Good HDL Can Become Bad HDL

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In assessing cardiovascular disease (CVD) risk, physicians generally assume that higher HDL-Cholesterol (HDL-C) is protective and anything that lowers "good" HDL-C levels will also likely increase the risk of CVD. Indeed, research has shown that is primarily HDL particles that pick up cholesterol from the periphery (including the artery wall) and bring it back to the liver for disposal via a process called "reverse cholesterol transport". In addition, HDL and one of its main proteins (apo A-1) have shown to have anti-inflammatory properties that appear to reduce CVD risk. People with elevated inflammation in their bodies as measured by CRP levels are at much higher risk of CVD events. Elevated CRP levels in some studies appear to as a good a predictor of increased CVD events as are elevated LDL-C level. [i] Current American Heart Association guidelines for assessing CVD risk assume higher HDL-C levels always confer a reduced risk of CVD.

When "Good" HDL Goes "Bad"

Dr. Corsetti at the University of Rochester recent study found that in patients with increased levels of CRP in their blood, those who also had high levels of HDL-C actually had an even higher risk of developing unstable angina, having a heart attack, or dying from CVD than those with lower HDL-C levels. This study followed 767 patients who had already suffered a previous heart attack for an average of 26 months to determine which CVD risk factors best predicted subsequent events. [ii]Dr. Corsetti's study showed patients with higher HDL-C levels were actually more prone to CVD events than those with more moderate HDL-C levels when they also elevated CRP levels in their blood. This suggests that a high CRP is a good marker for dysfunctional HDL particles that may actually be "bad" for artery health and increase the risk of CVD.

Current and the newly proposed US Dietary guidelines suggests dietary fat exceed 20% of calories in part because of concerns about lower HDL-C levels. AHA researchers have questioned the use of very-low-fat diets in part because of presumably adverse changes in fasting blood lipids including a drop in HDL-C.[iii]However, such concerns seem debatable since it is only very-low-fat diets that have been shown to dramatically reduce angina [iv] and reverse the atherosclerotic process in human clinical trials. [v] How can this seemingly apparently contradictory data be explained?

HDL-C is assumed to be "good" because it is involved in reverse cholesterol transport and because of its anti- inflammatory properties. However, it is now clear that HDL and its apo A-1 can lose these protective functions via changes in its lipid composition or modification of its proteins. [vi] Indeed reducing dietary fat reduces a host of inflammatory substances in the blood and alters HDL particles so they switch from anti-inflammatory to pro-inflammatory. Very low fat diets may lower HDL-C levels but also can restore their anti-inflammatory properties. [vii]

Research from the Pritikin Longevity Center has also shown a 45% reduction in CRP levels in just 12 days in on a very-low-fat diet. [viii]

Research has also shown that reverse cholesterol transport is not impaired when HDL-C levels drop as a result of reduced dietary fat intake.[ix]

Bottom Line: Reduced HDL-C levels that result from adopting a very-low-fat diet composed largely of fruits, vegetables and whole grains may be due largely to a reduction in dysfunctional inflammatory HDL particles that may actually be promoting atherosclerosis. Therefore, fears that diets very low in fat may promote atherosclerosis, because they may lower HDL-C, appear unwarranted.

By Dr. James J Kenney, PhD, FACN


[i] Parson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation2003;107:499-511

[ii] Corsetti JP, Ryan D, Rainwater L, et al. Cholesteryl ester transfer protein polymorphism (TaqIB) associates with risk in postinfarction patients with high C-reactive lipoprotein cholesterol levels. Arterioscler Thromb Vasc Biol 2010DOI:10.1161/ATVBAHA.110.207977

[iii] Lichstenstein AH, Van Horn L. Very low fat diets. Circulation 1998;98:935-9

[iv] Barnard RJ, Guzy PM, Rosenberg JM, et al. Effects of an intensive exercise and nutrition program on patients with coronary artery disease: Five year follow-up. J Cardiac Rehab 1983;3:183-90

[v] Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial. Lancet 1990;336:129-33

[vi] Smith JD. Dysfunctional HDL as a diagnostic and therapeutic target. Aterioscler Thromb Vasc Biol. 2101;30:151

[vii] Roberts CK, Ng C, Hama S, et al. Effect of short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular disease risk factors. J Appl Physiol 2006;101:1727-32

[viii] Wegge JK, et al. Effect of diet and exercise intervention on inflammatory and adhesion molecules in postmenopausal women on hormone replacement therapy and at risk for coronary artery disease. Metabolism 2004;53:377-81

[ix] Brinton EA, Eisenberg S, Breslow JL. A low-fat diet decrease high density lipoprotein cholesterol by decreasing HDL apoprotein transport rates. J Clin Invest 1990;85:144-51

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