Dave

Sorry, your appeals to authority don’t work. I know Nick loves reminding us of his credentials and you seem to fall for it. Well my USMLE scores are higher than 98 percent of all doctors globally, so you should trust me? Right? What’s yours? Hint it’s probably much lower. Nobody needs to understand metabolism or cholesterol to understand what bad science looks like. It’s actually baffling that you’re even trying to defend a blatantly flawed and biased n = 1 “case study” that’s obscuring >90% of measurements. Even more baffling that you don’t seem to understand the difference between exposure and a measurement. Hint, a single measurement ≠ exposure, especially post hoc. I guarantee you any decent researcher who’s never read a paper on metabolism will do a better job appraising studies than you will, evidently. All good though. I’m learning this scientific pretentiousness is pretty ubiquitous on X. When the science don’t make sense, the incentives always do

29 out of 30 obese men claimed they ate ~2500 kcal while actually eating ~4000 kcal a day. They were off 37%, ~1500 kcal. Enough to lose 3 lbs per week. Even when they knew they were being watched, they still underreported almost 500 kcal per day. The first step to losing fat is facing the truth about your intake and tracking your calories. If you can't do that, everything else fails.

Response to Rebuttals on: "Seven Years of 700 Cholesterol Without Coronary Atherosclerosis". It’s been really interesting to watch the first 24-hour response to this new paper. The overwhelming majority has been, if not fully enthusiastic, at least curious. And I sincerely appreciate that. That said, some of the pushback has also been revealing… even comical. So let me address the most common retorts. ⏳1. “He’s too young.” Asked and answered. HoFH Children with similar LDL and ApoB levels can develop measurable plaque within the first few years of life and even heart attacks by age 8 or 10. Other people around my age, using similar imaging technology, also show measurable plaque. “He’s young” is not a good explanation. 🙄2. “You have a conflict of interest because you’re the patient.” LMAO! This one might be my favorite. What exactly did I do? Go into the CT scanner and suck in my plaque like I was sucking in my gut? Ask the AI algorithm, “Hey, I’m the patient — do me a solid?” If you think this is a rebuttal, I suggest you don’t join any debate teams. 🦓3. “He’s an outlier.” Yes. At a population level, I am an outlier. I don’t have obesity, prediabetes, or metabolic syndrome. But that’s one of the broader points: We have a paucity of data on the risks of elevated LDL in metabolically healthy people without underlying genetic lipid disorders. Outliers are not reasons to stop thinking. They’re opportunities to learn. 🤷‍♂️4. “It’s a fluke. He’s a one-off.” What a remarkably uncurious response. Imagine an oncologist had a patient with stage IV pancreatic cancer (~3% five-year survival rate). And that patient somehow cured himself, then went on to win the 100 meters at the Olympics 12 years later. Would the oncologist say: “Meh… What’s for lunch?” Of course not. A good scientist or doctor (or curious human) would ask: what happened here? 🧬5. “Oh, you probably just have protective genetics.” Oh, really? My father had a 99% occlusion of his left anterior descending artery at age 44. My Lp(a) runs between 100 and 194. And on top of that, I have a history of inflammatory bowel disease, a condition associated with chronic systemic inflammation. 🫀6. “But what about the Keto-CTA paper?” If you’re trying to beat this drum like it’s a trump card, I’d guarantee you’re stuck in an echo chamber and have incomplete information. It has now been clarified repeatedly that the original CLEERLY dataset published on April 7th was not reliable. CLEERLY had unblinded scans, anomalously results, and refused to perform a quality-control check. And multiple independent analyses have since shown that the KETO-CTA group do not appear to be a high-progression group. This is why we, the authors, took the initiative to retract the paper (NOT the study). The KETO-CTA Heartflow and QAngio data are available as a pre-print. And I’ve seen nobody legitimately try to defend the CLEERLY dataset. Also, the data show that LDL and ApoB did not predict plaque progression, and even at high LDL and ApoB levels, confirmed regression was observed. 👇 For supporters, feel free to link this the next time you see someone try to deploy these arguments. For critics, I suggest taking a read and thinking carefully… either to avoid falling onto the pyramid… or to avoid giving me reason to expand it.