Thank you for introducing Dr. Cromwell to us. His easily understood discussion with you about the nuances of the lipid energy model and his thoughtful perspective about the implications of Dr Nick Norowitz’s Oreo self experiment, was fascinating. The whole LMHR position is equally as fascinating in the realm of possibilities it offers in understanding metabolic health. Dave, how satisfying for you and hard earned. Well deserved, too.
@@realDaveFeldman- "Easily understood....." ??? Please help. Can you explain the Forier(?) vs the Medusa studie that Dr Cromwell uses as examples. In both studies the statin treated groups had less cardiovascular events. What does he mean by referring to those studies answering the question if lowering LDL (or apoB) is crucial to reduce future cardiovascular events ???
Still bugs me that he emphatically says lipoproteins cause CVD. Actually they are at the scene but no mechanism has been shown. Plus reducing cholesterol by statin therapy has minute effects on MI.
@@realDaveFeldman How do you think about the SREBP pathway? Saturated fat can activate a protein called SREBP, which increases the expression of genes involved in fatty acid and cholesterol synthesis. This includes genes that suppress LDL receptor activity, reducing LDL clearance from the bloodstream.
What a GREAT conversation with a doctor who wants to understand what the “real” risks are in all cases - not just giving patients answers per the “guidelines”. Dave: you have good, thoughtful, open-minded, questioning people on your team. You are rocking the lipid world!!
Excellent conversation. Thank you for introducing Dr. Cromwell. So glad that finally a mainstream practitioner who is open minded to this model. Thank you Dave for your dedication & hard work in this topic. Looking forward to meeting you, Dr. Cromwell, Nick and the others this March in Las Vegas.
Well done Dave and team, long form discussions are extremely important for general understanding and to be able have one with a lipid specialist is fantastic. Respect to Dr. Cromwell for being willing to explore and learn, I would think that most regard their knowledge as complete when they arrive at his station.
The most important question answered by Dr. Cromwell is “Do we expect any plaque in lean mass hyper responders?” . The answer is ‘yes’. But he also said we don’t know how long it can take for this phenotype to get plaque, if any. He does say that there needs to be a different conversion for those who do not have plaque. Now it’s upto this phenotype to decide if they want to wait till they develop plaque .Some of them may never develop plaque, but it seems to be dependent on the individual ,and not the whole phenotype. He also mentions mortality. It’s possible that this phenotype may not have adverse outcomes as far as mortality is concerned. We don’t know yet
Very interesting topic! I became a LMHR in the past year of carnivore. I also have a documented 20+year history at the VA system of high total cholesterol, triglycerides and LDL, lowish HDL, normal fasting glucose and BMI no more that 23, During all these years, I tried to eat a 'balanced' diet and excercised frequently. Im just now 57yo and I had a CAC, echocardio and stress test to have as baseline once I became interested in this topic. The tests showed no damages and zero calcifications. I also have very good blood pressure. Yes, I took statins in the past (4yrs ago) for a 3 month period but had a severe adverse reaction and stopped. Grew paranoid and denied further trials of other statins. About two years ago, I also tried fenofibrates but these did not lower my triglycerides, in fact, they kept on creeping up to 500s and I felt muscle aches so I stopped them too. Then I found the carnivore diet in late 2022. I'm now what they call a LMHR and lowered my bmi to under 20. Never felt better and rather take the rist of a heart attack than going back to feeling bloated, inflamed and low energy like when I was on the SAD. BTW, is also believe is helping me overcome multiple myeloma blood cancer, no new tumors (had one on my L1 vert before carnivore) and low adverse effects during chemo. My blood markers are remarkedly good for being on chemo, according to my hema/onco team.
Thank you for sharing your story. I can only imagine, "feeling good" after all that gives you better quality of life. Hopefully Triglycerides come down with a high, healthy fat, carnivore lifestyle. At age 65 my Trig/HDL ratio is 0.3 so I really don't care what my LDL levels are.
@@kenadams5504 are you the LMHR police? lol? Yes, it took me over six months to get from trigs in the 500s to below 100. setting the bar at 70 or less seems excessive but whatever. Could care less if someone considers me lmhr or not but for the sake of argument, as of last week: tc399 tri85 hdh83 ldl293 vldl15 158lbs 6’1” 57yo. On my 12th week of chemo and feeling great.
Thanks, Dave, and thanks again for OwnYourLabs. I'm using it a LOT now as I "game" my lipid for my PCP before returning to my own LMHR self. Glad to "meet" Dr. Cromwell. You and Nick are getting incredible traction now, to the point that the mainstream medical field will have to be confronted with your research. Nick is getting amazing attention from the Oreo experiment. I would have done Oreos myself, except I simply can't burn that many calories and would probably feel super sick. (I weigh 101 lbs. and actually eat a lot for my size, so it's rice, a little fruit and more veggies for me.)
Thank you for being a voice of reason for the LMHR community. Like many of your viewers, I’m currently being pressured by an MD to try statin therapy. I’m a 58 year old female, 5’2”, 140#, CrossFit 4x weekly, run 3x weekly, 26% bmi by dexa, fasting insulin 1.0, CRP 2.6, A1C 5.0. My total cholesterol is 304, triglycerides 85, HDL 90, LDL direct 194. I was again pressured to take a statin. I responded with a request for an advanced fasting lipid panel. Results: NMR cholesterol 293, NMR triglycerides 82, NMR HDL 91, NMR 12:47 LDL 286, LDL P 1584, small LDL less than 165, large VLDL P 2.8, HDL P total 41, large HDL P 16.5, LDL particle size 22.8, VLDL size 51.3, HDL size 10.2. After this result, another statin recommended. I’ve responded with a request for a CAC score, and also have an echocardiogram and stress echo scheduled. Any other suggestions? Other than a history of PVC, I have no other cardiac issues. I feel like I’m being bullied. Low carb/keto 5.5 years and counting.
Thank you for bringing us this valuable knowledge and researchers (including yourself) which would otherwise be obscure to many of us. Good topic and work!
I love this kind of dialog, and that I can watch in near real time as novel data drives a better understanding of human metabolism. I hope more experts in the field get involved. On the one hand, we may learn something new and exciting about a subject many consider solved science. On the other hand, new experimental data may disprove the lipid energy model or provide needed nuance. Either way, science advances. Dr. Cromwell's points about considering context regarding treating LDL and APOB were refreshing. Most discussions on UA-cam talk in such black-and-white terms. Either LDL is the most significant thing to address or that it has no relevance at all.
Great conversation, Dave, thank you so much! I fit your LMHR criteria, and am metabolically healthy. If you need another person in your test group, let me know! I’d love to help move the cause forward! Keep up the great work!! Very appreciated!
This was such an excellent nuanced disucussion, and imo should be the go to resource for those with current questions about their ldl on a low carb keto diet
Terrific interview and well expressed with clear explanations. Cromwell is a gold mine among the coal mines of lipidologists. I wish some lipid researcher would introduce into their factors those of us with the APOE 4 allele. I am a strict keto dieter (7+ years) with a BMI of 23, TRGs of 69 and HDL of 52, and a fasting insulin of 6. Last summer I added MCT oil capsules to my regime and my LDL shot up 100 pts and my APOB is now in the high risk category! At the age of 74 with a CT Angiogram with Calcium Score of 0 less than a year ago, I am now considering taking a statin and Eztimibe, which I have always resisted doing. Scared me, but I removed the MCT oil from my supplement regime. I will continue to wear a CGM as it seems the only control I have over my crippled genetics by regulating my glucose metabolism.
I've been eating low carb for a while now. I'm a hyper responder with the same triad of elevated ldl, high hdl, low triglycerides. Ate massive amounts of salad a couple of months before my physical b/c I was worried about getting the same statin discussion with the Dr again. The ldl dropped naturally to the point where the statins were not pushed on me during my most recent Dr visit. Took the CAC test shortly after and scored 0 just to make sure things were ok. This study speaks volumes and I hope this study catches my Dr's eye without me having to mention it. I have sent him a link about hyper responders in the past but it may have fallen on deaf ears. I'm not saying I'm going to eat Oreos before my next Dr visit, but I may need to look into sweet potatoes or some kind of carb in general.
I found a better way how to decrease my LDL than to stuff myself with carbs. When my doctor wanted to put me on statins because very high LDL I told him, that I will try to change my diet first and will come in few months for new blood tests. During next few months I was still on the keto diet, but I replaced a big part of animal fats with plenty of olive oil and coconut oil. And it actually worked. My LDL dropped 60%. I am not sure what is exactly the mechanism behind it, but I recall vaguely a lecture done by Dr. Paul Mason, who was saying that if we replace animal fats with plant oils our cholesterol will drop and phytosterol in our blood will increase. Which is not necessarily a good thing, but at least I was spared the statins.
@@neilnewinger3059 That is interesting what you state about the coconut oil. I remember when first going low carb, I lost a ton of weight but back then blood work ldl was optimum. 3 years later my ldl crept up. It wasn't crazy high like what these guys speak of but it was in the 180s. Back when my ldl was really good 3 years ago, I used MCT oil pretty often. I put it in my coffee, two good yogurt, and took it by spoon as well. I wonder if the MCT oil may have had something to do with ldl lowering b/c I don't use it anymore. It is too pricey.
I was smiling when I read how you guys operate because I thought it was just me who deals with the doctor that way. I consider people like us are poor victims of the society authority norm. We are cornored to find our own way out. As Dave asked but Dr Cromwell didnt believe, this LMHR population (at least in a wider sense) is not small. Dr Cromwell said he never comes across any. Maybe that's because people in this population all operate the same way.
Thank you, Dr. Cromwell. It was very interesting to hear you speak about this. As you pointed out there are only two ways the body removes cholesterol from the system, LDL receptors on the liver and through the process of excreting bile with your waist. So the only two effects possible are in the exchange of LDL through the receptors or the recovery/excretion of bile cholesterol. I believe that the body has demonstrated the ability to rapidly adjust the various energy systems in the body to handle energy demands. I suspect that a change in the LDL receptors at the liver is more likely the cause rather than bile excretion. That is much more fitting with the biological purposes and drivers of the liver. I look forward to studies that can pin point the cause of the Oreo effect on LMHR.
Great job Dave! As usual, you and Nick have a gift of walking a delicate line of challenging mainstream theory without offending or insulting. Great work. I'm having a very, very difficult time trusting anything that Bill says because he is constantly trying to view new LMHR ideas through his old paradigm. He is very stuck in one way of thinking. He even contradicts his own platform. His platform measure many biomarkers like fasting insulin, glucose, HbA1c, insulin resistance, etc, yet he continues to insist that ApoB is the culprit. When we improve all biomarkers with low-carb, but ApoB goes up, how can he continue to insist that ApoB is the cause. I sometimes hear him say that it's not only ApoB, but when he says that it sounds like he doesn't believe those words. Anyway, great job Dave!
We need to understand the mechanics of these rapid changes. In the mean time, likely people with cholesterol issues should follow ~ conservative best practices.
I think an interesting study will be to randomize LMHRs into two groups. One group keeps up with a ketogenic diet, and the second group goes on a high carb diet, which will crash down their ApoB, and then look at plaque growth, instead of comparing LMHRs to general population
I love listening to conversations like this. There is so much information here and relatively easy to understand. I also like the experiences of Dr. Cromwell with patients. I learned a lot from this conversation. It makes a lot of things fall in their places. Which then also creates lots of (new) questions 🙂 For example: What are the views of Dave and Dr. Cromwell on the cyclic process of atherosclerosis. It seems to be a process that starts with endothelial damage, that then gets repaired, resulting in a plaque that is covered with an intact endothelial layer. After which endothelial damage happens again,. and the process repeats itself. First,... is this view correct and if so, what would be the trigger (or triggers) for each cycle to start? I doubt that it is the presence of LDL particles in the blood stream.
When you look at the transcriptome of the atherosclerotic process you will see TRPV4 and klf4 as two main players on the field. Too many carbs-> glucose and stimulate TRPV1 that stimulates insulin and causes low sodium/hyponatremia/hypoosmolality that triggers TRPV4. When TRPV1 increases insulin, insulin again increases TRPV1 that causes too much inflammatory factors including reactive oxygen species in mitochondria that oxidize lipids- your oxidized LDL gobbled up by macrophages that become foamy macrophages in plaque. Here’s a recent article: 2020 article Stem Cell Pluripotency Genes Klf4 and Oct4 Regulate Complex SMC Phenotypic Changes Critical in Late-Stage Atherosclerotic Lesion Pathogenesis
Dave love the air boreallis lights behind you beautiful …………and thanks for this video was so informative and spoke in layman’s terms brilliant !!! 👏👏👏👏👏🙏🙏♥️🇨🇦
I would very much appreciate a study for those of us who have reduced our CAC score. Mine is down 33% on Carnivore. The question is, in that process of reducing CAC, are particles released creating a higher risk of heart attack as that calcium moves toward existing narrowing?
I’m certainly a very big fan of greater research in those with a positive CAC but who are actively taking steps towards better metabolic health. In a roundabout way, our study out of Lunquist will give some peripheral data on this
I respect Mr Cromwell’s concern about the level of LDL. I feel the more important factor of plaque would be diet and hypertension as the cause which he alluded to at he end. On a population level most people fear weight from a poor diet, most don’t factor in poor health and disease as a concern.
Please help. Can anybody explain the Forier vs Medusa studies that Dr Cromwell uses as examples. In both studies the statin treated groups had less cardiovascular events. What does he mean by referring to those studies answering the question if lowering LDL (or apoB) is crucial to reduce future cardiovascular events ???
Dr in general is not worried about your health they are worried if you going to pay them - my son is a Dr and I must say the young Dris much more open to new info then the old ones - we must educate ourselves to take charge of our own health the same as looking ourselves after our own finances
Age 71 female LCHF 4yrs CAC 10 - report says the calcified plaque is located on mitral valve. Mini TIA (an overnight at hospital). Proved statin intolerant very quickly. Highly motivated to avert pre-diabetes which is rampant in the family. If there was a ‘next-step’ that could be taken, would this be Keto? Seems to have leanmasshyperresponder traits but since am considered to be in secondary prevention category, is there research to add light to context? Eg where to get more information. Loving the nerdy-ness, which I find positively challenging even with multiple re-listening. Big thanks to you both.
As a former Cardiovascular specialist at Abbott Labs. My perspective…..These LMHR’s may have a genetic benefit regarding reverse cholesterol transport. Eskimo tribes who eat massive amounts of omega 3 fat have very high LDL-C with zero plaque development. Now, genetic gifts aside, what are the LMHR’s APO b levels, LPa levels, HS-CRP levels, LDL-P numbers? Does this subset of people have genetic advantages with the above testing values as well? As stated by Dr Cromwell, it’s the patients with damaged clearance of atherogenic lipoproteins that make up the vast majority of folks with CVD. So again, please let us know the other lipid tests so that we can determine if this is indeed like the Eskimos who also have high LDL-C values yet no plaque. My 98 year old grandmother smoked 2 packs of cigarettes a day and a shot of scotch. Her physiology and genetics prevented what many others would have succumbed to…….Please get those other tests done and report back. Thx for the hard work.
He is so right about challenging mortality -since it is critical. Many years ago I read a piece stating that while mammography DETECTED cancers earlier they DID NOT INCREASE MORTALITY. The morality rate was higher for breast cancer patients WHO DISCOVERED THEIR LUMP IN A BREAST EXAM INSTEAD OF A MAMOGRAPHY. I stopped having them and had to fight my doctors for years to STOP RADIATING HEALTHY BREADT TISSUE. I don’t know if they have come to realize that and stopped recommending then ROUTINELY -as opposed to -unless you detect a lump- or not , but they don’t ever say anything to me about one. If I had radiated my healthy breast tissue every year for all these years I’d probably have breast cancer by now. IS ALL ABOUT MORTALITY RATE. THANK YOU. YOU ARE OUR HERO!! Thank you for sacrificing your salary to save lives!!! ❤️🙏🏻
Good. At around 1 hour, 20 minutes, Dave brings up metabolic dysfunction. It was my understanding that insulin resistance results in deleterious oxidation and inflammation that is correlated with plaque progression.
here's the problem for me, high LDL won't cause plaque in the absence of inflammation, as it only shows up to repair damage, so if low carb keeps inflammation markers low, then there shouldn't be a problem with plaque build up. And why aren't we discussing the role of blood clots and heart attacks? All I know is I have a CAC and a CTA of zero, and I have been under 10g of carbs a day (carni) for nearly 7 years now with no change in those scores, and I feel amazing. So for me, I am staying this way. tbh I would rather drop dead of a heart attack and feel fantastic up until that point, than be on 7 different drugs for health problems and live feeling like garbage and unable to actually enjoy the years I am given.
LDL is ok Oxidized LDL is not. Too many carb/sugar-> too much TRPV1 on mitochondria that produce too much reactive oxygen species (ROS) that oxidize lipids. Those oxidized lipids are eaten up by macrophages that are called foamy macrophages in plaque. Here’s an article that describes the atherosclerotic process: 2020 article Stem Cell Pluripotency Genes Klf4 and Oct4 Regulate Complex SMC Phenotypic Changes Critical in Late-Stage Atherosclerotic Lesion Pathogenesis
Doubt this. What I think you’re seeing is a genetically gifted subset with good RCT. Most of us have the opposite and need science and pharmaceutical life jackets. Many studies show LDL-C as “lower is better” for CVD. Infants have very low LDL-C and there’s a subset of the population with no APO-b and survive just fine. The brain manufacturers its own cholesterol so no worries there.
Do we know how good a CAC score is? I've heard doctors say that it doesn't really show anything untill the 11th hour. Kind of how liver enzymes can stay in normal range until there is serious trouble. Also Dave as a long time supporter / donator. Thank you for all you're doing. Its just as exciting for all of us out here.
CAC demonstrates calcified plaque. It's the soft plaque that kills. If you're worried, get a coronary CT Angiography (very detailed). While getting testing, rest a "treadmill" stress test to understand your fitness to cardiovascular health. If you find the right doctor, they will hook you up to VO2MAX test at the same time. Then you will have a big picture view.
A CAC score of 1 or more indicates you have heart disease. The higher the score, the more you have. Start with a CAC test first, as a score of zero means you really don't have much to worry about.
@@markopolo8845 Yes. I'm just curious if its senstive enough to show progression in such a short amount of time. Or if any of the methods we use can really show risk accurately.
Hi Dave - make sure to include the ldl mg years calculation of statin reduction in the comparison group as 26/80 Miami cohort had statin use (no idea for how long - you can get data?). If they reduced their apoB by 40% less than 14+ years, the Miami cohort may have a life time burden of higher ldl mg years. I think the risk however might be able to be a more compelling argument than lifetime ldl mg years comparison. Just something to keep in mind as you run your calculations.
I’m 1 yr into a keto diet and r today found out I’m clearly a LMHR. I’m in Canada and my Dr. said it was the highest cholesterol he had ever seen or heard of. Low triglycerides but cholesterol THROUGH THE ROOF! Can you possibly point me in the direction of some GTA area Doctors who understand Keto?
I hear very little about damaged LDL. LDL where the APO-b is unrecognizable so it is poorly recycled. Are there any studies showing the frequency of glucose binding to APO-b and causing its inactivation? Glucose binding to hemoglobin is so well characterized that we use it instead of fasting glucose testing in most cases. Population data correlating high LDL with disease obscures the contribution of damaged APO-b. Just a thought from a guy with an AA degree.
I find a problem with the idea of ldl receptor down regulation in that the ldl count would continually climb and would never stabilize. A high production rate of ldl and a stable count equals a high clearance rate. Sorta like elevated fasting glucose via gluconeogenisis without insulin resistance. Same clearance rate (it’s not climbing, but baseline is set at a higher level. Something is directing this level
Perspective from inside the LMHR set; It is nice we have lots of little models to discuss and argue over BUT my actual lipid-glucose-glutamine metabolism is a monster millions of years in the making. You can’t make it roll over and play tricks like a puppy. It has its own mind and will react as the gods have programmed it to react. Not all of our metabolism is defined in our individual genetics.
I do keto diet, cardio everyday, and intermittant Fasting .My ldl only increased after eating keto.I'm lean (bmi 23.5), with low trigs/high hdl and ldl 400! .Doc wants me on a statin ,so I learned about lmhr.I diagnose myself as a lean mass hyper-responder .My Doc never heard of lmhr . I am the lower scale of lmhr and could ,therefore, "normalise " my hypercholesterolemia in just 16 days (eating a packet of oreos per day) .I don't know if I want to lower my ldl when its a large and fluffy particle in a context of metabolic health. Lmhr ,it seems, is protective against cardio vascular disease .Why would I lessen a protection against a disease ?.
Forgive my ignorance, I’m not trying to compete with you guys. My cursory understanding is that the experiment results may have something to do with the person’s overall baseline of insulin resistance, which is developed over time of predominant ketosis. During my longer ketogenic phases I’ve experienced rapid recovery if I ‘dip out’ of ketosis. A recovery time that increases if I do a lot of ‘dipping out’. Somehow my overall metabolic baseline shifts. Dr Boz also refers to this. In other words, the lower success of the statin may be due to a lowered metabolism baseline
This was a study that had great difficulty finding enough people that fit the prototype. And in many instances subjects who otherwise fit, the prototype were excluded specifically because of elevated CAC scores. It is a little disingenuous to be proud of the fact that the people that were included had low CAC scores.
actually one of the main reasons people were exluded was they didn't have copies of verified old blood work showing normal cholesterol levels, I was one of them, my total cholesterol was always lauded by my doctors as it sat at around 135, with my LDL being at 70, but with no actual records to provide, I can't be used in a study like this
Because of its complexity and the large number of factors involved, it seems like this LDL- CVD risk conundrum is unlikely to be resolved through this very slow loop process of observation (from real life data) --> model hypothesis -> model testing -> debates --> more obersation --> model revision/new model. Being a software engineer, Dave, have you thought of using machne learning which is more capable than human to taking large number of factors into consideration? There are many machine learning for healthcare startups. Can we take advantage of the work they do? I heard data is the key. If we can find a way to collect electronic records of all the data under the many factor "lables" from blood test data, age (changes with time), to even symtoms patients experience, and any fator we can think of, we ask these startups to apply the best type of ML to determine the CVD risk or plaque size in quantitative terms. Make sense?
My Total Cholesterol dropped from 7 to 2.85 mmol/l from april 26 to may 10 on statins. So six week steady state does not apply to me. Checked with Mission 3:1 meter.
I’m going to say I tried to follow what these two gentlemen are saying but I am just a country bumpkin. I can barely understand what they’re talking about. I think the cause of heart attack and stroke and the calcification of arteries boils down to a few things: stress, harmful chemicals in the environment, harmful foods such as sugar-seed oils-hydrogenated oils-heavily processed food, processed carbohydrates. If we eat foods that are as nutritious and as close to its natural state then we will have a lot less problems and diseases.
Hi, I am from South Korea, 58yo female. I have been eating only beef, Ghee butter, salt, and water for more than a year now and almost healed 30 year old psoriasis and got so many other positive changes in my body. Dr.Feldman, I have a question. How can dietary fat raise LDL? According to Dr. Malcolm Kendrick who suggests thrombogenic hypothesis of CVD , all dietary fat including saturated fat completely BYPASSES liver when metabolized. Chylomicron, not LDL, delivers fat to sells and gets reabsorbed by liver. On the other hand, excessive dietary carbs(glucose) goes into liver, liver stores 900kcal worth of glucose as glucogen and turns the rest into TG, liver makes VLDL , loads it with TG and sends it out, VLDL delivers TG, becomes IDL and then LDL, which is reabsorbed by liver. LDL only comes from VLDL, and VLDL comes from liver.
Plaque comes from too much TRPV1. TRPV1 is stimulated by sugar, glp-1, capsaicin, insulin and certain drugs such as oxcarbazepine. What drugs, foods such as capsaicin did the person take?
Interesting some of the keto/carnivore MD’s dismiss high LDL as being a problem (except FH)at all. What about out of control diabetics who have a higher risk of heart attack w/o regard to LDL? @ 1 hour 25 mins finally gets to “metabolically healthy” which is probably the answer to the problem. He is just not used to treating many metabolically healthy individuals.
That is my impression too. Most doctors are used to mostly obese, prediabetic, metabolically dysregulated Oreo consumers who have probably just one "good" blood test number - LDL. There is a short supply of metabolically healthy individuals. So they consider those sick people to be the standard how to determine those "healthy" normal values.
You are confused. You can't have a heart attack without plaque, soft, inflamed plaque. And you can't have plaque without high levels of ApoB lipoprotein particles carrying LDL-C. High saturated fat diets lead to cholesterol synthesis and increased ApoB to transport it in the blood. These ApoB particles pass through the artery wall, get stuck there and oxidized, leading to plaque formation and this can happen even with a metabolically healthy person. So high saturated fat diets can be lethal, even in metabolically healthy individuals.
And the vast majority of the keto keto community are olympic level athletes yes? Theyre not. Most people looking to diet are metabolically unhealthy with high BMI. Like most of USA. Feldman's marketing of his study is probably killing them faster.
I don't think we have the lipid model correct. I have been on Keto-Vore for 5 years and my LDL is 327, HDL 98 and Trig 26. 5'5" 128 lbs. I'm not that lean, maybe average but have somewhat high LDL. I think if you are in Ketosis from high fat and low carb then your body will use fat for fuel and thus more LDL is in circulation. If you break that fat fueled Ketogenic state by adding larger quantities of carbohydrates, then your body will trigger the Ghrelin hormone which will trigger the Insulin hormone receptors to store fat for "the winter". Bears do this when they eat lots of berries and honey to fatten up and during winter when there is not much food and they hibernate; bears will live off of their own fat storage.
This is interesting…l don’t really think there is certain people that are only LMHR…l think personally anybody that go Keto is going to have higher LDL in the absence of carbohydrates…
@@maxwatermeyer4406 I generally eat pasture raised eggs and grass fed animals (butter, organs, meat) and wild fish. No seed oils, no veggies (except a little bit of Sauerkraut), very little nuts, a little fermented cheese (Brie, Parmesan, Kefir), and no fruits.
I am pessimistic that any benefit for health is going to come from these studies. I see Dave Feldman and colleagues taking victory laps already, but it doesn't seem justified to me. BTW, I am not a skeptical medical professional, I'm a layman, but I am skeptical. It's clear that Dr. Cromwell, who is a real scientist and understands the problems with Dave's and his colleague's research, is not convinced that it has any value for health, or limited value. One value would be that if a person on a high saturated fat keto diet developed plaque, with the right choice of a carb, might be able to quickly and sharply lower their LDL-C and their ApoB. The big problem with the explosion in LDL-C and ApoB that you get with eating a lot of saturated fat is time. Dr. Cromwell addressed this. The longer you have high LDL-C and ApoB, the higher the probability of getting plaque. That is what people on the high saturated fat keto diet are facing right now. The greater the amount of LDL-C in the blood, the greater the number of ApoB particles the body produces to transport them. When ApoB lipoprotein particles, which transport LDL-C particles in the blood rise above the physiological needs of the body, they can pass through the artery wall and get lodged in the "subspace." There they get oxidized which initiates plaque formation. Inflammation then kicks in. You don't need prior inflammation or insulin resistance for this to happen. This is what I have learned from Dr. Cromwell's interviews with Dr. Carvalho. I don't think that Dave's research is going to change this. People on the high saturated fat keto diet are going to get heart disease. It's just a question of time. Beyond this, I don't think that Dave has a scientific attitude. He is too emotionally committed to his views, to accept that they might be wrong. No matter what problems Dr. Cromwell raised with his work, he simply ignored them. And make no mistake, Dr. Cromwell is no believer. People should be paying attention, because until now, Dave and his colleagues have dominated the airwaves. Now we are hearing the facts from a real scientist.
@@newyorkguy158 the problem is we have no data from 200 years ago when NONE of us ate high carb and sugar the way we do now, so there is no indication that the higher LDL numbers are actually out of the norm, they are only out of the norm over the past 70 years or so, a blip in our timeline
I really want to know if I'm a lean mass hyper responder but my blood tests are in 'Canadian'. LDL 4.0, HDL 2.5 and Tryglicerides 0.4. Anyone that can help me out?
Arguing that this is a disorder, looking at my numbers might offer some insight. I have a low carb diet, am lean with very high HDL and very low trigs. But my LDL is in the normal range. Some how my LDL receptors are able to keep up.
what is your version of a low-carb diet? when I go under 10 grams of carbs a day my LDL jumps to over 500, but my HDL is 80 and trigs are mid 40's,, when I bump to 60g of carbs a day, my HDL and trigs remain the same, but my LDL drops to around 140, however if I go above 100g of carbs, my HDL drops to around 40 and my trigs jump to 120, my LDL then drops to under 100--- but my fasting bg bumps over 100 (75 on low carb) and I feel like complete shit
Or, the natural mechanism triggered by carbohydrate reintroduction is naturally more efficient than the statin as the statin might likely be affecting other things.
Gosh i just want someone to explain this for lay person. My biggest takeaway is bad science led to poor patient outcomes and cardiologists and pharma are sh*tting their pants.
Dr. Cromwell didn't answer the direct question about the risk reduction by LDL lowering drugs and EPA. Per what bigfarms published, it is up to 4% for whom who has higher than 2 hCRP. The rest of the cohort did not det any benefits
I’ll volunteer? I’m 55 172 , 6’3 , BMI 21 , I run a 7:30 minute mile , I weight training, been doing this my whole life, state Wrestling champion, and my Cholesterol is 270 I can’t get it lower! 62 triglycerides , HDL 82
If insulin causes separation of insulin receptor from LDL receptor, and subsequently increased activity of LDL-R, then why wouldn't we expect a high LDL, very low insulin state to very quickly yield an increase in LDL endocytosis in response to a sudden shift to episodic insulin bursts (with sugar consumption)? Your paper states point blank that the phenomenon cannot be attributable to insulin action. Can you clarify why you are confident that insulin is not playing a role here? What if, for example, Nick were to sustain normal nutritional ketosis and take low dose insulin injections? (Not to induce a hypo, just to evaluate LDL response.) If insulin isn't a contributor, the LDL should remain more or less high. If insulin is part of the LDL lowering mechanism, the LDL should drop significantly and substantially. Just wondering out loud because insulin is so involved in so many pathways, including LDL receptor function, that it strikes me as a plausible player in the overall mechanism. Yet you seem very confident that insulin can be disregarded. Great conversation, by the way. Thanks for sharing, as always.
Interesting speculation. Still...You should have more of a bioquantum focus not just molecular chemistry focus. Nature makes the most elaborate semiconducting photon/electron processes. I moved toward this five years ago having prior to this followed Dave years since 2016 and being a LMHR myself. My bias is being formerly a semiconductor researcher and now a biohacker SAD_survivor.
There really isn't a question. In an interview with Dr. Carvalho, Dr. Cromwell explained the process by which ApoB causes plaque, starting with the synthesis of saturated fat into LDL-C.
@@antoniodethomasis2583 I hope you are not referring to me. There are quack doctors on youtube who deny the science. Yes, they are like flat earthers. Dr. Brewer, for example. I used to respect him until I discovered the truth. For years he has been denying, without the slightest evidence that LDL-C causes heart disease. He says it's the fireman, not the fire. Completely wrong. Although it's really the ApoB that is the cause. And he says that saturated fats are not harmful, which follows from claiming that LDL-C is not causative. Wrong again. Everyone should watch Dr Carvalho's first interview with Dr. Cromwell in which he talks about science deniers like Dr. Brewer, though not mentioning him by name. Keep in mind that these doctors have monetized their channels, even developed large international telemed practices based on false information and are doubling down to prevent their clients from knowing the truth.
Reintroducing carbs back into zero carb or very low carb diets can restore health markers. Not only normal LDL levels but also free testosterone and SHBG. So, the take away from this experiment is that a balanced diet is the best diet.
So... the problem seems to be, there isn't enough data on how a healthy person functions on a diet that has been the norm for all human species (plural) for millions of years minus the last let's say 20.000 years with the onset of year round carbohydrate availability. Of course nobody pays money to figure out how "healthy" works.. maybe insurance companies might have an interest in that?
LDL alone is not a great predictor of heart disease. Your HDL/triglyceride ratio is a better indicator. The ideal is 2.0 or less. Most people are much higher than that. Look up "metabolic syndrome."
@@markopolo8845 ApoB is the best indicator and correlates often with LDL. HDL is not that great and too high values seem to also be correlated with worse outcomes.
I found a better way how to decrease my LDL than to stuff myself with unhealthy Oreos or other carbs. When my doctor wanted to put me on statins because of very high LDL I told him, that I will try to change my diet first and will come in few months for new blood tests. During next few months I was still on the keto diet, but I replaced a big part of animal fats with plenty of olive oil and coconut oil. And it actually worked. My LDL dropped 60%. I am not sure what is exactly the mechanism behind it, but I recall vaguely a lecture done by Dr. Paul Mason, who was saying that if we replace animal fats with plant oils our cholesterol will drop and phytosterol in our blood will increase. Which is not necessarily a good thing, but at least I was spared the statins.
What I found frustrating about this exchange was even if apoB contributes to plaques over time all else being equal so what? If I'm on statins for the last 30 years of my life and die of liver cancer age 90, but i dropped my CAC from 100 to 30, so what? Its been my observation that medicos are usually terrible logical thinkers.
Why only focus on one kind of statin? There are different statins that have different mechanisms of how they clear LDL. Maybe a different type would have worked as well as (or better than) the carbs.
The Lipid Energy Model (LEM) is probably not correct for the following reasons: 1. A person who is eating a keto diet, whether they are lean or fat, has depleted glycogen stores. Someone who has a higher BMI has more fat mass, but they would still be glycogen depleted on a keto diet. LEM posits that a fat person on a keto diet would have more glycogen than a lean person is probably not true. 2. For LEM to be correct, on a keto diet, a lean person's fat cells would release more free fatty acids than a fat person's. This is probably not correct as the opposite is true. The more fat a person has, the more free fatty acids are released into the blood. 3. LEM says that a large amount of free fatty acids are released into the blood in a lean person and the liver packages the FFA into VLDL. And yet we see a low amount of triglyceride in the blood, so where does the large amount of triglyceride in VLDL go? If they go back to the fat cells, then the body just wasted a lot of energy releasing fat and then putting fat back into fat cells - and this doesn't make sense. If the large amount of triglyceride go into muscle, why would a person with lower BMI need more energy than a person with higher BMI? The opposite is true, a person with higher BMI has a higher basal metabolic rate, and therefore need more energy. Also, the lipid test is done fasted in the morning, so the only energy used is overnight when the person is sleeping. So a lean person somehow needs more energy while sleeping than a fat person? It doesn't make sense. Hypothetically, the result would make sense after a person ran a marathon, because muscles used up a lot of energy. This is not the case, the lipid test is done in the morning after a overnight fast, not after a marathon. 4. The reintroduction of carbs lowering LDL does not provide evidence for LEM. Carbs lower LDL by another mechanism, not as described by LEM. I believe the major driver of very high LDL in LMHR is due to low insulin and thyroid hormone on a keto diet that reduce LDL receptor activity, resulting in less clearance of LDL from the blood. Addition of carbs raises insulin and thyroid hormone, restoring LDL receptor activity. 5. Why does a lean person have lower thyroid hormone than a fat person? Because the keto diet mimics fasting. Fasting is more dangerous for a lean person than a fat person because there is less fat reserve. So a lean person's body responds by lowering thyroid hormone to lower metabolism to conserve energy. Lower thyroid hormone results in less LDL receptor activity and therefore more LDL in the blood. Your recent experiment with women on keto diet shows that there's a correlation with thyroid hormone, which provides support for this explanation. 6. In order to show that LEM is correct, you have to provide experimental evidence that on a keto diet, a lean person's fat cells release more free fatty acids into the blood than a fat person's. And more VLDL's are released into the blood. The reintroduction of carbs doesn't provide any experimental support for LEM because it can be explained by other mechanisms as outlined above. Without evidence of greater release of FFA and VLDL, you don't have any support for LEM. My guess is that when you measure FFA and VLDL release, you'll find the opposite, which is that a lean person releases less FFA and VLDL than a fat person. 7. Lastly, it's not surprising that one can shift lipoproteins in a short period of time by changing diet given that the longest living lipoproteins, LDL and HDL, only last a few days in the blood.
Have to say I agree with this. I have yet to see any proof of causation - high LDL to plaque formation only association and assumptions. Also don't understand the use of ApoB if there is one per LDL particle irrespective of density then this takes no account of the normal HDL/LDL synthesis.
Wow that was a long comment. Can you site a source for your assertion that thyroid hormone regulates LDL receptors? I think you might be conflating gene expression and receptor regulation. The carbohydrate reintroduction is presented as significant because of the rapid drop in LDL not just the drop.
So people with a low BMI would have high LDL if and when they exercise or are low on calories and generally see their lipids vary a lot regardless of low carb/high carb? Do we see this? There is the other observation that those losing weight quickly on any sort of diet will have high LDL. Maybe due to suppression of thyroid. Fascinating comment.
Show me a plant based cholesterol worrier that looks healthy and strong and perhaps I’ll pay more attention to them. It’s always, without fail, obvious which person is the healthy one. Eat a species appropriate diet and forget all this crap about chasing down microscopic details of your lipids. Cromwell has been a useful idiot to the pharmaceutical industry for years. He’s made a ton of money pushing this crap. Feldman is way too patient with these idiots. He will never get them to budge.
Dr Cromwell at multiple points in time is trying to make Feldman understand (using evidence from 50 years of big studies) that high ApoB is worse than low ApoB for CVD, other things being the same. At no point does Feldman even seem like he understands that message, he has such a tunnel vision about his own LMHR phenotype and hypothesis. This was a hard watch because though Dr Cromwell ( who is the obvious expert here and Feldman is not) is willing to give consideration to Feldmans hypothesis, Feldman is already convinced of this own theory (yet to be even completed) and disregards all of previous evidence from much bigger and better studies on LDL/ApoB. The customary 'talk to your doctor' in the beginning is not sincere, and truth is half his followers will have active plaque formations and their high LDL keto diet will be worsening that accumulation. The other half will probably be fine regardless. As such, this whole line of study is a big negative given how wrongly it's been marketed without it even being completed.
I have had very high cholesterol always throughout my life. Please share your contact details - email so that I can seek your advice on how to proceed.
Thank you for introducing Dr. Cromwell to us. His easily understood discussion with you about the nuances of the lipid energy model and his thoughtful perspective about the implications of Dr Nick Norowitz’s Oreo self experiment, was fascinating. The whole LMHR position is equally as fascinating in the realm of possibilities it offers in understanding metabolic health. Dave, how satisfying for you and hard earned. Well deserved, too.
You have no idea. This is something I’ve waited for a very long time.
@@realDaveFeldman- "Easily understood....." ???
Please help. Can you explain the Forier(?) vs the Medusa studie that Dr Cromwell uses as examples.
In both studies the statin treated groups had less cardiovascular events.
What does he mean by referring to those studies answering the question if lowering LDL (or apoB) is crucial to reduce future cardiovascular events ???
Still bugs me that he emphatically says lipoproteins cause CVD. Actually they are at the scene but no mechanism has been shown. Plus reducing cholesterol by statin therapy has minute effects on MI.
@@realDaveFeldman How do you think about the SREBP pathway? Saturated fat can activate a protein called SREBP, which increases the expression of genes involved in fatty acid and cholesterol synthesis. This includes genes that suppress LDL receptor activity, reducing LDL clearance from the bloodstream.
@@kathya1956 you don't know what you're talking about
What a GREAT conversation with a doctor who wants to understand what the “real” risks are in all cases - not just giving patients answers per the “guidelines”. Dave: you have good, thoughtful, open-minded, questioning people on your team. You are rocking the lipid world!!
Outstanding guest Dave. Dr Cromwell explains things so well.
Excellent conversation. Thank you for introducing Dr. Cromwell. So glad that finally a mainstream practitioner who is open minded to this model. Thank you Dave for your dedication & hard work in this topic. Looking forward to meeting you, Dr. Cromwell, Nick and the others this March in Las Vegas.
Well done Dave and team, long form discussions are extremely important for general understanding and to be able have one with a lipid specialist is fantastic. Respect to Dr. Cromwell for being willing to explore and learn, I would think that most regard their knowledge as complete when they arrive at his station.
The most important question answered by Dr. Cromwell is “Do we expect any plaque in lean mass hyper responders?” . The answer is ‘yes’. But he also said we don’t know how long it can take for this phenotype to get plaque, if any.
He does say that there needs to be a different conversion for those who do not have plaque.
Now it’s upto this phenotype to decide if they want to wait till they develop plaque .Some of them may never develop plaque, but it seems to be dependent on the individual ,and not the whole phenotype.
He also mentions mortality. It’s possible that this phenotype may not have adverse outcomes as far as mortality is concerned. We don’t know yet
Very interesting topic! I became a LMHR in the past year of carnivore. I also have a documented 20+year history at the VA system of high total cholesterol, triglycerides and LDL, lowish HDL, normal fasting glucose and BMI no more that 23, During all these years, I tried to eat a 'balanced' diet and excercised frequently. Im just now 57yo and I had a CAC, echocardio and stress test to have as baseline once I became interested in this topic. The tests showed no damages and zero calcifications. I also have very good blood pressure. Yes, I took statins in the past (4yrs ago) for a 3 month period but had a severe adverse reaction and stopped. Grew paranoid and denied further trials of other statins. About two years ago, I also tried fenofibrates but these did not lower my triglycerides, in fact, they kept on creeping up to 500s and I felt muscle aches so I stopped them too. Then I found the carnivore diet in late 2022. I'm now what they call a LMHR and lowered my bmi to under 20. Never felt better and rather take the rist of a heart attack than going back to feeling bloated, inflamed and low energy like when I was on the SAD. BTW, is also believe is helping me overcome multiple myeloma blood cancer, no new tumors (had one on my L1 vert before carnivore) and low adverse effects during chemo. My blood markers are remarkedly good for being on chemo, according to my hema/onco team.
Thank you for sharing your story. I can only imagine, "feeling good" after all that gives you better quality of life. Hopefully Triglycerides come down with a high, healthy fat, carnivore lifestyle. At age 65 my Trig/HDL ratio is 0.3 so I really don't care what my LDL levels are.
@@garyjackson40540,3 , fantastic. Never heard a Nr like that. Will you tell me how much was your triglycerides and how much HDL ? Thank you very much
Lmhr lipids are : trigs 80 , ldl >200 . Without lipids like these , it ain't lmhr... (unless I missed something).
@@kenadams5504 are you the LMHR police? lol? Yes, it took me over six months to get from trigs in the 500s to below 100. setting the bar at 70 or less seems excessive but whatever. Could care less if someone considers me lmhr or not but for the sake of argument, as of last week: tc399 tri85 hdh83 ldl293 vldl15 158lbs 6’1” 57yo. On my 12th week of chemo and feeling great.
@@kenadams5504 LOL. The LMHR police is here. I didn't share my last lipid results. Anyways, FYI my last trigs 85 so not quite
Thanks, Dave, and thanks again for OwnYourLabs. I'm using it a LOT now as I "game" my lipid for my PCP before returning to my own LMHR self. Glad to "meet" Dr. Cromwell. You and Nick are getting incredible traction now, to the point that the mainstream medical field will have to be confronted with your research. Nick is getting amazing attention from the Oreo experiment. I would have done Oreos myself, except I simply can't burn that many calories and would probably feel super sick. (I weigh 101 lbs. and actually eat a lot for my size, so it's rice, a little fruit and more veggies for me.)
Thank you for being a voice of reason for the LMHR community. Like many of your viewers, I’m currently being pressured by an MD to try statin therapy. I’m a 58 year old female, 5’2”, 140#, CrossFit 4x weekly, run 3x weekly, 26% bmi by dexa, fasting insulin 1.0, CRP 2.6, A1C 5.0. My total cholesterol is 304, triglycerides 85, HDL 90, LDL direct 194. I was again pressured to take a statin. I responded with a request for an advanced fasting lipid panel. Results: NMR cholesterol 293, NMR triglycerides 82, NMR HDL 91, NMR 12:47 LDL 286, LDL P 1584, small LDL less than 165, large VLDL P 2.8, HDL P total 41, large HDL P 16.5, LDL particle size 22.8, VLDL size 51.3, HDL size 10.2. After this result, another statin recommended. I’ve responded with a request for a CAC score, and also have an echocardiogram and stress echo scheduled. Any other suggestions? Other than a history of PVC, I have no other cardiac issues. I feel like I’m being bullied. Low carb/keto 5.5 years and counting.
Thank you for bringing us this valuable knowledge and researchers (including yourself) which would otherwise be obscure to many of us.
Good topic and work!
Dr Cromwell is such an outstanding educator, thanks for this one hoping to see more collabs in the future as the research continues
Watching this with a big fat smile on my face.
Super fascinating.
I love this kind of dialog, and that I can watch in near real time as novel data drives a better understanding of human metabolism. I hope more experts in the field get involved. On the one hand, we may learn something new and exciting about a subject many consider solved science. On the other hand, new experimental data may disprove the lipid energy model or provide needed nuance. Either way, science advances.
Dr. Cromwell's points about considering context regarding treating LDL and APOB were refreshing. Most discussions on UA-cam talk in such black-and-white terms. Either LDL is the most significant thing to address or that it has no relevance at all.
Great conversation, Dave, thank you so much! I fit your LMHR criteria, and am metabolically healthy. If you need another person in your test group, let me know! I’d love to help move the cause forward! Keep up the great work!! Very appreciated!
Great questions, great discussion, Dave. The highlight was your question at 1:02:45 - that discussion is my main intrigue in LMHR.
We should chat. I think you’d agree there aren’t often moments like these in science…
Are you guys collaborating?
@realDaveFeldman
Aaaah, sooo. Cathartic indeed. Thank you.
Thank you. I've watched 5 videos so far, and this is the only one that was in a basic language that we all can understand. Thank you so much 😊
This was such an excellent nuanced disucussion, and imo should be the go to resource for those with current questions about their ldl on a low carb keto diet
Terrific interview and well expressed with clear explanations. Cromwell is a gold mine among the coal mines of lipidologists. I wish some lipid researcher would introduce into their factors those of us with the APOE 4 allele. I am a strict keto dieter (7+ years) with a BMI of 23, TRGs of 69 and HDL of 52, and a fasting insulin of 6. Last summer I added MCT oil capsules to my regime and my LDL shot up 100 pts and my APOB is now in the high risk category! At the age of 74 with a CT Angiogram with Calcium Score of 0 less than a year ago, I am now considering taking a statin and Eztimibe, which I have always resisted doing. Scared me, but I removed the MCT oil from my supplement regime. I will continue to wear a CGM as it seems the only control I have over my crippled genetics by regulating my glucose metabolism.
I've been eating low carb for a while now. I'm a hyper responder with the same triad of elevated ldl, high hdl, low triglycerides. Ate massive amounts of salad a couple of months before my physical b/c I was worried about getting the same statin discussion with the Dr again. The ldl dropped naturally to the point where the statins were not pushed on me during my most recent Dr visit. Took the CAC test shortly after and scored 0 just to make sure things were ok. This study speaks volumes and I hope this study catches my Dr's eye without me having to mention it. I have sent him a link about hyper responders in the past but it may have fallen on deaf ears. I'm not saying I'm going to eat Oreos before my next Dr visit, but I may need to look into sweet potatoes or some kind of carb in general.
I found a better way how to decrease my LDL than to stuff myself with carbs. When my doctor wanted to put me on statins because very high LDL I told him, that I will try to change my diet first and will come in few months for new blood tests. During next few months I was still on the keto diet, but I replaced a big part of animal fats with plenty of olive oil and coconut oil. And it actually worked. My LDL dropped 60%. I am not sure what is exactly the mechanism behind it, but I recall vaguely a lecture done by Dr. Paul Mason, who was saying that if we replace animal fats with plant oils our cholesterol will drop and phytosterol in our blood will increase. Which is not necessarily a good thing, but at least I was spared the statins.
@@neilnewinger3059 That is interesting what you state about the coconut oil. I remember when first going low carb, I lost a ton of weight but back then blood work ldl was optimum. 3 years later my ldl crept up. It wasn't crazy high like what these guys speak of but it was in the 180s. Back when my ldl was really good 3 years ago, I used MCT oil pretty often. I put it in my coffee, two good yogurt, and took it by spoon as well. I wonder if the MCT oil may have had something to do with ldl lowering b/c I don't use it anymore. It is too pricey.
I was smiling when I read how you guys operate because I thought it was just me who deals with the doctor that way. I consider people like us are poor victims of the society authority norm. We are cornored to find our own way out. As Dave asked but Dr Cromwell didnt believe, this LMHR population (at least in a wider sense) is not small. Dr Cromwell said he never comes across any. Maybe that's because people in this population all operate the same way.
Thank you. Great discussion.
amazing interview. Thank you so much.❤
Thank you, Dr. Cromwell. It was very interesting to hear you speak about this. As you pointed out there are only two ways the body removes cholesterol from the system, LDL receptors on the liver and through the process of excreting bile with your waist. So the only two effects possible are in the exchange of LDL through the receptors or the recovery/excretion of bile cholesterol. I believe that the body has demonstrated the ability to rapidly adjust the various energy systems in the body to handle energy demands. I suspect that a change in the LDL receptors at the liver is more likely the cause rather than bile excretion. That is much more fitting with the biological purposes and drivers of the liver. I look forward to studies that can pin point the cause of the Oreo effect on LMHR.
Very nicely done! Looking forward to what's to come!
Great job Dave! As usual, you and Nick have a gift of walking a delicate line of challenging mainstream theory without offending or insulting. Great work. I'm having a very, very difficult time trusting anything that Bill says because he is constantly trying to view new LMHR ideas through his old paradigm. He is very stuck in one way of thinking. He even contradicts his own platform. His platform measure many biomarkers like fasting insulin, glucose, HbA1c, insulin resistance, etc, yet he continues to insist that ApoB is the culprit. When we improve all biomarkers with low-carb, but ApoB goes up, how can he continue to insist that ApoB is the cause. I sometimes hear him say that it's not only ApoB, but when he says that it sounds like he doesn't believe those words. Anyway, great job Dave!
I loved this discussion 😊, thank you both 🙏
Using Oreos was GENIUS!😂😂😂a real “gotcha” to Big Pharma
👏👏 excellent conversation..
Thank you!
this was enjoyable - thanks. - Dr. Cromwell is great. appreciate.
We need to understand the mechanics of these rapid changes. In the mean time, likely people with cholesterol issues should follow ~ conservative best practices.
I think an interesting study will be to randomize LMHRs into two groups. One group keeps up with a ketogenic diet, and the second group goes on a high carb diet, which will crash down their ApoB, and then look at plaque growth, instead of comparing LMHRs to general population
I love listening to conversations like this. There is so much information here and relatively easy to understand. I also like the experiences of Dr. Cromwell with patients. I learned a lot from this conversation. It makes a lot of things fall in their places.
Which then also creates lots of (new) questions 🙂
For example: What are the views of Dave and Dr. Cromwell on the cyclic process of atherosclerosis. It seems to be a process that starts with endothelial damage, that then gets repaired, resulting in a plaque that is covered with an intact endothelial layer. After which endothelial damage happens again,. and the process repeats itself. First,... is this view correct and if so, what would be the trigger (or triggers) for each cycle to start? I doubt that it is the presence of LDL particles in the blood stream.
When you look at the transcriptome of the atherosclerotic process you will see TRPV4 and klf4 as two main players on the field. Too many carbs-> glucose and stimulate TRPV1 that stimulates insulin and causes low sodium/hyponatremia/hypoosmolality that triggers TRPV4.
When TRPV1 increases insulin, insulin again increases TRPV1 that causes too much inflammatory factors including reactive oxygen species in mitochondria that oxidize lipids- your oxidized LDL gobbled up by macrophages that become foamy macrophages in plaque.
Here’s a recent article: 2020 article
Stem Cell Pluripotency Genes Klf4 and Oct4 Regulate Complex SMC Phenotypic Changes Critical in Late-Stage Atherosclerotic Lesion Pathogenesis
Dave love the air boreallis lights behind you beautiful …………and thanks for this video was so informative and spoke in layman’s terms brilliant !!! 👏👏👏👏👏🙏🙏♥️🇨🇦
I would very much appreciate a study for those of us who have reduced our CAC score. Mine is down 33% on Carnivore. The question is, in that process of reducing CAC, are particles released creating a higher risk of heart attack as that calcium moves toward existing narrowing?
Your CAC score is lower?
How in the world did you accomplish lowering a CAC score?? I’m very interested to find out how to do this!!
I’m certainly a very big fan of greater research in those with a positive CAC but who are actively taking steps towards better metabolic health. In a roundabout way, our study out of Lunquist will give some peripheral data on this
How did you lower your CAC score?
@@paulettejackson1767 - it says in the post how it's lowered.
I respect Mr Cromwell’s concern about the level of LDL. I feel the more important factor of plaque would be diet and hypertension as the cause which he alluded to at he end. On a population level most people fear weight from a poor diet, most don’t factor in poor health and disease as a concern.
Net: lmhr LDL variations are a healthy, expected physiological response.
Please help. Can anybody explain the Forier vs Medusa studies that Dr Cromwell uses as examples.
In both studies the statin treated groups had less cardiovascular events.
What does he mean by referring to those studies answering the question if lowering LDL (or apoB) is crucial to reduce future cardiovascular events ???
Dr in general is not worried about your health they are worried if you going to pay them - my son is a Dr and I must say the young Dris much more open to new info then the old ones - we must educate ourselves to take charge of our own health the same as looking ourselves after our own finances
Age 71 female LCHF 4yrs CAC 10 - report says the calcified plaque is located on mitral valve. Mini TIA (an overnight at hospital). Proved statin intolerant very quickly. Highly motivated to avert pre-diabetes which is rampant in the family. If there was a ‘next-step’ that could be taken, would this be Keto? Seems to have leanmasshyperresponder traits but since am considered to be in secondary prevention category, is there research to add light to context? Eg where to get more information. Loving the nerdy-ness, which I find positively challenging even with multiple re-listening. Big thanks to you both.
you can always try a lower carb, but not keto approach- maybe 50 grams of carbs?
As a former Cardiovascular specialist at Abbott Labs. My perspective…..These LMHR’s may have a genetic benefit regarding reverse cholesterol transport. Eskimo tribes who eat massive amounts of omega 3 fat have very high LDL-C with zero plaque development. Now, genetic gifts aside, what are the LMHR’s APO b levels, LPa levels, HS-CRP levels, LDL-P numbers? Does this subset of people have genetic advantages with the above testing values as well? As stated by Dr Cromwell, it’s the patients with damaged clearance of atherogenic lipoproteins that make up the vast majority of folks with CVD.
So again, please let us know the other lipid tests so that we can determine if this is indeed like the Eskimos who also have high LDL-C values yet no plaque. My 98 year old grandmother smoked 2 packs of cigarettes a day and a shot of scotch. Her physiology and genetics prevented what many others would have succumbed to…….Please get those other tests done and report back. Thx for the hard work.
He is so right about challenging mortality -since it is critical. Many years ago I read a piece stating that while mammography DETECTED cancers earlier they DID NOT INCREASE MORTALITY. The morality rate was higher for breast cancer patients WHO DISCOVERED THEIR LUMP IN A BREAST EXAM INSTEAD OF A MAMOGRAPHY. I stopped having them and had to fight my doctors for years to STOP RADIATING HEALTHY BREADT TISSUE. I don’t know if they have come to realize that and stopped recommending then ROUTINELY -as opposed to -unless you detect a lump- or not , but they don’t ever say anything to me about one. If I had radiated my healthy breast tissue every year for all these years I’d probably have breast cancer by now. IS ALL ABOUT MORTALITY RATE. THANK YOU. YOU ARE OUR HERO!! Thank you for sacrificing your salary to save lives!!! ❤️🙏🏻
Good. At around 1 hour, 20 minutes, Dave brings up metabolic dysfunction. It was my understanding that insulin resistance results in deleterious oxidation and inflammation that is correlated with plaque progression.
here's the problem for me, high LDL won't cause plaque in the absence of inflammation, as it only shows up to repair damage, so if low carb keeps inflammation markers low, then there shouldn't be a problem with plaque build up. And why aren't we discussing the role of blood clots and heart attacks? All I know is I have a CAC and a CTA of zero, and I have been under 10g of carbs a day (carni) for nearly 7 years now with no change in those scores, and I feel amazing. So for me, I am staying this way. tbh I would rather drop dead of a heart attack and feel fantastic up until that point, than be on 7 different drugs for health problems and live feeling like garbage and unable to actually enjoy the years I am given.
But what if high functioning LDL has a positive effect on Plaque…what if lowering it is a net negative.
LDL is ok Oxidized LDL is not.
Too many carb/sugar-> too much TRPV1 on mitochondria that produce too much reactive oxygen species (ROS) that oxidize lipids.
Those oxidized lipids are eaten up by macrophages that are called foamy macrophages in plaque.
Here’s an article that describes the atherosclerotic process:
2020 article
Stem Cell Pluripotency Genes Klf4 and Oct4 Regulate Complex SMC Phenotypic Changes Critical in Late-Stage Atherosclerotic Lesion Pathogenesis
Are you stupid?
Doubt this. What I think you’re seeing is a genetically gifted subset with good RCT. Most of us have the opposite and need science and pharmaceutical life jackets. Many studies show LDL-C as “lower is better” for CVD. Infants have very low LDL-C and there’s a subset of the population with no APO-b and survive just fine. The brain manufacturers its own cholesterol so no worries there.
Do we know how good a CAC score is? I've heard doctors say that it doesn't really show anything untill the 11th hour. Kind of how liver enzymes can stay in normal range until there is serious trouble.
Also Dave as a long time supporter / donator. Thank you for all you're doing. Its just as exciting for all of us out here.
CAC demonstrates calcified plaque. It's the soft plaque that kills. If you're worried, get a coronary CT Angiography (very detailed). While getting testing, rest a "treadmill" stress test to understand your fitness to cardiovascular health. If you find the right doctor, they will hook you up to VO2MAX test at the same time. Then you will have a big picture view.
A CAC score of 1 or more indicates you have heart disease. The higher the score, the more you have. Start with a CAC test first, as a score of zero means you really don't have much to worry about.
Check out x.com/realdavefeldman/status/1492755168298881032?s=46
@@markopolo8845not true, with high ApoB you most probably already have soft plaque, even with a CAC score of 0.
@@markopolo8845 Yes. I'm just curious if its senstive enough to show progression in such a short amount of time. Or if any of the methods we use can really show risk accurately.
Hi Dave - make sure to include the ldl mg years calculation of statin reduction in the comparison group as 26/80 Miami cohort had statin use (no idea for how long - you can get data?). If they reduced their apoB by 40% less than 14+ years, the Miami cohort may have a life time burden of higher ldl mg years. I think the risk however might be able to be a more compelling argument than lifetime ldl mg years comparison. Just something to keep in mind as you run your calculations.
I’m 1 yr into a keto diet and r today found out I’m clearly a LMHR. I’m in Canada and my Dr. said it was the highest cholesterol he had ever seen or heard of. Low triglycerides but cholesterol THROUGH THE ROOF! Can you possibly point me in the direction of some GTA area Doctors who understand Keto?
I hear very little about damaged LDL.
LDL where the APO-b is unrecognizable so it is poorly recycled.
Are there any studies showing the frequency of glucose binding to APO-b and causing its inactivation? Glucose binding to hemoglobin is so well characterized that we use it instead of fasting glucose testing in most cases. Population data correlating high LDL with disease obscures the contribution of damaged APO-b.
Just a thought from a guy with an AA degree.
I find a problem with the idea of ldl receptor down regulation in that the ldl count would continually climb and would never stabilize. A high production rate of ldl and a stable count equals a high clearance rate. Sorta like elevated fasting glucose via gluconeogenisis without insulin resistance. Same clearance rate (it’s not climbing, but baseline is set at a higher level. Something is directing this level
Perspective from inside the LMHR set; It is nice we have lots of little models to discuss and argue over BUT my actual lipid-glucose-glutamine metabolism is a monster millions of years in the making. You can’t make it roll over and play tricks like a puppy. It has its own mind and will react as the gods have programmed it to react. Not all of our metabolism is defined in our individual genetics.
I do keto diet, cardio everyday, and intermittant Fasting .My ldl only increased after eating keto.I'm lean (bmi 23.5), with low trigs/high hdl and ldl 400! .Doc wants me on a statin ,so I learned about lmhr.I diagnose myself as a lean mass hyper-responder .My Doc never heard of lmhr . I am the lower scale of lmhr and could ,therefore, "normalise " my hypercholesterolemia in just 16 days (eating a packet of oreos per day) .I don't know if I want to lower my ldl when its a large and fluffy particle in a context of metabolic health. Lmhr ,it seems, is protective against cardio vascular disease .Why would I lessen a protection against a disease ?.
Can we have a study with beer vs statins? I'm just kidding. well.. sort of.
Forgive my ignorance, I’m not trying to compete with you guys. My cursory understanding is that the experiment results may have something to do with the person’s overall baseline of insulin resistance, which is developed over time of predominant ketosis. During my longer ketogenic phases I’ve experienced rapid recovery if I ‘dip out’ of ketosis. A recovery time that increases if I do a lot of ‘dipping out’. Somehow my overall metabolic baseline shifts. Dr Boz also refers to this.
In other words, the lower success of the statin may be due to a lowered metabolism baseline
This was a study that had great difficulty finding enough people that fit the prototype. And in many instances subjects who otherwise fit, the prototype were excluded specifically because of elevated CAC scores. It is a little disingenuous to be proud of the fact that the people that were included had low CAC scores.
I was thinking the same thing. They eliminated people who would have disproven their hypothesis.
actually one of the main reasons people were exluded was they didn't have copies of verified old blood work showing normal cholesterol levels, I was one of them, my total cholesterol was always lauded by my doctors as it sat at around 135, with my LDL being at 70, but with no actual records to provide, I can't be used in a study like this
Because of its complexity and the large number of factors involved, it seems like this LDL- CVD risk conundrum is unlikely to be resolved through this very slow loop process of observation (from real life data) --> model hypothesis -> model testing -> debates --> more obersation --> model revision/new model. Being a software engineer, Dave, have you thought of using machne learning which is more capable than human to taking large number of factors into consideration? There are many machine learning for healthcare startups. Can we take advantage of the work they do? I heard data is the key. If we can find a way to collect electronic records of all the data under the many factor "lables" from blood test data, age (changes with time), to even symtoms patients experience, and any fator we can think of, we ask these startups to apply the best type of ML to determine the CVD risk or plaque size in quantitative terms. Make sense?
My Total Cholesterol dropped from 7 to 2.85 mmol/l from april 26 to may 10 on statins.
So six week steady state does not apply to me.
Checked with Mission 3:1 meter.
Or, is the lipid energy model simply an accurate depiction of the most efficient functioning metabolic state.
It's a more complete description of energy states wrt diet and lipids.
I may have missed somewhere, but what is the change in ApoB?
Anyone remember the comedian/actor Joe E. Brown? This doctor resembles him!
Of course the next question is what about a SAD diet with high carb intake and high LDL
I’m going to say I tried to follow what these two gentlemen are saying but I am just a country bumpkin. I can barely understand what they’re talking about. I think the cause of heart attack and stroke and the calcification of arteries boils down to a few things: stress, harmful chemicals in the environment, harmful foods such as sugar-seed oils-hydrogenated oils-heavily processed food, processed carbohydrates. If we eat foods that are as nutritious and as close to its natural state then we will have a lot less problems and diseases.
Hi, I am from South Korea, 58yo female. I have been eating only beef, Ghee butter, salt, and water for more than a year now and almost healed 30 year old psoriasis and got so many other positive changes in my body.
Dr.Feldman, I have a question. How can dietary fat raise LDL?
According to Dr. Malcolm Kendrick who suggests thrombogenic hypothesis of CVD , all dietary fat including saturated fat completely BYPASSES liver when metabolized. Chylomicron, not LDL, delivers fat to sells and gets reabsorbed by liver.
On the other hand, excessive dietary carbs(glucose) goes into liver, liver stores 900kcal worth of glucose as glucogen and turns the rest into TG, liver makes VLDL , loads it with TG and sends it out, VLDL delivers TG, becomes IDL and then LDL, which is reabsorbed by liver. LDL only comes from VLDL, and VLDL comes from liver.
Plaque comes from too much TRPV1. TRPV1 is stimulated by sugar, glp-1, capsaicin, insulin and certain drugs such as oxcarbazepine. What drugs, foods such as capsaicin did the person take?
Or, rather than a disordered metabolism it is a designed metabolic response.
Interesting some of the keto/carnivore MD’s dismiss high LDL as being a problem (except FH)at all. What about out of control diabetics who have a higher risk of heart attack w/o regard to LDL? @ 1 hour 25 mins finally gets to “metabolically healthy” which is probably the answer to the problem. He is just not used to treating many metabolically healthy individuals.
That is my impression too. Most doctors are used to mostly obese, prediabetic, metabolically dysregulated Oreo consumers who have probably just one "good" blood test number - LDL. There is a short supply of metabolically healthy individuals. So they consider those sick people to be the standard how to determine those "healthy" normal values.
You are confused. You can't have a heart attack without plaque, soft, inflamed plaque. And you can't have plaque without high levels of ApoB lipoprotein particles carrying LDL-C. High saturated fat diets lead to cholesterol synthesis and increased ApoB to transport it in the blood. These ApoB particles pass through the artery wall, get stuck there and oxidized, leading to plaque formation and this can happen even with a metabolically healthy person. So high saturated fat diets can be lethal, even in metabolically healthy individuals.
And the vast majority of the keto keto community are olympic level athletes yes? Theyre not. Most people looking to diet are metabolically unhealthy with high BMI. Like most of USA. Feldman's marketing of his study is probably killing them faster.
@@ladagspa2008 Of course they are not, but their metabolic health improves significantly on that diet.
I don't think we have the lipid model correct. I have been on Keto-Vore for 5 years and my LDL is 327, HDL 98 and Trig 26. 5'5" 128 lbs. I'm not that lean, maybe average but have somewhat high LDL. I think if you are in Ketosis from high fat and low carb then your body will use fat for fuel and thus more LDL is in circulation. If you break that fat fueled Ketogenic state by adding larger quantities of carbohydrates, then your body will trigger the Ghrelin hormone which will trigger the Insulin hormone receptors to store fat for "the winter". Bears do this when they eat lots of berries and honey to fatten up and during winter when there is not much food and they hibernate; bears will live off of their own fat storage.
This is interesting…l don’t really think there is certain people that are only LMHR…l think personally anybody that go Keto is going to have higher LDL in the absence of carbohydrates…
@@maxwatermeyer4406 I generally eat pasture raised eggs and grass fed animals (butter, organs, meat) and wild fish. No seed oils, no veggies (except a little bit of Sauerkraut), very little nuts, a little fermented cheese (Brie, Parmesan, Kefir), and no fruits.
I am pessimistic that any benefit for health is going to come from these studies. I see Dave Feldman and colleagues taking victory laps already, but it doesn't seem justified to me. BTW, I am not a skeptical medical professional, I'm a layman, but I am skeptical. It's clear that Dr. Cromwell, who is a real scientist and understands the problems with Dave's and his colleague's research, is not convinced that it has any value for health, or limited value. One value would be that if a person on a high saturated fat keto diet developed plaque, with the right choice of a carb, might be able to quickly and sharply lower their LDL-C and their ApoB.
The big problem with the explosion in LDL-C and ApoB that you get with eating a lot of saturated fat is time. Dr. Cromwell addressed this. The longer you have high LDL-C and ApoB, the higher the probability of getting plaque. That is what people on the high saturated fat keto diet are facing right now. The greater the amount of LDL-C in the blood, the greater the number of ApoB particles the body produces to transport them. When ApoB lipoprotein particles, which transport LDL-C particles in the blood rise above the physiological needs of the body, they can pass through the artery wall and get lodged in the "subspace." There they get oxidized which initiates plaque formation.
Inflammation then kicks in. You don't need prior inflammation or insulin resistance for this to happen. This is what I have learned from Dr. Cromwell's interviews with Dr. Carvalho.
I don't think that Dave's research is going to change this. People on the high saturated fat keto diet are going to get heart disease. It's just a question of time. Beyond this, I don't think that Dave has a scientific attitude. He is too emotionally committed to his views, to accept that they might be wrong. No matter what problems Dr. Cromwell raised with his work, he simply ignored them. And make no mistake, Dr. Cromwell is no believer. People should be paying attention, because until now, Dave and his colleagues have dominated the airwaves. Now we are hearing the facts from a real scientist.
@@newyorkguy158 the problem is we have no data from 200 years ago when NONE of us ate high carb and sugar the way we do now, so there is no indication that the higher LDL numbers are actually out of the norm, they are only out of the norm over the past 70 years or so, a blip in our timeline
Please tell me what is considered a “borderline” LMHR?
I really want to know if I'm a lean mass hyper responder but my blood tests are in 'Canadian'.
LDL 4.0, HDL 2.5 and Tryglicerides 0.4. Anyone that can help me out?
Is the LDL elevation in a LMHR, pathological?
I’d like to see the variable of activity level
Arguing that this is a disorder, looking at my numbers might offer some insight. I have a low carb diet, am lean with very high HDL and very low trigs. But my LDL is in the normal range. Some how my LDL receptors are able to keep up.
what is your version of a low-carb diet? when I go under 10 grams of carbs a day my LDL jumps to over 500, but my HDL is 80 and trigs are mid 40's,, when I bump to 60g of carbs a day, my HDL and trigs remain the same, but my LDL drops to around 140, however if I go above 100g of carbs, my HDL drops to around 40 and my trigs jump to 120, my LDL then drops to under 100--- but my fasting bg bumps over 100 (75 on low carb) and I feel like complete shit
Or, the natural mechanism triggered by carbohydrate reintroduction is naturally more efficient than the statin as the statin might likely be affecting other things.
Gosh i just want someone to explain this for lay person. My biggest takeaway is bad science led to poor patient outcomes and cardiologists and pharma are sh*tting their pants.
Dr. Cromwell didn't answer the direct question about the risk reduction by LDL lowering drugs and EPA. Per what bigfarms published, it is up to 4% for whom who has higher than 2 hCRP. The rest of the cohort did not det any benefits
I’ll volunteer? I’m 55 172 , 6’3 , BMI 21 , I run a 7:30 minute mile , I weight training, been doing this my whole life, state Wrestling champion, and my
Cholesterol is 270 I can’t get it lower! 62 triglycerides , HDL 82
If insulin causes separation of insulin receptor from LDL receptor, and subsequently increased activity of LDL-R, then why wouldn't we expect a high LDL, very low insulin state to very quickly yield an increase in LDL endocytosis in response to a sudden shift to episodic insulin bursts (with sugar consumption)? Your paper states point blank that the phenomenon cannot be attributable to insulin action. Can you clarify why you are confident that insulin is not playing a role here?
What if, for example, Nick were to sustain normal nutritional ketosis and take low dose insulin injections? (Not to induce a hypo, just to evaluate LDL response.) If insulin isn't a contributor, the LDL should remain more or less high. If insulin is part of the LDL lowering mechanism, the LDL should drop significantly and substantially.
Just wondering out loud because insulin is so involved in so many pathways, including LDL receptor function, that it strikes me as a plausible player in the overall mechanism. Yet you seem very confident that insulin can be disregarded.
Great conversation, by the way. Thanks for sharing, as always.
Interesting speculation.
Still...You should have more of a bioquantum focus not just molecular chemistry focus. Nature makes the most elaborate semiconducting photon/electron processes.
I moved toward this five years ago having prior to this followed Dave years since 2016 and being a LMHR myself.
My bias is being formerly a semiconductor researcher and now a biohacker SAD_survivor.
The question remains. Does high ldl cause plaque? Does inflammation in your arteries?
There really isn't a question. In an interview with Dr. Carvalho, Dr. Cromwell explained the process by which ApoB causes plaque, starting with the synthesis of saturated fat into LDL-C.
@@newyorkguy158 I guess some people still believe the world is flat.
@@antoniodethomasis2583 I hope you are not referring to me. There are quack doctors on youtube who deny the science. Yes, they are like flat earthers. Dr. Brewer, for example. I used to respect him until I discovered the truth. For years he has been denying, without the slightest evidence that LDL-C causes heart disease. He says it's the fireman, not the fire. Completely wrong. Although it's really the ApoB that is the cause. And he says that saturated fats are not harmful, which follows from claiming that LDL-C is not causative. Wrong again. Everyone should watch Dr
Carvalho's first interview with Dr. Cromwell in which he talks about science deniers like Dr. Brewer, though not mentioning him by name. Keep in mind that these doctors have monetized their channels, even developed large international telemed practices based on false information and are doubling down to prevent their clients from knowing the truth.
This went well with 4 eggs for brunch.
Reintroducing carbs back into zero carb or very low carb diets can restore health markers. Not only normal LDL levels but also free testosterone and SHBG. So, the take away from this experiment is that a balanced diet is the best diet.
Dave you guys keep saying glycogen depleted but many studies show people keto adapted restore their glycogen. Please clarify
Aren't those studies about muscle glycogen?
So... the problem seems to be, there isn't enough data on how a healthy person functions on a diet that has been the norm for all human species (plural) for millions of years minus the last let's say 20.000 years with the onset of year round carbohydrate availability. Of course nobody pays money to figure out how "healthy" works.. maybe insurance companies might have an interest in that?
being on 12 oreo cookies (100g carb) for 14 days is not dangerous Dave.
What is EPA?
Eicosapentaenoic acid (omega-3)
What about people like me who have a CAC score of 24 with an average LDL of 82-111. Never had any "risk" factors. How is this explained?
Explained by the fact that LDL needs to typically be below 70 before atherosclerosis progression is halted.
Sounds good. No more LMHR carnivore for me. PSK 9, celery sticks, Oreos, prediabeties here I come...
LDL alone is not a great predictor of heart disease. Your HDL/triglyceride ratio is a better indicator. The ideal is 2.0 or less. Most people are much higher than that. Look up "metabolic syndrome."
@@markopolo8845 I agree. As an LMHR mine is 0.68. LDL 221. HDL 85 Trigs, 58.
@@markopolo8845 ApoB is the best indicator and correlates often with LDL. HDL is not that great and too high values seem to also be correlated with worse outcomes.
I found a better way how to decrease my LDL than to stuff myself with unhealthy Oreos or other carbs. When my doctor wanted to put me on statins because of very high LDL I told him, that I will try to change my diet first and will come in few months for new blood tests. During next few months I was still on the keto diet, but I replaced a big part of animal fats with plenty of olive oil and coconut oil. And it actually worked. My LDL dropped 60%. I am not sure what is exactly the mechanism behind it, but I recall vaguely a lecture done by Dr. Paul Mason, who was saying that if we replace animal fats with plant oils our cholesterol will drop and phytosterol in our blood will increase. Which is not necessarily a good thing, but at least I was spared the statins.
His echo or microphone quality spoils the piece
What I found frustrating about this exchange was even if apoB contributes to plaques over time all else being equal so what? If I'm on statins for the last 30 years of my life and die of liver cancer age 90, but i dropped my CAC from 100 to 30, so what? Its been my observation that medicos are usually terrible logical thinkers.
Frequent testing?
Sure, and you can have all of my test results
But who's going to pay for it?
Oreo cookies are not a health food? WTF.
You would never see us Bill, since we avoid you like ...
Why only focus on one kind of statin? There are different statins that have different mechanisms of how they clear LDL. Maybe a different type would have worked as well as (or better than) the carbs.
C'mon Dave you know you and Frank can't just disconnect me. I heard you talking.
Why would this guy entertain statins given the side effects
The Lipid Energy Model (LEM) is probably not correct for the following reasons:
1. A person who is eating a keto diet, whether they are lean or fat, has depleted glycogen stores. Someone who has a higher BMI has more fat mass, but they would still be glycogen depleted on a keto diet. LEM posits that a fat person on a keto diet would have more glycogen than a lean person is probably not true.
2. For LEM to be correct, on a keto diet, a lean person's fat cells would release more free fatty acids than a fat person's. This is probably not correct as the opposite is true. The more fat a person has, the more free fatty acids are released into the blood.
3. LEM says that a large amount of free fatty acids are released into the blood in a lean person and the liver packages the FFA into VLDL. And yet we see a low amount of triglyceride in the blood, so where does the large amount of triglyceride in VLDL go? If they go back to the fat cells, then the body just wasted a lot of energy releasing fat and then putting fat back into fat cells - and this doesn't make sense. If the large amount of triglyceride go into muscle, why would a person with lower BMI need more energy than a person with higher BMI? The opposite is true, a person with higher BMI has a higher basal metabolic rate, and therefore need more energy.
Also, the lipid test is done fasted in the morning, so the only energy used is overnight when the person is sleeping. So a lean person somehow needs more energy while sleeping than a fat person? It doesn't make sense. Hypothetically, the result would make sense after a person ran a marathon, because muscles used up a lot of energy. This is not the case, the lipid test is done in the morning after a overnight fast, not after a marathon.
4. The reintroduction of carbs lowering LDL does not provide evidence for LEM. Carbs lower LDL by another mechanism, not as described by LEM. I believe the major driver of very high LDL in LMHR is due to low insulin and thyroid hormone on a keto diet that reduce LDL receptor activity, resulting in less clearance of LDL from the blood. Addition of carbs raises insulin and thyroid hormone, restoring LDL receptor activity.
5. Why does a lean person have lower thyroid hormone than a fat person? Because the keto diet mimics fasting. Fasting is more dangerous for a lean person than a fat person because there is less fat reserve. So a lean person's body responds by lowering thyroid hormone to lower metabolism to conserve energy. Lower thyroid hormone results in less LDL receptor activity and therefore more LDL in the blood. Your recent experiment with women on keto diet shows that there's a correlation with thyroid hormone, which provides support for this explanation.
6. In order to show that LEM is correct, you have to provide experimental evidence that on a keto diet, a lean person's fat cells release more free fatty acids into the blood than a fat person's. And more VLDL's are released into the blood. The reintroduction of carbs doesn't provide any experimental support for LEM because it can be explained by other mechanisms as outlined above. Without evidence of greater release of FFA and VLDL, you don't have any support for LEM. My guess is that when you measure FFA and VLDL release, you'll find the opposite, which is that a lean person releases less FFA and VLDL than a fat person.
7. Lastly, it's not surprising that one can shift lipoproteins in a short period of time by changing diet given that the longest living lipoproteins, LDL and HDL, only last a few days in the blood.
Have to say I agree with this. I have yet to see any proof of causation - high LDL to plaque formation only association and assumptions. Also don't understand the use of ApoB if there is one per LDL particle irrespective of density then this takes no account of the normal HDL/LDL synthesis.
Wow that was a long comment.
Can you site a source for your assertion that thyroid hormone regulates LDL receptors? I think you might be conflating gene expression and receptor regulation.
The carbohydrate reintroduction is presented as significant because of the rapid drop in LDL not just the drop.
So people with a low BMI would have high LDL if and when they exercise or are low on calories and generally see their lipids vary a lot regardless of low carb/high carb? Do we see this? There is the other observation that those losing weight quickly on any sort of diet will have high LDL. Maybe due to suppression of thyroid. Fascinating comment.
Show me a plant based cholesterol worrier that looks healthy and strong and perhaps I’ll pay more attention to them. It’s always, without fail, obvious which person is the healthy one. Eat a species appropriate diet and forget all this crap about chasing down microscopic details of your lipids. Cromwell has been a useful idiot to the pharmaceutical industry for years. He’s made a ton of money pushing this crap. Feldman is way too patient with these idiots. He will never get them to budge.
Dr Cromwell at multiple points in time is trying to make Feldman understand (using evidence from 50 years of big studies) that high ApoB is worse than low ApoB for CVD, other things being the same. At no point does Feldman even seem like he understands that message, he has such a tunnel vision about his own LMHR phenotype and hypothesis. This was a hard watch because though Dr Cromwell ( who is the obvious expert here and Feldman is not) is willing to give consideration to Feldmans hypothesis, Feldman is already convinced of this own theory (yet to be even completed) and disregards all of previous evidence from much bigger and better studies on LDL/ApoB.
The customary 'talk to your doctor' in the beginning is not sincere, and truth is half his followers will have active plaque formations and their high LDL keto diet will be worsening that accumulation. The other half will probably be fine regardless. As such, this whole line of study is a big negative given how wrongly it's been marketed without it even being completed.
I have had very high cholesterol always throughout my life. Please share your contact details - email so that I can seek your advice on how to proceed.