Ultimately this is why I am skeptical of the LDL residence time stuff. Whether or not the gene variants affecting LDL concentration are increasing secretion or reducing clearance, it's the total concentration that the risk is tracking. https://t.co/PPxuvOhoDU https://t.co/RmkmqmYydM https://t.co/gUuP2JYfv7
Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease.
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Jan 2019 – Jul 2025Where it's discussed
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X / Twitter29 posts
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What people are saying
The discussions frequently emphasize the role of ApoB in cardiovascular risk, with users referencing specific studies and genetic evidence, such as the association of gene variants with heart disease. The tone ranges from supportive to skeptical, citing detailed research and expressing interest in how these findings might influence clinical practices, with expressions like 'strong evidence' and 'interesting support' suggesting an overall recognition of the research's importance.
Most discussions support the idea that triglyceride and LDL cholesterol reductions, especially via genetic traits related to ApoB, have similar effects on reducing heart disease risk, indicating a moderate to high level of consensus.
The posts demonstrate strong curiosity, with multiple discussions referencing detailed studies, gene variants, and mechanisms, showing high relevance and engagement with the topic.
Many users delve into technical aspects such as the roles of ApoB, genetic analyses, and the influence of diet or insulin on lipids, reflecting deep engagement beyond surface-level discussion.
While the debates highlight robust evidence regarding the importance of ApoB and lipid management, some skepticism about the clinical application or interpretation indicates moderate perceived impact, though there’s acknowledgment of the significance of g
Abstract in brief
- The study investigates whether lowering triglycerides or LDL cholesterol has a similar impact on reducing the risk of coronary heart disease by examining genetic variants in the LPL (triglyceride-lowering) and LDLR (LDL-lowering) genes.
- Results showed that genetic variants in LPL and LDLR affected levels of triglycerides, LDL cholesterol, and ApoB-containing lipoproteins differently, but both were linked to a similarly reduced risk of coronary heart disease.
- This suggests that reducing triglycerides through genetic means may lower heart disease risk as effectively as lowering LDL cholesterol, despite their differing effects on specific lipid levels.
Top posts
Most liked on X and Bluesky3/8 Extremely thorough Mendelian randomization analyses find a dose-dependent relationship between ApoB and CHD across approximately two dozen genetic variants across many independent pathways. Neither ApoA-1 nor pleiotropy can reasonably explain this. https://t.co/PPxuvO0lBU https://t.co/wJ3NJBKv5P
This was across 14 different data-sets. https://t.co/PPxuvOhoDU
@SABOURETCardio @DrMarthaGulati @robmentz @vbluml @AndrewJSauer @iamritu @khurramn1 @ErinMichos @dranulala @SantosGallegoMD @ShelleyZieroth @dramitkhera @AnnMarieNavar Actually I'm looking forward to knowing how they will expalin the failure. I wasn't surprised by the frustrating results since I read that MR study published 3 years ago by @ProfKausikRay and Brian Ference in @JAMA_current (doi:10.1001/jama.2018.20045)
Here is my take on this interesting study supporting the importance of Apo B in CVD risk. Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease https://t.co/A69vcesqaO via @practiceupdate
@JohnKastelein @Lpa_Doc “[need TG⬇️ >200mg/dL to show benefit comparable to 1mmol⬇️LDL-C]” He did say that here (1) in a 2016 interview & elsewhere. I thought his later work emphasized ⬇️ apoB containing lipoproteins. Ex:(2) (1) https://t.co/XT1EBafmc4 (2) https://t.co/88hQJ5hZJ3
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@jpegan10 @lipo_fan @JoshJwageman @drhungo He generally cites these studies to support that position: “Therefore, the clinical benefit of lowering triglyceride and LDL-C levels may be proportional to the absolute change in ApoB.” https://t.co/oSLHBxL28g “The association of genetically predicted TG with CAD persisted
@CarnivoreMeme @jpegan10 @TapaDaBoy @ethanjweiss @realDaveFeldman Take your pick. But in the case of people like Dave and Nick, the genetics are probably related to insulin. Insulin is an independent mediator of LDL receptor activity. Low carb diets just make their lipids high, most likely. https://t.co/PPxuvO0lBU
@cultistslayer @AldonSnow48246 @Drlipid @nationallipid @society_eas @TheFHFoundation @fhpatienteurope @drpablocorral If publishing yesterday isn't enough, let me know. 10.1056/NEJMoa2304146 And data on ApoB on Athero: 10.1001/jama.2018.20045 Does lowering Apo B works? Sure it does 10.1001/jamacardio.2021.5083
RT @pabeda1: @SABOURETCardio @DrMarthaGulati @robmentz @vbluml @AndrewJSauer @iamritu @khurramn1 @ErinMichos @dranulala @SantosGallegoMD @S…
@SABOURETCardio @DrMarthaGulati @robmentz @vbluml @AndrewJSauer @iamritu @khurramn1 @ErinMichos @dranulala @SantosGallegoMD @ShelleyZieroth @dramitkhera @AnnMarieNavar Actually I'm looking forward to knowing how they will expalin the failure. I wasn't surprised by the frustrating results since I read that MR study published 3 years ago by @ProfKausikRay and Brian Ference in @JAMA_current (doi:10.1001/jama.2018.20045)
3/8 Extremely thorough Mendelian randomization analyses find a dose-dependent relationship between ApoB and CHD across approximately two dozen genetic variants across many independent pathways. Neither ApoA-1 nor pleiotropy can reasonably explain this. https://t.co/PPxuvO0lBU https://t.co/wJ3NJBKv5P
@JohnKastelein @Lpa_Doc “[need TG⬇️ >200mg/dL to show benefit comparable to 1mmol⬇️LDL-C]” He did say that here (1) in a 2016 interview & elsewhere. I thought his later work emphasized ⬇️ apoB containing lipoproteins. Ex:(2) (1) https://t.co/XT1EBafmc4 (2) https://t.co/88hQJ5hZJ3
Pemafibrate lowers TG 40%-50%, but very small change in apoB. Outcome consistent with genetic studies by Ference and others. https://t.co/zjoJmHCT2L https://t.co/88hQJ5hZJ3 https://t.co/iYVWBaajyK
RT @The_Nutrivore: This was across 14 different data-sets. https://t.co/PPxuvOhoDU
This was across 14 different data-sets. https://t.co/PPxuvOhoDU
RT @The_Nutrivore: @ondrej_sibl @RChrisCC @zerohedge https://t.co/PPxuvOhoDU https://t.co/EE9l693PHh The association between CVD and LDL-C…
RT @The_Nutrivore: @ScepticalDoctor @professionaldog @enjoylife3D @NickEggleton @FoodFirst_Ty Show me evidence that dietary cholesterol inc…
RT @The_Nutrivore: @ondrej_sibl @RChrisCC @zerohedge https://t.co/PPxuvOhoDU https://t.co/EE9l693PHh The association between CVD and LDL-C…
@ondrej_sibl @RChrisCC @zerohedge https://t.co/PPxuvOhoDU https://t.co/EE9l693PHh The association between CVD and LDL-C is null after adjusting for ApoB. https://t.co/EULPjoPsPJ
RT @The_Nutrivore: Ultimately this is why I am skeptical of the LDL residence time stuff. Whether or not the gene variants affecting LDL co…
RT @The_Nutrivore: @ScepticalDoctor @professionaldog @enjoylife3D @NickEggleton @FoodFirst_Ty Show me evidence that dietary cholesterol inc…
Ultimately this is why I am skeptical of the LDL residence time stuff. Whether or not the gene variants affecting LDL concentration are increasing secretion or reducing clearance, it's the total concentration that the risk is tracking. https://t.co/PPxuvOhoDU https://t.co/RmkmqmYydM https://t.co/gUuP2JYfv7
@DaveKeto @skinnygaz https://t.co/v3AUyPGbIE IMO this is a pretty solid proof that ApoB is what matters the most. Impact of lower TG and/or LDL is proportional to ApoB reduction.
@ScepticalDoctor @professionaldog @enjoylife3D @NickEggleton @FoodFirst_Ty Show me evidence that dietary cholesterol increases ApoB as a general effect. We know it increases the cholesterol content of lipoproteins, sure. But the cholesterol content of lipoproteins isn't nearly as relevant as ApoB for CVD risk. https://t.co/PPxuvOhoDU
RT @PreKureOfficial: Here's something that helps explain this - genes that lower TGs, and genes that lower LDL, are equally protective agai…
Here's something that helps explain this - genes that lower TGs, and genes that lower LDL, are equally protective against IHD, But genes that lower LDL-C also lower TGs, while genes that lower TGs raise LDL-C. This makes LDL-C a Janus-faced marker. 7/n https://t.co/t7URzQ8TyX
Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease. https://t.co/gjlnuer8Yw
RT @EurekaMag: Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease https…
RT @EurekaMag: Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease https…
Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease https://t.co/T8Bkg0BRMz #eurekamag
Here is my take on this interesting study supporting the importance of Apo B in CVD risk. Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease https://t.co/A69vcesqaO via @practiceupdate
Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With Risk of Coronary Heart Disease https://t.co/gevmZ1FUbU via @practiceupdate
Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With CHD Risk https://t.co/O9yjZD7L6D
Association of Triglyceride-Lowering LPL Variants and LDL-C-Lowering LDLR Variants With CHD Risk https://t.co/DVsUAfqch5
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