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.
• 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