The Camberwell Collaborative Depression Study III. Depression and Adversity in the Relatives of Depressed Probands

McGuffin, Peter; Katz, Randy; Bebbington, Paul

doi:10.1192/bjp.152.6.775

Cited by 179 publications

(79 citation statements)

References 17 publications

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“…8 Considered together, early and proximal social factors explain a large proportion of depression in population-based samples. 8 However, these social factors account for relatively smaller proportion of depression in clinically ascertained samples 9,10 and fail to explain the grater differences in risk of depression between monozygotic compared to dizygotic twins. 11,12 The evidence for genetic influences on depression consists primarily of twin studies.…”

Section: The Interacting Causes Of Depressionmentioning

confidence: 99%

The implications of gene–environment interactions in depression: will cause inform cure?

Uher

2008

Mol Psychiatry

134

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In a number of human diseases, including depression, interactions between genetic and environmental factors have been identified in the absence of direct genotype-disorder associations. The lack of genes with major direct pathogenic effect suggests that genotype-specific vulnerabilities are balanced by adaptive advantages and implies aetiological heterogeneity. A model of depression is proposed that incorporates the interacting genetic and environmental factors over the life course and provides an explanatory framework for the heterogeneous aetiology of depression. Early environmental influences act on the genome to shape the adaptability to environmental changes in later life. The possibility is explored that genotype-and epigenotype-related traits can be harnessed to develop personalized therapeutic interventions. As diagnosis of depression alone is a weak predictor of response to specific treatments, aetiological subtypes can be used to inform the choice between treatments. As a specific application of this notion, a hypothesis is proposed regarding relative responsiveness of aetiological subtypes of depression to psychological treatment and antidepressant medication. Other testable predictions are likely to emerge from the general framework of interacting genetic, epigenetic and environmental mechanisms in depression.

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Section: The Interacting Causes Of Depressionmentioning

confidence: 99%

The implications of gene–environment interactions in depression: will cause inform cure?

Uher

2008

Mol Psychiatry

134

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“…22 We found no statistically significant differences in the reported gene-environment interaction when women were compared to men. Family history of psychological problems has been associated with both exposure 36 and outcome, 37 and thus should remain in the model. The independence from family history of our reported gene-environment interaction may suggest that there could be some specific role for the 5HTTLPR genotype (or the serotonin transporter gene) in its modification of the risk effect for depression conferred by previous TLEs.…”

Section: Novelty and Interestmentioning

confidence: 99%

The risk for depression conferred by stressful life events is modified by variation at the serotonin transporter 5HTTLPR genotype: evidence from the Spanish PREDICT-Gene cohort

et al. 2007

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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)).

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“…For example, Bebbington and colleagues McGuffin et al, 1988) have shown that levels of SLEs are increased in the relatives of depressed patients versus controls, although Farmer and colleagues (Farmer et al, 2000) suggested that familial similarities in SLEs with depression may largely result from shared experiences.…”

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confidence: 99%

Sources of Individual Differences in Stressful Life Event Exposure in Male and Female Twins

et al. 2004

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T he roles of genetic and environmental influences on stressful life events were examined in 3938 twin pairs (MZ, same-sex DZ, and opposite-sex DZ) using a sex-limitation model. Life events were assessed by personal interview, and were categorized as being either personal (i.e., events that occur directly to the individual) or network (i.e., events that occur to someone within the individual's social network, thus affecting the individual indirectly). Consistent with previous reports, genetic factors were found to exert more influence on personal events than network events. Genetic correlations between males and females suggest that many of the same genetic factors are acting within both genders.

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The Camberwell Collaborative Depression Study III. Depression and Adversity in the Relatives of Depressed Probands

Cited by 179 publications

References 17 publications

The implications of gene–environment interactions in depression: will cause inform cure?

The implications of gene–environment interactions in depression: will cause inform cure?

The risk for depression conferred by stressful life events is modified by variation at the serotonin transporter 5HTTLPR genotype: evidence from the Spanish PREDICT-Gene cohort

Sources of Individual Differences in Stressful Life Event Exposure in Male and Female Twins

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