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Elevated Plasma C-Reactive Protein in Chronically Distressed Subjects Who Carry the A Allele of the TNF-α −308 G/A Polymorphism

Bibliographic Data

ID20971197
AuthorsPascal Jeanmonod (Ecole polytechnique fédérale de Lausanne), Roland Von Känel (0000-0002-8929-5129), Friedrich E Maly, Jerome E Fischer (0000-0002-7543-1820, corresponding author), Joachim E Fischer
Year2004
Volume66
Issue4
Pages501-506
Publication date2004-07-01
Peer ReviewedYes
Open AccessNo
TypeARTICLE
VenuePsychosomatic Medicine (JOURNAL)
Journal identifiersISSN: 0033-3174 • E-ISSN: 1534-7796
PublisherOvid Technologies (Wolters Kluwer Health) (PUBLISHER)
DOI10.1097/01.psy.0000130903.78444.7d
PMID15272094
OpenAlexW2016888770
LanguageEN
Citations received3
References cited33

OBJECTIVE: Sustained psychological stress may result in a state operationalized as "vital exhaustion." Exhaustion predicted coronary artery disease (CAD) events whereby increased inflammatory activity might mediate this link. Moreover, there is an emerging importance of gene-environmental interactions in CAD. We investigated the effect of exhaustion severity on plasma levels of C-reactive protein (CRP) and whether exhaustion might regulate CRP levels via the -308G/A polymorphism of the tumor necrosis factor (TNF)-alpha gene. METHODS: We assessed exhaustion in 275 industrial employees (mean age +/- SD, 41 +/- 9 years, 88% men) using the Maastricht Questionnaire. Subjects were stratified as per exhaustion severity: none (N = 80), moderate (N = 128), and severe (N = 67). The TNF-alpha polymorphism was determined by real-time polymerase chain reaction, and plasma CRP levels were measured by a high-sensitivity immunoassay. RESULTS: There was a significant interaction between exhaustion and the TNF-alpha polymorphism, explaining 4.5% in the variance of plasma CRP values (F(5,271) = 2.47, p =.033); the result held after controlling for classic cardiovascular risk factors. Adjusted mean CRP levels across exhaustion strata in GA (N = 70) and AA (N = 3) carriers combined were 0.91 mg/l (none), 1.78 mg/l (moderate), and 2.61 mg/l (severe) as compared with 1.24 mg/l, 1.61 mg/l, and 1.36 mg/l for the GG wild-type (N = 202). CONCLUSION: The findings suggest that the A allele of the TNF-alpha -308 G/A polymorphism may mediate inflammation with exhaustion in a dose-response relationship, while with the GG wild-type exhaustion severity seems unrelated to CRP levels. The finding provides a rationale for gene-environmental interactions by which psychosocial factors may promote atherosclerosis and CAD

Allele · Biology · C-reactive protein · Coronary artery disease · Gene · Inflammation · Polymorphism (computer science) · Tumor necrosis factor alpha · Adipokines, Inflammation, and Metabolic Diseases · Endocrinology · Exercise and Physiological Responses · Genetics · Internal Medicine · Medicine · Stress Responses and Cortisol

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Unique citing works3
Citations per year0.15
Citation span2006 - 2007 (2)
Citation velocityhistorical
Highly citedNo
Citation typesNeutral: 3

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