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.
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.
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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.
How this study connects
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