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Open AccessJournal ArticleDOI

The moderation by the serotonin transporter gene of environmental adversity in the etiology of depression: 2009 update

Rudolf Uher, +1 more
- 01 Jan 2010 - 
- Vol. 15, Iss: 1, pp 18-22
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TLDR
An updated review of 34 human observational studies indicates that the length polymorphism of the serotonin transporter gene moderates the effect of environmental adversity in the development of depression.
Abstract
An updated review of 34 human observational studies indicates that the length polymorphism of the serotonin transporter gene moderates the effect of environmental adversity in the development of depression. This finding depends on the use of contextual or objective methods to assess environmental adversity and is attenuated when self-report instruments are used. Inconsistent findings in male adolescents suggest a developmental stage and sex-specific protective mechanism. These systematic relationships between method and results should be followed up to specify causal mechanisms leading to depression.

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Citations
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Journal ArticleDOI

Depression in adolescence

TL;DR: Unipolar depressive disorder in adolescence is common worldwide but often unrecognised, and the incidence, notably in girls, rises sharply after puberty and, by the end of adolescence, the 1 year prevalence rate exceeds 4%.
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From Stress to Inflammation and Major Depressive Disorder: A Social Signal Transduction Theory of Depression

TL;DR: A biologically plausible, multilevel theory is proposed that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental stress with internal biological processes that drive depression pathogenesis and may shed light on several important questions including how depression develops, why it frequently recurs, and why it is strongly predicted by early life stress.
Journal ArticleDOI

The serotonin transporter promoter variant (5-HTTLPR), stress, and depression meta-analysis revisited: evidence of genetic moderation.

TL;DR: In this article, the authors performed a meta-analysis on the entire body of work assessing the relationship between 5-HTTLPR, stress and depression and concluded that there is no evidence supporting the presence of genetic moderation.
Journal ArticleDOI

Differential susceptibility to the environment: an evolutionary--neurodevelopmental theory.

TL;DR: The differential susceptibility paradigm has far-reaching implications for understanding whether and how much child and adult development responds, for better and for worse, to the gamut of species-typical environmental conditions.
Journal ArticleDOI

Resilience as a dynamic concept.

TL;DR: Evidence on turning point effects associated with experiences that increase opportunities and enhance coping and Gene–environment interaction findings are considered, and it is noted that there is some evidence that the genetic influences concerns responsivity to all environments and not just bad ones.
References
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Journal ArticleDOI

Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene

TL;DR: Evidence of a gene-by-environment interaction is provided, in which an individual's response to environmental insults is moderated by his or her genetic makeup.
Journal ArticleDOI

Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene

TL;DR: Evidence of a gene-by-environment interaction is provided, in which an individual's response to environmental insults is moderated by his or her genetic makeup.
Journal ArticleDOI

Interaction Between the Serotonin Transporter Gene (5-HTTLPR), Stressful Life Events, and Risk of Depression: A Meta-analysis

TL;DR: This meta-analysis yielded no evidence that the serotonin transporter genotype alone or in interaction with stressful life events is associated with an elevated risk of depression in men alone, women alone, or in both sexes combined.

Interaction Between the Serotonin Transporter Gene (5-HTTLPR), Stressful Life Events, and Risk of Depression

TL;DR: Merikangas et al. as discussed by the authors showed that most common genetic risks, at least when studied individually, are modest in magnitude, with relative risks in the range of 1.3 or less.
Journal ArticleDOI

Strategy for investigating interactions between measured genes and measured environments.

TL;DR: It is suggested that in psychiatric genetics, ignoring nurture handicaps the field's capacity to make new discoveries about nature and the potential benefits of the measured-GxE approach for basic neuroscience and for gene hunting are explained.
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