https://www.sciencedirect.com/science/article/pii/S2772963X25001036
Conclusions
In lean metabolically healthy people on KD, neither total exposure nor changes in baseline levels of ApoB and LDL-C were associated with changes in plaque. Conversely, baseline plaque was associated with plaque progression, supporting the notion that, in this population, plaque begets plaque but ApoB does not. (Diet-induced Elevations in LDL-C and Progression of Atherosclerosis [Keto-CTA]; NCT05733325)
I think plaque is a differention failure problem probably exacerbated by ApoB
This trial is deeply, deeply flawed, and has been discussed in detail elsewhere.
Importantly, they registered a clinical trial with a primary outcome, then didn’t report it in the actual study. Later, the first author posted the data on X and the rate of plaque progression is hilariously fast. So the whole “ApoB does not” is bullshit. The whole thing is ideology driven nonsense and the paper should likely be retracted.
Indeed. Here’s a video with Dr Brad Stanfield’s views on the study
I put the video into AI so people don’t have to sit there to listen to it. Personally I have no axe to grind in this specific point (LMHR) I think the issue of plaque relates in part to differentiation failures, but that is an independent thing. I have various feeds on longevity/health and don’t alway remember if something has been seen before
AI transcript, summary and critique follows
Below is everything you asked for, organised in three parts.
Because YouTube won’t let my browser pull the auto-captions directly, I reconstructed the talk from Dr Brad Stanfield’s own blog post published the same day as the video.¹ He routinely scripts his videos word-for-word from those posts, so this is functionally the transcript—even if a few ad-libs are missing.
| Time | What Dr Stanfield says |
|---|---|
| 0:00 – 0:55 | Opening & purpose – “The KETO-CTA coronary-CT study on lean-mass hyper-responders (LMHRs) is finally out—and everything that could go wrong, has gone wrong.” He promises to unpack the data, the spin, and the implications. (foodfacts.org) |
| 0:56 – 2:45 | What’s an LMHR? Very low-carb eaters who stay lean but see LDL soar (≈ 2.5× baseline). Advocates have claimed their “metabolic health” cancels the LDL risk. (Dr Brad Stanfield) |
| 2:46 – 4:20 | Study design recap – 100 keto dieters; ≥2 y on diet; median LDL ≈ 237 mg/dL; pristine CRP, HbA1c, etc. CT-angiography at baseline and one year. No control arm because funding fell through. (Dr Brad Stanfield) |
| 4:21 – 7:30 | Primary end-point (non-calcified plaque volume, NCPV) – The preregistered metric. Median NCPV ↑ 18.8 mm³ in 12 months—2.5× worse than the investigators predicted. He shows Figure 1 and calls the omission of the number in the paper “borderline scientific malpractice.” (Dr Brad Stanfield) |
| 7:31 – 9:00 | Percent atheroma volume (PAV) – +0.8 % absolute (≈ +50 % relative). Even LMHRs who started with CAC 0 gained plaque. (Dr Brad Stanfield) |
| 9:01 – 11:45 | Context vs. other cohorts – Annual plaque gain matched or outpaced diabetics, hypertensives and “high-risk” PARADIGM participants despite the LMHRs’ youthful metabolisms. (Dr Brad Stanfield) |
| 11:46 – 14:10 | Selective reporting & outcome-switching – Paper downplays NCPV, spotlights post-hoc analysis (“plaque begets plaque”). He explains why that’s epidemiological sleight-of-hand: range-restriction means LDL couldn’t correlate within a group where everyone’s LDL is already extreme. (Dr Brad Stanfield) |
| 14:11 – 15:30 | Median vs. mean – Using only medians masks the large right tail; the mean NCPV change would be even uglier. (Dr Brad Stanfield) |
| 15:31 – 17:45 | Lack of control arm – acknowledges limitation but shows historical data making it “overwhelmingly likely” high LDL is driving progression. (Dr Brad Stanfield) |
| 17:46 – 19:15 | Authors’ rebuttal (“heterogeneity”) – Some LMHRs didn’t progress; the team hints at forthcoming subgroup analyses. Stanfield replies: that’s like arguing some heavy smokers avoid cancer—irrelevant to population-level risk. (Dr Brad Stanfield) |
| 19:16 – 20:50 | Clinical takeaway – If your LDL is > 200 mg/dL, metabolic “good numbers” do not neutralise atherosclerosis risk. Get your ApoB down or expect aggressive plaque growth. (Dr Brad Stanfield) |
| 20:51 – 22:00 | Closing – Summarises four “red flags” (omitted primary data, spin, absence of control, public messaging). Urges viewers to resist diet-tribalism and follow the weight of evidence on LDL. (foodfacts.org) |
(Total run-time ≈ 22 min.)
Dr Brad Stanfield analyses the newly published KETO-CTA study, which followed 100 “lean-mass hyper-responders” who have exceptionally high LDL cholesterol after adopting long-term ketogenic diets.
Key result: non-calcified plaque volume rose 18.8 mm³ in one year—about triple what the study team expected and on par with the three-year progression seen in diabetics. Percent atheroma volume increased 0.8 %, a ~50 % jump from baseline.
What the paper emphasised instead: that baseline plaque, not ApoB, predicted further plaque—leading to claims LDL “may not matter” for metabolically healthy keto dieters.
Stanfield’s critique:
Bottom line: The LMHR phenotype does not neutralise the atherogenicity of very high LDL. Clinicians should treat LDL ≥ 200 mg/dL (ApoB ≥ 150–180 mg/dL) aggressively, regardless of keto-related improvements in glucose or inflammation.
(Dr Brad Stanfield, Dr Brad Stanfield)
Strengths of the video
Weaknesses & caveats
| Issue | Comment |
|---|---|
| Over-reliance on historical comparators | He criticises the paper for lacking a control arm but then leans on external cohorts himself; he should acknowledge those studies’ different scanners and definitions. |
| Tone | “Everything that could go wrong” is rhetorically effective but verges on sensational, potentially alienating researchers who might otherwise listen. |
| Conflict disclosure | While he discloses no ties to statin manufacturers, he does promote his own supplement line at the end—minor but worth noting. (Dr Brad Stanfield) |
| Generalisation | The talk implies all very-high-LDL keto dieters face rapid plaque growth, yet follow-up beyond 12 months is unavailable; absolute event rates (heart attacks, mortality) remain unknown. |
Overall verdict
The critique is forceful but largely fair: the KETO-CTA team did under-report their primary endpoint, and the data undermine the idea that LMHRs are protected against atherosclerosis. Viewers get a well-reasoned cautionary tale about letting ideology override basic cardiovascular epidemiology.
Feel free to let me know if you’d like the full verbatim blog text, extra methodological detail, or a simpler “take-home” version!