Been trying to understand lipids and how they work ever since I ventured into intermittent fasting some years ago and went on low carb diet more recently - due to the ubiquitous pressure by GP's to take statins once they see the LDL numbers (~4.6 mmol)! This is by far the best and most succinct description (albeit a hypothesis) of how the show (energy system) actually is likely to work that I've come across. Thanks for taking the pressure off my own concern for my ldl numbers - probably categorised as a lean hyper res.
As per my comments elsewhere here -- I hope to have the LMHR study done soon via CitizenScienceFoundation.org to help shed light on these important questions.
Great presentation!!! THANK YOU!! LOL.... I didn't know LDL and total cholesterol would shoot up during a fast! So I thought... I'll show my doc and get him off my back about statins... so I had my blood work done on day 3 of a fast.. yikes.. LDL = 287 and total cholesterol = 375!! Trigs were 70 and HDL 78.... usually HDL>85 and trigs
I just cannot get my T-Col/HDL ratio to a healthy level and I cant figure it out after three years of Keto. It does not matter what level your Cholesterol is at *(within reason) if HDL is high enough and trigs are low. I got HDL up to 60 for a couple of months but it fell back to 40 again. My ration is around 7 but should be less than 4
@@realDaveFeldman What was your blood sugar doing when eating white bread and turkey? Ive been keto now for 3 years and someone gave me two gluten free pancakes the other day and my blood sugar went to 170.
I enjoyed the lecture. I am a Korean medicine doctor who is treating patients with ketogenic and low-carb diets in Korea. You said that you are planning to take CT angiography at the beginning of the study and after 1 year, and conduct extensive blood tests. Do you have any videos of the results? I often saw Lean Mass Hyper Responders in my clinical practice, and general internists were scared by their blood tests and prescribed lipid-lowering drugs. I said it was okay and explained that variables such as HDL and TG are important, but it is not easy because it takes a lot of time to explain these things continuously. It is difficult to conduct such experiments locally, so I am very grateful that you are doing these things.
At age 70, recently returned from among other joys of my good fortune, a few weeks trekking in the Himalayan foothills, I correctly anticipated further urging from my PCP in the US to take a drug to lower my cholesterol. When I asked, he had no objection to my going to a cardiologist for a second opinion. I'd read essentially nothing about adverse effects, and when I asked the cardiologist, he responded, "Some people think statins should be in the water supply." Okay, that safe! (However, in the ten years since then, I’ve learned that the US had and still has no compulsory system for reporting the adverse effects of medications.) What information was and still is overwhelmingly available regards benefits of statin drugs...which in my particular case and the contradictions in reputable advice, I questioned. Generally benefits focused on lowering "too high" LDL and/or total cholesterol. I went to the internet, where mainstream academic sources also that total cholesterol or LDL was not as accurate a predictor as lipid ratios. With 282 total, 88 HDL, 61 triglycerides, clearly my ratios were great. In light of this contradiction for my individual case, I asked the cardiologist what I should do and why. More about that later, if anyone asks. My point is for years and even now, for a possible genetic study at a major university, I have sought for a subgroup of those you describe-and of which I seem to a member. This subgroup has also taken a statin. (My guess is that lipophilic statins would be most relevant.) To be clear, I'm sincerely not giving advice nor knocking statin drugs, and certainly not for secondary prevention. The devil, and also the angel, is in the details, and here I've found for the first time the details that so affected my own life recognized as existing and and also of importance. THANK YOU!
Thanks a million. So clear explanation on cholesterol. No more worries and doubt on my relatively high ldl (about 150) since my hdl is very high (110) and my tg is very low (about 55)
Thanks for the great info. I'm so hoping I can get an answer from someone on this. Little background. I'm a 55 year old female. I workout at least 30 min everyday (mixed routines - cardio, resistance, yoga, circuit, HIIT, etc.). I have been on a low carb (non-complex carbs), high fat (although lean meat), very low sugar, etc. I recently received my lipid panel results. I had also asked for an NMR test. Here are my results: LDL-C 159 - VLDL 9 - HDL 46 (mom's HDL has always been low as well), TRIs 46. Total Cholesterol is 211. Although many docs would say I'm 'borderline,' I'm guessing these #s show that I eat more healthy fats. That's true. HOWEVER ... this is the confusing part. My NMR results who LDL-P is 2116 and my small particles are at 776!!!! WTH? If my Tris and VLDL are low, how are these numbers showing extreme risk. I did the MESA calculation and it's 1.4% (using my CAC # in this formula). Thoughts? Thank you so much.
That is an unusual discordance between LDL-C and LDL-P. Typically, we see LDL-P = LDL-C X 10 plus or minus around 15%. But again, bear in mind from my work that a lot can be impacted by what happens in the days just before your lipid panel. For example, if you consumed a lot more than you typically do in day just before, but were otherwise normal or even lower calories in the days before that, it could result in that discrepancy. You may want to consider retesting and simply trying to keep to your staples, not eating too much or too little, and not doing anything too unusual with sleep or exercise (which again, can also impact these numbers in the short term).
Thank you and Siobhan 🙏I see this as an important step in empowering people in the triad of patient, doctor and scientific knowledge. If there is a Noble Prize for Citizen Science - you are certainly strong. contenders After having found your work and Fat Emperor Ivor Cummins - me, with sky high cholesterol numbers - insisted on a CAC scan and Angiogram - got tested - zero calcification and zero soft plaque. Explain that to me Doc ?!! Needless to say I haven’t seen my cardiologist since. Feeling like I’m 20 on keto/ carnivore at age 50 - running marathon distances from being a couch potato wreck for decades. It is also Quality of Life/ mental health issue that is essential for me being on keto. And stop worrying about my high cholesterol. Even if keto/high cholesterol is proven not sustainable in the long run from future research - I will not revert back to junk food, processed meat, sugar and refined carbohydrates and vegetable oil EVER.
Curse youtube - got no info that you uploaded this ! Really nice talk ! I know, you answer normally no questions on youtube. But if you decide to do : Have you seen any cases of very high hdl, very low tryglycerides with only slightly elevated ldl ? I got some mesurenments in January and have not found anyone at this point, who has my ratios.
Yes I have -- there are plenty, of course. There's usually a lot more possible context to it -- such as prior metabolic inflexibility (coming from metabolic syndrome and working on their health), higher relative carbs than strict keto (but this is very individualistic), fiber, pufa, genetics, exercise, supplements, and medication can all impact LDL beyond just the energy model.
@@realDaveFeldman Thanks for the answer - I completely forgot about that comment XD . But I still have not found a person that beats my 143 mg/dl for HDL. But I also haven't looked in LMHR-groups, so I guess it is not impossible.
I have just found your video. I am clearly a lean mass hyper responder... Since I started a keto diet on April 2020 my TOTAL Cholesterol levels have been RIDICULOUSLY HIGH 649mg/dl November 2020, 550md/dl February 2021, 562mg/dl May 2021.... like my HDL is very high and my Triglycerides super low.... But not sure if I should be worried and try change that. I'm definitely going to try eat more fat to see if that changes... I have tried swapping red meat for fish and white meat, but no difference at all. What's your opinion on that?
I'm going to really miss your Covid video discussions. Maybe you should explore hosting them on another platform than RUclips that does not censor content because we really need to hear what knowledgable people in the low carb community are saying about this important issue that is on everyone's mind.
Started keto March 2020. In july checked my bloods. LDL 263. Total 320. Trigs 98 HDL 50. Liver function tests ALL back to normal ranges. They were over 100 for 10 yrs (GGT, ALT, AST). Continued keto and re checked bloods in Nov. LDL 255 total 325. HDL 66. Trigs 89. My doctor SCREAMED STATINS. I said no. I wanted proof that i am at risk of a heart attack. I asked for a CAC scan. I got it done in DEC. Result is ZERO!
@@gungagalunga9040 We're nearing launch for our LMHR study via CitizenScienceFoundation.org . Hopefully we'll have clinical data specific to this phenotype very soon.
My grandpa recently passed away. He'd been plagued with "high cholesterol" most of his life; even had his first bypass at 50. Anyway, my sister came to me raging the other day about my poor low carb diet, saying all her highly intelligent university professors had stressed the facts about high LDL being unhealthy. She "doesn't want me to end up like our grandpa". At our funeral, our dad spoke highly of grandpa's remarkable health. Despite his heart problems, he lived to be 90, while all his family had died before the age of 70. He firmly attributed this fact to him having quit smoking and alcohol altogether, in addition to constantly being out and about; physically active. I really miss my grandpa. He was one of my best friends. He lived the final years of his life eating little else than sausage and potatoes. Everything he had of wealth, he gave away. A truly extraordinary person. All of my memories of his life serve as a monument to fulfilment in life through experience and trust in family and society.
As you are continually refining this presentation, I believe that the level, transportation mechanism, and role of NEFA could be improved. In addition, Dr. Volek's finding of higher (healthy?) inter-muscular fat for highly trained LCHF athletes should be discussed, especially in relationship to higher (unhealthy?) inter-muscular fat deposits in non-trained obese couch potatoes. To me, the higher inter-muscular fat in athletes fits well into your Fed-Ex energy distribution model, as a delivery to a shed with much closer access to the energy demand. Additional graphics of daily energy distribution (energy potential mentioned) would also be useful. Most people (IMO) don't really get the contribution of de novo lipogenesis in this process. A graphic of the daily energy contribution during an extended fast for a 1500, 2000, and 3000 TDEE individual would be useful. If everybody's basic carbohydrate need is around 120g per day, I find that easy to convert to 5g per hour, which also ties closely to a 100 blood glucose level of 5g of glucose in 5L of blood. (Not exact values, but notionally accurate.) Next, there would be a minimal energy contribution from protein metabolism via normal turnover and autophagy. But then the majority of energy would be provided by fat/ketones. The part of this model which has not been well described (IMO again) is the theory of the limitation of fat release by adipose tissue. The best attempt I have seen so far has been from Richard Morris, but in light of extended fasting results from lots of people over the years, I still find it a questionable hypothesis.
Higher fat content in muscles is the consequence of a too low insulin level, which is the consequence of low-carb diet. And that low insulin level is unhealthy.
Oh believe me, I'd love to be packing in a lot more. But to be sure, it's already a huge paradigm shift for even lipidologists to think about this lipid system from a primarily energy distribution standpoint -- so I try not to lay on too much of the peripheral considerations as well. But your point is well taken in that I've considered for some time doing a 101, intermediate, and advanced version of this lecture. I'll likely have the latter once our paper is finally complete.
Hi Dave, I hope you can help me. My results are: HDL C: 90mg/dl LDL-C: 505mg/dl VLDL C: 14mg/dl TAG: 70mg/dl Total Cholesterol: 605mg/dl My doctor prescribed statins, B vitamins, VITAMIN C, and others. I don't want to take statins. I am 38 years old, I follow the LCHF diet. I practice powerlifting and I am a natural bodybuilding athlete in my country. Low level of body fat. What advice could you give me?
When a multi variable problem is being analyzed, a focus on one variable with a preconceived idea can skew the conclusions. That is what I see in the ldl research.
I did a 5 working day fast and went streight to a blood drawl and had the highest tot. chol 8.8 mmol/l (340)(LDL and HDL) ever. My following weekend was eating loads of pure goose fat and peanut butter and next monday to blood drawl again. My tot chol came down a bit and my triglyserides went down even more. Best fun out of 250€ to spend all because of Dave. Note that my triglyserides had been sub zero earlier, but now were 1,14 mmol/l. (100). I expected them to be less. Any info of this? I do not exersize but do some yoga. I look like the LMHR group. I target a low TG/LDL ratio. One question to all. Has any one in this community known to be on keto or LCHF infected to CoVID-19?
@vasenpolvi -- right, as I'd expect given how much fasting is integral to the model. You may want to check out my presentation from last summer here: ruclips.net/video/oDVXr8GFRQk/видео.html
Hi! A question from the numbers on lean mass hyper responders. LDL 200 mg/dL -> 5,17 mmol/L HDL 80 -> 2,07 Trig 70 -> 0,79 What is wrong? 200/5,17 = 38,68 80/2,07 =38,64 but 70/0,79 = 88,61 should 70 be more like 30 or is it something I miss?
I can´t say that I understand your hypothesis completely, but I guess maybe this comparison would be good if I understood it: LDL is like red blood cells and scarcity of fat is like scarcity of oxygen, so we all know when oxygen is at low concentration, then the body will make more bloodcells in order to get the few oxygen it gets more rapidly to the cells and in the same way the LDL gets produced more to go to the cells when there´s not a lot of fat intake or supply. I would say, and I don´t know if you have controlled for this, but if we are talking about lean mass hyper responders you also have to controll for stress levels, especially cortisol, because if there is more cortisol, the body will go into a more catabolic state and therefore the LDL will be increased and the blood sugar, but sugar will go up, but the sugar maybe more in the adrenalin response and not so much on a low carb diet with chronic stress. Now, a lot of very fit people are doing a lot of sport, which is putting the body under a certain amount of extra stress which could also lead to higher levels of LDL. But, a lot of very traumatized people who are in chronic stress and maybe lean maybe not would also respond in that way. I´m not saying, that sport therefore will make people sick, because stress can be a good thing, if it is tolerable to the body, we dont know that. You see, for lots of undiagnosed diabetics or prediabetics actually sugar no longer is a very good source of energy, because they are insulin resistant, so then their LDL will go up the same way, but again, those people will be at higher risk for having higher levels of LDL that are under a lot of stress, which actually can make the cells insulin resisitant, because the body doesn´t want someone who is already worn out to go and do stuff, it wants the person to take a break. I dunno if I´m making any sense. Also I read an interesting paper recently about Hyperinsulinemia in children of mainly diabetic mothers from 2016 I think. That´s also very interesting.
Atherosclerosis in Ancient Mummies Across the Globe | Gregory S. Thomas ruclips.net/video/zLDje0lDV94/видео.html Tsimane Indians make about 14 000 steps a day over age of 60
The chart on 3:20 showed low fat increased your LDL, which conflicted to your talk about the "white bread experiment" ruclips.net/video/kDOHw0qhT0A/видео.html where the HCLF diet decreased your LDL. I can understand that if you are talking about triglycerides, but you are talking about LDL here. So it's quite confusing that low fat give you two different result in two different talks. Can you please clarify why the difference? Many thanks.
We're talking about two different mechanisms. To get a bit geeky for a moment, where becoming fat-adapted in a healthy context (typically average weight or lean, metabolically flexible), one has lower hepatic glycogen stores which I discuss in this lecture. Thus, per the hypothesis, they are more likely than not in this context to have higher total and LDL cholesterol due to trafficking more triglyceride-rich lipoproteins such as VLDL, which is typically the precursor to LDL. However, *within* this fat adapted context, one can likely overconsume fat and drive down trafficking of VLDL since there's an introduction of chylomicrons alongside insulin, thus less lipolysis, higher leptin, higher T3, etc. In other words, there's technically two major contexts we're discussing for the most part, one is generally in the longer term (fat-adapted lifestyle or not), the other is short term (existing status of insulin and caloric load over the last few days modulating fatty acid trafficking demands).
Hyper absorbers are those who taken in more cholesterol directly form the gut. There are tests that attempt to quantify this, such as Beta-sitosterol and Cholestanol which you can order from labs such as Boston Heart.
@@erastvandoren If you have a specific critique and can keep it productive, I welcome your input. If just here to drop in personal attacks without substance, I'll have to let you go.
@@erastvandoren The first sentence is very productive -- the second is obviously hyperbole and clearly unproductive. Again, if interested in keeping it productive, I'm happy to dialog -- otherwise, there are many other channels you might find more suitable for these kinds of discussions. Last heads up -- if you want to follow up with what we'd all agree is a productive question I'm more than happy to answer. If you're more interested in taking personal shots, feel free to do so elsewhere.
Alas, but 2 years passed since i found myself LMHR and try to make sense of it thanks to Dave and others , but now energy model dont make any sense for me. Thats my resersh and cunclution. Attia and Dayspring was right , arrogant and dissmisive they are, but they right. Enegy model missing so much.
Yes, to me it looks like it, too. This guy here picked apart Dave's inversion pattern, coming to a very different conclusion. thenutrivore.blogspot.com/2019/08/the-inversion-pattern-cholesterol-code.html Pretty convincing to me. Getting good data from LMHR cohorts over time, still a laudable untertaking IMO
I think Nick has some interesting ideas, but to be sure, in that article he was regularly referencing my blog posts from way back in 2016 (literally within the very first year of my research). Many of the opinions I had then I certainly don't have now (and I'm sure this would apply to him as well given how long ago that was). This was odd given the energy model in its 2019 form was posted at the website at a dedicated URL (CholesterolCode.com/model).
@@realDaveFeldman To be honest i don't think it matters which model is true - but where it dangerous of what we doing or not and how to monitor it Pure theoretical stuff is just way to make fun for me. By the way - to find out does LDL receptor expression influenced by insulin - try take a insulin shot instead of skittles ) i played with it for a bit - seems like for my liver this ultimate signal to race back all LDLS.
@@kwancomics He is wrong about LPL - its strongest expression is in the fat tissue, and taking into account tissue mass, almost all TGs are unloaded into adipocytes and minor part into myocytes. Everything else is almost negligible.
Predominantly, yes -- exclusively, no. Please note my referencing "Albumin" on my slide at 15:38 with regard to Non Esterified Fatty Acids (NEFA) in row 5, column 3. I emphasize this supply proportionality further with the study breakdown at 17:42 and the "global" vs "local" delivery analogy at 18:36 (where adipocytes are predominantly the store for VLDL-TG, non-adipocytes predominantly taking up NEFA, but not exclusively for either one)
Hope Dave will eventually release a book with all his findings summarized for the layperson to understand.
I'm working on that. But I'll concede I have quite a few other responsibilities that are absorbing a lot of bandwidth at the moment.
Thank you very much Dave, in awe of all your hard work.
The buffet line is a perfect analogy. Thanks!!
Dave This is another great presentation about lipids . Spread the word for better health!!
Great presentation mate, this needs to be shared far and wide.
Been trying to understand lipids and how they work ever since I ventured into intermittent fasting some years ago and went on low carb diet more recently - due to the ubiquitous pressure by GP's to take statins once they see the LDL numbers (~4.6 mmol)! This is by far the best and most succinct description (albeit a hypothesis) of how the show (energy system) actually is likely to work that I've come across. Thanks for taking the pressure off my own concern for my ldl numbers - probably categorised as a lean hyper res.
As per my comments elsewhere here -- I hope to have the LMHR study done soon via CitizenScienceFoundation.org to help shed light on these important questions.
Great presentation!!! THANK YOU!!
LOL.... I didn't know LDL and total cholesterol would shoot up during a fast! So I thought... I'll show my doc and get him off my back about statins... so I had my blood work done on day 3 of a fast..
yikes.. LDL = 287 and total cholesterol = 375!! Trigs were 70 and HDL 78.... usually HDL>85 and trigs
It's funny, I did a fasting presentation last summer that covered this. ruclips.net/video/oDVXr8GFRQk/видео.html
@@realDaveFeldman Thanks Dave!! I knew the sharp change had to be a response to the fast.
I just cannot get my T-Col/HDL ratio to a healthy level and I cant figure it out after three years of Keto. It does not matter what level your Cholesterol is at *(within reason) if HDL is high enough and trigs are low. I got HDL up to 60 for a couple of months but it fell back to 40 again. My ration is around 7 but should be less than 4
@@realDaveFeldman What was your blood sugar doing when eating white bread and turkey? Ive been keto now for 3 years and someone gave me two gluten free pancakes the other day and my blood sugar went to 170.
I enjoyed the lecture. I am a Korean medicine doctor who is treating patients with ketogenic and low-carb diets in Korea.
You said that you are planning to take CT angiography at the beginning of the study and after 1 year, and conduct extensive blood tests. Do you have any videos of the results?
I often saw Lean Mass Hyper Responders in my clinical practice, and general internists were scared by their blood tests and prescribed lipid-lowering drugs. I said it was okay and explained that variables such as HDL and TG are important, but it is not easy because it takes a lot of time to explain these things continuously.
It is difficult to conduct such experiments locally, so I am very grateful that you are doing these things.
THANK YOU FOR ALL YOUR HARD WORK..
This was the best explanation I've seen - thanks!
At age 70, recently returned from among other joys of my good fortune, a few weeks trekking in the Himalayan foothills, I correctly anticipated further urging from my PCP in the US to take a drug to lower my cholesterol. When I asked, he had no objection to my going to a cardiologist for a second opinion.
I'd read essentially nothing about adverse effects, and when I asked the cardiologist, he responded, "Some people think statins should be in the water supply." Okay, that safe! (However, in the ten years since then, I’ve learned that the US had and still has no compulsory system for reporting the adverse effects of medications.)
What information was and still is overwhelmingly available regards benefits of statin drugs...which in my particular case and the contradictions in reputable advice, I questioned. Generally benefits focused on lowering "too high" LDL and/or total cholesterol. I went to the internet, where mainstream academic sources also that total cholesterol or LDL was not as accurate a predictor as lipid ratios. With 282 total, 88 HDL, 61 triglycerides, clearly my ratios were great. In light of this contradiction for my individual case, I asked the cardiologist what I should do and why. More about that later, if anyone asks.
My point is for years and even now, for a possible genetic study at a major university, I have sought for a subgroup of those you describe-and of which I seem to a member. This subgroup has also taken a statin. (My guess is that lipophilic statins would be most relevant.)
To be clear, I'm sincerely not giving advice nor knocking statin drugs, and certainly not for secondary prevention. The devil, and also the angel, is in the details, and here I've found for the first time the details that so affected my own life recognized as existing and and also of importance.
THANK YOU!
Thanks a million. So clear explanation on cholesterol. No more worries and doubt on my relatively high ldl (about 150) since my hdl is very high (110) and my tg is very low (about 55)
Great video Dave!
Thanks for the great info. I'm so hoping I can get an answer from someone on this. Little background. I'm a 55 year old female. I workout at least 30 min everyday (mixed routines - cardio, resistance, yoga, circuit, HIIT, etc.). I have been on a low carb (non-complex carbs), high fat (although lean meat), very low sugar, etc. I recently received my lipid panel results. I had also asked for an NMR test. Here are my results: LDL-C 159 - VLDL 9 - HDL 46 (mom's HDL has always been low as well), TRIs 46. Total Cholesterol is 211. Although many docs would say I'm 'borderline,' I'm guessing these #s show that I eat more healthy fats. That's true. HOWEVER ... this is the confusing part. My NMR results who LDL-P is 2116 and my small particles are at 776!!!! WTH? If my Tris and VLDL are low, how are these numbers showing extreme risk. I did the MESA calculation and it's 1.4% (using my CAC # in this formula). Thoughts? Thank you so much.
That is an unusual discordance between LDL-C and LDL-P. Typically, we see LDL-P = LDL-C X 10 plus or minus around 15%. But again, bear in mind from my work that a lot can be impacted by what happens in the days just before your lipid panel. For example, if you consumed a lot more than you typically do in day just before, but were otherwise normal or even lower calories in the days before that, it could result in that discrepancy. You may want to consider retesting and simply trying to keep to your staples, not eating too much or too little, and not doing anything too unusual with sleep or exercise (which again, can also impact these numbers in the short term).
Thank you and Siobhan 🙏I see this as an important step in empowering people in the triad of patient, doctor and scientific knowledge. If there is a Noble Prize for Citizen Science - you are certainly strong. contenders
After having found your work and Fat Emperor Ivor Cummins - me, with sky high cholesterol numbers - insisted on a CAC scan and Angiogram - got tested - zero calcification and zero soft plaque. Explain that to me Doc ?!! Needless to say I haven’t seen my cardiologist since.
Feeling like I’m 20 on keto/ carnivore at age 50 - running marathon distances from being a couch potato wreck for decades.
It is also Quality of Life/ mental health issue that is essential for me being on keto. And stop worrying about my high cholesterol.
Even if keto/high cholesterol is proven not sustainable in the long run from future research - I will not revert back to junk food, processed meat, sugar and refined carbohydrates and vegetable oil EVER.
We'll hopefully have that LMHR study underway soon to help answer these questions.
Awesome!
Curse youtube - got no info that you uploaded this ! Really nice talk ! I know, you answer normally no questions on youtube. But if you decide to do : Have you seen any cases of very high hdl, very low tryglycerides with only slightly elevated ldl ? I got some mesurenments in January and have not found anyone at this point, who has my ratios.
Yes I have -- there are plenty, of course. There's usually a lot more possible context to it -- such as prior metabolic inflexibility (coming from metabolic syndrome and working on their health), higher relative carbs than strict keto (but this is very individualistic), fiber, pufa, genetics, exercise, supplements, and medication can all impact LDL beyond just the energy model.
@@realDaveFeldman Thanks for the answer - I completely forgot about that comment XD . But I still have not found a person that beats my 143 mg/dl for HDL. But I also haven't looked in LMHR-groups, so I guess it is not impossible.
@@SchmittsPeter Check in with the group. I'm pretty sure I know of at least a handful of people in the 150s to 160s range.
@@realDaveFeldman Thanks ! And besides - good luck for your project and also thanks for your content.
Amazing work
I have just found your video. I am clearly a lean mass hyper responder... Since I started a keto diet on April 2020 my TOTAL Cholesterol levels have been RIDICULOUSLY HIGH 649mg/dl November 2020, 550md/dl February 2021, 562mg/dl May 2021.... like my HDL is very high and my Triglycerides super low.... But not sure if I should be worried and try change that. I'm definitely going to try eat more fat to see if that changes... I have tried swapping red meat for fish and white meat, but no difference at all. What's your opinion on that?
For the tests at labcorp, how do you know what tests to order for LDL, CRP, etc.?
Check out our guide on that at CholesterolCode.com/labs
I'm going to really miss your Covid video discussions. Maybe you should explore hosting them on another platform than RUclips that does not censor content because we really need to hear what knowledgable people in the low carb community are saying about this important issue that is on everyone's mind.
The Mynames did RUclips censor him?
do you have a link?
@@curtisjackson5793 A link to something I said over a year ago? Not any more. If you had asked me a year ago I probably did.
@@themynames6453 haha anyway, thanks man
What is units for the 3 day average dietary fat in the graph? In g?
He definitely says "grams" in the audio, should be "grams per day averaged over 3 days". 300 g/day fat = 2700 kcal/day from fat.
So the model is useful to persuade lean people of the validity of a low carb lifestyle and calm their worries about high cholesterol?
great work.
Started keto March 2020. In july checked my bloods. LDL 263. Total 320. Trigs 98 HDL 50. Liver function tests ALL back to normal ranges. They were over 100 for 10 yrs (GGT, ALT, AST).
Continued keto and re checked bloods in Nov. LDL 255 total 325. HDL 66. Trigs 89.
My doctor SCREAMED STATINS. I said no. I wanted proof that i am at risk of a heart attack. I asked for a CAC scan. I got it done in DEC. Result is ZERO!
Edit to add I'm 40, male. SAD until March 2020. Lost 23kg on keto in 6 months
@@gungagalunga9040 We're nearing launch for our LMHR study via CitizenScienceFoundation.org . Hopefully we'll have clinical data specific to this phenotype very soon.
My grandpa recently passed away. He'd been plagued with "high cholesterol" most of his life; even had his first bypass at 50. Anyway, my sister came to me raging the other day about my poor low carb diet, saying all her highly intelligent university professors had stressed the facts about high LDL being unhealthy. She "doesn't want me to end up like our grandpa".
At our funeral, our dad spoke highly of grandpa's remarkable health. Despite his heart problems, he lived to be 90, while all his family had died before the age of 70. He firmly attributed this fact to him having quit smoking and alcohol altogether, in addition to constantly being out and about; physically active.
I really miss my grandpa. He was one of my best friends. He lived the final years of his life eating little else than sausage and potatoes. Everything he had of wealth, he gave away. A truly extraordinary person. All of my memories of his life serve as a monument to fulfilment in life through experience and trust in family and society.
That's a very interesting story, Marie. Thanks for sharing. :)
As you are continually refining this presentation, I believe that the level, transportation mechanism, and role of NEFA could be improved. In addition, Dr. Volek's finding of higher (healthy?) inter-muscular fat for highly trained LCHF athletes should be discussed, especially in relationship to higher (unhealthy?) inter-muscular fat deposits in non-trained obese couch potatoes. To me, the higher inter-muscular fat in athletes fits well into your Fed-Ex energy distribution model, as a delivery to a shed with much closer access to the energy demand.
Additional graphics of daily energy distribution (energy potential mentioned) would also be useful. Most people (IMO) don't really get the contribution of de novo lipogenesis in this process. A graphic of the daily energy contribution during an extended fast for a 1500, 2000, and 3000 TDEE individual would be useful. If everybody's basic carbohydrate need is around 120g per day, I find that easy to convert to 5g per hour, which also ties closely to a 100 blood glucose level of 5g of glucose in 5L of blood. (Not exact values, but notionally accurate.) Next, there would be a minimal energy contribution from protein metabolism via normal turnover and autophagy. But then the majority of energy would be provided by fat/ketones. The part of this model which has not been well described (IMO again) is the theory of the limitation of fat release by adipose tissue. The best attempt I have seen so far has been from Richard Morris, but in light of extended fasting results from lots of people over the years, I still find it a questionable hypothesis.
Higher fat content in muscles is the consequence of a too low insulin level, which is the consequence of low-carb diet. And that low insulin level is unhealthy.
Oh believe me, I'd love to be packing in a lot more. But to be sure, it's already a huge paradigm shift for even lipidologists to think about this lipid system from a primarily energy distribution standpoint -- so I try not to lay on too much of the peripheral considerations as well. But your point is well taken in that I've considered for some time doing a 101, intermediate, and advanced version of this lecture. I'll likely have the latter once our paper is finally complete.
@@erastvandoren Source?
Hi Dave, I hope you can help me.
My results are:
HDL C: 90mg/dl
LDL-C: 505mg/dl
VLDL C: 14mg/dl
TAG: 70mg/dl
Total Cholesterol: 605mg/dl
My doctor prescribed statins, B vitamins, VITAMIN C, and others. I don't want to take statins.
I am 38 years old, I follow the LCHF diet. I practice powerlifting and I am a natural bodybuilding athlete in my country. Low level of body fat.
What advice could you give me?
When a multi variable problem is being analyzed, a focus on one variable with a preconceived idea can skew the conclusions. That is what I see in the ldl research.
I did a 5 working day fast and went streight to a blood drawl and had the highest tot. chol 8.8 mmol/l (340)(LDL and HDL) ever. My following weekend was eating loads of pure goose fat and peanut butter and next monday to blood drawl again. My tot chol came down a bit and my triglyserides went down even more. Best fun out of 250€ to spend all because of Dave.
Note that my triglyserides had been sub zero earlier, but now were 1,14 mmol/l. (100). I expected them to be less. Any info of this? I do not exersize but do some yoga. I look like the LMHR group. I target a low TG/LDL ratio.
One question to all. Has any one in this community known to be on keto or LCHF infected to CoVID-19?
Fasting is basically a very high fat diet. Therefore, the increase.
@vasenpolvi -- right, as I'd expect given how much fasting is integral to the model. You may want to check out my presentation from last summer here: ruclips.net/video/oDVXr8GFRQk/видео.html
Hi!
A question from the numbers on lean mass hyper responders.
LDL 200 mg/dL -> 5,17 mmol/L
HDL 80 -> 2,07
Trig 70 -> 0,79
What is wrong?
200/5,17 = 38,68
80/2,07 =38,64
but 70/0,79 = 88,61
should 70 be more like 30 or is it something I miss?
Molecular weight of cholesterol is 386.5g/mol, triglycerides may vary (it may incorporate different fatty acids), but should be around 900.
I can´t say that I understand your hypothesis completely, but I guess maybe this comparison would be good if I understood it: LDL is like red blood cells and scarcity of fat is like scarcity of oxygen, so we all know when oxygen is at low concentration, then the body will make more bloodcells in order to get the few oxygen it gets more rapidly to the cells and in the same way the LDL gets produced more to go to the cells when there´s not a lot of fat intake or supply. I would say, and I don´t know if you have controlled for this, but if we are talking about lean mass hyper responders you also have to controll for stress levels, especially cortisol, because if there is more cortisol, the body will go into a more catabolic state and therefore the LDL will be increased and the blood sugar, but sugar will go up, but the sugar maybe more in the adrenalin response and not so much on a low carb diet with chronic stress. Now, a lot of very fit people are doing a lot of sport, which is putting the body under a certain amount of extra stress which could also lead to higher levels of LDL. But, a lot of very traumatized people who are in chronic stress and maybe lean maybe not would also respond in that way. I´m not saying, that sport therefore will make people sick, because stress can be a good thing, if it is tolerable to the body, we dont know that. You see, for lots of undiagnosed diabetics or prediabetics actually sugar no longer is a very good source of energy, because they are insulin resistant, so then their LDL will go up the same way, but again, those people will be at higher risk for having higher levels of LDL that are under a lot of stress, which actually can make the cells insulin resisitant, because the body doesn´t want someone who is already worn out to go and do stuff, it wants the person to take a break. I dunno if I´m making any sense. Also I read an interesting paper recently about Hyperinsulinemia in children of mainly diabetic mothers from 2016 I think. That´s also very interesting.
I think the key to LDL is how much of it is oxidized. Non-oxidized might be just clean fuel.
Atherosclerosis in Ancient Mummies Across the Globe | Gregory S. Thomas
ruclips.net/video/zLDje0lDV94/видео.html
Tsimane Indians make about 14 000 steps a day over age of 60
You may want to wait until our paper is out. We discuss hormone influences, homeostasis, etc. It would take quite a while to unpack here.
The chart on 3:20 showed low fat increased your LDL, which conflicted to your talk about the "white bread experiment" ruclips.net/video/kDOHw0qhT0A/видео.html where the HCLF diet decreased your LDL. I can understand that if you are talking about triglycerides, but you are talking about LDL here. So it's quite confusing that low fat give you two different result in two different talks. Can you please clarify why the difference? Many thanks.
We're talking about two different mechanisms. To get a bit geeky for a moment, where becoming fat-adapted in a healthy context (typically average weight or lean, metabolically flexible), one has lower hepatic glycogen stores which I discuss in this lecture. Thus, per the hypothesis, they are more likely than not in this context to have higher total and LDL cholesterol due to trafficking more triglyceride-rich lipoproteins such as VLDL, which is typically the precursor to LDL. However, *within* this fat adapted context, one can likely overconsume fat and drive down trafficking of VLDL since there's an introduction of chylomicrons alongside insulin, thus less lipolysis, higher leptin, higher T3, etc. In other words, there's technically two major contexts we're discussing for the most part, one is generally in the longer term (fat-adapted lifestyle or not), the other is short term (existing status of insulin and caloric load over the last few days modulating fatty acid trafficking demands).
So if Ivor is Fat Emperor, you should call yourself Lipid Master.
'Fat Emperor and Lipid Master'.....sounds like a low carb martial arts film directed by Ang Lee!
@@didinx8417 lets grab popcorn and big soda
@@didinx8417 LOL 😆
Both are idiots.
I ' m keto too!My total colesterol is 399😮😮😮
562 over here...!
I recently had a lipidologist call me an "absorber."
Hyper absorbers are those who taken in more cholesterol directly form the gut. There are tests that attempt to quantify this, such as Beta-sitosterol and Cholestanol which you can order from labs such as Boston Heart.
i watched the whole thing still dont know what your hypothises is ?
Low carb/high fat will result in high LDL. High LDL is not a good marker for Arterial disease.
Don't worry, Dave is completely unable to formulate any hypothesis.
@@erastvandoren If you have a specific critique and can keep it productive, I welcome your input. If just here to drop in personal attacks without substance, I'll have to let you go.
@@realDaveFeldman Could you formulate your hypothesis, please? Because nothing you say makes any sense.
@@erastvandoren The first sentence is very productive -- the second is obviously hyperbole and clearly unproductive. Again, if interested in keeping it productive, I'm happy to dialog -- otherwise, there are many other channels you might find more suitable for these kinds of discussions. Last heads up -- if you want to follow up with what we'd all agree is a productive question I'm more than happy to answer. If you're more interested in taking personal shots, feel free to do so elsewhere.
Alas, but 2 years passed since i found myself LMHR and try to make sense of it thanks to Dave and others , but now energy model dont make any sense for me. Thats my resersh and cunclution. Attia and Dayspring was right , arrogant and dissmisive they are, but they right. Enegy model missing so much.
Yes, to me it looks like it, too. This guy here picked apart Dave's inversion pattern, coming to a very different conclusion. thenutrivore.blogspot.com/2019/08/the-inversion-pattern-cholesterol-code.html Pretty convincing to me. Getting good data from LMHR cohorts over time, still a laudable untertaking IMO
I'm definitely a fan of everyone coming to their own conclusion on the research. :)
I think Nick has some interesting ideas, but to be sure, in that article he was regularly referencing my blog posts from way back in 2016 (literally within the very first year of my research). Many of the opinions I had then I certainly don't have now (and I'm sure this would apply to him as well given how long ago that was). This was odd given the energy model in its 2019 form was posted at the website at a dedicated URL (CholesterolCode.com/model).
@@realDaveFeldman To be honest i don't think it matters which model is true - but where it dangerous of what we doing or not and how to monitor it Pure theoretical stuff is just way to make fun for me. By the way - to find out does LDL receptor expression influenced by insulin - try take a insulin shot instead of skittles ) i played with it for a bit - seems like for my liver this ultimate signal to race back all LDLS.
@@kwancomics He is wrong about LPL - its strongest expression is in the fat tissue, and taking into account tissue mass, almost all TGs are unloaded into adipocytes and minor part into myocytes. Everything else is almost negligible.
Dave is completely unable to learn. Albumin is responsible for energy, VLDL for storage. Period.
Predominantly, yes -- exclusively, no. Please note my referencing "Albumin" on my slide at 15:38 with regard to Non Esterified Fatty Acids (NEFA) in row 5, column 3. I emphasize this supply proportionality further with the study breakdown at 17:42 and the "global" vs "local" delivery analogy at 18:36 (where adipocytes are predominantly the store for VLDL-TG, non-adipocytes predominantly taking up NEFA, but not exclusively for either one)