scholarly journals Genetics of generalized anxiety disorder and related traits

2017 ◽  
Vol 19 (2) ◽  
pp. 159-168 ◽  
Keyword(s):  
Anxiety Disorder ◽  
Generalized Anxiety Disorder ◽  
Reuptake Inhibitor ◽  
Stressful Life Events ◽  
Association Studies ◽  
Twin Studies ◽  
Generalized Anxiety ◽  
Environment Interaction ◽  
Genome Wide Association Studies ◽  
Clinical Genetic

This review serves as a systematic guide to the genetics of generalized anxiety disorder (GAD) and further focuses on anxiety-relevant endophenotypes, such as pathological worry fear of uncertainty, and neuroticism. We inspect clinical genetic evidence for the familialityl heritability of GAD and cross-disorder phenotypes based on family and twin studies. Recent advances of linkage studies, genome-wide association studies, and candidate gene studies (eg, 5-HTT, 5-HT1A, MAOA, BDNF) are outlined. Functional and structural neuroimaging and neurophysiological readouts relating to peripheral stress markers and psychophysiology are further integrated, building a multilevel disease framework. We explore etiologic factors in gene-environment interaction approaches investigating childhood trauma, environmental adversity, and stressful life events in relation to selected candidate genes (5-HTT, NPSR1, COMT, MAOA, CRHR1, RGS2), Additionally, the pharmacogenetics of selective serotonin reuptake inhibitor/serotonin-norepinephrine reuptake inhibitor treatment are summarized (5-HTT, 5-HT2A, COMT, CRHR1). Finally, GAD and trait anxiety research challenges and perspectives in the field of genetics, including epigenetics, are discussed.

scholarly journals THE IMPACT OF STRESSFUL LIFE EVENTS ON RELAPSE OF GENERALIZED ANXIETY DISORDER

2012 ◽  
Vol 29 (5) ◽  
pp. 386-391 ◽  
Author(s):  
Jennifer L. Francis ◽  
Ethan Moitra ◽  
Ingrid Dyck ◽  
Martin B. Keller
Keyword(s):  
Anxiety Disorder ◽  
Life Events ◽  
Generalized Anxiety Disorder ◽  
Stressful Life Events ◽  
Stressful Life ◽  
Generalized Anxiety ◽  
The Impact

The impact of generalized anxiety disorder and stressful life events on risk for major depressive episodes

2006 ◽  
Vol 36 (6) ◽  
pp. 789-795 ◽  
Author(s):  
JOHN M. HETTEMA ◽  
JONATHAN W. KUHN ◽  
CAROL A. PRESCOTT ◽  
KENNETH S. KENDLER
Keyword(s):  
Anxiety Disorder ◽  
Life Events ◽  
Generalized Anxiety Disorder ◽  
Stressful Life Events ◽  
Stressful Life ◽  
Generalized Anxiety ◽  
Major Depressive ◽  
Major Depressive Episodes ◽  
Depressive Episodes ◽  
The Impact

Background. Both generalized anxiety disorder (GAD) and stressful life events (SLEs) are established risk factors for major depressive disorder, but no studies exist that examine the interrelationship of their impact on depressive onsets. In this study, we sought to analyze the joint effects of prior history of GAD and recent SLEs on risk for major depressive episodes, comparing these in men and women.Method. In a population-based sample of 8068 adult twins, Cox proportional hazard models were used to predict onsets of major depression from reported prior GAD and last-year SLEs rated on long-term contextual threat.Results. For all levels of threat, prior GAD increases risk for depression, with a monotonic relationship between threat level and risk. While females without prior GAD consistently show higher depressive risk than males, this is no longer the case in subjects with prior GAD who have experienced SLEs. Rather, males appear to be more vulnerable to the depressogenic effects of both prior GAD and SLEs.Conclusion. The effects of prior GAD and SLEs jointly increase the risk of depression in both sexes, but disproportionately so in males.

Genetics

2018 ◽  
Author(s):  
Carol Kan ◽  
Ma-Li Wong
Keyword(s):  
Complex Traits ◽  
Association Studies ◽  
Genetic Correlations ◽  
Twin Studies ◽  
Epidemiological Studies ◽  
Environment Interaction ◽  
Genome Wide Association Studies ◽  
Small Magnitude ◽  
Gene Environment ◽  
Genetic Overlap

An association between type 2 diabetes mellitus (T2DM) and depression has been reported in epidemiological studies. Finding a genetic overlap between T2DM and depression will provide evidence to support a common biological pathway to both disorders. Genetic correlations observed from twin studies indicate that a small magnitude of the variance in liability can be attributed to genetic factors. However, no genetic overlap has been observed between T2DM and depression in genome-wide association studies using both the polygenic score and the linkage disequilibrium score regression approaches. Clarifying the shared heritability between these two complex traits is an important next step towards better therapy and treatment. Another area that needs to be explored is gene–environment interaction, since genotypes can affect an individual’s responses to the environment and environment can differentially affect genotypes expression.

Generalized anxiety disorder and major depressive disorder comorbidity: an example of genetic pleiotropy?

2004 ◽  
Vol 19 (1) ◽  
pp. 27-33 ◽  
Author(s):  
P. Gorwood
Keyword(s):  
Major Depressive Disorder ◽  
Anxiety Disorder ◽  
Depressive Disorder ◽  
Generalized Anxiety Disorder ◽  
Twin Studies ◽  
Genetic Mutation ◽  
Generalized Anxiety ◽  
Major Depressive ◽  
Single Genetic Mutation ◽  
High Comorbidity

AbstractGeneralized anxiety disorder (GAD) and major depressive disorder (MDD) are the most common type of anxiety-mood comorbidity. Up to 80% of subjects with lifetime GAD also have a comorbid mood disorder during their lifetime. Many hypotheses have been raised to explain such high comorbidity. Pleiotropy, i.e. a single genetic mutation explains (apparently) different disorders, is one of them and is hereby reviewed. Importance and reliability of GAD and MDD comorbidity (1); Evidence in favour of co-aggregation of GAD and MDD within families (the risk of one disorder in a proband increasing the risk for the other in relatives) (2); substantial heredity for both disorders according to twin studies with evidence for genetic correlation of unity between the two disorders (3); existence of numerous mechanisms (4) potentially linking the two disorders to common vulnerability genes, are all in accordance with such a hypothesis. Some examples of potentially shared mechanisms (such as CRF dysregulation or abnormal transcription factors) and possible common vulnerability genes (for example, the serotonin transporter gene) are given to highlight the pleiotropy hypothesis.

scholarly journals When Anxiety Actually Hides an Overdose of Missing. The Therapeutic Approach of a Transgenerational Journey

2020 ◽  
Vol 11 (3sup1) ◽  
pp. 48-53
Author(s):  
Mioara Grigoraş ◽  
Keyword(s):  
Anxiety Disorder ◽  
General Population ◽  
Anxiety Disorders ◽  
Generalized Anxiety Disorder ◽  
Stressful Life Events ◽  
Early Adulthood ◽  
Panic Attacks ◽  
Generalized Anxiety ◽  
Cultural Aspects ◽  
Unrealistic Expectations

Many people suffer from anxiety and panic attacks, statistics showing that 1 in 3 people have their lives affected because of these worrying and annoying symptoms. One of the most common anxiety disorders observed in general medical practice and in the general population is the generalized anxiety disorder. In about 85% of cases, generalized anxiety does not appear alone, but is accompanied by other psychological problems, of which the most common are: depression, other anxiety disorders, substance abuse, digestive problems, etc. The patient diagnosed with Generalized Anxiety Disorder (GAD) usually has suffered from severe anxiety and worries about several different areas of their life for at least six months. It occurs in 5-9% of the population, and the incidence is twice as high in women as in men. Generalized anxiety usually begins in adolescence or early adulthood. GAG is caused by several factors: 30%-50% of it can be genetic in nature, but it also can be caused by experiences during childhood, recent stressful life events, unrealistic expectations about others and oneself, conflicts in relationships, alcohol consumption, coping skills and other factors (Ciubara et al., 2018). Studies show that the anxiety levels in the general population have risen over the past 50 years - probably due to declining social cohesion affecting communities, unrealistic expectations for quality of life, excessive focus on negative news, and other factors, social and cultural aspects.

Genetic Risk Factors of Depression

Depression ◽  
2019 ◽  
pp. 33-50
Author(s):  
Thorhildur Halldorsdottir ◽  
Hildur Ýr Hilmarsdottir
Keyword(s):  
Genetic Risk ◽  
Familial Aggregation ◽  
Association Studies ◽  
Twin Studies ◽  
Risk Scores ◽  
Environment Interaction ◽  
Genome Wide Association Studies ◽  
Gene By Environment Interaction ◽  
Genome Wide ◽  
Candidate Gene Studies

Research on the genetic underpinnings of depression has rapidly advanced in the past decade. This field of research provides a promising avenue toward improving the diagnosis of, prevention of, and treatment for this devastating disorder. The goal of this chapter is to review the main genetic and gene-by-environment interaction findings on depression. We first describe family and twin studies used to empirically study the familial aggregation of depression. Second, we provide a review of the genome-wide association studies (GWAS) published to date. Building on GWAS findings, we will discuss the use of polygenic risk scores in predicting depression. We also review the most robust candidate gene studies and gene-by-environment interaction studies. Finally, we discuss the clinical implications of the findings and promising strategies for making further progress within this field.

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