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The HDL paradox: what does it mean and how to manage low serum HDL cholesterol level?
Barbara Cybulska1, Longina Kłosiewicz-Latoszek
1National Food and Nutrition Institute, Warsaw, Poland. barbara.cybulska@wp.pl.
Insights
High-density lipoprotein (HDL) functionality, not just levels, is crucial in preventing atherosclerosis. Future research aims to boost functional HDL to reduce cardiovascular events.
Area of Science:
- Lipidology
- Cardiovascular Science
- Atherosclerosis Research
Background:
- Familial hypercholesterolemia and severe hypertriglyceridemia are significant lipidologic concerns.
- High-density lipoprotein cholesterol (HDL-C) levels are a focus in cardiovascular risk assessment.
- The role of HDL in atherogenesis requires further elucidation.
Purpose of the Study:
- To summarize current evidence on HDL's complex role in atherogenesis.
- To review therapeutic recommendations for patients with low HDL-C levels.
- To highlight the importance of HDL functionality over mere levels.
Main Methods:
- Review of current scientific evidence and expert views.
- Analysis of existing literature on HDL functionality in pathological conditions.
- Evaluation of therapeutic strategies targeting HDL.
Main Results:
- Available evidence suggests HDL's antiatherogenic properties are linked to functionality, not just quantity.
- HDL functionality is compromised in pathological conditions associated with inflammation.
- Low HDL-C levels may indicate dysfunctional HDL particles.
Conclusions:
- HDL's role in atherogenesis is complex and tied to its functionality.
- Inflammation significantly impacts HDL functionality, potentially impairing its protective effects.
- Future therapies should focus on increasing functional HDL to reduce cardiovascular events and improve clinical guidelines.
Abstract:
The topic of this article is an important practical lipidologic issue, along with familial hypercholesterolaemia and severe hypertriglyceridaemia which have also been recently reviewed in the Polish literature. In this paper, we attempted to summarise current scientific evidence and views on the complex role of HDL in atherogenesis, as well as therapeutic recommendations in patients with low HDL-C level. In summary, it should be noted that the available evidence does not indicate that HDL are not antiatherogenic lipoproteins but rather directs our attention towards their functionality and dysfunctionality accompanying numerous pathologic conditions associated with inflammation. It may be hoped that effective methods to increase the number of functional HDL in the plasma will be developed in future studies, translating to a reduction in CV events and thus deserving a place in clinical practice guidelines.
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