ArticleAtherosclerosis2008
Genetic and environmental influences on systemic markers of inflammation in middle-aged male twins.
Article in Atherosclerosis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 48 citations in OpenAlex.
- Heritability of carotid intima-media thickness and inflammatory factors of atherosclerosis in a Chinese population.Scientific reports · 2024Article
- Literary Identification of Differentially Hydroxymethylated DNA Regions for Type 2 Diabetes Mellitus: A Scoping Minireview.International journal of environmental research and public health · 2024Article
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- Abilities of Pre-Treatment Inflammation Ratios as Classification or Prediction Models for Patients with Colorectal Cancer.Diagnostics (Basel, Switzerland) · 2021Article
- Quantitative genetics of circulating Dickkopf-related protein 1 (DKK1) in community-based sample of UK twins.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2016Article
- Genetic and environmental determinants of population variation in interleukin-6, its soluble receptor and C-reactive protein: insights from identical and fraternal twins.Brain, behavior, and immunity · 2015Article
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- Genetic and environmental influences on the prospective correlation between systemic inflammation and coronary heart disease death in male twins.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
- Genetic insights into cardiometabolic risk factors.The Clinical biochemist. Reviews · 2014Review
- Effect of genetic and environmental influences on cardiometabolic risk factors: a twin study.Cardiovascular diabetology · 2011Article
- Genetic variants in LPL, OASL and TOMM40/APOE-C1-C2-C4 genes are associated with multiple cardiovascular-related traits.BMC medical genetics · 2011Article
- Temporal reliability of cytokines and growth factors in EDTA plasma.BMC research notes · 2010Article
- Mendelian randomization: potential use of genetics to enable causal inferences regarding HIV-associated biomarkers and outcomes.Current opinion in HIV and AIDS · 2010Review
- Heritability of renal function and inflammatory markers in adult male twins.American journal of nephrology · 2010Article
- Pleiotropy of C-reactive protein gene polymorphisms with C-reactive protein levels and heart rate variability in healthy male twins.The American journal of cardiology · 2009Article
- Serotonin transporter gene, depressive symptoms, and interleukin-6.Circulation. Cardiovascular genetics · 2009Article
- The relation of genetic and environmental factors to systemic inflammatory biomarker concentrations.Circulation. Cardiovascular genetics · 2009Article
- Inflammation and stress-related candidate genes, plasma interleukin-6 levels, and longevity in older adults.Experimental gerontology · 2009Article
- Common genetic contributions to depressive symptoms and inflammatory markers in middle-aged men: the Twins Heart Study.Psychosomatic medicine · 2009Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
objectivesThe aims of this study were to determine the relative influence of genetic and environmental contributions to inflammatory biomarkers, and to what extent correlations among these markers are due to genetic or environmental factors.
methodsWe performed univariate and multivariate genetic analyses of four inflammatory markers: interleukin-6 (IL-6), soluble IL-6 receptor (sIL-6R), C-reactive protein (CRP), and fibrinogen, in 166 (88 monozygotic and 78 dizygotic) middle-aged male twin pairs.
resultsThe mean age (+/-S.D.) of the twins was 54 (+/-2.93) years. Heritability was substantial for CRP (0.61, 95% CI: 0.47-0.72) and moderate to fair for IL-6 (0.31, 0.13-0.46), sIL-6R (0.49, 0.30-0.76) and fibrinogen (0.52, 0.34-0.65). IL-6, CRP and fibrinogen showed significant correlations, but not with sIL-6R. Multivariate genetic analysis found that these correlations could be best explained by a common pathway model, where the common factor explained 27%, 73% and 25% of the variance of IL-6, CRP and fibrinogen, respectively. About 46% (95% CI: 21-64%) of the correlations among the three inflammatory markers could be explained by the genetic factors. After adjusting for covariates known to influence inflammation levels, heritability estimates were slightly decreased but the overall results remained similar.
conclusionsA significant part of the variation in inflammatory marker levels is due to genetic influences. Furthermore, almost 50% of the shared variance among these biomarkers is due to a common genetic factor which likely plays a key role in the regulation of inflammation.
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