BACKGROUND: The relationship between personality and psychiatric illness is complex. It is not clear whether one directly causes the other. METHOD: In a population-based sample of male twins (n=3030), we attempted to predict major depression (MD) from neuroticism (N) and extraversion (E) and vice versa, to evaluate the causal, scar, state, and prodromal hypotheses. In a longitudinal, structural equation twin model, we decomposed the covariation between N and MD into (a) genetic and environmental factors that are common to both traits, as well as specific to each one and (b) direct causal effects of N at time 1 on subsequent MD, as well as between MD and subsequent N. RESULTS: E was negatively correlated with lifetime and one-year prevalence of MD. N predicted the new onset of MD, and was predicted by both current and past MD. It did not predict the time to onset of MD. All of the covariation between N and MD was due to additive genetic and individual-specific environmental factors shared by both traits and a direct causal path between MD and N assessed later. No genetic factors were unique to either trait. CONCLUSIONS: In men, N may be a vulnerability factor for MD but does not cause it directly. However, MD may have a direct causal effect on N. The genetic overlap between N and MD in men may be greater than in women.
BACKGROUND: The relationship between personality and psychiatric illness is complex. It is not clear whether one directly causes the other. METHOD: In a population-based sample of male twins (n=3030), we attempted to predict major depression (MD) from neuroticism (N) and extraversion (E) and vice versa, to evaluate the causal, scar, state, and prodromal hypotheses. In a longitudinal, structural equation twin model, we decomposed the covariation between N and MD into (a) genetic and environmental factors that are common to both traits, as well as specific to each one and (b) direct causal effects of N at time 1 on subsequent MD, as well as between MD and subsequent N. RESULTS: E was negatively correlated with lifetime and one-year prevalence of MD. N predicted the new onset of MD, and was predicted by both current and past MD. It did not predict the time to onset of MD. All of the covariation between N and MD was due to additive genetic and individual-specific environmental factors shared by both traits and a direct causal path between MD and N assessed later. No genetic factors were unique to either trait. CONCLUSIONS: In men, N may be a vulnerability factor for MD but does not cause it directly. However, MD may have a direct causal effect on N. The genetic overlap between N and MD in men may be greater than in women.
Authors: Alicia Colvin; Gale A Richardson; Jill M Cyranowski; Ada Youk; Joyce T Bromberger Journal: Arch Womens Ment Health Date: 2014-06-21 Impact factor: 3.633
Authors: G J Lewis; M S Panizzon; L Eyler; C Fennema-Notestine; C-H Chen; M C Neale; T L Jernigan; M J Lyons; A M Dale; W S Kremen; C E Franz Journal: Neuroimage Date: 2014-09-28 Impact factor: 6.556
Authors: Leah D Doane; Carol E Franz; Elizabeth Prom-Wormley; Lindon J Eaves; Sally P Mendoza; Dirk H Hellhammer; Sonia Lupien; Hong Xian; Michael J Lyons; William Kremen; Kristen C Jacobson Journal: Horm Behav Date: 2011-05-18 Impact factor: 3.587
Authors: Min-Tzu Lo; Yunpeng Wang; Karolina Kauppi; Nilotpal Sanyal; Chun-Chieh Fan; Olav B Smeland; Andrew Schork; Dominic Holland; David A Hinds; Joyce Y Tung; Ole A Andreassen; Anders M Dale; Chi-Hua Chen Journal: Hum Mol Genet Date: 2017-11-15 Impact factor: 6.150
Authors: Bertus F Jeronimus; Roman Kotov; Johan Ormel; Harriëtte Riese; Elisabeth H Bos; Benjamin Hankin; Judith G M Rosmalen; Albertine J Oldehinkel Journal: Clin Psychol Rev Date: 2013-04-29