Intergenerational transmission of ADHD behaviors: genetic and environmental pathways.

BACKGROUND: We investigate if covariation between parental and child attention-deficit hyperactivity disorder (ADHD) behaviors can be explained by environmental and/or genetic transmission. METHODS: We employed a large children-of-twins-and-siblings sample (N = 22 276 parents and 11 566 8-year-old children) of the Norwegian Mother, Father and Child Cohort Study. This enabled us to disentangle intergenerational influences via parental genes and parental behaviors (i.e. genetic and environmental transmission, respectively). Fathers reported on their own symptoms and mothers on their own and their child's symptoms. RESULTS: Child ADHD behaviors correlated with their mother's (0.24) and father's (0.10) ADHD behaviors. These correlations were largely due to additive genetic transmission. Variation in children's ADHD behaviors was explained by genetic factors active in both generations (11%) and genetic factors specific to the children (46%), giving a total heritability of 57%. There were small effects of parental ADHD behaviors (2% environmental transmission) and gene-environment correlation (3%). The remaining variability in ADHD behaviors was due to individual-specific environmental factors. CONCLUSIONS: The intergenerational resemblance of ADHD behaviors is primarily due to genetic transmission, with little evidence for parental ADHD behaviors causing children's ADHD behaviors. This contradicts theories proposing environmental explanations of intergenerational transmission of ADHD, such as parenting theories or psychological life-history theory.

Familial confounding or measurement error? How to interpret findings from sibling and co-twin control studies.

Epidemiological researchers often examine associations between risk factors and health outcomes in non-experimental designs. Observed associations may be causal or confounded by unmeasured factors. Sibling and co-twin control studies account for familial confounding by comparing exposure levels among siblings (or twins). If the exposure-outcome association is causal, the siblings should also differ regarding the outcome. However, such studies may sometimes introduce more bias than they alleviate. Measurement error in the exposure may bias results and lead to erroneous conclusions that truly causal exposure-outcome associations are confounded by familial factors. The current study used Monte Carlo simulations to examine bias due to measurement error in sibling control models when the observed exposure-outcome association is truly causal. The results showed that decreasing exposure reliability and increasing sibling-correlations in the exposure led to deflated exposure-outcome associations and inflated associations between the family mean of the exposure and the outcome. The risk of falsely concluding that causal associations were confounded was high in many situations. For example, when exposure reliability was 0.7 and the observed sibling-correlation was r = 0.4, about 30-90% of the samples (n = 2,000) provided results supporting a false conclusion of confounding, depending on how p-values were interpreted as evidence for a family effect on the outcome. The current results have practical importance for epidemiological researchers conducting or reviewing sibling and co-twin control studies and may improve our understanding of observed associations between risk factors and health outcomes. We have developed an app (SibSim) providing simulations of many situations not presented in this paper.

Prenatal maternal stress, child internalizing and externalizing symptoms, and the moderating role of parenting: findings from the Norwegian mother, father, and child cohort study.

BACKGROUND: Few studies have examined how parenting influences the associations between prenatal maternal stress and children's mental health. The objectives of this study were to examine the sex-specific associations between prenatal maternal stress and child internalizing and externalizing symptoms, and to assess the moderating effects of parenting behaviors on these associations. METHODS: This study is based on 15 963 mother-child dyads from the Norwegian Mother, Father, and Child Cohort Study (MoBa). A broad measure of prenatal maternal stress was constructed using 41 self-reported items measured during pregnancy. Three parenting behaviors (positive parenting, inconsistent discipline, and positive involvement) were assessed by maternal report at child age 5 years. Child symptoms of internalizing and externalizing disorders (depression, anxiety, attention-deficit hyperactivity disorder, conduct disorder, and oppositional-defiant disorder) were assessed by maternal report at age 8. Analyses were conducted using structural equation modeling techniques. RESULTS: Prenatal maternal stress was associated with child internalizing and externalizing symptoms at age 8; associations with externalizing symptoms differed by sex. Associations between prenatal maternal stress and child depression, and conduct disorder and oppositional-defiant disorder in males, became stronger as levels of inconsistent discipline increased. Associations between prenatal maternal stress and symptoms of attention-deficit hyperactivity disorder in females were attenuated as levels of parental involvement increased. CONCLUSIONS: This study confirms associations between prenatal maternal stress and children's mental health outcomes, and demonstrates that these associations may be modified by parenting behaviors. Parenting may represent an important intervention target for improving mental health outcomes in children exposed to prenatal stress.

Childhood personality and academic performance: A sibling fixed-effects study.

OBJECTIVE: This study investigated the associations between personality traits at age 8 and academic performance between ages 10 and 14, controlling for family confounds. BACKGROUND: Many studies have shown links between children's personality traits and their school performance. However, we lack evidence on whether these associations remain after genetic and environmental confounders are accounted for. METHOD: Sibling data from the Norwegian Mother and Child Cohort Study (MoBa) were used (n = 9701). First, we estimated the overall associations between Big Five personality traits and academic performance, including literacy, numeracy, and foreign language. Second, we added sibling fixed effects to remove unmeasured confounders shared by siblings as well as rating bias. RESULTS: Openness to Experience (between-person ß = 0.22 [95% CI: 0.21-0.24]) and Conscientiousness (between-person ß = 0.18 [95% CI 0.16-0.20]) were most strongly related to educational performance. Agreeableness (between-person ß = 0.06 [95% CI -0.08-0.04]) and Extraversion (between-person ß = 0.02 [95% CI 0.00-0.04]) showed small associations with educational performance. Neuroticism had a moderate negative association (between-person ß = -0.14 [95% CI -0.15-0.11]). All associations between personality and performance were robust to confounding: the within-family estimates from sibling fixed-effects models overlapped with the between-person effects. Finally, childhood personality was equally predictive of educational performance across ages and genders. CONCLUSIONS: Although family background is influential for academic achievement, it does not confound associations with personality. Childhood personality traits reflect unbiased and consistent individual differences in educational potential.

Positive maternal mental health attenuates the associations between prenatal stress and children's internalizing and externalizing symptoms.

Positive maternal mental health can improve perceptions of stressful situations and promote the use of adaptive coping strategies. However, few studies have examined how positive maternal mental health affects children's development. The aims of this study were to examine the associations between positive maternal mental health and children's internalizing and externalizing symptoms, and to ascertain whether positive maternal mental health moderated the associations between prenatal stress and children's internalizing and externalizing symptoms. This study is based on the Norwegian Mother, Father, and Child Cohort Study (MoBa), and comprised 36,584 mother-child dyads. Prenatal stress was assessed using 41 self-reported items measured during pregnancy. Positive maternal mental health (self-efficacy, self-esteem, and enjoyment) was assessed by maternal report during pregnancy and postpartum. Child internalizing and externalizing symptoms were assessed by maternal report at age 5. Structural equation modeling was used for analysis. Maternal self-efficacy, self-esteem, and enjoyment were negatively associated with internalizing and externalizing symptoms in males and females. The association between prenatal stress and internalizing symptoms in males was stronger at low than at high levels of maternal self-esteem and enjoyment, whereas for females, the association was stronger at low than at high levels of maternal self-esteem and self-efficacy. This study provides evidence of associations between positive maternal mental health and children's mental health, and suggests that higher positive maternal mental health may buffer against the impacts of prenatal stress. Positive maternal mental health may represent an important intervention target to improve maternal-child well-being and foster intergenerational resilience.

Educational attainment and mortality in schizophrenia.

BACKGROUND: Individuals suffering from schizophrenia have a reduced life expectancy with cardiovascular disease (CVD) as a major contributor. Low educational attainment is associated with schizophrenia, as well as with all-cause and CVD mortality. However, it is unknown to what extent low educational attainment can explain the increased mortality in individuals with schizophrenia. AIM: Here, we quantify associations between educational attainment and all-cause and CVD mortality in individuals with schizophrenia, and compare them with the corresponding associations in the general population. METHOD: All Norwegian citizens born between January 1, 1925, and December 31, 1959, were followed up from January 1, 1990, to December 31, 2014. The total sample included 1,852,113 individuals, of which 6548 were registered with schizophrenia. We estimated hazard ratios (HR) for all-cause and CVD mortality with Cox models, in addition to life years lost. Educational attainment for index persons and their parents were included in the models. RESULTS: In the general population individuals with low educational attainment had higher risk of all-cause (HR: 1.48 [95% CI: 1.47-1.49]) and CVD (HR: 1.59 [95% CI: 1.57-1.61]) mortality. In individuals with schizophrenia these estimates were substantially lower (all-cause: HR: 1.13 [95% CI: 1.05-1.21] and CVD: HR: 1.12 [95% CI: 0.98-1.27]). Low educational attainment accounted for 3.28 (3.21-3.35) life years lost in males and 2.48 (2.42-2.55) years in females in the general population, but was not significantly associated with life years lost in individuals with schizophrenia. Results were similar for parental educational attainment. CONCLUSIONS: Our results indicate that while individuals with schizophrenia in general have lower educational attainment and higher mortality rates compared with the general population, the association between educational attainment and mortality is smaller in schizophrenia subjects than in the general population.

Mechanisms linking parental educational attainment with child ADHD, depression, and academic problems: a study of extended families in The Norwegian Mother, Father and Child Cohort Study.

BACKGROUND: Low educational attainment in parents is associated with child psychopathology. It is not clear whether the associations are due to risk factors that family members share or due to effects of maternal or paternal education on the offspring. We investigate whether associations between maternal and paternal educational attainment and child symptoms of attention deficit/hyperactivity disorder (ADHD), depression, and academic problems are due to shared genetic factors, shared family environmental factors, or effects of the parental phenotype educational attainment itself. METHODS: This study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). The sample comprised 34,958 children (17,128 girls) in 28,372 extended-family units. We used data from related nuclear families linked by siblings in the parent generation. We applied a quasi-experimental extended children-of-twins design that included siblings in both generations and took account of nonrandom mating by including partners. Educational attainment was self-reported by mothers and fathers. Mothers reported children's symptoms of ADHD, symptoms of depression, and academic problems by questionnaire when the children were 8 years old. RESULTS: Children of lowly educated parents scored higher on all outcomes and had an approximate doubling of the risk of high symptom levels. The association between maternal and paternal educational attainment and child symptoms of ADHD and academic problems persisted after controlling for shared genetic and family environmental factors. Phenotypic transmission to depression was weaker and in the best fitting model fully explained by genetic factors shared by the two generations. CONCLUSIONS: Associations between educational attainment of mothers and fathers and child symptoms of ADHD and academic problems could not be ascribed to shared familial risk factors, whereas associations with symptoms of depression could. Parental education or resources and behaviors resulting from low education might be targets of interventions aimed at reducing symptoms of ADHD and academic problems.

Continuity of genetic and environmental influences on clinically assessed major depression from ages 18 to 45.

BACKGROUND: Studies on the stability of genetic risk for depression have relied on self-reported symptoms rather than diagnoses and/or short follow-up time. Our aim is to determine to what degree genetic and environmental influences on clinically assessed major depressive disorder (MDD) are stable between age 18 and 45. METHODS: A population-based sample of 11 727 twins (6875 women) born between 1967 and 1991 was followed from 2006 to 2015 in health registry data from primary care that included diagnoses provided by treating physicians. Individuals with schizophrenia or bipolar disorder (n = 163) were excluded. We modelled genetic and environmental risk factors for MDD in an accelerated longitudinal design. RESULTS: The best-fitting model indicated that genetic influences on MDD were completely stable from ages 18 to 45 and explained 38% of the variance. At each age, the environmental risk of MDD was determined by the risk at the preceding observation, plus new environmental risk, with an environmental correlation of +0.60 over 2 years. The model indicated no effects of shared environment and no environmental effects stable throughout the observational period. All long-term stability was therefore explained by genetic factors. CONCLUSIONS: Different processes unfolded in the genetic and environmental risk for MDD. The genetic component is stable from later adolescence to middle adulthood and accounted for nearly all long-term stability. Therefore, molecular genetic studies can use age-heterogenous samples when investigating genetic risk variants of MDD. Environmental risk factors were stable over a short span of years with associations rapidly decreasing and no evidence of permanent environmental scarring.

Joint factorial structure of psychopathology and personality.

BACKGROUND: Normative and pathological personality traits have rarely been integrated into a joint large-scale structural analysis with psychiatric disorders, although a recent study suggested they entail a common individual differences continuum. METHODS: We explored the joint factor structure of 11 psychiatric disorders, five personality-disorder trait domains (DSM-5 Section III), and five normative personality trait domains (the 'Big Five') in a population-based sample of 2796 Norwegian twins, aged 19‒46. RESULTS: Three factors could be interpreted: (i) a general risk factor for all psychopathology, (ii) a risk factor specific to internalizing disorders and traits, and (iii) a risk factor specific to externalizing disorders and traits. Heritability estimates for the three risk factor scores were 48% (95% CI 41‒54%), 35% (CI 28‒42%), and 37% (CI 31‒44%), respectively. All 11 disorders had uniform loadings on the general factor (congruence coefficient of 0.991 with uniformity). Ignoring sign and excluding the openness trait, this uniformity of factor loadings held for all the personality trait domains and all disorders (congruence 0.983). CONCLUSIONS: Based on our findings, future research should investigate joint etiologic and transdiagnostic models for normative and pathological personality and other psychopathology.

Genetically Informative Mediation Modeling Applied to Stressors and Personality-Disorder Traits in Etiology of Alcohol Use Disorder.

A statistical mediation model was developed within a twin design to investigate the etiology of alcohol use disorder (AUD). Unlike conventional statistical mediation models, this biometric mediation model can detect unobserved confounding. Using a sample of 1410 pairs of Norwegian twins, we investigated specific hypotheses that DSM-IV personality-disorder (PD) traits mediate effects of childhood stressful life events (SLEs) on AUD, and that adulthood SLEs mediate effects of PDs on AUD. Models including borderline PD traits indicated unobserved confounding in phenotypic path coefficients, whereas models including antisocial and impulsive traits did not. More than half of the observed effects of childhood SLEs on adulthood AUD were mediated by adulthood antisocial and impulsive traits. Effects of PD traits on AUD 5‒10 years later were direct rather than mediated by adulthood SLEs. The results and the general approach contribute to triangulation of developmental origins for complex behavioral disorders.

Explaining the association between anxiety disorders and alcohol use disorder: A twin study.

BACKGROUND: It is unknown whether social anxiety disorder (SAD) has a unique association with alcohol use disorder (AUD) over and beyond that of other anxiety disorders, how the associations develop over time, and whether the associations are likely to be causal. METHODS: Diagnoses of AUD, SAD, generalized anxiety disorder, panic disorder, agoraphobia, and specific phobias were assessed twice using the Composite International Diagnostic Interview among 2,801 adult Norwegian twins. The data were analyzed using logistic regression analyses and multivariate biometric structural equation modeling. RESULTS: SAD had the strongest association with AUD, and SAD predicted AUD over and above the effect of other anxiety disorders. In addition, SAD was prospectively associated with AUD, whereas other anxiety disorders were not. AUD was associated with a slightly elevated risk of later anxiety disorders other than SAD. Biometric modeling favored a model where SAD influenced AUD compared to models where the relationship was reversed or due to correlated risk factors. Positive associations between AUD and other anxiety disorders were fully explained by shared genetic risk factors. CONCLUSIONS: Unlike other anxiety disorders, SAD plausibly has a direct effect on AUD. Interventions aimed at prevention or treatment of SAD may have an additional beneficial effect of preventing AUD, whereas interventions aimed at other anxiety disorders are unlikely to have a similar sequential effect on AUD.

Genetic and Environmental Structure of DSM-IV Criteria for Antisocial Personality Disorder: A Twin Study.

Results from previous studies on DSM-IV and DSM-5 Antisocial Personality Disorder (ASPD) have suggested that the construct is etiologically multidimensional. To our knowledge, however, the structure of genetic and environmental influences in ASPD has not been examined using an appropriate range of biometric models and diagnostic interviews. The 7 ASPD criteria (section A) were assessed in a population-based sample of 2794 Norwegian twins by a structured interview for DSM-IV personality disorders. Exploratory analyses were conducted at the phenotypic level. Multivariate biometric models, including both independent and common pathways, were compared. A single phenotypic factor was found, and the best-fitting biometric model was a single-factor common pathway model, with common-factor heritability of 51% (95% CI 40-67%). In other words, both genetic and environmental correlations between the ASPD criteria could be accounted for by a single common latent variable. The findings support the validity of ASPD as a unidimensional diagnostic construct.

Mood, anxiety, and alcohol use disorders and later cause-specific sick leave in young adult employees.

BACKGROUND: Mental disorders strongly influence work capability in young adults, but it is not clear which disorders that are most strongly associated with sick leave, and which diagnoses that are stated on the sick leave certificates. Better knowledge of the impairments associated with different mental disorders is needed for optimal planning of interventions and prioritization of health services. In the current study, we investigate the prospective associations between eight mood, anxiety, and alcohol use disorders, and later sick leave granted for mental, somatic, or any disorder. METHODS: Lifetime mental disorders were assessed by structured diagnostic interviews in 2,178 young adults followed for eight years with registry data on sick leave. Relative risk ratios were estimated for the associations between each mental disorder and the different forms of sick leave. RESULTS: All included diagnoses were associated with later sick leave. In adjusted analyses, major depressive disorder and generalized anxiety disorder were the strongest predictors of sick leave granted for mental disorders, whereas social anxiety disorder and specific phobia were the strongest predictors of sick leave granted for somatic disorders. Specific phobia and major depressive disorder had the highest attributable fractions for all-cause sick leave. CONCLUSIONS: Mood and anxiety disorders constituted independent risk factors for all cause sick leave, whereas alcohol use disorders seemed to be of less importance in young adulthood. Disorders characterised by distress were most strongly associated with sick leave granted for mental disorders, whereas disorders characterised by fear primarily predicted sick leave granted for somatic conditions. A large part of all sick leave is related to specific phobia, due to the high prevalence of this disorder. The impairment associated with this common disorder may be under-acknowledged, and it could decrease work capacity among individuals with somatic disorders. This disorder has good treatment response and may be overlooked as a target for interventions aimed at prevention of sick leave.

Mental distress predicts divorce over 16 years: the HUNT study.

BACKGROUND: The association between mental distress and divorce is well established in the literature. Explanations are commonly classified within two different frameworks; social selection (mentally distressed people are selected out of marriage) and social causation (divorce causes mental distress). Despite a relatively large body of literature on this subject, selection effects are somewhat less studied, and research based on data from both spouses is scarce. The purpose of the present study is to investigate selection effects both at the individual level and the couple level. METHODS: The current study is based on couple-level data from a Norwegian representative sample including 20,233 couples. Long-term selection effects were tested for by means of Cox proportional hazard models, using mental distress in both partners at baseline as predictors of divorce the next 16 years. Three identical sets of analyses were run. The first included the total sample, whereas the second and third excluded couples who divorced within the first 4 or 8 years after baseline, respectively. An interaction term between mental distress in husband and in wife was specified and tested. RESULTS: Hazard of divorce was significantly higher in couples with one mentally distressed partner than in couples with no mental distress in all analyses. There was also a significant interaction effect showing that the hazard of divorce for couples with two mentally distressed partners was higher than for couples with one mentally distressed partner, but lower than what could be expected from the combined main effects of two mentally distressed partners. CONCLUSIONS: Our results suggest that mentally distressed individuals are selected out of marriage. We also found support for a couple-level effect in which spouse similarity in mental distress to a certain degree seems to protect against divorce.

Socioeconomic status and sick leave granted for mental and somatic disorders: a prospective study of young adult twins.

BACKGROUND: Low socioeconomic status (SES), indicated by low income and education, has consistently been found to be a strong predictor of sick leave. Several possible pathways from SES to sick leave have been described in previous literature, but there are also evidence indicating that the association can be confounded by common underlying factors. This study utilizes a population-based sample of employed young adult twins to estimate (i) the degree to which education and income are prospectively related to sick leave granted for mental, somatic, and any disorder, and (ii) whether these associations are confounded by familial factors. METHODS: Registry data on educational attainment and income at age 30 and subsequent sick leave were available for 6,103 employed young adult twins, among which there were 2,024 complete twin pairs. The average follow-up time was 6.57 years. Individual-level associations and fixed effects within twin pairs were estimated. RESULTS: Low education and income were associated with sick leave granted for both mental and somatic disorders, and with sick leave granted for any disorder. Associations were attenuated within dizygotic twin pairs and reduced to non-significance within monozygotic twin pairs, suggesting influence of familial factors on the associations between SES and sick leave. CONCLUSIONS: Low SES is associated with a higher level of sick leave granted for both mental and somatic disorders among young adults, but these associations are confounded by factors that are common to co-twins. Education and income are therefore not likely to strongly affect sick leave in young adulthood.

Genetic similarity between relatives provides evidence on the presence and history of assortative mating.

Assortative mating - the non-random mating of individuals with similar traits - is known to increase trait-specific genetic variance and genetic similarity between relatives. However, empirical evidence is limited for many traits, and the implications hinge on whether assortative mating has started recently or many generations ago. Here we show theoretically and empirically that genetic similarity between relatives can provide evidence on the presence and history of assortative mating. First, we employed path analysis to understand how assortative mating affects genetic similarity between family members across generations, finding that similarity between distant relatives is more affected than close relatives. Next, we correlated polygenic indices of 47,135 co-parents from the Norwegian Mother, Father, and Child Cohort Study (MoBa) and found genetic evidence of assortative mating in nine out of sixteen examined traits. The same traits showed elevated similarity between relatives, especially distant relatives. Six of the nine traits, including educational attainment, showed greater genetic variance among offspring, which is inconsistent with stable assortative mating over many generations. These results suggest an ongoing increase in familial similarity for these traits. The implications of this research extend to genetic methodology and the understanding of social and economic disparities.

The structure of psychiatric comorbidity without selection and assortative mating.

The widespread comorbidity observed across psychiatric disorders may be the result of processes such as assortative mating, gene-environment correlation, or selection into population studies. Between-family analyses of comorbidity are subject to these sources of bias, whereas within-family analyses are not. Because of Mendelian inheritance, alleles are randomly assigned within families, conditional on parental alleles. We exploit this variation to compare the structure of comorbidity across broad psychiatric polygenic scores when calculated either between-family (child polygenic scores) or within-family (child polygenic scores regressed on parental polygenic scores) in over 25,000 genotyped parent-offspring trios from the Norwegian Mother Father and Child Cohort study (MoBa). We fitted a series of factor models to the between- and within-family data, which consisted of a single genetic p-factor and a varying number of uncorrelated subfactors. The best-fitting model was identical for between- and within-family analyses and included three subfactors capturing variants associated with neurodevelopment, psychosis, and constraint, in addition to the genetic p-factor. Partner genetic correlations, indicating assortative mating, were not present for the genetic p-factor, but were substantial for the psychosis (b = 0.081;95% CI [0.038,0.124]) and constraint (b = 0.257;95% CI [0.075,0.439]) subfactors. When average factor levels for MoBa mothers and fathers were compared to a population mean of zero we found evidence of sex-specific participation bias, which has implications for the generalizability of findings from cohort studies. Our results demonstrate the power of the within-family design for better understanding the mechanisms driving psychiatric comorbidity and their consequences on population health.

Alcohol use and spousal mental distress in a population sample: the Nord-Trøndelag Health Study.

BACKGROUND: It is a widely held notion that alcohol abuse is related to mental distress in the spouse. Research has substantiated this notion by showing a tendency for spouses of alcohol abusers to experience more mental distress than spouses of non-abusers. However, the picture seems to be more complex, as some results do not show a significant effect or even less mental distress among spouses of alcohol abusers with the highest alcohol consumption. The present study investigates the association between spousal mental distress and both a high consumption of alcohol and having experienced alcohol related problems. METHODS: Norwegian population-based questionnaire data from the Nord-Trøndelag Health Study (HUNT 2) were analyzed. In total 11,584 couples were eligible for analysis. Alcohol consumption was measured by numerical indicators of alcohol amount and frequency of drinking, whereas alcohol-related problems (i.e. having been criticized for excessive drinking) were measured by the CAGE Alcohol Screening Questionnaire. Multivariate hierarchical regression analyses were performed. RESULTS: Results revealed that alcohol consumption was significantly associated with a decrease in spousal mental distress, whereas alcohol-related problems were associated with an increase in spousal mental distress when adjusted for each other. Interaction effects indicated that couples discordant for drinking problems experienced more mental distress than spouses concordant for drinking problems. CONCLUSIONS: The results of our study indicate that alcohol-related problems constitute a clear risk factor for spousal mental distress. On the other hand, a high consumption of alcohol per se was related to lower levels of spousal mental distress, after adjusting for the alcohol-related problems perceived by the alcohol consumer him/herself. All effect sizes were small, but the trends were clear, challenging the notion that a high consumption of alcohol is exclusively and under all circumstances negative for the spouse.

Social anxiety disorder is a risk factor for alcohol use problems in the National Comorbidity Surveys.

BACKGROUND: According to the self-medication and biopsychosocial models, individuals with social anxiety disorder (SAD) are at increased risk of developing an alcohol use disorder (AUD) as alcohol represents a maladaptive coping mechanism for some sufferers of SAD. The SAD-to-AUD causation was earlier supported in Norwegian longitudinal twin data and later questioned using longitudinal data from the USA. METHODS: We re-analyzed partly the same USA-based data (National Comorbidity Surveys, n = 5001), conducting theoretical and simulation analyses on different formulations of temporality and using real-data Logistic regression analysis to investigate whether baseline SAD was associated with AUD at the follow-up. RESULTS: Upon proper analysis of temporality, SAD preceded AUD. Specifically, SAD was the only one of the seven anxiety disorders that predicted 10-year later AUD after adjusting for all other anxiety disorders and AUD at the baseline (odds ratio was 1.70% and 95% confidence interval 1.12-2.57). SAD was also associated with incident AUD (OR = 1.64, 95% CI = 1.14-2.37). We provide formal, simulation-based, and data-based arguments on how certain flawed models of incidence attenuate the temporal association. CONCLUSIONS: We demonstrated temporality and specificity in SAD-to-AUD association, which are considered signs of causation. We further identified and discussed problems in previous statistical analyses with different conclusions. Our findings add support for models positing causal effects of SAD on AUD, such as the self-medication and biopsychosocial models. The available evidence suggests that treating SAD should incur better chances of preventing AUD compared to treating other anxiety disorders, which lack comparable evidence on causation.

The association between parental internalizing disorders and child school performance.

Parents play a crucial role in children's lives. Despite high prevalences of anxiety and depression, we do not know how these disorders among parents associate with child school performance in Norway. We use regression models to estimate associations between parental mental disorders and child school performance, while adjusting for some social and genetic confounders. Parental anxiety and depression were assessed from administrative registers of government funded health service consultations for all individuals in Norway with children born between 1992 and 2002. School performance was assessed as standardized grade point average at the end of compulsory education when children are 16 years old. Associations were also considered in samples of adoptees and among differentially affected siblings. We find that 18.8% of children have a parent with an anxiety or depression diagnosis from primary care during the last three years of compulsory education (yearly prevalence: 11.5%). There is a negative association between these parental mental disorders and child school outcomes (z = 0.43). This association was weakened, but statistically significant among differentially exposed siblings (z = 0.04), while disappearing in adoptee children. Many children experience that their parents have anxiety or depression and receive a diagnosis from primary care. On average, these children have lower school performance. The association is attenuated when comparing differentially exposed siblings and disappears in adoptee children. These results have a poor fit with the hypothesis that parental internalizing is an influential causal factor in determining children's educational success.