Interesting. Looking forward to the explanation of how others who did not have a lean mass (and may still not be lean), might end up with a LMHR lipid profile after going keto.
This is so fascinating for me(I'm 55). I'm 4.7 years animal product only eater and my TOTAL Cholesterol went from 5.99mmol/L in 2019 to 10.10mmol/L in 2022, HDL went from 1.63mmol/L in 2019 to 2.23mmol/L in 2022, Tri's went from 1.18 in 2019 to 0.88mmol/L......my LDL went from 3.82mmol/L in 2019 to 7.47mmol/L in 2022. My Dr freaked out because of that LDL but was mystified because my Chol/HDL (Risk Ratio) was 4.53 and normally she is happy as long as its under 4.9 so she was very confused but open to new information. My weight dropped from 240lbs in 2019 down to 170lbs 8months after starting carnivore and it's been so rock solid at 170 that we thought the scale was broken and bought a new one.....wasn't broken. Cheers
@boutthere3374 So you have no fears of developing plaque with LDL levels so high? Have you had a CAC test to at least establish a baseline? I would. Losing 70lbs of fat is gloriously good for you, but IMO I wouldn't put ALL my eggs into one basket. I would carefully monitor plaque and also not restrict myself to carnivore only. Most available evidence consistently back mediterranean and proper lifestyle.
@@drott150 I was nervous in the beginning and your suggestion isn't lost on me but I've lost so much faith in the so called "experts" since 2020 combined with all the improvements I've experienced that I'm no longer concerned.
@@boutthere3374 Yes I totally get what you're saying, especially with what happened since 2020. But we mustn't succumb to throwing the baby out with the bath water due to our frustration. Not all science is lies, not all of the experts are corrupted frauds. We must take up the challenge of researching studies and endure the struggle of sifting through the BS to get to the nuggets of truth. Like I said, if you haven't gotten a CAC test, it's so easy to get. 15 minutes in and out and not expensive if you have to pay out of pocket. At least then you will know what you're dealing with instead of putting a high LDL diet into your body in perpetuity without knowing your existing risk baseline. I lost 50 lbs on low carb and then switched to a balanced mediterranean diet afterwards. I've kept the weight off no problem since. Remember, we know what plaque is. It IS comprised of trapped cholesterol. The exact process of how it ends up as plaque is a more complicated question...but plaque IS accumulated, trapped LDL cholesterol. LDL plays some kind of role, there is no doubt about that. Letting it run at sky high levels may prove catastrophic.
@@drott150I was mostly vegetarian up to 2019... ldl 46, hdl 47, tri 65. Ran 80 to 100 miles weekly, rode just over 100 hundred miles weekly and played soccer 1 or twice a week, and had a heart attack 🤔. Prior to my MI, on my mostly vegetarian and was completely whole food, I lost almost every bit of testosterone... total 24. All my sex hormones completely screwed off. My cardio, supposedly the best around, cleared me 5 times, including 5 days prior to my MI.. i was having severe chest pain, weakness. After my MI, he prescribed me a statin with my already very low cholesterol. After 1 month my ldl went to 20, hdl and tri didn't budge, my cardio told me to stop the statin immediately. LDL is vitally important to cell structure. Without it, or low is worse than high. After I started carnivore, approximately 40 days, all more hormones where all back to numbers never seen by lab results previously. Also, my hdl, vit d rose and tri went down which pharmaceuticals or my whole food plant diet didn't accomplish. And, if the medical world knows so much about "heart disease" and how to handle it, why is it that every year the number of deaths increase, substantially? The medical field has put all the eggs in 1 basket. Statins, beta blocker and blood pressure medication based on a total cholesterol score without care of history or make up of cholesterol... thats irresponsible at minimum. IMO
@@johngalt3659 That's really interesting, thanks for sharing. I personally wouldn't consider a vegetarian diet healthy because I feel it is unnatural for humans. We are designed to eat at least some meat. Going without it can and does result in nutritional deficiencies that may be related to why you had your problems. Or, it may be you're simply a genetic outlier compared to the general population for reasons that are not communicated or known by you. If you consistently maintained such low cholesterol for your entire life, some other driving factor must have been responsible for your MI. For the most (not all) people, having cholesterol levels that consistently low helps to protect them from heart disease (barring any special problems peculiar to them). Today, most cardio science points to a combination of inflammation and high lipids together as primary causes for atherosclerosis. The inflammation part is largely tied to metabolic health, which includes excess sugar and carbohydrate consumption (especially refined carbs). As to why the number of deaths remains high and may be increasing is because so many people are obese and getting more obese every year. Entire generations are being raised on highly processed, refined foods that are high in saturated fat and sugar. This has caused skyrocketing rates of juvenile diabetes and early onset/advanced diabetes in adults. Obesity and diabetes are directly correlated with heart disease. So, the explanation for increasing heart disease rates is pretty straightforward, despite what modern medical science knows about what usually causes it.
I hope you are going to continue your lecture Professor Feldman! You are explaining things so well. Btw thank you also, (along with Siobhan Huggins), for giving us in this community Own Your Labs. My husband and I have gotten a boat load of labs done in the past 2 years; and VERY affordably to boot. It’s great that we can have these to assess our metabolic health (along with our health care provider). We love being Citizen Scientists as well as we’ve given permission for your foundation to use our results in your research.
summary of the video Introduction: - The video is simplifying the lipid energy model to explain high LDL cholesterol in "lean mass hyperresponders", especially for a lay audience. Biochemistry background: - Very low density lipoproteins (VLDL) are produced in the liver and transport lipids like triglycerides and cholesterol in the blood. - VLDL is rich in triglycerides originally from fat stores in the body. - The lipid energy model focuses on high turnover of triglyceride-rich VLDL. Key processes in VLDL turnover: 1. VLDL drops off its triglyceride cargo into cells as it circulates, transforming into triglyceride-poor LDL. 2. Nearby high-density lipoprotein (HDL) particles pick up components released during this process. 3. This results in higher LDL concentrations but also boosts HDL levels. Explanation for lean hyperresponders: - More VLDL secretion and turnover leads to higher LDL levels through the above mechanisms. - Increased HDL is also explained by more components being picked up during VLDL processing. - Lean, metabolically healthy individuals exhibit this effect due to high lipid flux and less dysfunctional fat cells. Role of fat cells: - Studies show large, dysfunctional visceral fat cells are associated with insulin resistance and a poor lipid profile. - Specifically linked to low HDL, high triglycerides and LDL. - Dysfunctional fat cells may limit triglyceride delivery to VLDL, reducing its processing. Proposed "traffic jam" mechanism: - Reduced triglyceride acceptance by fat cells means less VLDL conversion and HDL formation. - This could explain disease links if we're just seeing blocked lipid transport ("traffic jam"). Conclusion: - Failure of lipoproteins to effectively deliver lipids may underlie associated diseases, not just lipids themselves. - Keeping this delivery/trafficking perspective is important for understanding lipid metabolism.
You’re the best! I am a LMHR and also a post menopausal woman. Trying to explain to my pcp why I don’t need a statin - would actually be worse for me! I am going to send this to her!
Thank you Mr Feldman. I'm very much a layperson on these matters but although I had to watch your presentation a couple of times you did manage to drag me along to some kind of understanding of the gross features of your model. I'm looking forward to a part 2 of this simplified approach. Best regards.
@jamesdellaneve9005 Peter's always an arrogant jerk. Close your eyes while listening to him, or mute the sound while you're viewing his videos and you'll see that he's an arrogant jerk.
I don't think he's right about everything, but 1) be respectful, and 2) your comment is incoherent, which is not a good look when trying to lecture someone 😂
I find Attia, pretty knowledgeable and not the least bit arrogant. Found his information valuable as I do have high LDL, but low VLDL and triglycerides and blood glucose….
Excellent presentation!! Please continue to post more on your channel! ☺️ I believe you have found your knew destiny- training docs! You need to become a Professor Dave!
HDL also takes lipid efflux from macrophages when the ABC-A1 transporter is potentiated at an insulin nadir - lipids specifically Cholesterol which the macrophage has no other way to draw down (TG's it can use for energy, phospholipids it can bleb off). This is another reason why HDL-C goes up on a low carb diet (LMHR or OMNR - obese mass normo-responder), and one which is particularly important for atherosclerotic progression of macrophages in the arterial wall into foam cells.
I would like to see a deeper explanation of how the VLDL process at the beginning of the flow-chart gets started. The explanation of what happens after makes sense, but what exactly about low-carb/keto gets it started. I'm also interested in whether the resulting LDL has the same impact as LDL in a metabolically unhealthy person. BTW, I'm one of those folks who meet the LMHR triad (HDL consistently over 100, TG consistently under 50, LDL consistently over 200 but was higher when I was losing weight). BMI is 22.8, but I'm not an athlete. Just try to stay active enough to do the things I love, such as pickleball and hiking.
This is the video abstract for our Lipid Energy Model paper: ruclips.net/video/AkzxESsTJyM/видео.htmlsi=HwLcnwJSmDNPXgkK -- and of course, you can check out the paper itself (in link below it)
I’ve watched and read all of that, and I’m still a bit unclear on what triggers the initial dump of lipoprotein. Food? Exercise? Something else? Does it happen for everyone? Or am I an outlier?
Wow, this is the first time I've got an explanation why my HDL are low. I fit the body type of a LMHR and my cholesterol readings hyper responds to my diet. On a ketogenic diet my cholesterol levels skyrockets to: Tot: 360 mg/dl 9,0 mmol/L LDL: 280 mg/dl 7,0 mmol/L But my HDL is too low HDL: 24 mg/dl 0,6 mmol TGR: ? 1,9 mmol/ L I'm probably insulin resistent.
When you look at adipocytes of "skinny people," there is a sizable percentage that actually are metabolically unhealthy, and at the end of the day, that's the impact I believe, not actual weight. The swollen engorged adipocytes your video depicted matching an obese person isn't always the case. As you stated, the macrophages coming in to the presence of these adipocytes that are engorged and cannot take on anymore triglycerides seems to be the problem, and I wonder if THAT is the problem with cardiovascular disease. Instead of the smooth endothelial lining inside the arteries, you have inflamed endothelial lining, which allows fat cells to become lodged in, and the dysfunctional endothelium tries to build over that litter, over and over again. Does anybody else see it this way? It cannot be overstated, I appreciate SO MUCH what you are doing here.
I need to dive into this. I've been on a keto-carnivore diet for 6 months, lost 50 pounds, reversed a bunch of conditions, but my triglycerides skyrocketed into the thousands upon thousands and my HDL tanked.
That's the oposite of my KETO experience and I'm not a LMHR. My trigs were 360 and came down to 65 but I also started hiking and trail running so I'm not sure which had the biggest impact on trigs but the more I exercise the higher my HDL goes. Cardio exercise has more benefit than diet Just how many blood tests have you had? It sounds like an anomaly that needs retesting.
Oh so it’s very similar to FH 1) normal VLDL turnover (no VLDL and TG accumulation) 2) very high VLDL production and turnover to LDL 3) net accumulation of LDL due to overwhelmed clearance (LDL-R mediated in FH, unknown in LMHR) So functionally this is an FH picture… Important to remember that in FH the LDLR deficiency does NOT explain the high LDL-C levels (>200). This is because LDLr is a high affinity low capacity system that is easily saturated, most of LDL clearance happens with receptors not yet identified with low affinity but high capacity. FH patients have very high VLDL production with intact TRL turnover (similar to LMHR) which leads to accumulation of LDL (similar to LMHR) and high ASCVD risk (similar to LMHR?)
To think at one point in my life Triglycerides were around 300 and only traces of HDL could be detected in my blood. On my way to NASH liver disease at that point.
@@hikerJohn I had all the signs, but no official diagnosis at that point. At the time only a liver biopsy could officially determine it back then. I had the biopsy in 2002 and received the diagnosis of NASH.
@@hikerJohn Oh ok. They had me down for fatty liver disease via a sonogram of the abdomen. That, and splenomegaly both. NASH, and the stages leading up to it, including NAFLD, are all precursors to NASH involving years. Also, only a small, but ever growing percent, of these patients ever advance to NASH. At the time I experienced it the rate was less than five percent of patients with fatty liver ever advanced that far, but that was over twenty years ago.
I seem to have already have CAD. Keto for a year dropped 40lbs reversed diabetes but have high ldl 283! HDL has gone up to 50 trigs are 120ish. Cardiologist freaks me to take plavix and repatha because of heart scan (but they didn’t do a CAC score. So I don’t know what to do!
As a keto based athlete why is my HDL not going up like the LMHR model when everything else is the same. The more I train my aerobic capacity the higher my HDL goes but it has never gone above 63 but when not training it drops to as low as 26. That's the only thing that makes me NOT a LMHR. My Trigs have been as low as 47 but were as high as 215 when I was not training because of a knee injury. Trigs before kito and before aerobic training were as high as 357. Trigs are always highest when HDL is lowest. B=When my HDL is high and Trigs are low my LDL is still well over 200. My lowest LDL level was when my HDL was lowest and trigs were high. I wonder what role age has to do with all of this?
Genetics. Some people have low HDL due to genetics specially south Asians. My HDL is about 113, LDL 270 and all I do is 10000 steps a day and a few sets of sprints twice a week and a couple hundred push ups a week nothing extreme or athletic
The high LDL just shows your energy transport mechanism has been corrected by becoming fat adapted. You need to study those of us who respond, but TG, HDl are still a little out of whack and even are LDL-P pattern B. I would call myself a partial responder. I am sure it is a huge improvement, but not total.
Nice explanation. While like the lipid energy model.. though (as I recently commented to Nickolas ) where there were some comments about the LMHR name. I think the name could be problematic. Is there a strong reason to expect its only for lean people? this could mislead people, or their doctor, to exclude them from the group because they have higher BMI-- doctors might tell someone with a higher BMI or being overweight that the results don't apply to them. Maybe a better name would be Ketogenic HyperResponder. If one had normal LDL before keto but see it "hyperrespond" to keto, there is still a strong push by doctors for statins. But if there is something deeper that comes from your study, the name will result in many many doctors ignoring it for many patients.
Remember seeing one video, where they referenced a study where the harm from LDL particles was on a graph per size, and the difference between large and small LDL was something like 14% (cant remember the number exactly, but small anyway). Why are people concentrating so much on what their LDL size might be if they are both harmful, and the larger ones only slightly better?
Like the other patterns mentioned in this video, I think LDL size is likely a downstream result of this context more than it is a cause in and of itself. But this is why we need the LMHRstudy to better understand the risk involved.
@@realDaveFeldman yeah but my point was: why even bother with particle sizes, if that study I saw is correct and all the LDL particles are harmful and the risk varies only slightly? If that is correct then ApoB count is enough to know ones likely risk. If people on keto believe high ApoB/LDL doesn't affect them like other people, it would naturally be nice to see a study demonstrating that. I will be surprised if it pans out and low carb offers any protection against atherosclerosis.
Hi I think I’m that layman you’re trying to reach but having trouble applying it to my numbers. Trig 43, HDL 91, calc LDL 122. If the upcoming announcement shows LMHR doesn’t correlate with increased cardiovascular risk will it follow that my numbers are not likely to cause increased cardiovascular risk even though I don’t cross the LDL threshold for LMHR definition?
Just because you can mechanistically explain body's response to a diet, does not mean it is healthy!!! For example you can equally well explain diabetes, atherosclerosis and many more diseases, but that does not mean they are now not a problem since you understand them (better)... Understanding mechanism is not a justification.
I followed a high carb vegan diet for 6 years, then had a major heart attack. Now Im following a carnivore diet, but my LDL is about 4 times higher than when i was vegan. Doctors want me to take statins to lower it, but it was so low for many years prior to the attack. Im definitely a LMHR. Is eating this way the path to heal my damaged arteries, or is my high LDL dangerous BECAUSE my arteries are compromised??
One video showed some study, where the difference between LDL sizes for heart disease wasn't that significant, cant remember exactly but could have been only like 14% difference. So all LDL particles caused heart disease, the smaller ones a bit more.
I'm new, so forgive my Captain Obvious remark, but I would think one of the most pressing issues with the long-term validation of this theory would be allowing such a high level of LDL, despite whatever level of theoretical confidence there may be LDL>200 shouldn't be a problem for LMHRs specifically. So, for any trials that allow these prolonged 200+ LDL excursions, it would seem important to find a method that can very accurately detect small changes in both hard and soft hard plaque (amongst those that already have plaque) within relatively short time intervals. That way, if things aren't progressing as hoped, the trial can be halted rapidly with minimal harm to the participants. And with the plaque findings - either good, bad or neutral - further insights into the credibility of the proposed theory could be gleaned quickly. I recently read the following study: *"High-intensity interval training induces beneficial effects on coronary atheromatous plaques: a randomized trial."* In this study they used an intravascular method for measuring plaque I had never heard of before (being a layman). I'm not sure if it is capable of measuring both hard and soft plaque, but presumably it's superior to CAC and other methods currently available to make atherosclerotic measurements (albeit it is invasive). They use it over a short timeframe in this study, so one would assume it has the precision and fidelity to deliver the results they hang their hats on. Maybe it could be used for one of your studies? Here's an excerpt describing it: *_"multivessel intravascular imaging was performed when feasible by a combination IVUS- and near-infrared spectroscopy (NIRS) catheter using an automated pullback system (TVC-MC8 model system with a 3.2Fr 40 MHz catheter, Infraredx, Burlington, Massachusetts). Following administration of intracoronary nitroglycerine, the NIRS-IVUS catheter was positioned as distally as possible in the coronary artery. To ensure matching coronary segments at baseline and follow-up, the distal starting points of the pullbacks were recorded angiographically to assist in registration of the corresponding segments at follow-up."_*
To those who are familiar with the Randle cycle, it is not surprising that an LMHR should exist. More relevant is the question whether LMHRs (if they exist) are vulnerable to a long-term exposure to elevated levels of LDL. The answer to the above question is likely to be YES. From many studies, the mechanism behind LDL driven atherosclerosis seems pretty clear. In the aggregate, the studies point to oxidative damages, to arterial walls, from which people have harder time recovering as they age. That is, the elevated levels of LDL become an issue as one ages due to diminishing capabilities to handle oxidative damages. Consider, in general, why CVs occur more frequently in older people. Proving the above with a low p-value is difficult, because in the field of nutritional science, there are competing economic interests. On the other hand, to those who have been examining scientific literature for a long time with a modicum of objectivity, all the handwringing over the ketogenic diet and carnivore diet is ridiculous. Although the ketogenic diet and carnivore diet may show short-term benefits, they are very likely to accelerate age-dependent declines in CV functions.
You are eloquently explaining how vldl is dropping off triglycerides. I am wondering why you are calling it LDL cholesterol , VLDL cholesterol and HDL cholesterol. We need to demand these lipoproteins be called what they are, it is confusing to call them cholesterol. They carry a variety of fat based items, we don’t name them based on what they transport.
Interesting. Looking forward to the explanation of how others who did not have a lean mass (and may still not be lean), might end up with a LMHR lipid profile after going keto.
This is so fascinating for me(I'm 55). I'm 4.7 years animal product only eater and my TOTAL Cholesterol went from 5.99mmol/L in 2019 to 10.10mmol/L in 2022, HDL went from 1.63mmol/L in 2019 to 2.23mmol/L in 2022, Tri's went from 1.18 in 2019 to 0.88mmol/L......my LDL went from 3.82mmol/L in 2019 to 7.47mmol/L in 2022. My Dr freaked out because of that LDL but was mystified because my Chol/HDL (Risk Ratio) was 4.53 and normally she is happy as long as its under 4.9 so she was very confused but open to new information. My weight dropped from 240lbs in 2019 down to 170lbs 8months after starting carnivore and it's been so rock solid at 170 that we thought the scale was broken and bought a new one.....wasn't broken. Cheers
@boutthere3374 So you have no fears of developing plaque with LDL levels so high? Have you had a CAC test to at least establish a baseline? I would. Losing 70lbs of fat is gloriously good for you, but IMO I wouldn't put ALL my eggs into one basket. I would carefully monitor plaque and also not restrict myself to carnivore only. Most available evidence consistently back mediterranean and proper lifestyle.
@@drott150 I was nervous in the beginning and your suggestion isn't lost on me but I've lost so much faith in the so called "experts" since 2020 combined with all the improvements I've experienced that I'm no longer concerned.
@@boutthere3374 Yes I totally get what you're saying, especially with what happened since 2020. But we mustn't succumb to throwing the baby out with the bath water due to our frustration. Not all science is lies, not all of the experts are corrupted frauds. We must take up the challenge of researching studies and endure the struggle of sifting through the BS to get to the nuggets of truth. Like I said, if you haven't gotten a CAC test, it's so easy to get. 15 minutes in and out and not expensive if you have to pay out of pocket. At least then you will know what you're dealing with instead of putting a high LDL diet into your body in perpetuity without knowing your existing risk baseline. I lost 50 lbs on low carb and then switched to a balanced mediterranean diet afterwards. I've kept the weight off no problem since.
Remember, we know what plaque is. It IS comprised of trapped cholesterol. The exact process of how it ends up as plaque is a more complicated question...but plaque IS accumulated, trapped LDL cholesterol. LDL plays some kind of role, there is no doubt about that. Letting it run at sky high levels may prove catastrophic.
@@drott150I was mostly vegetarian up to 2019... ldl 46, hdl 47, tri 65. Ran 80 to 100 miles weekly, rode just over 100 hundred miles weekly and played soccer 1 or twice a week, and had a heart attack 🤔. Prior to my MI, on my mostly vegetarian and was completely whole food, I lost almost every bit of testosterone... total 24. All my sex hormones completely screwed off. My cardio, supposedly the best around, cleared me 5 times, including 5 days prior to my MI.. i was having severe chest pain, weakness. After my MI, he prescribed me a statin with my already very low cholesterol. After 1 month my ldl went to 20, hdl and tri didn't budge, my cardio told me to stop the statin immediately. LDL is vitally important to cell structure. Without it, or low is worse than high. After I started carnivore, approximately 40 days, all more hormones where all back to numbers never seen by lab results previously. Also, my hdl, vit d rose and tri went down which pharmaceuticals or my whole food plant diet didn't accomplish. And, if the medical world knows so much about "heart disease" and how to handle it, why is it that every year the number of deaths increase, substantially?
The medical field has put all the eggs in 1 basket. Statins, beta blocker and blood pressure medication based on a total cholesterol score without care of history or make up of cholesterol... thats irresponsible at minimum. IMO
@@johngalt3659 That's really interesting, thanks for sharing. I personally wouldn't consider a vegetarian diet healthy because I feel it is unnatural for humans. We are designed to eat at least some meat. Going without it can and does result in nutritional deficiencies that may be related to why you had your problems. Or, it may be you're simply a genetic outlier compared to the general population for reasons that are not communicated or known by you. If you consistently maintained such low cholesterol for your entire life, some other driving factor must have been responsible for your MI. For the most (not all) people, having cholesterol levels that consistently low helps to protect them from heart disease (barring any special problems peculiar to them).
Today, most cardio science points to a combination of inflammation and high lipids together as primary causes for atherosclerosis. The inflammation part is largely tied to metabolic health, which includes excess sugar and carbohydrate consumption (especially refined carbs).
As to why the number of deaths remains high and may be increasing is because so many people are obese and getting more obese every year. Entire generations are being raised on highly processed, refined foods that are high in saturated fat and sugar. This has caused skyrocketing rates of juvenile diabetes and early onset/advanced diabetes in adults. Obesity and diabetes are directly correlated with heart disease. So, the explanation for increasing heart disease rates is pretty straightforward, despite what modern medical science knows about what usually causes it.
I hope you are going to continue your lecture Professor Feldman! You are explaining things so well. Btw thank you also, (along with Siobhan Huggins), for giving us in this community Own Your Labs. My husband and I have gotten a boat load of labs done in the past 2 years; and VERY affordably to boot. It’s great that we can have these to assess our metabolic health (along with our health care provider). We love being Citizen Scientists as well as we’ve given permission for your foundation to use our results in your research.
What is the name of the lab?
@@joy_1939 Own Your Labs (google it)
@@joy_1939 Own Your Labs
everything is falling into place very elegantly 🤗
it would be really great if in your slide you mentioned the non-US units as well.
Decalitre? It sounds metric
summary of the video
Introduction:
- The video is simplifying the lipid energy model to explain high LDL cholesterol in "lean mass hyperresponders", especially for a lay audience.
Biochemistry background:
- Very low density lipoproteins (VLDL) are produced in the liver and transport lipids like triglycerides and cholesterol in the blood.
- VLDL is rich in triglycerides originally from fat stores in the body.
- The lipid energy model focuses on high turnover of triglyceride-rich VLDL.
Key processes in VLDL turnover:
1. VLDL drops off its triglyceride cargo into cells as it circulates, transforming into triglyceride-poor LDL.
2. Nearby high-density lipoprotein (HDL) particles pick up components released during this process.
3. This results in higher LDL concentrations but also boosts HDL levels.
Explanation for lean hyperresponders:
- More VLDL secretion and turnover leads to higher LDL levels through the above mechanisms.
- Increased HDL is also explained by more components being picked up during VLDL processing.
- Lean, metabolically healthy individuals exhibit this effect due to high lipid flux and less dysfunctional fat cells.
Role of fat cells:
- Studies show large, dysfunctional visceral fat cells are associated with insulin resistance and a poor lipid profile.
- Specifically linked to low HDL, high triglycerides and LDL.
- Dysfunctional fat cells may limit triglyceride delivery to VLDL, reducing its processing.
Proposed "traffic jam" mechanism:
- Reduced triglyceride acceptance by fat cells means less VLDL conversion and HDL formation.
- This could explain disease links if we're just seeing blocked lipid transport ("traffic jam").
Conclusion:
- Failure of lipoproteins to effectively deliver lipids may underlie associated diseases, not just lipids themselves.
- Keeping this delivery/trafficking perspective is important for understanding lipid metabolism.
You’re the best! I am a LMHR and also a post menopausal woman. Trying to explain to my pcp why I don’t need a statin - would actually be worse for me! I am going to send this to her!
Thank you Mr Feldman. I'm very much a layperson on these matters but although I had to watch your presentation a couple of times you did manage to drag me along to some kind of understanding of the gross features of your model. I'm looking forward to a part 2 of this simplified approach. Best regards.
Dr Attia R U listening?? Ignorance is bliss, what we do, so lets hear something for a change!
Yeah. Peter is a jerk. At least, he was when he interviewed Dave. The kind of arrogant Doctor that gives Doctors a bad name.
@@jamesdellaneve9005hubris is just so unappealing
@jamesdellaneve9005
Peter's always an arrogant jerk.
Close your eyes while listening to him, or mute the sound while you're viewing his videos
and you'll see that he's an arrogant jerk.
I don't think he's right about everything, but 1) be respectful, and 2) your comment is incoherent, which is not a good look when trying to lecture someone 😂
I find Attia, pretty knowledgeable and not the least bit arrogant. Found his information valuable as I do have high LDL, but low VLDL and triglycerides and blood glucose….
Well that makes complete sense…. And the rhetorical question is completely relevant…. What is causing the traffic jam…. We need to find out!!!
Excellent presentation!! Please continue to post more on your channel! ☺️ I believe you have found your knew destiny- training docs! You need to become a Professor Dave!
Best channel about the topic. Amazing!!!
Excellent video. Pointed and clear. Bravo!
Now THAT makes complete sense!
Fascinating - thank you for these videos to help me understand what is going on with me!! ;)
HDL also takes lipid efflux from macrophages when the ABC-A1 transporter is potentiated at an insulin nadir - lipids specifically Cholesterol which the macrophage has no other way to draw down (TG's it can use for energy, phospholipids it can bleb off). This is another reason why HDL-C goes up on a low carb diet (LMHR or OMNR - obese mass normo-responder), and one which is particularly important for atherosclerotic progression of macrophages in the arterial wall into foam cells.
I would like to see a deeper explanation of how the VLDL process at the beginning of the flow-chart gets started. The explanation of what happens after makes sense, but what exactly about low-carb/keto gets it started. I'm also interested in whether the resulting LDL has the same impact as LDL in a metabolically unhealthy person. BTW, I'm one of those folks who meet the LMHR triad (HDL consistently over 100, TG consistently under 50, LDL consistently over 200 but was higher when I was losing weight). BMI is 22.8, but I'm not an athlete. Just try to stay active enough to do the things I love, such as pickleball and hiking.
I'd advise getting your oxLDL measured (ideally want this below 60).
This is the video abstract for our Lipid Energy Model paper: ruclips.net/video/AkzxESsTJyM/видео.htmlsi=HwLcnwJSmDNPXgkK -- and of course, you can check out the paper itself (in link below it)
I’ve watched and read all of that, and I’m still a bit unclear on what triggers the initial dump of lipoprotein. Food? Exercise? Something else? Does it happen for everyone? Or am I an outlier?
Fantastic video, and great explanations..thank you !
Wow, this is the first time I've got an explanation why my HDL are low.
I fit the body type of a LMHR and my cholesterol readings hyper responds to my diet.
On a ketogenic diet my cholesterol levels skyrockets to:
Tot: 360 mg/dl 9,0 mmol/L
LDL: 280 mg/dl 7,0 mmol/L
But my HDL is too low
HDL: 24 mg/dl 0,6 mmol
TGR: ? 1,9 mmol/ L
I'm probably insulin resistent.
As someone living in Europe 🇪🇺 I probably won't ever have a "blood test " because I have never had any, not in 74 years. Carry On.
When you look at adipocytes of "skinny people," there is a sizable percentage that actually are metabolically unhealthy, and at the end of the day, that's the impact I believe, not actual weight. The swollen engorged adipocytes your video depicted matching an obese person isn't always the case. As you stated, the macrophages coming in to the presence of these adipocytes that are engorged and cannot take on anymore triglycerides seems to be the problem, and I wonder if THAT is the problem with cardiovascular disease. Instead of the smooth endothelial lining inside the arteries, you have inflamed endothelial lining, which allows fat cells to become lodged in, and the dysfunctional endothelium tries to build over that litter, over and over again. Does anybody else see it this way?
It cannot be overstated, I appreciate SO MUCH what you are doing here.
I need to dive into this. I've been on a keto-carnivore diet for 6 months, lost 50 pounds, reversed a bunch of conditions, but my triglycerides skyrocketed into the thousands upon thousands and my HDL tanked.
That's the oposite of my KETO experience and I'm not a LMHR. My trigs were 360 and came down to 65 but I also started hiking and trail running so I'm not sure which had the biggest impact on trigs but the more I exercise the higher my HDL goes. Cardio exercise has more benefit than diet
Just how many blood tests have you had? It sounds like an anomaly that needs retesting.
@@hikerJohn yeah, maybe something with the fasting period prior to the blood tests?
@@zlmdragon. You can't get that lean and function normally. You could maybe do it as an experiment but not as a lifestyle.
@@wocket42 You should fast for 9-10 hrs but not for a 24 hr period. You want to reduce the variables not increase them.
after your weight stabilizes wait a few months and check again
Oh so it’s very similar to FH
1) normal VLDL turnover (no VLDL and TG accumulation)
2) very high VLDL production and turnover to LDL
3) net accumulation of LDL due to overwhelmed clearance (LDL-R mediated in FH, unknown in LMHR)
So functionally this is an FH picture…
Important to remember that in FH the LDLR deficiency does NOT explain the high LDL-C levels (>200). This is because LDLr is a high affinity low capacity system that is easily saturated, most of LDL clearance happens with receptors not yet identified with low affinity but high capacity. FH patients have very high VLDL production with intact TRL turnover (similar to LMHR) which leads to accumulation of LDL (similar to LMHR) and high ASCVD risk (similar to LMHR?)
To think at one point in my life Triglycerides were around 300 and only traces of HDL could be detected in my blood. On my way to NASH liver disease at that point.
What do you mean by on your way to NASH liver disease? Did you have steatohepatitis?
@@hikerJohn I had all the signs, but no official diagnosis at that point. At the time only a liver biopsy could officially determine it back then. I had the biopsy in 2002 and received the diagnosis of NASH.
@@frankenz66 That makes sense. I was diagnosed with NAFLD from an MRI
@@hikerJohn Oh ok. They had me down for fatty liver disease via a sonogram of the abdomen. That, and splenomegaly both. NASH, and the stages leading up to it, including NAFLD, are all precursors to NASH involving years. Also, only a small, but ever growing percent, of these patients ever advance to NASH. At the time I experienced it the rate was less than five percent of patients with fatty liver ever advanced that far, but that was over twenty years ago.
Outstanding
I seem to have already have CAD. Keto for a year dropped 40lbs reversed diabetes but have high ldl 283! HDL has gone up to 50 trigs are 120ish. Cardiologist freaks me to take plavix and repatha because of heart scan (but they didn’t do a CAC score. So I don’t know what to do!
Thanks !
As a keto based athlete why is my HDL not going up like the LMHR model when everything else is the same. The more I train my aerobic capacity the higher my HDL goes but it has never gone above 63 but when not training it drops to as low as 26. That's the only thing that makes me NOT a LMHR. My Trigs have been as low as 47 but were as high as 215 when I was not training because of a knee injury. Trigs before kito and before aerobic training were as high as 357. Trigs are always highest when HDL is lowest. B=When my HDL is high and Trigs are low my LDL is still well over 200. My lowest LDL level was when my HDL was lowest and trigs were high.
I wonder what role age has to do with all of this?
Same for me. Trigs at 40, but HDL never gets above 70. No idea why.
Genetics. Some people have low HDL due to genetics specially south Asians. My HDL is about 113, LDL 270 and all I do is 10000 steps a day and a few sets of sprints twice a week and a couple hundred push ups a week nothing extreme or athletic
The high LDL just shows your energy transport mechanism has been corrected by becoming fat adapted. You need to study those of us who respond, but TG, HDl are still a little out of whack and even are LDL-P pattern B. I would call myself a partial responder. I am sure it is a huge improvement, but not total.
Nice explanation. While like the lipid energy model.. though (as I recently commented to Nickolas ) where there were some comments about the LMHR name. I think the name could be problematic. Is there a strong reason to expect its only for lean people? this could mislead people, or their doctor, to exclude them from the group because they have higher BMI-- doctors might tell someone with a higher BMI or being overweight that the results don't apply to them. Maybe a better name would be Ketogenic HyperResponder. If one had normal LDL before keto but see it "hyperrespond" to keto, there is still a strong push by doctors for statins. But if there is something deeper that comes from your study, the name will result in many many doctors ignoring it for many patients.
This sounds like "lipoprotein resistance" in the metabolically challenged - LOL!
Traffic ham analogy 🤔. How about submarine??? 🤔 💭
Remember seeing one video, where they referenced a study where the harm from LDL particles was on a graph per size, and the difference between large and small LDL was something like 14% (cant remember the number exactly, but small anyway). Why are people concentrating so much on what their LDL size might be if they are both harmful, and the larger ones only slightly better?
Like the other patterns mentioned in this video, I think LDL size is likely a downstream result of this context more than it is a cause in and of itself. But this is why we need the LMHRstudy to better understand the risk involved.
@@realDaveFeldman yeah but my point was: why even bother with particle sizes, if that study I saw is correct and all the LDL particles are harmful and the risk varies only slightly? If that is correct then ApoB count is enough to know ones likely risk.
If people on keto believe high ApoB/LDL doesn't affect them like other people, it would naturally be nice to see a study demonstrating that. I will be surprised if it pans out and low carb offers any protection against atherosclerosis.
Higher LDL because something is being delivered to downstream to an active consumer..
I loved the explanation. What is the name of the lab?
Hi I think I’m that layman you’re trying to reach but having trouble applying it to my numbers. Trig 43, HDL 91, calc LDL 122. If the upcoming announcement shows LMHR doesn’t correlate with increased cardiovascular risk will it follow that my numbers are not likely to cause increased cardiovascular risk even though I don’t cross the LDL threshold for LMHR definition?
Just because you can mechanistically explain body's response to a diet, does not mean it is healthy!!!
For example you can equally well explain diabetes, atherosclerosis and many more diseases, but that does not mean they are now not a problem since you understand them (better)...
Understanding mechanism is not a justification.
I followed a high carb vegan diet for 6 years, then had a major heart attack.
Now Im following a carnivore diet, but my LDL is about 4 times higher than when i was vegan. Doctors want me to take statins to lower it, but it was so low for many years prior to the attack.
Im definitely a LMHR.
Is eating this way the path to heal my damaged arteries, or is my high LDL dangerous BECAUSE my arteries are compromised??
I would also like to know this. Is it too good to be true?
👍👍
Thank you, very understandable. How do the small, dense lipoproteins initiate the atherosclerotic process? Anyone?
Maybe they don't in either case.
lipoproteins do not initiate anything, they are just a transport. Inflammation initiates the process.
One video showed some study, where the difference between LDL sizes for heart disease wasn't that significant, cant remember exactly but could have been only like 14% difference. So all LDL particles caused heart disease, the smaller ones a bit more.
I'm new, so forgive my Captain Obvious remark, but I would think one of the most pressing issues with the long-term validation of this theory would be allowing such a high level of LDL, despite whatever level of theoretical confidence there may be LDL>200 shouldn't be a problem for LMHRs specifically. So, for any trials that allow these prolonged 200+ LDL excursions, it would seem important to find a method that can very accurately detect small changes in both hard and soft hard plaque (amongst those that already have plaque) within relatively short time intervals. That way, if things aren't progressing as hoped, the trial can be halted rapidly with minimal harm to the participants. And with the plaque findings - either good, bad or neutral - further insights into the credibility of the proposed theory could be gleaned quickly.
I recently read the following study: *"High-intensity interval training induces beneficial effects on coronary atheromatous plaques: a randomized trial."* In this study they used an intravascular method for measuring plaque I had never heard of before (being a layman). I'm not sure if it is capable of measuring both hard and soft plaque, but presumably it's superior to CAC and other methods currently available to make atherosclerotic measurements (albeit it is invasive). They use it over a short timeframe in this study, so one would assume it has the precision and fidelity to deliver the results they hang their hats on. Maybe it could be used for one of your studies? Here's an excerpt describing it: *_"multivessel intravascular imaging was performed when feasible by a combination IVUS- and near-infrared spectroscopy (NIRS) catheter using an automated pullback system (TVC-MC8 model system with a 3.2Fr 40 MHz catheter, Infraredx, Burlington, Massachusetts). Following administration of intracoronary nitroglycerine, the NIRS-IVUS catheter was positioned as distally as possible in the coronary artery. To ensure matching coronary segments at baseline and follow-up, the distal starting points of the pullbacks were recorded angiographically to assist in registration of the corresponding segments at follow-up."_*
All interesting, but until safety is demonstrated it seems like playing Russian roulette.
To those who are familiar with the Randle cycle, it is not surprising that an LMHR should exist. More relevant is the question whether LMHRs (if they exist) are vulnerable to a long-term exposure to elevated levels of LDL.
The answer to the above question is likely to be YES. From many studies, the mechanism behind LDL driven atherosclerosis seems pretty clear. In the aggregate, the studies point to oxidative damages, to arterial walls, from which people have harder time recovering as they age. That is, the elevated levels of LDL become an issue as one ages due to diminishing capabilities to handle oxidative damages. Consider, in general, why CVs occur more frequently in older people.
Proving the above with a low p-value is difficult, because in the field of nutritional science, there are competing economic interests. On the other hand, to those who have been examining scientific literature for a long time with a modicum of objectivity, all the handwringing over the ketogenic diet and carnivore diet is ridiculous. Although the ketogenic diet and carnivore diet may show short-term benefits, they are very likely to accelerate age-dependent declines in CV functions.
Mr. Feldman,
So you take statin?
My cardiologist died from heart attack.
Well now he's an expert in his field..
@MrAnecro Everyone's heart goes into cardiac arrest eventually. Everyone.
You are eloquently explaining how vldl is dropping off triglycerides. I am wondering why you are calling it LDL cholesterol , VLDL cholesterol and HDL cholesterol. We need to demand these lipoproteins be called what they are, it is confusing to call them cholesterol. They carry a variety of fat based items, we don’t name them based on what they transport.