scholarly journals The structure of genetic and environmental risk factors for fears and phobias

2013 ◽  
Vol 44 (11) ◽  
pp. 2375-2384 ◽  
Author(s):  
E. K. Loken ◽  
J. M. Hettema ◽  
S. H. Aggen ◽  
K. S. Kendler

BackgroundAlthough prior genetic studies of interview-assessed fears and phobias have shown that genetic factors predispose individuals to fears and phobias, they have been restricted to the DSM-III to DSM-IV aggregated subtypes of phobias rather than to individual fearful and phobic stimuli.MethodWe examined the lifetime history of fears and/or phobias in response to 21 individual phobic stimuli in 4067 personally interviewed twins from same-sex pairs from the Virginia Adult Twin Study of Psychiatric and Substance Abuse Disorders (VATSPSUD). We performed multivariate statistical analyses using Mx and Mplus.ResultsThe best-fitting model for the 21 phobic stimuli included four genetic factors (agora-social-acrophobia, animal phobia, blood-injection-illness phobia and claustrophobia) and three environmental factors (agora-social-hospital phobia, animal phobia, and situational phobia).ConclusionsThis study provides the first view of the architecture of genetic and environmental risk factors for phobic disorders and their subtypes. The genetic factors of the phobias support the DSM-IV and DSM-5 constructs of animal and blood-injection-injury phobias but do not support the separation of agoraphobia from social phobia. The results also do not show a coherent genetic factor for the DSM-IV and DSM-5 situational phobia. Finally, the patterns of co-morbidity across individual fears and phobias produced by genetic and environmental influences differ appreciably.

2017 ◽  
Vol 47 (12) ◽  
pp. 2205-2215 ◽  
Author(s):  
T. Reichborn-Kjennerud ◽  
R. F. Krueger ◽  
E. Ystrom ◽  
F. A. Torvik ◽  
T. H. Rosenström ◽  
...  

BackgroundDSM-5 includes two conceptualizations of personality disorders (PDs). The classification in Section II is identical to the one found in DSM-IV, and includes 10 categorical PDs. The Alternative Model (Section III) includes criteria for dimensional measures of maladaptive personality traits organized into five domains. The degree to which the two conceptualizations reflect the same etiological factors is not known.MethodsWe use data from a large population-based sample of adult twins from the Norwegian Institute of Public Health Twin Panel on interview-based DSM-IV PDs and a short self-report inventory that indexes the five domains of the DSM-5 Alternative Model plus a domain explicitly targeting compulsivity. Schizotypal, Paranoid, Antisocial, Borderline, Avoidant, and Obsessive-compulsive PDs were assessed at the same time as the maladaptive personality traits and 10 years previously. Schizoid, Histrionic, Narcissistic, and Dependent PDs were only assessed at the first interview. Biometric models were used to estimate overlap in genetic and environmental risk factors.ResultsWhen measured concurrently, there was 100% genetic overlap between the maladaptive trait domains and Paranoid, Schizotypal, Antisocial, Borderline, and Avoidant PDs. For OCPD, 43% of the genetic variance was shared with the domains. Genetic correlations between the individual domains and PDs ranged from +0.21 to +0.91.ConclusionThe pathological personality trait domains, which are part of the Alternative Model for classification of PDs in DSM-5 Section III, appears to tap, at an aggregate level, the same genetic risk factors as the DSM-5 Section II classification for most of the PDs.


1996 ◽  
Vol 168 (S30) ◽  
pp. 68-75 ◽  
Author(s):  
Kenneth S. Kendler

In both clinical and epidemiological samples, major depression (MD) and generalised anxiety disorder (GAD) display substantial comorbidity. In a prior analysis of lifetime MD and GAD in female twins, the same genetic factors were shown to influence the liability to MD and to GAD. A follow-up interview in the same twin cohort examined one-year prevalence for MD and GAD (diagnosed using a one-month minimum duration of illness). Bivariate twin models were fitted using the program Mx. High levels of comorbidity were observed between MD and GAD. The best-fitting twin models, when GAD was diagnosed with or without a diagnostic hierarchy, found a genetic correlation of unity between the two disorders. The correlation in environmental risk factors was +0.70 when GAD was diagnosed non-hierarchically, but zero when hierarchical diagnoses were used. Our findings provide further support for the hypothesis that in women, MD and GAD are the result of the same genetic factors. Environmental risk factors that predispose to ‘pure’ GAD episodes may be relatively distinct from those that increase risk for MD.


2008 ◽  
Vol 65 (12) ◽  
pp. 1438 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Steven H. Aggen ◽  
Nikolai Czajkowski ◽  
Espen Røysamb ◽  
Kristian Tambs ◽  
...  

2006 ◽  
Vol 36 (11) ◽  
pp. 1583-1591 ◽  
Author(s):  
KENNETH S. KENDLER ◽  
NIKOLAI CZAJKOWSKI ◽  
KRISTIAN TAMBS ◽  
SVENN TORGERSEN ◽  
STEVEN H. AGGEN ◽  
...  

Background. The ‘odd’ or ‘Cluster A’ personality disorders (PDs) – paranoid, schizoid and schizotypal PDs – were created in DSM-III with little empirical foundation. We have examined the relationship between the genetic and environmental risk factors for dimensional representations of these three personality disorders.Method. These personality disorders were assessed using the Structured Interview for DSM-IV Personality (SIDP-IV) in 1386 young adult twin pairs from the Norwegian Institute of Public Health Twin Panel. Using Mx, a single-factor independent pathway twin model was fitted to the number of endorsed criteria for the three disorders.Results. The best-fit model included genetic and unique environmental common factors and genetic and unique environmental effects specific to each personality disorder. Total heritability was modest for these personality disorders and ranged from 21% to 28%. Loadings on the common genetic and unique environmental factors were substantially higher for schizotypal than for paranoid or schizoid PD. The proportion of genetic liability shared with all Cluster A disorders was estimated at 100, 43 and 26% respectively for schizotypal, paranoid and schizoid PDs.Conclusion. In support of the validity of the Cluster A construct, dimensional representations of schizotypal, paranoid and schizoid PD are all modestly heritable and share a portion of their genetic and environmental risk factors. No evidence was found for shared environmental or sex effects for these PDs. Schizotypal PD most closely reflects the genetic and environmental liability common to all three Cluster A disorders. These results should be interpreted in the context of the limited power of this sample.


1999 ◽  
Vol 29 (4) ◽  
pp. 925-934 ◽  
Author(s):  
T. WADE ◽  
N. G. MARTIN ◽  
M. C. NEALE ◽  
M. TIGGEMANN ◽  
S. A. TRELOAR ◽  
...  

Background. The study explored the genetic and environmental risk factors for both the behaviours and attitudes characteristic of disordered eating.Methods. In three waves of data collection, information was collected from female twins regarding their eating and attitudes towards eating, weight and shape. The first assessment consisted of a self-report questionnaire (1988–9) with 1682 women. The second assessment consisted of a semi-structured psychiatric interview schedule (1992–3), completed by 1852 women, many of whom had completed Wave 1 assessment. The third assessment, with 325 women chosen from Waves 1 and 2 (1995–6), consisted of a semi-structured interview (the Eating Disorder Examination).Results. As only one twin pair was concordant for lifetime bulimia nervosa at Wave 3 assessment, ordinal measures of all assessments were used in a multivariate genetic analysis. Results indicated that additive genetic and non-shared environmental influences best explained variance in liability to disordered eating, with about 60% (95% CI 50–68) of the variance explained by genetic factors. Comparison with a model allowing for the effects of shared environment indicated genetic factors accounted for a similar degree of variance (59%, 95% CI 36–68).Conclusion. Liability to the development of the behaviours and attitudes characteristic of eating disorders is best explained by both environmental and genetic factors, with covariation between the three measures best explained by a single latent phenotype of disordered eating which has a heritability of 60%.


2005 ◽  
Vol 7 (1) ◽  
pp. 69-80 ◽  

Genetic factors are clearly important in the etiology of schizophrenia, but the environment in which an individual's genes find expression is also crucial to the development of the illness. In this review of environmental risk factors for schizophrenia, we consider risks operating prenatally and perinatally, during childhood, and then later in life prior to illness onset Some of these risk factors have been well documented, for example, early hazards causing fetal growth retardation or hypoxia, and hazards nearer the onset of illness like drug abuse and migration. Others are much less certain. The importance of interaction between genetic and environmental risk is, however, undoubtedly important and there is emerging evidence for this from a range of sources. As the etiology of schizophrenia is unraveled, the picture becomes more complex, but also more obviously relevant to the plight of the individual patient.


2011 ◽  
Vol 168 (1) ◽  
pp. 29-39 ◽  
Author(s):  
Kenneth S. Kendler ◽  
Steven H. Aggen ◽  
Gun Peggy Knudsen ◽  
Espen Røysamb ◽  
Michael C. Neale ◽  
...  

2010 ◽  
Author(s):  
Thomas A. Wills ◽  
Pallav Pokhrel ◽  
Frederick X. Gibbons ◽  
James D. Sargent ◽  
Mike Stoolmiller

Sign in / Sign up

Export Citation Format

Share Document