Cardiovascular
Do remnant cholesterol and triglycerides cause cardiometabolic multimorbidity?
Open access · cc by · source: Europe PMC
In >300,000 UK Biobank participants, higher remnant cholesterol and triglycerides tracked—and MR supported a causal role in—progression to cardiometabolic multimorbidity, especially IHD plus type 2 diabetes.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Mendelian randomisation raises this above the observational association it accompanies.
Genetic instruments support a causal role for triglyceride-rich lipoproteins in cardiometabolic multimorbidity. Remnant cholesterol at or above 1.0 against below 0.4 mmol/L carried HR 2.46 for type 2 diabetes and 1.63 for ischaemic heart disease; causal odds per 1.0 mmol/L triglycerides were 1.21 for any multimorbidity, with associations for ischaemic heart disease and diabetes but not stroke.
Evidence for the claim as stated.
The randomised trial and the genetic study support different claims about the same molecules. The trial randomises a real dietary exposure but measures markers over four weeks in healthy volunteers; the Mendelian randomisation estimates lifelong effects on hard endpoints but from a single baseline lipid measurement in a healthier-than-average cohort, with instrument pleiotropy unresolved.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
The randomised trial and the genetic study support different claims about the same molecules. The trial randomises a real dietary exposure but measures markers over four weeks in healthy volunteers; the Mendelian randomisation estimates lifelong effects on hard endpoints but from a single baseline lipid measurement in a healthier-than-average cohort, with instrument pleiotropy unresolved.
- Supports · Does coconut oil raise LDL like butter?
Study at a glance
- Design
- Mendelian randomisation — UK Biobank multistate cohort plus one-sample Mendelian randomisation using 13 triglyceride-rich-lipoprotein SNPs.
- N
- N=334030 · Observational: 334,030 (remnant cholesterol) and 365,577 (triglycerides); MR: 376,712 and 411,930.
- Population
- UK Biobank adults free of diabetes, ischemic heart disease, and stroke at baseline (lipid-lowering users excluded from observational analyses).
- Outcome
- Progression from first cardiometabolic disease to multimorbidity (especially IHD plus type 2 diabetes), plus causal ORs from MR.
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
Do remnant cholesterol and triglycerides cause cardiometabolic multimorbidity?
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
Observational n was 334,030 (remnant cholesterol) and 365,577 (triglycerides).
334,030 (men% = 42.5%) and 365,577 (men% = 42.1%) eligible participants were included in the observational analysis of remnant cholesterol and triglycerides
Remnant cholesterol ≥1.0 mmol/L had T2D HR 2.46 and IHD HR 1.63 vs <0.4 mmol/L.
Participants with serum remnant cholesterol of ≥1.0 mmol/L had 146% (HR: 2.46; 95% CI: 2.23, 2.71; P for trend <0.001) and 63% (HR: 1.63; 95% CI: 1.52, 1.74; P for trend <0.001) higher risks of type 2 diabetes and ischemic heart disease
Key findings
Remnant cholesterol ≥1.0 vs <0.4 mmol/L: T2D HR 2.46 and IHD HR 1.63. Triglycerides ≥2.3 mmol/L: T2D HR 3.54. Causal TG ORs per 1.0 mmol/L were 1.21 (any multimorbidity) and 1.24 (IHD–T2D); remnant cholesterol ORs per 0.29 mmol/L were 1.23 and 1.26. Associations were for IHD and diabetes, not stroke.
Methodology
Used multistate models from first cardiometabolic disease (diabetes, IHD, or stroke) to multimorbidity, then one-sample MR with 13 biologically relevant SNPs in hundreds of thousands of UK Biobank participants.
Limitations
Single baseline lipids, possible instrument pleiotropy, and a healthier-than-average UK Biobank sample still limit how far causal estimates travel.
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