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Attentional Threat Avoidance and Familial Risk are Independently Associated with Childhood Anxiety Disorders

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Title: Attentional Threat Avoidance and Familial Risk are Independently Associated with Childhood Anxiety Disorders
Language: English
Authors: Brown, Hannah M., McAdams, Tom A., Lester, Kathryn J., Goodman, Robert, Clark, David M., Eley, Thalia C.
Source: Journal of Child Psychology and Psychiatry. Jun 2013 54(6):678-685.
Availability: Wiley-Blackwell. 350 Main Street, Malden, MA 02148. Tel: 800-835-6770; Tel: 781-388-8598; Fax: 781-388-8232; e-mail: cs-journals@wiley.com; Web site: http://www.wiley.com/WileyCDA/
Peer Reviewed: Y
Page Count: 8
Publication Date: 2013
Document Type: Journal Articles
Reports - Research
Descriptors: Anxiety Disorders, Children, Etiology, Family Influence, Bias, Attention, Twins, Correlation, Scores, Comparative Analysis, Environmental Influences, Genetics, Interviews, At Risk Persons, Parents, Visual Stimuli, Foreign Countries, Heredity, Nonverbal Communication, Regression (Statistics)
Geographic Terms: United Kingdom (London)
DOI: 10.1111/jcpp.12024
ISSN: 0021-9630
Abstract: 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 less than 0.05. 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 = 0.65 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. (Contains 3 tables and 1 figure.)
Abstractor: As Provided
Number of References: 40
Entry Date: 2014
Accession Number: EJ1013172
Database: ERIC
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  Value: <anid>AN0087694537;jyy01jun.13;2024Jun04.07:33;v2.2.500</anid> <title id="AN0087694537-1">Attentional threat avoidance and familial risk are independently associated with childhood anxiety disorders. </title> <p>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 (<reflink idref="bib548" id="ref1">548</reflink>) = 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.</p> <p>attention; children; familial risk; Anxiety</p> <p>Anxiety disorders are common, affecting between 10 and 15% of children and adolescents (Costello, Mustillo, Erkanli, Keeler, & Angold, 2003). Often diagnosed in childhood with a mean age of onset of 11 years (Kessler et al., 2005), they show stability into adulthood (Hofstra, Van der Ende, & Verhulst, 2000) and are associated with a range of impairments, such as in social relationships (La Greca & Lopez, 1998) and academic achievement (Van Ameringen, Mancini, & Farvolden, 2003). As a result, it is important to identify causal risk factors to inform intervention and prevention.</p> <hd id="AN0087694537-2">Familial‐risk factors for anxiety</hd> <p>Anxiety appears to aggregate in families (Eley, Collier, McGuffin, Owen, & Gottesman, 2002). A higher incidence in the offspring of adults with anxiety disorders than those without (e.g. Beidel & Turner, 1997) suggests familial factors are likely to play a causal role in anxiety development. A multitude of twin studies in childhood show that this family resemblance is due to both genetic and environmental factors. Model‐fitting analyses of childhood anxiety (e.g. Gregory & Eley, 2011) indicate moderate heritability (genetic influence) and modest shared environmental influences (i.e. environmental factors making family members similar). The remaining influence is attributed to nonshared environmental factors that make family members different.</p> <hd id="AN0087694537-3">Cognitive risk factors for anxiety</hd> <p>Cognitive models of childhood anxiety (Muris & Field, 2008) propose that attentional biases for environmental threats affect the development and maintenance of anxiety disorders. Various experimental paradigms have been developed to examine anxiety‐related attentional processes with both adults and children (Hadwin & Field, 2010). Dot‐probe tasks briefly present stimuli pairs (e.g. faces) of opposing emotional valence followed by a visual target probe in place of one of the stimuli. Participants identify the location or some differentiating feature of the probe as fast as possible. Attentional allocation is inferred by comparing reaction times across trial types. Faster reactions for probes replacing emotional relative to neutral stimuli indicate attentional vigilance for stimuli of that valence whilst slower reaction times indicate attentional avoidance. Dot‐probe studies with children repeatedly find associations between anxiety and preferential processing of negative/threatening stimuli (Bar‐Haim, Lamy, Pergamin, Bakermans‐Kranenburg, & van IJzendoorn, 2007). Although the direction of this bias is debated, it is generally accepted that differences in stimulus duration may in part explain mixed findings. Despite equivocal results, shorter durations (less than 500 ms) typically reveal attentional vigilance to threat (e.g. Waters, Mogg, Bradley, & Pine, 2008) whilst longer durations are more often associated with avoidance (e.g. Mansell, Clark, Ehlers, & Chen, 1999; Stirling, Eley, & Clark, 2006).</p> <p>The specificity of anxiety‐related attention is also unclear. Dot‐probe studies typically compare reaction times for probes in angry‐neutral and happy‐neutral face pairs. Some find anxiety‐related biases for angry faces alone (e.g. Mogg, Philippot, & Bradley, 2004) whilst others also find biases for happy faces (Waters et al., 2008), suggesting attentional biases for emotional faces generally. Some studies have examined negative facial expressions other than anger. Specifically, an earlier study by our research group identified avoidance of fear as well as angry faces with social anxiety but only an association with fear remained significant when controlling for other negative expressions (Stirling et al., 2006).</p> <hd id="AN0087694537-4">Aetiology of anxiety‐related cognitive biases</hd> <p>Attempts to identify mechanisms underpinning the development of these biases and their role in anxiety disorders are scarce. Some theorists propose that biases are learnt from observing and modelling parental responses to, and reflections on threat (e.g. Hadwin, Garner, & Perez‐Olivas, 2006). Studies showing attentional biases towards threat in children of parents with anxiety disorders support this notion (e.g. Pine et al., 2005). However, familial processes may not function in an entirely environmental manner. They may also reflect genetic influences shared between parent and child.</p> <p>Twin studies are needed disentangle the extent to which cognitive biases are attributable to genetic and environmental factors. There are few twin studies of anxiety‐related cognitive processes. The majority focus on anxiety sensitivity; hypervigilance towards symptoms of anxiety (attentional bias) with a belief (interpretation bias) they are harmful (Reiss & McNally, 1985). Four studies have shown moderate heritability of anxiety sensitivity (.33–.46) in adult (Stein, Jang, & Livesley, 1999), adolescent (Brown et al., 2012; Zavos, Gregory, & Eley, 2012) and child samples (Eley, Gregory, Clark, & Ehlers, 2007) with the remaining variance attributed to nonshared environmental factors. The absence of shared environmental influences suggests familial resemblance in cognitive biases is solely due to genetic factors although failure to detect shared environmental influences could be due to power issues.</p> <p>Two studies have used the twin design to examine genetic and environmental factors shared between cognitive biases and anxiety symptoms. These revealed a high genetic overlap between both anxiety sensitivity and anxiety symptoms in adolescence (.74; Zavos, Rijsdijk, Gregory, & Eley, 2010) and panic/somatic symptoms in childhood (.96; Eley et al., 2007). The latter revealed a genetic correlation of −.47 between heart beat perception (an experimental measure of attention to internal bodily symptoms) and panic/somatic symptoms, although this correlation was nonsignificant (95% CI = −1.00–1.00). These studies indicate that the same genetic factors influence both anxiety‐related cognitive biases and anxiety symptoms.</p> <hd id="AN0087694537-5">Current study</hd> <p>The current study sought to expand the limited understanding of the aetiology of attentional biases in childhood anxiety disorders. We used a face version of the dot‐probe paradigm in a sample of 600 twins making this the largest study exploring anxiety‐related attentional biases in children with anxiety disorders, to date. This study extended previous work by our group (Stirling et al., 2006), combining the face dot‐probe paradigm with genetically sensitive data regarding childhood anxiety diagnoses.</p> <p>First, we examined the nature of attentional biases in anxious compared with nonanxious children. As with studies using longer stimulus durations, we predicted anxiety disorders would be associated with greater attentional avoidance of negative faces. Additional exploratory analyses examined the specificity of attentional biases for different negative face types.</p> <p>Second, we examined the aetiology of anxiety‐related attentional bias by comparing correlations between monozygotic (MZ) and dizygotic (DZ) twins. We predicted that attentional avoidance of threat would show moderate genetic influence consistent with twin studies of other anxiety‐related cognitive processes and in line with intermediate phenotype theories (Meyer‐Lindenberg & Weinberger, 2006). Evidence of shared environmental influence was less expected.</p> <p>Finally, we examined the aetiological relationship between childhood anxiety and attentional bias. Due to the low prevalence of anxiety disorders in our sample, inferred genetic and familial‐risk indices (Kendler et al., 1995) were used instead of traditional twin modelling. The relationship between inferred risk, attentional bias and anxiety disorders was examined using a series of logistic regressions. We hypothesized that familial risk (representing both genetic and environmental factors) and attentional bias would predict the presence of anxiety disorders. We were also interested in the possibility that, if heritable, attentional bias might mediate familial effects on anxiety.</p> <hd id="AN0087694537-6">Method</hd> <hd id="AN0087694537-7">Participants</hd> <p>The ECHO (Emotion, Cognition, Heredity and Outcome) study consists of 300 twin pairs aged 8 years 2 months to 8 years 11 months recruited from a larger population twin study (Twins Early Development Study, TEDS; Trouton, Spinath, & Plomin, 2002). The Maudsley Hospital Ethics Committee, London, UK provided ethical approval. A selected extremes design was employed to maximize power. The majority of twins pairs (N = 247) were selected because one or both members scored highly (top 15%) for maternal‐reported anxiety at age seven. The remaining 53 pairs were selected from TEDS if neither twin scored highly for maternal‐reported anxiety to ensure anxiety scores covered those in the general population. Data from 11 twin pairs (4%) were excluded following data collection because at least one twin in that pair had known neurological or severe receptive language impairments, autistic spectrum disorder or attention difficulties or because researchers observed substantial difficulty completing the tasks. Twin pair zygosity was identified using a combination of parent‐rated questionnaire (Price et al., 2000) and DNA sequencing in uncertain cases. The sample consisted of 96 identical (monozygotic) pairs and 192 nonidentical (dizygotic) pairs and one pair of unknown zygosity who refused DNA clarification. As would be expected in a sample selected for high anxiety scores, the majority of children were girls (57%). The majority of twin pairs were white (N = 256, 87%) in line with the national average (93%; Scott, Pearce & Goldblatt, 2001). Mothers were somewhat more likely to be employed (N = 215, 74%) than the national average for mothers of children under 15 (64%; Huerta et al., 2011) and more likely to be educated to A‐level or higher (N = 157, 54%) than a nationally representative sample (32%; Meltzer, Gatward, Goodman, & Ford, 2000).</p> <hd id="AN0087694537-8">Procedure</hd> <p>Participating families completed a 2‐hr testing session at the Institute of Psychiatry, London. Parents gave written consent. Twins completed a range of questionnaires and experimental paradigms split into two halves by a break. Twin pairs completed the two halves in the opposite orders to counter‐balance any fatigue or learning effects. Parents of twins completed a range of questionnaires in a separate room. Tasks were counterbalanced across participants.</p> <hd id="AN0087694537-9">Measures</hd> <p>Anxiety  Anxiety was measured using the development and well‐being assessment interview (DAWBA; Goodman, Ford, Richards, Gatward, & Meltzer, 2000). The DAWBA is a self‐administered structured interview covering a range of emotional and behavioural symptoms. Diagnoses were made in line with the Diagnostic and Statistical Manual (DSM IV; American Psychiatric Association, 2000) based on the number and severity of symptoms present at assessment. The DAWBA demonstrates substantial diagnostic agreement with clinician ratings [Cohen’s Kappa(k) = .67; Goodman et al., 2000] and moderate agreement with other structured interviews (.38 to.48; Angold et al., 2012). In the current study, parents (typically mothers) completed the DAWBA on a computer. Closed‐ and open‐ended responses were coded using computer algorithms and clinician ratings by the first author of the measure (RG) respectively. These were combined to identify individuals with an anxiety disorder. Anxiety data were available for 93.7% of the sample (N = 562). Few reached the clinical cut‐off for each anxiety diagnosis; separation anxiety disorder = 14, specific phobia = 11, social phobia = 13, generalized anxiety disorder = 9, other anxiety disorder = 9. As a result, all anxiety disorders were combined for analyses, resulting in a total of 47 individuals with at least one anxiety disorder. Exploration of associations with specific anxiety diagnoses was not possible.</p> <hd id="AN0087694537-10">Attentional bias</hd> <p>Attentional biases were assessed using a face dot‐probe paradigm. We selected 32 facial expression models from a widely used set of photographs (Matsumoto & Ekman, 1988). Equal numbers of male/female and Caucasian/Japanese models were used. Each model portrayed three facial expressions; negative (angry, sad, fearful or disgust faces), neutral and positive (happy faces), resulting in 96 images. Each dot‐probe trial consisted of a centrally positioned fixation cross which was replaced by a face‐pair; each presented for 1,000 ms. Face pairs comprised two pictures of the same model presented horizontally next to one another. All combinations of face pairs were used for each model resulting in 96 trials in three blocks representing negative‐neutral, negative‐positive and neutral‐positive trials; 32 trials in each block. Negative‐neutral and negative‐positive blocks consisted of equal numbers of fear, sadness, anger and disgust faces (eight trials per emotion). Following presentation of face pairs, a probe display was presented consisting of either a triangle or a square in a location corresponding to the centre of one of the faces (see Figure 1 for schematic diagram). Probe shape and location were counterbalanced. Equal numbers of each probe type appeared in the location of each face type. Participants indicated which shape probe was displayed as quickly as possible by pressing one of two labelled buttons on a serial mouse. Probes remained on screen until participants responded. Trials were randomly presented within each block. Blocks were counterbalanced across participants.</p> <p>Participants completed the dot‐probe task individually and wore headphones to reduce sound distraction. The task was presented on a Toshiba Satellite Pro 4600 laptop with a 14 inch screen. Instructions were presented on screen and read by the researcher to ensure comprehension. Each child completed 12 practice trials before commencing 96 test trials. For analyses, only trial reaction times (RT) for correct responses were included. In addition, trials with RTs less than 100 ms or greater than 3,000 ms were excluded as they likely represent lack of attention to the task. The error and outlier rates were low (6% and.8%, respectively) and did not differ between children with and without anxiety. Mean RTs for probes replacing each emotional expression type (negative, neutral or positive) in each block were calculated for each participant if at least 80% of trials were nonmissing, resulting in four participants removed over all trial combinations. In addition, mean RTs for each negative emotion (anger, fear, sad, disgust) were calculated to explore specificity.</p> <hd id="AN0087694537-11">Genetic and familial risk</hd> <p>Given the low prevalence of anxiety disorders in this sample and the dichotomous nature of the outcome variable, inferred risk indices were used instead of traditional twin model fitting. The inferred genetic risk index (Kendler et al., 1995) assigns each member of a twin pair to one of four ‘genetic risk’ categories based on the anxiety diagnosis status of their co‐twin and the genetic relatedness between them. Assuming additive genetic influence, MZ twins are at highest risk for a disorder when their co‐twin is affected and at lowest risk when their co‐twin is unaffected. Similarly, DZ twins are at higher or lower genetic risk dependent on the diagnostic status of their co‐twin. However, this risk is reduced relative to MZ twins because of the decreased genetic similarity between them. As a result, MZ twins with an affected co‐twin were assigned a score of 1.0 representing the highest risk, DZ twins of affected co‐twins 0.5, DZ twins of unaffected co‐twins ‐0.5 and MZ twins of unaffected co‐twins −1.0 representing the lowest genetic risk. A familial‐risk index was also created to account for the possibility of shared environmental influences such that twins of affected co‐twins and twins of unaffected co‐twins were assigned a score of 1.0 and 0.0, respectively, regardless of zygosity.</p> <hd id="AN0087694537-12">Analyses</hd> <p>Attentional bias scores were calculated for each trial type (negative‐neutral, negative‐positive and neutral‐positive): bias score = PN‐PE where PN is the mean RT for probes replacing neutral faces and PE is the mean RT for probes replacing the emotional (negative or positive) face (MacLeod & Mathews, 1988). In negative‐positive trials, positive faces were used as the more neutral group. The t‐tests examined whether these differed significantly between those with and without anxiety. Further exploratory analyses examined the specificity of attentional bias using a within‐subjects analysis of variance (ANOVA) to compare biases for angry, fear, sad and disgust faces. MZ and DZ twin correlations for bias scores differing significantly between those with and without anxiety were compared to estimate genetic and environmental influences. Both MZ and DZ twins are assumed to share within‐pair environments to the same extent. However, because MZ twins are 100% genetically related, whilst DZ twins share only 50% of segregated genetic variance, any evidence of increased similarity for attentional biases between MZ, relative to DZ, twins suggests additive genetic influence. Shared environmental influences are estimated as the difference between the MZ correlation and genetic estimates (see Plomin, DeFries, McClearn, & McGuffin, 2007 for more detail). The remaining variance is attributed to nonshared environmental influences; although this estimate also includes measurement error.</p> <p>The proportion of children with an anxiety disorder in each of the inferred genetic and familial‐risk categories were compared to examine which index best represented the nature of risk for anxiety disorders in the sample. A greater proportion of probands in ‘MZ affected’ than ‘DZ affected’ risk categories is indicative of genetic influences on anxiety disorders. However, a larger proportion of probands in ‘affected’ than ‘unaffected’ categories regardless of zygosity suggests both genetic and shared environmental factors influence anxiety disorders.</p> <p>Regression analyses examined the relationship between attentional bias, inferred risk and anxiety disorders. Only bias scores which differed significantly between those with and without anxiety were included in regression models. The first model examined whether the available demographic variables (age, sex and ethnicity) predicted the presence of an anxiety disorder. Only significant predictors were retained. Subsequent models predicted the presence of anxiety disorders from both inferred risk and attentional bias both separately and simultaneously. All analyses were conducted in Stata version 10 (Statacorp, 2007) using the cluster robust command to account for genetic relatedness between participants.</p> <hd id="AN0087694537-13">Results</hd> <hd id="AN0087694537-14">Attentional bias</hd> <p>Mean reaction times and bias scores for each trial type on the dot‐probe task are shown in Table 1. Overall, children avoided negative faces in negative‐neutral trials, were vigilant for positive faces in neutral‐positive trials and avoided positive faces in negative‐positive trials. Those with an anxiety disorder were significantly more avoidant of negative faces in negative‐neutral trials than those without; t (<reflink idref="bib548" id="ref2">548</reflink>) = 2.44, p < .05, d = .37 (95% CI = .07–.67). There were no significant differences for any other trial type (Table 2). A within‐subjects ANOVA of each negative face type (anger, fear, sadness, disgust) from negative‐neutral trials indicated no significant differences in negative face‐specific bias scores between those with and without an anxiety disorder; F(<reflink idref="bib3" id="ref3">3</reflink>) = 1.92, ns. Twin correlations for negative bias scores from negative‐neutral trials were nonsignificant for monozygotic or dizygotic twins (rs = −.03 and −.07, respectively), indicating no genetic or shared environmental influences.</p> <p>1 Mean reaction times and bias scores (standard deviations) for each trial type from a face dot‐probe task completed by 8‐year‐old children</p> <p> <ephtml> <table><tr><th>Trial‐type</th><th>Probed image mean reaction time (ms)</th><th>Mean bias score</th><th>t</th><th>df</th></tr><tr><td /><td>Negative</td><td>Neutral</td><td /><td /><td /></tr><tr><td>Negative‐neutral</td><td>810.19 (192.71)</td><td>781.83 (186.83)</td><td>−28.63 (104.27)</td><td>6.63*</td><td>582</td></tr><tr><td /><td>Neutral</td><td>Positive</td><td /><td /><td /></tr><tr><td>Neutral‐positive</td><td>808.66 (189.93)</td><td>778.91 (185.45)</td><td>30.30 (102.06)</td><td>−7.19*</td><td>585</td></tr><tr><td /><td>Negative</td><td>Positive</td><td /><td /><td /></tr><tr><td>Negative‐positive</td><td>775.13 (182.26)</td><td>788.56 (179.93)</td><td>−13.79 (95.76)</td><td>−3.48*</td><td>582</td></tr></table> </ephtml> </p> <p>1 Negative and positive bias scores indicate avoidance and vigilance, respectively.</p> <ulist> <item>2 *p < .001.</item> <item>2 Mean bias scores (standard deviation) for anxious and nonanxious participants on each trial type in the face dot‐probe</item> </ulist> <p> <ephtml> <table><tr><th valign="bottom"> </th><th>Anxiety disorder status</th><th valign="bottom">t</th><th valign="bottom">df</th></tr><tr><th>Affected</th><th>Unaffected</th></tr><tr><td>Negative‐neutral</td><td>−65.83 (96.46)</td><td>−27.29 (103.07)</td><td>2.44*</td><td>548</td></tr><tr><td>Neutral‐positive</td><td>23.97 (78.54)</td><td>30.29 (103.50)</td><td>.40</td><td>551</td></tr><tr><td>Negative‐positive</td><td>−5.79 (92.59)</td><td>13.64 (95.34)</td><td>1.31</td><td>547</td></tr></table> </ephtml> </p> <p>3 *p < .05.</p> <p>To examine internal consistency, split‐half reliabilities were calculated by randomly halving the trials within each block. Raw reaction times and bias scores from each half were correlated (Schmukle, 2005). Split‐half correlations for raw reaction times were above.69 (p < .001) on all trial types. Split‐half correlations for bias scores were nonsignificant for negative‐neutral and negative‐positive trials (rs = .02 and −.08, ns) and.55 (p < .05) for positive‐neutral trials.</p> <hd id="AN0087694537-15">Inferred genetic/familial risk</hd> <p>Table 3 presents the proportion of probands in each inferred risk category. Whilst there was a higher proportion of individuals with an anxiety disorder in affected than unaffected co‐twin categories (.18 and.07, respectively), no distinction could be made between MZ and DZ twins within these groups. This suggests that having a twin with an anxiety disorder places the individual at greater risk of having an anxiety disorder regardless of the degree of genetic relatedness between them. Accordingly, the familial‐risk index was used in subsequent analyses.</p> <p>3 Proportion of twins in the sample with an anxiety disorder in each inferred genetic risk ( Kendler et al., 1995 ) and inferred familial‐risk category</p> <p> <ephtml> <table><tr><th /><th>N</th><th>Proportion (N) of affected twins</th></tr><tr><td>MZ co‐twin affected</td><td>14</td><td>.21 (3)</td></tr><tr><td>DZ co‐twin affected</td><td>32</td><td>.20 (6)</td></tr><tr><td>DZ co‐twin unaffected</td><td>339</td><td>.07 (25)</td></tr><tr><td>MZ co‐twin unaffected</td><td>173</td><td>.06 (10)</td></tr><tr><td>Affected co‐twin</td><td>43</td><td>.18 (9)</td></tr><tr><td>Unaffected co‐twin</td><td>510</td><td>.07 (35)</td></tr></table> </ephtml> </p> <p>4 Inferred genetic risk shown above the horizontal and inferred familial risk below. ‘Risk’ decreases reading down the table within each section.</p> <hd id="AN0087694537-16">Predicting anxiety disorders</hd> <p>Inferred familial risk and attentional bias scores from negative‐neutral trials were included in regression models predicting the presence of an anxiety disorder. Since bias scores were measured in milliseconds, they were standardized to aid interpretation of odd ratios (OR). Age (OR (95% CI) = 0.92 (0.16–5.24)), gender (OR = 1.16; (0.68–2.35) and ethnicity (OR = 0.97; (0.27–3.58) were not significant predictors of anxiety disorders so were dropped from subsequent models. Independent models for attentional bias and inferred familial risk revealed that attentional bias significantly predicted anxiety disorders [OR = 0.65 (0.50–0.85)]. Increased attentional bias scores, indicative of less attentional avoidance, predicted decreased risk of an anxiety disorder. Inferred familial risk approached significance as an independent predictor of anxiety disorders. Children with an affected co‐twin were 3.25 (95% CI = 0.98–10.77) times more likely to have an anxiety disorder themselves. When both attentional bias and inferred familial risk were entered into the model simultaneously attentional bias predicted anxiety disorders to the same extent as when entered independently whilst familial risk became a significant predictor of anxiety disorders. Children with an affected co‐twin were now 3.64 (95% CI = 1.05–12.60) times more likely to have an anxiety disorder themselves.</p> <hd id="AN0087694537-17">Discussion</hd> <p>This study examined aetiological associations between attentional bias, inferred familial risk and anxiety disorder diagnoses in the largest sample exploring attentional biases in children to date. The analyses showed anxious children were significantly more avoidant of negative faces than nonanxious children but attentional bias scores were not influenced by genetic or shared environmental factors. Risk for anxiety disorders was best described by a familial‐risk index, representing both genetic and shared environmental influences. Both attentional avoidance of negative faces and familial risk were significant independent predictors of anxiety disorders.</p> <hd id="AN0087694537-18">Anxiety‐related attentional avoidance of negative faces</hd> <p>Anxiety‐related attentional biases were identified for negative faces in negative‐neutral trials alone, consistent with previous studies revealing biases for negative but not positive stimuli (Mogg et al., 2004) and indicating a degree of specificity in anxiety‐related attentional processes. Exploratory analyses showed no significant difference in biases for specific negative facial expressions suggesting anxiety‐related biases for negative faces generally. This diverges with previous studies which identified anxiety‐related biases specific to certain negative expressions (Stirling et al., 2006). However, Stirling et al. (2006) focused specifically on social anxiety symptoms rather than disorders and it is worth noting that analyses in the current study were exploratory and bias scores for each negative facial expression were calculated from only eight trials.</p> <p>We found no evidence for genetic or shared environmental influence on dot‐probe bias scores suggesting attentional biases are solely influenced by nonshared environmental factors such as peer learning or independent stressful life events (Mogg, Bradley, & Hallowell, 1994). This is the first study to use a dot‐probe task in a twin sample, but findings diverge with those from previous twin studies of related constructs which find moderate genetic effects with little or no influence of shared environment (Eley et al., 2007). The lack of familial effects identified in the current study could in part be due to low statistical power. A priori power analysis in our sample of 300 twin pairs suggested we had 53% power to detect effects of the magnitude previously reported. However, we expected larger heritability estimates as we are tapping into underlying cognitive processes potentially closer to gene expression (Meyer‐Lindenberg & Weinberger, 2006). Failure to detect familial effects could also result from possible unreliability of dot‐probe tasks as implied my low split‐half correlations in the current study. In twin modelling, any unreliability increases estimates of nonshared environment which artificially decreases heritability making it harder to detect. As a result, this study presents an important first step in exploring the aetiology of anxiety‐related attentional bias but replication with larger samples is needed to clarify aetiological influences. In addition, we are currently exploring the psychometric properties of a range of cognitive bias paradigms with children to assess their suitability to explore aetiological questions and are unaware of any previous similar studies.</p> <hd id="AN0087694537-19">Familial risk for anxiety</hd> <p>In the current sample, risk for anxiety disorders was best described by a familial‐risk index representing both genetic and environmental factors. However, the inferred familial‐risk index is unable to disentangle the magnitude of influence attributable to genetic and shared environmental factors separately. Support for both genetic and shared environmental influences is found in twin modelling studies which reveal moderate genetic and modest shared environmental influences on a range of anxiety measures in childhood (Gregory & Eley, 2011).</p> <hd id="AN0087694537-20">Attentional bias, inferred familial risk and anxiety disorders</hd> <p>Regression analyses suggested attentional avoidance of negative faces and inferred familial risk have independent effects on anxiety disorders. This is divergent with previous twin studies showing large genetic correlations between anxiety symptoms and cognitive biases (e.g. Eley et al., 2007). Poor reliability of dot‐probe tasks could explain the lack of aetiological relationship identified between attentional bias and anxiety disorders in our sample. In addition, due to the cross‐sectional nature of the current study the causal role of attentional bias in childhood anxiety disorders cannot be established. However, experimental studies manipulating attentional biases for negative information reveal associated changes in anxiety (Hakamata et al., 2010) consistent with attentional biases representing causal risk factors for anxiety development. Future longitudinal studies should examine the causal role of existing attentional biases in later childhood anxiety.</p> <hd id="AN0087694537-21">Limitations</hd> <p>Although the largest study of anxiety‐related attentional biases in childhood to date, there was low statistical power for twin analyses. Due to financial constraints of in‐person testing, the current sample was smaller than in typical twin studies. Despite positive selection for high maternally reported anxiety at age seven, the incidence of anxiety diagnoses was low; only 47 children met diagnostic criteria for an anxiety disorder. This could in part be because the mean age of the sample was 8 years old and the mean onset age for anxiety disorders is 11 years old (Kessler et al., 2005). Recent evidence suggests that the DAWBA sets a higher threshold for anxiety disorders than some alternative measures (Angold et al., 2012). Consequently, children may have exhibited greater anxiety levels than the general population but failed to meet DAWBA criteria for a diagnosis. Furthermore, the DAWBA is based on current sympomatology rather than lifetime history so those identified as anxious at seven may not present the same symptoms at eight. Categorical inferred risk indices were therefore used instead of traditional twin modelling but a loss of variance compared with continuous parameter estimation further reduced power to identify aetiological relationships between attentional avoidance of threat and the presence of an anxiety disorder.</p> <hd id="AN0087694537-22">Conclusions</hd> <p>This study is one of only a few to examine the aetiological relationships between anxiety‐related cognitive processes and anxiety disorders in childhood and is only the second study to use an experimental paradigm rather than self‐report questionnaire to explore anxiety‐related cognitive biases in a twin design. Furthermore, studies using dot‐probe tasks rarely have samples as large as the one in the current study. As a result, this study represents novel research on the genetic and environmental interplay between cognitive processes and anxiety. We found that both familial risk, representing genetic and shared environmental influences, and attentional avoidance of threat stimuli independently predict the presence of anxiety disorders in middle childhood. Future research should aim to clarify the interplay between these risk factors in childhood anxiety.</p> <hd id="AN0087694537-23">Acknowledgements</hd> <p>The ECHO study is funded by a Career Development Award from the Medical Research Council to the senior author. Thanks goes to the participating families, Alice Gregory, Georgina Hosang, Jennifer Lau, Peter McGuffin, Maria Napolitano, Fiona McCleod, Robert Plomin, Fruhling Rijsdijk, Jasmine Singh and Lucy Stirling for their input at various stages of the project.</p> <p>The authors have declared that they have no competing or potential conflicts of interest.</p> <hd id="AN0087694537-24">Correspondence</hd> <p>Hannah Brown, PO Box 80, Institute of Psychiatry, 16 De Crespigny Park, London SE5 8AF, UK; Email: hannah.brown@kcl.ac.uk</p> <hd id="AN0087694537-25">Key points</hd> <p>• Childhood anxiety disorders are characterized by attentional biases for threatening aspects of the environment.</p> <p>• Twin studies indicate that this association is due in part to their genetic overlap.</p> <p>• This study found that anxiety‐related attentional avoidance of threatening faces and inferred familial risk were independently associated with childhood anxiety disorders, with no evidence for a genetic overlap.</p> <p>• These results suggest that targeting children’s attentional processes could prove useful in influencing the development of anxiety.</p> <p>• Implications and limitations are discussed.</p> <ref id="AN0087694537-26"> <title>Footnotes</title> <blist> <bibl id="bib1" type="bt">1</bibl> <bibtext>Conflict of interest statement: No conflicts declared. </bibtext> </blist> </ref> <ref id="AN0087694537-27"> <title>References</title> <blist> <bibtext>American Psychiatric Association. 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  Data: Attentional Threat Avoidance and Familial Risk are Independently Associated with Childhood Anxiety Disorders
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  Data: <searchLink fieldCode="AR" term="%22Brown%2C+Hannah+M%2E%22">Brown, Hannah M.</searchLink><br /><searchLink fieldCode="AR" term="%22McAdams%2C+Tom+A%2E%22">McAdams, Tom A.</searchLink><br /><searchLink fieldCode="AR" term="%22Lester%2C+Kathryn+J%2E%22">Lester, Kathryn J.</searchLink><br /><searchLink fieldCode="AR" term="%22Goodman%2C+Robert%22">Goodman, Robert</searchLink><br /><searchLink fieldCode="AR" term="%22Clark%2C+David+M%2E%22">Clark, David M.</searchLink><br /><searchLink fieldCode="AR" term="%22Eley%2C+Thalia+C%2E%22">Eley, Thalia C.</searchLink>
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  Data: <searchLink fieldCode="SO" term="%22Journal+of+Child+Psychology+and+Psychiatry%22"><i>Journal of Child Psychology and Psychiatry</i></searchLink>. Jun 2013 54(6):678-685.
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  Data: Wiley-Blackwell. 350 Main Street, Malden, MA 02148. Tel: 800-835-6770; Tel: 781-388-8598; Fax: 781-388-8232; e-mail: cs-journals@wiley.com; Web site: http://www.wiley.com/WileyCDA/
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  Data: <searchLink fieldCode="DE" term="%22Anxiety+Disorders%22">Anxiety Disorders</searchLink><br /><searchLink fieldCode="DE" term="%22Children%22">Children</searchLink><br /><searchLink fieldCode="DE" term="%22Etiology%22">Etiology</searchLink><br /><searchLink fieldCode="DE" term="%22Family+Influence%22">Family Influence</searchLink><br /><searchLink fieldCode="DE" term="%22Bias%22">Bias</searchLink><br /><searchLink fieldCode="DE" term="%22Attention%22">Attention</searchLink><br /><searchLink fieldCode="DE" term="%22Twins%22">Twins</searchLink><br /><searchLink fieldCode="DE" term="%22Correlation%22">Correlation</searchLink><br /><searchLink fieldCode="DE" term="%22Scores%22">Scores</searchLink><br /><searchLink fieldCode="DE" term="%22Comparative+Analysis%22">Comparative Analysis</searchLink><br /><searchLink fieldCode="DE" term="%22Environmental+Influences%22">Environmental Influences</searchLink><br /><searchLink fieldCode="DE" term="%22Genetics%22">Genetics</searchLink><br /><searchLink fieldCode="DE" term="%22Interviews%22">Interviews</searchLink><br /><searchLink fieldCode="DE" term="%22At+Risk+Persons%22">At Risk Persons</searchLink><br /><searchLink fieldCode="DE" term="%22Parents%22">Parents</searchLink><br /><searchLink fieldCode="DE" term="%22Visual+Stimuli%22">Visual Stimuli</searchLink><br /><searchLink fieldCode="DE" term="%22Foreign+Countries%22">Foreign Countries</searchLink><br /><searchLink fieldCode="DE" term="%22Heredity%22">Heredity</searchLink><br /><searchLink fieldCode="DE" term="%22Nonverbal+Communication%22">Nonverbal Communication</searchLink><br /><searchLink fieldCode="DE" term="%22Regression+%28Statistics%29%22">Regression (Statistics)</searchLink>
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  Data: 10.1111/jcpp.12024
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  Data: 0021-9630
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  Data: 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 less than 0.05. 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 = 0.65 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. (Contains 3 tables and 1 figure.)
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      – TitleFull: Attentional Threat Avoidance and Familial Risk are Independently Associated with Childhood Anxiety Disorders
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              Type: published
              Y: 2013
          Identifiers:
            – Type: issn-print
              Value: 0021-9630
          Numbering:
            – Type: volume
              Value: 54
            – Type: issue
              Value: 6
          Titles:
            – TitleFull: Journal of Child Psychology and Psychiatry
              Type: main
ResultId 1