Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: a meta-analysis

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Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: a meta-analysis
Authors: Neil Risch, Richard Herrell, Thomas Lehner, Kung-Yee Liang, Lindon Eaves, Josephine Hoh, Andrea Griem, Maria Kovacs, Jurg Ott, Kathleen Ries Merikangas
Citation: JAMA : the journal of the American Medical Association 301 (23): 2462-2461. 2009 June
Database(s): PubMed (PMID/19531786)
DOI: 10.1001/jama.2009.878.
PMCID:2938776
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Extract:

Interaction between the serotonin transporter gene (5-HTTLPR), stressful life events, and risk of depression: a meta-analysis reports a meta-analysis on the 5-HTTLPR polymorphism, stressful life events and depression.

There is a erratum[1] which corrects wording in the original article.

There was a number of comments on the article:

  1. K. C. Koenen, S. Galea, Gene-environment interactions and depression
  2. N. Rieckmann, M. A. Rapp, J. Müller-Nordhorn, Gene-environment interactions and depression
  3. Gene-environment interactions: biologically valid pathway or artifact?
  4. Jacob Peedicayil pointed to epigenetics as an explanation for gene-environment (GXE) interactions.[2]

The study Gene x environment interactions at the serotonin transporter locus also examined 5-HTTLPR and stressful life event interaction on depression.

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

Contents

[edit] Included studies

  1. Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene
  2. Gene-environment interaction analysis of serotonin system markers with adolescent depression
  3. The relationship between stressful life events, the serotonin transporter (5-HTTLPR) genotype and major depression
  4. Mental and physical distress is modulated by a polymorphism in the 5-HT transporter gene interacting with social stressors and chronic disease burden
  5. Social adversity, the serotonin transporter (5-HTTLPR) polymorphism and major depressive disorder
  6. Life events, first depression onset and the serotonin transporter gene
  7. Early family environment, current adversity, the serotonin transporter promoter polymorphism, and depressive symptomatology
  8. Relationship of 5-HTTLPR genotypes and depression risk in the presence of trauma in a female twin sample
  9. Family based association analyses between the serotonin transporter gene polymorphism (5-HTTLPR) and neuroticism, anxiety and depression
  10. No interaction between the serotonin transporter polymorphism (5-HTTLPR) and childhood adversity or recent stressful life events on symptoms of depression: results from two community surveys
  11. PREDICT Study Core Group. 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
  12. Interactions between life stressors and susceptibility genes (5-HTTLPR and BDNF) on depression in Korean elders
  13. 5-HTTLPR genotype, stressful life events and late-life depression: no evidence of interaction in a French population
  14. Interaction between the 5-HTTLPR serotonin transporter polymorphism and environmental adversity for mood and anxiety psychopathology: evidence from a high-risk community sample of young adults

[edit] Results

The three main results were [2]:

  1. No association of 5-HTTLPR on depression
  2. Association of stressful life events and depression
  3. No association of interaction between 5-HTTLPR and stressful life events on depression

[edit] External links

[edit] References

  1. missing author1 (2009). "Incorrect Wording in: Interaction Between the Serotonin Transporter Gene (5-HTTLPR), Stressful Life Events, and Risk of Depression: A Meta-analysis". JAMA 302(5): 492. doi: 10.1001/jama.302.5.492.
  2. Jacob Peedicayi (2009). "The role of epigenetics in gene-environment interactions". Arch. Gen. Psychiatry 66: 1287-1289. [1].
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