What is the genetic relationship between anxiety and depression?
ABSTRACT 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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ABSTRACT: In this article, I outline a general framework for the evolutionary analysis of mental disorders based on the concepts of life history theory. I synthesize and extend a large body of work showing that individual differences in life history strategy set the stage for the development of psychopathology. My analysis centers on the novel distinction between fast spectrum and slow spectrum disorders. I describe four main causal pathways from life history strategies to psychopathology, argue that psychopathology can arise at both ends of the fast–slow continuum of life history variation, and provide heuristic criteria for classifying disorders as fast or slow spectrum pathologies. I then apply the fast–slow distinction to a diverse sample of common mental disorders: externalizing disorders, schizophrenia and autism spectrum disorders, obsessive-compulsive disorders, eating disorders, and depression. The framework integrates previously disconnected models of psychopathology within a common frame of reference and has far-reaching implications for the classification of mental disorders.Psychological Inquiry 08/2014; 25(3-4):261. · 4.73 Impact Factor
- Psychological Inquiry 08/2014; 25(3-4):394-413. · 4.73 Impact Factor
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ABSTRACT: Chronic stress is a causative for the development of many psychopathological syndromes in humans, including major depression and anxiety disorders. There is a high degree of comorbidity of depression and anxiety. Therefore, the current study investigated whether the CUS can produce comorbid depression and anxieties like behaviour in rats.Rats were subjected to an experimental setting of CUS for 14 days. Escitalopram (5-20 mg/kg per oral, p.o) was administered to stressed and sham rats for 14 days during stress period. Following the CUS and treatment, rats were subjected to a rodent's behavioural test battery (depression/anxiety). The results revealed that, CUS rats significantly exhibited depression-like behaviour in open field exploration, socio-sexual interaction tests. In addition, an anxiety-like behaviour was observed in neophobic situation like elevated plus maze and social interaction test. Further chronic treatment with escitalopram prevented the CUS induced depression and anxiety like behaviour in rats. CUS induced behavioural deficits in rats were comparable to the element of comorbid depression and anxiety in humans. The present findings provide the information that, CUS can be the model for comorbid depression associated anxiety.International Journal of Preclinical and Pharmaceutical Research. 12/2010; 1(1):54-63.