Lipid subfraction testing provides detailed information about the types and amounts of lipids (fats) present in the blood. This test measures the different subfractions of lipids, such as low-density lipoprotein (LDL), high-density lipoprotein (HDL), and very low-density lipoprotein (VLDL).
Lipid subfraction testing is more comprehensive than standard lipid tests which only measure total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. By analysing the different subfractions of lipids, practitioners can get a more complete picture of a person's lipid profile and may better understand their risk for cardiovascular disease.
LDL cholesterol is often referred to as "bad" cholesterol because it can contribute to the buildup of plaque in the arteries, which can lead to heart disease. However, not all LDL cholesterol is equally harmful. Some subfractions of LDL cholesterol, such as small, dense LDL particles, are more harmful than others. Lipid subfraction testing can identify these subfractions and may help inform the risk for cardiovascular disease.
High levels of Lp(a) increase your risk of atherosclerosis and is an inherited genetic condition. The apo B/apo A-I ratio indicates the cholesterol balance between potentially atherogenic (bad) and anti-atherogenic (good) particles.
High levels of Lp(a) increase your risk of atherosclerosis and is an inherited genetic condition. As levels are genetically determined they are usually not lowered by lifestyle changes such as diet and exercise. Your level of Lp(a) remains virtually constant throughout your life.
Lipids and cholesterol are fat-like substances in your blood. Some are necessary for good health, but when you have a high level of cholesterol in your blood, a lot of it ends up being deposited in the walls of your arteries and other vital organs. Lifestyle choices including diet, exercise and alcohol intake can all influence cholesterol levels and your risk of developing heart disease.
Total cholesterol includes both HDL cholesterol and LDL cholesterol. Cholesterol is essential for many processes in the body, including the formation of cell membranes, the production of hormones, and the metabolism of vitamin D.
LDL cholesterol is often referred to as "bad" cholesterol, as it can contribute to the development of atherosclerosis, a condition where plaque builds up in the arteries and can increase the risk of heart disease.
VLDL is considered "bad" cholesterol because high levels can contribute to the buildup of plaque in the arteries. VLDL also has important functions in the body, such as providing energy to cells and helping to transport fat-soluble vitamins.
HDL cholesterol is often referred to as "good" cholesterol, as it helps remove excess cholesterol from the bloodstream and can protect against the development of heart disease.
Triglycerides are the main storage form of fatty acids in the body and a source of energy. High levels of triglycerides are associated with cardiovascular disease, obesity, type 2 diabetes, and metabolic syndrome.
Non-HDL cholesterol is considered an effective lipid measurement for assessing cardiovascular disease risk as it is believed to reflect levels of 'bad' cholesterol.
IDL is a transitional lipoprotein that is eventually converted to LDL. Elevated levels of IDL in the blood can contribute to the buildup of plaque in the arteries, just like LDL.
Intermediate Density Lipoprotein is a class of lipoproteins formed in the degradation of VLDLs.
Intermediate Density Lipoprotein is a class of lipoproteins formed in the degradation of VLDLs.
Intermediate Density Lipoprotein is a class of lipoproteins formed in the degradation of VLDLs.
Low-density lipoprotein (LDL) can be categorised into subfractions, which range from LDL-1 through to LDL-7 based on their size and density. Among these subfractions, LDL-1 and LDL-2 are thought to be less atherogenic than LDL-3 to LDL-7, meaning they may have a lower tendency to contribute to the development of atherosclerosis. This is due to the fact that LDL-1 and LDL-2 are larger and more buoyant than LDL-3 to LDL-7, which reduces their likelihood of penetrating the arterial wall and contributing to plaque formation.
LDL-1 is the largest and least dense subtype of LDL, and it has a buoyant density. LDL-1 is less likely to penetrate the arterial wall and contribute to the formation of plaque compared to smaller, denser LDL subfractions.
LDL-2 is the second largest and second least dense subtype of LDL, and it also has a buoyant density.
Research indicates that higher quantities of smaller, denser LDL3-7 particles are linked to inflammation and pose a greater risk of causing atherosclerosis compared to fewer, larger and more buoyant LDL1-2 particles. LDL3-7 particles are smaller and denser, and are more likely to permeate the arterial wall and participate in the formation of plaque.
Presence of small highly atherogenic dense Low Density Lipoprotein 3 through 7 are associated with 3 times greater risk for coronary artery disease independent of other risk factors.
Presence of small highly atherogenic dense Low Density Lipoprotein 3 through 7 are associated with 3 times greater risk for coronary artery disease independent of other risk factors.
Presence of small highly atherogenic dense Low Density Lipoprotein 3 through 7 are associated with 3 times greater risk for coronary artery disease independent of other risk factors.
Presence of small highly atherogenic dense Low Density Lipoprotein 3 through 7 are associated with 3 times greater risk for coronary artery disease independent of other risk factors.
LDL-7 is the smallest and densest subtype of LDL and has the highest atherogenicity, meaning it poses the greatest risk for contributing to the development of atherosclerosis and cardiovascular disease.
A low LDL mean particle size indicates the presence of LDLs of a size capable of penetrating the endothelial lining and causing the development of atheromatous plaques.
Risk is based on mean LDL particle size. Note that risk factors other than mean particle size may still require medical intervention.
Download and print your pathology form from your i-screen dashboard.
Fast from all food and drink (other than water) for at least 8 hours, and no more than 12 hours prior to your test.
Take your form to one of our affiliated collection centres to have your sample taken - no need for an appointment.
Results for this test available in 10-12 days and will be published in your online dashboard.