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Dave Feldman

Software engineer; citizen scientist (no medical training); founder, Citizen Science Foundation

Engineer who, after his LDL rose sharply on a ketogenic diet, began self-experimenting and built the Lipid Energy Model with academic collaborators. He coined the "lean mass hyper-responder" phenotype and co-organised the KETO-CTA imaging study. Notably empirical: he frames the high-LDL question as something to be tested rather than asserting LDL is harmless.

Position (a lossy summary - the nuance is below)

LDL: benign to causal

-0.50 (toward "LDL benign")

LDL benignLDL causal

Argues LDL elevation in lean, metabolically healthy keto dieters is an adaptive energy-trafficking response (the Lipid Energy Model) rather than automatically pathological - but stops short of declaring it safe, instead funding and running studies to test it. A cautious, empirical skeptic.

Statins: anti to pro

-0.20 (roughly centered between "Anti-statin" and "Pro-statin")

Anti-statinPro-statin

Not primarily a statin commentator; his focus is the phenotype and its research, and he tends to argue the question is unresolved rather than campaigning for or against statins.

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.

Key arguments

  • LDL rises on carbohydrate restriction as an adaptive energy-trafficking response (Lipid Energy Model).
  • The LMHR triad (high LDL, high HDL, low triglycerides) is the opposite of atherogenic dyslipidemia.
  • The question should be settled by imaging and outcomes, not assertion.

Positions on specific claims

Conflicts of interest

Founder of the Citizen Science Foundation, which crowdfunds the research he promotes; public identity is closely tied to the LMHR concept and the Lipid Energy Model.

Fair criticisms

  • The KETO-CTA pre-registered primary endpoint (non-calcified plaque volume) rose markedly at one year.
  • Peter Attia's "mass balance" objection questions whether the proposed mechanism quantitatively explains the huge LDL rise.
  • Small, self-selected cohort with no long-term cardiovascular event data.

Sources