Kenneth S. Kendler

CHILDHOOD SEPARATION ANXIETY DISORDER AND ADULT ONSET PANIC ATTACKS SHARE A COMMON GENETIC DIATHESIS

Childhood separation anxiety disorder (SAD) is hypothesized to share etiologic roots with panic disorder. The aim of this study was to estimate the genetic and environmental sources of covariance between childhood SAD and adult onset panic attacks (AOPA), with the primary goal to determine whether these two phenotypes share a common genetic diathesis.

RISK FACTORS FOR ANXIETY DISORDERS: COMMON AND SPECIFIC EFFECTS IN A NATIONAL SAMPLE

Anxiety disorders and major depressive disorder (MDD) often co‐occur and share a broad range of risk factors. The goal of this study was to examine whether the co‐occurrence of anxiety disorders and MDD could be explained by an underlying latent factor and whether the risk factors exert their effect exclusively through this factor, directly on each disorder, or through a combination of effects at both levels.

Generalized anxiety disorder and anorexia nervosa: evidence of shared genetic variation

Background: Previous studies have indicated a high prevalence of generalized anxiety disorder (GAD) in women with anorexia nervosa (AN). However, the shared genetic and environmental components of these disorders have not been explored. This study seeks to elucidate the shared genetic and environmental components between GAD and AN. Method: Using 2,083 women from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders, structural equation modeling was used to obtain maximum likelihood estimates of the environmental genetic, shared and unique environmental components in 496 women with GAD, 47 women with AN, 43 women with GAD + AN, and 1,497 women without GAD or AN. Results: Results show that the heritability of GAD was 0.32 and AN was 0.31, and the genetic correlation between the two disorders was 0.20, indicating a modest genetic contribution to their comorbidity. Unique environment estimate was 0.68 for GAD and 0.69 for AN, with a unique environmental correlation of 0.18. All common environmental parameters were estimated at zero. Conclusions: The modest shared genetic and unique environmental liability to both disorders may help explain the high prevalence of GAD in women with AN. This knowledge could help in the treatment and prevention of comorbid disorders. Depression and Anxiety, 2011.

EVIDENCE FOR DISTINCT GENETIC EFFECTS ASSOCIATED WITH RESPONSE TO 35% CO2

Carbon dioxide (CO2) hypersensitivity represents an individual difference response to breathing CO2 enriched air. People with a history of panic attacks or panic disorder are particularly prone to anxious response, suggesting that CO2 hypersensitivity is a robust risk marker of panic spectrum vulnerability.

A comparison of melancholic and nonmelancholic recurrent major depression in Han Chinese women.

Although the diagnosis of melancholia has had a long history, the validity of the current DSM‐IV definition remains contentious. We report here the first detailed comparison of melancholic and nonmelancholic major depression (MD) in a Chinese population examining in particular whether these two forms of MD differ quantitatively or qualitatively.

Association Study between GABA Receptor Genes and Anxiety Spectrum Disorders

Background: Human anxiety disorders are complex diseases with relatively unknown etiology. Dysfunction of the Gamma‐aminobutyric acid (GABA) system has been implicated in many neuropsychiatric conditions, including anxiety and depressive disorders. In this investigation, we explored four GABA receptor genes for their possible associations with genetic risk for anxiety disorders and depression.Methods: Our study sample consisted of 589 cases and 539 controls selected from a large population‐based twin registry based upon a latent genetic risk factor shared by several anxiety disorders, major depression, and neuroticism. We subjected these to a two‐stage protocol, in which all candidate genetic markers were screened for association in stage 1 (N=376), the positive results of which were tested for replication in stage 2 (N=752). We analyzed data from 26 single nucleotide polymorphisms (SNPs) from four GABA receptor genes: GABRA2, GABRA3, GABRA6, and GABRG2. Results: Of the 26 SNPs genotyped in stage 1, we identified two markers in GABRA3 that met the threshold (P≤.1) to be tested in stage 2. Phenotypic associations of these two markers failed to replicate in stage 2. Conclusions: These findings suggest that common variation in the GABRA2, GABRA3, GABRA6, and GABRG2 genes does not play a major role in liability to anxiety spectrum disorders. Depression and Anxiety 26:998–1003, 2009. Published 2009 Wiley‐Liss, Inc.

CHRONICITY OF DEPRESSION AND MOLECULAR MARKERS IN A LARGE SAMPLE OF HAN CHINESE WOMEN

Major depressive disorder (MDD) has been associated with changes in mean telomere length and mitochondrial DNA (mtDNA) copy number. This study investigates if clinical features of MDD differentially impact these molecular markers.

Psychiatric comorbidity does not only depend on diagnostic thresholds: an illustration with major depressive disorder and generalized anxiety disorder

High rates of psychiatric comorbidity are subject of debate: To what extent do they depend on classification choices such as diagnostic thresholds? This paper investigates the influence of different thresholds on rates of comorbidity between major depressive disorder (MDD) and generalized anxiety disorder (GAD).

Symptoms of major depression: Their stability, familiality, and prediction by genetic, temperamental, and childhood environmental risk factors

Psychiatry has long sought to develop biological diagnostic subtypes based on symptomatic differences. This effort assumes that symptoms reflect, with good fidelity, underlying etiological processes. We address this question for major depression (MD).

An examination of the etiologic overlap between the genetic and environmental influences on insomnia and common psychopathology

Insomnia is comorbid with internalizing and externalizing psychiatric disorders. However, the extent to which the etiologic influences on insomnia and common psychopathology overlap is unclear. There are limited genetically informed studies of insomnia and internalizing disorders and few studies of overlap exist with externalizing disorders.