Genome-Wide Environment Interaction Between Depressive State and Stressful Life Events

Ikeda, Masashi; Shimasaki, Ayu; Takahashi, Atsushi; Kondo, Kenji; Takeo, Satoshi; Kawase, Kohei; Esaki, Kosei; Otsuka, Yasuyo; Mano, Keiko; Kubo, Michiaki; Iwata, Nakao

doi:10.4088/jcp.15l10127

Cited by 27 publications

(20 citation statements)

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“…(1120 male and 1828 female subjects; age 37.0 6 15.2 years old) were genotyped as healthy control subjects; they had no personal history of mental disorders and were Japanese descent by self-report. Among them, 1108 subjects were nurses at Fujita Health University Hospital (21), while the others were recruited from the general population.…”

Section: Healthy Comparison Subjects a Total Of 2948 Subjectsmentioning

confidence: 99%

Pharmacogenomic Study of Clozapine-Induced Agranulocytosis/Granulocytopenia in a Japanese Population

Takeo

Ikeda

Mushiroda

et al. 2016

Biological Psychiatry

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Section: Healthy Comparison Subjects a Total Of 2948 Subjectsmentioning

confidence: 99%

Pharmacogenomic Study of Clozapine-Induced Agranulocytosis/Granulocytopenia in a Japanese Population

Takeo

Ikeda

Mushiroda

et al. 2016

Biological Psychiatry

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“…Therefore, we hypothesized that the ‘core’ symptoms of PegIFN‐induced depressive state are different from those of the ‘general’ depressive state, which is usually associated with SLE. To clarify whether the core symptoms of PegIFN‐induced depressive state were unique, we compared the effect size (increase in subscale change between the baseline and worst point) for all BDI items between the current results and our previous cohort data (see Appendix S1 for details of our previous report of general depressive state) . In this explorative analysis, we found that ‘somatic symptoms’ (larger changes observed in the PegIFN therapy group, including sleep disturbance, loss of appetite, and weight loss) showed a relatively small effect size in our previous data for general depressive state (Table ).…”

Section: Resultsmentioning

confidence: 75%

Risk factors and clinical characteristics of the depressive state induced by pegylated interferon therapy in patients with hepatitis C virus infection: A prospective study

Kawase

Kondo

Takeo

et al. 2016

Psychiatry Clin Neurosci

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Aim: Pegylated interferon (PegIFN) therapies for hepatitis C virus (HCV) infection often induce a depressive state. This study aimed to identify the risk factors for and clinical characteristics of PegIFNinduced depressive state.Methods: Sixty-nine subjects with HCV who received PegIFN therapy were enrolled. Before beginning therapy, all subjects were evaluated using the Neuroticism-Extraversion-Openness Five-Factor Inventory and the List of Threatening Events Questionnaire. Beck Depression Inventory (BDI) scores were also evaluated at baseline, 2-4 weeks after initiating therapy, and every 4 weeks thereafter.Results: During the study, 18 subjects (24.3%) developed a depressive state (BDI ≥ 10). A bimodal peak of onset was observed during the early (2-8 weeks) and late (after 20 weeks) therapy phases. Moreover, we observed that baseline BDI scores (odds ratio [OR] = 1.40, P = 0.0104) and neuroticism (OR = 1.14, P = 0.0275) were significant risk factors for developing a depressive state. To determine the specific characteristics of this condition, we compared the BDI subscales between the 'PegIFNinduced' and 'general' depressive state reported previously. We found that the score at 'somatic symptoms' was higher in the 'PegIFN-induced' group. Conclusion:Our results indicate the following: (i) PegIFN-induced depressive state most frequently develops during the first 8 weeks of therapy; (ii) baseline BDI and neuroticism scores are risk factors for PegIFN-induced depressive state; and (iii) the core symptoms of PegIFN-induced depressive state are different from those of 'general' depression.

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“…and, therefore, add validity to the diathesis-stress theory for depression. Empirically demonstrating the diathesis-stress theory for depression would validate recent 20-22,24 and future studies using a genome-wide approach to identify genetic mechanisms and interactive pathways involved in GxE underpinning the causative effect of “stress” in the development of depressive symptoms and mental illness in general. This study adds to our understanding of gene-by-environment interactions, although larger samples will be required to confirm differences in diathesis-stress effects between women and men.…”

Section: Discussionmentioning

confidence: 76%

A validation of the diathesis-stress model for depression in Generation Scotland

Arnau‐Soler

Adams

Clarke

et al. 2018

Preprint

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Depression has well-established influences from genetic and environmental risk factors. This has led to the diathesis-stress theory, which assumes a multiplicative gene-by-environment interaction (GxE) effect on risk. Recently, Colodro-Conde et al. empirically tested this theory, using the polygenic risk score for major depressive disorder (PRS, genes) and stressful life events (SLE, environment) effects on depressive symptoms, identifying significant GxE effects with an additive contribution to liability. We have tested the diathesis-stress theory on an independent sample of 4 919 individuals.We identified nominally significant positive GxE effects in the full cohort (R2 = 0.08%, p = 0.049) and in women (R2 = 0.19%, p = 0.017), but not in men (R2 = 0.15%, p = 0.07). GxE effects were nominally significant, but only in women, when SLE were split into those in which the respondent plays an active or passive role (R2 = 0.15%, p = 0.038; R2 = 0.16%, p = 0.033, respectively). High PRS increased the risk of depression in participants reporting high numbers of SLE (p = 2.86 × 10−4). However, in those participants who reported no recent SLE, a higher PRS appeared to increase the risk of depressive symptoms in men (β = 0.082, p = 0.016) but had a protective effect in women (β = −0.061, p = 0.037). This difference was nominally significant (p = 0.017). Our study reinforces the evidence of additional risk in the aetiology of depression due to GxE effects. However, larger sample sizes are required to robustly validate these findings.

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Genome-Wide Environment Interaction Between Depressive State and Stressful Life Events

Cited by 27 publications

References 0 publications

Pharmacogenomic Study of Clozapine-Induced Agranulocytosis/Granulocytopenia in a Japanese Population

Pharmacogenomic Study of Clozapine-Induced Agranulocytosis/Granulocytopenia in a Japanese Population

Risk factors and clinical characteristics of the depressive state induced by pegylated interferon therapy in patients with hepatitis C virus infection: A prospective study

A validation of the diathesis-stress model for depression in Generation Scotland

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