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Background: Despite being considered a measure of environmental risk, reported life events are partly heritable. One mechanism that may contribute to this heritability is genetic influences on sensitivity, relating to how individuals process and interpret internal and external signals. The aim of this study was to explore the genetic and environmental overlap between self-reported life events and measures of sensitivity., Methods: At age 17, 2,939 individuals from the Twins Early Development Study (TEDS) completed measures of anxiety sensitivity (Children's Anxiety Sensitivity Index), environmental sensitivity (Highly Sensitive Child Scale) and reported their experience of 20 recent life events. Using multivariate Cholesky decomposition models, we investigated the shared genetic and environmental influences on the associations between these measures of sensitivity and the number of reported life events, as well as both negative and positive ratings of life events., Results: The majority of the associations between anxiety sensitivity, environmental sensitivity and reported life events were explained by shared genetic influences (60%-75%), with the remainder explained by nonshared environmental influences (25%-40%). Environmental sensitivity showed comparable genetic correlations with both negative and positive ratings of life events (r A  = .21 and .15), anxiety sensitivity only showed a significant genetic correlation with negative ratings of life events (r A  = .33). Approximately 10% of the genetic influences on reported life events were accounted for by influences shared with anxiety sensitivity and environmental sensitivity., Conclusion: Differences in how individuals process the contextual aspects of the environment or interpret their own physical and emotional response to environmental stimuli may be one mechanism through which genetic liability influences the subjective experience of life events., (© 2022 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Background: Shame is considered a maladaptive self-conscious emotion that commonly co-occurs alongside depression and anxiety. Little is known, however, about the aetiology of shame and its associations with depression and anxiety. We estimated, for the first time, genetic and environmental influences on shame and on its associations with depression and anxiety in adolescence., Methods: The sample was twin and sibling pairs from the Genesis 1219 Study (Time 1, N = 2,685; males 42.8%, M age  = 14.95, SD = 1.67, age range: 12-21; Time 2, N = 1618; males 39.7%, M age  = 16.97, SD = 1.64, age range: 14-23). Participants completed validated questionnaires to measure shame (at Time 1), depression and anxiety (at Times 1 and 2)., Results: Shame was moderately to strongly associated with concurrent depression and anxiety. Prospectively, shame was significantly associated with an increase in depression, but not anxiety. Genetic analyses revealed that shame was moderately heritable with substantial nonshared environmental influence. The associations between shame and concurrent depression and anxiety were primarily accounted for by overlapping genetic influences. Prospectively, the association between shame and later depression was primarily accounted for by genetic and nonshared environmental influences shared with earlier depression. The unique association between shame and later depression was mostly explained by common nonshared environmental influences., Conclusions: The findings offer novel evidence regarding aetiology of shame-although moderately heritable, shame in adolescents may also result from nonshared environmental factors. Genetic and nonshared environmental influences contribute to the co-occurrence of shame with depression and anxiety., (© 2021 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

Background: Generalized anxiety and depression are extremely prevalent and debilitating. There is evidence for age and sex variability in symptoms of depression, but despite comorbidity it is unclear whether this extends to anxiety symptomatology. Studies using questionnaire sum scores typically fail to address this phenotypic complexity., Method: We conducted exploratory and confirmatory factor analyses on Generalized Anxiety Disorder (GAD-7) and Patient Health Questionnaire (PHQ-9) items to identify latent factors of anxiety and depression in participants from the Genetic Links to Anxiety and Depression Study (N = 35,637; 16-93 years). We assessed age- and sex-related variability in latent factors and individual symptoms using multiple logistic regression., Results: Four factors of mood, worry, motor, and somatic symptoms were identified (comparative fit index [CFI] = 0.99, Tucker-Lewis Index [TLI] = 0.99, root mean square error of approximation [RMSEA] = 0.07, standardized root mean square residuals [SRMR] = 0.04). Symptoms of irritability (odds ratio [OR] = 0.81) were most strongly associated with younger age, and sleep change (OR = 1.14) with older age. Males were more likely to report mood and motor symptoms (p < .001) and females to report somatic symptoms (p < .001)., Conclusion: Significant age and sex variability suggest that classic diagnostic criteria reflect the presentation most commonly seen in younger males. This study provides avenues for diagnostic adaptation and factor-specific interventions., (© 2021 The Authors. Depression and Anxiety published by Wiley Periodicals LLC.)

Background: Many studies detect associations between parent behaviour and child symptoms of anxiety and depression. Despite knowledge that anxiety and depression are influenced by a complex interplay of genetic and environmental risk factors, most studies do not account for shared familial genetic risk. Quantitative genetic designs provide a means of controlling for shared genetics, but rely on observed putative exposure variables, and require data from highly specific family structures., Methods: The intergenerational genomic method, Relatedness Disequilibrium Regression (RDR), indexes environmental effects of parents on child traits using measured genotypes. RDR estimates how much the parent genome influences the child indirectly via the environment, over and above effects of genetic factors acting directly in the child. This 'genetic nurture' effect is agnostic to parent phenotype and captures unmeasured heritable parent behaviours. We applied RDR in a sample of 11,598 parent-offspring trios from the Norwegian Mother, Father and Child Cohort Study (MoBa) to estimate parental genetic nurture separately from direct child genetic effects on anxiety and depression symptoms at age 8. We tested for mediation of genetic nurture via maternal anxiety and depression symptoms. Results were compared to a complementary non-genomic pedigree model., Results: Parental genetic nurture explained 14% of the variance in depression symptoms at age 8. Subsequent analyses suggested that maternal anxiety and depression partially mediated this effect. The genetic nurture effect was mirrored by the finding of family environmental influence in our pedigree model. In contrast, variance in anxiety symptoms was not significantly influenced by common genetic variation in children or parents, despite a moderate pedigree heritability., Conclusions: Genomic methods like RDR represent new opportunities for genetically sensitive family research on complex human traits, which until now has been largely confined to adoption, twin and other pedigree designs. Our results are relevant to debates about the role of parents in the development of anxiety and depression in children, and possibly where to intervene to reduce problems.

Do associations between maternal anxiety symptoms and offspring mental health remain after comparing differentially exposed siblings? Participants were 17,724 offspring siblings and 11,553 mothers from the Norwegian Mother and Child Cohort study. Mothers reported anxiety and depressive symptoms at 30 weeks' gestation, and 0.5, 1.5, 3, and 5 years postpartum. Child internalizing and externalizing problems were assessed at ages 1.5, 3, and 5, and modeled using multilevel analyses with repeated measures nested within siblings, nested within mothers. Maternal pre- and postnatal anxiety were no longer associated with child internalizing or externalizing problems after adjusting for maternal depression and familial confounding. Maternal anxiety when the children were in preschool age, however, remained significantly associated with child internalizing but not externalizing problems., (© 2018 Society for Research in Child Development.)

Background: Anxiety and depression are common, debilitating and costly. These disorders are influenced by multiple risk factors, from genes to psychological vulnerabilities and environmental stressors, but research is hampered by a lack of sufficiently large comprehensive studies. We are recruiting 40,000 individuals with lifetime depression or anxiety and broad assessment of risks to facilitate future research., Methods: The Genetic Links to Anxiety and Depression (GLAD) Study (www.gladstudy.org.uk) recruits individuals with depression or anxiety into the NIHR Mental Health BioResource. Participants invited to join the study (via media campaigns) provide demographic, environmental and genetic data, and consent for medical record linkage and recontact., Results: Online recruitment was effective; 42,531 participants consented and 27,776 completed the questionnaire by end of July 2019. Participants' questionnaire data identified very high rates of recurrent depression, severe anxiety, and comorbidity. Participants reported high rates of treatment receipt. The age profile of the sample is biased toward young adults, with higher recruitment of females and the more educated, especially at younger ages., Discussion: This paper describes the study methodology and descriptive data for GLAD, which represents a large, recontactable resource that will enable future research into risks, outcomes, and treatment for anxiety and depression., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Anxiety in parents is associated with anxiety in offspring, although little is known about the mechanisms underpinning these intergenerational associations. We conducted the first genetically sensitive study to simultaneously examine the effects of mother, father and child anxiety symptoms on each other over time., Method: Adoptive parent and child symptoms were measured at child ages 6, 7 and 8 years from 305 families involved in the Early Growth and Development Study, using a prospective adoption design. Children were adopted at birth to nonrelatives, and composite data on internalising problems within birth families were used as a proxy measure of offspring inherited risk for anxiety. Structural equation models were fitted to the data to examine prospective associations between adoptive mother, father and child symptoms, whilst accounting for individuals' symptom stability over time., Results: Child anxiety symptoms at age 7 predicted adoptive mothers' anxiety symptoms at age 8. No mother-to-child or child-to-father effects were observed. These results were consistent in sensitivity analyses using only paternal offspring reports and using a second measure of child anxiety symptoms. Fathers' anxiety symptoms at child age 6 prospectively predicted child symptoms, but only when paternal offspring reports were included in the model. Composite data on birth family internalising problems were not associated with child anxiety symptoms., Conclusions: Results show environmentally mediated associations between parent and child anxiety symptoms. Results support developmental theories suggesting that child anxiety symptoms can exert influence on caregivers, and mothers and fathers may play unique roles during the development of child symptoms. Further research is needed on the role of genetic transmission associated with anxiety symptoms in biologically related families. In the meantime, researchers and clinicians should strive to include fathers in assessments and consider the effects of child symptoms on caregivers., (© 2019 The Authors. Journal of Child Psychology and Psychiatry published by John Wiley & Sons Ltd on behalf of Association for Child and Adolescent Mental Health.)

The majority of those who experience clinical anxiety and/or depressive symptoms in the population do not receive treatment. Studies investigating inequalities in treatment outcomes rarely consider that individuals respond differently to their experience of the environment. Much of our environment is under genetic influence, via our behaviour, whereby individuals actively select their experiences. If genes influence who seeks and receives treatment, selection bias will confound genomic studies of treatment response. Furthermore, if some individuals are at high genetic risk of needing but not commencing treatment, then greater efforts could be made to engage them. The role of common genetic variation on four lifetime treatment-seeking behaviours (treatment-seeking, treatment-receipt, self-help, self-medication with alcohol/drugs) was examined in participants of the UK Biobank (sample size range: 48,106 - 75,322). Treatment-related behaviours were only modestly heritable in these data. Nonetheless, genetic correlations reveal substantial genetic overlap between lifetime treatment-related behaviours and psychiatric disorders, symptoms and behavioural traits. To our knowledge, this is the first study to examine genetic influences on treatment-related behaviours. Further work is required to determine whether genetic factors could be used alongside clinical, social and demographic factors to identify at risk groups and inform strategies which target early intervention., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The transition from primary to secondary school is often associated with a period of heightened anxiety and worry. For most children, any feelings of anxiety subside relatively quickly but for a small minority, emotional difficulties can continue into the first year of secondary school and beyond. This study recruited 109 children and measured their anxiety symptoms and school concerns toward the end of primary school and again at the end of their first term of secondary school. We investigated for the first time whether pre-transition measures of attentional and interpretation bias, and the magnitude of change in attentional bias toward and away from threat stimuli were associated with pre- and post-transition measures of anxiety and school concerns, and the change in these measures over time. Over 50% of the current sample exceeded clinical levels of anxiety at pre-transition. However, anxiety symptoms and school concerns had significantly reduced by post-transition. Higher levels of pre-transition anxiety or school concerns, and a greater magnitude of change in attentional bias towards threat stimuli predicted a larger reduction in anxiety symptoms and school concerns across the transition period. A greater interpretation bias toward threat was associated with higher pre-transition anxiety symptoms and school concerns but not post-transition scores, or the change in these scores. While many children experience heightened anxiety prior to school transition, this appears to be largely temporary and self-resolves. Nonetheless, the current findings highlight the importance of monitoring children's anxiety and concerns, and related cognitive processes during this important transition period.

Twin studies have shown that emotional problems (anxiety and depression) in childhood and adolescence are moderately heritable (~20-50%). In contrast, DNA-based 'SNP heritability' estimates are generally <15% and non-significant. One notable feature of emotional problems is that they can be somewhat transient, but the moderate stability seen across time and across raters is predominantly influenced by stable genetic influences. This suggests that by capturing what is in common across time and across raters, we might be more likely to tap into any underlying genetic vulnerability. We therefore hypothesised that a phenotype capturing the pervasive stability of emotional problems would show higher heritability. We fitted single-factor latent trait models using 12 emotional problems measures across ages 7, 12 and 16, rated by parents, teachers and children themselves in the Twins Early Development Study sample. Twin and SNP heritability estimates for stable emotional problems (N = 6110 pairs and 6110 unrelated individuals, respectively) were compared to those for individual measures. Twin heritability increased from 45% on average for individual measures to 76% (se = 0.023) by focusing on stable trait variance. SNP heritability rose from 5% on average (n.s.) to 14% (se = 0.049; p = 0.002). Heritability was also higher for stable within-rater composites. Polygenic scores for both adult anxiety and depression significantly explained variance in stable emotional problems (0.4%; p = 0.0001). The variance explained was more than in most individual measures. Stable emotional problems also showed significant genetic correlation with adult depression and anxiety (average = 52%). These results demonstrate the value of examining stable emotional problems in gene-finding and prediction studies.

Attentional control theory (ACT) proposes that anxiety is associated with executive functioning deficits. The theory has been widely investigated in adults. The current study tested whether symptoms of childhood anxiety and depression were associated with experimentally measured attentional control in the context of non-emotional and emotional stimuli. Sixty-one children (mean age = 9.23 years, range = 8.39-10.41) reported their trait anxiety and depression symptoms and completed three visual search tasks. The tasks used a variant of an irrelevant singleton paradigm and measured attentional capture by task-irrelevant non-emotional (color) and emotional (facial expressions) distractors. Significant attentional capture by both non-emotional and emotional distractors was observed, and was significantly correlated with trait anxiety and symptoms of depression. The strength of relationship between attentional capture and the symptoms did not differ significantly for non-emotional and emotional distractors. The results suggest that symptoms of childhood anxiety and depression are associated with poorer attentional control both in the presence of emotional and non-emotional stimuli, supporting ACT in younger populations. This attentional deficit in the context of non-emotional information might be as central to childhood internalizing symptoms as attentional biases often observed on tasks investigating processing of emotional stimuli.

Background: Mindfulness-based therapies have been shown to be effective in treating depression and reducing cognitive biases. Anxiety sensitivity is one cognitive bias that may play a role in the association between mindfulness and depressive symptoms. It refers to an enhanced sensitivity toward symptoms of anxiety, with a belief that these are harmful. Currently, little is known about the mechanisms underpinning the association between mindfulness, depression, and anxiety sensitivity. The aim of this study was to examine the role of genetic and environmental factors in trait mindfulness, and its genetic and environmental overlap with depressive symptoms and anxiety sensitivity., Methods: Over 2,100 16-year-old twins from a population-based study rated their mindfulness, depressive symptoms, and anxiety sensitivity., Results: Twin modeling analyses revealed that mindfulness is 32% heritable and 66% due to nonshared environmental factors, with no significant influence of shared environment. Genetic influences explained over half of the moderate phenotypic associations between low mindfulness, depressive symptoms, and anxiety sensitivity. About two-thirds of genetic influences and almost all nonshared environmental influences on mindfulness were independent of depression and anxiety sensitivity., Conclusions: This is the first study to show that both genes and environment play an important role in the etiology of mindfulness in adolescence. Future research should identify the specific environmental factors that influence trait mindfulness during development to inform targeted treatment and resilience interventions. Shared genetic liability underpinning the co-occurrence of low mindfulness, depression, and anxiety sensitivity suggests that the biological pathways shared between these traits should also be examined., (© 2015 The Authors. Depression and Anxiety published by Wiley Periodicals, Inc.)

Autism shows a high degree of comorbidity with anxiety disorders. Adolescence is a time of increased stress and vulnerability to internalising problems. This study addresses for the first time the degree of genetic and environmental overlap between autistic traits (total measure and subscales) and internalising traits in a community-based adolescent twin sample. Parents of 12-14-year-old twins (N = 3,232 pairs; 3,460 males, 3,004 females) reported on the twins' internalising and autistic traits. Autistic trait subscales were created using principal component analysis. Bivariate twin model-fitting was conducted. Autistic and internalising traits correlated moderately (r = 0.30). Genetic influences on individual traits were substantial but genetic overlap between traits was moderate (genetic correlation: males = 0.30, females = 0.12). Shared environmental influences were low for internalising traits and moderate for autistic traits, and showed considerable overlap (shared environmental correlation: males = 0.53, females = 1). Nonshared environmental influences were moderate for internalising traits and low for autistic traits and showed low overlap. A multiple component solution was found for autistic traits and of the derived subscales, autistic-like 'Social Unease' showed the most phenotypic and genetic overlap with internalising traits.

Background: Twin studies have shown that anxiety in a general population sample of children involves both domain-general and trait-specific genetic effects. For this reason, in an attempt to identify genes responsible for these effects, we investigated domain-general and trait-specific genetic associations in the first genome-wide association (GWA) study on anxiety-related behaviours (ARBs) in childhood., Methods: The sample included 2810 7-year-olds drawn from the Twins Early Development Study (TEDS) with data available for parent-rated anxiety and genome-wide DNA markers. The measure was the Anxiety-Related Behaviours Questionnaire (ARBQ), which assesses four anxiety traits and also yields a general anxiety composite. Affymetrix GeneChip 6.0 DNA arrays were used to genotype nearly 700,000 single-nucleotide polymorphisms (SNPs), and IMPUTE v2 was used to impute more than 1 million SNPs. Several GWA associations from this discovery sample were followed up in another TEDS sample of 4804 children. In addition, Genome-wide Complex Trait Analysis (GCTA) was used on the discovery sample, to estimate the total amount of variance in ARBs that can be accounted for by SNPs on the array., Results: No SNP associations met the demanding criterion of genome-wide significance that corrects for multiple testing across the genome (p<5×10(-8)). Attempts to replicate the top associations did not yield significant results. In contrast to the substantial twin study estimates of heritability which ranged from 0.50 (0.03) to 0.61 (0.01), the GCTA estimates of phenotypic variance accounted for by the SNPs were much lower 0.01 (0.11) to 0.19 (0.12)., Conclusions: Taken together, these GWAS and GCTA results suggest that anxiety--similar to height, weight and intelligence--is affected by many genetic variants of small effect, but unlike these other prototypical polygenic traits, genetic influence on anxiety is not well tagged by common SNPs.

The current study sought to examine the direction of influences on longitudinal associations between anxiety sensitivity, anxiety and depression. The continuity of genetic and environmental influences on these traits over adolescence was also investigated. Self reports of anxiety sensitivity, anxiety and depression were collected from approximately 1,300 twin and sibling pairs, on two occasions (mean ages 15 and 17). The direction and etiology of the associations between these traits were examined using longitudinal genetic cross-lagged models. All traits were stable over time and this stability accounted for the largest proportion of variance at time 2. There was, however, also evidence of reciprocal associations between variables over time. Genetic effects were fairly stable across time, although new genetic influences were evident at the second time point. Environmental effects tended to be more time specific. This study adds to our understanding of the direction of effects between anxiety sensitivity, anxiety and depression in adolescence, and the risks underlying their associations.

Background: Cognitive biases have long been hypothesized to influence the development and maintenance of symptoms of internalizing problems. Anxiety sensitivity represents one such bias and refers to sensitivity to the physical and emotional symptoms of anxiety and the belief that these are harmful. Twin studies indicate a role for both environmental and genetic influences on anxiety sensitivity. However, little work has been done specifying environments or genes involved in this phenotype. In light of this, we looked at the association between stressful life events, the serotonin transporter gene polymorphism (5HTTLPR), and anxiety sensitivity in a longitudinal sample of adolescents., Methods: Stressful life events and anxiety sensitivity were measured in over 1,500 individuals at three time points (mean ages 15, 17, and 20 years). 5HTTLPR was genotyped in 1,109 participants., Results: There was consistent evidence for an association between stressful life events and both anxiety sensitivity and change in anxiety sensitivity over time. Although the effect of independent stressful life events was relatively short lived, dependent stressful life events were associated with anxiety sensitivity over time. There was no evidence for a main effect of 5HTTLPR on anxiety sensitivity. 5HTTLPR genotype did not moderate the effect of stressful life events on anxiety sensitivity., Conclusions: The current study extends previous work by showing that stressful life events, independent of the individual, explained change in cognitions associated with anxiety and depression. This effect does not, however, appear to be moderated by genotype., (© 2012 Wiley Periodicals, Inc.)

We examined the aetiology of anxiety symptoms in an unselected population at ages 7 and 9, a period during which anxiety disorders first begin to develop (mean age at onset is 11 years). Specifically, the aim of the study was to investigate genetic and environmental continuity and change in components of anxiety in middle childhood. Parents of over 3,500 twin pairs completed the Anxiety-Related Behaviours Questionnaire (ARBQ) when twins were 7 and 9 years old. Multivariate-longitudinal analyses were conducted to examine genetic and environmental influences on stability and change in four anxiety scales: Negative Cognition, Negative Affect, Fear and Social Anxiety. We found moderate temporal stability in all four scales from 7 to 9 years (correlations ranging from 0.45 to 0.54) and moderate heritability (average 54%). Both shared and non-shared environmental influences were modest (average 18%-28% respectively). Genetic factors (68%) explained most of the homotypic continuity in anxiety. We show that homotypic continuity of Anxiety-Related Behaviours (i.e. the continuation of one specific type of anxiety over time) was largely driven by genetic factors. In contrast, though more varied, heterotypic continuity between some traits (i.e. the change from one type of anxiety-related behaviour into another over time) was mainly due to shared-environmental factors.

Objectives: Little is known about the aetiology of the links between sleep disturbance and anxiety and depression symptoms. The aim of this study was to estimate genetic and environmental influences on these associations., Methods: Questionnaires were completed by 1556 young adults from twin and sibling pairs (61.5% female)., Results: Sleep disturbance was moderately correlated with symptoms of anxiety (r=.39) and depression (r=.50). There was substantial overlap between genes influencing sleep disturbance and those influencing symptoms of anxiety (rA=.58) and depression (rA=.68). Overall, the associations between sleep and symptoms of both anxiety and depression were mainly due to genes (explaining 74% and 58% of the covariances respectively), with the remainder due to nonshared environmental factors., Conclusions: Moderate phenotypic and genetic correlations between the phenotypes support the view that sleep disturbance is related to the presence of various psychiatric difficulties, but also warrants independent consideration and treatment., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Anxiety and depression share genetic influences, and have been associated with similar cognitive biases. Psychological theories of anxiety and depression highlight threat interpretations of ambiguity. Little is known about whether genes influence cognitive style, or its links to symptoms. We assessed ambiguous word and scenario interpretations, anxiety and depression symptoms in 300 8-year-old twin pairs. There were significant correlations between both negative interpretations of ambiguous words and scenarios and depression symptoms after controlling for anxiety symptoms (r = .13 and .31, respectively), but no significant correlations with anxiety independent of depression. Genetic effects ranged from 16% for depression to 30% for ambiguous word interpretations. Non-shared environmental influences were large (68-70%). Both genetic and environmental influences contributed to the association between depression and ambiguous scenario interpretations. These findings support psychological theories, which emphasise the role of environmental stress both on the development of threat interpretations and on their links with symptoms. The data also support a role for genetic influence on threat interpretations, which may mediate responses to stress.

State and trait anxiety define different aspects of anxiety, and may represent environmentally and genetically mediated components of this phenotype. Furthermore their relationship, where trait anxiety is expressed through levels of state anxiety under threatening circumstances, may represent a process of interplay between a genetic vulnerability factor and an environmental stressor. To test these hypotheses, we explored genetic and environmental influences on measures of state and trait anxiety in a sample of 1058 twins (521 males and 537 females) aged 8-16. The results were consistent with these hypotheses. State anxiety is largely influenced by environmental factors in males and females whereas trait anxiety shows moderate genetic effects and substantial non-shared environment effects. Their association was accounted for by non-shared environmental effects, with modest genetic and shared environmental inputs. The implications of these results for vulnerability mechanisms involving stress reactivity on anxiety are discussed.

Anxiety and conduct problems covary, yet studies have not explored the genetic and environmental origins of this association. We analyzed parent-reported anxiety and conduct problems in 6,783 pairs of twins at 2-, 3-, and 4-years of age. As anxiety and conduct problems were fairly stable across the three ages (average 1-year correlation was .53), ratings from all three were combined. The aggregate anxiety and conduct ratings correlated .33 for boys and .30 for girls. Bivariate genetic analyses indicated fairly low genetic correlations (.31 for boys, .16 for girls), and high shared environmental correlations (1.0 for boys and 0.99 for girls) between anxiety and conduct problems. Most of the phenotypic correlation was accounted for by shared environmental mediation (65% for boys and 94% for girls), indicating that many of the same family environmental factors are responsible for the development of both anxiety and conduct problems.

Anxiety sensitivity is associated with both anxiety and depression and has been shown to be heritable. Little, however, is known about the role of genetic influence on continuity and change of symptoms over time. The authors' aim was to examine the stability of anxiety sensitivity during adolescence. By using a genetically sensitive design, the authors were also able to investigate the extent to which genetic and environmental factors influence anxiety sensitivity over time. Self-reports of anxiety sensitivity were obtained for over 1,300 twin and sibling pairs at 3 time points. Data were analyzed using multivariate genetic models. Anxiety sensitivity was moderately heritable at all time points with substantial nonshared environmental contributions. Time 1 genetic factors accounted for continuity of symptoms at Times 2 and 3. New genetic factors at Time 2 also influenced Time 3 symptoms. New nonshared environmental influences emerged at each time point. Analysis of a latent factor of trait anxiety sensitivity revealed some stable nonshared environmental influences. Genetic effects were generally stable over time, with new genetic influences emerging in late adolescence. Environmental influences on anxiety sensitivity were, on the whole, more time specific; however, some stable environmental influences were also found. (Contains 2 figures and 4 tables.)

Background: Despite theoretical and empirical support for an association between maternal control and child anxiety, few studies have examined the origins of this association. Furthermore, none use observer-ratings of maternal control within a genetically informative design. This study addressed three questions: 1) do children who experience maternal control report higher anxiety levels than those who do not?; 2) to what extent do genetic and environmental factors influence maternal control and child anxiety?; 3) to what extent do genetic and environmental factors influence the associations between child anxiety and maternal control? Method: Five hundred and thirty 8-year-old children (from 265 twin pairs) and their mothers were observed participating in an "etch-a-sketch" task from which maternal control was rated. Children rated their anxiety using the Screen for Child Anxiety Related Emotional Disorders. Results: Children who experienced maternal behaviour rated as "extreme control" reported higher anxiety levels than those who did not. Maternal control was highly heritable (A = 0.63), high self-rated anxiety less so (h[superscript 2][subscript g] = 0.36). The overlap between high child anxiety and maternal control was primarily due to shared genetic factors. Conclusions: These results suggest that maternal control is likely to have been elicited by children with high levels of anxiety.

Background: Little is known about mechanisms of genetic influence on panic, particularly in childhood. Cognitive theories of panic disorder highlight threatening interpretations of physical sensations, and increased awareness of such sensations. Specifically, anxiety sensitivity (AS) and heartbeat perception (HBP) have been associated with panic in adults and children. We examined genetic and environmental influences on childhood AS, HBP, panic/somatic ratings, and their associations. Methods: Self-ratings of AS and DSM-based anxiety (including panic/somatic items) were obtained from 300 eight-year-old twin pairs (600 individuals), selected for mother-rated child anxiety at age 7. HBP was also assessed. Results: Panic/somatic ratings were significantly correlated with both AS (r = 0.55) and continuous HBP error scores (r = -0.13). AS and HBP scores showed significantly greater correlations with panic/somatic ratings than with all other anxiety scales, except for HBP and school anxiety. Genetic influences on panic/somatic ratings were modest (15%), and moderate for both AS (37%), and HBP (30%). Non-shared environmental influences were substantial. The genetic correlations between panic/somatic ratings and both AS and HBP error scores were 0.98 (95% CI: 0.74-1.00) and -0.46 (95% CI: -1.00-1.00) respectively. Conclusions: Self-ratings of panic and AS overlap genetically. Future research should consider whether AS mediates genetic risk for panic disorder.

Attentional biases with regard to emotional facial expressions are associated with social anxiety in adults. We investigated whether similar relations exist in children. Seventy-nine 8- to 11-year-olds completed a probe detection task. On a given trial, 1 of 3 pairs of faces was presented: negative-neutral, negative-positive, and positive-neutral. The strongest association was between social anxiety symptoms and avoidance of negative faces from negative-neutral trials (r = - 0.32), with all other correlations less than half that size. This association was largely due to avoidance of angry and fearful expressions. These results provide preliminary evidence that anxiety is associated with attentional biases in children as in adults.

The objective of this study was to examine the associations between persistent childhood sleep problems and adulthood anxiety and depression. Parents of 943 children (52% male) participating in the Dunedin Multidisciplinary Health and Development Study provided information on their children's sleep and internalizing problems at ages 5, 7, and 9 years. When the participants were 21 and 26 years, adult anxiety and depression were diagnosed using a standardized diagnostic interview. After controlling for childhood internalizing problems, sex, and socioeconomic status, persistent sleep problems in childhood predicted adulthood anxiety disorders (OR (95% CI) = 1.60 (1.05-2.45), p = .030) but not depressive disorders (OR (95% CI) = .99 (.63-1.56), p = .959). Persistent sleep problems in childhood may be an early risk indicator of anxiety in adulthood.KEY WORDS: sleep problems; anxiety; depression.

Objective: To examine the etiologies of covariation of childhood sleep problems and other behavioral/emotional problems in young children. Method: The parents of more than 6,000 twin pairs provided information on their twins' anxiety, conduct, and hyperactivity at ages 3, 4, and 7 by completing the Strengths and Difficulties Questionnaire. Information on sleep problems was obtained at age 3/4. Results: Phenotypic correlations in preschool years between sleep problems and anxiety, conduct, and hyperactivity ranged from 0.17 to 0.22. These correlations were largely due to shared environmental factors (0.72-0.96) and less to heredity (0.05-0.26) and nonshared environment (0.00-0.06). Sleep problems at age 3/4 years predicted at age 7 years anxiety ([beta] = .12, p < .001), conduct problems ([beta] = .09, p < .001), and hyperactivity ([beta] = .07, p < .001), after accounting for stability of these problems. These predictive associations were also mainly mediated by shared environment (0.16-0.91), although genetic (0.02-0.84) and nonshared environmental (-0.03-0.09) factors were also influential. Conclusions: The modest associations between early sleep problems and later behavioral/emotional problems are largely accounted for by common psychosocial risk factors. Further research on which specific risks may mediate these connections is needed. J. Am. Acad. Child Adolesc. Psychiatry, 2004;43(6):744-751. Key Words: twins, sleep, behavioral/emotional problems.

Background: Emotional symptoms, such as anxiety and depressive symptoms, are common during adolescence, often persist over time, and can precede the emergence of severe anxiety and depressive disorders. Studies suggest that a vicious cycle of reciprocal influences between emotional symptoms and interpersonal difficulties may explain why some adolescents suffer from persisting emotional symptoms. However, the role of different types of interpersonal difficulties, such as social isolation and peer victimisation, in these reciprocal associations is still unclear. In addition, the lack of longitudinal twin studies conducted on emotional symptoms during adolescence means that the genetic and environmental contributions to these relationships during adolescence remain unknown. Methods: Participants (N = 15,869) from the Twins Early Development Study completed self‐reports of emotional symptoms, social isolation and peer victimisation at 12, 16 and 21 years old. A phenotypic cross‐lagged model examined reciprocal associations between variables over time, and a genetic extension of this model examined the aetiology of the relationships between variables at each timepoint. Results: First, emotional symptoms were reciprocally and independently associated with both social isolation and peer victimisation over time, indicating that different forms of interpersonal difficulties uniquely contributed to emotional symptoms during adolescence and vice versa. Second, early peer victimisation predicted later emotional symptoms via social isolation in mid‐adolescence, indicating that social isolation may constitute an intermediate pathway through which peer victimisation predicts longer‐term emotional symptoms. Finally, individual differences in emotional symptoms were mostly accounted for by non‐shared environmental factors at each timepoint, and both gene–environment and individual‐specific environmental mechanisms were involved in the relationships between emotional symptoms and interpersonal difficulties. Conclusions: Our study highlights the necessity to intervene early in adolescence to prevent the escalation of emotional symptoms over time and to consider social isolation and peer victimisation as important risk factors for the long‐term persistence of emotional symptoms. [ABSTRACT FROM AUTHOR]

Background: While studies from the start of the COVID-19 pandemic have described initial negative effects on mental health and exacerbating mental health inequalities, longer-term studies are only now emerging. Method: In total, 34 465 individuals in the UK completed online questionnaires and were re-contacted over the first 12 months of the pandemic. We used growth mixture modelling to identify trajectories of depression, anxiety and anhedonia symptoms using the 12-month data. We identified sociodemographic predictors of trajectory class membership using multinomial regression models. Results: Most participants had consistently low symptoms of depression or anxiety over the year of assessments (60%, 69% respectively), and a minority had consistently high symptoms (10%, 15%). We also identified participants who appeared to show improvements in symptoms as the pandemic progressed, and others who showed the opposite pattern, marked symptom worsening, until the second national lockdown. Unexpectedly, most participants showed stable low positive affect, indicating anhedonia, throughout the 12-month period. From regression analyses, younger age, reporting a previous mental health diagnosis, non-binary, or self-defined gender, and an unemployed or a student status were significantly associated with membership of the stable high symptom groups for depression and anxiety. Conclusions: While most participants showed little change in their depression and anxiety symptoms across the first year of the pandemic, we highlight the divergent responses of subgroups of participants, who fared both better and worse around national lockdowns. We confirm that previously identified predictors of negative outcomes in the first months of the pandemic also predict negative outcomes over a 12-month period. [ABSTRACT FROM AUTHOR]

Background: There is substantial variation in patient symptoms following psychological therapy for depression and anxiety. However, reliance on endpoint outcomes ignores additional interindividual variation during therapy. Knowing a patient's likely symptom trajectories could guide clinical decisions. We aimed to identify latent classes of patients with similar symptom trajectories over the course of psychological therapy and explore associations between baseline variables and trajectory class. Methods: Patients received high-intensity psychological treatment for common mental health problems at National Health Service Improving Access to Psychological Therapies services in South London (N = 16 258). To identify trajectories, we performed growth mixture modelling of depression and anxiety symptoms over 11 sessions. We then ran multinomial regressions to identify baseline variables associated with trajectory class membership. Results: Trajectories of depression and anxiety symptoms were highly similar and best modelled by four classes. Three classes started with moderate-severe symptoms and showed (1) no change, (2) gradual improvement, and (3) fast improvement. A final class (4) showed initially mild symptoms and minimal improvement. Within the moderate-severe baseline symptom classes, patients in the two showing improvement as opposed to no change tended not to be prescribed psychotropic medication or report a disability and were in employment. Patients showing fast improvement additionally reported lower baseline functional impairment on average. Conclusions: Multiple trajectory classes of depression and anxiety symptoms were associated with baseline characteristics. Identifying the most likely trajectory for a patient at the start of treatment could inform decisions about the suitability and continuation of therapy, ultimately improving patient outcomes. [ABSTRACT FROM AUTHOR]

Background: Previous research indicates that body dysmorphic disorder (BDD) is associated with risk of suicidality. However, studies have relied on small and/or specialist samples and largely focussed on adults, despite these difficulties commonly emerging in youth. Furthermore, the aetiology of the relationship remains unknown. Methods: Two independent twin samples were identified through the Child and Adolescent Twin Study in Sweden, at ages 18 (N = 6027) and 24 (N = 3454). Participants completed a self-report measure of BDD symptom severity. Young people and parents completed items assessing suicidal ideation/behaviours. Logistic regression models tested the association of suicidality outcomes with: (a) probable BDD, classified using an empirically derived cut-off; and (b) continuous scores of BDD symptoms. Bivariate genetic models examined the aetiology of the association between BDD symptoms and suicidality at both ages. Results: Suicidal ideation and behaviours were common among those with probable BDD at both ages. BDD symptoms, measured continuously, were linked with all aspects of suicidality, and associations generally remained significant after adjusting for depressive and anxiety symptoms. Genetic factors accounted for most of the covariance between BDD symptoms and suicidality (72.9 and 77.7% at ages 18 and 24, respectively), but with significant non-shared environmental influences (27.1 and 22.3% at ages 18 and 24, respectively). Conclusions: BDD symptoms are associated with a substantial risk of suicidal ideation and behaviours in late adolescence and early adulthood. This relationship is largely explained by common genetic liability, but non-shared environmental effects are also significant and could provide opportunities for prevention among those at high-risk. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to examine differences in fear conditioning between anxious and nonanxious participants in a single large sample. Materials and methods: We employed a remote fear conditioning task (FLARe) to collect data from participants from the Twins Early Development Study (n = 1,146; 41% anxious vs. 59% nonanxious). Differences between groups were estimated for their expectancy of an aversive outcome towards a reinforced conditional stimulus (CS+) and an unreinforced conditional stimulus (CS−) during acquisition and extinction phases. Results: During acquisition, the anxious group (vs. nonanxious group) showed greater expectancy towards the CS−. During extinction, the anxious group (vs. nonanxious group) showed greater expectancy to both CSs. These comparisons yielded effect size estimates (d = 0.26–0.34) similar to those identified in previous meta‐analyses. Conclusion: The current study demonstrates that remote fear conditioning can be used to detect differences between groups of anxious and nonanxious individuals, which appear to be consistent with previous meta‐analyses including in‐person studies. [ABSTRACT FROM AUTHOR]

Background: Sleep apnea is one of the most common sleep disorders and it is related to multiple negative health consequences. Previous studies have shown that sleep apnea is influenced by genetic factors. However, studies have not investigated the genetic and environmental influences of symptoms of sleep apnea in young adults. Furthermore, the underpinnings of the relationship between apnea symptoms and internalizing/externalizing problems are unknown. The objectives of this study were to estimate the magnitude of: (1) genetic and environmental influences on self-reported apnea symptoms; (2) the relationship between self-reported apnea symptoms and internalizing/externalizing traits; (3) genetic and environmental influences on the associations between self-reported apnea symptoms, internalizing behaviors and externalizing behaviors. Methods: In a twin/sibling study, univariate and multivariate models were fitted to estimate both individual variance and sources of covariance between symptoms of sleep apnea and internalizing/externalizing behaviors. Results: Our results show that genetic influences account for 40% of the variance in sleep apnea symptoms. Moreover, there are modest associations between depression, anxiety and externalizing behaviors with apnea symptoms (ranging from r = 0.22–0.29). However, the origins of these associations differ. For example, whereas most of the covariation between symptoms of depression and sleep apnea can be explained by genes (95%), there was a larger role for the environment (53%) in the association between symptoms of anxiety and sleep apnea. Conclusions: Genetic factors explain a significant proportion of variance in symptoms of apnea and most of the covariance with depression. [ABSTRACT FROM AUTHOR]

Background: Anxiety and depressive disorders can be classified under a bidimensional model, where depression and generalized anxiety disorder are represented by distress and the other anxiety disorders, by fear. The phenotypic structure of this model has been validated, but twin studies only show partial evidence for genetic and environmental distinctions between distress and fear. Moreover, the effects of genetic variants are mostly shared between anxiety and depression, but the genome-wide genetic distinction between distress and fear remains unexplored. This study aimed to examine the degree of common genetic variation overlap between distress and fear, and their associations with the psychosocial risk factors of loneliness and social isolation.Methods: We used genome-wide data from 157,366 individuals in the UK Biobank who answered a mental health questionnaire.Results: Genetic correlations indicated that depression and generalized anxiety had a substantial genetic overlap, and that they were genetically partially distinct from fear disorders. Associations with loneliness, but not social isolation, showed that loneliness was more strongly associated with both distress disorders than with fear.Conclusions: Our findings shed light on genetic and environmental mechanisms that are common and unique to distress and fear and contribute to current knowledge on individuals' susceptibility to anxiety and depression. [ABSTRACT FROM AUTHOR]

Background: Twin studies in children reveal that familial aggregation of anxiety disorders is due to both genetic and environmental factors. Cognitive biases for threat information are considered a robust characteristic of childhood anxiety. However, little is known regarding the underlying aetiology of such biases and their role in anxiety disorders. Method: A face version of the dot-probe task measuring attentional biases for negative (anger, fear, sad, disgust) and positive (happy) facial expressions was completed by 600, 8-year-old twins; the largest study of its kind. Twin correlations for attentional bias scores were compared to estimate genetic and environmental effects. Parent-report diagnostic interviews identified children with an anxiety disorder. Indices of inferred genetic and familial risk for anxiety disorders were created for each child. Data were analysed using a series of logistic regressions. Results: Anxious children showed greater attentional avoidance of negative faces than nonanxious children; t (548) = 2.55, p < .05. Attentional avoidance was not under genetic or shared environmental influence. Risk for anxiety disorders was predicted by familial factors. Both attentional avoidance and inferred familial risk were significant but independent predictors of anxiety disorders (ORs = .65 and 3.64, respectively). Conclusions: Anxiety-related attentional biases and familial risk play important but independent roles in childhood anxiety disorders. If replicated, these findings indicate that links between genetic risk and anxiety disorders lie outside the domain of attentional processes. [ABSTRACT FROM AUTHOR]

The Genesis 12–19 (G1219) Study is an ongoing longitudinal study of a sample of UK twin pairs, non-twin sibling pairs, and their parents. G1219 was initially designed to examine the role of gene–environment interplay in adolescent depression. However, since then data have continued to be collected from both parents and their offspring into young adulthood. This has allowed for longitudinal analyses of depression and has enabled researchers to investigate multiple phenotypes and to ask questions about intermediate mechanisms. The study has primarily focused on emotional development, particularly depression and anxiety, which have been assessed at multiple levels of analysis (symptoms, cognitions, and relevant environmental experiences). G1219 has also included assessment of a broader range of psychological phenotypes ranging from antisocial behaviors and substance use to sleep difficulties, in addition to multiple aspects of the environment. DNA has also been collected. The first wave of data collection began in the year 1999 and the fifth wave of data collection will be complete before the end of 2012. In this article, we describe the sample, data collection, and measures used. We also summarize some of the key findings to date. [ABSTRACT FROM AUTHOR]

Catastrophizing about sleeplessness is a cognitive process associated with sleep disturbance in adults. This study aimed to (1) examine whether children catastrophize about the consequences of not sleeping; (2) define the topics that children catastrophize about; (3) assess whether there is a link between catastrophizing and sleep disturbance in children; and (4) examine whether an association between catastrophizing and sleep in children is mediated by anxiety and depression symptoms. Children completed the sleep self-report and a catastrophizing interview. Testing took place in two inner-city schools in London, UK and participants comprised 123 children aged between 8 and 10 years (49% male). Thirty-four (28%) participants reported concerns in response to the catastrophizing questionnaire. The main topics being catastrophized were concerns about sleep, physiological issues and one’s own emotions. Catastrophes predicted sleep disturbance after controlling for age and sex ( β = 0.35, P < 0.001) but not when controlling additionally for anxiety and depression symptoms ( β = 0.15, P = 0.106). Symptoms of anxiety (Sobel test = 3.30, P < 0.001) and depression (Sobel test = 2.90, P = 0.004) mediated the influence of catastrophizing on sleep. A proportion of children catastrophized about the consequences of sleeplessness and this was associated with sleep disturbance, an association which was mediated through anxiety and depression symptoms. [ABSTRACT FROM AUTHOR]

Background: Anxiety-related behaviors (ARBs) are commonly observed during typical development, yet few studies have investigated their etiology in middle childhood. This study aimed to examine both the phenotypic and genetic differentiation of ARB subtypes within the general population at age 7 and 9. It constituted a follow-up to an earlier study of ARBs in preschool children. Methods: We investigated the phenotypic structure of ARBs in a large population-based twin sample, comprising 7,834 twin pairs at age 7 and 3,644 twin pairs at age 9. Quantitative genetic modeling techniques were then used to determine the relative influences of genetic and environmental factors upon different types of ARB and upon the covariation between them. Results: Factor analysis supported the presence of five ARB factors at both ages: negative cognitions, negative affect, fear, obsessive–compulsive behaviors, and social anxiety. Multivariate genetic analyses revealed significant genetic effects and a small but significant influence of shared environment for all ARB subtypes. There was a moderate level of genetic specificity for each subtype as well as some shared genetic effects. Shared environmental influences correlated highly across all types of ARB, whereas nonshared environmental effects were largely subtype specific. Conclusions: The current results suggest that ARBs can be differentiated both phenotypically and genetically within middle childhood, with subtypes reflecting symptom groupings of diagnosable disorders but also aspects of temperament. Although some etiological risk factors lead to a generalized vulnerability to anxiety, others may serve to differentiate between different types of ARBs. Depression and Anxiety, 2009. © 2009 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

It is becoming increasingly apparent that genetic research into psychiatric disorders would benefit from consideration of the environment because these risk mechanisms are likely to interact. Despite generalised anxiety disorder (GAD) being one of the most prevalent disorders presented in primary care, there is a paucity of published studies of gene-environment interactions (G × E) for this phenotype. This article describes how our current knowledge of GAD is useful in designing studies of G × E for GAD. To increase the chances of identifying replicable G × E for GAD further information is needed with regards to: defining and measuring GAD, difficulties co-occurring with GAD, quantitative genetic estimations for GAD, specific genes associated with GAD, and specific environmental risks for GAD. [ABSTRACT FROM AUTHOR]