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Recent work has suggested a high level of congruence between normative personality, most typically represented by the 'big five' factors, and abnormal personality traits. In 2,293 Norwegian adult twins ascertained from a population-based registry, the authors evaluated the degree of sharing of genetic and environmental influences on normative personality, assessed by the Big Five Inventory (BFI), and personality disorder traits (PDTs), assessed by the Personality Inventory for DSM-5-Norwegian Brief Form (PID-5-NBF). For four of the five BFI dimensions, the strongest genetic correlation was observed with the expected PID-5-NBF dimension (e.g., neuroticism with negative affectivity [+], conscientiousness with disinhibition [−]). However, neuroticism, conscientiousness, and agreeableness had substantial genetic correlations with other PID-5-NBF dimensions (e.g., neuroticism with compulsivity [+], agreeableness with detachment [−]). Openness had no substantial genetic correlations with any PID-5-NBF dimension. The proportion of genetic risk factors shared in aggregate between the BFI traits and the PID-5-NBF dimensions was quite high for conscientiousness and neuroticism, relatively robust for extraversion and agreeableness, but quite low for openness. Of the six PID-5-NBF dimensions, three (negative affectivity, detachment, and disinhibition) shared, in aggregate, most of their genetic risk factors with normative personality traits. Genetic factors underlying psychoticism, antagonism, and compulsivity were shared to a lesser extent, suggesting that they are influenced by etiological factors not well indexed by the BFI. [ABSTRACT FROM AUTHOR]

Background: While age-related increases of between-person variability in a variety of cognitive measures are commonly reported in cross-sectional studies, the nature of short-term intraindividual fluctuation in elderly people’s performance is relatively unexplored. Objective: The goal of the present study is to examine short-term fluctuations in elderly people’s sensorimotor functioning and their relations to individual differences in verbal and spatial memory. Methods: Fluctuations in old adults’ (mean = 75.71 years, SD = 6.93 years) sensorimotor performance were investigated by biweekly measurements spanning approximately 7 months. Sensorimotor performance was measured by three walking tasks, including the duration and the number of steps taken to walk a 360-degree circle and to walk 10 feet both at normal and fast pace. Performances of verbal and spatial memory were assessed by weekly measurements of digit memory span, memory for short text and spatial recognition. Results: The magnitude of intraindividual fluctuation in most sensorimotor and memory tasks examined was at least half as great as the level of individual differences across persons. In addition, intraindividual fluctuation in sensorimotor performance is a relatively stable individual attribute, which correlates positively with age and negatively with the levels of sensorimotor, text and spatial memory performance. Although a substantial amount of individual differences in intraindividual fluctuation was shared with mean performance level, variance component and hierarchical regression analyses showed that intraindividual fluctuation in walking steps added significant independent contribution over and above that given by level of performance in predicting text and spatial memory. Conclusion: Taking these results together, we suggest that intraindividual fluctuations in elderly people’s performance should not be ignored or simply treated as measurement error; rather, they are potentially important empirical variables for understanding sensory and cognitive aging and the nature of intraindividual response variations in general.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Genetic risk and environmental adversity-both important risk factors for major depression (MD)-are thought to differentially impact on depressive symptom types and associations. Does heterogeneity in these risk factors result in different depressive symptom networks in patients with MD?, Methods: A clinical sample of 5784 Han Chinese women with recurrent MD were interviewed about their depressive symptoms during their lifetime worst episode of MD. The cases were classified into subgroups based on their genetic risk for MD (family history, polygenic risk score, early age at onset) and severe adversity (childhood sexual abuse, stressful life events). Differences in MD symptom network structure were statistically examined for these subgroups using permutation-based network comparison tests., Results: Although significant differences in symptom endorsement rates were seen in 18.8% of group comparisons, associations between depressive symptoms were similar across the different subgroups of genetic and environmental risk. Network comparison tests showed no significant differences in network strength, structure, or specific edges (P-value > 0.05) and correlations between edges were strong (0.60-0.71)., Limitations: This study analyzed depressive symptoms retrospectively reported by severely depressed women using novel statistical methods. Future studies are warranted to investigate whether similar findings hold in prospective longitudinal data, less severely depressed patients, and men., Conclusions: Similar depressive symptom networks for MD patients with a higher or lower genetic or environmental risk suggest that differences in these etiological influences may produce similar symptom networks downstream for severely depressed women., (Copyright © 2017. Published by Elsevier B.V.)

Background: A clearer understanding of the etiological overlap between DSM-IV personality disorders (PDs) and alcohol use (AU) and alcohol use disorder (AUD) is needed. To our knowledge, no study has modeled the association between all 10 DSM-IV PDs and lifetime AU and AUD. The aim of the present study is to identify which PDs are most strongly associated with the phenotypic, genetic, and environmental risks of lifetime AU and AUD, and to determine if these associations are stable across time., Methods: Participants were Norwegian twins assessed at two waves. At Wave 1, 2801 twins were assessed for all 10 DSM-IV PD criteria, lifetime AU, and DSM-IV AUD criteria. At Wave 2, six of the 10 PDs were again assessed along with AU and AUD among 2393 twins. Univariate and multiple logistic regressions were run. Significant predictors were further analyzed using bivariate twin Cholesky decompositions., Results: Borderline and antisocial PD criteria were the strongest predictors of AU and AUD across the two waves. Despite moderate phenotypic and genetic correlations, genetic variation in these PD criteria explained only 4% and 3% of the risks in AU, and 5% to 10% of the risks in AUD criteria, respectively. At Wave 2, these estimates increased to 8% and 23% for AU, and 17% and 33% for AUD., Conclusions: Among a large Norwegian twin sample, borderline and antisocial PD criteria were the strongest predictors of the phenotypic and genotypic liability to AU and AUD. This effect remained consistent across time., (Copyright © 2017 Elsevier B.V. All rights reserved.)

The association between pregnancy and perinatal complications (PPCs) and risks for adult psychiatric disorders other than psychoses has received relatively limited attention. In this study, we aim to characterize the associations between PPCs and risks for anxiety, affective, substance use, and eating disorders in a population-based sample of twins. Personal interviews were conducted with 1,806 female twin subjects to assess their lifetime history of alcoholism, anorexia nervosa, bulimia nervosa, generalized anxiety disorder, major depression, panic disorder, simple phobias, and social phobias. PPCs were retrospectively assessed at personal interview with the subject's parents. The associations between PPCs and risks for psychiatric disorders are characterized using logistic regression. In this sample of twins, gestational age is associated with a significantly increased risk for anorexia nervosa and pregnancy complications are associated with a significantly increased risk for both anorexia nervosa and bulimia nervosa. Pregnancy and perinatal complications may be associated with an increased risk for eating disorders in women., (Copyright 2001 Wiley-Liss, Inc.)

Objective: Although family, twin and adoption studies have suggested that lifetime major depression (MD) is a heritable condition, nearly all these studies have relied for the diagnosis on long-term human memory, which is fallible and potentially biased. Could the estimates of heritability of MD be biased by the well-demonstrated genetic influences on memory?, Methods: Both members of 858 female-female twin pairs from a population-based registry were personally interviewed at least three times over 9 years. The interview assessed a history of depressive onsets and recoveries in the last year to the nearest month. We examine heritability of MD using four recall intervals: last year, last 6 months, last 3 months and current month., Results: Examining the occurrence of one or more depressive episodes across all three interviews, heritabilities of MD (95% CI) for the four time periods were: 0.41 (0.27-0.54), 0.41 (0.26-0.55), 0.35 (0.16-0.52) and 0.34 (0.11-0.55). These heritability estimates did not differ significantly from one another. A similar pattern was found if heritability was assessed for the number of interviews in which criteria for MD were met., Conclusion: Modelling results suggest that the heritability of MD was not influenced by the duration of the required recall. Genetic influences on human recall do not appear to contribute substantially to estimated heritability of MD.

Background: Alcoholism and depression frequently co-occur, but the origins of this comorbidity remain uncertain. Most previous family, twin, and adoption studies of these disorders have used cases ascertained through treatment settings, who may differ from cases in epidemiological samples. We studied the importance of genetic influences on risk for lifetime comorbidity of major depression and alcoholism by means of a population-based twin sample., Methods: Lifetime major depression (MD), alcohol abuse, and alcohol dependence were assessed by structured interview for both members of 3755 twin pairs from the Mid-Atlantic Twin Registry. Pair resemblance was analyzed by means of structural equation models., Results: Individuals with MD were at significantly increased risk for alcohol dependence and for a combined diagnosis of alcohol abuse and/or dependence. History of MD in a twin significantly increased the risk of cotwin alcohol dependence and alcohol abuse and/or dependence among identical male pairs and for alcohol abuse and/or dependence in identical female pairs, but not among male or female fraternal pairs. Results of structural modeling indicate that comorbidity occurs because the genetic and specific environmental sources of liability to MD overlap with those underlying alcohol dependence and alcohol abuse and/or dependence. This overlap was significant only within sex, not across sexes., Conclusions: In this population-based twin sample, the familial transmission of MD and alcohol dependence was largely disorder specific. Comorbidity appears to be due to sex-specific genetic and environmental risk factors. The factors underlying depression in women do not appear to arise from the same factors underlying alcoholism in men.

Background: Some studies suggest that cortisol may be under genetic control. The aims of our study were to investigate the familial resemblance in morning and evening cortisol secretion as assessed by saliva cortisol and to assess the influence of history of major depression., Methods: Women for this investigation were selected from an ongoing study in female-female twin pairs ascertained from the Virginia Twin Registry. Telephone screening assured that current inclusion/exclusion criteria were met. Subjects were asked to collect AM samples within 45 min after awakening, and evening samples immediately before bedtime for 14 days., Results: There was a high degree of correlation across weeks in both the AM and PM cortisol values, indicating significant stability across individuals. There was significant correlation between AM and PM cortisol in monozygotic twins. In twins with a history of major depression (n = 30), compared with the twins without past major depression (n = 28), there was a trend towards higher cortisol (p = .056)., Conclusions: These results suggest that around 40-45% of the total variance in salivary cortisol is shared by monozygotic twins. Although the increase in baseline cortisol in twins with a history of major depression is only significant at the trend level, the effect size is comparable to an "in episode" depressed population.

Background: There are substantial sex differences in all levels of alcohol involvement among U.S. adults. The goal of this study was to test whether the magnitude and sources of genetic and environmental influences on liability for alcohol abuse and dependence differ for men and women., Methods: Structured personal interviews were used to assess DSM-III-R- and DSM-IV-defined alcohol abuse and dependence among 5091 male and 4168 female twins (including 1546 identical, 1128 same-sex fraternal, and 1423 opposite-sex pairs) born in Virginia between 1934 and 1974. Twin correlations were analyzed using structural equation modeling., Results: The magnitude of twin-pair resemblance was similar across several definitions of alcoholism and was substantially higher among identical than fraternal pairs. The proportion of population variation in liability attributed to genetic factors was substantial among both women (55-66%) and men (51-56%), and we found little evidence of a role of environmental factors shared by family members. In all definitions studied, we could reject a model that the genetic sources of liability in the two sexes overlap completely., Conclusion: In this first population-based study of alcoholism among male and female twins from the U.S., we found that genetic factors play a major role in the development of alcoholism in both sexes, that the magnitudes of genetic influence were equally high for men and women, and that the genetic sources of vulnerability are partially, but not completely, overlapping in men and women.