Hi Layne - thank you again for your interest in our research. While I’ll do a more thorough breakdown at a later point in time (currently on a research trip), I would like to again emphasize a crucial component of the LEM is that both higher VLDL secretion is *coupled* with increased lipoprotein lipase turnover. Triglycerides are indeed a good proxy for VLDL that has yet to be turned over. But the LEM isn’t looking to only greater secretion, it is emphasizing the extremely high relevance of the turnover itself which is part of why you see higher HDL cholesterol as well. Again, we would love to come on and chat about it more at length to better explore this model for what it proposes.
What about LEM decreases the risk of ApoB? Even if turnover of any given particle is higher, endothelial intrusion is a diffusion process so concentration dependent, not dependent on the lifecycle of any given particle (the probability is not dependent on the history of a particle).
@scotbradesteems The LEM is seeking to explain this phenomenon in the context of high LDL/ApoB where seemingly metabolically healthy, fat-adapted. The specific risk association of high LDL/ApoB in this context is what we're researching with the LMHR Study out of Lundquist.
@@erastvandoren, "… then he can show us his biomarkers." He did show us the only one he was interested in for this experiment -- LDL-c. It took less than "at least a couple of weeks on Oreos" to see the effect on that one, so why should he be concerned about any others? If he was not, why are you? (Have you even seen his video explaining what this was all about?")
@@erastvandoren, So design and conduct a study to show the effects you are interested in. I would still suggest that you watch (or re-watch) Dr. Norwitz's video where he explains his intent for his experiment.
there is nothing to watch in Norton's videos then. Firstly, Layne himself admitted to errors while replying to this and suggested it's because he was dealing with his mother's surgery. Which is awkward because he sells Data>Feelings and yet he uses feelings to try to explain his deficiencies. As someone who follows the science myself, there is a reason why I follow both these guys, because getting 2 opposing views is essential for science. In fact I got to know Norwitz because of the study, bravo to him for using Oreos, that was provocative of him and it brought out the attention. Norton refusing to debate Norwitz is proving frustrating because I need to hear both opposing views with arguments for each. I didn't want to say this, but on this, as even Layne points out so clearl, Norwitz has his science and data correct, and we science followers should try to see beyond the superficial data and get beyond. Because that study raises more questions. And I appreciate even Layne saying the study raises questions. If Layne and his character sees the study as important, I wonder what type of person you are, really.@@erastvandoren
All this suggests that there is some aspect of the lipid metabolism mechanism that is currently not understood. Developing that understanding may help develop for the whole population, not just the lmhr, more optimal treatment options and nutrition.
It is understood fairly well, by the lipid energy model. It's misunderstood by laypeople and poorly educated/indoctrinated healthcare workers. I also think Layne has been spewing pseudo science on nutrition for decades including false information about cholesterol.
I find this video extremely interesting because I would actually have been eligible for the study. Got bloodwork 1 week out from my show last April around 6-7% body fat and had been on extremely low carb for many weeks prior (obviously). Total cholesterol was near 400ng/dL
Yea buddy, I think eligibility criteria also includes you need to be "natty". You cholesterol is sky high not because you're a LMHR, you're using PEDs 😂
I am fit the LMHR description to a "T". I was VLC/Carnivore for several years. I am lean (F/40 with bicep/shoulder vascularity, approx 18% bf). My triglycerides were well below 70 (usually 45-50), HDL sits around 108, but my LDL was creeping up, up, up; eventually hitting the high 300's. I track macros (using Carbon), so I flipped the fuel from fat to carbs and my LDL dropped so fast! Within 3 weeks, I was just a few points over the high end of ref range. My fasting/am BG barely bumped up from high 70's to low 80's and I feel more secure with better numbers. Also, my trigs and HDL have stayed the same. I agree that this possible phenotype may do perfectly fine on a LC diet, but I argue, much like Layne does here, that the shifting of fuel sources may serve us well. I'm enjoying the rice and bread, I must say.
I fit LMHR as well after years of high fat keto/carnivore diet. 37 year old male very muscular and fit with 10% BF. Blood markers very similar to yours. I’ve tried reintroducing carbs around workouts with some success but beyond 100g/day gives me awful brain fog. I just feel so damn good without carbs I’m torn on this. Really hope some more conclusive data comes out soon.
@@MmartinL On the other hand, if some carbs lead to elevating A1C, that could be bad too. It'd be nice to have low glucose/cholesterol/triglycerides, but it seems nearly impossible for some people to get all three in the low range unless they have great genetics. I can choose to lower either cholesterol or glucose, but not both. Triglycerides are low no matter what.
I was LMHR. LDL 400. I just added some carbs, remained low carb but not Keto, LDL dropped back. I think this is the way to go if you don't need Keto for a medical condition
Just wanted to thank you. I am a senior at UNLV in Nutrition/Dietetics field. Trying to take on a second major in Biochemistry. Everytime I feel overwhelmed by the stuff I am learning, or the stuff I feel like is way over my head to learn. I watch one of your videos and realize this is how it is done and it is going to take me a while to learn how to get to this point. Thanks
so, I come from the low-carb tribe, but this discussion is actually very well done, very fair, and one of the best layman's explanations of this topic I've heard.
This was a sensible response to this study. I fit the LMHR profile after being low carb high fat for about two years. Started out this journey obese with diabetes. Eating this way has put my diabetes into remission but my LDL is over 200. Adding back carbs will probably drop my LDL but push my glucose levels back up. Seems like a no win situation.
I have very weird digestive issues. I am extremely intolerant to starch and complex carbs are almost as problematic. We are talking massive blood loss. Trying to eat a “heart healthy” diet and resulted in my weight dropping down to 99 lbs, hair falling out, restless legs, and extremely low tissue iron. I went low carb once I realized starch was the main problem. At one point my cholesterol was over 500 when I was very low carb, almost carnivore. I had my arteries scanned four years ago and my calcium score was ZERO. I got concerned when my triglycerides were high a few years ago. I weigh 120 lbs now. Gastroenterologists were ridiculously unhelpful and I figured this out on my own. Like Layne said, some of us are just unicorns and standard advice makes matters worse. Last fall, I reluctantly tried a statin, and even on half the dose, I felt like a zombie, so I stopped. I added simple carbs, mostly in the form of honey and maple syrup. Occasional coconut flour and wheat bran,but I eat very little fiber and feel better that way. I am not into any nutritional dogma or diet culture. I will eat anything that I can digest without symptoms. I can’t tolerate “healthy” fats like nuts, avocados, olive or canola oil. I cut back on added fat in general, but do full fat diary because my mood and energy suffer if there is nit enough fat in my diet. My total cholesterol last time was 300, HDL and triglycerides both were 70. At age 66, I strength train, walk, and run as much as my twitchy insides allow, and consider myself very healthy.
@@troy3423 LOL. Go to a dietitian? Wow, I NEVER thought of that. Or probiotics. Or prebiotics. Or fiber. Or yogurt. Or butyrate. Or kombucha. Or other fermented foods. Or FMT. (Fecal microbiota transplant) Or low salicylate. Or SIBO. Or bone broth. Or any other suggestion that presumes I am uninformed and have not already tried everything and was left to manage this problem with no assistance from “experts.” Because someone has an RD after their name, are they gonna wave a wand and render me able to suddenly digest the things I cannot? Telling me to eat things I cannot digest won’t fix the problem. I once asked a dietitian for help with a low FODMAP diet and she had never heard of it. Fired more gastroenterologists than most people have seen, because the only thing they do is give you the same canned advice, over and over again, even after you have reiterated that you have ALREADY TRIED THESE THINGS and THEY DO NOT WORK. The worst was the time I was in the ER for uncontrollable hemorrhaging and the advice was to “eat more fiber”. Or perhaps the time a doctor put me on medication for intestinal cramps and I could not swallow as a result, and when I reported that she said she hoped I would not stop the drug because that was not a side effect. I stopped the drug, regained the ability to swallow, and needless to say, didn’t waste my time with her again.
I tried this myself and it was consistent with their results. On keto I had trippled my LDL and after starting sugar/honey my LDL dropped significantly (almost to baseline). I am relatively lean.
I used to do low carb (and I was one who thought it was "magic" somehow). Luckily, I have a super smart doctor (happens to be a powerlifter, too) who geeks out on nutrition and studies as much as I do. For the past 6 years or so, he has done lipid panels on me every three months, and back when the lean mass hyper responder stuff was trending and the small vs. large particle cholesterol was a big thing, he even checked my particle size. No matter what I did, even at a healthy to lower weight, my cholesterol was just high (close to 300). Consuming less saturated fat in favor of olive oil, etc. didn't help much. His advice was spot on, I think-- if I stayed at that level for a short time and being low carb helped me lose weight, it was okay. But I shouldn't stay there long term because high cholesterol is a proven mortality risk factor. He suggested I go up to moderate carb-- just taking carbs to around 100 instead of 20-40, and that significantly dropped my cholesterol levels. It's anecdotal, but I 100% believe that eating more carbs is what dropped my cholesterol levels. I'm not sure why, but it made a huge difference for me. I haven't done low carb in about three years. Now I track and eat a "balanced" diet. Not everyone is like me, but I'm definitely healthier for it. My cholesterol, while still on the high side, is not dangerously high and not high enough for a statin yet. Thanks for the video-- I'm sending it to my doctor!
I wouldn't be surprised if it was because of fiber. Soluble fiber is useful for the body to shed excess cholesterol. And high fiber diets are often considered to be overall quite healthy.
Thank you for your comment! I'm a nutrition student and we have spent a lot of time on this issue. The fiber found in carbohydrates have a wonderful ability to help lower LDL by binding to it so it can be excreted from the body. That's likely what happened for you. I'm glad you were able to find a good balance.
@@taylorhillard4868I agree. My TC was 8.0 ( New Zealand values). 1 month on high fibre foods with very low saturated fat and it dropped to 6.6. On whole foods. No statin yet ( I do have Pattern B) and hope its continuing its downward trajectory
I'm a physician, and this is my 2 cents based on what I know. LDL-C, VLDL-C, and even ILD-C are all just circulating lipids on a spectrum with different sizes and compositions, but in essence they are all just 1 apoB particle with different lipid composition. And there are people with low LDL-C on treatment but still have a residual CVD risk, and these in patients the residual risks are somewhat explained when used nonHDL-C or apoB (there are studies if I remember correctly). There are also patients who are insulin resistant who have low LDL-C because this population has very small lipid particles rich in triglyceride. What I think happened in this study is that person increase calories and carb intake, which elevated other components of his lipid profile (triglyceride in particular), causing most of his lipoprotein particles to become smaller and shifting the cholesterol concentration into other non-LDL particles. I think additional information about his total cholesterol and non-HDL-C will probably help, both of which I think will either elevate or stay the same (meaning same CVD risk). I would love to hear your opinion about this hypothesis.
The definition provided for a Lean Mass Hyper Responder (LMHR) is often misunderstood. It is crucial to clarify that an LMHR is characterized by specific lipid metrics: LDL-C ≥200mg/dl, HDL-C ≥80 mg/dl, and TG ≤ 70mg/dl. This definition is independent of Body Mass Index (BMI) and dietary patterns. Although LMHRs typically exhibit lower BMI and carbohydrate intake, which may intensify the phenotype, per the LEM, it is important to underscore that neither BMI nor diet are criteria for the LMHR definition. Concerning LDL-C exposure, the assertion that solely the exposure to LDL-C or APO-B containing lipoproteins leads to endothelial penetration raises questions. It is essential to consider whether arterial interaction with these particles, potentially for repair purposes, also plays a role. The context of elevated LDL levels in all studies does not account for individuals without lipid metabolism dysfunction. For instance, conditions like reduced LDL receptor activity or impaired APOB100 recognition. However, the individuals in question do not exhibit these dysfunctions. The LEM paper offers an in-depth analysis of this phenomenon. Nevertheless, the absence of studies specifically addressing LMHR individuals leaves a gap in understanding their risk for Atherosclerotic Cardiovascular Disease (ASCVD), a critical concern for those on ketogenic diets for medical reasons, seeking assurance on the relative safety of increased LDL levels. The critique regarding triglycerides (TG) is well-received. While I am not an authority on this subject, I look forward to the authors' response and the ensuing discussion, as they are known for engaging in insightful dialogue. One point to note from this LEM: it identifies three factors that can elevate your LDL levels: 1) Depleting liver glycogen stores. 2) Increasing energy expenditure. 3) Reducing body fat. In essence, possessing a lean physique, consuming minimal carbohydrates, and engaging in extensive physical activity are conditions that elevate the likelihood of higher LDL cholesterol. However, experiencing just one of these conditions may not necessarily lead to an increase in LDL.
@@yoso585 Every LDL that crosses endothelium can be gulped down by a macrophage. As far as I know, this process (fluid phase macrophage pinocytosis) is unregulated. We also know that inhibition of LDL transcytosis prevents atherosclerosis completely.
I think I may fit in this group. I went keto 6 years ago to keep from converting to a full blown diabetic. My LDL went into the mid 200s. Needless to say my Dr. freaked. He has been trying to get me to go on a statin ever since. This year he ran every cardiac test offered in our area. All were normal. Once every two weeks I eat more carbs so that I don't lose my ability to use glucose. Checked my lipids during this time and my LDL was lower as was my HDL. Trigs went up.. '
If your TG went up significantly in response to carbohydrates maybe you have not fixed the problem with insulin resistance yet. You just treated the symptoms. Which is ok, that‘s what meds do as well. We know that diabetes remission is not caused by cutting out carbs. It has been done on various diets and even happens after weight loss surgery. It is probably due to loosing fat. Why are you so sure your high LDL-C is not harmful and your doctors worries are nonsensical? What harm would be taking meds to be on the safe side? That‘s what I don‘t get tbh. I think it is dangerous to put a study, that excluded every LMHR with plaque and also is lacking a control group above randomized controlled trials and mendelian randomization studies. There needs to be more research to come to a proper conclusion and definitely of higher quality. One big question would be how many of the LMHR do not develop plaque and how many do not and if it’s more then people with low BMI and normal or slightly elevated LDL-C not on a low carb diet. There are people that do get no cardiovascular problems despite high LDL-C and not being metabolically healthy. My grandma for example. LDL-C in the 300eds elevated TG‘s and fasting glucose. No heart disease with 88. So should we not care about LDL-C and metabolic health then? There are always outliers. And a study cherry picking what might be outliers is largely used to depict all of the group. I see that very critical. What‘s also stange is you could predict their studies outcome - plaque does not build up over one year, but several or even decades. Don‘t get me wrong, I‘m fascinated with the phenomenon. But I do not think the lipid energy model is correct. It makes no sense. It proposes that LDL-C is high because of higher traffic of Triglycerides in LDL particles. But triglycerides are very low in LMHR and they do not have much small LDL typically carrying TG’s. No it is the reverse cholesterol transport, that is the issue in my opinion, where HDL but mostly LDL is involved. Both HDL-C and LDL-C increase in LMHR, indicating they are full of cholesterol. Reverse cholesterol transport is increased in fat loss, as not only the stored triglycerides leave the cells. This happens on low carb/keto more then on a carb rich diet. Fat tissue somehow protects from high cholesterol. If you look at BMI and LDL-C, you see only a rising linear relationship up to a BMI of 30, and then even a drop. I bet there is something wrong with the fat tissues in LMHR.
I have also seen a scenario like this with someone that had low triglycerides, highish HDL, high LDL, lean and fit that worked out. She was in my ER having a massive MI. Seeing skinny "fit" people having heart attacks made up my mind about LDL a long time ago. I can't for the life of me understand why anyone can sit with these numbers and feel okay with it
That doesn't mean the high LDL caused the MI. That's like saying you can't be involved in a car accident if you're not in a car. The idea of the study is to eventually disprove that LDL is a factor with the calcification of arteries leading to heart disease. There are many factors that can lead to a heart attack, and it isn't just heart disease. As there are other studies that show high LDL is associated with longevity, I am very interested to see where this study of LMHR's goes.
@@LucidAmethyst that wasn't the point of the study. Its stating that there is a subsection of the population, lean people on extremely low carb diets, who use LDL as a transporter in the lipid energy model. There is a hope that that does not lead to coronary plaque. However we know for certain that LDL is involved in the pathogenesis of coronary plaque development. It's not the only factor I agree.
@@LucidAmethyst You are wrong. I don't think they have any intention of trying to prove anything like that. They only care about LMHR. I'm also unaware of any study showing high LDL is associated with longevity. If you mean that there is data collected where old people developed high LDL and then died because of a ton of other factors, then yes that probably exists. Did they have high LDL their whole lives and that's why they lived long? No. Just look at people with Familial hypercholesterolemia. They tend to have cardiac events very young. They did not live extra due to high LDL. They died very young. It makes no sense to say high LDL is associated with longer life when all the data shows otherwise.
@@LucidAmethystafaik the association between high LDL and longevity is due to diseases like cancer, hepatitis, malnutrition etc which among other symptoms cause lower LDL. When researchers take care to exclude subjects with undiagnosed diseases from prospective studies, the association between high LDL and longevity disappears.
For those LMHR individuals who are concerned about their high LDL, this information comes from another case experiment (mine). A minimal dose of Rosuvastatin (5 mg) along with a minimal dose of Ezetimibe (5 mg; in my country, they only sell 10 mg dose pills, so I have to cut them in half) reduced my LDL from around 220 to around 40 mg/dL (the actual numbers were 218 and 43). Initially, using Rosuvastatin (10 mg) alone, I reduced it to 121, and in a first attempt of combining Rosuvastatin (5 mg) and Ezetimibe (10 mg), the resultant LDL was 38. BTW, I suspect that LMHR individuals are not so much 'unicorns'. I, who am not a particularly social person, know several.
I do similar, 7 mg simvastatin and 3mg Ezetimbe and 500 mg L Carnitine (for LP(a)). But I do not get anywhere near the reduction you do, I am at about 60-70mg/DL LDL. Mine started at 60 then bounced up to 70 six months later, I would expect yours will do the same.
@@Chris_P_, two reasons. The first one is a matter of control. When you start being permissive with something, at least in my case, it's very easy to slip down the slope. The second reason is that I had digestive issues (gastritis, GERD) that have improved significantly. Besides (I don't know if this is real or just suggestion, but just in case), my concentration and memory have also improved. I don't want to take risks. I'm not afraid of statins and have no side effects, apart from a couple of points increase in AST and ALT, but both are still below 24.
The commentary on carnivore channels surrounding these studies is so over the top. And Norwitz does nothing to counter the disinformation, while at the same time marketing directly to those same people.
I think is a pretty Bad one, that on this one he basically tried to insult someone who actually wanted him to collaborate on a ver interesting research. Layne showed that he has no scientific mind on this one . Layne showed that he is too, a zealot
Hi Dr. Norton, really interesting study and thanks for presenting it in such a fantastic balanced way. I was reading a bit into LDL and PCSK9 mutations (heart-1 trial from Verve therapeutics, Crispr trial for knocking out PSCK9 mutant in liver cells as a first trial for gene editing for familial hypercholesterolemia) and was wondering, if the study considered the genetic background of these specific people? I could imagine, that these people might have a different compensation mechanism, where low carb actually leads to increased LDL, since they might lack a specific enzyme or have lower levels of it. Moreover, I was wondering if they also checked the plaque formation/ degradation in the context of the diet. Thanks again for this amazing video and your honest style! Love it. Keep this great work! Many greetings!
THIS WAS AMAZING! I have a wicked nerd-on. Also I think your response to the hot takes is closer to “data + feelings”…I’d buy that t-shirt in a heartbeat.
Layne, please don't lump Nick and Dave in with all low carbers. Your video is implying that Nick/Dave are recklessly going rogue and making firm conclusions out of this. I think you know better. Nick and Dave have many of the same concerns.
This is very interesting. I have always been lean, great BMI, reasonable ammount of lean mass, low fat, always had normal cholersterol...and when i started IF a few years ago and migrated towards a low carb diet..my cholesterol went towards numbers such as 250-300 LDL...and none of the doctors couldn't explain it. I am looking forward to more data because it gives me hope.
@@KiwiBee21 Lol, I can just see the new marketing label. “clinically proven to reduce high cholestoral” with a big asterisk. Then, further super fine print somewhere on the bottom or back of the package somewhere referencing the asterisk stating: “ Individual results may greatly vary and results were based on a N of 1 study. We do not endorse our product as a substitution for medical advice, prescribed treatment or the consumption of oreos to prevent or treat high LDL. Please consult with your doctor.”. Having said that I have to confess as a side note, I am super jealous of the LMHR phenotype. I love me oreos, but cannot stop at one only, so find I need to totally avoid them. If I could eat 13 Oreos a day with impunity. Now, that would be heaven,,and a dream come true 🙂
As a breastfeeding mom, oreos are a staple in my diet. They are rich in calories, calcium and a chemical called sunflower lecithin. Sunflower Lecithin is an emulsifier which means it liquify the fat in my milk and makes it easier for it to flow from my breast to the baby or the pump. Our milk supply is crucial for us breastfeeding mothers so yes! We love oreos 😊
I'm almost in the camp you described. Without a statin, my LDL runs close to 180 (about 100 with 10 mg of Lipitor). Last I checked my HDL was 69, and triglycerides were 50. I'm thin and athletic, and work out quite a bit. It seems to me like the logical thing is to keep doing what I'm doing as far as exercise and diet are concerned, and keep taking my low-dose statin. The possible side effect is higher blood sugar levels, but my fasting glucose is still high 80s, and muscle pains, which I don't have. Why the aversion to statins in this scenario?
I'm glad to hear you get such significant results from a reasonable dose. At my last physical I found myself in nearly exactly the same situation (LDL 180 and everything else pretty good). I'm currently at the end of a six-month test to see if I can get results with 10 lbs weight loss and a higher-fiber, lower saturated fat diet, but I'm expecting to have to start statins next month.
Cognitive function I guess. I did try a statin for a while and my feeling was decreased Cognitive function, so much so, I couldn't compile data. Lol. I used to get gout bad. Meds looked like a life long thing, so I made better connections to what was good and rectified the issue. A side effect was much better numbers with ldl, hdl, triglyceride. Old habits started coming back and the numbers got worse again and that's when I tried a statin. Since then I have tried to make better habits easier to follow from making even better connections. I actually have optimal metabolic health now. If you can, it is clearly better to work with nature than fight against nature, such as using a statin. Not going to be possible with everyone, I guess.
Another limitation of the case study is that they measured LDL-C and not Apo B. I believe there are about 25 percent of people who can have low LDL-C, but high Apo B and we now that Apo B is more accurate marker of CVD risk.
High HDL/LDL and low Trig was how my blood work consistently came back when I consistently only ate Red Meat, fatty fish, veggies and fruit. Low blood pressure as well. I no longer eat strictly meat and veggies and my HDL/LDL is back to normal but my trigs hover around 100 and my blood sugar/A1C has been trending in a bad direction. (Typ 1 Diabetic)
Thanks for a balanced review Layne. Excuse my ignorance as I have no idea how LDL is measured from a blood sample, so my question is probably entirely stooopid… Is it possible that any of the ketone bodies (bhb, acetate etc) could be causing a misreading of the ldl numbers, thus artificially increasing the readings,?
I’m kinda like that subject I was doing yearly blood tests in the past, and I got the best results (122 total cholesterol) when I was having soda with deep fried food for breakfast and afternoon snack everyday. It doesn’t mean someone else would have the same results, also it doesn’t mean it’s healthier on the long run for myself. I also used to do an Oreo diet for bulking (super skinny), but nowadays I try to eat more lean and unprocessed food, and my body responds positively to it.
I’m glad you talked about inflammation since it is a big driver towards cardiovascular disease independent of cholesterol. More so in my opinion than LDL. Lower inflammation means less diseases to a certain point. By the way, there are no unicorns. Every person has thousands of people who respond just like they do. Maybe not millions but thousands. There are thousands of lean mass hyper responders in the wild. A minority sure, but not a unicorn.
These are not unicorns, and it's not about the people. It's about the model of what metabolism is, and the variety of ways in which it can function. Function in a healthy, natural way. I wonder what the typical LDL levels are for wild cats. I'll be looking into that...
I just read about someone this morning who lowered LDL by introducing milk into his diet. Milk is somewhat high in carbs. 5 years from now there will be some good studies coming out Recent study out of Europe I just read about has LDL as a minor risk factor
I disagree with your assessment of the topic because I think your argument is based on lipid hypothesis, ie,higher the concentration of LDL’s , higher the risk for atherosclerosis whereas the other side’s hypothesis is based on lipid energy model- see Dave Feldman’s explanation why people who are on ketogenic or carnivore diet have high LDL.
Although there was an intervention, this appears more mechanistic to me. clinically, most physicians who work with diet commonly see a greater physiological response with food than medication. I usually give most of my patients 1 month to drop their LDL by 30% in 4 weeks after we discuss a plan absent any statins. That period is too short for us to retest after prescribing statins other than assessing for side effects. Why statins didn't work as well? Assuming perfect adherence - it could simply be an absorption issue with the statins. The lipid profile may impede statin pharmacokinetics, this happens sometimes with diabetic patients and there is a lot of research about which statins are better to use in diabetics for this reason. Clinically, more health gurus are gonna claim statins are trash, high LDL is fine, and low carb is the best way to go now, so yay, work just got more fun because they guy who eats bacon and weighs 300lbs at 5'6 is gonna tell me his diet is scientifically proven to be heart healthy by adding in Oreos.
While interesting, the LMHR having LDL and by consequence Apo-B particle number similar to that of people with familial hypercholesterolemia, the risk elevation is so high for heart disease events and possible death that it would not be worthwhile to ever stay at such a lipid level. Especially since we know particle number is the key driver in ASCVD not size, and particle number tracks pretty well with mg/dL values often given in standard lipid panels. Moreover, the WHOs recent 2023 report with nearly 3.7 million people suggests reducesd risk for mortality, CHD incidence, and type 2 diabetes for substituting 5% saturated fat with PUFA MUFA and whole grain/slower digesting carbs. Not to mention this aligns with mountains of previous data corroborating high saturated fat and ASCVD risk via elevation in LDL cholesterol such as mensink 2016, Hooper et al 2020, Hegsted et al 1993, the seven countries study 50 year follow up data, the north Karelia project, Ference et al 2017, Kim et al 2021, and Mazidi et al. (2020) to make a few.
It would be interesting to have measured, if not already, whether the "Lean Mass Hyper-Responders" tend to be more hyper-absorbers of dietary cholesterol. EmpowerDX can measure absorption markers vs production markers of cholesterol and if on the high end of absorption, this can drastically increase LDL-C and ApoB if eating a low-carb diet that is high in cholesterol laden foods such as eggs and organ meat. In the study they did mention a baseline diet based on macros, but not amount of cholesterol ingestion and whether that changed when adding the oreos.
Nick made it clear Oreos were added it to the diet without and taking anything out. That means his saturated fat intake actually increased on Oreo phase
can you make a video on high protein diets and liver diseases like nafld . seems like there are many conflicting viewpoints on this topic and some people say high protein diets are good and other says they are bad for liver disease.
Nothing has been established about lmhr aside from a definition and basic baseline data. The Oreo experiment may apply to all lmhr. Though interesting, and not clear if response is from carbs or is from over feeding, it can remove one from the lmhr category. But what this has to do with demonstrating anything counter to the current ldl cvd relationship is absolutely nothing.
HDL has been proven to NOT be an individual risk factor for cardiovascular disease. Studies on HDL raising drugs have proved this. I believe there are studies on people who have high HDL for genetic reasons do the same but not sure.
I was initially hyped about the LMHR stuff, as I fitted into this criteria quite well (IF and Paleo zealot back then). Then I started digging deep in LDL and Apo-B literature - my enthusiasm faded. So the best lifestyle ever: be a KETO LMHR and on truck load of statins and PCSK9i-s. (joke, haha) Great analogy on smoking vs the lipids - I will keep it. All in all I follow their research as it can reveal crucial novel information.
Wouldn't that lipid model hypothesis be very easy to test by measuring ApoB directly? If by some miracle ApoB levels were indeed low despite huge LDL, then fine, maybe LMHR don't have higher risk of heart disease, but that is very unlikely. Also, given that it is a single individual, it is plausible that he could have some mutation in some enzyme involved in lipid or glucose metabolism that exacerbates those effects.
LMHRs can do this trick with any carb source. So that would be the advice, eat sweet potato and you’ll likely have similar lab values with a lower LDL, while still being low carb/keto. I believe Nick stayed in ketosis during this period. He may have supplemented to do it, but still possible.
@@Feed_Bleed_Read Yes he did, I have confirmation of this now. He used ketone supplements to stay in ketosis. However, even Nick states that some people, if they strategize correctly, may be able to carb cycle without supplements.
11:35 -- Well, first of all, the Oreo group was 'intervened' for less than 2.5 wks, while the Statin group was intervened for 6 wks. To me it looks like as if the Oreo curve was flattening out or may even rise later on, say, around 6 wks (?) (ha ha), while the statin provides a steadier control on the LDL levels...which is not surprising...time does matter, and we should try & look at longer term data, even if the subjects are fed Oreos for 6 wks -- I bet they all will like that! 😀 Also, the baseline levels of the Oreo group before starting the 'Oreo therapy' was btwn 384, while the baseline of the stating group was 421. This can affect the shape of the curves when dropping, esp. when the X-axes are not the same (days vs weeks)...which in turn can 'look dramatic'... Also, I'd like to see this study replicated -- a carefully designed, well-conducted study. As the Sagan Standard goes: "Extraordinary claims require extraordinary evidence."
This is a study by PhD, Harvard doctor bro. Even Layne with his bully attitude admits the data is correct, try anything else and stay away from the data being not conclusive. You can't get better data than this.
I don't think you have carefully examined the study. As far as I remember, the researchers conducted a Calcium Score on the participants, and the results showed that they had almost zero, which is less than people with normal LDL. Therefore, it is unlikely that if they had lower LDL, they would have a lower risk of cardiovascular diseases. It seems like you are biased, my friend. You always have the same perspective, which is why you have problems with the majority of researchers and doctors on social media.
So he did not understand the findings of the experiment and asks his PhD advisor who was clueless. But the explanation is in the study! Obviously here feelings blurred interpretation or interest in the data to actually study data. Nick predicted the outcome of the Oreo study so he obviously has some foundational knowledge which the majority of the mainstream medical professionals lack. Keep going Nick your quest for knowledge is severely lacking in many who rest in the current LDL story as being settled science and are dismissive of anyone who dares challenge their narrative.
the "rebound" was due to the subject testing another aspect of the lipid energy hypothesis, which is that increasing energy expenditure (exercise) would increase LDL-C. He intentionally doubled his steps for that final period and saw the predicted result.
because the docs he consulted said 6 weeks should be a fair "trial" period to see the likely lowering effects of the statin. these LMHR guys know they can raise and lower their LDL at will by throttling carb intake.
Since it was done with 1 subject, if outside factors were taken into account such as sleep & stress. Possibly just eating Oreos made the subject feel better (satisfied) which lowered stress levels for better sleep? Another factor could be going from Keto to Non-keto helped with bowel movements. During digestion, soluble fiber binds with cholesterol in bile and aids in its excretion. But the issue there is that there's no soluble fiber in Oreos.
No it's because LDL is used to transport fatty acids through the blood to be used as energy. When you're obese your cells have more than enough fuel so your LDL stays the same or even goes down on low carb but if you're very lean all that fat has to come from dietary fat which is transported in LDL to the cells. The reason the addition of carbs from oreo lower the LDL is because the body now also has extra glucose for fuel, meaning that it has to transport less fat to the cells for fuel.
Dr. Norton, ironically my cardiologist had me massively increase CBH while matching fat and protein concurrently to when Nick did he n=1. Due to autoimmune reactions to almost all CBH sources the only way I was able to do this was via homemade Christmas cookies(if I was gonna feel like shit from CBH, they were at least gonna be delicious) as they allowed me to match fatty acids to my animal-based diet. Anecdotally, I had LDL decrease from ≈460 to ≈230 and TG decrease ≈65 to ≈34. Nick Norowitz explains the decrease in TG because of hyperinsulinemia in a fasted state(he explains better, I’m not a lipidologist lol). Could this be true in the context of a diet that promotes glucose sparing and physiologic insulin resistance? Ergo, with the increase in CBH you see an insulin resistance like oversecretion of insulin? This has been something that I have not been able to get my head around but I am concerned about as my low CBH diet is because of autoimmune issues that take priority to LDL. Thank you, on the off chance you read/respond to this lol.
It's also important to note that Nick's experiment didn't even assess both major classes of statin. It only examined hydrophilic statins (like rosuvastatin), which tend to do a poorer job of LDL clearance than lipophilic statins, which have greater penetration into the liver. It's quite possible such a statin would have done as well as, or at least comparably to, the Oreos. It's a flawed, clickbait experiment that doesn't even demonstrate what it says it does. And it's being used without any context by low carb grifters to engage in further statin and LDL denialism. The takeaway for most lay people, I suspect, is "statins are garbage because they don't even work as well as Oreos!" Then the extremely online 65-year-old with metabolic disease ignores his cardiologist's advice because he heard Ken Berry and Shawn Baker mention this on TH-cam. I find the entire online low carb ecosystem to be completely insidious. My takeaway from the experiment, at best, is that (1) these kinds of diets may contain an inherent, and potentially morbid, risk factor for those with this phenotype in the form of extremely elevated LDL; and (2) it's probably a better approach for this phenotype to add at least the number of grams of carbs outlined in the experiment to their ketogenic diet in order to reduce this risk. I don't think the experiment successfully demonstrated that statins would be ineffective for this phenotype because it only assessed one kind of statin, as noted. And it's only testing one person, Nick, and his response could be idiosyncratic. The experiment could have just as easily tested a banana instead of Oreos, but it wouldn't get the headline. A banana would get people thinking they should eat more whole plant based, which isn't what low carb ideologues like Nick want.
Not necessarily, maybe it would be better for that person not to eat oreos and having high LDL. It is not exactly shown that such a high LDL in the context of LMHR is less healthy.
It's so important that this is one person. That may just happen to be the one in 8 billion who sees this dramatic a response. Even still, if I were on a low carb diet with high LDL but every other biomarker looking good, I'd just add like 200 calories of carbs a day and see if that lowered my LDL. You can stick to your low carb diet throughout the day then just add a couple pieces of fruit at the end of every day. Seems easy enough. Oh, I'd also take a statin if I didn't have adverse side effects to them. Why not both?
In my personal experience, Oreos have a similar effect to diet soda, they greatly reduce my anxiety. Having two Oreos for breakfast makes me not craving anything else all day long. But possibly it's an unicorn effect too.. 😆
Yes, it is interesting he used foods he objects/rejects and is now using them to promote his work/science and popularity. Maybe he finally saw the light and that all "foods" can be incorporated into a healthy diet.
I don't think there's enough consideration of what exactly low carb hyper responders are eating when they get high LDL, or what exactly they could be eating to lower LDL, other than Oreos. What do different types of carbs (whole or refined) do, and what does different types of fats (saturated or polyunsaturated) do. Knowing more about this could explain a lot. We need to know why some people are hyper responders in the first place. Does a ketogenic diet (or a certain kind of ketogenic diet) make them need more cholesterol in the same way that disease make people need more cholesterol? More experiments, please.
Good point, they should have done the study with some whole grain bread or fruit, but then it wouldn't have the same click bait result as Oreos do. Are they interested in science or social media clicks?
Oreo sitting back wishing this came out sooner so they could’ve advertised their magical LDL lowering abilities during the Super Bowl. They woulda got Pfizer rich overnight.
Nick consistantly emphasizes this was only a study of one, do not stop taking statins or in anyway think this proves anything it was only to provoke conversation. As for Nick himself this guy is brilliant and would destroy Layne in a debate on metabolism.
Skipped the video, went straight to the grocery store. Thanks doc!
Lmao funny.
Hi Layne - thank you again for your interest in our research. While I’ll do a more thorough breakdown at a later point in time (currently on a research trip), I would like to again emphasize a crucial component of the LEM is that both higher VLDL secretion is *coupled* with increased lipoprotein lipase turnover. Triglycerides are indeed a good proxy for VLDL that has yet to be turned over. But the LEM isn’t looking to only greater secretion, it is emphasizing the extremely high relevance of the turnover itself which is part of why you see higher HDL cholesterol as well. Again, we would love to come on and chat about it more at length to better explore this model for what it proposes.
What in blazes does that even mean.
You are out to lunch.
Thanks for all you do Dave! Can't wait for lmhr study this year on plaque.
What about LEM decreases the risk of ApoB? Even if turnover of any given particle is higher, endothelial intrusion is a diffusion process so concentration dependent, not dependent on the lifecycle of any given particle (the probability is not dependent on the history of a particle).
@scotbradesteems The LEM is seeking to explain this phenomenon in the context of high LDL/ApoB where seemingly metabolically healthy, fat-adapted. The specific risk association of high LDL/ApoB in this context is what we're researching with the LMHR Study out of Lundquist.
I watched Nick Norwitz's video on this. It that this was done specifically to start a conversation among researchers at large.
It seems to be doing that. ( 4:16 )
@@erastvandoren,
"… then he can show us his biomarkers."
He did show us the only one he was interested in for this experiment -- LDL-c. It took less than "at least a couple of weeks on Oreos" to see the effect on that one, so why should he be concerned about any others? If he was not, why are you? (Have you even seen his video explaining what this was all about?")
@@erastvandoren,
So design and conduct a study to show the effects you are interested in.
I would still suggest that you watch (or re-watch) Dr. Norwitz's video where he explains his intent for his experiment.
@erastvandoren you must not be a LMHR, it's okay fatty
there is nothing to watch in Norton's videos then. Firstly, Layne himself admitted to errors while replying to this and suggested it's because he was dealing with his mother's surgery. Which is awkward because he sells Data>Feelings and yet he uses feelings to try to explain his deficiencies. As someone who follows the science myself, there is a reason why I follow both these guys, because getting 2 opposing views is essential for science. In fact I got to know Norwitz because of the study, bravo to him for using Oreos, that was provocative of him and it brought out the attention. Norton refusing to debate Norwitz is proving frustrating because I need to hear both opposing views with arguments for each. I didn't want to say this, but on this, as even Layne points out so clearl, Norwitz has his science and data correct, and we science followers should try to see beyond the superficial data and get beyond. Because that study raises more questions. And I appreciate even Layne saying the study raises questions. If Layne and his character sees the study as important, I wonder what type of person you are, really.@@erastvandoren
All this suggests that there is some aspect of the lipid metabolism mechanism that is currently not understood. Developing that understanding may help develop for the whole population, not just the lmhr, more optimal treatment options and nutrition.
Yes. It seems odd that so many people would be so resistant to that.
It is understood fairly well, by the lipid energy model. It's misunderstood by laypeople and poorly educated/indoctrinated healthcare workers. I also think Layne has been spewing pseudo science on nutrition for decades including false information about cholesterol.
I find this video extremely interesting because I would actually have been eligible for the study. Got bloodwork 1 week out from my show last April around 6-7% body fat and had been on extremely low carb for many weeks prior (obviously). Total cholesterol was near 400ng/dL
mg/dL*
Yea buddy, I think eligibility criteria also includes you need to be "natty". You cholesterol is sky high not because you're a LMHR, you're using PEDs 😂
Thank you for the balanced review and the ability to say "I don't know," it's why I am a big fan and keep coming back to this channel!
I am fit the LMHR description to a "T". I was VLC/Carnivore for several years. I am lean (F/40 with bicep/shoulder vascularity, approx 18% bf). My triglycerides were well below 70 (usually 45-50), HDL sits around 108, but my LDL was creeping up, up, up; eventually hitting the high 300's. I track macros (using Carbon), so I flipped the fuel from fat to carbs and my LDL dropped so fast! Within 3 weeks, I was just a few points over the high end of ref range. My fasting/am BG barely bumped up from high 70's to low 80's and I feel more secure with better numbers. Also, my trigs and HDL have stayed the same. I agree that this possible phenotype may do perfectly fine on a LC diet, but I argue, much like Layne does here, that the shifting of fuel sources may serve us well. I'm enjoying the rice and bread, I must say.
I fit LMHR as well after years of high fat keto/carnivore diet. 37 year old male very muscular and fit with 10% BF. Blood markers very similar to yours. I’ve tried reintroducing carbs around workouts with some success but beyond 100g/day gives me awful brain fog. I just feel so damn good without carbs I’m torn on this. Really hope some more conclusive data comes out soon.
Has your weight training performance increased since you brought carbs back in?
Can you say something about your performance and hormonal levels? Did they change? How do you feel better?
@@bcjammer87can you say something about your performance and hormonal levels in both situations? How do you feel about?
@@bcjammer87have you tested possible food sensitivities? Not all carbs are equal.
LMHR here. LDL went to 200+ on keto and 300+ on carnivore. HDL, trigs, etc were perfect.
Eat some carbs
It is not shown whether this high LDL is harmless. Maybe it is healthier if you had a lower LDL by eating some carbs.
@@MmartinL I think that is likely correct. I do not eat this way now, I was just experimenting with those diets to see how I responded.
@@MmartinL The lower you can get your LDL the better.
@@MmartinL On the other hand, if some carbs lead to elevating A1C, that could be bad too. It'd be nice to have low glucose/cholesterol/triglycerides, but it seems nearly impossible for some people to get all three in the low range unless they have great genetics. I can choose to lower either cholesterol or glucose, but not both. Triglycerides are low no matter what.
My insurance won't cover Oreos, thanks Obama
need to get a prescription from your doc ;-)
@@JoeS97756😂😂😂He is joking about insurance.
😅😅use Medicare!
😂
@@saintjulien6126 I know, as was I. lol
I was LMHR. LDL 400. I just added some carbs, remained low carb but not Keto, LDL dropped back.
I think this is the way to go if you don't need Keto for a medical condition
Just wanted to thank you. I am a senior at UNLV in Nutrition/Dietetics field. Trying to take on a second major in Biochemistry. Everytime I feel overwhelmed by the stuff I am learning, or the stuff I feel like is way over my head to learn. I watch one of your videos and realize this is how it is done and it is going to take me a while to learn how to get to this point. Thanks
so, I come from the low-carb tribe, but this discussion is actually very well done, very fair, and one of the best layman's explanations of this topic I've heard.
You mean, Layne-man's explanation! Aha! 😂
nice one bro hah@@rixxlx
You mean explanation to a layman? Because Layne-man is not a layman.
This was a sensible response to this study. I fit the LMHR profile after being low carb high fat for about two years. Started out this journey obese with diabetes. Eating this way has put my diabetes into remission but my LDL is over 200. Adding back carbs will probably drop my LDL but push my glucose levels back up. Seems like a no win situation.
Cholesterol is the fireman, not the fire
I have very weird digestive issues. I am extremely intolerant to starch and complex carbs are almost as problematic. We are talking massive blood loss. Trying to eat a “heart healthy” diet and resulted in my weight dropping down to 99 lbs, hair falling out, restless legs, and extremely low tissue iron. I went low carb once I realized starch was the main problem. At one point my cholesterol was over 500 when I was very low carb, almost carnivore. I had my arteries scanned four years ago and my calcium score was ZERO. I got concerned when my triglycerides were high a few years ago. I weigh 120 lbs now.
Gastroenterologists were ridiculously unhelpful and I figured this out on my own. Like Layne said, some of us are just unicorns and standard advice makes matters worse.
Last fall, I reluctantly tried a statin, and even on half the dose, I felt like a zombie, so I stopped.
I added simple carbs, mostly in the form of honey and maple syrup. Occasional coconut flour and wheat bran,but I eat very little fiber and feel better that way. I am not into any nutritional dogma or diet culture. I will eat anything that I can digest without symptoms. I can’t tolerate “healthy” fats like nuts, avocados, olive or canola oil. I cut back on added fat in general, but do full fat diary because my mood and energy suffer if there is nit enough fat in my diet.
My total cholesterol last time was 300, HDL and triglycerides both were 70.
At age 66, I strength train, walk, and run as much as my twitchy insides allow, and consider myself very healthy.
Dairy, not diary. Oops
Calcium score is a late-stage finding. If you find calcium you are very close to a hear attack.
You should probably go see a Dietitian
@@troy3423 LOL.
Go to a dietitian? Wow, I NEVER thought of that. Or probiotics. Or prebiotics. Or fiber. Or yogurt. Or butyrate. Or kombucha. Or other fermented foods. Or FMT. (Fecal microbiota transplant) Or low salicylate. Or SIBO. Or bone broth. Or any other suggestion that presumes I am uninformed and have not already tried everything and was left to manage this problem with no assistance from “experts.”
Because someone has an RD after their name, are they gonna wave a wand and render me able to suddenly digest the things I cannot? Telling me to eat things I cannot digest won’t fix the problem. I once asked a dietitian for help with a low FODMAP diet and she had never heard of it. Fired more gastroenterologists than most people have seen, because the only thing they do is give you the same canned advice, over and over again, even after you have reiterated that you have ALREADY TRIED THESE THINGS and THEY DO NOT WORK. The worst was the time I was in the ER for uncontrollable hemorrhaging and the advice was to “eat more fiber”. Or perhaps the time a doctor put me on medication for intestinal cramps and I could not swallow as a result, and when I reported that she said she hoped I would not stop the drug because that was not a side effect. I stopped the drug, regained the ability to swallow, and needless to say, didn’t waste my time with her again.
@@kostisapostolidis1821 my score was zero.
I tried this myself and it was consistent with their results. On keto I had trippled my LDL and after starting sugar/honey my LDL dropped significantly (almost to baseline). I am relatively lean.
I used to do low carb (and I was one who thought it was "magic" somehow). Luckily, I have a super smart doctor (happens to be a powerlifter, too) who geeks out on nutrition and studies as much as I do. For the past 6 years or so, he has done lipid panels on me every three months, and back when the lean mass hyper responder stuff was trending and the small vs. large particle cholesterol was a big thing, he even checked my particle size.
No matter what I did, even at a healthy to lower weight, my cholesterol was just high (close to 300). Consuming less saturated fat in favor of olive oil, etc. didn't help much. His advice was spot on, I think-- if I stayed at that level for a short time and being low carb helped me lose weight, it was okay. But I shouldn't stay there long term because high cholesterol is a proven mortality risk factor.
He suggested I go up to moderate carb-- just taking carbs to around 100 instead of 20-40, and that significantly dropped my cholesterol levels. It's anecdotal, but I 100% believe that eating more carbs is what dropped my cholesterol levels. I'm not sure why, but it made a huge difference for me.
I haven't done low carb in about three years. Now I track and eat a "balanced" diet. Not everyone is like me, but I'm definitely healthier for it. My cholesterol, while still on the high side, is not dangerously high and not high enough for a statin yet.
Thanks for the video-- I'm sending it to my doctor!
I wouldn't be surprised if it was because of fiber. Soluble fiber is useful for the body to shed excess cholesterol. And high fiber diets are often considered to be overall quite healthy.
Sounds like an awesome doctor!
Thank you for your comment! I'm a nutrition student and we have spent a lot of time on this issue. The fiber found in carbohydrates have a wonderful ability to help lower LDL by binding to it so it can be excreted from the body. That's likely what happened for you. I'm glad you were able to find a good balance.
There are so many vegans with LDL of 50-70. So carbs definitely help.
@@taylorhillard4868I agree. My TC was 8.0 ( New Zealand values). 1 month on high fibre foods with very low saturated fat and it dropped to 6.6. On whole foods. No statin yet ( I do have Pattern B) and hope its continuing its downward trajectory
I'm a physician, and this is my 2 cents based on what I know. LDL-C, VLDL-C, and even ILD-C are all just circulating lipids on a spectrum with different sizes and compositions, but in essence they are all just 1 apoB particle with different lipid composition. And there are people with low LDL-C on treatment but still have a residual CVD risk, and these in patients the residual risks are somewhat explained when used nonHDL-C or apoB (there are studies if I remember correctly). There are also patients who are insulin resistant who have low LDL-C because this population has very small lipid particles rich in triglyceride. What I think happened in this study is that person increase calories and carb intake, which elevated other components of his lipid profile (triglyceride in particular), causing most of his lipoprotein particles to become smaller and shifting the cholesterol concentration into other non-LDL particles. I think additional information about his total cholesterol and non-HDL-C will probably help, both of which I think will either elevate or stay the same (meaning same CVD risk). I would love to hear your opinion about this hypothesis.
The definition provided for a Lean Mass Hyper Responder (LMHR) is often misunderstood. It is crucial to clarify that an LMHR is characterized by specific lipid metrics: LDL-C ≥200mg/dl, HDL-C ≥80 mg/dl, and TG ≤ 70mg/dl. This definition is independent of Body Mass Index (BMI) and dietary patterns. Although LMHRs typically exhibit lower BMI and carbohydrate intake, which may intensify the phenotype, per the LEM, it is important to underscore that neither BMI nor diet are criteria for the LMHR definition.
Concerning LDL-C exposure, the assertion that solely the exposure to LDL-C or APO-B containing lipoproteins leads to endothelial penetration raises questions. It is essential to consider whether arterial interaction with these particles, potentially for repair purposes, also plays a role. The context of elevated LDL levels in all studies does not account for individuals without lipid metabolism dysfunction. For instance, conditions like reduced LDL receptor activity or impaired APOB100 recognition. However, the individuals in question do not exhibit these dysfunctions. The LEM paper offers an in-depth analysis of this phenomenon. Nevertheless, the absence of studies specifically addressing LMHR individuals leaves a gap in understanding their risk for Atherosclerotic Cardiovascular Disease (ASCVD), a critical concern for those on ketogenic diets for medical reasons, seeking assurance on the relative safety of increased LDL levels.
The critique regarding triglycerides (TG) is well-received. While I am not an authority on this subject, I look forward to the authors' response and the ensuing discussion, as they are known for engaging in insightful dialogue.
One point to note from this LEM: it identifies three factors that can elevate your LDL levels:
1) Depleting liver glycogen stores.
2) Increasing energy expenditure.
3) Reducing body fat.
In essence, possessing a lean physique, consuming minimal carbohydrates, and engaging in extensive physical activity are conditions that elevate the likelihood of higher LDL cholesterol. However, experiencing just one of these conditions may not necessarily lead to an increase in LDL.
Endothelial penetration? 😅 🤡
Transcytosis of LDL is absolutely normal and happens in everyone.
@@erastvandoren Layne says it in the video..... aging Is normal and happens in everyone, but who wants to accelerate that process??
@@erastvandoren so then, every ldl that passes through is detrimental?
@@davidflorez1196 yes, we don't want to accelerate LDL transcytosis. That's why we need to keep inflammation, blood glucose and pressure down.
@@yoso585 Every LDL that crosses endothelium can be gulped down by a macrophage. As far as I know, this process (fluid phase macrophage pinocytosis) is unregulated. We also know that inhibition of LDL transcytosis prevents atherosclerosis completely.
I think I may fit in this group. I went keto 6 years ago to keep from converting to a full blown diabetic. My LDL went into the mid 200s. Needless to say my Dr. freaked. He has been trying to get me to go on a statin ever since. This year he ran every cardiac test offered in our area. All were normal. Once every two weeks I eat more carbs so that I don't lose my ability to use glucose. Checked my lipids during this time and my LDL was lower as was my HDL. Trigs went up..
'
If your TG went up significantly in response to carbohydrates maybe you have not fixed the problem with insulin resistance yet. You just treated the symptoms. Which is ok, that‘s what meds do as well.
We know that diabetes remission is not caused by cutting out carbs. It has been done on various diets and even happens after weight loss surgery.
It is probably due to loosing fat.
Why are you so sure your high LDL-C is not harmful and your doctors worries are nonsensical?
What harm would be taking meds to be on the safe side? That‘s what I don‘t get tbh.
I think it is dangerous to put a study, that excluded every LMHR with plaque and also is lacking a control group above randomized controlled trials and mendelian randomization studies. There needs to be more research to come to a proper conclusion and definitely of higher quality.
One big question would be how many of the LMHR do not develop plaque and how many do not and if it’s more then people with low BMI and normal or slightly elevated LDL-C not on a low carb diet. There are people that do get no cardiovascular problems despite high LDL-C and not being metabolically healthy. My grandma for example. LDL-C in the 300eds elevated TG‘s and fasting glucose. No heart disease with 88. So should we not care about LDL-C and metabolic health then? There are always outliers.
And a study cherry picking what might be outliers is largely used to depict all of the group. I see that very critical.
What‘s also stange is you could predict their studies outcome - plaque does not build up over one year, but several or even decades.
Don‘t get me wrong, I‘m fascinated with the phenomenon. But I do not think the lipid energy model is correct. It makes no sense. It proposes that LDL-C is high because of higher traffic of Triglycerides in LDL particles. But triglycerides are very low in LMHR and they do not have much small LDL typically carrying TG’s.
No it is the reverse cholesterol transport, that is the issue in my opinion, where HDL but mostly LDL is involved. Both HDL-C and LDL-C increase in LMHR, indicating they are full of cholesterol. Reverse cholesterol transport is increased in fat loss, as not only the stored triglycerides leave the cells. This happens on low carb/keto more then on a carb rich diet.
Fat tissue somehow protects from high cholesterol. If you look at BMI and LDL-C, you see only a rising linear relationship up to a BMI of 30, and then even a drop. I bet there is something wrong with the fat tissues in LMHR.
“Supplementation with Oreo cookies” a sentence is never thought I’d hear 😂😂
I have also seen a scenario like this with someone that had low triglycerides, highish HDL, high LDL, lean and fit that worked out. She was in my ER having a massive MI. Seeing skinny "fit" people having heart attacks made up my mind about LDL a long time ago. I can't for the life of me understand why anyone can sit with these numbers and feel okay with it
That doesn't mean the high LDL caused the MI. That's like saying you can't be involved in a car accident if you're not in a car. The idea of the study is to eventually disprove that LDL is a factor with the calcification of arteries leading to heart disease. There are many factors that can lead to a heart attack, and it isn't just heart disease. As there are other studies that show high LDL is associated with longevity, I am very interested to see where this study of LMHR's goes.
Did she happen to be vaccinated
@@LucidAmethyst that wasn't the point of the study. Its stating that there is a subsection of the population, lean people on extremely low carb diets, who use LDL as a transporter in the lipid energy model. There is a hope that that does not lead to coronary plaque. However we know for certain that LDL is involved in the pathogenesis of coronary plaque development. It's not the only factor I agree.
@@LucidAmethyst You are wrong. I don't think they have any intention of trying to prove anything like that. They only care about LMHR. I'm also unaware of any study showing high LDL is associated with longevity. If you mean that there is data collected where old people developed high LDL and then died because of a ton of other factors, then yes that probably exists. Did they have high LDL their whole lives and that's why they lived long? No. Just look at people with Familial hypercholesterolemia. They tend to have cardiac events very young. They did not live extra due to high LDL. They died very young. It makes no sense to say high LDL is associated with longer life when all the data shows otherwise.
@@LucidAmethystafaik the association between high LDL and longevity is due to diseases like cancer, hepatitis, malnutrition etc which among other symptoms cause lower LDL. When researchers take care to exclude subjects with undiagnosed diseases from prospective studies, the association between high LDL and longevity disappears.
Thanks for helping sort this out. Its Interesting for sure
Been waiting for this video, thanks, Layne
For those LMHR individuals who are concerned about their high LDL, this information comes from another case experiment (mine). A minimal dose of Rosuvastatin (5 mg) along with a minimal dose of Ezetimibe (5 mg; in my country, they only sell 10 mg dose pills, so I have to cut them in half) reduced my LDL from around 220 to around 40 mg/dL (the actual numbers were 218 and 43). Initially, using Rosuvastatin (10 mg) alone, I reduced it to 121, and in a first attempt of combining Rosuvastatin (5 mg) and Ezetimibe (10 mg), the resultant LDL was 38.
BTW, I suspect that LMHR individuals are not so much 'unicorns'. I, who am not a particularly social person, know several.
I do similar, 7 mg simvastatin and 3mg Ezetimbe and 500 mg L Carnitine (for LP(a)). But I do not get anywhere near the reduction you do, I am at about 60-70mg/DL LDL. Mine started at 60 then bounced up to 70 six months later, I would expect yours will do the same.
@@robertdaymouse3784, maybe the Lp(a) is the point. Mine is below 1. Or maybe not. I have bloodwork scheduled for next week. We'll see.
@@robertdaymouse3784 Maybe the point is the Lp(a). Mine is below 1 mmol/L. Or maybe not. I have blood work scheduled for next week. We'll see.
I’m curious why you’d want to take the statins, but not just increase carb consumption a bit?
@@Chris_P_, two reasons. The first one is a matter of control. When you start being permissive with something, at least in my case, it's very easy to slip down the slope. The second reason is that I had digestive issues (gastritis, GERD) that have improved significantly. Besides (I don't know if this is real or just suggestion, but just in case), my concentration and memory have also improved. I don't want to take risks. I'm not afraid of statins and have no side effects, apart from a couple of points increase in AST and ALT, but both are still below 24.
The commentary on carnivore channels surrounding these studies is so over the top. And Norwitz does nothing to counter the disinformation, while at the same time marketing directly to those same people.
Feldman and norwitz are grifters
This was one of your best videos yet on an extremely weird study and result!
I think is a pretty Bad one, that on this one he basically tried to insult someone who actually wanted him to collaborate on a ver interesting research. Layne showed that he has no scientific mind on this one . Layne showed that he is too, a zealot
Hi Dr. Norton, really interesting study and thanks for presenting it in such a fantastic balanced way. I was reading a bit into LDL and PCSK9 mutations (heart-1 trial from Verve therapeutics, Crispr trial for knocking out PSCK9 mutant in liver cells as a first trial for gene editing for familial hypercholesterolemia) and was wondering, if the study considered the genetic background of these specific people? I could imagine, that these people might have a different compensation mechanism, where low carb actually leads to increased LDL, since they might lack a specific enzyme or have lower levels of it. Moreover, I was wondering if they also checked the plaque formation/ degradation in the context of the diet.
Thanks again for this amazing video and your honest style! Love it. Keep this great work! Many greetings!
I’m only going to watch the first 10 seconds of this video and assume it’s fact to help justify the sleeve of Oreos I’m about to smash. Thanks Layne!
That answer is simple. If you are low carb and find out you have high ldl, eat some damn oreos and retest.
THIS WAS AMAZING! I have a wicked nerd-on. Also I think your response to the hot takes is closer to “data + feelings”…I’d buy that t-shirt in a heartbeat.
Thanks for your great content!! Best explanation about this study I've seen.
Layne, please don't lump Nick and Dave in with all low carbers. Your video is implying that Nick/Dave are recklessly going rogue and making firm conclusions out of this. I think you know better. Nick and Dave have many of the same concerns.
This is very interesting. I have always been lean, great BMI, reasonable ammount of lean mass, low fat, always had normal cholersterol...and when i started IF a few years ago and migrated towards a low carb diet..my cholesterol went towards numbers such as 250-300 LDL...and none of the doctors couldn't explain it. I am looking forward to more data because it gives me hope.
This video is above my scientific abilities.
Sadly, I can just see makers of oreos taking this study out of context and falsely using this to further market the sales of oreos
Only thing this study is being falsely used for is by the ketotards who are now claiming statins are useless, and that high LDL in keto is safe.
Anticipating the buy in from legacy media
@@KiwiBee21 Lol, I can just see the new marketing label. “clinically proven to reduce high cholestoral” with a big asterisk. Then, further super fine print somewhere on the bottom or back of the package somewhere referencing the asterisk stating: “ Individual results may greatly vary and results were based on a N of 1 study. We do not endorse our product as a substitution for medical advice, prescribed treatment or the consumption of oreos to prevent or treat high LDL. Please consult with your doctor.”. Having said that I have to confess as a side note, I am super jealous of the LMHR phenotype. I love me oreos, but cannot stop at one only, so find I need to totally avoid them. If I could eat 13 Oreos a day with impunity. Now, that would be heaven,,and a dream come true 🙂
FDA won't allow it.
As a breastfeeding mom, oreos are a staple in my diet. They are rich in calories, calcium and a chemical called sunflower lecithin. Sunflower Lecithin is an emulsifier which means it liquify the fat in my milk and makes it easier for it to flow from my breast to the baby or the pump. Our milk supply is crucial for us breastfeeding mothers so yes! We love oreos 😊
I disagree with some of your takes, but this was a good video and levelheaded take. Cheers.
I just googled “Do Oreos lower cholesterol?” like just a minute ago. I go on TH-cam and bam, this video pops up. Trippy
I mean, you know it’s Nick, right? Did you even read the study?
He was being professional
@@stargazerbird or stupid and he didn’t even read the study fully.
Doesn't this study just show that......carbs are good? LOL
I'm almost in the camp you described. Without a statin, my LDL runs close to 180 (about 100 with 10 mg of Lipitor). Last I checked my HDL was 69, and triglycerides were 50. I'm thin and athletic, and work out quite a bit.
It seems to me like the logical thing is to keep doing what I'm doing as far as exercise and diet are concerned, and keep taking my low-dose statin. The possible side effect is higher blood sugar levels, but my fasting glucose is still high 80s, and muscle pains, which I don't have. Why the aversion to statins in this scenario?
I'm glad to hear you get such significant results from a reasonable dose. At my last physical I found myself in nearly exactly the same situation (LDL 180 and everything else pretty good). I'm currently at the end of a six-month test to see if I can get results with 10 lbs weight loss and a higher-fiber, lower saturated fat diet, but I'm expecting to have to start statins next month.
Cognitive function I guess. I did try a statin for a while and my feeling was decreased Cognitive function, so much so, I couldn't compile data. Lol. I used to get gout bad. Meds looked like a life long thing, so I made better connections to what was good and rectified the issue. A side effect was much better numbers with ldl, hdl, triglyceride. Old habits started coming back and the numbers got worse again and that's when I tried a statin. Since then I have tried to make better habits easier to follow from making even better connections. I actually have optimal metabolic health now. If you can, it is clearly better to work with nature than fight against nature, such as using a statin. Not going to be possible with everyone, I guess.
There's concern about mental cognition if you have familiars with Alzheimer's disease bit if not I think your safe
I'm glad you're solving your statin deficiency so succesfully. Layne is truly an amazing guy right!
Thanks for your take on this, Layne. And thank you for disclosing bias. I wish all influencers did that.
Another limitation of the case study is that they measured LDL-C and not Apo B. I believe there are about 25 percent of people who can have low LDL-C, but high Apo B and we now that Apo B is more accurate marker of CVD risk.
High HDL/LDL and low Trig was how my blood work consistently came back when I consistently only ate Red Meat, fatty fish, veggies and fruit. Low blood pressure as well. I no longer eat strictly meat and veggies and my HDL/LDL is back to normal but my trigs hover around 100 and my blood sugar/A1C has been trending in a bad direction. (Typ 1 Diabetic)
Be right back buying Oreos and stopping my medication without talking to my doctor. (I'm joking, PLEASE DON'T DO THAT)
Thanks for a balanced review Layne. Excuse my ignorance as I have no idea how LDL is measured from a blood sample, so my question is probably entirely stooopid… Is it possible that any of the ketone bodies (bhb, acetate etc) could be causing a misreading of the ldl numbers, thus artificially increasing the readings,?
I’m kinda like that subject
I was doing yearly blood tests in the past, and I got the best results (122 total cholesterol) when I was having soda with deep fried food for breakfast and afternoon snack everyday.
It doesn’t mean someone else would have the same results, also it doesn’t mean it’s healthier on the long run for myself. I also used to do an Oreo diet for bulking (super skinny), but nowadays I try to eat more lean and unprocessed food, and my body responds positively to it.
Actually it does because this lipid energy model predicts exactly what you're describing.
Layne could you look at the recent U of Pittsburgh study linking high protein with atherosclerosis?
I remember clicking on a video titled "Are You a Lean Mass Hyper Responder?", expecting a video about hypertrophy. Boy was I wrong! LOL 🤣
I’m glad you talked about inflammation since it is a big driver towards cardiovascular disease independent of cholesterol. More so in my opinion than LDL. Lower inflammation means less diseases to a certain point. By the way, there are no unicorns. Every person has thousands of people who respond just like they do. Maybe not millions but thousands. There are thousands of lean mass hyper responders in the wild. A minority sure, but not a unicorn.
It's not independent of cholesterol. It's an accelerator of cholesterol.
All the choppiness at the intro just shows how difficult it was for him to not throw a ton of shade lol
These are not unicorns, and it's not about the people. It's about the model of what metabolism is, and the variety of ways in which it can function. Function in a healthy, natural way. I wonder what the typical LDL levels are for wild cats. I'll be looking into that...
I just read about someone this morning who lowered LDL by introducing milk into his diet. Milk is somewhat high in carbs.
5 years from now there will be some good studies coming out
Recent study out of Europe I just read about has LDL as a minor risk factor
data > feelings !
I disagree with your assessment of the topic because I think your argument is based on lipid hypothesis, ie,higher the concentration of LDL’s , higher the risk for atherosclerosis whereas the other side’s hypothesis is based on lipid energy model- see Dave Feldman’s explanation why people who are on ketogenic or carnivore diet have high LDL.
Although there was an intervention, this appears more mechanistic to me. clinically, most physicians who work with diet commonly see a greater physiological response with food than medication. I usually give most of my patients 1 month to drop their LDL by 30% in 4 weeks after we discuss a plan absent any statins. That period is too short for us to retest after prescribing statins other than assessing for side effects. Why statins didn't work as well? Assuming perfect adherence - it could simply be an absorption issue with the statins. The lipid profile may impede statin pharmacokinetics, this happens sometimes with diabetic patients and there is a lot of research about which statins are better to use in diabetics for this reason.
Clinically, more health gurus are gonna claim statins are trash, high LDL is fine, and low carb is the best way to go now, so yay, work just got more fun because they guy who eats bacon and weighs 300lbs at 5'6 is gonna tell me his diet is scientifically proven to be heart healthy by adding in Oreos.
Maybe a new mic to celebrate 500 k subs? Just saying, for the algorithm.
While interesting, the LMHR having LDL and by consequence Apo-B particle number similar to that of people with familial hypercholesterolemia, the risk elevation is so high for heart disease events and possible death that it would not be worthwhile to ever stay at such a lipid level. Especially since we know particle number is the key driver in ASCVD not size, and particle number tracks pretty well with mg/dL values often given in standard lipid panels. Moreover, the WHOs recent 2023 report with nearly 3.7 million people suggests reducesd risk for mortality, CHD incidence, and type 2 diabetes for substituting 5% saturated fat with PUFA MUFA and whole grain/slower digesting carbs. Not to mention this aligns with mountains of previous data corroborating high saturated fat and ASCVD risk via elevation in LDL cholesterol such as mensink 2016, Hooper et al 2020, Hegsted et al 1993, the seven countries study 50 year follow up data, the north Karelia project, Ference et al 2017, Kim et al 2021, and Mazidi et al. (2020) to make a few.
Great video!
The information should be automatically disregarded because of only one participant in the study.
It would be interesting to have measured, if not already, whether the "Lean Mass Hyper-Responders" tend to be more hyper-absorbers of dietary cholesterol. EmpowerDX can measure absorption markers vs production markers of cholesterol and if on the high end of absorption, this can drastically increase LDL-C and ApoB if eating a low-carb diet that is high in cholesterol laden foods such as eggs and organ meat. In the study they did mention a baseline diet based on macros, but not amount of cholesterol ingestion and whether that changed when adding the oreos.
Nick made it clear Oreos were added it to the diet without and taking anything out. That means his saturated fat intake actually increased on Oreo phase
Great video. thanks
can you make a video on high protein diets and liver diseases like nafld . seems like there are many conflicting viewpoints on this topic and some people say high protein diets are good and other says they are bad for liver disease.
Nothing has been established about lmhr aside from a definition and basic baseline data. The Oreo experiment may apply to all lmhr. Though interesting, and not clear if response is from carbs or is from over feeding, it can remove one from the lmhr category. But what this has to do with demonstrating anything counter to the current ldl cvd relationship is absolutely nothing.
💯
Can you do a video on Eric Berg claiming eating eggs increases or even causes your risk for heart disease?
I bought a dozen cases of oreos. Thanks doc! Ill eat a case a day
Would have been nice if he took fruit instead of oreos. Whole foods Meat + Fruit would be a very fun diet that also allows to stay lean.
HDL has been proven to NOT be an individual risk factor for cardiovascular disease. Studies on HDL raising drugs have proved this. I believe there are studies on people who have high HDL for genetic reasons do the same but not sure.
I was initially hyped about the LMHR stuff, as I fitted into this criteria quite well (IF and Paleo zealot back then). Then I started digging deep in LDL and Apo-B literature - my enthusiasm faded.
So the best lifestyle ever: be a KETO LMHR and on truck load of statins and PCSK9i-s. (joke, haha)
Great analogy on smoking vs the lipids - I will keep it.
All in all I follow their research as it can reveal crucial novel information.
Wouldn't that lipid model hypothesis be very easy to test by measuring ApoB directly? If by some miracle ApoB levels were indeed low despite huge LDL, then fine, maybe LMHR don't have higher risk of heart disease, but that is very unlikely. Also, given that it is a single individual, it is plausible that he could have some mutation in some enzyme involved in lipid or glucose metabolism that exacerbates those effects.
You didn't address their CTA's would love to hear your thoughts on that.
LMHRs can do this trick with any carb source. So that would be the advice, eat sweet potato and you’ll likely have similar lab values with a lower LDL, while still being low carb/keto. I believe Nick stayed in ketosis during this period. He may have supplemented to do it, but still possible.
@@Feed_Bleed_Read Yes he did, I have confirmation of this now. He used ketone supplements to stay in ketosis. However, even Nick states that some people, if they strategize correctly, may be able to carb cycle without supplements.
9:50 right this unicorn LDL population is so small and not how most people with broken metabolism behave that it's basically irrelevant. #1SubjectONE
It is not irrelevant to them.
11:35 -- Well, first of all, the Oreo group was 'intervened' for less than 2.5 wks, while the Statin group was intervened for 6 wks. To me it looks like as if the Oreo curve was flattening out or may even rise later on, say, around 6 wks (?) (ha ha), while the statin provides a steadier control on the LDL levels...which is not surprising...time does matter, and we should try & look at longer term data, even if the subjects are fed Oreos for 6 wks -- I bet they all will like that! 😀
Also, the baseline levels of the Oreo group before starting the 'Oreo therapy' was btwn 384, while the baseline of the stating group was 421. This can affect the shape of the curves when dropping, esp. when the X-axes are not the same (days vs weeks)...which in turn can 'look dramatic'...
Also, I'd like to see this study replicated -- a carefully designed, well-conducted study. As the Sagan Standard goes: "Extraordinary claims require extraordinary evidence."
This is a study by PhD, Harvard doctor bro. Even Layne with his bully attitude admits the data is correct, try anything else and stay away from the data being not conclusive. You can't get better data than this.
@@jimmymuthami7130 🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣🤣
Well, it’s just returning to the pre keto state. The original carb fed state. These are hyper responders. Boom up. Boom down.
@@jimmymuthami7130 You mean Harvard clown.
I don't think you have carefully examined the study. As far as I remember, the researchers conducted a Calcium Score on the participants, and the results showed that they had almost zero, which is less than people with normal LDL. Therefore, it is unlikely that if they had lower LDL, they would have a lower risk of cardiovascular diseases. It seems like you are biased, my friend. You always have the same perspective, which is why you have problems with the majority of researchers and doctors on social media.
So he did not understand the findings of the experiment and asks his PhD advisor who was clueless. But the explanation is in the study!
Obviously here feelings blurred interpretation or interest in the data to actually study data.
Nick predicted the outcome of the Oreo study so he obviously has some foundational knowledge which the majority of the mainstream medical professionals lack.
Keep going Nick your quest for knowledge is severely lacking in many who rest in the current LDL story as being settled science and are dismissive of anyone who dares challenge their narrative.
"Full disclosure, I have beef with guy, and this guy, and this guy, .... "
Yep, so true
Full disclosure: Layne is on statins
@SullivanKelly85 so are a lot of cardiologist and longevity Drs...
@@brownshit1 the irony there is not lost on me 😆
Excellent travail
Maybe the effect of Oreos was brief and if they continued for 6 weeks vs 16 days they could’ve seen the same rebound as the statin.
the "rebound" was due to the subject testing another aspect of the lipid energy hypothesis, which is that increasing energy expenditure (exercise) would increase LDL-C. He intentionally doubled his steps for that final period and saw the predicted result.
@@dkeener13 why only 16 days of Oreo but 6 weeks of statin?
because the docs he consulted said 6 weeks should be a fair "trial" period to see the likely lowering effects of the statin. these LMHR guys know they can raise and lower their LDL at will by throttling carb intake.
All this suggest to me that carbs fuel some important fonctions in our organism, other than the already important one of providing energy.
Since it was done with 1 subject, if outside factors were taken into account such as sleep & stress. Possibly just eating Oreos made the subject feel better (satisfied) which lowered stress levels for better sleep? Another factor could be going from Keto to Non-keto helped with bowel movements. During digestion, soluble fiber binds with cholesterol in bile and aids in its excretion. But the issue there is that there's no soluble fiber in Oreos.
No it's because LDL is used to transport fatty acids through the blood to be used as energy. When you're obese your cells have more than enough fuel so your LDL stays the same or even goes down on low carb but if you're very lean all that fat has to come from dietary fat which is transported in LDL to the cells. The reason the addition of carbs from oreo lower the LDL is because the body now also has extra glucose for fuel, meaning that it has to transport less fat to the cells for fuel.
Nick has IBD. He has to be in a keto state to avoid serious gut issues. He was probably grossed out and stressed when he had to eat Oreos.
Dr. Norton, ironically my cardiologist had me massively increase CBH while matching fat and protein concurrently to when Nick did he n=1. Due to autoimmune reactions to almost all CBH sources the only way I was able to do this was via homemade Christmas cookies(if I was gonna feel like shit from CBH, they were at least gonna be delicious) as they allowed me to match fatty acids to my animal-based diet. Anecdotally, I had LDL decrease from ≈460 to ≈230 and TG decrease ≈65 to ≈34.
Nick Norowitz explains the decrease in TG because of hyperinsulinemia in a fasted state(he explains better, I’m not a lipidologist lol). Could this be true in the context of a diet that promotes glucose sparing and physiologic insulin resistance? Ergo, with the increase in CBH you see an insulin resistance like oversecretion of insulin? This has been something that I have not been able to get my head around but I am concerned about as my low CBH diet is because of autoimmune issues that take priority to LDL.
Thank you, on the off chance you read/respond to this lol.
It's also important to note that Nick's experiment didn't even assess both major classes of statin. It only examined hydrophilic statins (like rosuvastatin), which tend to do a poorer job of LDL clearance than lipophilic statins, which have greater penetration into the liver. It's quite possible such a statin would have done as well as, or at least comparably to, the Oreos.
It's a flawed, clickbait experiment that doesn't even demonstrate what it says it does. And it's being used without any context by low carb grifters to engage in further statin and LDL denialism. The takeaway for most lay people, I suspect, is "statins are garbage because they don't even work as well as Oreos!" Then the extremely online 65-year-old with metabolic disease ignores his cardiologist's advice because he heard Ken Berry and Shawn Baker mention this on TH-cam. I find the entire online low carb ecosystem to be completely insidious.
My takeaway from the experiment, at best, is that (1) these kinds of diets may contain an inherent, and potentially morbid, risk factor for those with this phenotype in the form of extremely elevated LDL; and (2) it's probably a better approach for this phenotype to add at least the number of grams of carbs outlined in the experiment to their ketogenic diet in order to reduce this risk. I don't think the experiment successfully demonstrated that statins would be ineffective for this phenotype because it only assessed one kind of statin, as noted. And it's only testing one person, Nick, and his response could be idiosyncratic. The experiment could have just as easily tested a banana instead of Oreos, but it wouldn't get the headline. A banana would get people thinking they should eat more whole plant based, which isn't what low carb ideologues like Nick want.
so you’re saying in the context of that one person, they would be better off eating the oreos than not eating them?
Not necessarily, maybe it would be better for that person not to eat oreos and having high LDL. It is not exactly shown that such a high LDL in the context of LMHR is less healthy.
It's so important that this is one person. That may just happen to be the one in 8 billion who sees this dramatic a response. Even still, if I were on a low carb diet with high LDL but every other biomarker looking good, I'd just add like 200 calories of carbs a day and see if that lowered my LDL. You can stick to your low carb diet throughout the day then just add a couple pieces of fruit at the end of every day. Seems easy enough.
Oh, I'd also take a statin if I didn't have adverse side effects to them. Why not both?
The study also doesn’t say if this is just a temporal effect.
Around minute 8, you say that the genes that affect ldl do not affect anything else in the metabolism. Are you certain this is true ?
FHC includes higher clotting.
I've been waiting on this.
In my personal experience, Oreos have a similar effect to diet soda, they greatly reduce my anxiety. Having two Oreos for breakfast makes me not craving anything else all day long. But possibly it's an unicorn effect too.. 😆
One black swan is sufficient to debunk all swans are white. Right? 🤣
When they create whole body scanners and programs to identify each person’s perfect diet like in star trek, things will be nice.
Ooooh I was waiting for this one! Nick just won't stop talking about this. So annoying! THANK YOU!
Yes, it is interesting he used foods he objects/rejects and is now using them to promote his work/science and popularity. Maybe he finally saw the light and that all "foods" can be incorporated into a healthy diet.
@@profhaub You... you don't understand whats happening do you?
@@profhaubhe purposely used Oreos because almost no one would think they are healthy at all. Any carbs will cause lower LDL in LMHS.
@markhaubphd ahh no you missed the whole point, just like 90% of Layne fan base. 😂😂 fucking bots
I don't think there's enough consideration of what exactly low carb hyper responders are eating when they get high LDL, or what exactly they could be eating to lower LDL, other than Oreos. What do different types of carbs (whole or refined) do, and what does different types of fats (saturated or polyunsaturated) do. Knowing more about this could explain a lot.
We need to know why some people are hyper responders in the first place. Does a ketogenic diet (or a certain kind of ketogenic diet) make them need more cholesterol in the same way that disease make people need more cholesterol? More experiments, please.
Good point, they should have done the study with some whole grain bread or fruit, but then it wouldn't have the same click bait result as Oreos do. Are they interested in science or social media clicks?
First comment, 6 seconds in, Im stalking you Lane
First reply to your comment. 16 mins in. I’m stalking you Marco
The hunter becomes the hunted...
@@damiku-8866 🤣🤣🤣
That actually made me laugh 🤣
Sane analysis!
BRB, calculating Bayesian 95% CI of my 1 participant from unknown UNICORN prior 🦄
Love Layne’s videos. I literally use every app this man has and everyone of them are golden
does inflammation need to be present to cause the LDL to penetrate the endothelial walls?
No. The LDL entering the wall itself causes localised inflammation. Watch the video of Gil Carvalho with lipidologist William Cromwell
Oreo sitting back wishing this came out sooner so they could’ve advertised their magical LDL lowering abilities during the Super Bowl. They woulda got Pfizer rich overnight.
Nick consistantly emphasizes this was only a study of one, do not stop taking statins or in anyway think this proves anything it was only to provoke conversation. As for Nick himself this guy is brilliant and would destroy Layne in a debate on metabolism.