Where HDL is concerned, “you can’t be too thin,” Castelli says. One report found about a 1 percent rise in HDL for every pound of fat lost. This doesn’t mean you have to turn yourself into a toothpick, but that you should work on getting rid of excess flab as you add muscle. (Use a body-fat monitor rather than a scale to chart your progress.) Fortunately, fat loss is likely to go hand in hand with the exercise and dietary modifications that also raise HDL levels.
However, although low levels of HDL predict increased cardiovascular risk, particularly in healthy individuals with no history of cardiovascular events, the relationship between HDL and CHD risk is complex, with HDL-C and cardiovascular disease having a nonlinear relationship. For example, research found that HDL levels above approximately 60 mg/dL showed no further improvement in prognosis, and the EPIC (European Prospective Investigation into Cancer and Nutrition)-Norfolk and IDEAL (Incremental Decrease in End Points through Aggressive Lipid Lowering) studies showed that very high levels of HDL may actually be associated with an increased risk of atherosclerotic disease. [5, 6, 2]
While cholesterol is normally kept in balance, an unhealthy diet high in hydrogenated fats and refined carbohydrates can disrupt this delicate balance, leading to increased cholesterol levels. This imbalance is manifested in elevated LDL (bad cholesterol) and low HDL (good cholesterol), which increases the risk of heart attack or stroke. Other causes can include physical inactivity, diabetes, stress and hypothyroidism.
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While cholesterol is normally kept in balance, an unhealthy diet high in hydrogenated fats and refined carbohydrates can disrupt this delicate balance, leading to increased cholesterol levels. This imbalance is manifested in elevated LDL (bad cholesterol) and low HDL (good cholesterol), which increases the risk of heart attack or stroke. Other causes can include physical inactivity, diabetes, stress and hypothyroidism.
HDL serves as a chemical shuttle that transports excess cholesterol from peripheral tissues to the liver. This pathway is called the RCT system. In this system, plasma HDL takes up cholesterol from the peripheral tissues, such as fibroblasts and macrophages. (A study by El Khoury et al indicated that in persons with HALP, macrophages have an increased plasma cholesterol efflux capacity. [18] ) This may occur by passive diffusion or may be mediated by the adenosine triphosphate (ATP)–binding cassette transporter 1. The latter interacts directly with free apo A-I, generating nascent, or so-called discoidal, HDL. Cholesterol undergoes esterification by lecithin-cholesterol acyltransferase (LCAT) to produce cholesteryl ester, which results in the production of the mature spherical HDL. Cholesterol is also taken up from triglyceride-rich lipoproteins in a process mediated by a phospholipid transfer protein (ie, CETP). [19, 20, 21, 22]
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