Heart Attacks: It All Boils Down to LDL-P

…according to Drs. Thomas Dayspring and JamesUnderberg. By LDL-P, they mean LDL cholesterol particle number. I don’t know if these guys are right or not. I bet it’s more complicated than LDL particle number.

Most heart attacks (aka myocardial infarctions) indeed seem to be caused by acute rupture of an atherosclerotic plaque that’s been present for years. Two key questions are:

  1. What causes the plaque?
  2. Why causes them to rupture?

Underberg and Dayspring write:

The only absolute requirement for plaque development is the presence of cholesterol in the artery: although there are additional heart risk factors like smoking, hypertension, obesity, family history, diabetes, kidney disease, etc., none of those need to be present. Unfortunately, measuring cholesterol in the blood, where it cannot cause plaque, until recently has been the standard of risk-testing. That belief was erroneous and we now have much better biomarkers to use for CV risk-assessment. The graveyard and coronary care units are filled with individuals whose pre-death cholesterol levels were perfect. We now understand that the major way cholesterol gets into the arteries is as a passenger, in protein-enwrapped particles, called lipoproteins.

Particle entry into the artery wall is driven by the amount of particles (particle number) not by how much cholesterol they contain. Coronary heart disease is very often found in those with normal total or LDL-cholesterol (LDL-C) levels in the presence of a high LDL particle number (LDL-P). By far, the most common underlying condition that increases LDL particle concentration is insulin resistance, or prediabetes, a state where the body actually resists the action of the sugar controlling hormone insulin. This is the most common scenario where patients have significant heart attack risk with perfectly normal cholesterol levels. The good news is that we can easily fix this, sometimes without medication. The key to understanding how comes with the knowledge that the driving forces are dietary carbohydrates, especially fructose and high-fructose corn syrup. In the past, we’ve often been told that elimination of saturated fats from the diet would help solve the problem. That was bad advice. The fact is that until those predisposed to insulin resistance drastically reduce their carbohydrate intake, sudden deaths from coronary heart disease and the exploding diabetes epidemic will continue to prematurely kill those so afflicted.

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 And for goodness’ sake, if you want to live longer, start reducing the amount of dietary carbohydrates, including bread, potatoes, rice, soda and sweetened beverages (including fruit juices), cereal, candy – the list is large).

Underberg and Dayspring don’t mention don’t mention LDL particle size, such as small/dense and large/fluffy; the former are thought by many to be much more highly atherogenic. Is that outdated?

Whoever figures out the immediate cause of plaque rupture and how to reliably prevent it will win a Nobel Prize in Medicine.

Read the whole enchilada.

Steve Parker, M.D.

About Dayspring and Underberg:

Thomas Dayspring MD, FACP, FNLA   Director of Cardiovascular Education, The Foundation for Health Improvement and Technology, Richmond, VA. Clinical Assistant Professor of Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School.

James Underberg MD, FACP, FNLA   Clinical Assistant Professor of Medicine in the Division of General Internal Medicine at NYU Medical School and the NYU Center for Cardiovascular Disease Prevention . Director of the Bellevue Hospital Primary Care Lipid Management Clinic.

Steve Parker, M.D.

h/t Dr. Axel Sigurdsson

2 responses to “Heart Attacks: It All Boils Down to LDL-P

  1. Size of the LDL particles is now seen as more of a reflection of their absolute concentration. In other words, if you have 100 mg/dL or LDL cholesterol (the stuff inside the particles) and you have small LDL particles (the containers) then you will obviously need more LDL particles to carry the cholesterol around. The key question is how many?

    Once you adjust the statistical model of LDL size for the number of LDL particles, then size becomes an statistically insignificant. An example is people who have familial hypercholesterolemia. They typically have big LDL particles, but too many of them. They die in their 30’s if they don’t receive aphoresis. Size doesn’t help them one bit!

    • Tom, you remind me of a case I saw 20 years ago: woman in her 30s, familial hypercholesterolemia, serum cholesterol about 500 mg/dl. She’d already had coronary artery bypass grafting. Many in her family didn’t live past 40. We weren’t measuring particle size or number back then.