Brief reportHarm avoidance in subjects with obsessive-compulsive disorder and their families
Introduction
OCD is a severe psychiatric disorder that aggregates in families (Black et al., 1992, Pauls et al., 1995, Nestadt et al., 2000, Grabe et al., 2006a, Grabe et al., 2006b). However, the specific genetic and familial behavioural risk factors for OCD are largely unknown. Some studies have found an increase of anxiety disorders, namely generalized anxiety disorder (Nestadt et al., 2001) in first degree relatives of OCD cases, suggesting a familial predisposition to anxiety related traits. This line of thinking leads to the question to which extent biosocial personality traits contribute to the familial aggregation of psychiatric disorders (Brown et al., 1992).
R. Cloninger's biopsychosocial model of personality conceptualizes personality traits to be predominantly influenced by biological (Temperament) or environmental (Character) factors (Cloninger et al., 1993).
Temperament is defined as a heritable set of automatic responses to emotional stimuli, which follow the rules of associative conditioning or procedural learning. In contrast to character which is defined as our voluntary goals and values that are based on experience and insight learning. In his psychobiological model of personality, Cloninger integrated results from genetic studies, long-term studies of psychological development, pharmacological studies and psychometrical studies. In the first version of his personality questionnaire Cloninger postulated three genetic determined temperamental factors: harm avoidance (HA), novelty seeking (NS) and reward dependence (RD). Those three temperament factors built the Tridimensional Personality Questionnaire (TPQ). Later on he added persistence (P) as a fourth independent factor. In twin studies, every one of those four temperament factors has been found to be heritable, homogenous and independent (Heath et al., 1994). Certain configurations of temperament and character traits can be helpful in the diagnosis of personality disorders (Svrakic et al., 2002), in developing clinical profiles in mood disorders (Cloninger et al., 1998) or risk factors for depression (Elovainio et al., 2004).
In his work on “psychobiological approach to psychiatric assessment” Cloninger and Svrakic (1997) state that individual configurations in personality structure influence the risk of all forms of psychopathology as well as the responses on pharmacological treatment and psychotherapy. Especially HA has widely been associated with anxiety disorders (Fossey et al., 1989, Starcevic et al., 1996, Ampollini et al., 1999, Wiborg et al., 2005) and OCD (Richter et al., 1996, Bejerot et al., 1998). Subjects with high HA are described to worry a lot and see future in a pessimistic way, they are anxious and doubtful, shy and easy to exhaust.
Lyoo et al. (2001) compared OCD patients with healthy controls and found significantly higher HA scores which were additionally associated with greater severity of OCD. Recently, functional brain imaging demonstrated a tight coupling between perigenual cingulate and amygdala, acting as a feedback circuit during perceptual processing of fearful stimuli. The magnitude of this coupling inversely predicted almost 30% of variation in HA. Carriers of the short allele of a functional 5′ promoter polymorphism of the serotonin transporter gene (5-HTTLPR) showed relative uncoupling of this circuit (Pezawas et al., 2005). Thus, these genotype-related alterations in anatomy and function of an amygdala–cingulate feedback circuit critical for emotion regulation implicate a developmental, systems-level mechanism underlying normal emotional reactivity and genetic susceptibility for HA and possibly also for anxiety disorders and OCD.
The present study investigates the hypothesis that HA is elevated in OCD cases and in their first degree relatives compared to control families.
Section snippets
Method
The investigation is part of the German Epidemiologic Network for OCD Studies (GENOS) a large family study of OCD carried out at four different sites. GENOS was established to study the familial aggregation of OCD, to identify psychological, neuropsychological and genetic factors that are related to the familiality of OCD, and to characterize subtypes of OCD. The study was approved by the local ethics committees at the four study sites and all participants gave written informed consent before
Results
There were no significant differences in age (t = − 1.4, df = 148, n.s.) or sex (χ2 = 0.028, df = 1, n.s.) between cases (37.7, SD = 12.6 years, 65% females) and controls (41.2, SD = 17.1 years, 63% females). The same was true for the respective relatives (age: t = 1.4, df = 293, n.s.; Mean1°OCD 48.2, SD = 17.5 years; Mean1°CON 45.5, SD = 16.8 years; sex χ2 = 0.78, df = 1, n.s.; 58% versus 63% females, respectively).
OCD subjects (MeanOCD = 22.20, SD = 6.67) showed significantly higher scores of HA (t = 7.67, df = 148, p ≤ 0.001)
Discussion
The present study supports the role of HA as a putative familiar risk factor for OCD. Independent from current comorbid disorders, cases with OCD and their first degree relatives had significantly elevated scores of HA. This finding supports the assumption of a diathesis of anxiety related traits in families of OCD cases, predisposing the subjects to exaggerated anxiety responses facing unfamiliar or stressful situations and stimuli. Thus, in families of OCD cases children may be put at two
Role of funding source
The funding source was not involved in the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript.
Conflicts of interest
No conflict declared.
Acknowledgement
This research work was funded by the German Research Foundation (DFG) and in part by grants from the German Federal Ministry for Education and Research (BMBF, grant no. 01ZZ96030), from the Ministry for Education, Research and Cultural Affairs and the Ministry for Social Affairs of the State Mecklenburg-Western Pomerania.
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Both authors contributed equally to the paper.