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

doi:10.1016/j.atherosclerosis.2007.12.009

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 journal › Article › peer-review

38 Scopus citations

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 language	English (US)
Pages (from-to)	213-220
Number of pages	8
Journal	Atherosclerosis
Volume	200
Issue number	1
DOIs	https://doi.org/10.1016/j.atherosclerosis.2007.12.009
State	Published - Sep 2008
Externally published	Yes

Keywords

Common genes
Heritability
Inflammatory markers
Middle-aged males
Twin study

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

Access to Document

10.1016/j.atherosclerosis.2007.12.009

Cite this

@article{93aef8ef49714595b7ba25d4b8db7461,

title = "Genetic and environmental influences on systemic markers of inflammation in middle-aged male twins",

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.",

keywords = "Common genes, Heritability, Inflammatory markers, Middle-aged males, Twin study",

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

note = "Funding Information: The United States Department of Veterans Affairs provides financial support for the development and maintenance of the Vietnam Era Twin (VET) Registry. Numerous organizations have provided invaluable assistance in the conduct of this study, including: the Department of Defense; the National Personnel Records Center, National Archives and Records Administration; the Internal Revenue Service; the National Institutes of Health; the National Opinion Research Center; the National Research Council, National Academy of Sciences; the Institute for Survey Research, Temple University. Most importantly, the authors gratefully acknowledge the continued cooperation and participation of the members of the VET Registry and their families. Without their contribution this research would not have been possible. This study was supported by K24HL077506, R01 HL68630 and R01 AG026255 from the National Institutes of Health; by the Emory University General Clinical Research Center MO1-RR00039 and by Grant no. 0245115N from the American Heart Association.",

year = "2008",

month = sep,

doi = "10.1016/j.atherosclerosis.2007.12.009",

language = "English (US)",

volume = "200",

pages = "213--220",

journal = "Atherosclerosis",

issn = "0021-9150",

publisher = "Elsevier Ireland Ltd",

number = "1",

}

TY - JOUR

T1 - Genetic and environmental influences on systemic markers of inflammation in middle-aged male twins

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

N1 - Funding Information: The United States Department of Veterans Affairs provides financial support for the development and maintenance of the Vietnam Era Twin (VET) Registry. Numerous organizations have provided invaluable assistance in the conduct of this study, including: the Department of Defense; the National Personnel Records Center, National Archives and Records Administration; the Internal Revenue Service; the National Institutes of Health; the National Opinion Research Center; the National Research Council, National Academy of Sciences; the Institute for Survey Research, Temple University. Most importantly, the authors gratefully acknowledge the continued cooperation and participation of the members of the VET Registry and their families. Without their contribution this research would not have been possible. This study was supported by K24HL077506, R01 HL68630 and R01 AG026255 from the National Institutes of Health; by the Emory University General Clinical Research Center MO1-RR00039 and by Grant no. 0245115N from the American Heart Association.

PY - 2008/9

Y1 - 2008/9

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

UR - http://www.scopus.com/inward/record.url?scp=49749128111&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=49749128111&partnerID=8YFLogxK

U2 - 10.1016/j.atherosclerosis.2007.12.009

DO - 10.1016/j.atherosclerosis.2007.12.009

M3 - Article

C2 - 18243214

AN - SCOPUS:49749128111

SN - 0021-9150

VL - 200

SP - 213

EP - 220

JO - Atherosclerosis

JF - Atherosclerosis

IS - 1

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this