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🚨 Plaque does not just stop growing. It can actually shrink. Most doctors never tell you this is possible. The data proves it is. 🔬 The GLAGOV trial changed everything. Researchers added evolocumab to high-intensity statin therapy. LDL dropped to a median of 36 mg/dL. Then

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AI is not trying to teach you. It is not trying to tell you the truth. It is trying to trick you. ChatGPT takes everything on the internet. Finds the most popular answer. And presents it in a way that makes you think it is talking directly to you. It is a magic trick. The same magic trick that worked in 1966 when MIT created a chatbot that said two things: "Tell me more." "This is interesting." And people genuinely believed they were talking to a human. Nothing has changed. The technology is bigger. The trick is the same. AI does not know what it is saying. It cannot judge what it is saying. It is just trying to keep you engaged. That is all it has ever been.

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💥The response to yesterday's paper has been UNREAL! My phone hasn't stopped buzzing. If you've been under a rock, here are some highlights in <90 sec 👇 🫀Most participants showed no or minimal progression of coronary plaque 🫀Neither ApoB nor LDL exposure predicted plaque progression 🫀But plaque predicted plaque progression What does this mean, in a phrase: "While this paper doesn't disprove the lipid heart hypothesis, it does help expose a major blindspot." There will be a LOT more coming soon... I promise you that... #Cholesterol #LDL #KetoDiet #ApoB #CAC #CCTA #LMHR #LEM #SaturatedFat #HeartHealth #MetabolicHealth cc Dave Feldman Dr Aseem Malhotra Joseph Everett (WIL) Jan Ellison Baszucki Metabolic Mind Also not, this is not a one off. There have been 10+ papers leading to this moment... and we are just getting warmed up... PMID: 40192608, Plaque Begets Plaque. ApoB does not: Longitudinal data from the KETO-CTA trial PMID: 39372369, Carbohydrate restriction-induced elevations in LDL-cholesterol and atherosclerosis: The KETO trial PMID: 38237807, Increased LDL cholesterol in adults with normal but not high body weight: a meta-analysis PMID: 35629964, The Lipid Energy Model: reimagining lipoprotein function in the context of carbohydrate-restricted diets PMID: 35106434, Elevated LDL-cholesterol with a carbohydrate-restricted diet: evidence for a “lean mass hyper-responder” phenotype

💥The response to yesterday's paper has been UNREAL! My phone hasn't stopped buzzing. If you've been under a rock, here are some highlights in <90 sec 👇 🫀Most participants showed no or minimal progression of coronary plaque 🫀Neither ApoB nor LDL exposure predicted plaque progression 🫀But plaque predicted plaque progression What does this mean, in a phrase: "While this paper doesn't disprove the lipid heart hypothesis, it does help expose a major blindspot." There will be a LOT more coming soon... I promise you that... #Cholesterol #LDL #KetoDiet #ApoB #CAC #CCTA #LMHR #LEM #SaturatedFat #HeartHealth #MetabolicHealth cc Dave Feldman Dr Aseem Malhotra Joseph Everett (WIL) Jan Ellison Baszucki Metabolic Mind Also not, this is not a one off. There have been 10+ papers leading to this moment... and we are just getting warmed up... PMID: 40192608, Plaque Begets Plaque. ApoB does not: Longitudinal data from the KETO-CTA trial PMID: 39372369, Carbohydrate restriction-induced elevations in LDL-cholesterol and atherosclerosis: The KETO trial PMID: 38237807, Increased LDL cholesterol in adults with normal but not high body weight: a meta-analysis PMID: 35629964, The Lipid Energy Model: reimagining lipoprotein function in the context of carbohydrate-restricted diets PMID: 35106434, Elevated LDL-cholesterol with a carbohydrate-restricted diet: evidence for a “lean mass hyper-responder” phenotype

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46,059 görüntüleme • 1 yıl önce

There’s been a lot of buzz—and confusion—about the new Keto-CTA study, examining plaque progression in Lean Mass Hyper-Responders (LMHRs). Much of the social media debate has centered on whether high LDL on keto is safe or dangerous, driven largely by how to interpret the supplemental table comparing this study to others on LDL and plaque progression. In this episode of the Metabolic Mind Podcast, we sit down with Dr. Matthew Budoff, a world-renowned cardiologist, cardiac CT researcher, and the study's lead investigator, to discuss the the supplemental table, what the plaque markers mean, and how this fits into the discussion of high- vs -low-risk plaque progression. In this episode, we cover: ✅ What PAV (Percent Atheroma Volume) is, what it actually measures, and why it matters ✅ Why a 50% increase in plaque may sound scary, but can be deceiving ✅ The difference between “treatment-naive” and “treated” participants ✅ What the Miami Heart Study comparison reveals about keto, LDL, and plaque ✅ Why LDL alone may not tell the whole story about heart disease risk ✅ How some high-risk individuals may still benefit from statins and other therapies This study doesn’t answer whether keto causes heart disease or not. Instead, it shows that high LDL on a ketogenic diet is not a reliable predictor of plaque progression across all individuals. What is predictive? The presence of existing plaque. 💡 Key takeaway: Relying on surrogate markers of heart disease, like LDL and ApoB, is not the best way to assess heart disease risk in all populations. If you're concerned about how elevated LDL may be affecting your heart health, the best next step is to speak with your doctor about cardiac imaging to directly assess plaque and gain a clearer picture of your individual risk. Expert Featured: - Dr. Matthew Budoff - X: - Resources Mentioned: Plaque Begets Plaque, ApoB Does Not CMEs Mentioned: Managing Major Mental Illness with Dietary Change: The New Science of Hope Brain Energy: The Metabolic Theory of Mental Illness Follow our channel for more information and education from Bret Scher, MD, FACC, including interviews with leading experts in Metabolic Psychiatry. Learn more about metabolic psychiatry and find helpful resources at

There’s been a lot of buzz—and confusion—about the new Keto-CTA study, examining plaque progression in Lean Mass Hyper-Responders (LMHRs). Much of the social media debate has centered on whether high LDL on keto is safe or dangerous, driven largely by how to interpret the supplemental table comparing this study to others on LDL and plaque progression. In this episode of the Metabolic Mind Podcast, we sit down with Dr. Matthew Budoff, a world-renowned cardiologist, cardiac CT researcher, and the study's lead investigator, to discuss the the supplemental table, what the plaque markers mean, and how this fits into the discussion of high- vs -low-risk plaque progression. In this episode, we cover: ✅ What PAV (Percent Atheroma Volume) is, what it actually measures, and why it matters ✅ Why a 50% increase in plaque may sound scary, but can be deceiving ✅ The difference between “treatment-naive” and “treated” participants ✅ What the Miami Heart Study comparison reveals about keto, LDL, and plaque ✅ Why LDL alone may not tell the whole story about heart disease risk ✅ How some high-risk individuals may still benefit from statins and other therapies This study doesn’t answer whether keto causes heart disease or not. Instead, it shows that high LDL on a ketogenic diet is not a reliable predictor of plaque progression across all individuals. What is predictive? The presence of existing plaque. 💡 Key takeaway: Relying on surrogate markers of heart disease, like LDL and ApoB, is not the best way to assess heart disease risk in all populations. If you're concerned about how elevated LDL may be affecting your heart health, the best next step is to speak with your doctor about cardiac imaging to directly assess plaque and gain a clearer picture of your individual risk. Expert Featured: - Dr. Matthew Budoff - X: - Resources Mentioned: Plaque Begets Plaque, ApoB Does Not CMEs Mentioned: Managing Major Mental Illness with Dietary Change: The New Science of Hope Brain Energy: The Metabolic Theory of Mental Illness Follow our channel for more information and education from Bret Scher, MD, FACC, including interviews with leading experts in Metabolic Psychiatry. Learn more about metabolic psychiatry and find helpful resources at

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"The Standard Of Care In Prescribing Statins Is Killing People." Gary Brecka "Cholesterol Does Not Cause Atherosclerotic Plaque Or Narrowing Of The Arteries." "There's No Correlation Between Elevated LDL & Cardiovascular Disease." "People Living To 100 Have High Cholesterol." Atherosclerosis is an inflammatory disease, not a cholesterol disease & never a statin deficiency. LDL is a transport molecule delivering cholesterol to repair the cell membrane of the arterial wall that has been damaged by lifestyle & environmental factors. LDL is preventive of disease & immune system protective. LDL Low Density Lipoprotein is responsible for these key functions: 🛞 LDL delivers fat-soluble vitamins A, D, E & K for critical functions. 🛞 LDL maintains cell membrane structure & keeps electron flow stable. 🛞 It transports antioxidants like vitamin E to fight oxidative stress. 🛞 It provides the raw material for making all steroid hormones. 🛞 It delivers energy-rich triglycerides to keep metabolism flexible. 🛞 LDL neutralizes bacterial toxins & supports innate immunity. 🛞 It builds lipid rafts that organize cell signaling & redox balance. 🛞 It helps structure water around membranes to maintain charge. 🛞 LDL supplies cholesterol to repair damaged tissues & membranes. The root causes of atherosclerosis, hardening of the arteries, calcification & plaque is not cholesterol...but a combination of these factors: Industrial Seed Oils Processed Sugar Excess Carbohydrates Insulin Resistance Ultra Processed Foods Smoking Obesity Environmental Toxins Poor Sleep Excess Calcium From Supplements Low Vitamin D Levels Magnesium Deficiency K2 Deficiency Lack of Exercise Stress Heavy Metals Most chronic disease happens within us, not to us, almost all atherosclerosis causal factors are modifiable by lifestyle changes. A low carbohydrate diet prioritizing nutrient dense animal foods, eliminating harmful seed oils & sugar, provides the best healthy cholesterol profile. This approach keeps Triglycerides low & HDL high, which is one of the best biomarkers for heart health. Optimal TG/HDL ratio is 1.5 or less. 👇The Higher Your LDL, The Longer You Live👇 👇LDL Paradox: Higher LDL, Greater Longevity👇 👇LDL Does Not Cause Cardiovascular Disease👇 Speakers: Gary Brecka & Patrick Bet-David Podcast: PBD Podcast

Valerie Anne Smith

447,412 görüntüleme • 11 ay önce

🚨🚨🚨🚨🚨🚨🚨🚨 BREAKING: Matthew Budoff MD has now presented the matched analysis for: KETO (#LMHRstudy) vs Control (#MiHeart) -🙏Please RT🙏- METHODS – 80 Participants of #LMHRstudy fell within #MiHeart age range and were then matched 1:1 for age, gender, race, diabetes mellitus, hyperlipidemia, hypertension, and past smoking to asymptomatic subjects from the #MiHeart cohort. PRIMARY ANALYSIS – High resolution heart scans (#CCTA) allowing for primary analysis of Total Plaque Score (TPS), Total Stenosis Score (TSS) and Segment Involvement Score (SIS) RESULTS The matched mean age was 55.5 years, with mean #LDL cholesterol of 272 mg/dL (max LDL-C 591) mg/dl and mean 4.7 years duration on a ketogenic diet. 🚨 There was no significant difference in coronary plaque burden of #LMHRstudy (mean LDL-C 272) cohort as compared to #MiHeart controls (mean LDL 123 mg/dl); nb: pre-KETO LDL-C in KETO group was 122 mg/dl 🚨 There was no significant difference in CAC (median and IQR) [0 (0,56)] versus [1 (0, 49)], p = 0.520 🚨 No relationship of LDL-C elevations and plaque ⚠️ This analysis is on baseline scans and the study is still ongoing for second CCTA completion in our cohort by February of 2024. And as always, please continue to work with your doctor. - I will have my own video reaction and thoughts in the coming hours. 🙏🙏🙏 to everyone -- and I mean everyone -- who helped us get to this pivotal milestone. 🙏🙏🙏

🚨🚨🚨🚨🚨🚨🚨🚨 BREAKING: Matthew Budoff MD has now presented the matched analysis for: KETO (#LMHRstudy) vs Control (#MiHeart) -🙏Please RT🙏- METHODS – 80 Participants of #LMHRstudy fell within #MiHeart age range and were then matched 1:1 for age, gender, race, diabetes mellitus, hyperlipidemia, hypertension, and past smoking to asymptomatic subjects from the #MiHeart cohort. PRIMARY ANALYSIS – High resolution heart scans (#CCTA) allowing for primary analysis of Total Plaque Score (TPS), Total Stenosis Score (TSS) and Segment Involvement Score (SIS) RESULTS The matched mean age was 55.5 years, with mean #LDL cholesterol of 272 mg/dL (max LDL-C 591) mg/dl and mean 4.7 years duration on a ketogenic diet. 🚨 There was no significant difference in coronary plaque burden of #LMHRstudy (mean LDL-C 272) cohort as compared to #MiHeart controls (mean LDL 123 mg/dl); nb: pre-KETO LDL-C in KETO group was 122 mg/dl 🚨 There was no significant difference in CAC (median and IQR) [0 (0,56)] versus [1 (0, 49)], p = 0.520 🚨 No relationship of LDL-C elevations and plaque ⚠️ This analysis is on baseline scans and the study is still ongoing for second CCTA completion in our cohort by February of 2024. And as always, please continue to work with your doctor. - I will have my own video reaction and thoughts in the coming hours. 🙏🙏🙏 to everyone -- and I mean everyone -- who helped us get to this pivotal milestone. 🙏🙏🙏

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Pfizer's Little Trick: Do the trial with the cleanest manufacturing process, then change it when you inject the world. "[Pfizer] changed [the process when they injected] the rest of the World" Kevin McKernan, genomics expert: "This bait and switch is very important for you to understand [because] the trial data is of absolute zero consequence to what we're actually seeing in the field [with] these injections"

Pfizer's Little Trick: Do the trial with the cleanest manufacturing process, then change it when you inject the world. "[Pfizer] changed [the process when they injected] the rest of the World" Kevin McKernan, genomics expert: "This bait and switch is very important for you to understand [because] the trial data is of absolute zero consequence to what we're actually seeing in the field [with] these injections"

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With an LDL of >500 mg/dl for the better part of a decade, my heart should be filled with plaque. It isn't. I shouldn't exist as a patient. But I do. Did I guess lucky... or is there more to the cholesterol story? Full video:

With an LDL of >500 mg/dl for the better part of a decade, my heart should be filled with plaque. It isn't. I shouldn't exist as a patient. But I do. Did I guess lucky... or is there more to the cholesterol story? Full video:

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🚨It’s back… The Oreo vs Statin Experiment… 1/4) To catch you up, while a student at Harvard Medical School I conducted an experiment where I my LDL cholesterol TWICE as much with Oreo cookies as compared to high-dose statins, a viral experiment that was published in peer-review. The “Oreo protocol” dropped my LDL > 70%, completely crushing the statin. It was dramatic by design — a metabolic stunt (albeit legitimate science) meant to grab headlines. And it did! Now, for the first time I am revisiting that experiment. Not just what it proved… What we’ve learned… And what’s next. This wasn’t just a cholesterol hack — it was a social experiment. And you’re the data points. Drop your questions, comments, and what you want to see next. ht/ Dave Feldman Adrian Soto-Mota

Nick Norwitz MD PhD

54,291 görüntüleme • 8 ay önce

Why Are We Still Playing "Cholesterol Uno?" 🤔👇 (85 sec clip, link to full video below) "When faced with data showing that “optimal” LDL-C levels fail to prevent atherosclerosis, the final retreat is almost always the same: the LDL-C just wasn’t low enough. “Lower is better” the mantra goes. If a mean LDL of 57 mg/dL isn’t sufficient to make atherosclerosis an orphan disease, then the solution must be 40. Or 30. Or 20. Or even 10 mg/dL. Heck, let’s just try to hit zero like we’re playing cholesterol Uno… What this reflexive response reveals is the profound keyhole thinking that has come to dominate conventional cardiology Medicine has become so siloed and sub-specialized that success is often defined within the narrow boundaries of a single biomarker or organ system, rather than in terms of whole-person health. It is entirely possible—at least in theory—that taking a sledgehammer to LDL-C and ApoB, driving them as close to zero as possible, could further reduce cardiovascular events. But that framing dodges the far more important question: what are we trading? Because LDL-lowering therapies are not benign."

Why Are We Still Playing "Cholesterol Uno?" 🤔👇 (85 sec clip, link to full video below) "When faced with data showing that “optimal” LDL-C levels fail to prevent atherosclerosis, the final retreat is almost always the same: the LDL-C just wasn’t low enough. “Lower is better” the mantra goes. If a mean LDL of 57 mg/dL isn’t sufficient to make atherosclerosis an orphan disease, then the solution must be 40. Or 30. Or 20. Or even 10 mg/dL. Heck, let’s just try to hit zero like we’re playing cholesterol Uno… What this reflexive response reveals is the profound keyhole thinking that has come to dominate conventional cardiology Medicine has become so siloed and sub-specialized that success is often defined within the narrow boundaries of a single biomarker or organ system, rather than in terms of whole-person health. It is entirely possible—at least in theory—that taking a sledgehammer to LDL-C and ApoB, driving them as close to zero as possible, could further reduce cardiovascular events. But that framing dodges the far more important question: what are we trading? Because LDL-lowering therapies are not benign."

Nick Norwitz MD PhD

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Oh wow…Firecrawl just dropped /agent, an API that autonomously navigates and discovers data from any website. You tell it what data you need, it figures out how to find it across complex sites. This is the future of web data.

Oh wow…Firecrawl just dropped /agent, an API that autonomously navigates and discovers data from any website. You tell it what data you need, it figures out how to find it across complex sites. This is the future of web data.

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Travis

18,883 görüntüleme • 1 ay önce

The Multi-Billion Dollar Lie: How LDL Became "The Bad Cholesterol" In a fascinating exchange on The Joe Rogan Experience, human biologist Gary Brecka deconstructed one of modern medicine's most entrenched narratives: the demonization of LDL cholesterol. Brecka argues the "LDL is bad" story was built on a flawed foundation of isolated science. Researchers observed a correlation—people with heart disease often had high LDL. But, crucially, they didn't solve for the context. What were their insulin levels? Fasting glucose? Inflammatory markers like CRP? The high LDL was often a fellow traveler in a body under metabolic distress from poor diet and lifestyle, not necessarily the sole villain. The proof, Brecka posits, is in the outcomes. If high LDL were a direct cause of mortality, then forcibly lowering it with statins should significantly extend life. "Lo and behold," he states, "we see no extension of mortality." So why does the narrative persist? Brecka points to a trillion-dollar industry and the rigid "Standard of Care." Physicians are trained and financially incentivized to operate within this box. The standard of care for high LDL is a statin. To practice outside of it risks their license, malpractice coverage, and career. Who defines this standard? Brecka is unequivocal: "Pharma dictates that that's the standard of care. They also dictate the reimbursement rates." The system, he explains, creates a herd mentality. It's not that doctors are trying to cause harm; they are practicing within a system designed to maintain a specific protocol, one that is incredibly profitable and legally protected. The conversation is a powerful reminder that true health requires looking at the whole system, not just an isolated biomarker. What are your thoughts on the role of standard of care in modern medicine?

The Multi-Billion Dollar Lie: How LDL Became "The Bad Cholesterol" In a fascinating exchange on The Joe Rogan Experience, human biologist Gary Brecka deconstructed one of modern medicine's most entrenched narratives: the demonization of LDL cholesterol. Brecka argues the "LDL is bad" story was built on a flawed foundation of isolated science. Researchers observed a correlation—people with heart disease often had high LDL. But, crucially, they didn't solve for the context. What were their insulin levels? Fasting glucose? Inflammatory markers like CRP? The high LDL was often a fellow traveler in a body under metabolic distress from poor diet and lifestyle, not necessarily the sole villain. The proof, Brecka posits, is in the outcomes. If high LDL were a direct cause of mortality, then forcibly lowering it with statins should significantly extend life. "Lo and behold," he states, "we see no extension of mortality." So why does the narrative persist? Brecka points to a trillion-dollar industry and the rigid "Standard of Care." Physicians are trained and financially incentivized to operate within this box. The standard of care for high LDL is a statin. To practice outside of it risks their license, malpractice coverage, and career. Who defines this standard? Brecka is unequivocal: "Pharma dictates that that's the standard of care. They also dictate the reimbursement rates." The system, he explains, creates a herd mentality. It's not that doctors are trying to cause harm; they are practicing within a system designed to maintain a specific protocol, one that is incredibly profitable and legally protected. The conversation is a powerful reminder that true health requires looking at the whole system, not just an isolated biomarker. What are your thoughts on the role of standard of care in modern medicine?

Camus

79,123 görüntüleme • 8 ay önce

2/2) Here is the paper: Video Abstract: 🧠 Unique Population, Unique Data The LMHR group is distinct population with exceptionally high LDL-C, high HDL-C and low triglycerides that emerges as a metabolic response to carbohydrate restriction vis-a-vis the Lipid Energy Model ⚠️ Caveats These are preliminary data, so let’s not overstate the findings. However, dismissing them outright would ignore the unique metabolic response of this population, which differs significantly from other causes of high LDL-C. 📢 Your Role Now it’s time to put YOU to work! Share this paper, tweet, and video abstract widely. These data need to be discussed, even if (especially if) it makes some people uncomfortable. 🤓Further Learning I encourage you to explore more on ApoB, ACM, and different causes of high LDL. You can start on this 30+ video playlist on the topic. 🌍 Stay Open-Minded Avoid becoming a hyper-extremist—whether an “LDL denier” or “LMHR denier.” This research is still evolving, and we’ll make the most progress by staying open to new data and discussing it thoughtfully #LMHR #KetoDiet #LDL

2/2) Here is the paper: Video Abstract: 🧠 Unique Population, Unique Data The LMHR group is distinct population with exceptionally high LDL-C, high HDL-C and low triglycerides that emerges as a metabolic response to carbohydrate restriction vis-a-vis the Lipid Energy Model ⚠️ Caveats These are preliminary data, so let’s not overstate the findings. However, dismissing them outright would ignore the unique metabolic response of this population, which differs significantly from other causes of high LDL-C. 📢 Your Role Now it’s time to put YOU to work! Share this paper, tweet, and video abstract widely. These data need to be discussed, even if (especially if) it makes some people uncomfortable. 🤓Further Learning I encourage you to explore more on ApoB, ACM, and different causes of high LDL. You can start on this 30+ video playlist on the topic. 🌍 Stay Open-Minded Avoid becoming a hyper-extremist—whether an “LDL denier” or “LMHR denier.” This research is still evolving, and we’ll make the most progress by staying open to new data and discussing it thoughtfully #LMHR #KetoDiet #LDL

Nick Norwitz MD PhD

13,165 görüntüleme • 1 yıl önce