by Dr John Limansky | Jul 3, 2023 | Lipid Status, Primary Health Markers
A waxy, fat like substance that travels throughout the body in carrier lipoproteins (HDL, LDL, and VLDL); a precursor to steroid hormones and bile salts. May be elevated due to poor thyroid function, insulin resistance, blood glucose dysregulation, magnesium deficiency, dehydration, kidney disease, familial hypercholesterolemia. May be decreased due to liver dysfunction, oxidative stress, inflammation, malabsorption, anaemia.
by Dr John Limansky | Jul 3, 2023 | Cardic Risk Profile, Cardiovascular Risk, Lipid Status
Apolipoprotein A is the taxi driver. It activates the enzymes that load cholesterol from the tissues into HDL and allows HDL to be recognised and bound by receptors in the liver at the end of the transport. There are two forms of apolipoprotein A, apo A-I and apo A-II. Apo A-I is found in greater proportion than apo A-II (about 3 to 1). The concentration of apo A-I can be measured directly, unlike HDL, and tends to rise and fall with HDL levels. This has led some experts to think that apo A-I may be a better indicator of the risk of coronary artery disease from the build-up of atheroma than the HDL test, but this has yet to be proven definitively.
by Dr John Limansky | Jul 3, 2023 | Cardic Risk Profile, Cardiovascular Risk, Lipid Status
Laboratory tests for apo B typically measure only apo B-100 but are often reported as simply apo B. Apo B-100 concentrations tend to mirror the concentration of LDL-C. Many experts think that in the future, the concentration of apo B may eventually prove to be a better indicator of risk of cardiovascular disease (CVD) than LDL-C. However, the clinical use of apo B and that of other emerging cardiac risk markers such as apo A-I, Lp(a), and hs-CRP is not fully established.
by Dr John Limansky | Jul 3, 2023 | Cardic Risk Profile, Cardiovascular Risk, Lipid Status
“Lp(a) may accelerate atherosclerotic damage (atheroma) by increasing the size of plaque/atheroma in artery walls. It is retained in the artery wall more than LDL cholesterol as it binds to the artery lining through apolipoprotein (a). Lp(a) is also thought to increase risk of heart attacks by interfering with clotting mechanisms and therefore promoting clot development on the inner surface of blood vessels.
This dual action may explain the role of Lp(a) in the promotion of cardiovascular disease (CVD).
Lp(a) concentrations within the blood are genetically determined and will remain fairly constant in an individual over a lifetime. Concentration is not affected by diet, exercise, and other lifestyle modifications used to lower lipids within the blood. Lp(a) concentrations are slightly lower in men than in women and increase slightly in women after the menopause. The concentration of Lp(a) also varies with ethnicity: patients of African American descent can have concentrations up to 4 times higher than Caucasians, but they may not have a higher risk for CAD.”
by Dr John Limansky | Jul 3, 2023 | Cardic Risk Profile, Cardiovascular Risk, Inflammation, Lipid Status
The PLAC test measures the amount of lipoprotein associated phospholipase (Lp-PLA2) in blood. Lp-PLA2 is an enzyme primarily associated with low density lipoprotein (LDL). LDL carries Lp-PLA2 to the coronary artery walls where it activates an inflammatory response. This makes plaque, if present, more prone to rupture. Because this enzyme is associated with causing inflammation of coronary artery walls, high levels of Lp-PLA2 would therefore seem to indicate an increased risk of heart attack or stroke. Traditional inflammatory markers, such as hsCRP, and CRP, whilst recognised as being useful systemic inflammatory markers are not as sensitive for identifying inflammation of the coronary artery walls. As a result, the PLAC Test, which is measuring levels of Lp-PLA2, serves as a specific independent coronary marker.
by Dr John Limansky | Jul 3, 2023 | Cardic Risk Profile, Cardiovascular Risk, Lipid Status
The Omega-6 to Omega-3 ratio in the cell membranes is key to the development of inflammatory disorders such as rheumatoid arthritis and heart disease. The ratio of Omega-6 to Omega-3 in the West is around 15 to 1, fifteen times more Omega-6 on the cell membrane promoting inflammation. Having twice as much Omega-6 is considered by most experts to be the optimal amount ie a ratio of 2:1 Many people are aware of the health benefits of Omega-3 but the supplementation to achieve optimal health is erratic. Being able to test for Essential Red Cell Fatty Acids (Omega-6/Omega-3 ratio) identifies a person’s current status and is sufficiently specific to allow an accurate supplementation recommendation to be made.