The Keto CTA study is back on my feed today, and the authors are reiterating that it was retracted at their request. That’s fine. I’m actually open to the idea that the Cleerly data was flawed. My much, much larger problem is with the way the science was communicated. As they say, “Trust takes years to build, seconds to break, and forever to repair.” At launch, the message was “no association of ApoB with plaque” and “most participants showed NO OR MINIMAL progression.” (Pictures below.) But when the authors requested the retraction, the exact same data was suddenly the problem. Plaque progression was so high and so one directional, that it was said to be statistically implausible. So what is it? No or minimal progression or progression so consistent and so bad that the data must be flawed? Second, it’s worth remembering how science is supposed to be communicated. Plaque progression was the PRIMARY OUTCOME cited for the Keto CTA study. But plaque progression was not reported. The authors later apologized (which, to their credit, is good!) for not including the number in the graph they provided. But while putting the number in the figure would have been nice, that is not how you DISCUSS your primary outcome in the DISCUSSION of a paper. Let’s compare this to how @BradStanfieldMD discussed the primary outcome of his Rapamycin study, a study he put a tremendous amount of reputation behind and, quite literally put a second mortgage on his house to get over the finish line: “4.1 Principal Findings This randomised, double-blind, exploratory trial evaluated whether once-weekly sirolimus (rapamycin) 6 mg, timed to avoid peak training windows, could enhance functional adaptations to a 13-week resistance and endurance programme in sedentary older adults. Contrary to the ‘cycling hypothesis’ derived from preclinical models, we found no evidence of benefit. Instead, sensitivity analyses (complete-case and per-protocol) revealed a statistically significant blunting of functional gains in the sirolimus arm. Specifically, participants taking the drug performed fewer chair-stand repetitions and showed non-significant trends toward reduced walking distance and grip strength compared with placebo. Safety monitoring identified a higher burden of minor AEs and one serious infection (pneumonia) in the treatment arm.” He was clear. The study did not meet his primary endpoint, and instead, the intervention appeared to have worsened it. That is how science is communicated. I asked Grok to write the Discussion the Keto CTA should have had for its primary endpoint, had it been written the way Dr Stanfield did. Here is what Grok wrote: "Discussion Principal Findings This prospective, single-arm observational study evaluated whether long-term exposure to elevated LDL-C and ApoB (in the lean-mass hyper-responder phenotype on a ketogenic diet) was associated with progression of noncalcified coronary plaque over one year, as quantified by coronary CT angiography. The pre-specified primary endpoint was change in noncalcified plaque volume (NCPV). Contrary to the hypothesis that these elevations would not drive measurable plaque progression in this metabolically healthy cohort, we observed a median increase in NCPV of 18.9 mm³ (IQR 9.3–47.0 mm³), corresponding to a 42.8% relative change. The mean change was 31.5 mm³ (SD 31.5 mm³), reflecting substantial inter-individual heterogeneity. Most participants showed an increase in NCPV." That is how you discuss your primary endpoint. It’s not supposed to be a number on a chart (which was omitted anyway).