RaiderOS

@MohammedAlo @AmmousMD @MohammedAlo Are these guys trolling? Or just that dense? I don’t get it

The fact the you cite Uffe Rasnakov is laughable. Do you not understand the irony? That's an opinion piece by the way, in case you didn't know. He's a known cholesterol conspiracy theorist that made up his own studies to sell books. Welcome to the 2016 cholesterol denier grift. (Just so you know, the major Griftologists have moved past Uffe Rasnakov now.)

Have you read a textbook or study in the last 100 years? Point to one single study that shows harm from statins? When you look at every study ever done on statins, they consistently show a reduction in all cause morality, not just CV outcomes and events.

@Rholm22 How did Roger’s do.

Good to see the rookies play today. Caleb Rogers played entire game at RG, Darien Porter started and played roughly 3 quarters after injury to Kelly, Jack Bech led team with 6 catches on 6 targets, Tonka Hemingway recorded a sack. #RaiderNation

@SBakerMD The only people that think this are those who want to be blind to the results. The results show they are a high risk cohort until proven otherwise. It’s concerning. Don’t hurt people with your bias. You lose all credibility if you say differently.

Biggest takeaway of the Keto-CTA study is that a control group is sorely needed! Any other conclusions are largely worthless imo

@ryan_uhhh @realDaveFeldman @nicknorwitz But We just had an actual, “study,” showing the opposite. That it does affect keto and carnivore. Significantly. The topic of this post. A single person eating Oreos doesn’t change the results of this study.

@Raider_OS @realDaveFeldman You should look into the Oreo study done by @nicknorwitz , cholesterol doesn’t matter on keto/carnivore - you can eat as much fat as you want

Alas, I have to correct myself. Deleting original tweet, but posting here for posterity. I originally stated if looking at "Δ%NCPV between Cleerly scans suggests it's a high risk cohort" -- assuming we could indeed look only at the rate alone as allowable, but I've not been able to make that work, even with the AI for neutral weigh in... My prompt: Give a brief summary of the quantitative data of our table, how it compares to other studies, and give an overall assessment of its risk level as a cohort. #ChatGPT: Summary of Quantitative CCTA Data from Keto-CTA (V1 vs V2) 1. Metrics Reviewed Non-Calcified Plaque Volume (NCPV) Total Calcified Plaque Volume (TCPV) Percent Atheroma Volume (PAV) 2. Summary Statistics (One-Year Interval) MetricV1 Median (IQR)V2 Median (IQR)Median Δ (1-year)NCPV (mm³)44.05 (±86.78)66.00 (±137.93)+21.95TCPV (mm³)0.30 (±19.78)0.95 (±24.22)+0.65PAV0.02 (±0.04)0.03 (±0.06)+0.01 Note: All three metrics show an upward shift over the year, especially for NCPV, but the absolute magnitudes are small in comparison to higher-risk cohorts. 3. Comparison to Other Studies NCPV: The Miami Heart study reported 47.1 mm³ median NCPV at follow-up (4.7 years) in a matched low-risk cohort — almost identical to V2 in this cohort (66 mm³ median at just 1 year). Most high-risk populations in statin trials show annual NCPV increases of 10–20 mm³ despite lipid-lowering. Keto-CTA cohort shows a comparable increase over just one year without lipid-lowering, though with high inter-individual variability. TCPV: Low at baseline and follow-up, suggesting minimal calcification burden. Values are significantly lower than in cohorts with advanced atherosclerosis or aging populations. PAV: Rarely reported in low-risk populations due to scan complexity. In trials like GLAGOV and REVERSAL, PAV changes of 0.5–1.0% were linked to clinical significance. The +0.01 median increase in this cohort is orders of magnitude lower, reinforcing low global burden. 4. Overall Risk Assessment The plaque volume levels are low to moderate, but non-zero progression is observed, particularly in NCPV. Calcified burden remains negligible, aligning with the semi-quantitative CAC=0 results. PAV increase is extremely modest, suggesting only minor overall vessel wall burden increase. Risk implications: By traditional volume metrics, this cohort still profiles as low risk — especially given low TCPV and minimal PAV. However, the significant individual variability and measurable NCPV growth hint at possible early-stage activity in a subset. The disconnect between low CAC/TPS and higher NCPV suggests that relying solely on semi-quantitative scores may underestimate risk in metabolically unique populations like this. Via #Grok: (... Skipping to conclusion): The KETO-CTA cohort exhibits a low-risk profile with predominantly zero TPS and CAC scores, comparable to asymptomatic, low-risk populations in MESA and SCAPIS. The slight increase in TPS and CAC over one year indicates minimal plaque progression, consistent with stable, early atherosclerosis. A small subset with CAC >100 or TPS >3 is at moderate to high risk, warranting targeted interventions. Semi-quantitative measures align with prior studies but may underestimate non-calcified plaque, emphasizing the value of quantitative CCTA analysis (e.g., Cleerly AI). The cohort’s risk level supports conservative management for most, with intensified strategies for the minority with higher scores.

This generation's greatest defender

@JerryEngelmann Great video.

A video of Draymond's defense in game 3 He was especially great in the 4th quarter

@DrNadolsky @bohdyone @realDaveFeldman @MurseDarius What a Clown show. They just won’t admit it either.

There was major contention on not including those with a history of coronary artery calcium. I was vetoed despite the PI agreeing with me, but he didn’t care enough to force the change. Then there was major contention on the ethics behind using the baseline preliminary data to recruit more people and promote this phenotype as being benign. After speaking with a few dozen extremely brilliant researchers and scientists on the behind the scenes, it was unanimous that I should leave as this would be a train wreck that we see now. That’s the gist.

I sat down for an interview with @MurseDarius. His questions were tough but fair. We openly discussed several missteps in the rollout of the recent Keto-CTA longitudinal paper from April 7th: - The numeric Δ%NCPV should've been clearly presented. - Our social media coordination needed improvement. - Our handling of the formal journal process could’ve been stronger. As I emphasized in our conversation, I've spearheaded this project, and ultimately, the buck stops with me. My sincere apologies for any confusion caused—we've learned a lot as a team, and we're committed to doing better going forward. In the interview, I also explain why social media engagement will be quieter in the coming days as we carefully address Letters to the Editor through JACC Advances. My genuine thanks to both supporters and critics—often one and the same. Moments like these are humbling, but ultimately, they strengthen our science and reinforce our commitments moving forward. There's much more ahead, and I remain optimistic about what we'll discover together. youtu.be/xP0jK39yHds

@DoctorTro You sound insane. Calm down. Eat a carb

Let’s see how quickly you walk this back You will likely request more time so you can “study up” So let’s do it RIGHT NOW happy to demonstrate that you won’t do it

I’m happy to do it right now

@dr__idz Do it @DoctorTro But we know you won’t.

Alright then, seeing as though you’re so highly experienced in research and nutrition and know far more than myself, let’s do a live IG debate on your interpretation of the KETO CTA study and what it means for the general population. You’re so confident behind a keyboard let’s see what happens in an actual debate for all to see.

@dr__idz Great post.

🚨 Tro is moving the goalpost and manipulating study results to affirm his low carb bias - the exact same thing the KETO CTA study authors are doing. 🚨 1. Moving the goalpost = The primary outcome of interest is not PAV change. It’s NCPV (as per their own study protocol and it was the main point of our commentary letter. The NCPV increase after 1 year was 18.8mm^3 for the KETO dieters. That’s almost a 4x INCREASE in plaque for their PRIMARY outcome vs other healthy cohorts (e.g. NATURE CT study)❗️🤦🏽‍♂️ 2. The reason NCPV is more appropriate in this context is because statins tend to increase the amount of calcified plaque (to help stabilise it), thus changing the composition of plaque to be more protective. Using PAV is inappropriate in this context as it includes both calcified and non calcified plaque - people on statins may still increase PAV even if non-calcified plaque volume hasn’t increased much. This is backed by the PARADIGM cohort itself (PMID: 30789215); “However, under the effect of statins, CACS progression indicates only calcified PV progression, but not non-calcified PV progression.” When we look at the PRIMARY OUTCOME, the data is not good for these keto dieters.❗️ 3. You keep bringing up the nonsensical point of: “why didn’t they find a correlation between their LDL and plaque progression?” As we explained in the commentary letter —> in order to detect a robust dose response relationship, you need sufficient variability in exposure = analyse those with high LDL vs those with low LDL.❗️You need a large enough exposure contrast. Checking for an association between LDL and plaque progression when everyone has high LDL is a meaningless analysis without a low exposure group. It’s like assessing if skin wrinkles is associated with age, but the only age brackets you’re testing are those who are aged 70-85 years old 🤦🏽‍♂️ 4. Even if you want to hang your hat on a made up outcome (Percent Atheroma Volume) that wasn’t mentioned in the protocol as being an outcome of interest 🤔 —> the low risk group in PARADIGM were still overweight on average (BMI 24.9), had more hypertension (40ish%), diabetes, smoking, largely inactive and 70% had atypical chest pain - so if your argument is now that “metabolically healthy” fit and lean Keto dieters who have a CAC score of 0 at baseline, with no other risk factors for CVD other than high LDL/ApoB —> progress plaque at the same rate as metabolically unhealthy, hypertensive, diabetic and overweight medicated smokers following a generally unhealthy diet —> then it’s not looking good bruv. ❗️What you’re saying is the healthiest keto dieters with high LDL gain plaque at the same rates as your average overweight hypertensive Joe… And you think LDL is not an issue? Sorry you can’t be this stupid. 🥴 5. When you look at PAV change across the entire KETO cohort (0.8% increase), that’s HIGHER than the HIGH risk group in PARADIGM (most were overweight, 70% were hypertensive, 50% had diabetes and 32% were smokers).❗️ You’re doing the same thing these researchers tried to do @realDaveFeldman @nicknorwitz - change the narrative, avoid the primary outcome of interest and spin very alarming study results to suit your low carb bias. But quite frankly you failed just as catastrophically as them. 💀 No matter how you try and frame it, no matter what insults you use, you remain out of your research interpretation depth and facts remain facts = 🚨These “metabolically healthy” lean keto dieters increase their plaque at similar or faster rates than metabolically unhealthy cohorts and MUCH faster than healthy cohorts.🚨 @drgarymcgowan @Richie_Kirwan @PatrickElliott0 @DrNadolsky @drmatthewnagra

@MohammedAlo @SBakerMD I’m guessing he won’t respond to this

@SBakerMD How about when we compare it to studies using the same CT scan technology (Cleerly)? Looks even worse for LMHR.

To all of the critiques of the Keto-CTA study that compare it to other trials, claiming the results were worse - it may be a shock to you to find out that different CT scanners and different software systems can make huge difference in results What needs to happen (and I believe it is being planned) is to have a comparison groups using the exact same measurement protocols on exact same machines

@SBakerMD You are hurting people. And I can’t tell if you are doing it to push your narrative or if you have difficulty comprehending outcomes from studies .

Not based on this study, but one could make the argument that LMHR is as effective as a statin for limiting progression based on PAV changes for some individuals

@upRootNutrition Would love to see it.

I might have to put my systematic Norwitz debunk on the backburner to tackle this paper, haha. My god. 🤣

@benjamincowen Give the man his flowers !

After all these years, #ETH has finally entered into the lower logarithmic regression trend line 🥲

@toreroromero @SuiNetwork Can someone genuinely explain to me what people are buying and swapping on sui? How is the volume so high yet memes etc aren’t moving ? Thanks in advance.

$SUI token surpasses $315 billion in total swap volume, up 16.43% in the past 30 days.

@eclipse_L1 Is there any information on what ThorFi Node holders will get on this move to eclipse?

We're ONLY 5 days away from the biggest upgrade! 📅 #Avalanche9000 is unlocking the future of #Web3gaming, and Eclipse Gaming L1 is leading the charge. With dedicated L1s, Eclipse offers developers a scalable, low-latency chain tailored for immersive gameplay. Gamers benefit from seamless cross-chain asset transfers and game discoverability through tools like Eclipse Deck. This interoperability, combined with streamlined onboarding powered by Avalanche9000’s upgrades, lowers barriers for developers to create and scale their games effortlessly. Meanwhile, tools like GameLoop and Capsule are transforming the player economy with instant transactions and thriving in-game marketplaces. This isn’t just an upgrade—it’s the foundation for the next generation of gaming experiences. 🚀 #AVAX

@GraphkRaider Do you have a Link ?

Schedule set let’s run it 😤 #RaiderNation

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@De_pedro_1 @ItsShinybob @AliensOnInj @ToxicAliensINJ Any idea on utility of this token?