What is the genetic relationship between anxiety and depression?

Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, VA 23298-0126, USA.
American Journal of Medical Genetics Part C Seminars in Medical Genetics (Impact Factor: 3.91). 05/2008; 148C(2):140-6. DOI: 10.1002/ajmg.c.30171
Source: PubMed


Anxiety and depression share a long, close history in psychiatric nosology and treatment. The anxiety disorders, individually and as a group, exhibit remarkably high rates of comorbidity with each other and with major depression. Analyses done in large-scale epidemiologic surveys have identified major patterns of phenomenological overlap between these conditions. Researchers have tested hypotheses of shared genetic etiologies as a potential basis of this relationship. In general, available family studies have found mixed evidence for co-aggregation of anxiety and depressive disorders, while twin studies more definitively indicate that shared genetic risk factors largely account for this comorbidity. Some of this appears to be accounted for by genetic variation in personality traits that broadly predispose to anxiety and depression. Molecular genetic studies of these conditions, though too early to draw firm conclusions, thus far provide tentative support for specific genetic loci that may generally influence susceptibility across the anxiety-depressive spectrum.

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    • "This efficacy indicates that the serotonin system is very involved in stress and worrying; more accurately, drugs that interfere with the activity of the serotonergic system can be used to treat disorders that are accompanied by stress reactions and cognitive anxious and/or depressed symptoms. Symptoms of anxiety and depression commonly co-occur[5], and at least some evidence has been found for shared genetic aetiologies between these conditions[6]. Moreover, experiments with 'serotonergic' interventions led to the defining of a new subtype of depression, designated as 'anxiety/aggression-driven depression'[7]. "
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    ABSTRACT: The introduction of selective serotonin reuptake inhibitors has gradually changed the borders of the major depression disease class. Anhedonia was considered a cardinal symptom of endogenous depression, but the potential of selective serotonin reuptake inhibitors to treat anxiety disorders has increased the relevance of stress-induced morbidity. This shift has led to an important heterogeneity of current major depressive disorder. The complexity can be disentangled by postulating the existence of two different but mutually interacting neuronal circuits regulating the intensity of anhedonia (lack of pleasure) and dysphoria (lack of happiness). These circuits are functionally dominated by partly closed limbic (regulating misery-fleeing behaviour) and extrapyramidal (regulating reward-seeking behaviour) cortico-striato-thalamo-cortical (CSTC) circuits. The re-entry circuits include the shell and core parts of the accumbens nucleus, respectively. Pleasure can be considered to result from finding relief from the hypermotivation to exhibit rewarding behaviour, and happiness from finding relief from negative or conflicting circumstances. Hyperactivity of the extrapyramidal CSTC circuit results in craving, whereas hyperactivity of the limbic system results in dysphoria.
    Full-text · Article · Feb 2016 · Medical Hypotheses
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    • "A degree of clustering was introduced to account for patterns of shared liabilities between individual disorders above and beyond those introduced by life history variation. Specifically, MDD and GAD were part of a depression/GAD cluster (see Hettema, 2008; Lahey et al., 2011), whereas schizophrenia and mania were part of a psychosis cluster (see Cosgrove & Suppes, 2013; Crespi, Stead, & Elliot, 2010; International Schizophrenia Consortium, 2009). In the life history model, the autogenous subtype of OCD (but not the reactive subtype) is regarded as a functional correlate of the psychosis spectrum (Del Giudice, 2014a); to reflect this assumption, OCD was included in two overlapping clusters—the psychosis cluster and a separate OCD cluster. "
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    ABSTRACT: In recent years, tremendous progress has been made in mapping the structure of comorbidity between psychiatric disorders. In particular, empirical findings have suggested the existence of a general p factor of susceptibility to psychopathology. In the present study, simulation methods were used to test whether the observed structure of psychiatric disorders can be reproduced by the life history model of psychopathology, a recent classification model based on evolutionary theory. The assumptions of the life history model were used to generate virtual epidemiological samples, which were then analyzed with the methods used by earlier researchers. Analyses of simulated data successfully replicated the key findings by these researchers, including the emergence of the p factor and the switch from positive to negative correlation between internalizing and externalizing symptoms after inclusion of the p factor. These results offer initial support for the validity of the life history model.
    Full-text · Article · Aug 2015 · Clinical Psychological Science
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    • "We present robust findings of a gender–age interaction with a male preponderance before puberty and a female preponderance after. The gender–age interaction is present for both depressive disorders and anxiety disorders, supporting existing theories of an affective-anxious spectrum (Hudson et al. 2003; Middeldorp et al. 2005; Weissman et al. 2005; Hettema, 2008; Gardner & Boles, 2011). We hypothesize that males have a generalized prepubertal vulnerability towards a broader spectrum of mental disorders, rather than just neurodevelopmental disorders. "
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    ABSTRACT: Background: The post-pubertal association of female gender with emotional disorder is a robust finding. However, studies exploring the association of gender and emotional disorders before puberty are few and present diverging results. The aim of this study was to present gender-specific incidence rates of emotional disorders throughout childhood. Method: This is a population-based cohort study of 907,806 Danish 3- to 18-year-olds. The outcome was assignment of an emotional disorder diagnosis based on in-patient and out-patient data from The Danish Psychiatric Central Register. Outcome measures were incidence rates and cumulative incidences for unipolar depressive disorder (ICD-10: F32-F33), anxiety disorders (ICD-10: F40-F42), and emotional disorders with onset specific to childhood (ICD-10: F93). Results: Pre-pubertal incidence rates for depressive and anxiety disorders were higher for boys than girls. At age 12 years the pattern reversed. The cumulative incidence for any emotional disorder (F32-F33, F40-F42, F93) on the 11th birthday was 0.52% (95% CI 0.50-0.55) for boys and 0.31% (95% CI 0.29-0.33) for girls. On the 19th birthday cumulative incidence was 2.33% (95% CI 2.24-2.43) for boys and 3.77% (95% CI 3.64-3.90) for girls. The pre-pubertal male preponderance was also significant for depressive disorders (F32-F33, p = 0.00144) and anxiety disorders (F40-F42, F93, p < 0.00001) separately. Conclusions: Emotional disorders seem to display a male preponderance before the age of 12 years and a female preponderance thereafter. Studies exploring this gender-age interaction are needed. Still, the results question the general assumption that females throughout the lifespan are more at risk for emotional disorders than males.
    Full-text · Article · Aug 2014 · Psychological Medicine
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