The DOI matches its Crossref record; 37 of the 37 references it cites were found in a registry or an index.
Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study
Open accessAbstract
Background High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease processes, mendelian randomisation can be used to test the hypothesis that the association of a plasma biomarker with disease is causal.Methods We performed two mendelian randomisation analyses. First, we used as an instrument a single nucleotide polymorphism (SNP) in the endothelial lipase gene (LIPG Asn396Ser) and tested this SNP in 20 studies (20,913 myocardial infarction cases, 95,407 controls). Second, we used as an instrument a genetic score consisting of 14 common SNPs that exclusively associate with HDL cholesterol and tested this score in up to 12,482 cases of myocardial infarction and 41,331 controls. As a positive control, we also tested a genetic score of 13 common SNPs exclusively associated with LDL cholesterol.Findings Carriers of the LIPG 396Ser allele (2·6% frequency) had higher HDL cholesterol (0·14 mmol/L higher, p=8×10(-13)) but similar levels of other lipid and non-lipid risk factors for myocardial infarction compared with non-carriers. This difference in HDL cholesterol is expected to decrease risk of myocardial infarction by 13% (odds ratio [OR] 0·87, 95% CI 0·84-0·91). However, we noted that the 396Ser allele was not associated with risk of myocardial infarction (OR 0·99, 95% CI 0·88-1·11, p=0·85). From observational epidemiology, an increase of 1 SD in HDL cholesterol was associated with reduced risk of myocardial infarction (OR 0·62, 95% CI 0·58-0·66). However, a 1 SD increase in HDL cholesterol due to genetic score was not associated with risk of myocardial infarction (OR 0·93, 95% CI 0·68-1·26, p=0·63). For LDL cholesterol, the estimate from observational epidemiology (a 1 SD increase in LDL cholesterol associated with OR 1·54, 95% CI 1·45-1·63) was concordant with that from genetic score (OR 2·13, 95% CI 1·69-2·69, p=2×10(-10)).Interpretation Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.Funding US National Institutes of Health, The Wellcome Trust, European Union, British Heart Foundation, and the German Federal Ministry of Education and Research.
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In the citing paper
“Mendelian randomization studies further support the notion that HDL-C may not be causally related to CHD risk”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [111]
Experimental — accuracy not yet measuredIn the citing paper
“In contrast, Mendelian randomization studies do not provide compelling evidence that HDL-C is causally associated with the risk of ASCVD [49,61,62].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [61]
In the citing paper
“The causative role of HDL-C for protection against CVD has been questioned in several studies utilizing Mendelian randomization. 87,89,91,92”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [92]
In the citing paper
“As described below, findings from GWAS have increasing translational impact through identification of novel therapeutic targets67, prioritization (and deprioritization) of existing ones68 and development of polygenic scores that quantify individual genetic risk69.”
From A brief history of human disease genetics (2020) · cites this paper as [68]
In the citing paper
“The causative role of HDL-C for protection against CVD has been questioned in several studies utilizing Mendelian randomization.87,89,91,92”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [92]
In the citing paper
“Dietary interventions which raise HDL-C may not necessarily translate into CVD risk reduction, as serum HDL-c has recently been called into question regarding its role in the causal pathway of CVD (110).”
From Food Consumption and its Impact on Cardiovascular Disease: Importance of Solutions Focused on the Globalized Food System (2015) · cites this paper as [110]
In the citing paper
“With increasing availability of large-scale phenotyping (and genotyping), MR is being widely applied to quantitative traits (e.g. markers or adiposity, such as body mass index 13-16 ; blood lipids such as HDL-cholesterol 17-19 ; inflammation-related proteins such as interleukin-6 receptor 20,21 12 ) with the aim of discovering modifiable risk factors for disease that are causal and amenable to the”
From Integrating genomics with biomarkers and therapeutic targets to invigorate cardiovascular drug development (2021) · cites this paper as [20]
In the citing paper
“For example, whilst inflammation in general has long been postulated to influence vascular disease 49,50 , MR has been able to test whether particular elements in the inflammatory response cause 20 or are caused by 51 disease.”
From Integrating genomics with biomarkers and therapeutic targets to invigorate cardiovascular drug development (2021) · cites this paper as [20]
In the citing paper
“The interleukin 6 receptor (IL6R) is a drug target that alters CRP (see Figure 3 ), and for which genetic evidence supports a causal role of IL6R in CHD 20 54”
From Integrating genomics with biomarkers and therapeutic targets to invigorate cardiovascular drug development (2021) · cites this paper as [20]
In the citing paper
“In contrast, recent studies have failed to demonstrate that high HDL-C acquired naturally or pharmacologically, is associated with reduced CVD risk.5-11,18”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [11]
In the citing paper
“Similarly, a Mendelian randomization study failed to identify polymorphisms associated with high HDL-C that correlate with reduced CVD risk.11”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [11]
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Citations
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Teslovich, T. M., Musunuru, K., Smith, A. V., Edmondson, A. C., Stylianou, I. M., Koseki, M., Pirruccello, J. P., Ripatti, S., Chasman, D. I., Willer, C. J., et al. (2010) · Nature · doi:10.1038/nature09270 · Cited by 3,487 · cited 4×
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“…of disease effects of factor 7, which primarily affects high-density lipoprotein (HDL) cholesterol, and factor 11, which affects CRP, is consistent with Mendelian randomization studies that have shown no effect of HDL cholesterol or CRP on heart disease after adjusting for other traits 35–37 .”
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“Prior genetic evidence concerning HDL-C and atherosclerotic cardiovascular disease offers context [38], although stroke excluding SAH encompasses more than ischemic stroke and is not a direct replication of that phenotype.”
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“…- lish HDL-C as a directly protective agent; the inverse asso - ciation is more plausibly interpreted as reflecting HDL-C’s role as a marker of overall atherogenic lipoprotein burden, consistent with contemporary evidence that HDL-C levels themselves do not causally modify atherosclerosis [32, 33].”
Metadata
- Authors
- Voight, B. F., Peloso, G. M., Orho-Melander, M., Frikke-Schmidt, R., Barbalic, M., Jensen, M. K., Hindy, G., Hólm, H., Ding, E. L., Johnson, T., Schunkert, H., Samani, N. J., Clarke, R., Hopewell, J. C., Thompson, J. F., Li, M., Thorleifsson, G., Newton-Cheh, C., Musunuru, K., Pirruccello, J. P., Saleheen, D., Chen, L., Stewart, A. F., Schillert, A., Thorsteinsdottir, U., Thorgeirsson, G., Anand, S., Engert, J. C., Morgan, T., Spertus, J., Stoll, M., Berger, K., Martinelli, N., Girelli, D., McKeown, P. P., Patterson, C. C., Epstein, S. E., Devaney, J., Burnett, M.-S., Mooser, V., Ripatti, S., Surakka, I., Nieminen, M. S., Sinisalo, J., Lokki, M.-L., Perola, M., Havulinna, A., de Faire, U., Gigante, B., Ingelsson, E., Zeller, T., Wild, P., de Bakker, P. I. W., Klungel, O. H., Maitland-van der Zee, A.-H., Peters, B. J. M., de Boer, A., Grobbee, D. E., Kamphuisen, P. W., Deneer, V. H. M., Elbers, C. C., Onland-Moret, N. C., Hofker, M. H., Wijmenga, C., Verschuren, W. M., Boer, J. M., van der Schouw, Y. T., Rasheed, A., Frossard, P., Demissie, S., Willer, C., Do, R., Ordovas, J. M., Abecasis, G. R., Boehnke, M., Mohlke, K. L., Daly, M. J., Guiducci, C., Burtt, N. P., Surti, A., Gonzalez, E., Purcell, S., Gabriel, S., Marrugat, J., Peden, J., Erdmann, J., Diemert, P., Willenborg, C., König, I. R., Fischer, M., Hengstenberg, C., Ziegler, A., Buysschaert, I., Lambrechts, D., Van de Werf, F., Fox, K. A., El Mokhtari, N. E., Rubin, D., Schrezenmeir, J., Schreiber, S., Schäfer, A., Danesh, J., Blankenberg, S., Roberts, R., McPherson, R., Watkins, H., Hall, A. S., Overvad, K., Rimm, E., Boerwinkle, E., Tybjaerg-Hansen, A., Cupples, L. A., Reilly, M. P., Melander, O., Mannucci, P. M., Ardissino, D., Siscovick, D., Elosua, R., Stefansson, K., O'Donnell, C. J., Salomaa, V., Rader, D. J., Peltonen, L., Schwartz, S. M., Altshuler, D., & Kathiresan, S.
- Affiliations
- University of Pennsylvania (US)
- Boston University (US)
- Harvard University (US)
- Lund University (SE)
- deCODE Genetics (Iceland) (IS)
- Brigham and Women's Hospital (US)
- Queen Mary University of London (GB)
- University of Lübeck (DE)
- University of Leicester (GB)
- University of Oxford (GB)
- Broad Institute (US)
- University of Cambridge (GB)
- Ottawa Heart Institute (CA)
- Population Health Research Institute (CA)
- McGill University (CA)
- Vanderbilt University (US)
- University of Missouri–Kansas City (US)
- University of Münster (DE)
- University of Verona (IT)
- Queen's University Belfast (GB)
- MedStar Washington Hospital Center (US)
- GlaxoSmithKline (United States) (US)
- University of Helsinki (FI)
- Helsinki University Hospital (FI)
- Finnish Institute for Health and Welfare (FI)
- Karolinska Institutet (SE)
- Johannes Gutenberg University Mainz (DE)
- Utrecht University (NL)
- University Medical Center Utrecht (NL)
- University Medical Center Groningen (NL)
- St. Antonius Ziekenhuis (NL)
- National Institute for Public Health and the Environment (NL)
- Center for Non-Communicable Diseases (PK)
- University of Michigan (US)
- Massachusetts General Hospital (US)
- University of North Carolina at Chapel Hill (US)
- Hospital del Mar Research Institute (ES)
- University Hospital Regensburg (DE)
- Universitair Ziekenhuis Leuven (BE)
- University of Edinburgh (GB)
- University Hospital Schleswig-Holstein (DE)
- Max Rubner Institut (DE)
- Christian-Albrechts-Universität zu Kiel (DE)
- University of Leeds (GB)
- Aarhus University (DK)
- The University of Texas Health Science Center at Houston (US)
- Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico (IT)
- Ospedale di Parma (IT)
- University of Washington (US)
- Corresponding author
- Kathiresan, Sekar
- ORCID
- Voight, Benjamin F
- Peloso, Gina M
- Jensen, Majken K
- Hindy, George
- Hólm, Hilma
- Ding, Eric L
- Johnson, Toby
- Schunkert, Heribert
- Samani, Nilesh J
- Clarke, Robert
- Hopewell, Jemma C
- Thompson, John F
- Li, Mingyao
- Musunuru, Kiran
- Pirruccello, James P
- Saleheen, Danish
- Chen, Li
- Stewart, Alexandre FR
- Schillert, Arne
- Anand, Sonia
- Engert, James C
- Morgan, Thomas
- Spertus, John
- Stoll, Monika
- Martinelli, Nicola
- Girelli, Domenico
- McKeown, Pascal P
- Patterson, Christopher C
- Mooser, Vincent
- Ripatti, Samuli
- Surakka, Ida
- Nieminen, Markku S
- Sinisalo, Juha
- Lokki, Marja-Liisa
- Perola, Markus
- Havulinna, Aki
- Gigante, Bruna
- Ingelsson, Erik
- Zeller, Tanja
- Wild, Philipp
- Klungel, Olaf H
- Peters, Bas J M
- Grobbee, Diederick E
- Kamphuisen, Pieter W
- Deneer, Vera H M
- Elbers, Clara C
- Wijmenga, Cisca
- Verschuren, WM Monique
- Boer, Jolanda MA
- Demissie, Serkalem
- Willer, Cristen
- Do, Ron
- Abecasis, Gonçalo R
- Boehnke, Michael
- Mohlke, Karen L
- Daly, Mark J
- Burtt, Noël P
- Purcell, Shaun
- Gabriel, Stacey
- Marrugat, Jaume
- Erdmann, Jeanette
- König, Inke R
- Fischer, Marcus
- Hengstenberg, Christian
- Ziegler, Andreas
- Buysschaert, Ian
- Lambrechts, Diether
- Fox, Keith A
- Schreiber, Stefan
- Danesh, John
- Blankenberg, Stefan
- McPherson, Ruth
- Watkins, Hugh
- Hall, Alistair S
- Overvad, Kim
- Rimm, Eric
- Boerwinkle, Eric
- Cupples, L Adrienne
- Reilly, Muredach P
- Melander, Olle
- Mannucci, Pier M
- Ardissino, Diego
- Siscovick, David
- Salomaa, Veikko
- Rader, Daniel J
- Peltonen, Leena
- Altshuler, David
- Kathiresan, Sekar
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2012-08
- Volume
- 380
- Issue
- 9841
- Pages
- 572-580
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC3419820
- OpenAlex
- W1240353884
- Cited by
- 148
- References
- 36
- Citations by year
- 2026: 11 · 2025: 4 · 2024: 5 · 2023: 8 · 2022: 9 · 2021: 19 · 2020: 16 · 2019: 9 · 2018: 10 · 2017: 8 · 2016: 12 · 2015: 8 · 2014: 9 · 2013: 6 · 2012: 13
- FWCI
- 1.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- The Lancet (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- University of Regensburg Publication Server (University of Regensburg) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Leicester Research Archive (University of Leicester) (submittedVersion, other-oa)
- Lund University Publications (Lund University) (submittedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- Rivm Repository (Netherlands National Institute for Public Health and the Environment) (submittedVersion)
- Hirsla (Landspítali University Hospital) (submittedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- OpenAgrar (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- WOS
- Funders
- Wellcome Trust (090532)
- British Heart Foundation (RG/08/014/24067)
- National Institutes of Health (n01hc25195-41-0-1)
- National Heart, Lung, and Blood Institute (N01-HC-025195)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- HDL cholesterol, myocardial infarction, causal inference, endothelial lipase, genetic score, LDL cholesterol, cardiovascular risk, genetic instruments, single nucleotide polymorphisms, lipid biomarkers, confounding by indication, reverse causality
- MeSH terms
- Gene Frequency, Humans, Lipase, Cholesterol, HDL, Cholesterol, LDL, Myocardial Infarction, Prospective Studies, Risk Factors, Biomarkers, Case-Control Studies, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Mendelian Randomization Analysis
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