Dr Chris Huff

I want to make explicit the absurdity of this pivot from Norwitz: He is using a subset of 8 Cleerly scan pairs (setting aside the preposterous level of clinical research violations this involves) to argue that the original 100 pairs, which were burdened by unmanageable levels of intra-assay variance, were invalid. The same test. With less power. But now, since they see less progression, it’s exonerating. The only appropriate consideration left was to say the methodology was invalid and retract. Put together a new analysis with heartflow or Qangio if you want, but claiming this is exonerating is absurd. If you had any doubt remaining that this is an exercise of narrative building, you need not have it anymore.

@ifixhearts Cardiovascular disease is complex and multi factorial, but to answer your question, I suspect it’s mainly due to your poor understanding of lipidology and what is normal.

@jimmy_muthami @SamaHoole If this is your take away from the keto-cta trial, you need help with interpretation of scientific research.

@hufcm @SamaHoole There was, the keto-cta study that showed some people with sky high LDL levels showing plaque regression, the direct opposite of the LDL hypothesis. LDL didn't also predict the levels of plaque, as the lipid hypothesis states.

LDL goes up on carnivore because you're burning body fat. LDL transports fat. More fat burning = more LDL transport vehicles. It's not pathological. It's physiological. But we've medicalised a normal metabolic process because the number looks scary on paper.

@SamaHoole Replace glucose with cholesterol and your statements are fact.

Glucose is an essential molecule in the human body. Glucose is not an essential nutrient in the human diet. This is a huge distinction. The body has no issues creating all of its own glucose as long you support it with enough dietary fat.

@DrSuneelDhand I’m beginning to think this is a parody account.

I will never understand why people spend thousands on Ozempic when they could just do intermittent fasting for free and have way more health benefits

@DoctorTro You ate too much of it.

@drozcanyucel @drgarymcgowan “Certainly not”…that’s bold, especially given the overwhelming RCT data that says otherwise.

I have personally witnessed 35 of the last 40 years you mentioned. The decline in deaths from heart disease is certainly not due to cholesterol-lowering drugs. The most important reason is the widespread adoption and advancement of interventional cardiology! Elevated LDL itself does not cause deaths.

Statins are not miraculous, but they do reduce risk of CVD death, particularly in those at high risk. “Near universal prescription” is just made-up. LDL is one risk factor among others which remain widespread. Deaths from CVD have ⬇️ in the last 40yrs.

@drgarymcgowan @drozcanyucel 💯

@drozcanyucel I didn’t claim it was relate to cholesterol-lowering drugs, but that is absolutely part of it. You cannot be certain that these medications have not played a role. That is false. It’s a combination of PCI, meds, smoking cessation, BP control, cholesterol-lowering, and other.

@drgarymcgowan Also, given that the initial diagnosis of CAD is often in the setting of acute MI, many of these deaths occur pre-statin. Lipid lowering therapy has resulted in a profound reduction in secondary events.

@drgarymcgowan In metabolic dysfunction, the LDL particles carry more fat and less cholesterol. So while LDL-c is lower, the LDL particle number is still high.

LDL-ApoB discordance ⚖️ ➡️ most pronounced in metabolically unhealthy obesity ➡️ metabolic dysfunction, more than obesity, drives increased apoB–LDL-C discordance lipidjournal.com/article/S1933-…

@sguyenet @DrSuneelDhand Have you review his other posts? Just one of many idiotic takes.

@DrSuneelDhand This has got to be one of the dumbest opinions I've seen expressed by an MD on X. There are literally hundreds of placebo-controlled randomized trials showing that many common drugs, including GLP-1s, reduce the rate of the targeted illness.

LOL What a tool. No pharmaceutical product in history has ever resulted in lower rates of the illness or fewer prescriptions of said product

@drgarymcgowan High SFA intake also increases hepatic de novo lipogenesis. Double whammy.

Saturated Fat & LDL-Cholesterol: How Does LDLc ⬆️?! - When comparing high vs low SFA diets, LDLc is reduced in the low SFA condition - High SFA intake suppresses LDL-receptor (LDLr) expression - ⬇️ LDLr = reduced clearance of LDL particles (+ ⬇️LDLc) pubmed.ncbi.nlm.nih.gov/9101427/

@DrPlantel Master grifter Mark Hyman…and people eat it up.

No, Mark. People aren’t tired from “poor methylation.” They’re tired from busting their a$$ day in, day out. They’re tired from working nonstop, raising kids, caring for everyone else, and doing it all with barely any time or resources to take care of themselves. No supplement from your website will fix that.

@drgarymcgowan Yep. All hard facts.

5 uncontroversial facts: 1.) Cristiano Ronaldo is the GOAT. 2.) LDL-C causes atherosclerosis. 3.) Vaccines saved millions of lives. 4.) Pepsi Max over Coke Zero all day. 5.) Obesity is a major cause of chronic disease. We all agree, right?

Are you a clown? 🤡 If you think a median NCPV change of 18.8mm³ over one year qualifies as "no or minimal" plaque progression, you might be a clown. If you think that "plaque begets plaque" is an insightful statement, you might be a clown. If you think that self-applying a label that includes the word 'hyper" gives you superpowers, you might be a clown. If you think it's reasonable to convert continuous variables to discrete categories without scientific justification, you might be a clown. If you think that underpowered exploratory analyses should be the centerpiece of your publication, you might be a clown. If you think that reporting your primary outcome in a tweet is a hallmark of scientific rigour, you might be a clown. If you think that it isn't misleading for researchers to report their prospective cohort study as a trial, you might be a clown. If you think that repeatedly shouting "heterogeneity" turns shitty results into good results, you might be a clown. If you think it's reasonable to tell people to count pixels to extract your primary endpoint, you might be a clown. If you think an underpowered secondary analysis of 100 butter-chuggers upends 70+ years of medical science, you might be a clown. If you think it's reasonable for a senior author to publicly throw their co-authors under the bus with a bunch of lies, you might be a clown. If you think that purveying hallucinated models of metabolism will save you from an atherogenic lifestyle, you might be a clown. If you think that repeatedly using the taglines "stay curious" and "cautiously optimistic" will make your lack of scientific integrity any less obvious to the world, you might be a clown.

@professionaldog Yep. He and the Boetcher brothers are the ultimate grifters. Anti science garbage playing on emotion and conspiracy to fuel their income.

James is a classic grifter Puts forward a view based on beliefs then refuses to change mind based on much harder data because it doesn't fit his bias.

Nick fails to address the best criticisms post the publishing of his keto ‘trial’. The fact is approx 95/100 participants had plaque progression with a large % of these having much more rapid progression than observed in truly healthy subjects. Are there a few outliers… sure - like anything there are outliers (likely explained by genetics). But overall this data suggests LMHRs as a group are not a metabolically healthy low risk cohort. I suggest Nick responds to the below LTE including the ApoB part. osf.io/preprints/osf/…

I used the same prompt (ChatGPT o3), and it reported the following (note I am not suggesting that we base conclusions on which AI tool is right lol): "Key quantitative take-aways from your table ( n = 100, 1-year follow-up): Incidence of progression: 93 % had any PAV increase; 43 % met the widely-used “rapid progression” definition of ≥1 % PAV/year; 7 % converted from no visible plaque to new plaque within a year. How this compares with other cohorts: Bottom line: the LMHR ketogenic cohort is experiencing ≈ 3–6 × faster plaque growth than seen in most observational registries of comparable age, and a far higher proportion meet the “rapid progression” threshold. Overall cardiovascular-risk assessment for the cohort: Traditional risk markers: LDL-C ≥ 190 mg/dL and ApoB > 120 mg/dL (values reported for this study) place individuals in a “severe hypercholesterolaemia” category that guidelines already treat as high ASCVD risk, independent of imaging. Imaging findings: Median CAC = 0 suggests low short-term (5-year) event risk, yet the presence and rapid expansion of non-calcified plaque is worrisome because NCP is the most rupture-prone subtype. A 1 percentage-point rise in PAV per year is itself linked to higher event rates; 43 % of participants exceed that. Predictors within the cohort: Consistent with the 2025 JACC paper, baseline plaque—not LDL or ApoB—best predicts further growth (“plaque begets plaque”). Nevertheless, the whole group’s very high ApoB exposure remains biologically atherogenic, even if intra-group variance doesn’t explain progression. Integrated view: Although these lean, insulin-sensitive ketogenic dieters start with little calcification, the speed and composition of plaque progression point to at least a moderate-to-high future ASCVD risk if the current trajectory continues. Close follow-up (repeat CCTA or CAC at ≤2-year intervals), aggressive LDL-lowering therapy, and shared-decision making around diet/lipid management are advisable."

@drgarymcgowan @Drlipid 🤦‍♂️

Message from concerned man in his 30s w/ LDL-C 234 mg/dL (>99th %) His bro & mom have similar LDL-C, ?FH. Started statins but doubted & stopped, his doc says he doesn’t need meds as he is young and healthy. Why are we still waiting for disease? #PreventionFirst @Drlipid