Evidence map›Paper›PMID 25082230›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2014

Genetic and environmental influences on the prospective correlation between systemic inflammation and coronary heart disease death in male twins.

Sheng-Hui Wu, Michael C Neale, Anthony J Acton, Robert V Considine, Ruth E Krasnow, Terry Reed, Jun Dai

Open access · bronzeAbstract readComparative StudyTwin Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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 · 2016
    Article
  7. Observational
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Sheng-Hui WuFrom the Division of Epidemiology, Department of Medicine, Institute of Medicine and Public Health, Vanderbilt University Medical Center, Nashville, TN (S.-H.W., J.D.); Department of Psychiatry (M.C.N.) and Department of Human and Molecular Genetics (M.C.N.), Virginia Commonwealth University, Richmond; Division of Endocrinology (A.J.A., R.V.C.) and Department of Medical and Molecular Genetics (T.R.), Indiana University School of Medicine, Indianapolis; and Center for Health Sciences, Biosciences Division, SRI International, Menlo Park, CA (R.E.K.).
Michael C NealeFrom the Division of Epidemiology, Department of Medicine, Institute of Medicine and Public Health, Vanderbilt University Medical Center, Nashville, TN (S.-H.W., J.D.); Department of Psychiatry (M.C.N.) and Department of Human and Molecular Genetics (M.C.N.), Virginia Commonwealth University, Richmond; Division of Endocrinology (A.J.A., R.V.C.) and Department of Medical and Molecular Genetics (T.R.), Indiana University School of Medicine, Indianapolis; and Center for Health Sciences, Biosciences Division, SRI International, Menlo Park, CA (R.E.K.).
Anthony J ActonFrom the Division of Epidemiology, Department of Medicine, Institute of Medicine and Public Health, Vanderbilt University Medical Center, Nashville, TN (S.-H.W., J.D.); Department of Psychiatry (M.C.N.) and Department of Human and Molecular Genetics (M.C.N.), Virginia Commonwealth University, Richmond; Division of Endocrinology (A.J.A., R.V.C.) and Department of Medical and Molecular Genetics (T.R.), Indiana University School of Medicine, Indianapolis; and Center for Health Sciences, Biosciences Division, SRI International, Menlo Park, CA (R.E.K.).
Robert V ConsidineFrom the Division of Epidemiology, Department of Medicine, Institute of Medicine and Public Health, Vanderbilt University Medical Center, Nashville, TN (S.-H.W., J.D.); Department of Psychiatry (M.C.N.) and Department of Human and Molecular Genetics (M.C.N.), Virginia Commonwealth University, Richmond; Division of Endocrinology (A.J.A., R.V.C.) and Department of Medical and Molecular Genetics (T.R.), Indiana University School of Medicine, Indianapolis; and Center for Health Sciences, Biosciences Division, SRI International, Menlo Park, CA (R.E.K.).
Ruth E KrasnowFrom the Division of Epidemiology, Department of Medicine, Institute of Medicine and Public Health, Vanderbilt University Medical Center, Nashville, TN (S.-H.W., J.D.); Department of Psychiatry (M.C.N.) and Department of Human and Molecular Genetics (M.C.N.), Virginia Commonwealth University, Richmond; Division of Endocrinology (A.J.A., R.V.C.) and Department of Medical and Molecular Genetics (T.R.), Indiana University School of Medicine, Indianapolis; and Center for Health Sciences, Biosciences Division, SRI International, Menlo Park, CA (R.E.K.).
Terry ReedFrom the Division of Epidemiology, Department of Medicine, Institute of Medicine and Public Health, Vanderbilt University Medical Center, Nashville, TN (S.-H.W., J.D.); Department of Psychiatry (M.C.N.) and Department of Human and Molecular Genetics (M.C.N.), Virginia Commonwealth University, Richmond; Division of Endocrinology (A.J.A., R.V.C.) and Department of Medical and Molecular Genetics (T.R.), Indiana University School of Medicine, Indianapolis; and Center for Health Sciences, Biosciences Division, SRI International, Menlo Park, CA (R.E.K.).
Jun DaiFrom the Division of Epidemiology, Department of Medicine, Institute of Medicine and Public Health, Vanderbilt University Medical Center, Nashville, TN (S.-H.W., J.D.); Department of Psychiatry (M.C.N.) and Department of Human and Molecular Genetics (M.C.N.), Virginia Commonwealth University, Richmond; Division of Endocrinology (A.J.A., R.V.C.) and Department of Medical and Molecular Genetics (T.R.), Indiana University School of Medicine, Indianapolis; and Center for Health Sciences, Biosciences Division, SRI International, Menlo Park, CA (R.E.K.). jun.dai@vanderbilt.edu.
Indiana University – Purdue University Indianapolis · USVirginia Commonwealth University · US

Funding

Quality Assurance and Quality Control Project Management: Improving Submissions and Study Conduct in the Human Subjects Research Prior Approval ProcessUL1TR002529 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI MOE, SHARON M, WIEHE, SARAH ELIZABETH · 2018 to 2022
$27.2M
Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
CVD RISK FACTORS AND BRAIN MORPHOLOGY IN NHLBI TWINSR01HL051429 · NHLBI · SRI INTERNATIONAL · PI SWAN, GARY E · 1995 to 2001
$1.8M
NCATS NIH HHS UL1 TR001108NHLBI NIH HHS HL51429NHLBI NIH HHS R01 HL051429
6 · The paper itself

Abstract

objectiveBecause of lack of evidence, we aimed to examine to what degree low-grade systemic inflammation and coronary heart disease (CHD) death shared common genetic and environmental substrates. APPROACH AND

resultsFrom the 41-year prospective National Heart, Lung, and Blood Institute Twin Study, we included 950 middle-aged male twins at baseline (1969-1973). Low-grade systemic inflammation was measured with plasma levels of interleukin-6 (IL-6) and C-reactive protein. Univariate and bivariate structural equation models were used, adjusted for a risk score for CHD death. The score-adjusted heritability was 19% for IL-6, 27% for C-reactive protein, and 22% for CHD death. The positive phenotypic correlation of IL-6 with CHD death (radjusted=0.27; 95% confidence interval [CI], 0.08-0.43) was driven by additive genetic factors (contribution [relative contribution], 0.30 [111%]) but attenuated by unique environment (-0.03 [-11%]). The genetic correlation between IL-6 and CHD death was 0.74 (95% CI, 0.21-1.00), whereas the unique environmental correlation was -0.05 (95% CI, -0.35 to 0.25). The proportion of genetic variance for CHD death shared with that for IL-6 was 74%. The phenotypic correlation of C-reactive protein with CHD death (radjusted=0.10; 95% CI, -0.02 to 0.22) was explained by additive genetic factors (0.20 [149%]) but was attenuated by the unique environment (-0.09 [-49%]). The genetic correlation of C-reactive protein with CHD death was 0.63 (95% CI, -0.07 to 1.00), whereas the unique environmental correlation was -0.07 (95% CI, -0.29 to 0.17).

conclusionsLow-grade systemic inflammation, measured by IL-6, and long-term CHD death share moderate genetic substrates that augment both traits.

Indexed as

Gene-Environment InteractionBiomarkersBody Mass IndexCoronary DiseaseC-Reactive ProteinDiseases in TwinsGenetic Predisposition to DiseaseHumansInflammationInterleukin-6LipidsMaleMiddle AgedPhenotypeProspective StudiesTwins, DizygoticBiomarkersC-Reactive ProteinIL6 protein, humanInterleukin-6Lipidscoronary diseaseC-reactive proteingenesinterleukin-6mortalitytwins

Identifiers

PMID25082230
PMCPMC4163972
OpenAlexW2108051410

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.