ArticlePloS one2008
Does high C-reactive protein concentration increase atherosclerosis? The Whitehall II Study.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 3 of them syntheses that pooled 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.
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.
Who cites it
23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 45 citations in OpenAlex.
- Global assessment of C-reactive protein and health-related outcomes: an umbrella review of evidence from observational studies and Mendelian randomization studies.European journal of epidemiology · 2021Pooled it
- The interleukin-6 receptor as a target for prevention of coronary heart disease: a mendelian randomisation analysis.Lancet (London, England) · 2012Pooled it
- Evaluating the causal relevance of diverse risk markers: horizontal systematic review.BMJ (Clinical research ed.) · 2009Pooled it
- Left atrial appendage velocity, association with inflammatory indices in non-valvular atrial fibrillation patients.Future cardiology · 2025Article
- Article
- Investigating causal relationships between obesity and skin barrier function in a multi-ethnic Asian general population cohort.International journal of obesity (2005) · 2023Article
- Article
- C-Reactive Protein Levels and Risk of Cardiovascular Diseases: A Two-Sample Bidirectional Mendelian Randomization Study.International journal of molecular sciences · 2023Article
- Causal graphs for the analysis of genetic cohort data.Physiological genomics · 2020Review
- Mendelian Randomization Analysis in Observational Epidemiology.Journal of lipid and atherosclerosis · 2019Review
- Age modification of the relationship between C-reactive protein and fatigue: findings from Understanding Society (UKHLS).Psychological medicine · 2018Article
- C-reactive protein and diabetic retinopathy in Chinese patients with type 2 diabetes mellitus.International journal of ophthalmology · 2016Article
- Association of two variants in the interleukin-6 receptor gene and premature coronary heart disease in a Chinese Han population.Molecular biology reports · 2013Article
- C-reactive protein as a predictor of hypertension in the Hong Kong Cardiovascular Risk Factor Prevalence Study (CRISPS) cohort.Journal of human hypertension · 2012Article
- Genetic variants, immune function, and risk of pre-eclampsia among American Indians.American journal of reproductive immunology (New York, N.Y. : 1989) · 2012Article
- Anti-depressant medication use and C-reactive protein: results from two population-based studies.Brain, behavior, and immunity · 2011Article
- Abdominal obesity and other risk factors largely explain the high CRP in indigenous Australians relative to the general population, but not gender differences: a cross-sectional study.BMC public health · 2010Article
- Bayesian methods for meta-analysis of causal relationships estimated using genetic instrumental variables.Statistics in medicine · 2010Article
- Usefulness of Mendelian randomization in observational epidemiology.International journal of environmental research and public health · 2010Review
- Mendelian randomization in nutritional epidemiology.Nutrition reviews · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundC-reactive protein (CRP), a marker of systemic inflammation, is associated with risk of coronary events and sub-clinical measures of atherosclerosis. Evidence in support of this link being causal would include an association robust to adjustments for confounders (multivariable standard regression analysis) and the association of CRP gene polymorphisms with atherosclerosis (Mendelian randomization analysis). METHODOLOGY/PRINCIPAL
findingsWe genotyped 3 tag single nucleotide polymorphisms (SNPs) [+1444T>C (rs1130864); +2303G>A (rs1205) and +4899T>G (rs 3093077)] in the CRP gene and assessed CRP and carotid intima-media thickness (CIMT), a structural marker of atherosclerosis, in 4941 men and women aged 50-74 (mean 61) years (the Whitehall II Study). The 4 major haplotypes from the SNPs were consistently associated with CRP level, but not with other risk factors that might confound the association between CRP and CIMT. CRP, assessed both at mean age 49 and at mean age 61, was associated both with CIMT in age and sex adjusted standard regression analyses and with potential confounding factors. However, the association of CRP with CIMT attenuated to the null with adjustment for confounding factors in both prospective and cross-sectional analyses. When examined using genetic variants as the instrument for serum CRP, there was no inferred association between CRP and CIMT. CONCLUSIONS/SIGNIFICANCE: Both multivariable standard regression analysis and Mendelian randomization analysis suggest that the association of CRP with carotid atheroma indexed by CIMT may not be causal.
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Registered trials
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.