Guest guest Posted July 29, 2004 Report Share Posted July 29, 2004 The problem with just looking at HDL-C as a single number or focusing on it as a marker of risk reduction, is that it is not all HDL particles act the same. Some HDL particles protect against atherosclerosis but there are other HDL particles that have been shown to atherogenic. The latter are found more commonly in people consuming a lot of saturated fat and cholesterol. There are also HDL particles that seem to have little effect on atherosclerosis. A recent large review was unable to demonstrate that changes in HDL levels with drugs impacts the risk of CAD. Other research has shown a drop in HDL as a result of eating a healthy low fat diet does not lower the protective HDL particles that are involved in reverse cholesterol transport or taking cholesterol from the periphery back to the liver. So, low-fat diets may lower total HDL-C levels but do not impair reverse cholesterol transport. So a high HDL-C level is no guarantee that atherosclerosis will not progress. It depends not only on the total amount of HDL-C but also on the type of HDL particles that make up that total. In general apo A-1 levels are more predictive of a protective effect than is the cholesterol content of all the HDL particles combined. A lot of American women with HDL-C levels above 70 die of heart attacks even when their LDLs are " normal " for Americans. Unlike raising HDL-C levels using diet and/or drugs to lower LDL-C has consistently been proven to slow, stop and even reverse atherosclerosis and reduce heart attacks. So lowering LDL-C levels is often appropriate for women who have multiple CAD risk factors like smoking, diabetes, hypertension or clinical evidence of significant plaque. So, in the study posted, I would be more concerned about the negative of the LDL going up than the " proposed " positive of the HDL going up. Quote Link to comment Share on other sites More sharing options...
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