A recent genome wide association study reported evidence for association between rs1344706 within ZNF804A (encoding zinc finger protein 804A) and schizophrenia (P=1.61 ×10−7), and stronger evidence when the phenotype was broadened to include bipolar disorder (P=9.96 ×10−9). Here we provide additional evidence for association through meta-analysis of a larger dataset (schizophrenia/schizoaffective disorder N = 18945, schizophrenia plus bipolar disorder N =21274, controls N =38675). We also sought to better localize the association signal using a combination of de novo polymorphism discovery in exons, pooled de novo polymorphism discovery spanning the genomic sequence of the locus and high density LD mapping. Meta-analysis provided evidence for association between rs1344706 that surpasses widely accepted benchmarks of significance by several orders of magnitude for both schizophrenia (P=2.5 ×10−11, OR=1.10, 95% CI 1.07–1.14) and schizophrenia and bipolar disorder combined (P=4.1 ×10−13, OR=1.11, 95% CI 1.07–1.14). After de novo polymorphism discovery and detailed association analysis, rs1344706 remained the most strongly associated marker in the gene. The allelic association at the ZNF804A locus is now one of the most compelling in schizophrenia to date, and supports the accumulating data suggesting overlapping genetic risk between schizophrenia and bipolar disorder.
Introduction: Studies suggest that initial smoking pleasure influences future smoking behavior. We investigated how initial reactions to cigarettes or Swedish smokeless tobacco (snus) were associated with future use among 10,708 adults from the Swedish Twin Registry.
Methods: The Early Smoking Experience questionnaire captured physiologic reactions to initial tobacco use. Binary recursive partitioning (BRP) identified combinations of initial reactions predictive of regular tobacco use. Analyses, stratified by sex, were conducted separately among those who experimented with only cigarettes (EC), only snus (ES), and both products (EC+S).
Results: Among EC, 39.8% of men and 43.7% of women became smokers, while among ES, 78.6% of men and 53.7% of women became snus users. Among EC+S, 31.3% of men and 20.0% of women became dual users. BRP identified different reactions as predictive of future smoking for men (buzz) and women (dizziness, difficulty inhaling). No initial reaction predicted future snus use among men, but pleasant sensations, later age at first use, and relaxation predicted future snus use for women. Among EC+S, future exclusive use of either product was associated with a favorable initial reaction to that product. Dual users experienced higher prevalence of pleasant reactions and lower prevalence of unpleasant reactions in response to both products.
Conclusions: Our findings support that those who progress to regular tobacco use may be sensitive to the rewarding effects of nicotine but suggest that initial reactions differ by tobacco type. A high proportion of men became regular snus users regardless of initial reactions.
Previous studies have found an association between early age at first sexual intercourse and subsequent psychosocial maladjustment. Using a quasi-experimental approach, we examined the extent to which this observed association may be due to familial confounds not explored in prior research.
Using a population-based cohort of Swedish adult twins (ages 19–47; N = 12,126), we examined the nature of the association between early sexual intercourse (i.e., first intercourse occurring before age 16) and various outcomes reflecting psychosocial health, including substance use, depression, criminal convictions, and adolescent childbearing. We used two methods—discordant-twin analyses and bivariate twin modeling—to estimate the extent to which genetic and environmental confounds explained observed associations.
Individuals who engaged in early intercourse were at greater risk for most of the adverse psychosocial health outcomes measured in this study. Twin pairs discordant for engaging in early intercourse, however, did not differ significantly in their risk for psychosocial maladjustment. Our results indicated that early age at first sexual intercourse and subsequent psychosocial maladjustment may be associated due to familial factors shared by twins.
Early intercourse may be associated with poor psychosocial health largely due to shared familial influences rather than through a direct causal connection. Effective and efficient interventions, therefore, should address other risk factors common to both early intercourse and poor psychosocial health.
adolescence; sexual behavior; sex-education programs; behavior genetics
Previous studies have suggested that children who experience parental suicide at earlier ages are at higher risk of future hospitalization for suicide attempt. However, how the trajectories of risk differ by offspring age at the time of parental suicide is currently unknown.
To study time at risk to hospitalization for suicide attempt among offspring after experiencing parental suicide or accidental death by offspring developmental period at the time of parental death.
Population-based retrospective cohort study
26,096 offspring who experienced parental suicide and 32,395 offspring of accident decedents prior to age 25 from 1973-2003.
Main Outcome Measures
Hospitalization for suicide attempt. Parametric survival analysis was used to model the time to hospitalization for suicide attempt across offspring who lost a parent during early childhood (0-5 years old), later childhood (6-12), adolescence (13-17) and young adulthood (18-24).
The risk in offspring who lost a parent during early or late childhood surpassed the other two age groups’ hazards approximately 5 years after the origin and, for the youngest group, continued to rise over the course of decades. Offspring who lost a parent during adolescence or young adulthood were at greatest risk within 1 to 2 years after parental suicide, and risk declined over time. The shape of hospitalization risk was similar among those who experienced parental fatal accident. When the shape of hospitalization for suicide attempt at each developmental period was fixed to be the same between the two groups, offspring who lost a parent to suicide had earlier risk to hospitalization for suicide attempt hospitalization than offspring who lost a parent to an accident.
The hospitalization risk for suicide attempt in offspring who lost a parent during their childhood is different from those who lost a parent during adolescence or young adulthood. The results suggest critical windows for careful monitoring and intervention for suicide attempt risk, especially 1-2 years after parental death for the older age groups and over decades for childhood survivors of parental death.
In a study based on 96% of the roughly 28,000 patients with multiple sclerosis (MS) in Sweden, Westerlind et al. report relative and absolute MS risks for relatives of patients. Risks were lower than most of those previously reported, with an MS sibling risk seven times that of randomly selected controls.
Data on familial recurrence rates of complex diseases such as multiple sclerosis give important hints to aetiological factors such as the importance of genes and environment. By linking national registries, we sought to avoid common limitations of clinic-based studies such as low numbers, poor representation of the population and selection bias. Through the Swedish Multiple Sclerosis Registry and a nationwide hospital registry, a total of 28 396 patients with multiple sclerosis were identified. We used the national Multi-Generation Registry to identify first and second degree relatives as well as cousins, and the Swedish Twin Registry to identify twins of patients with multiple sclerosis. Crude and age corrected familial risks were estimated for cases and found to be in the same range as previously published figures. Matched population-based controls were used to calculate relative risks, revealing lower estimates of familial multiple sclerosis risks than previously reported, with a sibling recurrence risk (λs = 7.1; 95% confidence interval: 6.42–7.86). Surprisingly, despite a well-established lower prevalence of multiple sclerosis amongst males, the relative risks were equal among maternal and paternal relations. A previously reported increased risk in maternal relations could thus not be replicated. An observed higher transmission rate from fathers to sons compared with mothers to sons suggested a higher transmission to offspring from the less prevalent sex; therefore, presence of the so-called ‘Carter effect’ could not be excluded. We estimated the heritability of multiple sclerosis using 74 757 twin pairs with known zygosity, of which 315 were affected with multiple sclerosis, and added information from 2.5 million sibling pairs to increase power. The heritability was estimated to be 0.64 (0.36–0.76), whereas the shared environmental component was estimated to be 0.01 (0.00–0.18). In summary, whereas multiple sclerosis is to a great extent an inherited trait, the familial relative risks may be lower than usually reported.
familial recurrence; multiple sclerosis; familial risk; twin study
A persistent debate in psychiatry concerns whether schizophrenia and bipolar disorder are the clinical realizations of discrete versus shared etiological processes.
We linked the Multi-Generation Register, containing information about children and their parents of all Swedes, and the Hospital Discharge Register, covering all public psychiatric inpatient hospitalizations in Sweden. We identified 9,009,202 unique individuals in more than 2 million nuclear families. Risks for schizophrenia, bipolar disorder and their co-morbidity were calculated for biological and adoptive parents, offspring, full siblings and half-siblings of probands with the diseases. A multivariate generalized linear mixed model was used to estimate genetic and environmental contributions to liability for schizophrenia, bipolar disorder, and their co-morbidity.
There were increased risks of both schizophrenia and bipolar disorder to first degree relatives of probands with either disorder. Half-sibs had a significantly increased risk, albeit substantially lower than the full-siblings. When relatives of probands with bipolar disorder were analysed, increased risks for schizophrenia were present for all relationships, including offspring adopted away. Heritability for schizophrenia was 64% and for bipolar disorder 59%. Shared environmental effects were small but significant for both disorders. The co-morbidity between the disorders was primarily (63%) due to additive genetic effects common to both disorders.
Similar to molecular genetic studies, we found compelling evidence that schizophrenia and bipolar disorder partially share a common genetic etiology. These results challenge the current nosological dichotomy between schizophrenia and bipolar disorder, and are consistent with a reappraisal of these disorders as distinct diagnostic entities.
Adverse childhood experiences and substance use have been identified as potential causal risk factors for early-onset sexual intercourse. While it is possible that exposure to these risk factors directly increases the likelihood of engaging in early intercourse, an alternative explanation is that observed associations between these variables are due to shared familial confounds. These unmeasured confounds may increase the likelihood of being exposed to these risk factors and of engaging in early intercourse. Participants drawn from a population-based study of Swedish adult twins (ages 19–47 years; N = 12,126) reported on their history of exposure to early physical and sexual trauma, cigarette use, and cannabis use. We investigated the nature of the association between these risk factors and young age at first intercourse, using a comparison of twins differentially exposed to each risk factor. When compared to non-exposed, unrelated individuals, participants who reported adverse childhood experiences or who engaged in early cigarette use or cannabis use were more likely to engage in early intercourse. However, co-twin comparisons indicated that observed associations between these risk factors and early intercourse may be due to familial factors shared within twin pairs, and risk factor exposure may not lead directly to early intercourse. Our results suggest that preventing trauma exposure or preventing or delaying adolescents’ cigarette smoking or cannabis use may not effectively delay intercourse onset; instead, other aspects of the adolescent’s environment should be addressed.
adolescence; sexual behavior; substance use; child abuse; co-twin comparison; behavioral genetics
Attention deficit hyperactivity disorder (ADHD) is a common disorder that is associated with criminal behavior. Pharmacological treatment is available for ADHD and may reduce the risk of criminality
We gathered information on all individuals with a diagnosis of ADHD (N=25,656), their pharmacological treatment, and subsequent criminal convictions in Sweden during 2006 to 2009 using Swedish national registers. We used stratified Cox regression analyses to compare the rate of criminality while on ADHD medication, compared with the rate for the same individual while off medication.
Compared to non-medication periods, the criminality rate while on medication was significantly decreased by 32% (stratified Cox Regression hazard ratio: 0.68; 95 % confidence interval: 0.63-0.73) for men and 41% (hazard ratio: 0.59; 95 % confidence interval: 0.50-0.70) for women. The rate reduction remained between 17-46% in sensitivity analyses among males, including different exposures (e.g., type of treatment – stimulant and non-stimulant) and outcomes (e.g., type of crime - less severe, violent, and substance-related conviction).
We found statistically significant associations between ADHD medication and criminality in within-individual comparisons, with lower rates of criminality observed during periods on treatment. These findings raise the possibility that medication treatment reduces the risk of criminality among patients with ADHD.
Epilepsy is associated with high rates of premature mortality, but the contribution of psychiatric comorbidity is uncertain. We assessed the prevalence and risks of premature mortality from external causes such as suicide, accidents, and assaults in people with epilepsy with and without psychiatric comorbidity.
We studied all individuals born in Sweden between 1954 and 2009 with inpatient and outpatient diagnoses of epilepsy (n=69 995) for risks and causes of premature mortality. Patients were compared with age-matched and sex-matched general population controls (n=660 869) and unaffected siblings (n=81 396). Sensitivity analyses were done to investigate whether these odds differed by sex, age, seizure types, comorbid psychiatric diagnosis, and different time periods after epilepsy diagnosis.
6155 (8.8%) people with epilepsy died during follow-up, at a median age of 34·5 (IQR 21·0–44·0) years with substantially elevated odds of premature mortality (adjusted odds ratio [aOR] of 11·1 [95% CI 10·6–11·6] compared with general population controls, and 11·4 [10·4–12·5] compared with unaffected siblings). Of those deaths, 15·8% (n=972) were from external causes, with high odds for non-vehicle accidents (aOR 5·5, 95 % CI 4·7–6·5) and suicide (3·7, 3·3–4·2). Of those who died from external causes, 75·2% had comorbid psychiatric disorders, with strong associations in individuals with co-occurring depression (13·0, 10·3–16·6) and substance misuse (22·4, 18·3–27·3), compared with patients with no epilepsy and no psychiatric comorbidity.
Reducing premature mortality from external causes of death should be a priority in epilepsy management. Psychiatric comorbidity plays an important part in the premature mortality seen in epilepsy. The ability of health services and public health measures to prevent such deaths requires review.
Wellcome Trust, the Swedish Prison and Probation Service, and the Swedish Research Council.
Early maturing girls are at increased risk for disordered eating. However, it is unclear if the association between puberty and disordered eating continues throughout pubertal development and if a similar association is exhibited in boys.
Participants included 1340 same- and 624 opposite-sex twins from the Swedish Twin Study of Child and Adolescent Development. Pubertal development was assessed at age 13–14 with the Pubertal Development Scale. General disordered eating, measured with the Eating Disorder Inventory-2 (EDI) was assessed at age 16–17, and dieting and purging behaviors were assessed at both ages 16–17 and 19–20. We applied analysis of variance and logistic regression analyses to determine whether pubertal development in early-to-mid adolescence predicted eating disorder-related behaviors in late adolescence and young adulthood
Pubertal development in early-to-mid adolescence was significantly associated with EDI scores and dieting in late adolescence. No significant association was observed between pubertal development and dieting and purging in young adulthood.
Complex combinations of cultural and biological influences likely converge during pubertal development increasing vulnerability to disordered eating. The impact of pubertal development on disordered eating appears to be limited to the adolescent period.
disordered eating; eating disorder; puberty; pubertal development; development; adolescence
An early age at menarche is associated with disordered eating in women. However, it is unclear whether they share genetic factors. The goal of the current study is to delineate the genetic correlation between age at menarche and disordered eating.
Participants included 427 monozygotic and 329 dizygotic 16-17 year-old female twins from the Swedish Twin Study of Child and Adolescent Development. Disordered eating was assessed with the Eating Disorder Inventory-2. Age at menarche was assessed via self-report. A bivariate correlated factors model was used to delineate the genetic correlation between age at menarche and disordered eating.
The analysis revealed a negative genetic correlation of −.18 in the best-fit model indicating that the genetic factors that influence younger age at menarche are associated with increased liability for disordered eating.
Future research should examine possible causes for this correlation such as the estrogen system and gene-environment interactions.
disordered eating; puberty; adolescence; twin study
Identifying children with childhood-onset neurodevelopmental problems (NDPs, defined here as autism spectrum disorders [ASDs], attention-deficit/hyperactivity disorder [AD/HD], tic disorders [TDs], learning disorders [LDs] and development coordination disorder), using easily administered screening instruments, is a prerequisite for epidemiological research. Such instruments are also clinically useful to prioritize children for comprehensive assessments, to screen risk groups, and to follow controls.
Autism–Tics, ADHD, and other Co-morbidities inventory (A-TAC) was developed to meet these requirements; here the A-TAC’s prospective and psychometric properties are examined, when used in a population-based, epidemiological setting.
Since 2004, parents of all Swedish twins have been asked to take part in an ongoing, nation-wide twin study (The Child and Adolescent Twin Study in Sweden). The study includes the A-TAC, carried out as a telephone interview with parents of twins aged 9 or 12. In the present study, screen-positive twins from three birth year cohorts (1993–1995) were invited to a comprehensive clinical follow-up (blinded for previous screening results) together with their co-twins and randomly selected, healthy controls at age 15 (Total N = 452).
Sensitivity and specificity of A-TAC scores for predicting later clinical diagnoses were good to excellent overall, with values of the area under the receiver operating characteristics curves ranging from 0.77 (AD/HD) to 0.91 (ASDs). Among children who were screen-positive for an ASD, 48% received a clinical diagnosis of ASDs. For AD/HD, the corresponding figure was also 48%, for LDs 16%, and for TDs 60%. Between 4% and 35% of screen-positive children did not receive any diagnosis at the clinical follow-up three years later. Among screen-negative controls, prevalence of ASDs, AD/HD, LDs, and TDs was 0%, 7%, 4%, and 2%, respectively.
The A–TAC appeared to be a valid instrument to assess NDPs in this population-based, longitudinal study. It has good-to-excellent psychometric properties, with an excellent ability to distinguish NDPs (mainly ASDs) from non-NDPs at least three years after the screening evaluations, although specific diagnoses did not correspond closely to actual clinical diagnoses.
Autism; Tics; AD/HD, and other Co-morbidities inventory; A-TAC; Screening; Mental disorders diagnosed in childhood; Co-morbidity; Cohort studies; Predictive value of tests; Sensitivity and specificity
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