E Thiery

Heritability of borderline personality disorder features is similar across three countries

BACKGROUND Most of our knowledge about borderline personality disorder features has been obtained through the study of clinical samples. Although these studies are important in their own right, they are limited in their ability to address certain important epidemiological and aetiological questions such as the degree to which there is a genetic influence on the manifestation of borderline personality disorder features. Though family history studies of borderline personality disorder indicate genetic influences, there have been very few twin studies and the degree of genetic influence on borderline personality disorder remains unclear. METHOD Data were drawn from twin samples from The Netherlands (n=3918), Belgium (n=904) and Australia (n=674). In total, data were available on 5496 twins between the ages of 18 and 86 years from 3644 families who participated in the study by completion of a mailed self-report questionnaire on borderline personality disorder features. RESULTS In all countries, females scored higher than males and there was a general tendency for younger adults to endorse more borderline personality disorder features than older adults. Model-fitting results showed that additive genetic influences explain 42% of the variation in borderline personality disorder features in both men and women and that this heritability estimate is similar across The Netherlands, Belgium and Australia. Unique environmental influences explain the remaining 58% of the variance. CONCLUSION Genetic factors play a role in individual differences in borderline personality disorder features in Western society.

Unveiling patterns of affective responses in daily life may improve outcome prediction in depression: A momentary assessment study

OBJECTIVE Daily life affective responses are closely linked to vulnerability and resilience in depression. Prediction of future clinical course may be improved if information on daily life emotional response patterns is taken into account. METHOD Female subjects with a history of major depression (n=83), recruited from a population twin register, participated in a longitudinal study using momentary assessment technology with 4 follow-up measurements. The effect of baseline daily life emotional response patterns (affect variability, stress-sensitivity and reward experience) on follow-up depressive symptomatology was examined. RESULTS Both reward experience (B=-0.30, p=0.001) and negative affect variability (B=0.46, p=0.001) predicted future negative affective symptoms independent of all other dynamic emotional patterns and conventional predictors. CONCLUSION Daily life information on dynamic emotional patterns adds to the prediction of future clinical course, independent of severity of symptoms and neuroticism score. Better prediction of course may improve decision-making regarding quantitative and qualitative aspects of treatment.

Mechanisms of gene–environment interactions in depression: evidence that genes potentiate multiple sources of adversity

BACKGROUND Previous work suggests that daily life stress-sensitivity may be an intermediary phenotype associated with both genetic risk for depression and developmental stress exposures. In the current analysis we hypothesized that genetic risk for depression and three environmental exposures over the course of development [prenatal stress, childhood adversity and adult negative life events (NLEs)] combine synergistically to produce the phenotype of stress-sensitivity. METHOD Twin pairs (n=279) participated in a momentary assessment study using the Experience Sampling Method (ESM), collecting appraisals of stress and negative affect (NA) in the flow of daily life. Prospective data on birthweight and gestational age, questionnaire data on childhood adversity and recent NLEs, and interview data on depression were used in the analyses. Daily life stress-sensitivity was modelled as the effect of ESM daily life stress appraisals on ESM NA. RESULTS All three developmental stress exposures were moderated by genetic vulnerability, modelled as dizygotic (DZ) or monozygotic (MZ) co-twin depression status, in their effect on daily life stress-sensitivity. Effects were much stronger in participants with MZ co-twin depression and a little stronger in participants with DZ co-twin depression status, compared to those without co-twin depression. NLE main effects and NLE genetic moderation were reducible to birthweight and childhood adversity. CONCLUSIONS The findings are consistent with the hypothesis that adult daily life stress-sensitivity is the result of sensitization processes initiated by developmental stress exposures. Genes associated with depression may act by accelerating the process of stress-induced sensitization.

Does reactivity to stress cosegregate with subclinical psychosis? A general population twin study

Objective:  This study assessed the relationship between stress reactivity (trait 1) and psychosis (trait 2) across genetically related persons (cross‐twin, cross‐trait design) to examine whether stress reactivity is an uncontaminated and unconfounded familial marker of psychosis risk.

Meeting risk with resilience: high daily life reward experience preserves mental health

Geschwind N, Peeters F, Jacobs N, Delespaul P, Derom C, Thiery E, van Os J, Wichers M. Meeting risk with resilience: high daily life reward experience preserves mental health.

Subtle gene–environment interactions driving paranoia in daily life

It has been suggested that genes impact on the degree to which minor daily stressors cause variation in the intensity of subtle paranoid experiences. The objective of the present study was to test the hypothesis that catechol‐O‐methyltransferase (COMT) Val158Met and brain‐derived neurotrophic factor (BDNF) Val66Met in part mediate genetic effects on paranoid reactivity to minor stressors. In a general population sample of 579 young adult female twins, on the one hand, appraisals of (1) event‐related stress and (2) social stress and, on the other hand, feelings of paranoia in the flow of daily life were assessed using momentary assessment technology for five consecutive days. Multilevel regression analyses were used to examine moderation of daily life stress‐induced paranoia by COMT Val158Met and BDNF Val66Met genotypes. Catechol‐O‐methyltransferase Val carriers displayed more feelings of paranoia in response to event stress compared with Met carriers. Brain‐derived neurotrophic factor Met carriers showed more social‐stress‐induced paranoia than individuals with the Val/Val genotype. Thus, paranoia in the flow of daily life may be the result of gene–environment interactions that can be traced to different types of stress being moderated by different types of genetic variation.

Heritability estimates of intelligence in twins: Effect of chorion type.

This study investigates the basic assumption of homogeneity of monozygotic (MZ) twins: are there differences according to the timing of the zygotic splitting, early in dichorionic (DC) and later in monochorionic (MC) pairs? We assessed the IQ of 451 same-sexed twin pairs of known zygosity and chorion type with the Wechsler Intelligence Scale for Children-Revised (WISC-R). The variances of within-pair differences were compared for monochorionic (MC), dichorionic monozygotic (DC-MZ) and dizygotic same-sexed (DZ) twins and structural equation modeling was applied. High heritability estimates were found for almost all subscales and IQ-scores. A significant effect of chorion type was found: the MC twins resembled each other more than the DC-MZ twins on the subscales Arithmetic and Vocabulary. The effect accounts for respectively 14% and 10% of the total variance.

Cognition as predictor of current and follow-up depressive symptoms in the general population

Objective:  Previous studies have reported an association between depression and poor cognitive functioning. Unknown is to what degree such associations are merely state‐related or reflect an enduring depression vulnerability. This study examined whether cognitive deficits predict current and/or follow‐up (sub)clinical depressive symptoms in the general population.

Evidence that genes for depression impact on the pathway from trauma to psychotic-like symptoms by occasioning emotional dysregulation

BACKGROUND Genes for depression may act by making individuals more sensitive to childhood trauma. Given that childhood adversity is a risk factor for adult psychosis and symptoms of depression and psychosis tend to cluster within individuals and families, the aim was to examine whether the association between childhood adversity and psychotic-like symptoms is moderated by genetic liability for depression. A secondary aim was to determine to what degree a depression-related increase in stress sensitivity or depressive symptoms themselves occasioned the moderating effect. METHOD Female twins (n=508) completed both prospective and retrospective questionnaires regarding childhood adversity [the Symptom Checklist-90 - Revised (SCL-90-R) and SCID-I (psychotic symptoms)] and psychotic trait liability [the Community Assessment of Psychic Experiences (CAPE)]. Stress sensitivity was indexed by appraisals of event-related stress and negative affect (NA) in the flow of daily life, assessed with momentary assessment technology for five consecutive days. Multilevel regression analyses were used to examine moderation of childhood adversity by genetic liability for depression in the prediction of follow-up psychotic experiences. RESULTS The effect of childhood adversity was significantly moderated by genetic vulnerability for depression in the model of both follow-up psychotic experiences (SCL-90-R) and follow-up psychotic trait liability (CAPE). The moderation by genetic liability was mediated by depressive experience but not by stress sensitivity. CONCLUSIONS Genetic liability for depression may potentiate the pathway from childhood adversity to psychotic-like symptoms through dysfunctional emotional processing of anomalous experiences associated with childhood trauma.

Child psychopathology and lower cognitive ability: a general population twin study of the causes of association

Previous work has demonstrated associations between lower cognitive ability and childhood and adult non-psychotic psychopathology. As both cognitive ability (CA) and child psychopathology (CP) are influenced by genetic factors, one explanation for the association is that they are the pleiotropic manifestations of the same underlying genetic factors. The present paper examines three possible causes of the association: additive genetic factors, common environmental factors and individual-specific environmental factors. Three hundred and seventy-six twin pairs from the East Flanders Prospective Twin Survey were examined with the Child Behaviour Checklist and the Wechsler Intelligence Scale for Children-Revised. The cross-twin within-variable, within-twin cross-variable and cross-twin cross-variable correlations were calculated. Using structural equation modelling, bivariate models were fitted. The best fitting model was chosen, based on likelihood and parsimony. The observed phenotypic correlation between CP and CA was −0.19 (95% CI: −0.09, −0.27), with genetic factors accounting for about 84% of the observed correlation. Bivariate model fitting quantified the genetic correlation between CP and CA at −0.27 (95% CI: −0.12, −0.42) and the individual-specific environmental correlation at −0.17 (95% CI: −0.03, −0.31). In children, three different genetic factors may exist: one that solely affects the liability to CP, one that has only an effect on CA and one that influences both CP and CA. While individual-specific environmental factors can influence the liability to both traits, our results suggest that most of the environmental factors that increase the risk of CP do not influence CA and vice versa.