scholarly journals Evidence for distinct genetic and environmental influences on fear acquisition and extinction

2021 ◽  
pp. 1-9
Author(s):  
K. L. Purves ◽  
G. Krebs ◽  
T. McGregor ◽  
E. Constantinou ◽  
K. J. Lester ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Age Of Onset ◽  
Environmental Influences ◽  
Genetic Correlations ◽  
Fear Learning ◽  
Shared Environment ◽  
Conditioning Experiment ◽  
Preventative Measures ◽  
Genetic Overlap ◽  
Experimental Approaches

Abstract Background Anxiety disorders are highly prevalent with an early age of onset. Understanding the aetiology of disorder emergence and recovery is important for establishing preventative measures and optimising treatment. Experimental approaches can serve as a useful model for disorder and recovery relevant processes. One such model is fear conditioning. We conducted a remote fear conditioning paradigm in monozygotic and dizygotic twins to determine the degree and extent of overlap between genetic and environmental influences on fear acquisition and extinction. Methods In total, 1937 twins aged 22–25 years, including 538 complete pairs from the Twins Early Development Study took part in a fear conditioning experiment delivered remotely via the Fear Learning and Anxiety Response (FLARe) smartphone app. In the fear acquisition phase, participants were exposed to two neutral shape stimuli, one of which was repeatedly paired with a loud aversive noise, while the other was never paired with anything aversive. In the extinction phase, the shapes were repeatedly presented again, this time without the aversive noise. Outcomes were participant ratings of how much they expected the aversive noise to occur when they saw either shape, throughout each phase. Results Twin analyses indicated a significant contribution of genetic effects to the initial acquisition and consolidation of fear, and the extinction of fear (15, 30 and 15%, respectively) with the remainder of variance due to the non-shared environment. Multivariate analyses revealed that the development of fear and fear extinction show moderate genetic overlap (genetic correlations 0.4–0.5). Conclusions Fear acquisition and extinction are heritable, and share some, but not all of the same genetic influences.

scholarly journals Evidence for distinct genetic and environmental influences on fear acquisition and extinction

2020 ◽  
Author(s):  
K. L. Purves ◽  
G. Krebs ◽  
T. McGregor ◽  
E. Constantinou ◽  
K.J. Lester ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Age Of Onset ◽  
Environmental Influences ◽  
Genetic Correlations ◽  
Fear Learning ◽  
Shared Environment ◽  
Conditioning Experiment ◽  
Preventative Measures ◽  
Genetic Overlap ◽  
Experimental Approaches

AbstractBackgroundAnxiety disorders are highly prevalent with an early age of onset. Understanding the aetiology of disorder emergence and recovery is important for establishing preventative measures and optimising treatment. Experimental approaches can serve as a useful model for disorder and recovery relevant processes. One such model is fear conditioning. We conducted a remote fear conditioning paradigm in monozygotic and dizygotic twins to determine the degree and extent of overlap between genetic and environmental influences on fear acquisition and extinction.Methods1937 twins aged 22-25 years, including 538 complete pairs from the Twins Early Development Study (TEDS) took part in a fear conditioning experiment delivered remotely via the Fear Learning and Anxiety Response (FLARe) smartphone app.In the fear acquisition phase participants were exposed to two neutral shape stimuli, one of which was repeatedly paired with a loud aversive noise, while the other was never paired with anything aversive. In the extinction phase the shapes were repeatedly presented again, this time without the aversive noise. Outcomes were participant ratings of how much they expected the aversive noise to occur when they saw either shape, throughout each phase.ResultsTwin analyses indicated a significant contribution of genetic effects to the initial acquisition and consolidation of fear, and the extinction of fear (15%, 30% and 15% respectively) with the remainder of variance due to the non-shared environment. Multivariate analyses revealed that the development of fear and fear extinction show moderate genetic overlap (genetic correlations .4-.5).ConclusionsFear acquisition and extinction are heritable, and share some, but not all of the same genetic influences.

scholarly journals Validating the Use of a Smartphone App for Remote Administration of a Fear Conditioning Paradigm

2019 ◽  
Author(s):  
Kirstin Lee Purves ◽  
Elena Constantinou ◽  
Thomas McGregor ◽  
Kathryn J. Lester ◽  
Tom Joseph Barry ◽  
...  
Keyword(s):  
Individual Differences ◽  
Fear Conditioning ◽  
Reliability And Validity ◽  
Fear Learning ◽  
Group Differences ◽  
Smartphone App ◽  
Total N ◽  
Conditioning Paradigm ◽  
Large Samples ◽  
Conditioning Experiment

Fear conditioning models key processes related to the development, maintenance and treatment of anxiety disorders and is associated with group differences in anxiety. However, laboratory administration of tasks is time and cost intensive, precluding assessment in large samples, necessary for analysis of individual differences. This study introduces a newly developed smartphone app that delivers a fear conditioning paradigm remotely. Three groups of participants (total n=152) took part in three studies involving a differential fear conditioning experiment to assess the reliability and validity of a smartphone administered fear conditioning paradigm. This comprised of fear acquisition, generalisation, extinction, and renewal phases. We show that smartphone app delivery of a fear conditioning paradigm results in a pattern of fear learning comparable to traditional laboratory delivery, and is able to detect individual differences in performance that show comparable associations with anxiety to the prior group differences literature.

Genetic and Environmental Influences on Executive Functions and Intelligence in the ABCD Study

2020 ◽  
Author(s):  
Samantha M Freis ◽  
Claire Morrison ◽  
Jeffrey M. Lessem ◽  
John K. Hewitt ◽  
Naomi P. Friedman
Keyword(s):  
Cognitive Development ◽  
Executive Functions ◽  
Genetic Correlation ◽  
Middle Childhood ◽  
Middle Age ◽  
Environmental Influences ◽  
Genetic Correlations ◽  
Twin Studies

Executive functions (EFs) and intelligence (IQ) are phenotypically correlated and heritable; however, they show variable genetic correlations in twin studies spanning childhood to middle age. We analyzed data from over 11,000 children (9-10-year-olds, including 749 twin pairs) in the Adolescent Brain Cognitive Development (ABCD) Study to examine the phenotypic and genetic relations between EFs and IQ in childhood. We identified two EF factors – Common EF and Updating-Specific, which were both related to IQ (rs = .64-.81). Common EF and IQ were heritable (53-67%), and their genetic correlation (rG = .86) was not significantly different than 1. These results suggest that EFs and IQ are phenotypically but not genetically separable in middle childhood.

scholarly journals Fear conditioning and stimulus generalization in association with age in children and adolescents

2021 ◽  
Author(s):  
Julia Reinhard ◽  
Anna Slyschak ◽  
Miriam A. Schiele ◽  
Marta Andreatta ◽  
Katharina Kneer ◽  
...  
Keyword(s):  
Children And Adolescents ◽  
Fear Conditioning ◽  
Repeated Measures ◽  
Conditioned Fear ◽  
Fear Learning ◽  
Stimulus Generalization ◽  
Healthy Children ◽  
Older Individuals ◽  
Age Related ◽  
Current Task

AbstractThe aim of the study was to investigate age-related differences in fear learning and generalization in healthy children and adolescents (n = 133), aged 8–17 years, using an aversive discriminative fear conditioning and generalization paradigm adapted from Lau et al. (2008). In the current task, participants underwent 24 trials of discriminative conditioning of two female faces with neutral facial expressions, with (CS+) or without (CS−) a 95-dB loud female scream, presented simultaneously with a fearful facial expression (US). The discriminative conditioning was followed by 72 generalization trials (12 CS+, 12 GS1, 12 GS2, 12 GS3, 12 GS4, and 12 CS−): four generalization stimuli depicting gradual morphs from CS+ to CS− in 20%-steps were created for the generalization phases. We hypothesized that generalization in children and adolescents is negatively correlated with age. The subjective ratings of valence, arousal, and US expectancy (the probability of an aversive noise following each stimulus), as well as skin conductance responses (SCRs) were measured. Repeated-measures ANOVAs on ratings and SCR amplitudes were calculated with the within-subject factors stimulus type (CS+, CS−, GS1-4) and phase (Pre-Acquisition, Acquisition 1, Acquisition 2, Generalization 1, Generalization 2). To analyze the modulatory role of age, we additionally calculated ANCOVAs considering age as covariate. Results indicated that (1) subjective and physiological responses were generally lower with increasing age irrespective to the stimulus quality, and (2) stimulus discrimination improved with increasing age paralleled by reduced overgeneralization in older individuals. Longitudinal follow-up studies are required to analyze fear generalization with regard to brain maturational aspects and clarify whether overgeneralization of conditioned fear promotes the development of anxiety disorders or vice versa.

scholarly journals Sex differences and developmental stability in genetic and environmental influences on psychoactive substance consumption from early adolescence to young adulthood

2011 ◽  
Vol 41 (9) ◽  
pp. 1907-1916 ◽  
Author(s):  
J. H. Baker ◽  
H. H. Maes ◽  
H. Larsson ◽  
P. Lichtenstein ◽  
K. S. Kendler
Keyword(s):  
Substance Use ◽  
Young Adulthood ◽  
Early Adolescence ◽  
Illicit Drug ◽  
Common Factor ◽  
Environmental Influences ◽  
Genetic Effects ◽  
Shared Environment ◽  
Males And Females ◽  
Substance Consumption

BackgroundGenetic and environmental factors are important in the etiology of substance use. However, little is known about the stability of these factors across development. We aimed to answer three crucial questions about this etiology that have never been addressed in a single study: (1) Is there a general vulnerability to substance consumption from early adolescence to young adulthood? (2) If so, do the genetic and environmental influences on this vulnerability change across development? (3) Do these developmental processes differ in males and females?MethodSubjects included 1480 twin pairs from the Swedish Twin Study of Child and Adolescent Development who have been followed since 1994. Prospective, self-reported regular smoking, alcohol intoxication and illicit drug use were assessed at ages 13–14, 16–17 and 19–20 years. Structural modeling was performed with the program Mx.ResultsAn underlying common factor accounted for the association between smoking, alcohol and illicit drug consumption for the three age groups. Common genetic and shared environmental effects showed substantial continuity. In general, as participants aged, the influence of the shared environment decreased, and genetic effects became more substance specific in their effect.ConclusionsThe current report answers three important questions in the etiology of substance use. The genetic and environmental risk for substance consumption is partly mediated through a common factor and is partly substance specific. Developmentally, evidence was strongest for stability of common genetic effects, with less evidence for genetic innovation. These processes seem to be the same in males and females.

Are prescription misuse and illicit drug use etiologically distinct? A genetically-informed analysis of opioids and stimulants

2021 ◽  
pp. 1-8
Author(s):  
Genevieve F. Dash ◽  
Nicholas G. Martin ◽  
Arpana Agrawal ◽  
Michael T. Lynskey ◽  
Wendy S. Slutske
Keyword(s):  
Illicit Drugs ◽  
Environmental Influences ◽  
Genetic Influence ◽  
Prescription Opioid ◽  
Future Research ◽  
Shared Environment ◽  
Opioid Use ◽  
Stimulant Use ◽  
Prescription Opioid Misuse ◽  
Illicit Opioid Use

Abstract Background Drug classes are grouped based on their chemical and pharmacological properties, but prescription and illicit drugs differ in other important ways. Potential differences in genetic and environmental influences on the (mis)use of prescription and illicit drugs that are subsumed under the same class should be examined. Opioid and stimulant classes contain prescription and illicit forms differentially associated with salient risk factors (common route of administration, legality), making them useful comparators for addressing this etiological issue. Methods A total of 2410 individual Australian twins [Mage = 31.77 (s.d. = 2.48); 67% women] were interviewed about prescription misuse and illicit use of opioids and stimulants. Univariate and bivariate biometric models partitioned variances and covariances into additive genetic, shared environmental, and unique environmental influences across drug types. Results Variation in the propensity to misuse prescription opioids was attributable to genes (41%) and unique environment (59%). Illicit opioid use was attributable to shared (71%) and unique (29%) environment. Prescription stimulant misuse was attributable to genes (79%) and unique environment (21%). Illicit stimulant use was attributable to genes (48%), shared environment (29%), and unique environment (23%). There was evidence for genetic influence common to both stimulant types, but limited evidence for genetic influence common to both opioid types. Bivariate correlations suggested that prescription opioid use may be more genetically similar to prescription stimulant use than to illicit opioid use. Conclusions Prescription opioid misuse may share little genetic influence with illicit opioid use. Future research may consider avoiding unitary drug classifications, particularly when examining genetic influences.

Genetic and environmental influences on teacher ratings of the Child Behavior Checklist

2000 ◽  
Vol 24 (3) ◽  
pp. 373-381 ◽  
Author(s):  
Hilary Towers ◽  
Erica Spotts ◽  
Jenae M. Neiderhiser ◽  
Robert Plomin ◽  
E. Mavis Hetherington ◽  
...  
Keyword(s):  
Child Behavior ◽  
Child Behavior Checklist ◽  
Social Problems ◽  
Genetic Factors ◽  
Environmental Influences ◽  
Teacher Ratings ◽  
Attention Problems ◽  
Shared Environment ◽  
Sibling Pairs ◽  
Self Reports

The knowledge we have of childhood and adolescent behaviour is, to some extent, a function of the unique perspective of the rater. Although many behavioural genetics studies have used parent and child self-reports in their assessments of child and adolescent adjustment, few have included teacher ratings of behaviour. It is possible that genetic and environmental contributions to teacher reports are different from those using parent and self-reports. The present study examined genetic and environmental influences on six subscales of the Child Behavior Checklist Teacher Report Form (CBC-TRF) using a normative sample of adolescents. The sample consisted of 373 same-sex twin and sibling pairs of varying degrees of genetic relatedness participating in the Nonshared Environment in Adolescent project (NEAD). For all of the CBC subscales, except attention problems and social problems, nonshared environmental influence was the most important source of variance. Additive genetic factors were of moderate importance for externalising behaviours, whereas nonadditive genetic factors contributed to the anxious/depressed, attention problems, withdrawn, and social problems subscales. For none of the constructs was shared environment a significant influence. Three alternative models testing for contrast effects, differences in twin and nontwin siblings, and differences in nondivorced and stepfamilies were examined. In most cases, the best-fitting model was a model that did not include any of these effects, suggesting that these factors do not critically affect the basic model. However, some of the patterns of correlations and parameter estimates were unusual and may warrant future investigation.

scholarly journals Genetic overlap between Alzheimer’s disease and depression mapped onto the brain

2021 ◽  
Author(s):  
Jennifer Monereo Sánchez ◽  
Miranda T. Schram ◽  
Oleksandr Frei ◽  
Kevin O’Connell ◽  
Alexey A. Shadrin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genome Wide Association Study ◽  
Brain Mri ◽  
Genetic Correlations ◽  
Gaussian Mixture ◽  
Brain Morphology ◽  
Uk Biobank ◽  
Genetic Overlap ◽  
The Uk

ABSTRACTBackgroundAlzheimer’s disease (AD) and depression are debilitating brain disorders that are often comorbid. Shared brain mechanisms have been implicated, yet findings are inconsistent, reflecting the complexity of the underlying pathophysiology. As both disorders are (partly) heritable, characterizing their genetic overlap may provide etiological clues. While previous studies have indicated negligible genetic correlations, this study aims to expose the genetic overlap that may remain hidden due to mixed directions of effects.MethodsWe applied Gaussian mixture modelling, through MiXeR, and conjunctional false discovery rate (cFDR) analysis, through pleioFDR, to genome-wide association study (GWAS) summary statistics of AD (n=79,145) and depression (n=450,619). The effects of identified overlapping loci on AD and depression were tested in 403,029 participants of the UK Biobank (mean age 57.21 52.0% female), and mapped onto brain morphology in 30,699 individuals with brain MRI data.ResultsMiXer estimated 98 causal genetic variants overlapping between the two disorders, with 0.44 concordant directions of effects. Through pleioFDR, we identified a SNP in the TMEM106B gene, which was significantly associated with AD (B=-0.002, p=9.1×10−4) and depression (B=0.007, p=3.2×10−9) in the UK Biobank. This SNP was also associated with several regions of the corpus callosum volume anterior (B>0.024, p<8.6×10−4), third ventricle volume ventricle (B=-0.025, p=5.0×10−6), and inferior temporal gyrus surface area (B=0.017, p=5.3×10−4).DiscussionOur results indicate there is substantial genetic overlap, with mixed directions of effects, between AD and depression. These findings illustrate the value of biostatistical tools that capture such overlap, providing insight into the genetic architectures of these disorders.

scholarly journals Genetic Overlap Between Alzheimer’s Disease and Depression Mapped Onto the Brain

2021 ◽  
Vol 15 ◽  
Author(s):  
Jennifer Monereo-Sánchez ◽  
Miranda T. Schram ◽  
Oleksandr Frei ◽  
Kevin O’Connell ◽  
Alexey A. Shadrin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Genome Wide Association Study ◽  
Third Ventricle ◽  
Brain Mri ◽  
Genetic Correlations ◽  
Gaussian Mixture ◽  
Brain Morphology ◽  
Genetic Overlap ◽  
Ventricle Volume

Background: Alzheimer’s disease (AD) and depression are debilitating brain disorders that are often comorbid. Shared brain mechanisms have been implicated, yet findings are inconsistent, reflecting the complexity of the underlying pathophysiology. As both disorders are (partly) heritable, characterising their genetic overlap may provide aetiological clues. While previous studies have indicated negligible genetic correlations, this study aims to expose the genetic overlap that may remain hidden due to mixed directions of effects.Methods: We applied Gaussian mixture modelling, through MiXeR, and conjunctional false discovery rate (cFDR) analysis, through pleioFDR, to genome-wide association study (GWAS) summary statistics of AD (n = 79,145) and depression (n = 450,619). The effects of identified overlapping loci on AD and depression were tested in 403,029 participants of the UK Biobank (UKB) (mean age 57.21, 52.0% female), and mapped onto brain morphology in 30,699 individuals with brain MRI data.Results: MiXer estimated 98 causal genetic variants overlapping between the 2 disorders, with 0.44 concordant directions of effects. Through pleioFDR, we identified a SNP in the TMEM106B gene, which was significantly associated with AD (B = −0.002, p = 9.1 × 10–4) and depression (B = 0.007, p = 3.2 × 10–9) in the UKB. This SNP was also associated with several regions of the corpus callosum volume anterior (B &gt; 0.024, p &lt; 8.6 × 10–4), third ventricle volume ventricle (B = −0.025, p = 5.0 × 10–6), and inferior temporal gyrus surface area (B = 0.017, p = 5.3 × 10–4).Discussion: Our results indicate there is substantial genetic overlap, with mixed directions of effects, between AD and depression. These findings illustrate the value of biostatistical tools that capture such overlap, providing insight into the genetic architectures of these disorders.

Genetic and environmental influences on the relationship between adult ADHD symptoms and self-reported problem drinking in 6024 Dutch twins

2014 ◽  
Vol 44 (12) ◽  
pp. 2673-2683 ◽  
Author(s):  
E. M. Derks ◽  
J. M. Vink ◽  
G. Willemsen ◽  
W. van den Brink ◽  
D. I. Boomsma
Keyword(s):  
Alcohol Use ◽  
Adult Adhd ◽  
Rating Scales ◽  
Problem Drinking ◽  
Environmental Influences ◽  
Genetic Correlations ◽  
Self Report ◽  
Adhd Symptoms ◽  
Phenotypic Correlations ◽  
Dutch Twins

BackgroundCross-sectional and longitudinal studies have shown a positive association between attention deficit hyperactivity disorder (ADHD) and problematic alcohol use in adults. To what extent this association is explained by genetic and environmental factors is largely unknown.MethodData on ADHD and alcohol consumption were collected by self-report in 6024 adult Dutch twins. ADHD symptoms were assessed by three subscales of the Conners' Adult ADHD Rating Scales – Self-Report: Screening Version (CAARS–S:SV): inattentiveness, hyperactivity and the ADHD index (ADHD-I). Problem drinking was defined as at least two self-reported alcohol-related problems on the CAGE questionnaire. Structural equation modelling was applied to the bivariate twin data to estimate genetic and environmental influences.ResultsHeritability of ADHD symptoms ranged between 32% and 40% and heritability of problem drinking was 50%. The positive correlation between ADHD symptoms and problem drinking was confirmed in this general population sample, with phenotypic correlations between 0.20 and 0.28 and genetic correlations between 0.39 and 0.50. Phenotypic correlations are primarily (61–100%) explained by genetic influences with non-shared environmental influences explaining the remaining covariance. No significant quantitative or qualitative gender differences in covariance structure were found.ConclusionsThis study convincingly shows that ADHD symptoms and problem drinking are moderately but significantly correlated in adults and that genetic correlations are primarily underlying this association. This suggests that early interventions are required to prevent adolescents with ADHD from developing problematic levels of alcohol use. Furthermore, clinicians who treat alcohol-dependent patients should be aware that the patient may have a co-morbid condition of ADHD; integrated interventions are required.

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