INTRODUCTION: This study investigates the role of harm avoidance (HA) as a possible risk factor in the familiality of obsessive-compulsive disorder (OCD). HA is considered to be a genetically influenced personality trait with an increasingly understood neuroanatomical basis. METHOD: 75 subjects with OCD from hospital sites and a community sample and their 152 first degree relatives and 75 age and sex matched controls with their 143 first degree relatives were evaluated with structured clinical interviews (DSM-IV). HA was assessed with Cloninger's Tridimensional Personality Questionnaire (TPQ). RESULTS: Subjects with OCD had higher scores of HA than controls (p<or=0.001). First degree relatives of OCD cases also showed higher HA than relatives of control subjects (p=0.001).These results remained stable when comparing only OCD subjects versus controls (p<or=0.001) and relatives of OCD cases versus relatives of controls (p=0.005) without current comorbid disorders. LIMITATIONS: The investigation of HA alone does not allow to disentangle the transmission of biological versus psychological factors related to an elevated level of anxiety in families of OCD cases. CONCLUSION: This is the first study to extent previous findings of elevated HA in OCD cases to their first degree relatives. Thus, HA may partially mediate the familial risk for OCD.
INTRODUCTION: This study investigates the role of harm avoidance (HA) as a possible risk factor in the familiality of obsessive-compulsive disorder (OCD). HA is considered to be a genetically influenced personality trait with an increasingly understood neuroanatomical basis. METHOD: 75 subjects with OCD from hospital sites and a community sample and their 152 first degree relatives and 75 age and sex matched controls with their 143 first degree relatives were evaluated with structured clinical interviews (DSM-IV). HA was assessed with Cloninger's Tridimensional Personality Questionnaire (TPQ). RESULTS: Subjects with OCD had higher scores of HA than controls (p<or=0.001). First degree relatives of OCD cases also showed higher HA than relatives of control subjects (p=0.001).These results remained stable when comparing only OCD subjects versus controls (p<or=0.001) and relatives of OCD cases versus relatives of controls (p=0.005) without current comorbid disorders. LIMITATIONS: The investigation of HA alone does not allow to disentangle the transmission of biological versus psychological factors related to an elevated level of anxiety in families of OCD cases. CONCLUSION: This is the first study to extent previous findings of elevated HA in OCD cases to their first degree relatives. Thus, HA may partially mediate the familial risk for OCD.
Authors: Cheri A Levinson; Stephanie C Zerwas; Leigh C Brosof; Laura M Thornton; Michael Strober; Bernadette Pivarunas; James J Crowley; Zeynep Yilmaz; Wade H Berrettini; Harry Brandt; Steven Crawford; Manfred M Fichter; Katherine A Halmi; Craig Johnson; Allan S Kaplan; Maria La Via; James Mitchell; Alessandro Rotondo; D Blake Woodside; Walter H Kaye; Cynthia M Bulik Journal: Eur Eat Disord Rev Date: 2018-08-22
Authors: Joseph R Cohen; Benjamin L Hankin; Brandon E Gibb; Constance Hammen; Nicholas A Hazel; Denise Ma; Shuqiao Yao; Xiong Zhao Zhu; John R Z Abela Journal: J Clin Child Adolesc Psychol Date: 2012-12-13
Authors: Karin J H Verweij; Brendan P Zietsch; Sarah E Medland; Scott D Gordon; Beben Benyamin; Dale R Nyholt; Brian P McEvoy; Patrick F Sullivan; Andrew C Heath; Pamela A F Madden; Anjali K Henders; Grant W Montgomery; Nicholas G Martin; Naomi R Wray Journal: Biol Psychol Date: 2010-08-04 Impact factor: 3.251