I'm a LMHR (LDL 221, HDL 84, TG 41). Exercise 2 hours a day. OMAD (low carb wholefood omnivore). Reversed over a decade of pre-diabetes, hypertension, sleep apnea and other chronic diseases (while on statins and other prescription drugs, LDL 80)... Thank you Dave for opening my eyes. I quit all prescription drugs (cold turkey) 4 years ago. I've never felt better in my life.
Amazing. I have almost the exact same numbers. 221 LDL, 85HDL, 58 Trigs. I'm 52. I run 3-5 miles per day, 13% bodyfat. My Dr hates it. He said with my LDL alone, no other risk markers, I have a 50% chance (yes 50% chance) of a heart attack in the next 10 year's, if I don't start statins immediately...
@@chrissypearson5597 Peter Attia was on Keto for a few years then stopped. He was into fasting for a few years then stopped. If you don't like his opinion now, check back in a few years... Now he's in the camp of dropping LDL as much as possible. He's on PCSK9 inhibitor drug. He seems to have developed some fondness recently toward big pharmas. I do enjoy Peter's podcasts but take what he said with a grain of salt.
I gave chatGPT the transcrypt of this video to sumerize it: _________________________________ The video uses an analogy to explain complex aspects of cholesterol metabolism, particularly focusing on Apolipoprotein B (apoB) and its relation to Lean Mass Hyperresponders (LMHR) in the context of a ketogenic diet. Here's a summary of the key points from the transcript: Pizza Box Analogy: LDL particles are likened to empty pizza boxes. In a neighborhood (the body), after a pizza party (food consumption), empty boxes (LDL particles) accumulate. Some houses (cells) fail to recycle these boxes properly, leading to a pile-up. ApoB and Lipoproteins: All lipoproteins from the liver contain one copy of apoB. These include Very Low-Density Lipoproteins (VLDL), which are triglyceride-rich, and Low-Density Lipoproteins (LDL), which are triglyceride-poor. Metabolism of Lipoproteins: Under normal conditions, VLDL delivers triglycerides to cells, then shrinks to Intermediate-Density Lipoprotein (IDL), and eventually to LDL. LDL remains in circulation longer (2-4 days). Issues with Triglyceride Clearance: If cells don't accept triglycerides efficiently (e.g., due to insulin resistance), triglyceride-rich lipoproteins stay in circulation longer. This increases overall apoB levels and leads to higher triglyceride levels. Lean Mass Hyperresponders: On a ketogenic diet, some individuals experience a significant increase in LDL and apoB levels. The hypothesis is that their cells are highly efficient at utilizing triglycerides, leaving more "empty pizza boxes" (LDL particles) but very low triglycerides in the blood. Comparing this to current knowledge: ApoB as a Marker: ApoB is a recognized marker for cardiovascular risk, as each apoB-containing lipoprotein particle is potentially atherogenic. LDL and Cardiovascular Risk: High levels of LDL cholesterol are traditionally linked with an increased risk of heart disease. However, the analogy suggests that the context (e.g., presence of triglycerides, insulin resistance) matters. Ketogenic Diet and Cholesterol: It's known that ketogenic diets can significantly alter lipid profiles, often increasing LDL cholesterol. The LMHR phenomenon aligns with this, though the long-term cardiovascular implications are not fully understood. Triglyceride Metabolism: The emphasis on triglyceride-rich lipoproteins and their clearance is in line with current understanding. Poor clearance (due to insulin resistance or other factors) is associated with cardiovascular risk. ____________________________ I then asked it if and how this disagrees with current consensus on cholesterol metabolism: ____________________________ Points of Disagreement: Impact of LDL Levels: The video's theory that high LDL may not be uniformly detrimental in all contexts (like in LMHRs) is a significant departure from the consensus that high LDL is generally a risk factor for heart disease. Dietary Fat and Cholesterol: The theory implies that dietary changes like a ketogenic diet, high in fats, might not uniformly raise cardiovascular risk, which can contrast with traditional advice on reducing saturated fat intake to lower cholesterol levels. Conclusion: The theory presented in the video diverges from the traditional consensus mainly in its interpretation of the role of LDL cholesterol and the impact of dietary fats in certain contexts. It highlights the complexity and individual variability in lipid metabolism and cardiovascular risk. However, it's important to note that while this theory provides an interesting perspective, especially for individuals like LMHRs, it has not replaced the broader consensus in the medical community, which still emphasizes the importance of managing LDL cholesterol levels for cardiovascular health. Research in this area is ongoing, and a more nuanced understanding may emerge with time.
I want to believe you, but I don't. It is too well put-together to be written by an AI!... In fact, I think this explanation is even clearer than Dave's in the video! But I've seen so much magic by the ChatGPT that I might actually believe you after all! xD
I sincerely hate to say this (being a critic of ChatGP), but that cleared up the confusion I had after watching the video... Now it's perfectly clear what the vid was trying to convey, and I thank you for helping me out. Now, back to my troglodyte ways...
Jeff, sorry that you can't make friends but there's no excuse for being a militant detractor. Are you at least paid by comment? You clearly follow this channel and Ken Berry, whom I personally dislike, and try to respond everyone on every video with the same B's. You're looking like a bot. Probably a vegan one. If you're not a bot, either you have no job or your job is attacking these channels.
Love the pizza boxes analogy. This is the most understandable explanation of LMHR that I've seen so far. You're also explaining why LDL correlates with disease states in the general population.
As a person who has lost 110 lbs of fat and added lean muslce mass at 54 yrs old in the last 9 months through keto/carnivore, this is absolutely one of the best videos I have watched in helping me better understand why LDL may increase as I continue to shrink my BMI and keep/add my lean muscle mass!!! Thank-you for putting this in more simple terms and the pizza box illustration is brilliant. I am NOT a credentialed scientist, but I consider myself informed due to my research and desire to always learn more about our biology. With that said, this makes so much sense to me!! The work you and your colleagues are doing around LDL is absolutely impressive. Thank-you!
Hi, I am a low-carb eater too (not keto). I have decreased lots of body fat as well. But I don't really gain much skeletal muscle mass (SMM). can I ask how you managed to gain SMM?
My total cholesterol was always 180 up untill age 57 when i started not feeling well (gallbladder issues). I switched to a low carb diet and a year later cholesterol was up to 280, but triglycerides down from 90 to 52, HDL up to 69, vLDL down to 3. Doc freaked out about high cholesterol, but everything else looked great. Im healthier than ive been in years and feel great, and am very athletic. I eat a healthy organic animal based foods diet with fermented food, berries, some nuts, avocados some purple sweet potatoes. NO sugars, prossessed foods, acholic, seed oils. Pasta, grains, flour. Think im fine.
It is so sad that a doctor cannot see beyond the paradigm in their text books. Patient looks and acts healthy but the text book says they are basically on deaths doorstep. It is absurd.
I always thought VLDL was calculated from your tyg. It's always 20% of your trg. So @ 52 it should be 10.2. I always use my tyg to calculate it and it always matches with with the lab result of the VLDL. So I am puzzled that your VLDL is 3??? My trg was 50 and my VLDL was 10, and all my past tests works out to be the same.
Thank you for this explanation! Thank you sincerely for your research! 🙏 Serendipitous timing for myself as my Dr (UK) has called me in to discuss my high cholesterol! It’s worrying, but I hope this explains it and your hypothesis is confirmed. I fit the LMHR phenotype. Low Triglycerides, high HDL, very high LDL. Actually need to gain weight! Female. 41yrs. BMI 18.6 . Low carb real food diet (30-80g CHO naturally a day, in ketosis when test), since reading Phinney, Volek, and Westman’s work and especially “The art and science of low carbohydrate living / Performance “ (2017). The late Barry Groves opened my eyes first. Recommend to anyone wanting layman’s terms also the late pioneering biochemist Fred Kummerow work and his down to earth book/ explanation in “Cholesterol is not the Culprit”. Thank you again from the bottom of my heart!
Really great video, but I must say that subtitles are really annoying and present a problem if I want to share this video with auto translation for my friends that only speak spanish.
Great simple but powerful explanation. I am a LMHR with an LDL of 329 but Triglycerides of 52 and HDL of 114. But i have a high LP (a) of 48 mg/dl - normal range is 0-30 which is my main concern regarding potential vascular disease with this keto lifestyle. I also took Lipitor for more than 10 years, and my CAC score of 255 shows it. Of course, the PCP & Cardiologist insist that I return to daily statins, but I've refused for the past 2 years. Passed a treadmill test with flying colors, too. I walk 3 miles 6xwk and resistance train 30 mins 2x wk, use a CGM due to major glucose rise (>60 points) for more than 3 hrs before nearing baseline with any type of carb eating. A lot to worry about at age 69. . 8:03
I had a heart attack with similar numbers, but my triglycerides were in the 40's. I was briefly on the keto diet and didn't do well at all, so I went off it. I don't remember how long it was after that, that I had the attack. My insulin was a 6 at the time. I also past a stress test because I'm thin and exercise.
Saturated fat lowers LP(a) and if you want to know about risks concerning lipid sub types and risk look up Bart Kay. Google saturated fat and LP(a). Saturated fat increases LDL size and health as well.
Of course, that's what a statin does is calcify your arteries all in the name of plaque stabilization. But unfortunately, it doesn't stop a heart attack. Reversing my CAC with the Linus Pauling Heart Protocol so far 30% in 20 months.
Thanks Dave, These concepts are awesome, keep it up, as it is helping US understand whats going on. Just got labs back today, and everthing is about same, except trigs dropped from 47 to 36!, Sure hope thats a good sign. Cardio doc is old and not having any LMHR talk, would love to send this to him, bet he is to entrenched in his "old" school way of conceptualizing. Friday we may hear more!
Dave, you are doing an excellent job making these videos, and the analogy using pizza boxes was perfect! Please keep making videos on cholesterol so the world can understand the science behind it! I believe your theory is correct! We can’t wait to see more results on your lean mass hyper responder study! Thank you for all that you are doing! Have a great day Dave! ☺️
Great analogy Dave. It is not easy to identify true cause in a complex system. Very easy to jump to a conclusion that a marker is THE cause. Especially, if your future funding depends upon It………… You have to keep testing the current hypothesis. That is what science is..
Thank you SO MUCH! I’m pretty sure I’m LMHR. Just got APO-b results of 134 & have been freaking out bc of that info on top of all my high numbers. I thought high APO-b destroyed my hypothesis that I’m LMHR. My dr wants me on a statin & on lower fat, Mediterranean diet.(He hasn’t seen this latest blood work, just my previous results.) I feel validated, especially since I feel so good! Got my pre-diabetes in check & lost 18 pounds starting 18 months ago. My BMI=20, I’m 5’5” female, 116 pounds, 73 years old. Would love to be in this study, especially since there’s FH!
I wish you would go beyond LHMR to help the scientific community realize that LDL is not always bad and can be a result of improving metabolic health even when the individual wasn’t healthy before. Consider someone who goes keto after many years of eating a standard diet with seed oils but then does keto only to see their LDL go up
But we simply don;t know that keto diets are as healthy/safe as are very lowfat WFPB diets, so It would be premature to preach anything to the scientific community. Feldman doesn't have ANY hard evidence on long term health outcomes for any of this.
An additional aspect of this topic is the case of Paul Saladino as he now eats lots of honey and fruit juice along with meat but feels it is not problematic since his vldl levels continue to be low. But his vldl size has exploded, so what about that? Though it is correct to describe vldl as TG-rich and ldl as TG-poor its important to note that not all vldl is equal. Some vldl is highly TG-rich like Paul's and some (such as lmhr's) are much more TG-poor. This point doesn't really belong in this video as it is a special case, but its of interest because the LP-IR blood test that so powerfully predicts cvd events (Dugani et al 2021) is so dependent on vldl size irrespective of absolute vldl levels.
If you *_ONLY_* consider the lipoprotein angle, you won't see the full picture related to fructose consumption and human health. In other words, even if there is no negative impact on lipids from consuming fructose, there are health issues created in other areas of the body. For example, the process of metabolizing fructose is different than for metabolizing other sugars. In order to metabolize fructose, phosphates (the "P" in "ATP") from ATP have to be "stolen." The more fructose that needs to be dealt with, the more phosphates get stripped from ATP. This results in ATP being reduced to AMP - it goes from a TRIphosphate to a MONOphosphate. Now you have a bunch of AMP. When the body deals with AMP, uric acid is produced as a byproduct. See where this is going? When you eat fructose, you end up depleting ATP and producing uric acid. This is not a good situation to maintain long-term.
You mean that Apo-B may not be the Be-all, End-all--or the final word on atherosclerotic particles? Go figure. It bothers me how definitive people like Attia speak about it. I think there is a lot more science that needs to occur before it can be blamed as causally linked to CVD.
@@dmmcmah1 he definitely has establishment bias… Which makes sense from his background. Given time, I think he’ll wake up, but it’ll take a lot of his current beliefs to be proven wrong. What bothers me is his confidence that he’s absolutely correct, where he is so completely dismissive specifically of carnivore.
ApoB is causal and necessary for CVD. There may be additional factors, further nuance, but this is established as a fact. ApoB particles embed in artery walls regardless of oxidation or inflammation. Higher volumes of ApoB particles have been shown to lead to more particles in artery walls. Again, there are processes in the body to clear these embedded ApoB particles. And oxidation makes the arterial lesions worse, as does inflammation. But the LMHR hypothesis is just a guess that needs to be tested to see if some of the other factors at play mitigate the CVD risk of elevated ApoB particle counts.
I agree, the whole fear LDLs act is getting out of hand and anyone with a brain should question this cause something ain't right. I theorize that it may have more to do with autoimmune disorder than just too much LDLs. How an immune disorder affects the LDLs themselves.
I think he does. I came to this video bc of APO-b. Basically he says that it will be high if LDL is high & you’re LMHR. I had to stop the video a few times to absorb it. Going to watch again soon. I’m just very relieved! Best wishes!
Great video and explanation with pizza boxes. Curious, you mentioned APOB and VLDL are the same. Can you clarify? My APOB and VLDL numbers are not correlated at all.
Dave’s explanation above demonstrates once again that *high LDL cholesterol is not a problem* as long as we avoid chronic glycation, inflammation, oxidative stress, and metabolic dysfunction (i.e. *insulin resistance*). These conditions can be had via proper diet (low carb, high fat) and proper lifestyle (stress management, regular exercise, and intermittent fasting). Get these down, and you will never have a problem with plaque, or with cardiovascular disease. Focus on triglycerides, and don't worry about LDL.
Dave mentioned that the "explanation" is a mechanistic hypothesis and is not yet demonstrated with evidence to be correct. You want the thing you say here to be true, but they are not demonstrated to be true. The current balance of evidence shows that people with high ApoB (and LDL) have elevated risk of CVD. There may be a special sub-population like LMHR that don't exhibit elevated CVD risk, but this is just an idea to investigate at this point, not established scientific consensus.
You're right, but I honestly think the reason is because they have no focal vitamin C deficiency. This makes their endothelial superior like a shield 🛡. As for me, I'm restoring my focal vitamin C deficiency, and as a result, my CAC is reversing dramatically, and I'm not religious about diet. And that's pretty amazing!
Thank you very much for this interesting presentation. I am following the latest LDL presentations. I just don't get what risks of cardiovascular disease are there for a metabolically not very healthy person on Kero diet. Should I continue with the low carb diet if I have genetical Hypercholesterolemia and Dyslipidemia? My total cholesterol has been already higher before the ketogenic diet and my LDL has doubled since 2021 up to 200. I also have a hypothyroidism treated with euthyrox 75. I am female, 50yo. Thank you 🙏
My lipid fraction fasted versus not fasted: my TG dropped and HDL, LDL, apoB rose. This showed excellent lipid processing. My grade for both fraction tests were A -least likely to have a cardiac event, and both tests had high LDL and apoB with normal HDL and TG.
@@susanbeever5708 Pretty amazing isn't it. But for someone who follows standard medicine it would be pretty scary. Want a real education read Dr. Thomas Levy's book "Stop America's #1 Killer " Proof that the Origin of All Coronary Heart Disease is Clearly Reversible Arterial Scurvy. Wouldn't you think that hard calcium is harder to remove than soft plague? My last CAC was with contrast and yet not one word was spoken about plague burden. I had already been on the Pauling Protocol for 20 months intensely meaning 20-30 grams of ascorbic acid in divided doses with Lysine and proline used as binding inhibitors of Lp-a. I even had an ultrasound echo tee. I can only believe they saw little or no plaque build-up. I use a multi-pronged approach to heart disease.
I'm often censored, Susan. But yes, I'm aware of the possibilities, but it's highly unlikely with the Linus Pauling Heart Protocol. Know anyone reversing their CAC?
5:10 What I don't get is what is the proposed mechanism of action through which VLDL would be athero*genic*? I understand how it could be a risk factor or correlated with atherosclerosis, but I don't understand how it could *cause* it.
So, I'm an ultra-endurance athlete and I train a lot, mostly low-intensity fat-burning effort. I eat a whole-food, plant-based diet (95% of the time, occasional processed vegetarian foods when out at a restaurant or traveling). I am not on a low-carb diet, I fuel with carbs daily, but to hit my calorie targets I end up with a moderately large percentage of my calories from fat, 40-50% (mostly avocado, nuts, and seeds). My lipid panel values for HDL and TG meet the criteria for LMHR (87 and 61, respectively) but my LDL is "healthy" at 71. I am also very lean and have been my whole life, 7-12% body fat since I first got measured in college and now I am 52 years old. All of this makes me wonder if my LDL would shoot through the roof if I tried keto, if I am a LMHR but in the carb-fed low-LDL state. Based on genetic testing, I know I have exceptionally high risk for high ApoB and CVD. My understanding is that my diet and lifestyle are helping to manage that CVD risk by keeping my ApoB lower and improving my metabolic health. Does this research on the LMHR phenotype have implications for me?
Lmhr are defined pretty much by high or relatively high ldl (apob) thus imo you don't have that...your plant based might be the main reason thus, you don't qualify. I don't either but quite opposite. I consume meat/fat, but not as much and I eat more carb than keto/low carb folks and I exercise, but pretty minimal (2 days week)...but more than average folks 130/140's ldl 45/50 hdl 70/80 triglycerides RHR 60's BP 115/75
If I were to simplify this further, am I right to say that as long as Triglycerides (i.e the pizzas) are found to be low in number, the amount of LDL (empty pizza boxes) present does not cause any health issues and so is not a concern, since it is the excess Triglycerides (i.e. unconsumed pizzas) that will damage the body (i.e. uneaten pizzas left over long periods of time will rot and become toxic)?
Dave clearly stated that the CVD risk associated with high LDL not known to be different for individuals with the LMHR phenotype and that the possibility of a difference is a hypothesis at this point. The outcomes are bad for people with high LDL and there is a proven causal link between high LDL and CVD so it will be very surprising to find out that within the high-LDL population there is a subgroup (LMHR) that do not suffer dangerously elevated CVD risk. It MAY BE that LMHR with high LDL does not experience elevated CVD risk, but that has not been established based on credible evidence at this time.
While LMHR has low triglycerides like 50 mine are 100 and my HDL is just 36 yet I am reversing my CAC on the Linus Pauling Heart Protocol dramatically.
Perhaps this can explain why LDL can spike during extended fasting, too? I made the mistake of getting a screening deep into an extended fast, and my LDL was way out of range (I'm not a LMHR.)
So, how does the recent "Oreo Cookie" study and dramatic reduction of LDL seen fit into this and the dramatic clearing of the "empty pizza boxes" fit in this analogy ?
Lets say a LMHR ate an extremely high carbohydrate diet for many years, then had a major heart attack. Now they are eating a carnivore diet with an LDL more than 4 times higher than what is was prior to the heart attack. Could this way of eating help fix the issues caused by the high carbs for so long?
Thanks, Dave. I would like to live without eating carbohydrates just to lower my LDL, I am waiting for the hypothesis to be proven and to know the consequences. While I will continue to try to keep my LDL below 250.
@@yshraybman My Latin diet damaged my metabolism, a lot of rice, corn and wheat. That's 30 years of eating poorly. The Keto diet changed my life, I feel very good being in ketosis, when I try to do low carb I am hungrier, that hunger keeps me thinking about food all day, but in ketosis I am very happy.
Is your position that the main problem is pizza, not boxes ? And normally those track well together but they don’t in LMHR (higher than expected empty pizza boxes)
I'm not an LHMR by definition, but my HDL is higher than triglycerides, but LDL is less than 200. Probably because my carbs intake is still higher than a keto diet
Hi, thanks for this analogy!! I am a 58 year old male borderline LMHR... And after a high Apob blood score as well as the usual high Ldl I decided to have a CAC scan. Score = 0. My Medical Aid ranks me as a high risk individual yet refused to pay for my scan🤔🤐
How does high Lipoprotein(A) figure into all this???? that the famous Bob Harper fitness guru to the stars had high levels of & went into cardiac arrest in the gym a few years ago, but survived since there was a cardiac nurse & doctor in the gym at the same time & they had an diffibulator at the gym....
My recent blood test on low carb diet for 18 months is - Total cholesterol: 290 mg/dL - Triglycerides: 305 mg/dL - HDL cholesterol: 50 mg/dL - LDL cholesterol: 179 mg/dL - VLDL: 61 mg/dL Why is my triglycerides high and should I be concerned?. If so how to reduce? Anyone?
I am on keto and for many many years have high cholesterol, high triglycerides along with elevated liver enzyme numbers. The exciting message I got from this is that the triglycerides represent too much fuel so the body is refusing it. So my guess is that fasting should bring triglycerides and liver numbers down. Also I am hoping that OpenLabs has a Fibroscan prescription as my doctor is ignoring my please saying these numbers are no big deal. Wait another year they are not significant. 😢
CinthiaArmstrong7 I had a similar situation myself and on Keto... the only 2 things that helped reverse all my conditions of Fatty Liver (very elevated liver enzymes), completely heal my GERD, SIBO, Candida, Reflux & put my asthma in remission, lower my Triglycerides & so much more... was to 1) fast... basically OMAD (One Meal A Day) & 2) move from Keto to full on Carnivore! You may want to look into that... just for a while to see if it helps you with your liver enzymes & Triglycerides. Good health to you. Meat on. Heal on. 🧈 🥓 🥩 🍗 🍳🍖🦐
So in a big ol' fat guy like me, with a little too much gluconeogenesis going on because of hepatic IR, My cells won't be taking pizza deliveries because they still have lots of glucose. (despite the fact that I'm not eating carbs). So wouldn't my VLDL sky rocket?
Dave, So are you on keto/carnivore diet or not right now? Do you respond to comments? I don't think you do. If yes, share you NMR lipoprofile in the description of all your videos. It is the right thing to do. In other words practice your hypothosis. Other people don't consider what you are saying as hypothesis. They actually view it as something very scienitifically sound and good.
When I posted my blood test results to cholesterol code several years ago, I was told I might be a LMHR because of my numbers after several years of the keto diet. But I did not have any blood tests done before I adopted that diet, to compare before and after, so unfortunately I did not meet the criteria for being among the test subjects.
Dave, I've been a fan of yours since I started keto 5 years ago. And I'm a lean mass hyper responder (not in your study) so this subject is very important to me. I did not like your pizza analogy, I found it more confusing than speaking about the real thing. Why are the people ordering so much pizza when they are full? Does that mean they are eating too much? What is the plaque in the pizza analogy? All analogies break down at some point and this pizza one is no exception. The subject is TOO complicated to explain completely with a simple analogy.
Its still wrong becsuse it is based on the cholesterol hypothesis for the cause of disease. The habitual high glucose from a starch foundation diet is the cause of the arterial damage that cholesterol has to repair habitually leading to a buildup of cholesterol like a scar. Its obvious and yet everyone is still chasing cholesterol or lipids as the cause of damage and its flat wrong. If not then why is high glucose the cause of all the damage in diabetics. You eat a high glycemic, high starch diet you have habitually high spiking blood glucose. Blaming cholesterol is like blaming the paramedic who is trying to save your life for the accident. Additionally why arent there pizza boxes all over our veinous system if cholesterol were the cause.
The fact that elevated glucose is unhealthy does not mean that elevated LDL cholesterol is not also unhealthy. There can be more than one unhealthy pattern. Why do you think that statins lower CVD risk?
@@christopherbrand5360 Statins dont lower cardio vascular risk and in fact older people with higher cholesterol are at lower risk. Beyond that to reiterate if cholesterol is the cause why doesnt it attack the Veins?
@@christopherbrand5360 epidemiological studies bought and paid for by drug companies are not proof they are propaganda. Correlation does not equal causation. Just because cholesterol is at the scene of the crime does not make it the perpetrator. Like i said, we know glucose causes damage we also know one of cholesterols many roles is repair. Then its not hard to see why cholesterol is at the site of damage.
@@christopherbrand5360 i already answered, bought and paid for studies by drug companies are proof of anything except profits. Correlation does not equal causation. If you dont understand what that means i cant help you.
Thanks for this video, Dave! This is your most concise and easy to understand explanation of the lipid energy model to date. I will be linking it in the description of all of my videos related to this topic.
Also, there is another lipoprotein that has the ApoB receptor: Lp(a). Lp(a) has Apo (a) on its' surface as well. Lp (a) goes to damaged areas in the arterial lining to stabilized the clots formed. LDL is blamed for going into the artery walls and causing plaques (which are old blood clots), when it is actually a repair mechanism using Lp (a). Unless you look for ApoA using special testing, you won't know which lipoprotein it is. Malcolm Kendricks explains this better...
I am a 61 yr old guy, I'm overfat at 290lbs or so, AND I've been following a Carnivore diet for 3 months now. I just had my cholesterol checked and of course my LDL is high, my HDL isn't great. However, my lipo-B is elevated at 122, and my Lipo- A is in range at 140. I can't see myself as a "Lean mass hyper responder" yet I am otherwise healthy. I had a CAC test done and had zero plaque? Just sharing.
The analogy works for 85% of people with monogenic FH specifically those with LDLR and APOB gene mutations. Not sure about the polygenic FH... So blocking production is counterproductive. and yes they are looking at it backwards.
I guess I’m one of those who has a ‘severe genetic abnormality’ because I thought I was a lean mass hyper responder or maybe I am because I consistently have triglycerides in the 50s, HDL in the high 60’s and fasting insulin at 5.1 and I’m lean and have exercised hard for close to 50 years. Unfortunately I had a heart attack about 3 weeks ago and had severe blockage in 4 major arteries and had to have 4 stents put in. I’ve been carnivore-ish and keto-ish for close to 8 years but not perfect. I’ve had a lot of stress lately that I’m sure contributed to my heart attack but my father had a quintuple bypass surgery when he was 80 but I assumed it was because he didn’t exercise at all. I feel fine but I’m kinda traumatized by it. I’m on a high dose of Lipitor and a couple other drugs for now. I’m going to try going strictly keto and see what happens. I’ve always been lean but I guess I’m a TOFI (thin on the outside and fat on the inside). I resisted taking statins but maybe I’m one of those that needs to be on at least a low dose one. Thankfully my heart is strong otherwise I very well could have died.
@@anneeasterling9961 No. My doctor gave me a prescription for a CAC test a few months ago but I’d put it off but was going to schedule one this month. I don’t see a need for it now but I’m dealing with my cardiologist who wants to reduce my LDL levels down to 50. What I want to do is eliminate carbs and sugar and see if the LDL particles change in size and oxidative levels. I’m a sugar addict but always had low triglyceride levels and my A1c was relatively low but creeping up the past couple years to 5.6. Confronting my carb and sugar addiction is the core challenge for me. I’ve trained very hard my whole adult life and even that was a kind of addiction and allowed me to rationalize eating more sugar and carbs than the average person.
1:52 Remnants are what's left after chylomicrons have been depleted, and they get absorbed by the liver. VLDL is brand new lipoprotein, released by the liver, so it makes no sense to refer to that as a remnant.
@@franciscoadolfo5805 That still doesn't make sense. A remnant is what is left over after something else has been altered. You could call LDL a remnant of VLDL, since it is a TG-depleted version of it, but it's still better to stick with the existing "chylomicron remnant" when referring to lipoproteins and not confuse things by calling newly-made liporoteins, remnants.
Hello Dave, I am German, sorry for the english grammer. I already wrote in the comment section to Dr. Nick but have not gotten a response. I am a lifelong exerciser, BMI 23, Trig in low 70, HDL high 80, LDLD about 140. In my family (Mother, her Brother, their Father and Mother) all died of a heart attack. I am 60, I needed one stent at age 40. My Dr. says I have FH and need to be on low fat diet and take a statin's. I eat low Carb, low fat and high protein, What do you think? Oh yes, Chol, is 231, my ApoB 73.
I'm a LMHR (LDL 221, HDL 84, TG 41). Exercise 2 hours a day. OMAD (low carb wholefood omnivore). Reversed over a decade of pre-diabetes, hypertension, sleep apnea and other chronic diseases (while on statins and other prescription drugs, LDL 80)... Thank you Dave for opening my eyes. I quit all prescription drugs (cold turkey) 4 years ago. I've never felt better in my life.
"Exercise 2 hours a day."
Why are you doing that, and what does your "exercise" consist of?
@@aliendroneservices6621
Exercise is the most important tool to achieve good health IMO. I do walking, running and resistance exercise.
Attia claims the TG/HDL Ratio is NG. Who knows???
Amazing. I have almost the exact same numbers. 221 LDL, 85HDL, 58 Trigs. I'm 52. I run 3-5 miles per day, 13% bodyfat. My Dr hates it. He said with my LDL alone, no other risk markers, I have a 50% chance (yes 50% chance) of a heart attack in the next 10 year's, if I don't start statins immediately...
@@chrissypearson5597
Peter Attia was on Keto for a few years then stopped. He was into fasting for a few years then stopped. If you don't like his opinion now, check back in a few years... Now he's in the camp of dropping LDL as much as possible. He's on PCSK9 inhibitor drug. He seems to have developed some fondness recently toward big pharmas. I do enjoy Peter's podcasts but take what he said with a grain of salt.
I gave chatGPT the transcrypt of this video to sumerize it:
_________________________________
The video uses an analogy to explain complex aspects of cholesterol metabolism, particularly focusing on Apolipoprotein B (apoB) and its relation to Lean Mass Hyperresponders (LMHR) in the context of a ketogenic diet. Here's a summary of the key points from the transcript:
Pizza Box Analogy: LDL particles are likened to empty pizza boxes. In a neighborhood (the body), after a pizza party (food consumption), empty boxes (LDL particles) accumulate. Some houses (cells) fail to recycle these boxes properly, leading to a pile-up.
ApoB and Lipoproteins: All lipoproteins from the liver contain one copy of apoB. These include Very Low-Density Lipoproteins (VLDL), which are triglyceride-rich, and Low-Density Lipoproteins (LDL), which are triglyceride-poor.
Metabolism of Lipoproteins: Under normal conditions, VLDL delivers triglycerides to cells, then shrinks to Intermediate-Density Lipoprotein (IDL), and eventually to LDL. LDL remains in circulation longer (2-4 days).
Issues with Triglyceride Clearance: If cells don't accept triglycerides efficiently (e.g., due to insulin resistance), triglyceride-rich lipoproteins stay in circulation longer. This increases overall apoB levels and leads to higher triglyceride levels.
Lean Mass Hyperresponders: On a ketogenic diet, some individuals experience a significant increase in LDL and apoB levels. The hypothesis is that their cells are highly efficient at utilizing triglycerides, leaving more "empty pizza boxes" (LDL particles) but very low triglycerides in the blood.
Comparing this to current knowledge:
ApoB as a Marker: ApoB is a recognized marker for cardiovascular risk, as each apoB-containing lipoprotein particle is potentially atherogenic.
LDL and Cardiovascular Risk: High levels of LDL cholesterol are traditionally linked with an increased risk of heart disease. However, the analogy suggests that the context (e.g., presence of triglycerides, insulin resistance) matters.
Ketogenic Diet and Cholesterol: It's known that ketogenic diets can significantly alter lipid profiles, often increasing LDL cholesterol. The LMHR phenomenon aligns with this, though the long-term cardiovascular implications are not fully understood.
Triglyceride Metabolism: The emphasis on triglyceride-rich lipoproteins and their clearance is in line with current understanding. Poor clearance (due to insulin resistance or other factors) is associated with cardiovascular risk.
____________________________
I then asked it if and how this disagrees with current consensus on cholesterol metabolism:
____________________________
Points of Disagreement:
Impact of LDL Levels: The video's theory that high LDL may not be uniformly detrimental in all contexts (like in LMHRs) is a significant departure from the consensus that high LDL is generally a risk factor for heart disease.
Dietary Fat and Cholesterol: The theory implies that dietary changes like a ketogenic diet, high in fats, might not uniformly raise cardiovascular risk, which can contrast with traditional advice on reducing saturated fat intake to lower cholesterol levels.
Conclusion:
The theory presented in the video diverges from the traditional consensus mainly in its interpretation of the role of LDL cholesterol and the impact of dietary fats in certain contexts. It highlights the complexity and individual variability in lipid metabolism and cardiovascular risk. However, it's important to note that while this theory provides an interesting perspective, especially for individuals like LMHRs, it has not replaced the broader consensus in the medical community, which still emphasizes the importance of managing LDL cholesterol levels for cardiovascular health. Research in this area is ongoing, and a more nuanced understanding may emerge with time.
I want to believe you, but I don't. It is too well put-together to be written by an AI!... In fact, I think this explanation is even clearer than Dave's in the video! But I've seen so much magic by the ChatGPT that I might actually believe you after all! xD
@@Kiihhu2 Dave is always very clear in what he communicates. That definitely helps chatGPT to write a good summery.
I sincerely hate to say this (being a critic of ChatGP), but that cleared up the confusion I had after watching the video... Now it's perfectly clear what the vid was trying to convey, and I thank you for helping me out. Now, back to my troglodyte ways...
In the mean time I’ll try and get my triglycerides as low as I can and not eat the pizza crust😂
Great use of ChatGPT! Thanks for this summary. Very helpful!
Great analogy!
Another science denier making comments.
Jeff, sorry that you can't make friends but there's no excuse for being a militant detractor. Are you at least paid by comment? You clearly follow this channel and Ken Berry, whom I personally dislike, and try to respond everyone on every video with the same B's. You're looking like a bot. Probably a vegan one. If you're not a bot, either you have no job or your job is attacking these channels.
Love the pizza boxes analogy. This is the most understandable explanation of LMHR that I've seen so far. You're also explaining why LDL correlates with disease states in the general population.
Yes. Better than a bus, because pizza boxes are used once and recycled.
As a person who has lost 110 lbs of fat and added lean muslce mass at 54 yrs old in the last 9 months through keto/carnivore, this is absolutely one of the best videos I have watched in helping me better understand why LDL may increase as I continue to shrink my BMI and keep/add my lean muscle mass!!! Thank-you for putting this in more simple terms and the pizza box illustration is brilliant. I am NOT a credentialed scientist, but I consider myself informed due to my research and desire to always learn more about our biology. With that said, this makes so much sense to me!! The work you and your colleagues are doing around LDL is absolutely impressive. Thank-you!
Hi, I am a low-carb eater too (not keto). I have decreased lots of body fat as well. But I don't really gain much skeletal muscle mass (SMM). can I ask how you managed to gain SMM?
My total cholesterol was always 180 up untill age 57 when i started not feeling well (gallbladder issues). I switched to a low carb diet and a year later cholesterol was up to 280, but triglycerides down from 90 to 52, HDL up to 69, vLDL down to 3. Doc freaked out about high cholesterol, but everything else looked great. Im healthier than ive been in years and feel great, and am very athletic. I eat a healthy organic animal based foods diet with fermented food, berries, some nuts, avocados some purple sweet potatoes. NO sugars, prossessed foods, acholic, seed oils. Pasta, grains, flour. Think im fine.
It is so sad that a doctor cannot see beyond the paradigm in their text books. Patient looks and acts healthy but the text book says they are basically on deaths doorstep. It is absurd.
I always thought VLDL was calculated from your tyg. It's always 20% of your trg. So @ 52 it should be 10.2. I always use my tyg to calculate it and it always matches with with the lab result of the VLDL. So I am puzzled that your VLDL is 3??? My trg was 50 and my VLDL was 10, and all my past tests works out to be the same.
VLDL is always calculated. They simply never measure it. That's why it's called remnant. It's the result of a substation from the total.
Thank you for this explanation! Thank you sincerely for your research! 🙏
Serendipitous timing for myself as my Dr (UK) has called me in to discuss my high cholesterol! It’s worrying, but I hope this explains it and your hypothesis is confirmed. I fit the LMHR phenotype. Low Triglycerides, high HDL, very high LDL. Actually need to gain weight! Female. 41yrs. BMI 18.6 . Low carb real food diet (30-80g CHO naturally a day, in ketosis when test), since reading Phinney, Volek, and Westman’s work and especially “The art and science of low carbohydrate living / Performance “ (2017). The late Barry Groves opened my eyes first. Recommend to anyone wanting layman’s terms also the late pioneering biochemist Fred Kummerow work and his down to earth book/ explanation in “Cholesterol is not the Culprit”. Thank you again from the bottom of my heart!
I like the way you explain this hypothesis to us. Thank you, Dave!
This is an excellent explanation. Great work Dave!
Great explanation, Dave. Thanks.
I'm starting to get my head around the APoB thing. Thank you.
Thank you, Dave Feldman! I am very interested, it's personal!
Fantastic summation! Thank you.
Really great video, but I must say that subtitles are really annoying and present a problem if I want to share this video with auto translation for my friends that only speak spanish.
Thanks Dave, well done. Makes sense to me, cheers!
Great simple but powerful explanation. I am a LMHR with an LDL of 329 but Triglycerides of 52 and HDL of 114. But i have a high LP (a) of 48 mg/dl - normal range is 0-30 which is my main concern regarding potential vascular disease with this keto lifestyle. I also took Lipitor for more than 10 years, and my CAC score of 255 shows it. Of course, the PCP & Cardiologist insist that I return to daily statins, but I've refused for the past 2 years. Passed a treadmill test with flying colors, too.
I walk 3 miles 6xwk and resistance train 30 mins 2x wk, use a CGM due to major glucose rise (>60 points) for more than 3 hrs before nearing baseline with any type of carb eating. A lot to worry about at age 69.
. 8:03
I had a heart attack with similar numbers, but my triglycerides were in the 40's. I was briefly on the keto diet and didn't do well at all, so I went off it. I don't remember how long it was after that, that I had the attack. My insulin was a 6 at the time. I also past a stress test because I'm thin and exercise.
Saturated fat lowers LP(a) and if you want to know about risks concerning lipid sub types and risk look up Bart Kay.
Google saturated fat and LP(a). Saturated fat increases LDL size and health as well.
Of course, that's what a statin does is calcify your arteries all in the name of plaque stabilization. But unfortunately, it doesn't stop a heart attack. Reversing my CAC with the Linus Pauling Heart Protocol so far 30% in 20 months.
Dave Feldman is a genius...
Thanks Dave, These concepts are awesome, keep it up, as it is helping US understand whats going on. Just got labs back today, and everthing is about same, except trigs dropped from 47 to 36!, Sure hope thats a good sign. Cardio doc is old and not having any LMHR talk, would love to send this to him, bet he is to entrenched in his "old" school way of conceptualizing. Friday we may hear more!
You have come a long way since that first little experiment on yourself. Congratulations, you may wind up helping millions.
Dave isn't risking 'the sound is low' comments anymore and is just going phat subs all the way instead 😂
So amazing Dave! Great explanation. It's all about FLUX and metabolism, not concentration of a poison!
Dave, you are doing an excellent job making these videos, and the analogy using pizza boxes was perfect! Please keep making videos on cholesterol so the world can understand the science behind it! I believe your theory is correct! We can’t wait to see more results on your lean mass hyper responder study! Thank you for all that you are doing!
Have a great day Dave! ☺️
Great analogy Dave. It is not easy to identify true cause in a complex system. Very easy to jump to a conclusion that a marker is THE cause. Especially, if your future funding depends upon It………… You have to keep testing the current hypothesis. That is what science is..
Curious how it feels to be making history? This is so cool to watch from the outside. Absolutely amazing!
You’ll never feel it personally, so there’s that
Thank you SO MUCH! I’m pretty sure I’m LMHR. Just got APO-b results of 134 & have been freaking out bc of that info on top of all my high numbers. I thought high APO-b destroyed my hypothesis that I’m LMHR. My dr wants me on a statin & on lower fat, Mediterranean diet.(He hasn’t seen this latest blood work, just my previous results.) I feel validated, especially since I feel so good! Got my pre-diabetes in check & lost 18 pounds starting 18 months ago. My BMI=20, I’m 5’5” female, 116 pounds, 73 years old. Would love to be in this study, especially since there’s FH!
Brilliant. Love the analogy!
I wish you would go beyond LHMR to help the scientific community realize that LDL is not always bad and can be a result of improving metabolic health even when the individual wasn’t healthy before. Consider someone who goes keto after many years of eating a standard diet with seed oils but then does keto only to see their LDL go up
But we simply don;t know that keto diets are as healthy/safe as are very lowfat WFPB diets, so It would be premature to preach anything to the scientific community. Feldman doesn't have ANY hard evidence on long term health outcomes for any of this.
An additional aspect of this topic is the case of Paul Saladino as he now eats lots of honey and fruit juice along with meat but feels it is not problematic since his vldl levels continue to be low. But his vldl size has exploded, so what about that? Though it is correct to describe vldl as TG-rich and ldl as TG-poor its important to note that not all vldl is equal. Some vldl is highly TG-rich like Paul's and some (such as lmhr's) are much more TG-poor. This point doesn't really belong in this video as it is a special case, but its of interest because the LP-IR blood test that so powerfully predicts cvd events (Dugani et al 2021) is so dependent on vldl size irrespective of absolute vldl levels.
Great added input. Thank you!
If you *_ONLY_* consider the lipoprotein angle, you won't see the full picture related to fructose consumption and human health.
In other words, even if there is no negative impact on lipids from consuming fructose, there are health issues created in other areas of the body.
For example, the process of metabolizing fructose is different than for metabolizing other sugars.
In order to metabolize fructose, phosphates (the "P" in "ATP") from ATP have to be "stolen."
The more fructose that needs to be dealt with, the more phosphates get stripped from ATP.
This results in ATP being reduced to AMP - it goes from a TRIphosphate to a MONOphosphate.
Now you have a bunch of AMP. When the body deals with AMP, uric acid is produced as a byproduct.
See where this is going?
When you eat fructose, you end up depleting ATP and producing uric acid. This is not a good situation to maintain long-term.
lots of honey and fruit juice is definitely not normal. i'd like to see this guy in 20 years.
thank you for this video Dave you are amazing in the way you explain things I can’t wait for December 8.❤
Excellent! Keep extending this analogy. What causes the damage?
Read Dr Malcom Kendrick’s book The Clot Thickens
It’s a coagulation issue not fat deposits.
You mean that Apo-B may not be the Be-all, End-all--or the final word on atherosclerotic particles? Go figure. It bothers me how definitive people like Attia speak about it. I think there is a lot more science that needs to occur before it can be blamed as causally linked to CVD.
Attia is a hack.
@@dmmcmah1 he definitely has establishment bias… Which makes sense from his background. Given time, I think he’ll wake up, but it’ll take a lot of his current beliefs to be proven wrong. What bothers me is his confidence that he’s absolutely correct, where he is so completely dismissive specifically of carnivore.
ApoB is causal and necessary for CVD. There may be additional factors, further nuance, but this is established as a fact. ApoB particles embed in artery walls regardless of oxidation or inflammation. Higher volumes of ApoB particles have been shown to lead to more particles in artery walls. Again, there are processes in the body to clear these embedded ApoB particles. And oxidation makes the arterial lesions worse, as does inflammation. But the LMHR hypothesis is just a guess that needs to be tested to see if some of the other factors at play mitigate the CVD risk of elevated ApoB particle counts.
I agree, the whole fear LDLs act is getting out of hand and anyone with a brain should question this cause something ain't right. I theorize that it may have more to do with autoimmune disorder than just too much LDLs. How an immune disorder affects the LDLs themselves.
I'm not so sure it is a fact that it actually causes it. But it is a fact that it is present. There is definitely nuances
Great video. Tell us now how apoB factors in. The latest boogeyman.
I think he does. I came to this video bc of APO-b. Basically he says that it will be high if LDL is high & you’re LMHR. I had to stop the video a few times to absorb it. Going to watch again soon. I’m just very relieved! Best wishes!
Great video and explanation with pizza boxes. Curious, you mentioned APOB and VLDL are the same. Can you clarify? My APOB and VLDL numbers are not correlated at all.
Thanks for this analogy. I understand for the first time. 👍
Dave’s explanation above demonstrates once again that *high LDL cholesterol is not a problem* as long as we avoid chronic glycation, inflammation, oxidative stress, and metabolic dysfunction (i.e. *insulin resistance*). These conditions can be had via proper diet (low carb, high fat) and proper lifestyle (stress management, regular exercise, and intermittent fasting). Get these down, and you will never have a problem with plaque, or with cardiovascular disease. Focus on triglycerides, and don't worry about LDL.
Dave mentioned that the "explanation" is a mechanistic hypothesis and is not yet demonstrated with evidence to be correct. You want the thing you say here to be true, but they are not demonstrated to be true. The current balance of evidence shows that people with high ApoB (and LDL) have elevated risk of CVD. There may be a special sub-population like LMHR that don't exhibit elevated CVD risk, but this is just an idea to investigate at this point, not established scientific consensus.
You're right, but I honestly think the reason is because they have no focal vitamin C deficiency. This makes their endothelial superior like a shield 🛡. As for me, I'm restoring my focal vitamin C deficiency, and as a result, my CAC is reversing dramatically, and I'm not religious about diet. And that's pretty amazing!
Thank you very much for this interesting presentation. I am following the latest LDL presentations. I just don't get what risks of cardiovascular disease are there for a metabolically not very healthy person on Kero diet. Should I continue with the low carb diet if I have genetical Hypercholesterolemia and Dyslipidemia? My total cholesterol has been already higher before the ketogenic diet and my LDL has doubled since 2021 up to 200.
I also have a hypothyroidism treated with euthyrox 75. I am
female, 50yo. Thank you 🙏
Why doesn’t the liver remove more LDL when there is more of it with LMHR. Shouldn’t the half life of LDL be shorter than 3 days with LMHR ?
My lipid fraction fasted versus not fasted: my TG dropped and HDL, LDL, apoB rose. This showed excellent lipid processing. My grade for both fraction tests were A -least likely to have a cardiac event, and both tests had high LDL and apoB with normal HDL and TG.
apoB is causal
You think it is! My CAC is reversing because I'm restoring my focal vitamin C deficiency so far 30% in 20 months, that's 200 points!
@@SET12DSP that’s wonderful, I am trying to let you know that you must be aware of the plaque burden and the potential for blockage and thrombosis.
@@susanbeever5708 Pretty amazing isn't it. But for someone who follows standard medicine it would be pretty scary. Want a real education read Dr. Thomas Levy's book "Stop America's #1 Killer " Proof that the Origin of All Coronary Heart Disease is Clearly Reversible Arterial Scurvy. Wouldn't you think that hard calcium is harder to remove than soft plague?
My last CAC was with contrast and yet not one word was spoken about plague burden. I had already been on the Pauling Protocol for 20 months intensely meaning 20-30 grams of ascorbic acid in divided doses with Lysine and proline used as binding inhibitors of Lp-a. I even had an ultrasound echo tee. I can only believe they saw little or no plaque build-up. I use a multi-pronged approach to heart disease.
I'm often censored, Susan. But yes, I'm aware of the possibilities, but it's highly unlikely with the Linus Pauling Heart Protocol. Know anyone reversing their CAC?
I love that you were able to find stock photos of pizza boxes in various locations around houses. 😂
It would be interesting to see how Eurythrocyte Sedimentation Rate (ESR) correlates with APOB and/or LDL
How does one determine if they are a “lean mass hyper-responder”?
5:10 What I don't get is what is the proposed mechanism of action through which VLDL would be athero*genic*? I understand how it could be a risk factor or correlated with atherosclerosis, but I don't understand how it could *cause* it.
there is no proof VLDL sticking to artery wall like some gunk
5 years high saturated animal fat carnivore here.
Best decision of my life.
Very nice analogy. Thank U very much.❤
Does this mean LMHRs shouldn’t eat low carb diets? Or that they are fine eating low carb?
So, I'm an ultra-endurance athlete and I train a lot, mostly low-intensity fat-burning effort. I eat a whole-food, plant-based diet (95% of the time, occasional processed vegetarian foods when out at a restaurant or traveling). I am not on a low-carb diet, I fuel with carbs daily, but to hit my calorie targets I end up with a moderately large percentage of my calories from fat, 40-50% (mostly avocado, nuts, and seeds). My lipid panel values for HDL and TG meet the criteria for LMHR (87 and 61, respectively) but my LDL is "healthy" at 71. I am also very lean and have been my whole life, 7-12% body fat since I first got measured in college and now I am 52 years old. All of this makes me wonder if my LDL would shoot through the roof if I tried keto, if I am a LMHR but in the carb-fed low-LDL state. Based on genetic testing, I know I have exceptionally high risk for high ApoB and CVD. My understanding is that my diet and lifestyle are helping to manage that CVD risk by keeping my ApoB lower and improving my metabolic health. Does this research on the LMHR phenotype have implications for me?
Lmhr are defined pretty much by high or relatively high ldl (apob) thus imo you don't have that...your plant based might be the main reason thus, you don't qualify.
I don't either but quite opposite. I consume meat/fat, but not as much and I eat more carb than keto/low carb folks and I exercise, but pretty minimal (2 days week)...but more than average folks
130/140's ldl
45/50 hdl
70/80 triglycerides
RHR 60's
BP 115/75
Thanks. You are an excellent teacher.
I, too, am a LMHR. (LDL 231, HDL 79, TG 63) OMAD. 5'7 140, 60 years old. Feel like I'm 20.
If I were to simplify this further, am I right to say that as long as Triglycerides (i.e the pizzas) are found to be low in number, the amount of LDL (empty pizza boxes) present does not cause any health issues and so is not a concern, since it is the excess Triglycerides (i.e. unconsumed pizzas) that will damage the body (i.e. uneaten pizzas left over long periods of time will rot and become toxic)?
Dave clearly stated that the CVD risk associated with high LDL not known to be different for individuals with the LMHR phenotype and that the possibility of a difference is a hypothesis at this point. The outcomes are bad for people with high LDL and there is a proven causal link between high LDL and CVD so it will be very surprising to find out that within the high-LDL population there is a subgroup (LMHR) that do not suffer dangerously elevated CVD risk. It MAY BE that LMHR with high LDL does not experience elevated CVD risk, but that has not been established based on credible evidence at this time.
While LMHR has low triglycerides like 50 mine are 100 and my HDL is just 36 yet I am reversing my CAC on the Linus Pauling Heart Protocol dramatically.
Bravo! Now, where can I get a copy of that presentation?...
I love the analogy: Pizza Boxes filled fatty cargo! Do chylomicrons deliver LDLs? If so, roving pizza cats (or vans) looking for customers?
Perhaps this can explain why LDL can spike during extended fasting, too? I made the mistake of getting a screening deep into an extended fast, and my LDL was way out of range (I'm not a LMHR.)
Outstanding video! Keep doing this great job!
I apologize for not subscribing before now.
Sounds like it’s not a problem.
Ah Dave, you are my Cholesterol Jesus, always with a insightful parable to help me understand life!
So, how does the recent "Oreo Cookie" study and dramatic reduction of LDL seen fit into this and the dramatic clearing of the "empty pizza boxes" fit in this analogy ?
Lets say a LMHR ate an extremely high carbohydrate diet for many years, then had a major heart attack.
Now they are eating a carnivore diet with an LDL more than 4 times higher than what is was prior to the heart attack.
Could this way of eating help fix the issues caused by the high carbs for so long?
Excellent analogy!
Dave you are a legend
Thanks, Dave. I would like to live without eating carbohydrates just to lower my LDL, I am waiting for the hypothesis to be proven and to know the consequences. While I will continue to try to keep my LDL below 250.
humans are perfectly adapted to eat carbs, overeating it is a problem. overeating protein and fats is also as bad.
@@yshraybman My Latin diet damaged my metabolism, a lot of rice, corn and wheat. That's 30 years of eating poorly. The Keto diet changed my life, I feel very good being in ketosis, when I try to do low carb I am hungrier, that hunger keeps me thinking about food all day, but in ketosis I am very happy.
If you need another test subject Im available. My vldl hovers around 2 to 5 most tests.
Is your position that the main problem is pizza, not boxes ? And normally those track well together but they don’t in LMHR (higher than expected empty pizza boxes)
I'm not an LHMR by definition, but my HDL is higher than triglycerides, but LDL is less than 200. Probably because my carbs intake is still higher than a keto diet
Awesome explanation!
But then atherosclerosis would correlate much closer with triglyceride than apoB? Do we see that? If not, why not? Triglyceride lifecycle too short?
Share to all heart association in your country
Hi, thanks for this analogy!! I am a 58 year old male borderline LMHR... And after a high Apob blood score as well as the usual high Ldl I decided to have a CAC scan. Score = 0. My Medical Aid ranks me as a high risk individual yet refused to pay for my scan🤔🤐
How does high Lipoprotein(A) figure into all this???? that the famous Bob Harper fitness guru to the stars had high levels of & went into cardiac arrest in the gym a few years ago, but survived since there was a cardiac nurse & doctor in the gym at the same time & they had an diffibulator at the gym....
My recent blood test on low carb diet for 18 months is
- Total cholesterol: 290 mg/dL
- Triglycerides: 305 mg/dL
- HDL cholesterol: 50 mg/dL
- LDL cholesterol: 179 mg/dL
- VLDL: 61 mg/dL
Why is my triglycerides high and should I be concerned?. If so how to reduce?
Anyone?
did you fast when you had the blood test?
@@DorotheaGem no
@@SelyChangampally you have to fast 12-14 hrs to get correct results. Go to them again and I m pretty sure your Trigs will be under 100 :-)
Gold
I am on keto and for many many years have high cholesterol, high triglycerides along with elevated liver enzyme numbers. The exciting message I got from this is that the triglycerides represent too much fuel so the body is refusing it. So my guess is that fasting should bring triglycerides and liver numbers down. Also I am hoping that OpenLabs has a Fibroscan prescription as my doctor is ignoring my please saying these numbers are no big deal. Wait another year they are not significant. 😢
CinthiaArmstrong7
I had a similar situation myself and on Keto... the only 2 things that helped reverse all my conditions of Fatty Liver (very elevated liver enzymes), completely heal my GERD, SIBO, Candida, Reflux & put my asthma in remission, lower my Triglycerides & so much more... was to 1) fast... basically OMAD (One Meal A Day) & 2) move from Keto to full on Carnivore! You may want to look into that... just for a while to see if it helps you with your liver enzymes & Triglycerides.
Good health to you. Meat on. Heal on. 🧈 🥓 🥩 🍗 🍳🍖🦐
So in a big ol' fat guy like me, with a little too much gluconeogenesis going on because of hepatic IR, My cells won't be taking pizza deliveries because they still have lots of glucose. (despite the fact that I'm not eating carbs). So wouldn't my VLDL sky rocket?
Dave, So are you on keto/carnivore diet or not right now? Do you respond to comments? I don't think you do.
If yes, share you NMR lipoprofile in the description of all your videos. It is the right thing to do. In other words practice your hypothosis. Other people don't consider what you are saying as hypothesis. They actually view it as something very scienitifically sound and good.
Amazing work 👏🏻
Can you address particle size.? Please.
When I posted my blood test results to cholesterol code several years ago, I was told I might be a LMHR because of my numbers after several years of the keto diet. But I did not have any blood tests done before I adopted that diet, to compare before and after, so unfortunately I did not meet the criteria for being among the test subjects.
Dave, I've been a fan of yours since I started keto 5 years ago. And I'm a lean mass hyper responder (not in your study) so this subject is very important to me. I did not like your pizza analogy, I found it more confusing than speaking about the real thing. Why are the people ordering so much pizza when they are full? Does that mean they are eating too much? What is the plaque in the pizza analogy? All analogies break down at some point and this pizza one is no exception. The subject is TOO complicated to explain completely with a simple analogy.
the question is then, how do we become LMHR?
I find your pizza box analogy to be confusing. It made it harder to follow your argument. It probably worked with someone else, just not me.
LDL at 256
VLDL at 10
HDL at 73
ApoA at 172
ApoB at 151
27 yo, daily reaining, pretty fir and lean, low carb
👍💪
Why not a box of chocolates?
I knew pizza was good for something,..analogy
I want pizza now. Thanks.
So if I eat loads more pizza and get rid of all the boxes my doctor won't have a clue what's going on 🙃
Its still wrong becsuse it is based on the cholesterol hypothesis for the cause of disease.
The habitual high glucose from a starch foundation diet is the cause of the arterial damage that cholesterol has to repair habitually leading to a buildup of cholesterol like a scar. Its obvious and yet everyone is still chasing cholesterol or lipids as the cause of damage and its flat wrong.
If not then why is high glucose the cause of all the damage in diabetics. You eat a high glycemic, high starch diet you have habitually high spiking blood glucose.
Blaming cholesterol is like blaming the paramedic who is trying to save your life for the accident.
Additionally why arent there pizza boxes all over our veinous system if cholesterol were the cause.
The fact that elevated glucose is unhealthy does not mean that elevated LDL cholesterol is not also unhealthy. There can be more than one unhealthy pattern. Why do you think that statins lower CVD risk?
@@christopherbrand5360 Statins dont lower cardio vascular risk and in fact older people with higher cholesterol are at lower risk. Beyond that to reiterate if cholesterol is the cause why doesnt it attack the Veins?
@@christopherbrand5360 epidemiological studies bought and paid for by drug companies are not proof they are propaganda. Correlation does not equal causation. Just because cholesterol is at the scene of the crime does not make it the perpetrator. Like i said, we know glucose causes damage we also know one of cholesterols many roles is repair. Then its not hard to see why cholesterol is at the site of damage.
@@GregariousAntithesis Why do you say that statins don't lower CVD? That is hilarious. Science much?
@@christopherbrand5360 i already answered, bought and paid for studies by drug companies are proof of anything except profits. Correlation does not equal causation. If you dont understand what that means i cant help you.
Got it! The LMHR folks are hungry for pizzas, I knew it.
Well presented Dave, following from Athens Greece, looking forward to the outcomes of the LMHR study and your cookie 🍪 experiment
So, if the pizza boxes are the lipoproteins and the pizzas are the triglycerides, what is cholesterol? The topping?
Cholesterol is the grease on the box after the pizza is gone
Thanks for this video, Dave! This is your most concise and easy to understand explanation of the lipid energy model to date. I will be linking it in the description of all of my videos related to this topic.
Makes perfect sense to me.
Great analogy that drives home the point. Thank you for the good work you do.
Does anyone want pizza 🍕 now?
Also, there is another lipoprotein that has the ApoB receptor: Lp(a). Lp(a) has Apo (a) on its' surface as well. Lp (a) goes to damaged areas in the arterial lining to stabilized the clots formed.
LDL is blamed for going into the artery walls and causing plaques (which are old blood clots), when it is actually a repair mechanism using Lp (a). Unless you look for ApoA using special testing, you won't know which lipoprotein it is.
Malcolm Kendricks explains this better...
I am a 61 yr old guy, I'm overfat at 290lbs or so, AND I've been following a Carnivore diet for 3 months now. I just had my cholesterol checked and of course my LDL is high, my HDL isn't great. However, my lipo-B is elevated at 122, and my Lipo- A is in range at 140. I can't see myself as a "Lean mass hyper responder" yet I am otherwise healthy. I had a CAC test done and had zero plaque? Just sharing.
The analogy works for 85% of people with monogenic FH specifically those with LDLR and APOB gene mutations. Not sure about the polygenic FH... So blocking production is counterproductive. and yes they are looking at it backwards.
I guess I’m one of those who has a ‘severe genetic abnormality’ because I thought I was a lean mass hyper responder or maybe I am because I consistently have triglycerides in the 50s, HDL in the high 60’s and fasting insulin at 5.1 and I’m lean and have exercised hard for close to 50 years. Unfortunately I had a heart attack about 3 weeks ago and had severe blockage in 4 major arteries and had to have 4 stents put in. I’ve been carnivore-ish and keto-ish for close to 8 years but not perfect. I’ve had a lot of stress lately that I’m sure contributed to my heart attack but my father had a quintuple bypass surgery when he was 80 but I assumed it was because he didn’t exercise at all. I feel fine but I’m kinda traumatized by it. I’m on a high dose of Lipitor and a couple other drugs for now. I’m going to try going strictly keto and see what happens. I’ve always been lean but I guess I’m a TOFI (thin on the outside and fat on the inside). I resisted taking statins but maybe I’m one of those that needs to be on at least a low dose one. Thankfully my heart is strong otherwise I very well could have died.
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I'm curious.... before your heart attack, did you have any heart studies done? I'm particularly interested in CAC score.
@@anneeasterling9961 No. My doctor gave me a prescription for a CAC test a few months ago but I’d put it off but was going to schedule one this month. I don’t see a need for it now but I’m dealing with my cardiologist who wants to reduce my LDL levels down to 50. What I want to do is eliminate carbs and sugar and see if the LDL particles change in size and oxidative levels. I’m a sugar addict but always had low triglyceride levels and my A1c was relatively low but creeping up the past couple years to 5.6. Confronting my carb and sugar addiction is the core challenge for me. I’ve trained very hard my whole adult life and even that was a kind of addiction and allowed me to rationalize eating more sugar and carbs than the average person.
What was your A1C? Fasting insulin isn't the only important marker.
@@dmmcmah1 5.6
1:52 Remnants are what's left after chylomicrons have been depleted, and they get absorbed by the liver. VLDL is brand new lipoprotein, released by the liver, so it makes no sense to refer to that as a remnant.
Remnant cholesterol (RC) is TC - LDL - HDL. Which is VLDL. High RC is not favorable since it means vldl is pilling up, full of triglycerides.
@@franciscoadolfo5805 That still doesn't make sense. A remnant is what is left over after something else has been altered.
You could call LDL a remnant of VLDL, since it is a TG-depleted version of it, but it's still better to stick with the existing "chylomicron remnant" when referring to lipoproteins and not confuse things by calling newly-made liporoteins, remnants.
Hello Dave, I am German, sorry for the english grammer. I already wrote in the comment section to Dr. Nick but have not gotten a response. I am a lifelong exerciser, BMI 23, Trig in low 70, HDL high 80, LDLD about 140. In my family (Mother, her Brother, their Father and Mother) all died of a heart attack. I am 60, I needed one stent at age 40. My Dr. says I have FH and need to be on low fat diet and take a statin's. I eat low Carb, low fat and high protein, What do you think? Oh yes, Chol, is 231, my ApoB 73.