My whole way I view LDL has changed. I don’t believe a word that they say about it and don’t fear it … to the point that I don’t even care what mine is. So many of my health issues have been resolved since going on keto that I will never trust our medical & pharmaceutical industries ever again.
@@LiberatedMind1 "It’s easier to fool people than to convince them that they have been fooled" I am not referring to Bruce.... For a liberated mind you might need to open your eyes and look at what the health recommendations have done to the general population over the last 50 years. Its time to change. The system is broken.
@@1ProudAmerican You better take your own advice. Americans dont follow the guidelines, and their cholesterol levels are typically above them. Around the world there is a robust linear relationship between blood ldl levels and heart attack rates. Ive done extensive nutrition research, you clearly haven’t. Open your own mind, instead of resorting to condescension. The only fool here is yourself, and people like yourself. You are confident but clueless. A prime example of the Dunning Kruger effect.
I don't understand; he doesn't make a statin claim in this video, other than a small amount of carbs can reduce LDL-C in some people. What's your point?
I remember 1972 when the public was told steak, bacon and eggs, and butter cause heart disease. So "Mother Nature" did her TV advertisements for Chiffon margarine. People bought Margarin as a butter substitute so they wouldn't clog up their arteries. But it was just hydrogenated oils. ru-vid.com/video/%D0%B2%D0%B8%D0%B4%D0%B5%D0%BE-gDkiq5jD5Hc.html
I can still remember the day my mother came home with margarine and threw out the butter because of the scare back in the day. She thought she was making a healthy choice for the family. 50 years later, she still uses margarine because he doctor told her to. She’s on a fairly high does of statins because of “high cholesterol”.
@@darylaarons6625 Thank you for sharing that. I look back on the pictures from the 70's. We were a very skinny nation back then. A lot of people had Mic Jagger's build. I certainly did. To think the worst year for heart disease in the US was 1968 when we were a skinny nation.
Two questions, what was the HDL/LDL ratio in these people with low body mass index? Is LDL really the problem or was that correlation to heart disease not an indicator of cause?
@@jasoncdebussy, It is like someone saying "car-people" or "bus-people" if they are talking about things that transport people, if I understand it correctly. I am still trying to educate myself on this stuff and find it very confusing for people who know so much more about it than I do to speak about it that way.
@@ArcoZakus That is an absolutely ridiculous and nonsensical analogy! Did you think it up by yourself? 🤣 These are all different molecules and have different functions. There are so many myths, lies and much propaganda around nutrition - it's important to be scientific in order to get to the truth
I have had 5 great aunts die in the past 20yrs. They all were in their mid to late 90s. They were all active until right before they past. They lived their lives on a Southern diet, high in fat, eggs, vegetables.their ldl was high, but had no heart disease,or other disease. Just arthritis from old age & working forever. My doctor doesn't believe that would work today as its a different time. My diet is like theirs , but no vegetable oils used, just butter or bacon fat. It seems to work . My ldl is elivated but not high. My aunts swore by collard & turnip greens. So do i.
In the early 80s I read an English study that showed heart disease in the north was higher than the south with the diet was margarine in the north and butter in the south.
All so big pharma and medicine could save you with their pills, surgery and their “life saving” stents. If you had dropped the carbs/sugar and kept the butter, beef and eggs you wouldn’t need them. Follow the money. The corruption is pervasive in our society.
@@LakeOuachita Actually there was a clinical trial conducted by Ancel Keys, but it was never published "Minnesota Coronary Experiment In 1968, about ten years after the beginning and two years after the first publication of the results of the Seven Countries Study, Keys and Ivan Frantz initiated a large randomized control trial, replacing saturated fats by food items with naturally high or artificially raised content of linoleic acid in an intervention group. The randomized and blinded experiment ended in 1973. Results were not published until only much later in form of smaller excerpts as part of conference talks or doctoral theses. The raw data and analysis were discovered in 2013 in the estate of the principal investigator, Ivan Frantz. The study shows no positive effects of the altered dietary intake. Cardiovascular mortality of patients over 65 years of age increased by the replacement of saturated fats."
I just checked you OREO-Statin study. All I can say is that I wish you a long and fruitful science career. You deserve it. And humanity deserve it (if you stay at hospital/university and do not sell yourself to the "industry"). Congratulations. The results are so staggering, that an RCT should follow. I think some guys in Australia have a group of high LDLs that are keto/low carb long-timers.
My wife’s endocrinologist is practically vegetarian, runs marathons and takes medication for his HIGH cholesterol - his take is that cholesterol is produced by the body and there is nothing that can be done drastically reduce it. Just earthy healthy fresh foods and exercise…
People have been eating steaks, bacon, eggs, and butter for thousands of years, and nutritionists and doctors decided that they were suddenly bad for you?
Nick, you've done an excellent job. When I started keto for diabetes, I did not consume fatty meats, dairy, or high-SFA plant oils and lost a lot of weight. My LDL skyrocketed. A year later, I started adding fatty meats and dairy, and my LDL hardly fluctuated.
@user-kk4ix9uv9v I'm glad you liked it. It reflects my health transformation on lowcarb, and I now have much less health drama than I ever did when I was plant-based.
I am very definitely in the lean mass category of fit people. I cycle on and off on ketogenic diets. I have high LDL. VERY low triglycerides. High HDL. Abnormally LOW BLOOD SUGAR. Still, I am not going to discount that research that LDL is bad for you. I don't think this is well enough understood. I am going to stick with the theory that too much of anything is BAD.
Saturated fat is by far the safest dietary energy source. Stearic acid (common in beef) also increases mitochondrial biogenesis, which speeds up metabolism.
It’s important to note (which Nick has in other videos) that this hypothesis doesn’t apply to those with familial hypercholesterolemia or familial hyperlipedemia or FH. In that population (of which I am a member) we have a genetic disorder where we don’t have enough of or have faulty LDL receptors on our liver. It affects about 1% of the population.
No - it's the same. high LDL is bad for anyone and causal of atherosclerosis. Hopefully you are on a statin and PCSK9 inhibitor - it's realistic to treat to normal levels now.
@@jimsturt Wrong. High LDL is correlated with cvd not causal. Come on man, we’ve been eating and thriving on meat for over 2 million years. It’s why we were able to grow our big brains and it’s why our digestive system shrank from one of fermentation to one that took a lot less energy so our brains could utilize the extra energy. Now all of a sudden we can’t tolerate LDL particles? Or is it that with the advent and over abundance of processed foods with sugar, refined flour, seed oils and artificial ingredients NOW we can’t handle ldl. Do you not think that the processed foods and sugars and seed oils cause oxidative stress, inflammation and glycation? Ridiculous.
My best friend has FH - no diabetes, not overweight, never took the statins his doctor told him to start in high school. Hear attack last year at age 34 with two arteries over 90% blocked, ended up with 4 stents. you can shout oxidative stress or whatever other BS you want but at the end of the day it is simply LDL levels.
@@jimsturt People with FH have the propensity to clot which contributes to the dilemma. They’re different than LMHR’s in that they have the receptors to remove excess particles from the blood. It sounds like your friend may have the homozygous form which can affect kids.
I’m a good example. Age 52, I went on keto, but didn’t increase my consumption of saturated fat. All I did was eliminate chips and sugary snacks and added veggies. My hdl and triglycerides improved but my ldl doubled (80 to 160). This is freaking out my doc who now wants me on a statin. But I lost 30 pounds in 3 months. My bmi fell from 28ish to 25 and working on getting into the low 20s (probably another 10 to 15 pounds). I did all of this with zero exercise. I’m now adding weight training to hopefully get my ldl down so my doc gets off my back about going on statin. Hopefully my further leanness doesn’t worsen my ldl. I have no plans on following my docs advice to go on statins. I will do calcium scores every year if necessary (last one was zero). Don’t smoke or drink either so see no need to go on statin. It’s funny that I lost weight and technically eating much healthier but somehow that makes me a candidate for pharmaceutical intervention.
Why is RU-vid cutting out people's comments? Your comment ends like this: " I did all of this with zero exercise. I'm now...." My own comment up there also cut no matter how many times edited it or re-did it. . Weird if you ask me.
@@mjr7991 Right. For some weird reason I don't see "more" at all. Crazy alright. Oh, wait a minute, more weird stuff. My comment has been moved down below and there I do see "read more". Now I also see yours. I refreshed the page. But that is still totally nuts. 🙂 Aside from that, the main theme of my comment is that to those of us whose cholesterol shoots high it is not due to eating meat and fat and also has nothing to do with being lean, not lean etc. No relevance to any of it. It is in fact caused by burning body fat. So what does this translate to if I may? It has two causes. 1. It is genetics. 2. It is caused by fasting. In other words, just fast and your cholesterol shoots sky high. So what is happening is that keto/carnivore imitates fasting as far as your body is concerned. And of course, also some folks, their cholesterol goes way way higher than the others. Not every one of us is the same. However, it does level off. It won't just keep going up to 10000. So meat, no meat. lean, not lean. So long as you are burning fat for energy, that is the cause. That wraps it up. But what i find rather puzzling is why no experts clearly mention this. Notice how the dude Nick just by eating cookies his cholesterol dropped. Well, that is because when he eats the carbs, he no longer is burning fat. Plain and simple. That is all. Notice with you? When you begin to lose weight, your cholesterol shoots up and when you eat meat, it has nothing to do with it. In fact, if you exercise, fast, eat meat.... Whatever it takes, the minute you run out of carbs your body begins to use fat for energy, your cholesterol shoots up. Nobody actually clearly sees this. It took me a while to see it. I tell you what. Once you get the weight you want, balance your diet and you will see your cholesterol subside. Just eat carbs to keep you out of ketosis and no more. Because if you eat more then you will gain weight. As your body will turn the extra carbs and stores it as fat. My personal opinion is 100 grams of carbs a day is a good place once you reach your weight loss goal. But you just have to experiment.
@@jakubchrobry3701 I think that’s a bit of an over simplification. Similar to stating higher ldl alone with no other data will absolutely result in heart disease.
Great job Nicholas! Saturated fat does not stimulate glp-1 production that leads to insulin secretion but PUFAs do as they stimulate TRPA1 in the intestines a known receptor that stimulates glp-1 production that then stimulates the glp-1 receptor that is a g protein coupled receptor that lowers the threshold of TRP receptors TRPV1 and TRPA1. This leads to the neurosecretion of insulin in the pancreas and hormone secretion in the hypothalamus and pituitary.
@@shawshank6015 if you do a simple google search you will find research articles that delineate everything that I have stated. Not all neatly described in one simple to comprehend remedial place but reported in incremental steps per article. Obviously a challenge for some to comprehend. The science over thirty years since Dr. Julius discovered human TRPV1 has been enormous and has led him to sharing the Nobel Prize in 2021 with Dr. Patapoutian who discovered the piezo-1 channel, in the category of physiology and or medicine.
I had to consult ChatGPT for this, lol "The statement you provided contains several elements related to fat types, GLP-1 production, and insulin secretion. I'll break down the components to provide some clarification: Saturated fat and GLP-1 production: The statement suggests that saturated fat does not stimulate GLP-1 production. While it's true that different types of fats may have varying effects on GLP-1 secretion, the relationship is complex and not solely determined by the saturation of the fat. Dietary fats, including saturated fats, can influence GLP-1 release, but the mechanisms are multifaceted and may involve factors beyond just the type of fat. PUFAs (Polyunsaturated Fatty Acids) and TRPA1 activation: The statement implies that PUFAs stimulate TRPA1 in the intestines, which then leads to GLP-1 production. However, the direct connection between PUFAs, TRPA1 activation, and GLP-1 secretion is not universally established. While there is research on the effects of fatty acids on various receptors, the specific pathway mentioned may not be widely accepted or fully elucidated. GLP-1 receptor and G protein coupled receptor (GPCR): The statement correctly mentions that the GLP-1 receptor is a GPCR. Activation of GLP-1 receptors can indeed lead to various physiological responses, including the modulation of other receptors. TRP receptors (TRPV1 and TRPA1): The statement suggests that GLP-1 receptor activation lowers the threshold of TRP receptors (TRPV1 and TRPA1). The intricate interplay between GLP-1 and TRP receptors is an interesting concept, and there is some research on the interactions between gut hormones and TRP channels. However, the details and mechanisms may not be as straightforward as described. Neurosecretion of insulin and hormone secretion in the hypothalamus and pituitary: While GLP-1 can stimulate insulin secretion from the pancreas, the direct involvement of TRP receptors in neurosecretion of insulin and hormone secretion in the hypothalamus and pituitary is not universally accepted or well-documented. In summary, the statement outlines some interesting concepts, but the relationships between dietary fats, GLP-1 production, and the mentioned receptors are complex and may not be accurately captured in the presented sequence of events. The field of research on these topics is continually evolving, and new findings may provide more insights into these mechanisms."
@@LawrenceAugust_ very interesting and entertaining coming from a bot. Nice way of starting to think about things. At least there is thinking. The neurosecretion of insulin affects the pancreas via glp-1-> its GPCR receptor the glp-1R that lowers the threshold for TRPV1 on the nerves that stimulate the pancreatic beta cell tissues. The glp-1 RA such as semaglutide folks utilize this. The glp-1R in the paraventricular region of the hypothalamus lowers the threshold for TRPV1 and activation of TRPV1 leads to stimulation of the pituitary to release antidiuretic hormone. This can lead to hyponatremia, hypoosmolality and stimulate TRPV4 seen in active, inflammatory atherosclerosis. Glp-1R lowers the TRPA1 threshold in the hypothalamus that leads to suppression of appetite. This is what the glp-1 RA drugs such as semaglutide folks are so excited about. Fat stimulation of insulin is minimal as anyone wearing a continuous glucose monitor will attest however looking specifically at glp-1 secretion by enteroendocrine cells lining the gut PUFAs stimulate TRPA1. This is seen when people eat the TRPA1 agonist cinnamon also. Capsaicin a powerful TRPV1 agonist is taken in capsules as a diet supplement too but beware it can cause heart failure at high doses. My point is that TRP receptors are key to understanding the relationship between what is ingested and how insulin is produced. We do not yet know the complete answer how glp-1 rises so quickly after eating and there are more TRP channels such as TRPV2 and TRPV4 associated with glp-1 release. When we have hyperglycemia and the cells become resistant to the insulin receptor high insulin stimulates TRPV1 to get glucose out of the blood and into the cell because TRPV1 does not need the insulin receptor. TRPV1 utilizes GLUT4 without the insulin receptor to get glucose into the cell. Who knows this? Force feeding cells glucose-> too much oxidation-> oxidative imbalance while TRPV1 on mitochondria also -> too much reactive oxygen species in excess of antioxidant supply. This all leads to lipid oxidation and inflammatory damage of the mitochondria, cell and other tissues. So not including TRP channels is a disservice to our understanding of the serious metabolic health issues we face.
@@LawrenceAugust_ here are a couple of nice articles: Stimulation of glucagon-like peptide-1 secretion downstream of the ligand-gated ion channel TRPA1 G protein-coupled receptors in the hypothalamic paraventricular and supraoptic nuclei - serpentine gateways to neuroendocrine homeostasis Yes, they are working out testing techniques however the glp-1R is there as are TRP channels.
I’m still navigating here. 237/170/54 (total cholesterol, ldl, hdl in 2020. Now I’m 170/91/68. What did I do? Statins already but added ezitimibe. That made a bit of difference. What I did though after made the most and my other changes were same. Fiber, I was hitting 120% of daily soluble fiber for 6 months and that made a bigger impact it seems. I’m agnostic to everything, open to anything. We’re all trying to live our best life here.
Dr. Nicholas Norwitz you are thee most thought provoking scientist of this new LMHR awakening. This is taking off astronomical, may you be super successful in your endeavor to get doctors and scientist to sit down and have conversations ! 👏
Great clip. Edifying and more entertaining than your other clips. Might I suggest you produce more of these clips, with 10 minutes being the maximum length? Humor, brevity, conciseness-this triad opens the door to YT success. Helpful work and research-thank you.
Please slow down your delivery and pause after significant points. I know your excitement in your explanations but its a little tough to follow and digest! Keep it coming!😀
That's not rigid. Large LDL can deposit, too. And when they do, they have a bigger load, tho they're not as dangerous as small, which oxidizes easier. But small has less on board... So there's that.
I found you recently and really enjoy your content. I kept keto for a long time then careened into a pile of processed carbs I could not get out of. I need inspiration and you provide it with easy to understand information
I’m curious if in your research you’ve looked at any lean mass non-responders (I made up term) as comparison points against LMHR. My BMI is 21 and heavy exerciser. Saw no increase in LDL-C going to ketogenic diet; in fact LDL-C reduced ~20% and trigs decreased >90% compared to whole foods plant based.
@@Frostbiker Trigs a little under 40mg/dL. A1c 5.3~5.4%. Haven’t tested insulin in a couple years but it was quite low. Can’t remember the number now. Exercise is always fasted, first thing after wakeup.
My wife falls into your category and I fall into the LMHR on the exact same diet. One thing we have noticed however she gets sick a couple of times a year and I have not been sick in over 40yrs. Not sure why but my theory is the high LDL seems to be pretective.
Oh come on, be serious. In the Oreos experiment you changed two parameters: sugars and saturated fats. It doesn't make any sense that here you sell the drop in LDL-C levels as "oh, I increased saturated fat and my LDL-C dropped". Also, Figure 4 of your own paper on the American Journal of Clinical Nutrition shows that, for a given BMI, the higher the saturated fat intake, the higher the mean LDL change.
A lot to digest. I am lean, BMI 22.5, exercise daily, good BP, high ldl, low triglycerides, keto/low carb. My ldl doubled, going from a bit high to very, very high on keto/low carb. This may have changed as Nick’s research has continued, but I watched an interview with him in which he stated that they did not know if the LDL increase seen in lmhrs was injurious to heart health. I do find encouraging the research that shows eating saturated fat foods does not cause LDL to increase. I have adapted to low carb, and now prefer it because I rarely have carb cravings, and the adaptation was made easier by liberal consumption of foods with relatively high saturated fat. Thanks for the informative video.
So basically the liver produces high ldl on a low carb diet when the body detects depleted serum blood sugars from inadequate carbs but as soon as the carbs are restored the liver down regulates the production of ldl. This still doesn’t answer if it is healthy or not for the liver to produce high levels of ldl or whether moderate blood sugars in the blood is healthier ?
Are you syre you want to hear the answer to your question? Countless studies have shown that *high LDL in metabolically healthy people is a benefit, not a liability,* especially in older people. It dramatically reduces all-cause mortality.
Mortality raises when cholesterol is low, mortality decreases and general health improves when cholesterol is higher between 100-160mg/dl… The Japan study of 26k men and women.
Nick Norwitz, you are incorrect in some assumptions. At 3:35, you said you dropped your LDL eating Oreo cookies, even though they have saturated fat as well. This is a very inappropriate comparison - a 100 grams of Oreo cookies has 6 grams of saturated fat; a 100 grams of butter has 52 grams of saturated fat. That's over 8 times of difference in saturated fat content. You can't say "Even though Oreo cookies have saturated fat, my LDL dropped." You can only say this, if you conducted a second experiment, in which you eat an increased amounts of butter and your LDL drops. And you very much know this will not be the case, unless you eat more calories than you need, which forces the body to store fat and as a result, LDL drops. Therefore dietary saturated fats do have an impact on serum saturated fats, but this depends on caloric intake (and I am sure this is not the only factor at play here). In reality, the small amount of saturated fats in Oreos didn't drive your LDL down. It was the high carbohydrate content (Oreos have 68 grams per 100 gram; butter has 0.1 grams per 100 grams) - this provokes an insulin response and your LDL drops. As I've posted previously, I've conducted this experiment myself, by testing after changing my diet. Eating only plant foods for a couple of days lowers total and LDL cholesterol, eating only animal products (with the exception of fish - they have very low total and saturated fats) drives LDL higher. Again, saturated fat and total fat of consumed foods have very much to do with your total serum lipid profile. However, there are many additional factors at play here, which you don't consider. One example is the mass chronic problem of low vitamin D, which causes dyslipidemia and especially high LDL. In a research paper* it was shown that LDL (also total cholesterol and triglycerides, but not HDL) drops with higher vitamin D concentrations. You don't take this into account with the Lipid-energy model and especially in LMHR studies. And I bet you that vitamin D is just one of many factors, that we don't understand or consider. As far as your observation that some people who consume high saturated fat foods have lower LDL (again, how about their vitamin D status?) - have you considered that the ratio of the lipids carried by the LDL structure can change, and as a result so will the total LDL particles produced by the liver? Keep up your good work. * pubmed.ncbi.nlm.nih.gov/31407792/
@@KenJackson_US It's always best to see the research results. My opinion is not worth more than any other person's at this point. If you need to hear it - I don't believe in the LMHR phenotype. Yes, I agree genetics play a role and some people fit nicely in the LMHR phenotype, but I think this is just focusing on a group of people, because it looks nice on paper, instead of realizing this is the normal response for everyone and it varies from person to person. To put it differently, I think that this is the normal metabolic response for a typical human, on a carnivore diet, who has normal BMI, and is not consuming more calories than he needs. Yes, some carnivores with normal BMI have lower LDL, others have much higher LDL, but as I mentioned above, there are many factors to contribute to this - types of food consumed, vitamin and mineral status, thyroid and liver function, mental state of the person, environment, etc. What I think is that high LDL on its own is harmless - the body knows what it's doing on carnivore, because that's historically appropriate food for us. But we must behave historically appropriate as well - movement, sunlight (vitamin D, right?), good sleep. Not behaving properly or abusing substances results in damaged lipid transport particles like HDL and LDL - the latter, being in question, is dangerous if its receptor is no longer recognized and can't be recycled by the liver - it grows smaller and smaller, as it gives off the lipids it transports. The more small dense LDL (sdLDL) particles we have, the more likely we will have cardiovascular problems - they are the ones that lodge themselves in arteries and are covered in macrophages, because the body thinks they are foreign structures that need to be contained. Since measuring sdLDL levels is expensive, we should be very grateful that a relationship between sdLDL and triglyceride/HDL ratio was discovered. The lower your triglyceride/HDL ratio, the less sdLDL particles you have. If I remember correctly, at a ratio of 0.5, only 4% of LDL particles are sdLDL; under 0.3, almost no particles are sdLDL. So what's the worst thing that you can do as a carnivore with high LDL? Eat a lot of sugar at once and damage all that LDL traveling around your body. Eat a piece of cake on your or someone else's birthday and enjoy it. Drink a beer. That's a dozen times per year. But don't eat the entire cake at once and don't get wasted on alcohol. Remember, historically, we have eaten fruits every autumn to get fat - the body tolerates this just fine. But we are not supposed (and we shouldn't be able) to eat all the fruits from the tree at once. Sugar and alcohol allow us to abuse this mechanism. Hope that helps :)
@@randombitsofreality your right the worse thing I saw some in the carnivore diet is adding honey which is pure fructose, on the other hand what are your thoughts of APO B should we measure it if it's possible and you think is a better biomarker than just plane LDL?
Hey Nick, appreciate your efforts to educate the public on the topic of energy metabolism. I still feel like our current understanding of the interplay between the energy substrates is far from satisfactory and doesn’t take into account the diversity of the contexts. While I don’t blame anyone but myself for not retesting earlier, after going low-carb/ high fat (
Reason 4 reminds me of "The Science and Art of Low Carbohydrate Living" by Volek and Phinnek. Iirc they say while in a ketogenic state ingested saturated fat becomes the preferred field (as opposed to your body's stores). So is the reasoning basically not investing saturated fat -> higher LDL to supply energy around. Increase saturated fat intake lowers LDL since now there's less reason to take it from internal sources. This is why the Feldman protocol of increasing saturated fat works?
What do you think about the studies that have been done in regards to Apoe4 genotype where they analyzed how Saturated Fat and NonSatured Fat have different outcomes on Alzheimer irrelevant of plaque. They do conclude Saturated Fat is a major impact. I know you know this but i want your opinion on that! Thanks
I'd like (someday) for someone to be able to clear up, at what point are we talking about BMI measurements in LMHRs? For example I started my keto diet at a BMI of around 32, with type 2 diabetes and an LDL in the 60's. 80 lbs of weight loss later, on keto, and type 2 diabetes was reversed but LDL more than quadrupled to the 270s (this while on a statin). I'm now in the triad with trigs of 49, HDL of 98 and LDL of 275 and a BMI of 24. Is there such a thing as a Fat-to-lean-mass hyper responder? The other thing I'll throw in is that, as a kid, I was always extremely lean to the point that it was difficult to purchase clothing that would be long enough, yet skinny enough. No one checked cholesterol in the 1960s, especially in children, so I have no idea what my blood work would have been like back then. Perhaps once a LMHR, always a LMHR, even it you get fat and diabetic? I'd almost rather go back to eating pizza, bread and pasta again, just to relieve the brow beating I get from my doctors, none of whom can even spell lipid energy model. Thank you for looking for answers!
I'm going to be curious in June I get my blood work again, but back when I was BMI over 35 on keto my blood work looked great. I went off keto and maintained bmi 24 but the brain fog and the stiff joints returned so I decided to go on it again and sure enough brain fog gone and joint pain/stiff even only a couple weeks, much less. Awesome to be able to jump out of bed or get out of the car without having to take a moment. I can't wait for this comparison study. I know I have mild calcification just from a generic ct scan of my chest, that makes a TON of sense with my prior life, thankful it is still "mild". I'm also on a cancer med that could raise it. I may not live long, but I feel great. Quality over quantity. Thankfully I know what is on the other side for me so this is all just interesting to watch play out. I'm expecting my cardiologist to freak, but it will be interesting.
Thank you for your continued videos on this. As i near my BMI, my LDL shot up, and doc thinks i have FH...😂😂🤦🏼♀️🤦🏼♀️..yet, have no family history of this...
I have to ask. What is the thumbnail supposed to be? As a guitar player it looks like a guitar pedal made from butter, which is amazing. I’ll have one of those please. Great buttery tone.
Big shock that this channel puts out another ketovore conspiracy theory grift with clickbait titles/thumbnails bending over backwards and cherry picking to confirm your bias
Yet again you're making the claims of conspiracy, grift, reaching, cherry picking, and bias and yet again you have not provided any evidence for that claim.
Interesting effect in a small specific group (perhaps due to genetics?). Whatever causes the large increase, the major question still remains whether it is safe or not.
Agreed. I find the lipid energy model quite convicing for explaining the LMHR phenotype. However, I don't see why this would somehow neutralize the atherogenic effects of high LDL in LMHs. Presumably, LMHRs would have fewer risk factors for heart disease overall but, as far as I know, high ApoB can cause heart disease even without any other risk factors.
Exactly, while I understand the need for influencers to create clickbaity content, he seems to imply that we were only worried in the first place about the super high LDL levels of a very small subsection of the population and if this not explained by saturated fat intake, that means that saturated fats don’t raise LDL (in general)? All this LMHR stuff, seems to jump from the highly specific to generalizations and back again, and this reveals a lot about the motivation behind these studies. He likes to talk about the importance of nuance, but I don’t think that he’s actually that naive to believe that this is even remotely realistic in the keto/carnivore space.
Thanks Nicholas, but at this point what could be the driver of high LDL in a low carb diet? The 2 biggest culprits have always been saturated fats and/or carbs (sugar).
Physionic released a video yesterday (about the possibility of reversing atherosclerosis) where he claims that high LDL (whether large or small) will cause plaque because Apo B is somehow magically attracted to the endothelium of blood vessels (he explains this in detail - something to do with electric charge). He based himself on some studies which he probably linked in the description, I didn't look at them. I wish you made a video to address this 🙏🙏🙏
because studies clearly show CVD risk increases with high LDL C and Apo B. Slightly confused why you ask where is the proof when there's literally hundreds of studies indicating this?
@@destro1989 there are no studies that separate and single out LDL as a definitive factor, you need a study on carnivores/keto for 20 years to prove/disprove something. A lot of marathon runners are on the brink of dying, yet running is one of the best ways to keep one healthy.
@@miraak8523 how do you work that out? There are literally no studies that prove your point. There are plenty that show causality for LDL cholesterol and Apo B.
Hello Nick, One thing I haven't seen yet, among those who promote carnivore, is a comparison of why meat fat congeals in drain pipes, but not in arteries. It would be nice to see a study on that. Also, how does hydrogenated fats clog the arteries? Thank you for your videos. They're very informative.
2 reasons. Fairly simple. Fat in drains is just a big lump that cools enough to become solid, it can't mix with water even if liquid so disrupts flow and stuff and can build up over time. In your blood it is small clumps of fat precisely sized by your body's machinery and then packaged in a protein called a "lipoprotein" so it can mix with the water in your blood safely without building up. Second if it did get out for some reason it would be very hot because your body is above the melting point of all fats it will be liquid, then your immune cells can clear it out like any other problem. Hydrogenated fat does not clog arteries no fat clogs arteries, that was an unproven theory that really needs to go away tbh. The thing that causes heart attacks is coagulated blood, a blood clot. The thing that causes narrowed arteries is damaged arteries that need repairing and produce unstable low-density scar tissue. If it is allowed to heal it will become strong arterial tissue and calcified tissue.
What are we saying here? Are we saying if we eat well, exercise and keep lean, our ldl will increase? If we pig out and put weight on, it will decrease? Is an increase in ldl important to maintaining a healthy lifestyle?
My perspection is, that the leaner you are, the higher ldl you will have. If you will eat the same as fat man. I think its because leaner ppl can`T absorb that much 😂❤🎉 and have in blood more non-storable carry-on reserves.
Thanks for your Videos ! Went from 103kg to 80kg (182cm) on KETO and my LDL went up above 280 , so my Doctor almost forced me to go on statins ! He didn´t care about my drop, of TG from 175 to 70 and my big improvement of HDL and Liver Values ! All these doctors are seeing is, LDL is too high , take a pill !
Hi Nick! Did you track blood LPS, blood TMAO, leaky gut (Cyrex Array 2), and activity of Human herpesviruses in your personal case study of you on a ketogenic diet? The foods used on your ketogenic diet may have increased LDL cholesterol due to an immune response to LPS, etc. Children with certain active infections will have greatly increased LDL.
Hi! I just watched a video about your study and if I understood correctly when you were on statins exercise increased your ldl, is that true? Does that apply generally if there isnt enough carbs in circulation?
Hi Nick ,on you Oreo experiment what happened to your triglycerides and HDL ? I would guess triglycerides went higher and HDL lower? I am a LMHR with a ldl of 380
Did I hear this correctly? (Played it several times) The leaner you are the higher your LDL? This is ironic because sometimes in my blood work my LDL is higher than it should be. My HDL is within range, and my triglycerides are in range but the bump in LDL brings my total cholesterol slightly higher than normal and it always makes me upset! So I should not be too concerned about this? My Dr doesn't seem to be concerned as all my other markers and heart rate and blood pressure are all remarkably good. At my physical this year which I am always stressed out about my blood pressure was 110 over 66 which was surprising to me. My Dr was very happy with those numbers. Any insight into this would be greatly appreciated. 007
Why is LDL-C such an important endpoint for you? You seem to base your entire reasoning about saturated fat on that LDL-C is so important. In your opinion, is LDL-C a cause of anything?
The explanation of point 5 seems unreasonable. Being lean causes the LDL increase? lol, no, that's a tendentious way to put it. Going on a low carb diet caused the LDL increase for these lean people. I see no myths busted here. A reasonable hypothesis for the meta-analysis finding is just that people with high BMI have high uncontrolled caloric intake, including high saturated fat intake, so any kind of structured diet will lower their LDL levels. Conversely, people who are low BMI have a baseline low calorie intake (and so low saturated fat intake), and shifting to eating a lot more fat increases their LDL levels.
So glad to know I can figure out my BMI by testing cholesterol. Seriously though, thanks for pursuing this. I am also interested in those who are lean who are not hyper responders.
After a year on low carb, I lost 50 pounds. Sadly LDL increased 50%. I am certainly not a LMHR but my LDL must think I am. I heard Dave Feldman mention that the study parameters for the Trig/HDL/LDL might be expanded to include people like me who do not exactly meet the LMHR guidelines? I hope this is true because we, not so lean mass low carb people, need some good arguments to present to our doctors. Doc is happy about the drop in A1c to normal, 50-pound weight loss, higher HDL, and lower triglycerides, but they are VERY upset with me when I say no to a statin increase.
I am new to carnivore and watching lots of videos- one of them mentioned you and I was so excited to hear of a smart young man searching for the truth about food and going into the medical field!❤❤ I noticed your two beautiful dogs in your video and I wanted to ask how you feed them. I know it’s off topic but it’s been really bothering me for a couple years that my dogs’ food is just processed fake food. I’ve been giving a little less portions and adding whatever meat I’m eating that day into their food. Thoughts?
I've been following your research. My BMI is on the low side, I'm lean and physically active but my cholesterols are not under the LMHR category. LDL has been volatile over the years ranging from 82 to 180. I don't follow the keto diet. More towards the Mediterranean diet. Now I'm experimenting with increased carbohydrates intake to see if my LDL can push lower. Last LDL = 123 on 8/Feb. Will report back my finding if I can achieve under 100s again.
How did you come up with the "dosage" size of the Oreo cookies (one sleeve/day, I believe)? Based on my blood test results after nearly a year of carnivore, my total cholesterol is at 228. I'm definitely not an LMHR, but it would be fun to see if I could get my total cholesterol below 200 simply by eating the occasional orange or banana. I don't want to over-do it, however.
Question: I'm very lean ~10% and definitely am a hyper responder to LCHF. I do not fit the triad pattern, however. Do you often see individuals who are lean and will have their LDL/APOB/NMR particle counts skyrocket - like triple - if doing keto or carnivore but HDL stays low and TGs don't lower (my case they stubbornly hover in the mid 100s)? In terms of risk markers like LP-IR, LDL:HDL, TG:HDL, TC:HDL they look very unfavorable. Other metabolic markers improve of course but looking at the high particle #s in the context of those lipid measures may be problematic. It just struck me as odd that the only marker that seemed to move much at all is LDL and it goes absolutely bonkers. I've had LDL go to almost 600 so I just went back to a primal type mixed diet.
For me, everything happened exactly as he said. i was lean, went low carb(prediabetes). ldl went up ( a little) hdl went up. triglycerides went down ( a little )
Saturated fat for most people does not raise their LDL, but in the few that do, this can cause heart disease in the long term. People with familial hypercholesterolaemia often develop heart disease even though they have large LDL particles, low triglycerides, and are not diabetic. The difference between those with FH and the LMHRs is that those with FH have had high cholesterol since birth whereas LMHRs likely had high cholesterol for only a few years after going on a low carbohydrate diet that is higher in saturated fat. Not everyone with FH develops heart disease but that does not mean high cholesterol is safe because some smokers do not develop lung cancer and some diabetics do not become blind or lose their limbs. Dietary cholesterol from egg yolks do not raise cholesterol in most people, but a minority of people will hyperabsorb dietary cholesterol and this group also needs to be on a low cholesterol diet.
Great video. I remember asking you to put up an image in a past video... now I think your video editor is going over the top. Educational videos don't need to be flashy, the flashier the video is, the more fictional I expect it to be, just from experience.
So if you do a very low fat high carb diet as a lean person who is very active what do you see? I would be interested to see what the effect of a lower calorie intake plus high carb does. So far the drop in LDL in LMHR occurs when they either add sufficient calories to be in a slight excess or add carbs. Maybe if you switch it to the other extreme of high carb you still get high LDL during exercise or weight loss. That would further confirm the model that it’s the need to draw down fat reserves for energy that is the cause. Deplete the glucogen stores with a sprint or three and then do a longer run and then test. One confounder in your Oreo experiment was you added them onto a stable calorie intake so were in a calorie excess. How did you know if it was the extra calories or the carbs that made the difference? Fasting and quick weight loss will raise LDL. Never get a blood test on a diet.
I'm much more interested in LDL-C to LDL-P ratio. It's well established the most of our cholesterol is made in the cells, and very little is from our diet.
Nick a question, does everyone who are considered Lean Massive(how is this defined?) when going on a low-carb diet (how is that defined?) turn out to be LMHR(meaning their LDL will increase by say up to five hundred percent). It begs the question has there been anybody where their LDL doesn't rise? Nick I'm nearly 60 and been able to hear all your other videos with no problem up to now but this one I haven't clue what you said because I was fighting the overpowering music, so which is the more important - the information you want to get across or the annoying music in the background?
I'm 173 cm height and only 55kg. After eating mostly fatty meat and fruit for 1 year my LDL went from 80 to 360. I feel good but what concerns me is high ApoB, 2.36 g/L ... I will try to replace unsaturated fat with polyunsaturated fat (no proccessed seed oils of course) for about 2 months and see what happens with my numbers...
My LDL was over 500 in my last lipid panel. My TGs were 330. HDL is always over 70. My BMI is about 20. I'm thinking it's because my blood was taken after a 3 day fat fast (nothing except 30-50g butter per day). I didn't fast for a full 12 hours before the test. Also, I drank coffee. I'm thinking maybe I have a coffee sensitivity, or it's the inversion pattern at work. I've decided to buy a decent home cholesterol monitor and start experimenting to see just what affects my numbers, especially TGs, so dramatically.
That's just if you follow a keto diet, right? My LDL-C was too high, so I made some changes to my diet and became very active. I became very lean and completely eliminated saturated fat-rich animal products: both my triglycerides and my LDL-C plummeted while my HDL-C remained the same. I lost 20 pounds. My only significant sources of saturated fats are a modest consumption of dark chocolate, nuts, seeds, peanuts. I eat plenty of carbs from whole foods, but mostly maintain a caloric deficit. I would NEVER attempt a keto diet, though. Give me carbs.
What if any is the correlation between saturated fat intake and apoB, in various human groups. The correlation between high apoB levels and cardiac risk is pretty strong...
I'm on a ketogenic diet and my BMI is perfect for a man of my height. Consequently I'm pretty sure I have higher cholesterol. So is this support research paper and RU-vid video suggesting that to lower this LDL count one should consume saturated fats such as butter?
"Attia is rolling his eyes." He's tearing his clothes and banging his head against a wall, for he knows that he is being left behind. Science is marching on without him.
What really matter at the end of the day is what factors causes atherosclerosis, and only time will give the reason either the people with low carb diets but high saturated fat, or the people that follow a low carb and low saturated fat too
