Transition from stress sensitivity to a depressive state: longitudinal twin study (original) (raw)
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Genetic risk of depression and stress-induced negative affect in daily life
British Journal of Psychiatry, 2007
BackgroundA bias to develop negative affect in response to daily life stressors may be an important depression endophenotype, but remains difficult to assess.AimsTo assess this mood bias endophenotype, uncontaminated by current mood, in the course of daily life.MethodThe experience samping method was used to collect multiple appraisals of daily life event-related stress and negative affect in 279 female twin pairs. Cross-twin, cross-trait associations between daily life mood bias and DSM – IV depression were conducted.ResultsProbands whose co-twins were diagnosed with lifetime depression showed a stronger mood bias to stress than those with co-twins without such a diagnosis, independent of probands' current depressive symptoms and to a greater extent in monozygotic twins than in dizygotic twins.ConclusionsGenetic liability to depression is in part expressed as the tendency to display negative affect in response to minor stressors in daily life. This trait may represent a true de...
Cognitive Therapy and Research, 2000
Variation in the promoter region of the serotonin transporter gene (5-HTTLPR) has been linked to various cognitive-affective indices of stress sensitivity hypothesized to underlie vulnerability to depression. The current study examined the association of 5-HTTLPR with appraisals of naturally occurring acute life stressors in a community sample of 384 youth at elevated risk for depression due to oversampling for maternal
Psychological Medicine, 2009
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.
2007
We report results from the PREDICT-Gene case-control study nested in a prospective cohort designed to identify predictors of the onset of depression among adult primary-care attendees. We tested the potential gene-by-environment interaction between 5HTTLPR genotype at the serotonin transporter gene and previous exposure to threatening life events (TLEs) in depression. A total of 737 consecutively recruited participants were genotyped. Additional information was gathered on exposure to TLEs over a 6-month period, socio-demographic data and family history of psychological problems among first-degree relatives. Diagnoses of depression were ascertained using the Composite International Diagnostic Interview (CIDI) by trained interviewers. Two different depressive outcomes were used (ICD-10 depressive episode and ICD-10 severe depressive episode). Both the s/s genotype and exposure to increasing number of TLEs were significantly associated with depression. Moreover, the 5HTTLPR s/s genotype significantly modified the risk conferred by TLEs for both depressive outcomes. Thus, s/s homozygous participants required minimal exposure to TLE (1 TLE) to acquire a level of risk for depression that was only found among l/s or l/l individuals after significantly higher exposure to TLEs (two or more TLEs). The interaction was more apparent when applied to the diagnosis of ICD-10 severe depressive episode and after adjusting for gender, age and family history of psychological problems. Likelihood ratios tests for the interaction were statistically significant for both depressive outcomes (ICD-10 depressive episode: LR X 2 = 4.7, P = 0.09 (crude), LR-X 2 = 6.4, P = 0.04 (adjusted); ICD-10 severe depressive episode: LR X 2 = 6.9, P = 0.032 (crude), LR-X 2 = 8.1, P = 0.017 (adjusted)).
PloS one, 2016
The low transcriptionally efficient short-allele of the 5HTTLPR serotonin transporter polymorphism has been implicated to moderate the relationship between the experience of stressful life events (SLEs) and depression. Despite numerous attempts at replicating this observation, results remain inconclusive. We examined this relationship in young-adult Non-Hispanic white males and females between the ages of 22 and 26 (n = 4724) participating in the National Longitudinal Study of Adolescent to Adult Health (Add Health) with follow-up information every six years since 1995. Linear and logistic regression models, corrected for multiple testing, indicated that carriers of one or more of the S-alleles were more sensitive to stress than those with two L-alleles and at a higher risk for depression. This relationship behaved in a dose-response manner such that the risk for depression was greatest among those who reported experiencing higher numbers of SLEs. In post-hoc analyses we were not ab...
Development and Psychopathology, 2014
Previous research supports gene-environment interactions for polymorphisms in corticotrophin hormone receptor (CRHR1) and the serotonin transporter (5-HTTLPR) genes in predicting depression, but has rarely considered genetic influences on stress sensitization processes, whereby early adversities (EA) increase depressive reactivity to proximal stressors later in life. The current study tested a gene-environment-environment interaction (G ! E ! E; specifically gene-EA-proximal stress interaction) model of depression in a 20-year longitudinal study. Participants were assessed prospectively for EA up to age 5 and recent chronic stress and depressive symptoms at age 20 and genotyped for CRHR1 SNP rs110402 and 5-HTTLPR. EA predicted stronger associations between recent chronic stress and depression, and the effect was moderated by genes. CRHR1 A alleles and 5-HTTLPR short alleles were associated with greater stress sensitization (i.e., greater depressive reactivity to chronic stress for those also exposed to high levels of EA). Results are consistent with the notion that EA exposure results in neurobiological and cognitive-emotional consequences (e.g., altered hypothalamic-pituitaryadrenal [HPA] axis functioning) leading to emotional distress in the face of recent stressors among those with certain genetic characteristics, although further research is needed to explore explanatory mechanisms.
Journal of Psychiatric Research, 1990
To determine the etiology of self-reported depressive symptoms and their co-occurrence in the general population, multivariate genetic models were fitted to the responses of 771 female twin pairs (463 MZ, 308 DZ) to a 20-item epidemiological depression inventory (CES-D scale). A model which contained one common genetic factor, one shared environmental factor, and four unique environmental factors provided a useful account of symptom covariation. Under this model, the four non-shared environmental factors explained the largest proportion of variance in response to the CES-D scale, whereas a single common genetic factor explained substantially less of the variation in symptomatology. Consistent with previous findings (KENDLER, HEATH, MARTIN, & EAVES, Archives of Genera/ Psychiafry 43, 213-221, 1986) shared environmental influences were found to play a relatively minor role in the report of depressive symptoms. These results suggest that while genetic factors do contribute to the covariation among symptoms of depression, it is the largely non-shared environmental factors that account for the co-occurrence of symptoms in the general population. 1NTRODUCTlON EVIDENCE from numerous twin, family, and adoption studies has demonstrated the importance of both genetic and environmental factors in affective illness. In a review of the twin literature on affective disorders GERSHON, BUNNEY, LECKMAN, VAN EERDEWEGH, and DEBAUCHE (1976) reported an overall concordance rate of 69.2% for monozygotic twins and 13.3% for dyzygotic twin pairs, providing support for a genetic predisposition to this disorder. Genetic effects have been relatively well established in bipolar depression (WINOKUR &