Genetic and environmental influences on systemic markers of inflammation in middle-aged male twins

Shaoyong Su, Harold Snieder, Andrew H. Miller, James Ritchie, J. Douglas Bremner, Jack Goldberg, Jun Dai, Linda Jones, Nancy V. Murrah, Jinying Zhao, Viola Vaccarino

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Objectives: The 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. Methods: We 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. Results: The 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. Conclusions: A 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.

Original languageEnglish (US)
Pages (from-to)213-220
Number of pages8
JournalAtherosclerosis
Volume200
Issue number1
DOIs
StatePublished - Sep 1 2008
Externally publishedYes

Fingerprint

Interleukin-6 Receptors
C-Reactive Protein
Fibrinogen
Interleukin-6
Inflammation
Multivariate Analysis
Biomarkers

Keywords

  • Common genes
  • Heritability
  • Inflammatory markers
  • Middle-aged males
  • Twin study

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Su, S., Snieder, H., Miller, A. H., Ritchie, J., Bremner, J. D., Goldberg, J., ... Vaccarino, V. (2008). Genetic and environmental influences on systemic markers of inflammation in middle-aged male twins. Atherosclerosis, 200(1), 213-220. https://doi.org/10.1016/j.atherosclerosis.2007.12.009

Genetic and environmental influences on systemic markers of inflammation in middle-aged male twins. / Su, Shaoyong; Snieder, Harold; Miller, Andrew H.; Ritchie, James; Bremner, J. Douglas; Goldberg, Jack; Dai, Jun; Jones, Linda; Murrah, Nancy V.; Zhao, Jinying; Vaccarino, Viola.

In: Atherosclerosis, Vol. 200, No. 1, 01.09.2008, p. 213-220.

Research output: Contribution to journalArticle

Su, S, Snieder, H, Miller, AH, Ritchie, J, Bremner, JD, Goldberg, J, Dai, J, Jones, L, Murrah, NV, Zhao, J & Vaccarino, V 2008, 'Genetic and environmental influences on systemic markers of inflammation in middle-aged male twins', Atherosclerosis, vol. 200, no. 1, pp. 213-220. https://doi.org/10.1016/j.atherosclerosis.2007.12.009
Su, Shaoyong ; Snieder, Harold ; Miller, Andrew H. ; Ritchie, James ; Bremner, J. Douglas ; Goldberg, Jack ; Dai, Jun ; Jones, Linda ; Murrah, Nancy V. ; Zhao, Jinying ; Vaccarino, Viola. / Genetic and environmental influences on systemic markers of inflammation in middle-aged male twins. In: Atherosclerosis. 2008 ; Vol. 200, No. 1. pp. 213-220.
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abstract = "Objectives: The 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. Methods: We 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. Results: The 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. Conclusions: A 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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AU - Su, Shaoyong

AU - Snieder, Harold

AU - Miller, Andrew H.

AU - Ritchie, James

AU - Bremner, J. Douglas

AU - Goldberg, Jack

AU - Dai, Jun

AU - Jones, Linda

AU - Murrah, Nancy V.

AU - Zhao, Jinying

AU - Vaccarino, Viola

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N2 - Objectives: The 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. Methods: We 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. Results: The 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. Conclusions: A 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.

AB - Objectives: The 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. Methods: We 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. Results: The 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. Conclusions: A 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.

KW - Common genes

KW - Heritability

KW - Inflammatory markers

KW - Middle-aged males

KW - Twin study

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