On: Stress testing the lipid energy model.
Episode: 19
Date: October 2018
Key Subjects:
- Lean Mass Hyper-Responder (LMHR):
- Athletic, lean, low carb (and high fat).
- High levels of LDL-C and LDL-P.
- High levels of HDL-C.
- Low levels of TG.
- Feldman Thesis:
- LMHR have high rate of VLDL secretion.
- Needed to deliver the TG to cells for energy.
- Under these conditions, high LDL-C (or LDL-P) may not be a bad thing.
- Attia response:
- Feldman Thesis doesn’t explain how or why cholesterol goes up.
- If cholesterol doesn’t go up, the increased number of VLDL particles (needed to carry around the fat) should be cholesterol depleted, but they are not.
- So why is the cholesterol mass higher and where does it come from.
- Reasons that cholesterol goes up:
- More synthesized.
- More reabsorbed.
- Less cleared.
- Counter thesis:
- Higher intake of saturated fat results in higher cholesterol because it activates some cholesterol synthesis pathway (or prevents cholesterol clearance – see Cholesterol write-up)
- Can be avoided by replacing saturated fats with MUFA.
- Feldman Thesis doesn’t explain how or why cholesterol goes up.
- Both agree:
- LDL-C is one of three necessary ingredients for increased CVD risk (other two: oxidation / inflammation, damaged endothelial walls).
- Importance of testing oxidized LDL.
- Lipoproteins are energy delivery system for much more than cholesterol and TG (phospholipids, etc.).
Key Takeaways:
- Measure oxidized LDL to check for level of inflamed particles.
- Get sterol panel to understand how much cholesterol you synthesize and reabsorb.
Worth Listening:
Feldman thesis is a helpful reminder that lipoproteins are necessary as (energy) delivery system of more than just cholesterol to cells.
An interesting perspective, but Attia’s core thesis seems more convincing: high LDL-P is bad over time specifically for increased risk of CVD in the presence of inflammation and damaged arterial walls.
7/10