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The remainder of the serum cholesterol after subtracting the HDL is the non-HDL cholesterol. The concentration of these other components, which may cause atheroma, is known as the non-HDL-C. This is now preferred to LDL-C as a secondary marker as it has been shown to be a better predictor and it is more easily calculated. [10]
Cholesterol is tested to determine for "normal" or "desirable" levels if a person has a total cholesterol of 5.2 mmol/L or less (200 mg/dL), an HDL value of more than 1 mmol/L (40 mg/dL, "the higher, the better"), an LDL value of less than 2.6 mmol/L (100 mg/dL), and a triglycerides level of less than 1.7 mmol/L (150 mg/dL).
As with statins, this decrease in intra-hepatic (liver) LDL levels may induce hepatic LDL receptor up-regulation, also decreasing plasma LDL levels. As always, a key issue is how benefits and complications of such agents compare with statins—molecular tools that have been analyzed in large numbers of human research and clinical trials since ...
LDL circulates and is absorbed by the liver and peripheral cells. Binding of LDL to its target tissue occurs through an interaction between the LDL receptor and apolipoprotein B-100 on the LDL particle. Absorption occurs through endocytosis, and the internalized LDL particles are hydrolyzed within lysosomes, releasing lipids, chiefly cholesterol.
Levels of LDL or non-HDL cholesterol both predict future coronary heart disease; which is the better predictor is disputed. [39] High levels of small dense LDL may be particularly adverse, although measurement of small dense LDL is not advocated for risk prediction. [39] In the past, LDL and VLDL levels were rarely measured directly due to cost.
The chemical reaction is the same as the total cholesterol measurement, except that the enzymes are blocked from acting on non-HDL lipoproteins by the reagent and their own PEG tails. [8] From these three data LDL may be calculated. According to Friedewald's equation: [9] [LDL] = [Total cholesterol] − [HDL] − [Triglycerides] / 5