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.
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.
@@jeffj318 LOL!!! Do you even realize how many people this amazing doctor has saved from early deaths and disease?! Apparently not!!! Science? Safe and effective? What number are you on? blahahaha!!!
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...
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?
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.
Great analogy. Really helps to explain a complex topic in simple terms and gives us a potential mechanism to explain LMHR and why it seems to be a healthy phenotype.
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!
Dave Feldman is a true "citizen scientist" of the very first order. I am a retired physician and a ketogenic diet as done absolutely wonderful thing. In the setting of a HIGH HDL (60 or greater and a TRIGLYCERIDE LEVEL of 60 or less) s, I have tended to believe that a HIGH LDL is of little if any concern. I look forward to more research by Dave Feldman, and more TH-cam videos. I am intrigued when he says we may be looking at ApoB backwards, and I think his explanation of why this might be so makes a lot of sense.
You should be looking at focal vitamin C deficiency. On the Linus Pauling Heart Protocol, I am reversing my CAC so far by 30% or 200 points in just 20 months. Without worrying about cholesterol at all.
Thank you 😊 after 5 years i did my labs, 39 labs. The Dr office call me only because I have high colesterol, incredible, i stop them, sy, what about Insulin, triglycerides, HDL , ratio, my oxygen, my blood pressure etc. Everything perfect, 55 years old female, 127 pounds, with a lot of energy, healthy no meds. With my organs. Thanks again for this analogy ❤❤
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...
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.
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.
I couldn’t understand the pizza box scenario at all, but did inderstand the actual explanation easily. Pizza boxes just caused weird confusion that wasn’t needed Dave.
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 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..
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.
You're eating more saturated fats, that down regulates the ldl receptors on the liver thus leaving more atherosclerosis causing ApoB particles in circulation, resulting in increased LDL. Having a low CAC score just means you don't have calcified plaque, you could have plenty of soft plaque which is more harmful. Get a good quality CIMT test done.
The perfect video to better understand the LMHR phenotype without speaking English 😁 when translating the videos a lot of information is lost, so the visual work and analogy is of great help 🙏
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!
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.
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 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.
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 🙏
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.
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!
Borderline here. Refused a statin for over 12 years now. Looking forward to your study results and what is learned. I am planning on keeping my high LDL because I believe it is healthy.
Not in my book! Though I am mostly Keto grain and sugar-free, I am not religious about it. Reversing my CAC Score dramatically on the Linus Pauling Heart Protocol without going to extremes.
This was very helpful thank you. Glad you are doing this type of research. I think I might be one of those types as my LDL is high but triglycerides are not. Doctor suggested red yeast rice and eat healthy fats which I already do. My mom had high cholesterol they put her on statins. I wonder if her ALS was a result of these drugs.
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.
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?
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.
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.
I was on heavy keto, avacado every day low or very low carbs. APOB 220, I was shocked. I think I am LMHR, triglicerides 66. Male 126 lbs., 71 yr old. I exercise. Lipoprotein test was also high. I was so shocked I stopped eating avacados.
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 ?
The explanation is great though Dave. I’d just read a 2024 paper as it happens which was highlighting just how much more associated VLDL particles were with atherosclerosis than uLDL. Your explanation chimes completely with the findings of the paper. The paper wasn’t even concerned with Lean Mass Hyper-Responders, merely average populations. It just seems so sad that the profession are still struggling on with the LDL/ApoB deadend.
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.
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!
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?
Are you actually measuring the lipoprotein composition and particle sizes of these individuals? The previous theory stated that in case of a keto dieter who has high HDL, low triglycerides and high LDL, the LDL does not contain much ApoLipoB, but consists mainly of the larger, fluffy LDL particles which are not atherogenic. Did you count ApoLipoB in these people and found their numbers to be higher than the numbers of the larger fluffy LDL particles?
Look into how lipoproteins get cleared from the body. One primary mechanism for eliminating it is soluble fiber. LMHR may be partly a profile for fiber deficiency.
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.
Not sure but I think I am LMHR. Total cholesterol 330....HDL 70....triglycerides 49....LDL 253....remnant 7. Been ketovore since 2011. Currently at 16% body fat
Low energy, brain fog, insulin resistance and muscle wasting. I didn’t experience this on a regular diet taking a statin for 10 + years (not the brain fog and low energy anyway). I’d attribute the low energy to reduced fuel delivery lipoproteins. Statins promote calcium and diabetes (higher glucose). Avoid. The injectable PCSK9 inhibitors lower LDL way down to < 40 and are very much in experimental right now. You are the human trials If you take it. Malpractice. People are going to have dementia because of this crap.
The current scientific consensus is that such a LMHR on statins would be expected to have substantially lower CVD risk than one with higher LDL-C (or ApoB).
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
![Why your Low Carb Diet is hurting your Heart, and How to Improve it. [11 Studies]](http://i.ytimg.com/vi/tla-JrqhhHI/mqdefault.jpg)
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.
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.
@@jeffj318 LOL!!! Do you even realize how many people this amazing doctor has saved from early deaths and disease?! Apparently not!!! Science? Safe and effective? What number are you on? blahahaha!!!
@@jeffj318you showed him
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!
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?
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.
I like the way you explain this hypothesis to us. Thank you, Dave!
I'm starting to get my head around the APoB thing. Thank you.
Fantastic summation! Thank you.
Great explanation, Dave. Thanks.
Perfect video for anyone who wants to understand science better.
Thank you, Dave Feldman! I am very interested, it's personal!
Great analogy. Really helps to explain a complex topic in simple terms and gives us a potential mechanism to explain LMHR and why it seems to be a healthy phenotype.
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!
This is an excellent explanation. Great work Dave!
You have come a long way since that first little experiment on yourself. Congratulations, you may wind up helping millions.
Great analogy that drives home the point. Thank you for the good work you do.
Brilliant analogy! Now I finally understand. I became a LMHR when I started keto with IF. Feel healthier and stronger than ever before in my 50s
So amazing Dave! Great explanation. It's all about FLUX and metabolism, not concentration of a poison!
Dave Feldman is a true "citizen scientist" of the very first order. I am a retired physician and a ketogenic diet as done absolutely wonderful thing. In the setting of a HIGH HDL (60 or greater and a TRIGLYCERIDE LEVEL of 60 or less) s, I have tended to believe that a HIGH LDL is of little if any concern. I look forward to more research by Dave Feldman, and more TH-cam videos. I am intrigued when he says we may be looking at ApoB backwards, and I think his explanation of why this might be so makes a lot of sense.
You should be looking at focal vitamin C deficiency. On the Linus Pauling Heart Protocol, I am reversing my CAC so far by 30% or 200 points in just 20 months. Without worrying about cholesterol at all.
thank you for this video Dave you are amazing in the way you explain things I can’t wait for December 8.❤
Brilliant analogy! Thank you!
Thank you 😊 after 5 years i did my labs, 39 labs. The Dr office call me only because I have high colesterol, incredible, i stop them, sy, what about Insulin, triglycerides, HDL , ratio, my oxygen, my blood pressure etc. Everything perfect, 55 years old female, 127 pounds, with a lot of energy, healthy no meds. With my organs. Thanks again for this analogy ❤❤
Dave Feldman is a genius...
Thanks for this analogy. I understand for the first time. 👍
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...
Well presented Dave, following from Athens Greece, looking forward to the outcomes of the LMHR study and your cookie 🍪 experiment
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.
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.
Thank you🎉
Brilliant. Love the analogy!
Makes perfect sense to me.
Thank you Dave! This makes so much sense to me.
I couldn’t understand the pizza box scenario at all, but did inderstand the actual explanation easily. Pizza boxes just caused weird confusion that wasn’t needed Dave.
Dave you are a legend
Thanks. You are an excellent teacher.
Thanks Dave, well done. Makes sense to me, cheers!
Amazing presentation. Well done.
Does this mean LMHRs shouldn’t eat low carb diets? Or that they are fine eating low carb?
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!
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.
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..
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.
You're eating more saturated fats, that down regulates the ldl receptors on the liver thus leaving more atherosclerosis causing ApoB particles in circulation, resulting in increased LDL. Having a low CAC score just means you don't have calcified plaque, you could have plenty of soft plaque which is more harmful. Get a good quality CIMT test done.
The perfect video to better understand the LMHR phenotype without speaking English 😁 when translating the videos a lot of information is lost, so the visual work and analogy is of great help 🙏
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
I love that you were able to find stock photos of pizza boxes in various locations around houses. 😂
Very nice analogy. Thank U very much.❤
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!
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
I, too, am a LMHR. (LDL 231, HDL 79, TG 63) OMAD. 5'7 140, 60 years old. Feel like I'm 20.
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
Dave isn't risking 'the sound is low' comments anymore and is just going phat subs all the way instead 😂
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 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.
Awesome explanation!
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 🙏
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.
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!
Borderline here. Refused a statin for over 12 years now. Looking forward to your study results and what is learned. I am planning on keeping my high LDL because I believe it is healthy.
Is there a relation between LMHR and being in ketosis? Like do you need to be in ketosis to become a LMHR.
Not in my book! Though I am mostly Keto grain and sugar-free, I am not religious about it. Reversing my CAC Score dramatically on the Linus Pauling Heart Protocol without going to extremes.
Excellent analogy!
This was very helpful thank you. Glad you are doing this type of research. I think I might be one of those types as my LDL is high but triglycerides are not. Doctor suggested red yeast rice and eat healthy fats which I already do. My mom had high cholesterol they put her on statins. I wonder if her ALS was a result of these drugs.
Very easy to digest.😁 Thanks.
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.
A nice way to test if you got the analogy right is if you now want to have only the cheese and meat from the pizza from now on
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?
So what would be the implications for current treatment protocols?
Brilliant thank you
Bravo! Now, where can I get a copy of that presentation?...
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.
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.
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 ?
The trigliceride measurement in blood lab results include all triglicerides in blood, that in fasted state come from vldl, idl and ldl?
But then atherosclerosis would correlate much closer with triglyceride than apoB? Do we see that? If not, why not? Triglyceride lifecycle too short?
I was on heavy keto, avacado every day low or very low carbs. APOB 220, I was shocked. I think I am LMHR, triglicerides 66. Male 126 lbs., 71 yr old. I exercise. Lipoprotein test was also high. I was so shocked I stopped eating avacados.
Outstanding video! Keep doing this great job!
In summery: lipo proteins do *not cause* artheroscleroses.
You are correct! Focal vitamin C deficiency is the real issue. Reversing my CAC on the Linus Pauling Heart Protocol.
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 ?
How does one determine if they are a “lean mass hyper-responder”?
The explanation is great though Dave.
I’d just read a 2024 paper as it happens which was highlighting just how much more associated VLDL particles were with atherosclerosis than uLDL. Your explanation chimes completely with the findings of the paper. The paper wasn’t even concerned with Lean Mass Hyper-Responders, merely average populations. It just seems so sad that the profession are still struggling on with the LDL/ApoB deadend.
Apols, typo. uLDL should’ve read LDL above, but TH-cam won’t let me edit comments. I’ll link the paper in a separate comment.
It would be interesting to see how Eurythrocyte Sedimentation Rate (ESR) correlates with APOB and/or LDL
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.
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!
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?
I love the analogy: Pizza Boxes filled fatty cargo! Do chylomicrons deliver LDLs? If so, roving pizza cats (or vans) looking for customers?
Basically, what you are saying is that lean mass hyper responder is simply someone on a carnivore diet . Am I correct?
5 years high saturated animal fat carnivore here.
Best decision of my life.
Are you actually measuring the lipoprotein composition and particle sizes of these individuals? The previous theory stated that in case of a keto dieter who has high HDL, low triglycerides and high LDL, the LDL does not contain much ApoLipoB, but consists mainly of the larger, fluffy LDL particles which are not atherogenic. Did you count ApoLipoB in these people and found their numbers to be higher than the numbers of the larger fluffy LDL particles?
Very good analogy. I can understand the process better now.
Why doesn't the pizza boxes get recycled as quick as the cells gobble up the pizzas ? Isn't there an imbalance there in LHMRs ?
Look into how lipoproteins get cleared from the body. One primary mechanism for eliminating it is soluble fiber. LMHR may be partly a profile for fiber deficiency.
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.
Amazing work 👏🏻
Ah Dave, you are my Cholesterol Jesus, always with a insightful parable to help me understand life!
Gold
Not sure but I think I am LMHR. Total cholesterol 330....HDL 70....triglycerides 49....LDL 253....remnant 7. Been ketovore since 2011. Currently at 16% body fat
If you need another test subject Im available. My vldl hovers around 2 to 5 most tests.
What happens to a LMHR who takes statin to lower LDL-C, which leads to low LDL-c, low TG, and high HDL-c? Is that a a desirable condition?
lol god knows... And u have been hooked by the BS media
Low energy, brain fog, insulin resistance and muscle wasting. I didn’t experience this on a regular diet taking a statin for 10 + years (not the brain fog and low energy anyway). I’d attribute the low energy to reduced fuel delivery lipoproteins. Statins promote calcium and diabetes (higher glucose). Avoid. The injectable PCSK9 inhibitors lower LDL way down to < 40 and are very much in experimental right now. You are the human trials If you take it. Malpractice. People are going to have dementia because of this crap.
The current scientific consensus is that such a LMHR on statins would be expected to have substantially lower CVD risk than one with higher LDL-C (or ApoB).
@@christopherbrand5360 U might be the BOT, king of buzzwords.
@@250txc ???? 🤣
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
I apologize for not subscribing before now.