@article{ref1,
title="Preliminary evidence that the short allele of 5-HTTLPR moderates the association of psychiatric symptom severity on suicide attempt: the example in obsessive-compulsive disorder",
journal="Frontiers in psychiatry",
year="2022",
author="Harika-Germaneau, Ghina and Lafay-Chebassier, Claire and Langbour, Nicolas and Thirioux, Bérangère and Wassouf, Issa and Noel, Xavier and Jaafari, Nemat and Chatard, Armand",
volume="13",
number="",
pages="e770414-e770414",
abstract="BACKGROUND: The severity of symptoms represents an important source of distress in patients with a psychiatric disease. However, the extent to which this endogenous stress factor interacts with genetic vulnerability factors for predicting suicide risks remains unclear. <br><br>METHODS: We evaluated whether the severity of symptoms interacts with a genetic vulnerability factor (the serotonin transporter gene-linked promoter region variation) in predicting the frequency of lifetime suicide attempts in patients with a psychiatric disease. Symptom severity and 5-HTTLPR polymorphism were collected from a sample of 95 patients with obsessive-compulsive disorder (OCD). Lifetime suicide attempt was the primary outcome, and antecedent of multiple suicide attempts was the secondary outcome. <br><br>RESULTS: The gene-by-symptoms interaction was associated with an excess risk of suicide attempts (OR = 4.39, 95CI[1.44, 13.38], p < 0.009) and of multiple suicide attempts (OR = 4.18, 95CI[1.04, 16.77], p = 0.043). Symptom severity (moderate, severe, or extreme) was associated with an approximately five-fold increase in the odds of a lifetime suicide attempt in patients carrying one or two copies of the short allele of 5-HTTLPR. No such relationship was found for patients carrying the long allele. <br><br>CONCLUSION: This study provides preliminary evidence for the gene-by-stress interaction on suicide attempt when stress is operationalized as symptom severity. Progress in suicide research may come from efforts to investigate the gene-by-symptoms interaction hypothesis in a variety of diseases.<p /> <p>Language: en</p>",
language="en",
issn="1664-0640",
doi="10.3389/fpsyt.2022.770414",
url="http://dx.doi.org/10.3389/fpsyt.2022.770414"
}