Monday, June 4, 2012

HDL Cholesterol - Is More Better ?

HDL cholesterol ( the good cholesterol )

HDL's Job
 One of HDL cholesterol's primary duties is remove LDL cholesterol ( The bad cholesterol ) from Inflammatory cells , called macrophages , in our arteries and move the LDL back to our liver for disposal.

More is better ?
Research over the years have shown that people with high HDL are better protected from the risk of heart disease than those of us with lower HDL levels. This has pushed physicians and patients to find ways of increasing HDL levels in us genetically less fortunate souls. Efforts to increase HDL levels  has not been met with any great success and in some cases seem to increase a person risk of an early exit.

Functional ability is better ?
The problems associated with increasing the amount of HDL  has increased interest in the idea that the functional ability of our HDL may be more important than the amount of HDL circulating around in our blood. This may be good news for those of us who always just a little below the recommended targets for HDL .

I have attached a copy of article from the New England journal of Medicine on this subject.
One defination that you may not be familiar with is Apo Lipoprotein A1.
Apo A1 is a major component of HDL and may contribute to the function of HDL.

Have Fun , Be Smart.   Lipids and Diabetes is a fascinating long term learning process
David calder,MD

Cholesterol Efflux Capacity, High-Density Lipoprotein Function, and Atherosclerosis

Amit V. Khera, M.D., Marina Cuchel, M.D., Ph.D., Margarita de la Llera-Moya, Ph.D., Amrith Rodrigues, M.S., Megan F. Burke, B.A., Kashif Jafri, B.A., Benjamin C. French, Ph.D., Julie A. Phillips, Ph.D., Megan L. Mucksavage, M.Sc., Robert L. Wilensky, M.D., Emile R. Mohler, M.D., George H. Rothblat, Ph.D., and Daniel J. Rader, M.D.
N Engl J Med 2011; 364:127-135January 13, 2011
Citing Articles (92)


High-density lipoprotein (HDL) may provide cardiovascular protection by promoting reverse cholesterol transport from macrophages. We hypothesized that the capacity of HDL to accept cholesterol from macrophages would serve as a predictor of atherosclerotic burden.


We measured cholesterol efflux capacity in 203 healthy volunteers who underwent assessment of carotid artery intima–media thickness, 442 patients with angiographically confirmed coronary artery disease, and 351 patients without such angiographically confirmed disease. We quantified efflux capacity by using a validated ex vivo system that involved incubation of macrophages with apolipoprotein B–depleted serum from the study participants.


The levels of HDL cholesterol and apolipoprotein A-I were significant determinants of cholesterol efflux capacity but accounted for less than 40% of the observed variation. An inverse relationship was noted between efflux capacity and carotid intima–media thickness both before and after adjustment for the HDL cholesterol level. Furthermore, efflux capacity was a strong inverse predictor of coronary disease status (adjusted odds ratio for coronary disease per 1-SD increase in efflux capacity, 0.70; 95% confidence interval [CI], 0.59 to 0.83; P<0.001). This relationship was attenuated, but remained significant, after additional adjustment for the HDL cholesterol level (odds ratio per 1-SD increase, 0.75; 95% CI, 0.63 to 0.90; P=0.002) or apolipoprotein A-I level (odds ratio per 1-SD increase, 0.74; 95% CI, 0.61 to 0.89; P=0.002). Additional studies showed enhanced efflux capacity in patients with the metabolic syndrome and low HDL cholesterol levels who were treated with pioglitazone, but not in patients with hypercholesterolemia who were treated with statins.


Cholesterol efflux capacity from macrophages, a metric of HDL function, has a strong inverse association with both carotid intima–media thickness and the likelihood of angiographic coronary artery disease, independently of the HDL cholesterol level. (Funded by the National Heart, Lung, and Blood Institute and others.)


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    David Calder,MD


Your comments and questions are appreciated. David Calder,MD