People
Where prominent voices sit on two axes - whether LDL is causal, and whether to use statins. These scores are a deliberately lossy summary; the real nuance is on each person's page, with sources. Conflicts of interest are recorded for everyone, mainstream and skeptic alike.
Note: this seed set is currently weighted toward skeptics. The mainstream scientific case is carried by the studies and the EAS guideline; a stronger mainstream lipidology voice is a documented next addition.
Aseem Malhotra, MBBS
British cardiologist (MBBS); former NHS cardiology registrar/consultant roles
One of the most prominent credentialed cardiologists to challenge the lipid hypothesis, emphasising insulin resistance and lifestyle. His specific points on relative-vs-absolute statin benefit overlap with serious critiques, but his framing is contested and his wider credibility is compromised.
LDL benign-0.80LDL causalAnti-statin-0.90Pro-statinDave Feldman
Software engineer; citizen scientist (no medical training); founder, Citizen Science Foundation
The originator of the LMHR concept. His strongest contribution is methodological - actually imaging the arteries of high-LDL keto dieters rather than arguing from theory - though the cohort is small and the long-term outcome is unknown.
LDL benign-0.50LDL causalAnti-statin-0.20Pro-statinIvor Cummins
Biochemical/chemical engineer (not a physician); known as "The Fat Emperor"
A radical skeptic by training an engineer. His advocacy for CAC scoring as a direct disease measurement is genuinely valuable; his wholesale dismissal of LDL goes further than most skeptical physicians and his literature reading is self-taught.
LDL benign-0.85LDL causalAnti-statin-0.50Pro-statinMalcolm Kendrick, MBChB
Scottish general practitioner (GP); author and medical blogger
A radical skeptic whose thrombogenic hypothesis reframes atherosclerosis as damage-clot-repair rather than cholesterol deposition. His emphasis on endothelial and glycocalyx health is interesting; his claim that LDL cannot cross the endothelium is contradicted by transcytosis research.
LDL benign-0.95LDL causalAnti-statin-0.70Pro-statinNadir Ali, MD
Interventional cardiologist (30+ years); former Chairman of Cardiology, Clear Lake Regional Medical Center
One of few actively practising interventional cardiologists who openly disputes LDL causality. His mechanistic arguments for LDL''s biological functions are interesting; his core evidence (clinical observation) is uncontrolled and vulnerable to confounding and selection.
LDL benign-0.85LDL causalAnti-statin-0.60Pro-statinPaul Saladino, MD
Physician (MD); ancestral/animal-based-diet advocate; podcaster and author
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.
LDL benign-0.85LDL causalAnti-statin-0.70Pro-statinPeter Attia, MD
MD (Stanford); former surgeon, Johns Hopkins; longevity physician
The strongest informed counterweight to the "LDL is irrelevant" camp: he agrees the skeptics ask some right questions (LDL-C alone is insufficient) but reach the wrong conclusion (that atherogenic particles do not matter). His refrain to a metabolically healthy person with high LDL would be: "Great triglyceride/HDL ratio - now I want your ApoB."
LDL benign0.70LDL causalAnti-statin0.60Pro-statinThomas Dayspring, MD, FACP, FNLA
MD; clinical lipidologist; Fellow of the American College of Physicians and the National Lipid Association
The strongest specialist counterweight on the mainstream side: a career lipidologist who holds that apoB lipoproteins cause atherosclerosis and that the practical task is to measure apoB and lower it, early and substantially, in people at risk. To a metabolically healthy person with a high LDL he would still want the apoB measured and, if high, treated.
LDL benign0.90LDL causalAnti-statin0.90Pro-statin