (N=1,439,215 with final grades from compulsory school 1988–2006). To investigate the mechanisms, we studied offspring to schizophrenic patients and controls within the same extended families. We investigated genetic effects by stratifying analyses of parent-child associations according to genetic relatedness (half-cousins, full cousins, and half-siblings). Environmental effects were investigated by comparing school performance of offspring to schizophrenic fathers and to schizophrenic mothers, respectively, and by stratifying the analyses according to environmental relatedness while controlling genetic relatedness (paternal and maternal half-cousins, paternal and maternal half-siblings).
Offspring to parents with schizophrenia had poorer overall school performance than unrelated offspring to non-schizophrenic parents (−0.31 SD). Variability in genetic relatedness greatly moderated the strength of the within-family association (β=−0.23 within exposure-discordant half-cousins, β=−0.13 within exposure-discordant full cousins, and β=0.04 within exposure-discordant half-siblings), while no evidence was found that the environment affected offspring school performance.
Genetic factors account for poorer school performance in children of parents with schizophrenia. This supports that cognitive deficits found in individuals with schizophrenia and their relatives might be genetically inherited. Early detection of prodromal signs and impaired functioning of offspring to patients with schizophrenia could lead to earlier and better tailored interventions.
school performance; offspring; schizophrenia; genetics; environments
Autism spectrum disorder (ASD) is a neurodevelopmental disorder of complex etiology. Whereas strong evidence supports the causal role of genetic factors, a number of environmental risk factors have also been implicated. This study employed a cotwin-control design to investigate low birth weight as a risk factor for ASD.
A population-based sample of 3,715 same-sex twin-pairs participating in the Child and Adolescent Twin Study of Sweden were studied. ASD was assessed using a structured parent interview for screening of ASD and related developmental disorders, based on DSM-IV criteria. Birth weight was obtained from medical birth records maintained by the Swedish Medical Birth Registry.
Lighter twins in birth weight and ASD discordant twin-pairs (n= 34) were over three times more likely to meet criteria for ASD than heavier twins (OR = 3.25). Analyses of birth weight as a continuous risk factor showed a 13% reduction in risk of ASD per 100 gram increase in birth weight (n=78). Analysis of the effect of birth weight on ASD symptoms in the entire population (most of whom did not have ASD) showed a modest association. That is, for every 100 gram increase in birth weight a 2% decrease in severity of ASD indexed by A-TAC scores would be expected in the sample as a whole.
Data are consistent with the hypothesis that low birth weight confers risk to ASD. Thus, even though genetic effects are of major importance, non-genetic influence associated with birth weight may contribute to the development of ASDs.
Autism; Twin; Birth weight
Maternal smoking during pregnancy (SDP) is associated with lower academic achievement in offspring. The current study, which was based on all births in Sweden from 1983 through 1991, explored the possible causal processes underlying the association between SDP and offspring school grades and a standardized assessment of mathematic proficiency at age 15. The analyses compared relatives who varied in their exposure to SDP and who varied in their genetic relatedness. Although SDP was statistically associated with academic achievement when comparing unrelated individuals, the results suggest that SDP does not cause poorer academic performance, as full siblings differentially exposed to SDP did not differ in their academic scores. The pattern of results suggests that genetic factors shared by parents and their offspring explain significant variance in why offspring opposed to SDP have lower levels of academic achievement. Nevertheless, SDP impacts pregnancy-related outcomes. Reducing SDP, therefore, remains a major public health issue.
We assessed the impact of reducing the binge eating frequency and duration thresholds on the diagnostic criteria for bulimia nervosa (BN) and binge eating disorder (BED).
We estimated the lifetime population prevalence of BN and BED in 13,295 female twins from the Swedish Twin study of Adults: Genes and Environment employing a range of frequency and duration thresholds. External validation (risk to co-twin) was used to investigate empirical evidence for an optimal binge eating frequency threshold.
The lifetime prevalence estimates of BN and BED increased linearly as the frequency criterion decreased. As the required duration increased, the prevalence of BED decreased slightly. Discontinuity in co-twin risk was observed in BN between at least four times per month and at least five times per month. This model could not be fit for BED.
The proposed changes to the DSM-5 binge eating frequency and duration criteria would allow for better detection of binge eating pathology without resulting in a markedly higher lifetime prevalence of BN or BED.
Aim. To establish the prevalence of restrictive eating problems, the overlap and association with attention-deficit/hyperactivity disorder (ADHD), and autism spectrum disorders (ASD) and to estimate the heritability of eating problems in a general population sample of twins aged 9 and 12. Methods. Parents of all Swedish 9- and 12-year-old twin pairs born between 1993 and 1998 (n = 12,366) were interviewed regarding symptoms of ADHD, ASD, and eating problems (EAT-P). Intraclass correlations and structural equation modelling were used for evaluating the influence of genetic and environmental factors. Cross-twin, cross-trait correlations were used to indicate a possible overlap between conditions. Results. The prevalence of eating problems was 0.6% in the study population and was significantly higher in children with ADHD and/or ASD. Among children with eating problems, 40% were screened positive for ADHD and/or ASD. Social interaction problems were strongly associated with EAT-P in girls, and impulsivity and activity problems with EAT-P in boys. The cross-twin, cross-trait correlations suggested low correlations between EAT-P and ADHD or EAT-P and ASD. Genetic effects accounted for 44% of the variation in liability for eating problems. Conclusions. In the group with eating problems, there was a clear overrepresentation of individuals with ADHD and/or ASD symptoms.
Previous epidemiological, animal, and human cognitive neuroscience research suggests that maternal smoking during pregnancy causes increased risk of offspring substance use/problems.
To determine the extent to which the association between SDP and offspring substance use/problems depends on confounded familial background factors by using a quasi-experimental design.
We used two separate samples, from the United States and from Sweden, respectively. The analyses prospectively predicted multiple indices of substance use and problems while controlling for statistical covariates and comparing differentially exposed siblings to minimize confounding.
Sample 1: Offspring of a representative sample of women in the United States. Sample 2: The total Swedish population born over 13 years.
Patients or Other Participants
Sample 1: Adolescent offspring of the women in the National Longitudinal Survey of Youth 1979 (n=6,094). Sample 2: All offspring born in Sweden from 1983 through 1995 (n=1,187,360).
Main Outcome Measures
Sample 1: Self-reported adolescent alcohol, cigarette, and marijuana use, and early onset (before age 14 years) of each substance. Sample 2: Substance-related convictions and hospitalizations for an alcohol- or drug-related problem.
The same pattern emerged for each index of substance use/problems across the two samples. At the population level maternal smoking during pregnancy predicted every measure of offspring substance use/problems in both samples, ranging from adolescent alcohol use (HRmoderate=1.32, CI=1.22–1.43; HRhigh=1.33, CI=1.17=1.53) to a narcotic convictions (HRmoderate=2.23, CI=2.14–2.31; HRhigh=2.97, CI=2.86–3.09). When comparing differentially exposed siblings to minimize genetic and environmental confounds, however, the association between SDP and each measure of substance use/problems was minimal and not statistically significant.
The association between maternal smoking during pregnancy and offspring substance use/problems was likely due to familial background factors, not a causal influence, because siblings had similar rates of substance use and problems regardless of their specific exposure to smoking during pregnancy.
To assess the relative risk of amyotrophic lateral sclerosis (ALS) in families of ALS patients.
We conducted a cohort study based on the Swedish Multi-Generation Register (MGR) in 1961-2005. Among 6,671 probands (first ALS case in the family), 1,909 full siblings, 13,947 children, and 5,405 spouses were identified (exposed group). Other persons in MGR, who were siblings, children, or spouses to persons without ALS, served as the reference group. Relative risks of ALS among the exposed group, compared to the reference group, were calculated from Poisson regression models. Concurrence of ALS within twins was assessed in 86,441 twin pairs registered in the Swedish Twin Register.
Nine cases of ALS were noted among the siblings and 37 cases among the children of the probands, giving a 17-fold risk among the siblings (95% confidence interval [CI], 8.1-30.4) and a 9-fold risk among the children (95% CI, 6.2-12.0), compared to the reference group. Siblings and children had a higher excess risk if the proband was diagnosed at younger age, and the excess risks decreased with increasing age at diagnosis of the proband (p < 0.001). Spouses had no significantly increased risk (p = 0.27). Two cases were identified among the co-twins of ALS probands, giving a relative risk of 32 (95% CI, 5.2-102.6).
The siblings and children of ALS patients have an around 10-fold risk of ALS compared to the reference group. The excess risks vary with both age and kinship, indicating a major genetic role in familial ALS.
This article reviews existing research at the intersection of genetics and economics, presents some new findings that illustrate the state of genoeconomics research, and surveys the prospects of this emerging field. Twin studies suggest that economic outcomes and preferences, once corrected for measurement error, appear to be about as heritable as many medical conditions and personality traits. Consistent with this pattern, we present new evidence on the heritability of permanent income and wealth. Turning to genetic association studies, we survey the main ways that the direct measurement of genetic variation across individuals is likely to contribute to economics, and we outline the challenges that have slowed progress in making these contributions. The most urgent problem facing researchers in this field is that most existing efforts to find associations between genetic variation and economic behavior are based on samples that are too small to ensure adequate statistical power. This has led to many false positives in the literature. We suggest a number of possible strategies to improve and remedy this problem: (a) pooling data sets, (b) using statistical techniques that exploit the greater information content of many genes considered jointly, and (c) focusing on economically relevant traits that are most proximate to known biological mechanisms.
genetics; heritability; GWAS
In specific vole and primate species the neuropeptide Oxytocin (OT) plays a central role in the regulation of pair-bonding behavior. Here we investigate to what extent genetic variants in the oxytocin receptor gene (OXTR) are associated with pair-bonding and related social behaviors in humans.
We first genotyped twelve Single Nucleotide Polymorphisms (SNPs) in the Twin and Offspring Study in Sweden (TOSS, N=2309) and the Swedish Twin Study of CHild and Adolescent Development (TCHAD, N=1240) comprising measures of self-reported pair-bonding behavior. In the TOSS-sample we further investigated one the SNPs for measures of marital status and quality. Moreover, in the TCHAD sample we explored the longitudinal relationship between precursors of pair-bonding during childhood and subsequent behavior in romantic relationships. Finally, in TCHAD and in the Child and Adolescent Twin Study of Sweden (CATSS, N=1771) the association between the same SNP and childhood behaviors was investigated.
One SNP (rs7632287) in OXTR was associated with traits reflecting pair-bonding in women in the TOSS and TCHAD samples. In girls the rs7632287 SNP was further associated with childhood social problems, which longitudinally predicted pair-bonding behavior in the TCHAD-sample. This association was replicated in the CATSS-sample in which an association between the same SNP and social interaction deficit symptoms from the autism spectrum was detected.
These results suggest an association between variation in OXTR and human pair-bonding and other social behaviors, possibly indicating that the well described influence of OT on affiliative behavior in voles could also be of importance for humans.
Monogamy; Neuropeptide; Polymorphism; Autism; Affiliative behavior; Social Problems
These three studies examined the hypothesis that prenatal exposure to sex hormones influences twins’ risk for eating disorders based on co-twin sex, such that individuals with a female co-twin would be more likely than individuals with a male co-twin to meet diagnostic criteria for an eating disorder.
Male and female twins from the United States (N=2,607), Norway (N=2,796) and Sweden (N=16,458) with known co-twin sex and zygosity were assessed for eating disorders.
In the U.S. and Swedish samples, sex was significantly associated with eating disorder diagnoses, and although co-twin sex was not associated with eating disorders overall, it was associated with broadly defined bulimia nervosa in the Swedish sample. The effects for bulimia were not sustained when monozygotic twins were excluded, suggesting that the effects of prenatal sex hormones play a minor role in influencing eating disorders. Sex and co-twin sex were not associated with eating disorders in the Norwegian sample.
The prenatal sex hormone hypothesis, which proposes that prenatal hormone exposure is associated with later eating disorder symptomatology, was not supported in these three population-based twin samples.
eating disorders; estrogen; opposite sex twin pairs; prenatal hormone exposure; testosterone; twin study