Raising levels of high-density lipoprotein (HDL) cholesterol has regularly been suggested to provide protection against cardiovascular disease (CVD) – with a raft of nutrition science linking whole foods and specific nutrients, and dietary changes to an increase in ‘good’ HDL cholesterol.
From cutting out sugary drinks, to eating more wholegrain and fish intakes, and increasing intakes of sea buckthorn, there is a wealth of research suggesting nutrition can not only lower ‘bad’ LDL-cholesterol, but also increase ‘good’ HDL-cholesterol – and that this is a good thing for your risk of heart disease.
However, a number of recent studies have suggested that a single focus on cholesterol – and especially total cholesterol – may be ‘thwarting CVD prevention’, while a study last year suggested ‘good cholesterol’ itself might actually be bad.
Now, researchers from the University of Toronto suggest that rather than increasing concentrations of HDL cholesterol, it is an altered functioning of HDL cholesterol that is associated with lower heart disease risk.
Writing in the British Journal of Pharmacology, the review looks at a variety of data, and finds that fundamental studies suggest that HDL metabolism, and interaction with adipose tissue and systemic inflammation – rather than HDL concentration – is important for its cardio-protective qualities
"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 senior author Dr Demidmaa Tuvdendorj. “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 team said current strategies aimed at lowering ‘bad’ LDL-cholesterol and rising ‘good’ HDL cholesterol, may not necessarily provide an optimal strategy for altering HDL metabolism and function, “and thus, further research is required to supplement this mechanistic approach for preventing the progression of CVD.”
Source: British Journal of Pharmacology
Published online ahead of print, doi: 10.1111/bph.13743
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