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Cited by 30Lipoproteins and Cardiovascular HealthGenetic Associations and EpidemiologyCholesterol and Lipid Metabolism

Cholesterol not particle concentration mediates the atherogenic risk conferred by apolipoprotein B particles: a Mendelian randomization analysis

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Helgadottir, Anna, Thorleifsson, Gudmar, Snaebjarnarson, Audunn, Stefansdottir, Lilja, Sveinbjornsson, Gardar, Tragante, Vinicius, Björnsson, Eyþór, Steinthorsdottir, Valgerdur +57 more·2022·European Journal of Preventive Cardiology
DOI 10.1093/eurjpc/zwac219
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Abstract

Background and aims: The causal contribution of apolipoprotein B (apoB) particles to coronary artery disease (CAD) is established. We examined whether this atherogenic contribution is better reflected by non-high-density lipoprotein cholesterol (non-HDL-C) or apoB particle concentration. Method and results: We performed Mendelian randomization (MR) analysis using 235 variants as genetic instruments; testing the relationship between their effects on the exposures, non-HDL-C and apoB, and on the outcome CAD using weighted regression. Variant effect estimates on the exposures came from the UK Biobank (N = 376 336) and on the outcome from a meta-analysis of five CAD datasets (187 451 cases and 793 315 controls). Subsequently, we carried out sensitivity and replication analyses. In univariate MR analysis, both exposures associated with CAD (βnon-HDL-C = 0.40, P = 2.8 × 10−48 and βapoB = 0.38, P = 1.3 × 10−44). Adding effects on non-HDL-C into a model that already included those on apoB significantly improved the genetically predicted CAD effects (P = 3.9 × 10−5), while adding apoB into the model including non-HDL-C did not (P = 0.69). Thirty-five per cent (82/235) of the variants used as genetic instruments had discordant effects on the exposures, associating with non-HDL-C/apoB ratio at P < 2.1 × 10−4 (0.05/235). Fifty-one variants associated at genome-wide significance. Conclusion: Many sequence variants have discordant effects on non-HDL-C and apoB. These variants allowed us to show that the causal mechanism underlying the relationship between apolipoprotein B particles and CAD is more associated with non-HDL-C than apoB particle concentration.

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  • The results of all prospective observational discordance analyses, with a single exception, are consistent that the number of apoB particles is a more accurate index of cardiovascular risk than the mass of cholesterol within them.

    “Importantly, with a single exception,2 the results of all the prospective observational discordance analyses, irrespective of the method employed, are consistent: namely, that the number of apoB particles is a more accurate index of cardiovascular risk than the mass of cholesterol within them.”

    From Discordance among apoB, non-high-density lipoprotein cholesterol, and triglycerides: implications for cardiovascular prevention (2024) · cites this paper as [2]

    The citation is attached to the phrase “a single exception.” The source’s Discussion and Conclusion provide an exception to the asserted apoB advantage: its Mendelian-randomization analyses find that non-HDL cholesterol better captures the atherogenic contribution of apoB-containing particles. But the paper explicitly says it does not assess the relative strength of their associations in an epidemiological setting, so it cannot be identified as an exception among prospective observational discordance analyses. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • All reports since 2019, with one exception, including observational studies and randomized clinical trials, have confirmed that apoB is a more accurate marker of cardiovascular risk than LDL-C or non-HDL-C.

    “Moreover, all reports since then, with one exception,2 including observational studies and randomized clinical trials,3–13 have confirmed that apoB is a more accurate marker of cardiovascular risk than LDL-C or non-HDL-C, reinforcing the validity of the evaluation by the 2019 EAS/ESC Guidelines as to the superiority of apoB.”

    From Discordance among apoB, non-high-density lipoprotein cholesterol, and triglycerides: implications for cardiovascular prevention (2024) · cites this paper as [2]

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Authors
Helgadottir, A., Thorleifsson, G., Snaebjarnarson, A., Stefansdottir, L., Sveinbjornsson, G., Tragante, V., Björnsson, E., Steinthorsdottir, V., Gretarsdottir, S., Helgason, H., Saemundsdottir, J., Olafsson, I., Thune, J. J., Raja, A. A., Ghouse, J., Olesen, M. S., Christensen, A., Jacobsen, R. L., Dowsett, J., Bruun, M. T., Nielsen, K., Knowlton, K., Nadauld, L., Benediktsson, R., Erikstrup, C., Pedersen, O. B., Banasik, K., Brunak, S., DBDS Genomic Consortium, Andersen, S., Banasik, K., Brunak, S., Burgdorf, K., Didriksen, M., Dinh, K. M., Erikstrup, C., Gudbjartsson, D., Hansen, T. F., Hjalgrim, H., Jemec, G., Jennum, P., Johansson, P. I., Larsen, M. A. H., Mikkelsen, S., Nielsen, K. R., Nyegaard, M., Ostrowski, S. R., Pedersen, O. B., Stefansson, K., Stefánsson, H., Sækmose, S., Sørensen, E., Þorsteinsdóttir, U., Brun, M. T., Ullum, H., Werge, T., Bundgaard, H., Ostrowski, S. R., Sulem, P., Arnar, D. O., Thorgeirsson, G., Thorsteinsdottir, U., Gudbjartsson, D. F., Stefansson, K., & Holm, H.
Affiliations
  • deCODE Genetics/Amgen, Inc. , Sturlugata 8, Reykjavik 101 , Iceland
  • deCODE Genetics (Iceland) (IS)
  • Department of Clinical Biochemistry, Landspitali – The National University Hospital of Iceland , Reykjavik 101 , Iceland
  • University of Copenhagen (DK)
  • Copenhagen University Hospital (DK)
  • Odense University Hospital (DK)
  • Aalborg University Hospital (DK)
  • Intermountain Healthcare (US)
  • National University Hospital of Iceland (IS)
  • Department of Clinical Immunology, Zealand University Hospital-Køge , Køge , Denmark
  • Copenhagen Business School (DK)
  • Glostrup Hospital (DK)
  • Statens Serum Institut (DK)
  • Aarhus University Hospital (DK)
  • Department of Clinical Immunology, Copenhagen University Hospital, Rigshospitalet , Copenhagen , Denmark
  • Department of Clinical Medicine, University of Copenhagen , Copenhagen , Denmark
ORCID
Venue
European Journal of Preventive Cardiology
Publisher
Oxford University Press (OUP)
Published
2022-09-20
Volume
29
Issue
18
Pages
2374-2385
ISSN
  • 2047-4873 (ISSN-L)
  • 2047-4881
DOI
10.1093/eurjpc/zwac219
OpenAlex
W4296777909
Cited by
30
References
25
Citations by year
2026: 2 · 2025: 3 · 2024: 12 · 2023: 10 · 2022: 3
FWCI
6.69
Type
journal article
Language
en
Open access
Licence
Locations
  • European Journal of Preventive Cardiology (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, cc-by-nc)
  • Opin vísindi (Opin vísindi) (submittedVersion, cc-by-nc-sa)
  • VBN Forskningsportal (Aalborg Universitet) (submittedVersion, cc-by-nc)
  • University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion, cc-by-nc)
  • Opin vísindi (Opin vísindi) (submittedVersion, other-oa)
  • CBS Research Portal (Copenhagen Business School) (submittedVersion, cc-by-nc)
Funders
  • NordForsk (90580)
  • Innovation Fund Denmark
  • IFD (8114-00033B)
Topics
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
Keywords
apolipoprotein B, non-HDL cholesterol, coronary artery disease, atherogenic risk, genetic variants, causal inference, dyslipidemia
MeSH terms
Apolipoproteins B, Cholesterol, Coronary Artery Disease, Humans, Lipoproteins, Cholesterol, HDL, Cholesterol, LDL, Risk Factors, Atherosclerosis, Apolipoprotein B-100, Mendelian Randomization Analysis

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