Advanced lipid testing provides a more comprehensive evaluation of a person’s cholesterol and lipid levels than standard cholesterol tests. Advanced lipid testing measures not only total cholesterol, but also the levels of different types of cholesterol, including LDL (low-density lipoprotein), HDL (high-density lipoprotein), and VLDL (very low-density lipoprotein).
In addition, our advanced lipid test includes measurements of other lipids and lipoproteins, including triglycerides, lipoprotein(a), and Apolipoprotein A and B. These additional measurements can help provide a more detailed picture of a person’s cardiovascular risk and help identify potential underlying causes of high cholesterol.
High levels of Lp(a) increase your risk of atherosclerosis and is an inherited genetic condition. The apo B/apo A-1 ratio indicates the cholesterol balance between potentially atherogenic (bad) and anti-atherogenic (good) particles.
Apo A is a protein carried in HDL (“good”) cholesterol. It helps start the process for HDL to remove bad types of cholesterol from your body. In this way, apolipoprotein A can help to lower your risk for cardiovascular disease.
Apo B containing lipoproteins are the ones most likely to enter the wall of the arteries. They are capable of trafficking cholesterol into the artery wall, and if present in increased numbers may be the main initiating factor in atherosclerosis.
The apo B/apo A-1 ratio indicates the cholesterol balance between potentially atherogenic (bad) and antiatherogenic (good) particles. The ratio is strongly related to risk of cardiovascular disease.
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.
Fast from all food and drink (other than water) for at least 8 hours, and no more than 12 hours prior to your test.
Download and print your pathology form from your i-screen dashboard.
Take your form to one of our affiliated collection centres to have your sample taken.
Results for this test typically available in 2 weeks and will be published in your online dashboard.
