Diet and Lp(a): Does Dietary Change Modify Residual Cardiovascular Risk Conferred by Lp(a)?

Lipoprotein(a) [Lp(a)] is an independent, causal, genetically determined risk factor for cardiovascular disease (CVD). We provide an overview of current knowledge on Lp(a) and CVD risk, and the effect of pharmacological agents on Lp(a). Since evidence is accumulating that diet modulates Lp(a), the f...

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Bibliographic Details
Published in:Nutrients 2020-07, Vol.12 (7), p.2024
Main Authors: Enkhmaa, Byambaa, Petersen, Kristina S, Kris-Etherton, Penny M, Berglund, Lars
Format: Article
Language:English
Subjects:
Adult
Aged
Apolipoproteins
Atherosclerosis
Calcification
Carbohydrates
Cardiology
Cardiovascular disease
Cardiovascular diseases
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - therapy
Cholesterol
Cholesterol, LDL - blood
Cholesterol, LDL - metabolism
Clinical trials
Diet
Diet - methods
Dietary Fats - administration & dosage
Fatty Acids - administration & dosage
Female
Health risk assessment
Health risks
Heart Disease Risk Factors
Heterogeneity
Humans
Hypolipidemic Agents - therapeutic use
Lipids
Lipoprotein(a) - blood
Lipoprotein(a) - metabolism
Lipoproteins
Low density lipoprotein
Lp(a), cardiovascular risk
Male
metabolic feeding trials
Middle Aged
Plasma
Polymorphism
Review
Risk analysis
Risk factors
Stroke
Task forces
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Summary:Lipoprotein(a) [Lp(a)] is an independent, causal, genetically determined risk factor for cardiovascular disease (CVD). We provide an overview of current knowledge on Lp(a) and CVD risk, and the effect of pharmacological agents on Lp(a). Since evidence is accumulating that diet modulates Lp(a), the focus of this paper is on the effect of dietary intervention on Lp(a). We identified seven trials with 15 comparisons of the effect of saturated fat (SFA) replacement on Lp(a). While replacement of SFA with carbohydrate, monounsaturated fat (MUFA), or polyunsaturated fat (PUFA) consistently lowered low-density lipoprotein cholesterol (LDL-C), heterogeneity in the Lp(a) response was observed. In two trials, Lp(a) increased with carbohydrate replacement; one trial showed no effect and another showed Lp(a) lowering. MUFA replacement increased Lp(a) in three trials; three trials showed no effect and one showed lowering. PUFA or PUFA + MUFA inconsistently affected Lp(a) in four trials. Seven trials of diets with differing macronutrient compositions showed similar divergence in the effect on LDL-C and Lp(a). The identified clinical trials show diet modestly affects Lp(a) and often in the opposing direction to LDL-C. Further research is needed to understand how diet affects Lp(a) and its properties, and the lack of concordance between diet-induced LDL-C and Lp(a) changes.
ISSN:2072-6643
2072-6643
DOI:10.3390/nu12072024