Social support and the serotonin transporter genotype (5-HTTLPR) moderate levels of resilience, sense of coherence, and depression.

Gene x environment interactions have mainly been investigated in models of psychopathology. However, the putative interplay between genes and beneficial environmental conditions on positive outcomes has rarely been addressed. We therefore examined the interaction between the serotonin transporter linked polymorphic region (5-HTTLPR) and social support on the sense of coherence (SOC), resilience, and depressive symptoms. Furthermore, we scrutinized our examinations by differentiating between individuals with and without childhood abuse. The sample included 1,811 participants from the general population (Study of Health in Pomerania, Germany). The triallelic genotype of 5-HTTLPR was determined and longitudinal data of social support were used. Among individuals with high social support no significant differences between 5-HTTLPR genotypes regarding all outcome variables were found. However, among those with low social support, carriers of at least one short allele reported significantly increased levels of SOC and resilience, as well as less depressive symptoms than carriers of the l/l genotype. This result was not modified by differentiating between those with childhood abuse and those without. In less supportive social environments the impact of distinct genotypes on behavioral outcomes might be more relevant than in supportive environments where social compensation might take place. Our findings indicate that both alleles of 5-HTTLPR contribute to the adaptability to different environmental conditions.

Neuroticism developmental courses--implications for depression, anxiety and everyday emotional experience; a prospective study from adolescence to young adulthood.

BACKGROUND: Neuroticism is frequently discussed as a risk factor for psychopathology. According to the maturity principle, neuroticism decreases over the course of life, but not uniformly across individuals. However, the implications of differences in personality maturation on mental health have not been well studied so far. Hence, we hypothesized that different forms of neuroticism development from adolescence to young adulthood are associated with differences in depression, anxiety and everyday emotional experience at the age of 25. METHODS: A sample of 266 adolescents from the general population was examined three times over ten years (age at T0: 15, T1: 20 and T2: 25) using questionnaires, interviews and ecological momentary assessment (EMA). At all measurement points, neuroticism was assessed with the NEO inventory. At T2, diagnoses of major depression and anxiety disorders were captured with a structured clinical interview (M-CIDI). Phone-based EMA was used to assess emotional experience and affective instability over a two-week period at T2. RESULTS: The best fitting model was a latent class growth analysis with two groups of neuroticism development. Most individuals (n = 205) showed moderate values whereas 61 participants were clustered into a group with elevated neuroticism levels. In both groups neuroticism significantly changed during the ten year period with a peak at the age of 20. Individuals with a higher absolute level were at 14-fold increased risk for depression and 7-fold risk for anxiety disorders at the age of 25. In EMA, increased negative affect and arousal as well as decreased positive emotions were found in this high group. CONCLUSIONS: Other than expected, personality did not mature in our sample. However, there was a significant change of neuroticism values from adolescence to young adulthood. Further, over 20% of our participants showed a neuroticism development which was associated with adverse outcomes such as negatively toned emotional experience and a heightened risk to suffer from depressive and anxiety disorders in young adulthood. These high-risk persons need to be identified early to provide interventions supporting continuous personality maturation.

High social support buffers the effects of 5-HTTLPR genotypes within social anxiety disorder.

An interaction between genetic aspects and environmental stressors has been suggested with regard to the etiology of social anxiety disorder (SAD). However, potential protective interplays which might decrease the risk of SAD have not been considered so far. Thus, we analyzed the interaction between 5-HTTLPR and differing levels of social support regarding SAD. The sample was based on participants of the Study of Health in Pomerania, Germany. We used the triallelic genotype of 5-HTTLPR and longitudinal data of social support. Final analyses were conducted in 79 individuals with SAD and 1,708 without. The diagnosis of SAD was derived from diagnostic interviews in accordance with DSM-IV. Considering the risk of SAD, a general protective effect of high social support was shown independent of variation in 5-HTTLPR genotype. In contrast, the risk of SAD was increased for both genotypes within those individuals with low social support. Additionally, the odds ratio for suffering from SAD was about two times higher for carriers of the l/l genotype compared to those with at least one short allele in those perceiving less-supportive social environments. The findings suggest that SAD is influenced by a protective and a contributing gene × environment interaction. High social support might act in a protective and low social support in an increasing manner on the risk of SAD especially within carriers of the l/l genotype. Therefore, effects of 5-HTTLPR might be buffered by high social support with respect to the risk of SAD.

Longitudinal transmission pathways of borderline personality disorder symptoms: from mother to child?

BACKGROUND: There is evidence that the borderline symptomatology of the mother longitudinally predicts the number of borderline criteria met by the children. However, possible underlying mechanisms have rarely been examined. In line with transactional models of borderline personality disorder (BPD), we analyzed a broad concept of maladaptive mother-child interactions of mothers with BPD symptoms towards their children, including insensitive parenting and mother-child discrepancies, in reporting the child's psychopathological behavior. SAMPLING/METHODS: The sample was drawn from the population-based Greifswald Family Study and consisted of 295 children and their biological mothers. Both were examined at two points in time, first when the children were about 15 years old (T0) and again 5 years later (T1), using path analyses. RESULTS: Maladaptive mother-child interactions (especially an overprotective and rejecting parenting style and high discrepancies regarding internalizing problems) mediate the longitudinal transmission of borderline symptoms from mother to child. Furthermore, our data revealed that this result is consistent for various youth symptoms which are associated with BPD such as impulsivity or dissociation. CONCLUSION: The data of the current study imply that the transmission of borderline symptoms from mother to child is mediated by maladaptive mother-child interactions. For this reason early and professional support may be useful to prevent these children from developing severe psychopathology.

Testing the diathesis-stress model: 5-HTTLPR, childhood emotional maltreatment, and vulnerability to social anxiety disorder.

Regarding the development of social anxiety disorder (SAD), a diathesis-stress paradigm including biological vulnerabilities and environmental stressors can be assumed. However, studies dealing with the etiology of SAD did not integrate both aspects so far. We examined a particular diathesis-stress model for SAD in which we included a functional polymorphism of the serotonin transporter (5-HTTLPR) as a genetic vulnerability factor and childhood emotional maltreatment (CEM) as an environmental stressor. Current analyses were based on individuals who participated in the Study of Health in Pomerania. Psychiatric disorders were assessed with diagnostic interviews according to DSM-IV criteria. The triallelic genotype of 5-HTTLPR was determined. Statistical analyses were performed in 78 individuals with SAD and 1,035 without an axis I disorder. Logistic regression analysis revealed that the experience of CEM (odds ratio [OR] 4.56; 95% confidence interval [CI] 2.65-7.84), the l/l genotype of 5-HTTLPR (OR 2.13; 95% CI 1.31-3.48), female gender (OR 3.03; 95% CI 1.80-5.08) and younger age (OR 1.04; 95% CI 1.02-1.06) increased the odds for SAD. The data suggest that CEM, the l/l genotype of 5-HTTLPR, female gender and younger age are risk factors for SAD. This is in favor of the tested diathesis-stress model.

The association between depressive symptoms and emotion recognition is moderated by emotion regulation.

In this study, we examined the associations between depression and aspects of emotional functioning, namely emotion recognition, affectivity and interpersonal problems. Particularly, the moderating role of emotion regulation in these interrelations was tested in a sample of 85 women, who exhibited a wide range of depressive symptoms (Composite International Diagnostic Interview (CIDI), Beck Depression Inventory (BDI)). Emotion recognition was assessed with a paradigm displaying a widely used set of photographs of the six basic emotions in graded intensities. Further, participants were examined regarding emotion regulation (Emotion Regulation Questionnaire (ERQ)), interpersonal problems (Inventory of Interpersonal Problems-Circumplex (IIP-C)) and affectivity (Affect Intensity Measure (AIM), Positive and Negative Affect Schedule (PANAS)). Besides correlation analyses, Johnson-Neyman technique for probing interactions in linear regression models was applied to test for possible moderating effects. Depressive symptoms were positively correlated with error rates in anger recognition, but not with the other basic emotions. This association was moderated by suppression in that regard that more severely depressed women who more frequently used suppression showed superior recognition of angry faces than those with lower suppression values. Further, suppression was associated with an affective imbalance and interpersonal problems in women with current depressive disorder. In sum, our results emphasize the importance of differentiating subtypes of depression depending on emotion regulation capabilities for research on or treatment of emotional functioning in depression.

Maternal transmission of borderline personality disorder symptoms in the community-based Greifswald Family Study.

The authors longitudinally investigated the familial transmission of mothers' BPD symptoms to their offspring, taking maternal depression into consideration. The sample consisted of 323 offspring and their mothers from the community-based Greifswald Family Study. These families were examined for the first time when the children were about 15 years old (T(0)), and again 5 years later (T(1)), using self-ratings and interviews. Regression analyses revealed that maternal BPD symptoms and depression at T(0) were significant predictors of a number of BPD criteria that offspring met at T(1). Furthermore, the analyses also predicted offspring's general psychopathology. In sum, the authors' findings provide evidence for familial aggregation of BPD symptoms and heightened levels of general psychopathology in offspring of mothers with high levels of BPD features, pointing to the need for providing early intervention for this high-risk group.