Low fat diet and statins do not prevent heart attack because they only lower levels of large boyant LDL-C
It’s true that fewer people are actually dying of heart attacks in the US and other high-income countries (although low-income countries still have high mortality rates). But that statistic belies the truth. While fewer are dying of heart attacks, more people are suffering them. Of course rising numbers could be due to improved recognition, ambulance response time, emergency room functioning, the clot-buster tissue plasminogen activator (tPA), and heart attack post-care. But the real story is that more people are suffering heart attacks with lower LDL-C levels than before, because the standard fasting lipid profile—the blood test ordered by your practitioner to test your cholesterol—assumes that all LDL particles are the same.
There are two different LDLs, but the lipid profile test measures them together. The majority (80 percent) of circulating LDL species are called large buoyant or type A LDL, which are increased by dietary fat consumption. This is the species reduced by eating low-fat or by taking statins. However, large buoyant LDL is cardiovascularly neutral—meaning it’s not the particle driving the accumulation of plaque in the arteries leading to heart disease. Then there’s a second, less common (only 20 percent) LDL species called small dense or type B LDL.
There is some debate as to whether or not it’s the actual perpetrator of the plaque, but it doesn’t matter; small dense LDL is predictive of risk for a heart attack. The problem is that statins will lower your LDL-C because they’re lowering the type A LDL, which is 80 percent of the total; but they’re not doing anything to the type B LDL, which is the problematic particle.
References
- Lustig, Robert. (2021). Metabolical Chapter 2. “Modern Medicine” Treats Symptoms, Not Disease (p. 45). New York, NY: HarperCollins Publishers.
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