Paul Saladino, MD
Physician (MD); ancestral/animal-based-diet advocate; podcaster and author
A physician and high-profile advocate of animal-based diets who argues that native (unoxidised) LDL is not atherogenic and that high LDL is dangerous only when oxidised or in a "hostile" inflamed, insulin-resistant metabolic environment. He centres hs-CRP and fasting insulin as the markers that decide whether a high LDL is benign transport or a real risk signal.
Position (a lossy summary - the nuance is below)
LDL: benign to causal
-0.85 (strongly toward "LDL benign")
Argues only oxidised LDL drives foam-cell formation and plaque, that native LDL is a protective antioxidant with immune and transport roles, and that the LDL-CVD association is strong only when HDL is low - so a high LDL with high HDL and good metabolic markers is benign. A strong rejection of LDL quantity as the risk.
Statins: anti to pro
-0.70 (strongly toward "Anti-statin")
Argues statins show minimal benefit in primary prevention and that the focus on lowering LDL is misplaced relative to addressing oxidation and insulin resistance.
The figure this project''s framing centres on. His "context over quantity" argument (oxLDL, inflammation, insulin) captures a real point - context matters - but his stronger claim, that native LDL quantity is essentially irrelevant, runs against the Mendelian-randomization and trial evidence for causality.
Key arguments
- Native (unoxidised) LDL is not atherogenic; only oxidised LDL initiates plaque.
- Seed-oil-derived linoleic acid in LDL makes it oxidation-prone - so lowering LDL with seed oils may backfire.
- hs-CRP and fasting insulin determine whether high LDL is benign; LDL-CVD risk is strong only when HDL is low.
Positions on specific claims
- Does metabolic health change how dangerous a given LDL level is?
Core position: oxidation and metabolic context, not LDL quantity, determine risk.
- Does LDL cholesterol actually cause heart disease?
Rejects native-LDL causality; attributes plaque to oxidised LDL.
- Is very high LDL safe in a lean, metabolically healthy person on a low-carb diet?
Reads metabolically-healthy high-LDL (LMHR-like) profiles as low risk.
Conflicts of interest
Substantial commercial interests aligned with his position: book sales ("The Carnivore Code"), a large subscription podcast/media brand, and involvement with animal-based nutrition and supplement businesses. Surfaced here on the same basis as pharmaceutical ties are surfaced for mainstream figures.
Fair criticisms
- The "only oxidised LDL matters" claim does not negate that higher native LDL/ApoB particle exposure is causally linked to ASCVD in genetic and trial evidence.
- Leans on n-of-1 anecdote (his own LDL 533 with CAC 0) and a selective reading of Framingham/HDL interaction.
- Commercial brand is tightly coupled to the contrarian position.