Lipoprotein Checklist:
Intermediate-density lipoproteins (IDL)
After a meal, our bodies are meant to clear the
by-products of eating from our blood within 4–6 hours. However,
approximately 20% of people with coronary plaque have after-eating
by-products, called post-prandial lipoproteins, or PPLs, linger for
24 hours or longer. When PPLs linger, they exert damaging effects on
vascular structures. PPL particles insert themselves into
atherosclerotic plaque and fuel growth, and cause atherosclerosis
through other pathways.
- PPLs block natural artery relaxing agents, nitric oxide and endothelin, and thereby induce endothelial dysfunction (abnormal artery constriction), a fundamental process in atherosclerotic plaque formation.
- PPLs trigger increased blood levels of cellular adhesion molecules (CAM) like intracellular adhesion molecule-1, vascular cellular adhesion molecule VCAM-1, and E-selectin. When blood levels of CAMs are increased, inflammatory white blood cells adhere more readily to the artery wall and gain entry, leading to atherosclerotic plaque formation.
- PPLs activate blood clotting via increases in clotting factors VII and reduction of PAI-1, an inhibitor of clotting.
- PPLs trigger formation of a cascade of other abnormal lipoprotein particles that are potent causes of heart and vascular disease, e.g., small LDL particles.
Because triglycerides are a principal ingredient in PPLs, elevated
fasting triglycerides can serve as an indirect index of increased
PPLs. If triglycerides are ≥100 mg/dl, PPLs are likely to be
present. But fasting triglycerides are not foolproof, and
substantial PPL excess can still occur with triglyceride levels of
<100 mg/dl.
The best method to assess whether PPLs are present is to measure
intermediate-density lipoproteins (IDL) in fasting blood. (Direct
PPL measurement is a research tool unavailable to use.) A normal
amount of IDL is none—none whatsoever should be detected in fasting
blood. If present, IDL triggers atherosclerotic plaque growth. It is
also a potent cause of abdominal and thoracic aneurysms of the
aorta. IDL has also been shown to heighten the likelihood of pure
soft plaque in carotid arteries, the sort that easily fragment,
release debris, and cause strokes.
How to Manage and Reduce IDL
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