Gene×environment interactions at the serotonin transporter locus
Abstract
Background Although it is universally accepted that human disease and behavior depend upon both environmental and genetic variation, a view supported by family and twin studies, examples of environmental interactions with genes identified at the molecular level (G x E) are not so well established. Methods We carried out a systematic review and meta-analysis of the serotonin transporter (5-HTTLPR) polymorphic region x stressful life event (SLE) literature and investigated to what extent the main effects reported in this literature are consistent with a number of G x E hypotheses. Our aim was to provide a framework in which to assess the robustness of the claim for the presence of an interaction. Results The results from our systematic review and meta-analysis indicate that the main effect of 5-HTTLPR genotype and the interaction effect between 5-HTTLPR and SLE on risk of depression are negligible. We found that only a minority of studies report a replication that is qualitatively comparable to that in the original report. Conclusions Given reasonable assumptions regarding likely genetic and environmental effect sizes, our simulations indicate that published studies are underpowered. This, together with other aspects of the literature, leads us to suggest that the positive results for the 5-HTTLPR x SLE interactions in logistic regression models are compatible with chance findings.
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Heterogeneity in adversity exposure in previous samples may explain why gene-by-environment associations have been inconsistently replicated.
“In fact, heterogeneity in adversity exposure in previous samples may explain inconsistent replication of gene-by-environment associations (Kim-Cohen et al., 2006; Munafò et al., 2009).”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Munafò et al., 2009
Candidate gene studies need adequate numbers of subjects exposed and unexposed to the stressful environment to ensure adequate power.
“It is important that the study sample contains adequate numbers of subjects exposed and unexposed to the stressful environment to ensure adequate power”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Munafo et al. 2009
Munafo et al. (2009) meta-analysis concluded that most available studies were underpowered and that findings using logistic regression models were compatible with chance.
“Munafo et al. (2009) conducted a meta-analysis which led them to conclude that most of the available studies were underpowered, and that findings using logistic regression models were “compatible with chance.””
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Munafo et al. (2009)
Meta-analyses have not supported the MDD serotonin transporter gene-environment interaction finding.
“Meta-analyses have supported 111,112 and not supported 113,114 this finding.”
From Genetic architectures of psychiatric disorders: the emerging picture and its implications (2012) · cites this paper as [114]
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- Authors
- Munafò, M. R., Durrant, C., Lewis, G., & Flint, J.
- Affiliations
- Centre for Human Genetics (GB)
- University of Bristol (GB)
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 65
- Issue
- 3
- Pages
- 211-219
- ISSN
- 0006-3223 (ISSN-L)
- OpenAlex
- W2122246853
- Cited by
- 576
- References
- 34
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 2 · 2023: 5 · 2022: 5 · 2021: 10 · 2020: 55 · 2019: 18 · 2018: 17 · 2017: 34 · 2016: 40 · 2015: 50 · 2014: 45 · 2013: 51 · 2012: 80
- FWCI
- 4.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- gene-environment interaction, serotonin transporter, 5-HTTLPR polymorphism, life events, depression risk, replication robustness, statistical power, genetic effect size
- MeSH terms
- Computer Simulation, Environment, Genotype, Humans, Life Change Events, Stress, Psychological, Logistic Models, Serotonin Plasma Membrane Transport Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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