Cholesterol will not mix with water, and therefore, needs some assistance to travel throughout the bloodstream. With the help of a form of cholesterol HDL (high-density lipoprotein), packets of cholesterol are formed to help move cholesterol through the blood. HDL helps remove cholesterol from the body by transporting it to the liver. Another form of cholesterol is LDL (low-density lipoprotein). LDL does not aid in the transportation of cholesterol out of the body, instead it deposits cholesterol onto the vessel wall. LDL molecules contain much more cholesterol than HDL molecules.
|How to Increase HDL|
|How to Decrease LDL|
The total cholesterol/HDL ratio is more indicative of cardiovascular disease than TC (total cholesterol). The amount of HDL and LDL in the blood are added together, this number for all practical purposes, indicates the amount of total cholesterol. Therefore, if your HDL count is low, the LDL count will account for the remainder of the total. For men, an acceptable ratio of TC/HDL is 4.5 or below, and women are 4.0 or below.
|Ratio of total Cholesterol to HDL|
|Very low (1/2 average)||<3.4||<3.3|
|Moderate risk (2x average)||9.5||7.0|
|High risk (3x risk)||>23||>11|
|>= 500||Very High|
|Ratio of LDL to HDL|
|Very low (1/2 average)||1||1.5|
|Moderate risk (2x average)||6.3||5.0|
|High risk (3x risk)||8||6.1|
HDL levels have an inverse relationship with coronary heart disease. The ability of HDL to predict the development of coronary atherosclerosis has been estimated to be four times greater than LDL and eight times greater than TC. Treatment is recommended for those with an HDL level below 40 mg/dL. An HDL of 60 mg/dL is considered a protection against heart disease.
New MNR imaging tests assess the size of LDL particles. Small LDL particles are associated with a higher risk of cardiovascular disease.
Elevated triglycerides in the blood increase the risk of heart disease. Triglycerides do not come directly from dietary fats. Instead, they are produced in the liver from any excess carbohydrates that have not been used for energy.
Adults 20 years and older should undergo cholesterol screening (total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides) every 5 years. Blood samples should be obtained after fasting.
|LDL Cholesterol (mg/dl)|
|> 190||Very High|
|Total Cholesterol (mg/dl)|
|HDL Cholesterol (mg/dl)|
The National Cholesterol Education Program (May 16, 2001), Journal of the American Medical Association
After consuming a meal containing fat, the blood undergoes a transient increase in lipids, particularly triacylglycerols, lasting several hours. This is known as postprandial lipemia. Individuals consuming a typical Western diet spend approximately 18 hours per day in this state.
Exogenous fat transport begins in the intestine where dietary fats are packaged into lipoprotein particles called chylomicrons. Chylomicrons enter the bloodstream and deliver their triglyceride to adipose tissue and muscle. The remnant of chylomicrons is removed from the circulation by the liver.
Endogenous fat transportation begins when the liver secretes a Very Low-Density Lipoprotein particle (VLDL). When a VLDL particle reaches the capillary of muscle or adipose tissue, its triglyceride is extracted, leaving an Intermediate Density Lipoprotein (IDL). Half of the IDL particles are removed from circulation by the liver within two to six hours of their formation. The remaining IDL transforms into Low-Density Lipoproteins (LDL) which circulate for approximately two and a half days before binding to LDL receptors in the liver and other tissues.
Small dense low-density lipoprotein (LDL) are more atherogenic than larger LDL particles because they are
- more easily enter the vessel wall
- more prone to oxidative modification
- bind more tightly to the arterial wall
- cleared more slowly
The composition of triglyceride-rich lipoproteins (TRLs) is metabolically linked to LDL. LDL particle size is primarily affected by the plasma TG levels. Postprandial hyperlipidemia is associated with an increase in the proportion of small, dense LDL. Furthermore, prolonged lipemia promotes the transfer of core lipids between TRLs and high-density lipoprotein (HDL) leading to a reduction in HDL cholesterol levels. This combination is known as the lipid triad or atherogenic lipoprotein profile:
- high plasma TG concentrations
- increased small dense LDL
- low HD
Bravo E, Napolitano M, and Botham KM (2010). Postprandial Lipid Metabolism: The Missing Link Between Life-Style Habits and the Increasing Incidence of Metabolic Diseases in Western Countries? The Open Translational Medicine Journal, 2010, 2, 1-13
Elevated circulating cholesterol reduces the cell's ability to make its own cholesterol by turning off the production of HMG CoA reductase, which interrupts a step in the biosynthetic pathway of cholesterol. Incoming LDL derived cholesterol promotes the storage of cholesterol in the cell by activating ACAT which attaches a fatty acid to excess cholesterol molecules. This results in cholesterol esters that are deposited in storage droplets. The accumulation of cholesterol within the cell drives a feedback mechanism that stops the cell's synthesis of new LDL receptors. The cell adjusts its receptors, so only enough cholesterol is brought in to supply its needs.
With Familial Hypercholesterolemia, an inherited mutant gene causes the absence of LDL receptors. High circulating levels of LDL are found to be caused by increased production and a decrease in the removal of LDL. Consequently, Familial Hypercholesterolemia leads to high blood cholesterol and heart attacks in the young.