Background and aims: Substantial correlations between normal and abnormal personality traits have been found, but there is still little knowledge regarding the extent to which the underlying genetic and environmental influences are shared. Methods: 2,282 Norwegian twins were assessed for DSM-IV criteria for personality disorders using structured interviews. Ten years later years the twins were re-interviewed, and normal personality was assessed using the Big Five Inventory. Multivariate twin models were fitted to the five domains of normal personality and dimensional measures of each of the personality disorders individually. Results: While the heritability of the number endorsed criteria for the personality disorders ranged from 0.2 to 0.41, the proportion of genetic variance that was unique to each PD ranged from 19% for Avoidant to 79% for Schizotypal, with a median of 58% across all PDs. Conversely, the proportion of environmental variance unique to the personality disorder criteria ranged from 79% to 99%, with median of 97%. Conclusion: Our results suggest that a considerable proportion of the genetic variance and virtually all environmental variance is unique to the personality disorders, and not shared with the five broad domains of normal personality.
Backgroundand Aims: The stability over time for avoidant personality disorder (AVPD) and obsessive-compulsive personality disorder (OCPD) has previously been found to be moderate. However, the mechanisms underlying this temporal development are not well understood. In the present study we estimate the influence of genetic and environmental factors on stability and change in AVPD and OCPD. Methods: AVPD and OCPD traits were assessed using the Structured Interview for DSM-IV Personality in 2,793 young adult twins from the Norwegian Institute of Public Health Twin Panel (wave 1). On average 10 years later (wave 2) 2,282 of these were re-interviewed. Longitudinal biometric models were fitted to dimensional representations of AVPD and OCPD. Results: The number of endorsed sub-threshold criteria for both PDs decreased 31% from wave 1 to wave 2. The correlations between the numbers of traits endorsed at the two time points were 0.54 for AVPD and 0.37 for OCPD. Genetic factors contributed 67% and 53%, respectively, to the stability of AVPD and OCPD. The correlations between the genetic factors influencing AVPD and OCPD at the two time points were 1.00 and 0.72 respectively, while the environmental influences correlated 0.26 and 0.23, respectively. The correlation between the stable risk factors for AVPD and OCPD was 0.39 of which 63% was attributable to genetic influences. Conclusion: Both AVPD and OCPD were moderately stable from young to middle adulthood. Stability was in large part due to genetic factors, whereas environmental influences contributed to change.
Background and Aims: Antisocial personality disorder (ASPD) and borderline personality disorder (BPD) share genetic and environmental risk factors. Little is known about the temporal stability of these etiological factors in adulthood. Methods: DSM-IV criteria for ASPD and BPD were assessed using structured interviews in 2,282 Norwegian twins in early adulthood and approximately 10 years later. Longitudinal biometric models were used to analyze the number of endorsed criteria. Results: The mean criterion count for ASPD and BPD decreased 40% and 28% respectively from early to middle adulthood. Rank-order stability was 0.58 for ASPD and 0.45 for BPD. The best-fitting longitudinal twin model included only genetic and individual-specific environmental factors. Genetic effects, both those shared by ASPD and BPD, and those specific to each disorder remained completely stable. The unique environmental effects, however, changed substantially, with a correlation across time of 0.19 for the shared effects, and 0.39 and 0.15 respectively for those specific to ASPD and BPD. Genetic effects accounted for 71% and 72% of the stability over time for ASPD and BPD respectively. The genetic and environmental correlations between ASPD and BPD were 0.73, and 0.43 respectively at both time points. Conclusion: ASPD and BPD traits were moderately stable from early to middle adulthood, mostly due to genetic risk factors which did not change over the10 year assessment period. Environmental risk factors were mostly transient, and appear to be the main source of phenotypic change. Genetic liability factors were, to a large extent, shared by ASPD and BPD.
Objective: To measure the impact of the personality traits of Negative Affectivity and General Self-Efficacy measured during pregnancy to predict breastfeeding status at 4-months postpartum, adjusting for cesarean section, premature birth, parity, maternal age, and years of maternal education. Design: Prospective cohort study. Setting: The data collection was conducted as part of the Norwegian Mother and Child Cohort Study at the Norwegian Institute of Public Health. The national sample of 29,581 mothers completed assessment of Negative Affectivity and General Self-Efficacy at gestation weeks 17 and 30 and completed a self-report questionnaire at 6-months postpartum capturing detailed information about nutrition from birth thru 6 months. Outcome Measures: Mothers were classified with a cut-off at 4 months in the groups full breastfeeding, mixed breastfeeding, and bottle feeding. Results: We found that each interval of high Negative Affectivity increased the odds ratio of mixed breastfeeding (OR, 1.39; 95% CI, 1.27-1.51) and bottle feeding (OR, 1.56; 95% CI, 1.39-1.76), compared to full breastfeeding. Each interval of high General Self-Efficacy decreased the odds ratio of bottle feeding at 4 months (OR, 0.89; 95% CI, 0.83-0.96) but not of mixed breastfeeding (OR, 1.00; 95% CI, 0.95-1.04), compared to full breastfeeding. Conclusions: Our results support the hypothesis that Negative Affectivity and General Self-Efficacy are important antenatal predictors of breastfeeding 4 months postpartum. Adequately addressing the concerns and difficulties of mothers high in Negative Affectivity and low in General Self-Efficacy during prenatal and antenatal care could help prevent difficulties to sustain full breastfeeding.
Svekkelse av kognitive funksjoner som hukommelse og språkforståelse er en utbredt følge av traumatisk hjerneskade. De senere årene har flere studier undersøkt feilfri læring ("errorless learning") som metode for kognitiv rehabilitering etter traumatisk hjerneskade. Studiene rapporterer at feilfri læring gir bedre læringsresultater enn læring gjennom prøving og feiling ("errorful learning"). Feilfri læring baseres på et prinsipp for læring der anledningen til å gjøre feil reduseres eller elimineres. Den aktuelle pasientgruppen regnes som spesielt sårbar for at de feil som gjøres i en læringssituasjon, kan forstyrre innlæringen av riktig informasjon. Så langt har forskning på dette feltet vært konsentrert om kontrollerte, eksperimentelle situasjoner, og har i liten grad dokument klinisk anvendelse av feilfri læring som metode for rehabilitering. Målsetningene for denne studien er 1) å undersøke mulige forbedringer eller raffineringer av læringsteknikker basert på feilfri læring, og 2) evaluere feilfri læring i klinisk rehabilitering av personer som har vært utsatt for traumatisk hjerneskade.