23 Mar 2017 --- A new review has addressed the mysteries behind “good” HDL cholesterol and why boosting its levels may not necessarily provide protection from cardiovascular risk for patients.
For 50 years, HDL-C has been considered as the atheroprotective “good” cholesterol because of its strong inverse association with the progression of CVD. Thus, interventions to increase the concentration of HDL-C have been successfully tested in animals. However, clinical trials were unable to confirm the cardiovascular benefits of pharmaceutical interventions aimed at increasing HDL-C levels.
The new study suggests that enhancing the function of HDL cholesterol, rather than its concentration, is key to reducing cardiovascular risk.
The review details the manner in which tissue and systemic inflammation affects the metabolism of HDL cholesterol via several pathways, pointing to ways to improve its production and function.
“Our own clinical studies as well as in vitro and animal studies performed by other groups have demonstrated the significance of adipose, or fat, tissue for optimal HDL cholesterol metabolism and function,” said Dr. Demidmaa Tuvdendorj, senior author of the British Journal of Pharmacology article.
“Currently, it is accepted that adipose tissue inflammation is one of the hallmarks of systemic inflammation, thus, it is our hypothesis that addressing adipose tissue–associated systemic inflammation will support the atheroprotective role of HDL.”
The report adds, “Our current review of the literature positively demonstrates the negative impact of systemic and tissue (i.e. adipose tissue) inflammation in the healthy metabolism and function of HDL-C.”
“Our survey indicates that HDL-C may be a good marker of adipose tissue health, independently of its atheroprotective associations.”
“It is evident that the therapeutic agents currently available may not provide the optimal strategy for altering HDL-C metabolism and function, and thus, further research is required to supplement this mechanistic approach for preventing the progression of CVD.”
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