Stressful life events and the serotonin transporter gene (5-HTT) in recurrent clinical depression

Helen L. Fisher; Sarah Cohen-Woods; Georgina M. Hosang; Rudolf Uher; Georgia Powell-Smith; Robert Keers; Maria Tropeano; Ania Korszun; Lisa Jones; Ian Jones; Mike Owen; Nick Craddock; Ian W. Craig; Anne E. Farmer; Peter McGuffin

doi:10.1016/j.jad.2011.09.016

Stressful life events and the serotonin transporter gene (5-HTT) in recurrent clinical depression

Helen L. Fisher, Sarah Cohen-Woods, Georgina M. Hosang, Rudolf Uher, Georgia Powell-Smith, Robert Keers, Maria Tropeano, Ania Korszun, Lisa Jones, Ian Jones, Mike Owen, Nick Craddock, Ian W. Craig, Anne E. Farmer, Peter McGuffin

Research output: Contribution to journal › Article › peer-review

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Abstract

Background: An interaction between recent stressful life events (SLEs) and a serotonin transporter promoter polymorphism (5-HTTLPR) in depression has been inconsistently reported. Some of this variability may be due to a previous focus on sub-clinical depression, inclusion of individuals at the lower or upper ends of the age-span, or assumptions concerning the degree of dominance of the low expressing allele. Therefore, a large sample of patients with recurrent clinically diagnosed depression and controls screened for absence of depression was utilised to examine the moderating effect of each 5-HTTLPR genetic model on the association between SLEs and severe depressive episodes. Method: A sample of 1236 recurrent unipolar depression cases and 598 age-matched, never psychiatrically ill controls completed the List of Threatening Experiences Questionnaire to assess the number of SLEs experienced in the 6 months prior to the most severe depressive episode (cases) or interview (controls). DNA extracted from blood or cheek swabs was genotyped for the short (s) and long (l) alleles of 5-HTTLPR. Results: A greater number of SLEs were reported by cases than controls and this held across all genotypic groups. There was no main effect of 5-HTTLPR on depression and no evidence of interaction between total SLEs and any of the 5-HTTLPR genetic models. The results were the same for men and women. Limitations: Utilisation of retrospective self-reported SLEs may have reduced the accuracy of the findings and the cross-sectional design prevents causal inference. Conclusions: This study failed to find evidence of gene-environment interplay in recurrent clinical depression.

Original language	English
Pages (from-to)	189-193
Number of pages	5
Journal	Journal of Affective Disorders
Volume	136
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jad.2011.09.016
Publication status	Published - Jan 2012
Externally published	Yes

Bibliographical note

Funding Information:
Funding for the DeCC study was provided by the MRC. BACCs data collection was supported by GlaxoSmithKline, Research and Development. Helen L. Fisher and Georgina M. Hosang are supported by UK Medical Research Council (MRC) and Economic and Social Research Council interdisciplinary postdoctoral fellowships. Sarah Cohen-Woods is funded by a postdoctoral fellowship from the National Institute for Health Research (NIHR) Specialist Biomedical Research Centre for Mental Health at the South London and Maudsley NHS Foundation Trust and the Institute of Psychiatry, King's College London. The funding organisations had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication.

ASJC Scopus Subject Areas

Clinical Psychology
Psychiatry and Mental health

PubMed: MeSH publication types

Journal Article
Research Support, Non-U.S. Gov't

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.jad.2011.09.016

Cite this

Fisher, H. L., Cohen-Woods, S., Hosang, G. M., Uher, R., Powell-Smith, G., Keers, R., Tropeano, M., Korszun, A., Jones, L., Jones, I., Owen, M., Craddock, N., Craig, I. W., Farmer, A. E., & McGuffin, P. (2012). Stressful life events and the serotonin transporter gene (5-HTT) in recurrent clinical depression. Journal of Affective Disorders, 136(1-2), 189-193. https://doi.org/10.1016/j.jad.2011.09.016

Fisher, HL, Cohen-Woods, S, Hosang, GM, Uher, R, Powell-Smith, G, Keers, R, Tropeano, M, Korszun, A, Jones, L, Jones, I, Owen, M, Craddock, N, Craig, IW, Farmer, AE & McGuffin, P 2012, 'Stressful life events and the serotonin transporter gene (5-HTT) in recurrent clinical depression', Journal of Affective Disorders, vol. 136, no. 1-2, pp. 189-193. https://doi.org/10.1016/j.jad.2011.09.016

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title = "Stressful life events and the serotonin transporter gene (5-HTT) in recurrent clinical depression",

abstract = "Background: An interaction between recent stressful life events (SLEs) and a serotonin transporter promoter polymorphism (5-HTTLPR) in depression has been inconsistently reported. Some of this variability may be due to a previous focus on sub-clinical depression, inclusion of individuals at the lower or upper ends of the age-span, or assumptions concerning the degree of dominance of the low expressing allele. Therefore, a large sample of patients with recurrent clinically diagnosed depression and controls screened for absence of depression was utilised to examine the moderating effect of each 5-HTTLPR genetic model on the association between SLEs and severe depressive episodes. Method: A sample of 1236 recurrent unipolar depression cases and 598 age-matched, never psychiatrically ill controls completed the List of Threatening Experiences Questionnaire to assess the number of SLEs experienced in the 6 months prior to the most severe depressive episode (cases) or interview (controls). DNA extracted from blood or cheek swabs was genotyped for the short (s) and long (l) alleles of 5-HTTLPR. Results: A greater number of SLEs were reported by cases than controls and this held across all genotypic groups. There was no main effect of 5-HTTLPR on depression and no evidence of interaction between total SLEs and any of the 5-HTTLPR genetic models. The results were the same for men and women. Limitations: Utilisation of retrospective self-reported SLEs may have reduced the accuracy of the findings and the cross-sectional design prevents causal inference. Conclusions: This study failed to find evidence of gene-environment interplay in recurrent clinical depression.",

author = "Fisher, {Helen L.} and Sarah Cohen-Woods and Hosang, {Georgina M.} and Rudolf Uher and Georgia Powell-Smith and Robert Keers and Maria Tropeano and Ania Korszun and Lisa Jones and Ian Jones and Mike Owen and Nick Craddock and Craig, {Ian W.} and Farmer, {Anne E.} and Peter McGuffin",

note = "Funding Information: Funding for the DeCC study was provided by the MRC. BACCs data collection was supported by GlaxoSmithKline, Research and Development. Helen L. Fisher and Georgina M. Hosang are supported by UK Medical Research Council (MRC) and Economic and Social Research Council interdisciplinary postdoctoral fellowships. Sarah Cohen-Woods is funded by a postdoctoral fellowship from the National Institute for Health Research (NIHR) Specialist Biomedical Research Centre for Mental Health at the South London and Maudsley NHS Foundation Trust and the Institute of Psychiatry, King's College London. The funding organisations had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication. ",

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AU - Fisher, Helen L.

AU - Cohen-Woods, Sarah

AU - Hosang, Georgina M.

AU - Uher, Rudolf

AU - Powell-Smith, Georgia

AU - Keers, Robert

AU - Tropeano, Maria

AU - Korszun, Ania

AU - Jones, Lisa

AU - Jones, Ian

AU - Owen, Mike

AU - Craddock, Nick

AU - Craig, Ian W.

AU - Farmer, Anne E.

AU - McGuffin, Peter

N1 - Funding Information: Funding for the DeCC study was provided by the MRC. BACCs data collection was supported by GlaxoSmithKline, Research and Development. Helen L. Fisher and Georgina M. Hosang are supported by UK Medical Research Council (MRC) and Economic and Social Research Council interdisciplinary postdoctoral fellowships. Sarah Cohen-Woods is funded by a postdoctoral fellowship from the National Institute for Health Research (NIHR) Specialist Biomedical Research Centre for Mental Health at the South London and Maudsley NHS Foundation Trust and the Institute of Psychiatry, King's College London. The funding organisations had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication.

PY - 2012/1

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N2 - Background: An interaction between recent stressful life events (SLEs) and a serotonin transporter promoter polymorphism (5-HTTLPR) in depression has been inconsistently reported. Some of this variability may be due to a previous focus on sub-clinical depression, inclusion of individuals at the lower or upper ends of the age-span, or assumptions concerning the degree of dominance of the low expressing allele. Therefore, a large sample of patients with recurrent clinically diagnosed depression and controls screened for absence of depression was utilised to examine the moderating effect of each 5-HTTLPR genetic model on the association between SLEs and severe depressive episodes. Method: A sample of 1236 recurrent unipolar depression cases and 598 age-matched, never psychiatrically ill controls completed the List of Threatening Experiences Questionnaire to assess the number of SLEs experienced in the 6 months prior to the most severe depressive episode (cases) or interview (controls). DNA extracted from blood or cheek swabs was genotyped for the short (s) and long (l) alleles of 5-HTTLPR. Results: A greater number of SLEs were reported by cases than controls and this held across all genotypic groups. There was no main effect of 5-HTTLPR on depression and no evidence of interaction between total SLEs and any of the 5-HTTLPR genetic models. The results were the same for men and women. Limitations: Utilisation of retrospective self-reported SLEs may have reduced the accuracy of the findings and the cross-sectional design prevents causal inference. Conclusions: This study failed to find evidence of gene-environment interplay in recurrent clinical depression.

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Stressful life events and the serotonin transporter gene (5-HTT) in recurrent clinical depression

Abstract

Bibliographical note

ASJC Scopus Subject Areas

PubMed: MeSH publication types

UN SDGs

Access to Document

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