BREAKING - New Heart Scan Data on High LDL Keto

[@cgArtsy5]

I know it is always recommended that “ we check with our medical doctor” but that is usually why we are all here. I am a nurse and my medical doctor and many medical doctors are not up to date cholesterol and nutrition. A visit to your medical doctor for any issue usually results in a prescription for a medication. Thank you for the information and research you all provide!

[@apolopinov.8594]

Summary: In keto cohort, there's very strong evidence of no correlation between: - total plaque score and LDL particle count - total plaque score and small dense LDL - total plaque score and Lp(a) - total plaque score and OxPL Howerever, something quite interesting showed up: for both samples (keto and MiHeart), total non calcified plaque volume was almost the same, diverging on calcified plaque which was higher on the MiHeart sample. Both samples were of healthy people with median age of 50 who were not taking cholesterol lowering meds.

[@OIOnaut]

Yes but remember.. Miami were all non vaxxed!

[@jeffreyadams648]

Thanks.

[@terryolay4613]

Thanks so much.

[@wbonney411]

I went keto 19 months ago. Blood sugar good ,hdl to triglycerides ratio 1.74 , ideal. Yet my family doctor throws his hands in the air and fights with me because my ldl is 225. I truly can't wait for the medical profession to get off the statin kick back money and back to reality of science

[@Ozzie-n8t]

This concerning, is it not? People doing keto have given up all meds and stopped having any medical checks (carnivores even more so), believing they’re “protected” from all cardiovascular risk - and yet here we are, keto people who are only in their FIFTIES have the SAME amount of plaque as people eating standard diets.

[@colinvankeith4814]

To my knowledge this is the first study to analyze a sub-population who, on the surface, appear to have optimal metabolic health as well as being in prime health overall and looking at how their diet and lipid markers differ from the general population that recent studies have confirmed have at minimum some level of metabolic dysfunction ( 92%) and record amounts of chronic disease, obesity, and mental disorders. I propose that we have much to learn by studying healthy people. For me it’s personal. Since adopting a mostly ketogenic and carnivore diet my health and well being has never been better, yet, for the most part the medical community, friends, and family have not only provided zero support for my journey to better health, but have tried to sabotage my efforts, albeit, generally having good intentions. I’m 75 year old, very low carb for 12 years and mostly carnivore for the last 4 years with LDL of 584.

[@DrTomMD]

Are you willing to at least have annual, if not bi annual, carotid artery ultrasound checks?

[@colinvankeith4814]

@@DrTomMD Yes I am willing to have these tests repeated, however I cannot afford to pay for them and in BC medical insurance does not cover annual or bi annual testing; just the initial testing that were normal/optimal. Perhaps if I started to have symptoms they would do additional testing provided any positive tests would then inform a new treatment plan.

[@DrTomMD]

@@colinvankeith4814 if I were your physician, believe me, I could find the coding to get it covered. Your life is worth more than the cost of a carotid ultrasound

[@ematise]

@@colinvankeith4814 The Best thing or governments can do is to provide easier access to all kinds of health tests. The situation is the same in all parts of the world. Only then we can hope, as population, to become healthier.

[@StanDupp6371]

There is no such thing as Keto according to centenarians who don't have health problems. High carb centenarians. 2010 study title: "Discovery of Novel Sources of Vitamin B12 in Traditional Korean Foods from Nutritional Surveys of Centenarians." These Korean centenarians consume a high carb diet with 87% of plant foods and 13% from animal foods. They have almost no access to synthetic vitamins, supplements or fortified foods. Centenarian men take in about 1700 calories per day and about 300 grams of carbs per day. These people are set in their ways they do not play games with diets or experiment with any type of money making fad diet.

[@ronelpieterse933]

I am so grateful for your courage, hard work and the hope you give those of us who don't have a choice but to eat very low carb. You guys are epic.

[@nicknorwitzPhD]

Cue Avengers Music!

[@thomass5169]

Dave, congratulations to you and your team. Exciting results to say the least. The level of advancing new knowledge you are responsible for is not to be ignored. Just awesome Dave.

[@mikewagenbach5585]

Who knew totally flat lines could be so amazing?!? Looking forward to more of this work.

[@nicknorwitzPhD]

Great comment.

[@realDaveFeldman]

@@nicknorwitzPhD Also agree

[@JohnWilliams-gy5yc]

Er... Hope you guys ain't trying to jinx it unnecessarily. I wonder if we can really trust TPS and CPS 100%? To falsify statins and psk9i argument is only to measure preemptively if one is developing any soft plagues somewhere or not. I think I personally can't boldly pitch this theory to someone who already had heart attacks or strokes in the past without a proper scientific measurement. The pharma will *_ALWAYS_* have a standing ground on fear as long as we still don't have the "killing" (not to jinx) measurement.

[@w-k-w6200]

Phew! I'm so glad you had the Lp(a) data. Mine recently measured 187 after going carnivore for a few weeks for elimination reasons. The internet told me to worry! I'm so glad I decided to stay calm and wait for your study results. I suspected I might be an LMHR and my typical lipid panel changes after going carnivore responded accordingly. My hs-CRP is 0.6. I'm a fit/healthy 59 white male, no meds. I am considering getting a TPS, with AI-assist. Thanks for all the hard work guys!

[@nicknorwitzPhD]

"for elimination reasons" -- now I'm curious. Actually Adrian and I have a paper coming out on Carnivore and IBD probably on 9/2.

[@JoniSchwalbach]

@@nicknorwitzPhD looking forward to checking it

[@MeatingWellness]

This data was so interesting. Can't wait to see the longitudinal data as well.

[@LivingRadiant]

Thank you All! David, I have been waiting on this release, you have mentioned it last weekend!

[@JennyMitich]

This was mind blowing!! Can’t wait for the longitudinal data 👏🏼👏🏼👏🏼

[@StanDupp6371]

Here is the longitudinal data for over a century. High carb centenarians. 2010 study title: "Discovery of Novel Sources of Vitamin B12 in Traditional Korean Foods from Nutritional Surveys of Centenarians." These Korean centenarians consume a high carb diet with 87% of plant foods and 13% from animal foods. They have almost no access to synthetic vitamins, supplements or fortified foods. Centenarian men take in about 1700 calories per day and about 300 grams of carbs per day. These people are set in their ways they do not play games with diets or experiment with any type of money making fad diet. Get your CIMT test and then you learn.

[@JennyMitich]

@@StanDupp6371 I was referring to the longitudinal data for this particular study.

[@StanDupp6371]

@@JennyMitich Don't pay any attention to fake studies just stick to real humans long term track record as you can't fool real people for over a century but anyone can write bought and paid for studies to fool the gullible.

[@justanother240]

@@StanDupp6371 There's a survivalship bias built into these studies. Many factors play into being a centenarian around the turn of the century. I suspect the fact that they survived famine, war, and disease, without reliable access to modern medicine attests to their superior genetic makeup compared to the average population. For all we know, they would've lived longer eating an animal based diet.

[@HollyGeee]

Thanks Dave and hope to watch the documentary soon.

[@vanwander]

Absolutely amazing work. Keep it up. This work has repercussions to more than just the LMHR phenotype, as I believe it will lead to the finding of better markers of CVD risk. Likely composite markers.

[@ArcoZakus]

"... it will lead to the finding of better markers ..." Not without great resistance from drug companies that are making so much money selling drugs to treat current markers -- unless they can find new drugs to treat the better newer markers.

[@tomgoff7887]

Risk aren't necessarily the same thing as risk factors.

[@Krunch2020]

The lipid hypothesis seems to have been fabricated to sell medications.

[@tomgoff7887]

@@Krunch2020 How do you figure that out? The evidence that lowering cholesterol reduced major adverse cardiovascular events, came before the drugs were invented. In fact that is the exact reason why they were developed.

[@richardb8267]

Fantastic work guys! You will all save millions of lives!

[@josephvacquier6968]

Thank you for all your time and effort guys, really appreciate your work, which is such an important contribution to human health, ground breaking 🙏🏻

[@kelleyfrances490]

Extremely grateful for your diligence. Can't wait to show the final results to every statin-pushing doctor I know.

[@sjaron23]

Love the low key approach- letting the data speak for themselves.

[@RobertWinter2]

I'd nominate Dave, Nick, and Adrian for a Nobel Prize if I could. The science they are doing regarding lipid metabolism is as pioneering as the work by Brown and Goldstein.

[@nicknorwitzPhD]

"is as" - love this for many reasons only a few will understand... it's subtly speaks to an open mind and anti-tribalism

[@atoms-to-atoms]

Malcolm Kendrick needs a mention!

[@csmith5611]

@@atoms-to-atoms I was just about to add Dr Kendrick, a dogged and special pioneer .

[@OIOnaut]

Nobel prize is an indication of competitive peer centralised corruption. R. Faynman did not want to collect his.

[@andrewrivera4029]

It’s interesting to see doctors striving to improve health instead of practicing manipulating data to justify flawed models and engaging in double speak.

[@cmc6295]

True

[@MeatHeals]

Great stuff everyone. So grateful for your work.

[@sarahb.6475]

Thank you Dave! 😊 I am a LMHR. I am 52 years old and my resting heart rate is 53. Just feel really good and have lots of energy on this diet ( as long as I avoid all of my allergens). Pretty much eating what I can eat. Which puts me on a meat based diet. Very low carb high fat. Ken Berry says that's the Proper Human Diet. If I had a bunch of that calcified stuff that clogs arteries I seriously doubt if my resting heart rate would be 53! And it definitely goes into the 40s when i am asleep.

[@stuwhite2337]

I don't think you can correlate heart rate with atherosclerosis

[@lls66]

Heart rate is correlated with Vo2 max and a general sign of fitness which counteracts cvd but doesn’t guarantee it.

[@stuwhite2337]

@@lls66 I had a family member who's resting heart rate was 45. He still had a heart attack.

[@sgill4833]

It doesn't matter what your resting heart is. Your heart rate during prolonged exertion or vo2 max is what's important

[@ShoppingEmail-dr1fs]

it's not the 'proper human diet' at all - it' ignores all the evidence that people ate a huge variety of foods and were in good health. Study indigenous Australians, and Kitavan islanders and so on. Humans ate whatever they could find in the area they were.... including tubers, insects, (forrest dwellers) snakes, fish etc. Yes we ate meat, but we also ate nuts, berries, and tubers, bark, fungi, and shellfish and reptiles and so on.

[@larsnystrom6698]

It's really great work that we hope will change medical practices, sometime in the distant future, probably. I have low triglycerides and high HDL, so I've always ignored LDL levels. But it would be nice to have doctors utilize better things than just LDL levels as their diagnostics, and the mandatory following statins prescriptions.

[@pattia983]

LDL 350. 0 calcium score and totally normal no blockages nuclear stress test.carnivore

[@HEARTANDSOULOFMINE]

How old are you?

[@pattia983]

@@HEARTANDSOULOFMINE 64

[@nicolereid4467]

Appreciate your work so much!

[@XaqNautilus]

Thank you Mr. Feldman.

[@mbrochh82]

Here's a ChatGPT summary: - Preliminary data on high LDL keto diet presented at the symposium of metabolic health. - Emphasis on the preliminary nature of the data and the importance of consulting with a doctor. - Collaboration with Dr. Adrian Sodomota and Nick Norwitz on mechanistic publications. - Comparison between the Lean Mass Hyporesponder (Keto CTA) study and the Miami Heart (MI Heart) study. - Explanation of the Total Plaque score, which quantifies plaque in 15 segments of the heart. - Spearman correlations between lipid metrics and Total Plaque score show significant differences between the Keto cohort and Miami Heart. - LDL cholesterol in Miami Heart shows a near-significant correlation with Total Plaque score, unlike in the Keto cohort. - Different populations show different strengths of associations with biomarkers. - LDL cholesterol's association with plaque progression varies based on the etiology of high LDL. - Lean Mass Hyporesponder group shows no significant correlation between LDL cholesterol and Total Plaque score. - Total Plaque score versus lipid particle count (LDLP) in the Keto cohort shows no correlation. - Total Plaque score versus small dense LDL particles also shows no correlation. - Total Plaque score versus Lp(a) and oxidized phospholipid ApoB shows no correlation. - AI-guided analysis of CCTA scans reveals plaque in all participants, highlighting the importance of resolution. - Quantitative analysis shows similar total non-calcified plaque volume between the Keto group and Miami Heart. - Excluding participants on cholesterol-lowering medication still shows similar results between the two groups. - Main message: Preliminary data suggests that high LDL levels in a keto diet do not correlate with increased plaque volume, challenging traditional lipid hypotheses.

[@Rocketscientist66]

I absolutely love these discussions! Just fascinating. I am not a doctor or researcher (okay, I take that back ;-) I research and analyse everything. I’m pretty sure I was a doctor in a previous life.

[@consistentme22]

I would love to watch and learn from this video, however I do not have an hour to view it. Shorter formats would accommodate many. Keep up the great work!

[@danellekelly1214]

Why not just watch 15 minutes of it per day?

[@csmith5611]

So demeaning to all the time and effort spent by these scientists on your behalf.

[@perrysebastian6928]

Good work fellas!!

[@TOMGARVEYtheKETOCOOK]

Very interesting, hello from Las Vegas. Need to send this to my Dr. my argument for 4 years now!

[@realDaveFeldman]

Back at'cha from Vegas as well. 🫡

[@TOMGARVEYtheKETOCOOK]

If you ever need me to do anything Dave I'm here!!!​@@realDaveFeldman

[@qui1766]

The fact we as patients even HAVE to argue with our doctors, even when we provide strong medical literature and meta analyses is ridiculous frankly… our state of healthcare is sad.

[@rpearce25]

​@@qui1766I'm not picking sides here, but the preponderance of existing evidence is not on the keto/carnivore side. Perhaps that will change over time, I don't care, but for now medical providers have to stick with the data with a higher degree of certainty with regard to long term health outcomes. If your doc went to the comment section before mainstream scientific consensus to inform their medical practice they would be getting sued all over the place.

[@qui1766]

@@rpearce25 I don’t disagree, but I’m saying in general docs don’t keep up with medical literature, and it’s not their fault they don’t. Docs have way too many patients and are overworked as is. As someone who has a special interest in hormones, the way that many doctors including endocrinologists prescribe hormones is based on info from the 1960s when we knew basically nothing. I’m not even talking cutting edge science like this, I’m talking things that were easily disproven from years ago being common practice with doctors. When I have talked with doctors about certain things, they often tell me about random things they read online rather than peer reviewed research. What is being taught in medical schools on hormones (which is barely taught for GPs) and nutrition (which also essentially has no classroom time) it’s all information that’s been disproven from the 60s that isn’t even based in serious science. The medical education system for general practitioners has been teaching a lot of really outdated information. And instead of being open minded when presented with a number of peer reviewed medical analyses, patients are told they don’t know anything because they don’t have an MD. This isn’t every doctor obviously, but it’s the experience I’ve had with 80% of the doctors on Medicaid, and countless others have had bad experiences with this. One of my testicles died, upon their examination and determination, and doctors wouldn’t even refer me to a urologist or endo. Refused to get my testosterone levels checked and I had to figure everything else out myself. Told me I was “too young to worry about it”.

[@CaptainSteve777]

Great discussion and information. Thank you all. I've been ketovore for a few years now and CAC went down (177 on my old diet down to 143 on keto). Cheers

[@lls66]

When this is all said and done (with both pre and post ctas) a separate analysis of looking at another AI analysis focused on arterial inflammation using caristo cariheart software (FAI) from Oxford would be potentially eye popping and further explain differences between lmhr with and without plaque. Their Lancet ORFAN study shows astronomical association between specific types of inflammation and events with a max of 29x hazard ratio for the most inflamed. I’m sure they would happily finance that study with free AI scans.

[@fokcuk]

Dave, I love these updates, but do you mind doing a summary at the end for "normal people" that by the end of the video forget what was discussed in the middle and what were the outcomes

[@HimoftheBoat1967]

😂I know the feeling....🤦‍♂️

[@JMK-vo8pv]

This was an outstanding discussion. Question for you gentlemen-If the LDL and Lp(a) particles are actually "firefighters," and NOT fire/inflammation "accelerants" (i.e. "wood"), then doesn't it make sense that we would want as many of these "firefighter" particles floating around in our blood at all times? If my supposition is correct, then it seems that treatment with statins and/or PCSK9 inhibitors would be a really BAD idea for those people who are trying to fight the atherosclerosis process!

[@sgill4833]

That is correct. However having too many firefighters sitting around doing nothing isn't helping either.

[@ivanmatusic5540]

It's actually good for immunity and clearing out of toxins, incidence of sepsis goes down as LDL increases. Could be ldl are "firefighters" but become "wood" on standard american diet ie metabolic syndrome.

[@ingeamanda]

Con la dieta cetogenica en cinco meses revertí la resistencia a la insulina, en ocho meses perdí 24 kilos: bajé de 78 kilos a 54 kilos, mi IMC es 20.4. mi insulina es 3.7 uU/ml en ayunas y 4.3 post prandial, glucosa en ambos casos menor de 85, mis triglicéridos bajaron a 80, mi HDL aumentó un 50 % subiendo a 62, mi presión arterial se redujo a 115/70, pero por LDL alto (223). La médica que visité y llamaré Doctora estatina, no entiende razones y me quiere formular estátinas.

[@Oscar_AH]

Pasa de ella. Mi LDL es 569 y nunca me he sentido mejor. Si comes más grasa 3 días antes del siguiente test, dará más bajo también.

[@CindyCorporon]

@@Oscar_AHhello there, mine is 749 and probably rising. But my other labs are good. My Dr. Is concerned. wants me to take statins, and see a cardiologist. But I am not convinced that statins are beneficial. I asked her to check thyroid. I am mostly animal based. Less then 20 grams of vegetable carb a day. I am a senior woman. So if I got this far in life and feel healthy & active I will take my chances. We all die of something in the end.

[@brianwnc8168]

I'd like to see keto calcified plaque compared against what's considered a truly healthy Mediterranean diet where people are eating 12 cups of vegetables and salad a day and doing all the things in the best food categories such as when eating grains, only eating them in their whole form from 3 grains only. Quinoa, buckwheat, and amaranth. Plus having mushrooms a few times a week, high polyphenols, etc. A modified super Mediterranean diet where starchy carbs are cooled after eating to create digestive resistant starch, Etc

[@newdata]

how come dont see the arsonist that is main calprit ? sugar levels !

[@larrywong7834]

Am I missing SOMETHING. At minute 55:35 we are comparing n=54 subjects. Apparently they these 54 have very little TPS plaque. But the earlier studies by Dave and Budoff on LMHR had n=80 subjects. With many many with TPS 40 to 80. A score of 50 is very serious!!! Why are we not Looking at these peoples. Guess theres 26 subjects of the n=80 thats Not Lucky with diet. Including LMHR peoples. What can these n=26 peoples with Lots Heart Plaque eat???? Do they need control Lipoproteins?

[@ericzarahn9343]

The assertion made @3:38 that statistical significance (implicitly, p

[@CashMoneyMoore]

Can't wait to see the influencers dealing with that lipid-lowering excluded comparison, who am I kidding they'll probably ignore it. Can't wait to see when it becomes so big they can't ignore it and have to grapple with what this data is suggesting. I can't get over those R and P values for ldl in LMHR, it's literally what Dave and others have been hypothesizing for years "Perhaps ldl in this very different cohort is behaving differently". Also, shame that Miami heart didn't have lipid particle information, also I really wish there was a 1 to 5 year followup on Miami heart to see what "normal" or perhaps not normal but quite healthy compared to general population but not quite lmhrs, what their plaque progression looks like to compare to the LMHR followup. Hopefully there will be little to no plaque development, but if there is it would be great to have something to compare it to

[@realDaveFeldman]

- Yes, I wish MiHeart had longitudinal data as well - Of course, I should level-set that I fully expect the LMHR cohort to have some degree of plaque progression at a population level, given the average age is 55. I've said this dozens of times across podcasts even before the second scans came given the age of our mean. That said, I like speculate it will be lower than most if not all other major longitudinal studies, but that won't say a lot given they are all high risk (and I think both supporters and detractors alike are in agreement our cohort is probably not "high risk" relative to those cohorts). This is why the MiHeart match data was likely to be as interesting - and for many, *more* interesting -- than the longitudinal data of our study without a clear comparator (so far).

[@CashMoneyMoore]

Even hearing detractors argue that lmhrs are not high risk will be great ​@@realDaveFeldman

[@CashMoneyMoore]

It's wild to me that ldl is pushing statistical significance with total plaque in Miami heart but not lmhr

[@CashMoneyMoore]

@@realDaveFeldman Even hearing detractors saying that LMHR's are not high risk would be a big win

[@Ozzie-n8t]

Their risk is TOTALLY dependent on their coronary artery plaque burden and blockage percentages. The total plaque scores are the SAME in keto as in the general group.

[@manarsamad7378]

I request Gil Carvalho, MD, PhD, to watch this and share his perspectives.

[@justsaying7065]

Part 2 of why the Lipid Energy Model is probably not correct. This is an addition to my comment earlier. The reason why lean people see a greater increase in LDL than fat people is because doing keto is like 1) fasting and 2) being in winter. Keto is similar to fasting because you burn fat while fasting. Keto is similar to being in winter because there are very few plant foods (if any) in winter; so not eating carbs is like being in winter. Both fasting and being in winter are difficult conditions for the body. Fasting is self-explanatory. Being in winter means needing more energy to stay warm while being in an environment with harsh weather conditions and scarcity of foods. So when someone is doing keto, the body thinks that it's fasting or it's in winter and responds by conserving energy as a protective measure. It does that by lowering thyroid hormones to lower BMR. This has a side effect of lowering LDL receptors as well, which results in increased LDL in the blood. Since fasting and being in winter are more dangerous for lean people than for fat people because they have less fat reserves, lean people's bodies have a greater protective response, which results in a higher increase in LDL. That's why there is a correlation between BMI and the increase in LDL for people on keto. Reintroduction of carbs to the diet, as in the Oreo experiment, sends a signal to the body that 1) fasting or 2) winter is over. So the body can now relax and raise the thyroid hormones and BMR. In doing so, LDL receptors are restored as well, lowering LDL in the blood.

[@dianavp9054]

Thank you, your explanation was totally intelligible. :)

[@GJJC13]

I honestly do not know if the above explanation of the keto/winter, etc... is accurate but it seems to make a lot of sense and very well explained .

[@csmith5611]

Thank you so much, a really interesting and compelling hypothesis. Whole-body thinking.

[@GJJC13]

I read this yesterday and re-read it now and it is such a clear and logical way to explain the high LDL increase for fit, healthy people doing IF and low-carb. Wouldn't it be great if so many other KZbinrs that are deep into this topic and actually know the above had the capability of explaining this issue so clearly and in just a few paragraphs like @justsaying7065 has above: simple terms and so efficiently. Thank you for your contribution.

[@justsaying7065]

@@GJJC13 Thank you so much for your kind words! I try my best to uncover the truth.

[@Roberto-cg2gr]

Please include MRI visceral fat and Kraft insulin Assay Test for LMHR

[@kathycoe58]

Have you ever compared LMHR, FH and homozygous ApoE4 lipids? I’m a 4/4 and my lipids are very similar to these findings. I’ve been lowcarb 35 years. I’m very lean and muscular

[@lls66]

Have you done CTA clearly like imaging? Or a CAC or CIMT? Very curious

[@Metal_Stacking]

Remember the medical community is to treat not prevent medical conditions.

[@vadimesharak726]

To make it even more robust, would you, guys adopt it in the correlation with the Randle Cycle?

[@garyjackson4054]

Hi Dave we met briefly at the PHC conference earlier this year. I would be interested to see if there is any correlation between high levels of blood oxalates and hypertension with plaque formation? i.e. could oxalates under pressure be damaging epithellial tissue over time. Particularly where this scenario coincides with fluctuating blood sugar levels.

[@DrTomMD]

Greetings from Copenhagen at the annual ARDD (age related drug development) conference. Lipidologist and past president of the National Board of Physician Nutrition Specialists and current question writer for the American Board of Internal Medicine here. Starting to get my head wrapped around the LMHR phenotype. I’m skeptical of the level of ‘ASCVD resistance’ being hypothesized. But I’m a healthy skeptic so willing to be proven wrong. Nevertheless, initial observations and some questions: 10:30 - the result of ‘massive flux’ should still be a lower ApoB steady state. But maybe, just maybe, there’s a relative resistance to influx across the endothelial wall (whether between cells or through cells irrespectively) and enhanced efflux - problem in terms of plausibility not being so much the former as the latter (ie nothing about keto that is consistent with improved sub endothelial efflux - resistance to influx is more plausible to me, and maybe that’s all that’s necessary… Though I’m still skeptical that LMHR’s have “Teflon arteries“ Q1: What is the average “length of exposure”? Ie Subjects presumably we’re not on keto for life and therefore lifetime exposure to “stratospheric” levels of ApoB. ASCVD is a very slow process in terms of plaque progression (as opposed to plaque rupture). So far, what I believe is driving the extremely high ApoB is a combination of ultra high saturated fat intake resulting in hypersuppression of LDL particle receptor expression at surface of hepatocyte combined with supranormal dietary cholesterol intake. And the posit is that the endothelia arena is somehow resistant, net result anyway, to influx and potentiallysupranormal efflux. Whether keto is driving the slower progression towards detectable ASCVD w/ above average endothelial cell layer resistance to net LDL particle retention or if driven by genotype (eg I presume these subjects are largely more naturally lean vs lean as a result of keto, no?) and a resulting possibly very low inflammatory state is still in question or other factors, if this is real at all gentlemen because, with all due respect as you know, “great claims require great evidence“. And this level of claim is so great that we are nowhere near, in my professional opinion, the level of great evidence necessary to accept LMHR are “heroically” resistant to subendothelial ApoB particle accumulation. Were any correlations with hs-CRP, Lp-PLA2, MPO, IL-6, urine albumin/creatinine ratio sought?

[@CashMoneyMoore]

Answer to question 1) 4.7 years. 2) I believe they would argue that saturated fat has very little to do with it, Sat fat perhaps explaining 5-10% of the effect, as they have some cases of extremely high ldl with quite low sat fat but very high mufa and pufa ldls of 500+. Look at Nick Norwitz' Oreo experiment, which was a demonstration of the lmhr model where he added a dozen Oreos a day (adding quite a bit more sat fat per day) but also adding more carbs which reversed the lmhr phenomenon and brought his ldl from I believe 500 down to the mid 100s. He also did a washout and comparison with a high strength statin and th le extra sat fat Oreos brought down his ldl more than Statin. He's the gentleman in the bottom on the presentation and you can find his presentation of the Oreo study online. Nick or the others can perhaps take up your questions where I can't or correct anything that I have gotten wrong.

[@realDaveFeldman]

Greetings back to you as well, @DrTomMD - "Starting to get my head wrapped around the LMHR phenotype" > Given your questions ahead, I'd love if you could visit the hub page for our published papers: CholesterolCode.com/papers -- it's a fantastic resource that also includes the video abstracts to better understand the Lipid Energy Model as well. - "Q1: What is the average “length of exposure”? Ie Subjects presumably we’re not on keto for life and therefore lifetime exposure to “stratospheric” levels of ApoB." > Please be sure to check out our PI's presentation on the prelim data here: kzbin.info/www/bejne/aXrXgpiagrWhqbs with abstract published here: linkinghub.elsevier.com/retrieve/pii/S0026049524000805 (full paper coming shortly) Avg LDL-C was 122 for Keto-CTA pre-keto, 272 for mean of 4.7 years after. Avg LDL-C for MiHeart was 123 to matched age of 55.5. So the back of the envelop delta for LDL-C exposure ("Cholesterol-years") is (272 - 123) * 4.7 = 700.3 mg/dL. Both populations would have 50.8 years at nearly the same LDL-C exposure before the keto group moved into the LMHR-like phenotype -- so a little over 5 decades before. - "ASCVD is a very slow process in terms of plaque progression (as opposed to plaque rupture). " > I reference Brown and Goldstein frequently in my presentations for this study, even before it began. It's been long considered the strongest indicator for high exposure resulting in extremely rapid plaque development to symptomatic ASCVD in just a few years. Most existing RCTS are < 4.7 years and are looking at changes that are far less than the 700.3 mg/dL delta mentioned above. This is why these data are extremely fascinating in light of the more simplistic consideration of the Lipid Hypothesis as context independent. (ie, any population, regardless of context, is higher risk if at higher levels of LDL/ApoB) "So far, what I believe is driving the extremely high ApoB is a combination of ultra high saturated fat intake resulting in hypersuppression of LDL particle receptor expression at surface of hepatocyte combined with supranormal dietary cholesterol intake. And the posit is that the endothelia arena is somehow resistant, net result anyway, to influx and potentiallysupranormal efflux. " --> I think you'll find our existing published meta-analysis as very compelling (www.sciencedirect.com/science/article/pii/S0002916524000091?via%3Dihub) . If high saturated fat alone drove the high LDL-C levels we see in LMHRs, we'd see it across body compositions, particularly those with higher BMI. Note these are 41 different RCTs that we could find where at least one arm was adopting LC/keto and the results are quite consistent. - "Whether keto is driving the slower progression towards detectable ASCVD w/ above average endothelial cell layer resistance to net LDL particle retention or if driven by genotype (eg I presume these subjects are largely more naturally lean vs lean as a result of keto, no?) and a resulting possibly very low inflammatory state is still in question or other factors, if this is real at all gentlemen because, with all due respect as you know, “great claims require great evidence“. And this level of claim is so great that we are nowhere near, in my professional opinion, the level of great evidence necessary to accept LMHR are “heroically” resistant to subendothelial ApoB particle accumulation." --> To be sure, we're not asserting LMHR are somehow immune from ASCVD -- in fact, I've quite literally speculated our cohort of average 55yr olds will likely show at least some population level increase in non-calc plaque (our longitudinal endpoint) -- but that's because I'm confident all populations of mostly male 55 year olds will develop ASCVD. In short, no population is immune, which is also why I stressed everyone work with their doctors for their individual context. With all this said, ours is the first prospective study on a population with extremely high LDL cholesterol that excludes those with molecular FH or any major risk factor for ASCVD - which is great as I think this provides us a scientific opportunity to better see the independent atherogenicity of LDL/ApoB at a population level in this group of people.

[@realDaveFeldman]

"Were any correlations with hs-CRP, Lp-PLA2, MPO, IL-6, urine albumin/creatinine ratio sought?" --> on this I cannot answer yet as I'm blinded to those data. But I believe those markers we do have will likely come forward in future papers. (Can't say more than that for reasons I'm sure you understand -- but feel free to reach out privately if interested in what our roadmap is atm)

[@QuantumOverlord]

How long were they on the keto diet for? You wouldn't expect a robust asociation between instantaneous serum LDL and plaque score unless its representative of the cumulative exposure. If, prior to these diets, this cohort had low LDL then the results are simply consistent with the exposure not being long enough for it to generate a statistically significant result in the study.

[@mistahtom]

In addition to the fraudulent Ancel Keyes research, it’s also important to remind people of the history behind the original studies that link LDL elevations, saturated fat consumption, and CV disease were conducted during a time when many many people smoked manufactured cigarettes.

[@tomgoff7887]

There was no fraudulent Ancel Keys research. That is just a slur invented by people trying to sell sensational mass market 'health' books.

[@broccoli-dev]

What parts of Keyes' research do you believe are fraudulent?

[@fitmill8001]

@@broccoli-dev The fact that Keys studied 21 populations but included only 7 in the publication makes the study fraudulent in my opinion.

[@pasta_heals]

@@fitmill8001 What publication? If you're referring to Seven Countries then it's clear you've never read it because 1) he didn't study 21 populations and 2) for Seven Countries he studied sixteen cohorts individually.

[@EduardQualls]

"Manufactured" cigarettes? The problem with all tobacco products is not the manufacturing, but tobacco, itself. Tobacco is naturally radioactive, in that it concentrates both radioactive lead (Pb-210) and polonium (Po-210). Radioactivity is present in canned tobacco, cigarettes, cigars, snuff, in fact, in all forms of tobacco. All plants will concentrate radioactivity found in the soil and precipitation whenever present, and this is why ALL smoking, no matter the plant source, is pollution that is damaging to the face, mouth, throat and lungs. (For example, areas of trees within the US Northeast concentrated the precipitated radioactivity released from Three Mile Island [1979 ], to the point that fireplace ash from those trees reached the radioactivity levels of radioactive hospital waste.)

[@hectorviscenciobrambila3943]

Given that plaque formation may have several causes, then it may be worthwhile to use statistical multivariate models to try to explain it. It is a well-known fact that you may increase R-square coefficients by adding more variables to the model; in particular, when the variable selection has a sound foundation. I urge to use these kinds of tools.

[@Dr_Boult]

On the clacified plaque difference.. is there any theory suggesting that inflammation, which is lower on keto, accelerates the calcification? At the "oldest" period of their plaque progression, the keto folks may not be converting to calcified form -- that would be very interesting to explore and may be shown in the 1year data.

[@camperjack2620]

Interested in this topic, but sorry, I can't watch a 58 minute discussion. I'm looking for the 10 minute summary. Thanks for alll your work in this area.

[@shiftgood]

Start at 50:00

[@brucemckay6615]

Do better

[@qui1766]

That will likely be coming soon

[@GameofTrees]

I will choose to listen to the whole video:)

[@AnneMB955]

I have this going on while playing some iPhone games. 58 minutes of important info.

[@jaymckoskey25]

Remarkable data and nice analysis. The need for individualized medicine is real. I do think the Mi Heart population data is skewed by the statin usage, though. The group not on statins is skewed by having been sorted by doctors determining they don't need statins.

[@buppus]

Faridi et al just came out with an analysis of Miami Heart that included a subgroup analysis of only those with "Optimal risk factors" (n= 184) This was defined as, "not on lipid-lowering therapy and without hypertension, diabetes, or active tobacco use, optimal risk factors were further defined as having all of the following: systolic blood pressure

[@drcirocampos]

Excellent work! I am a cardiologist in Brazil, and I practice ketogenic and carnivore strategies. This data raised a question for me: does the KETO population have the same amount of non-calcified plaques as the MiHeart population, right? Could this be due to a shorter exposure time to a risk factor (in this case, dyslipidemia/elevated LDL)? However, upon further reflection, LDL levels and other particles did not appear to be predictors of plaque in the MiHeart study either. I sincerely hope this is not the case. I am eagerly awaiting the developments in this story.

[@lls66]

Please do super deep dives on every one of these graphs.

[@davidb9670]

The follow-up scans in the keto group were completed about 6 months ago. Still no results?!

[@gray45374]

I imagine they will be saving them for the paper to preserve some novelty.

[@dilettanter]

Can you do the HDL/triglyceride ratio correlation to TPS also? Or next time?

[@larrywong7834]

Dave____ Time Stamp 50:37. Table 3. Thats great Match results for the Median of LMHR compared to Median of MiHeart. Great low Plaque volume in BOTH. Was'nt it reported that both cohorts at Median had CAC= 0. THUS when they are not proned to CHD, CVD you would expect great matching numbers. What happens when we get off the Median. Looking at both cohorts when they have concerning levels of CAC. How well do both cohorts compare then. Which group then will have the most soft plaque. Developed from their respective Diets.

[@justsaying7065]

This study is not compelling because they excluded people on keto who have lots of plaque from the study, so of course the results look good. This study doesn’t inform an average person who wants to do keto what their risk of developing plaque is because this average person could be like the selected participants and not develop much plaque, or they could be like the people who are excluded from the study who have a tendency to develop lots of plaque. The difference could be due to genetics. So in essence, the study can’t tell, for an average person, if their risk of developing plaque increases, decreases, or stays the same, if they switch from a mixed diet to keto.

[@lls66]

This study is very compelling for science because it challenges the notion that ldl is always causal. It is a unique group of subjects. Like they repeatedly said, this is not medical advice and in your case, if you don’t fit lmhr profile, it isn’t necessarily applicable to you.

[@richardb8267]

This study is beyond compelling for science. This study is challenging the hypothesis that exist for more than half a century telling people that high ldl is the main cause of CVD (Atherosclerosis). But the data in this study suggest that LDL is NOT causal.

[@BeefNEggs057]

They didn’t want people who already broke their bodies and then went keto to try to fix it. They wanted to see lean people and see how their numbers tracked over time with high LDL. This is very compelling to me to see how these people track through time. This is what heart researcher should be doing instead of accepting the old tired assumptions that just aren’t true.

[@rmpenniv]

If they had selected individuals with existing plaque burden (vs excluding them) it would’ve completely undermined the point of this prospective study given it’s a comparison of plaque progression among healthy individuals with a matched Miami heart cohort lol.

[@larrywong7834]

​@@rmpennivLooks to me they compared the Median of each the n=80 LMHR to MiHeart n= 80. The Median of both was CAC= 0. Thus Median wise both groups had very low TPS total plaque score. Peoples below the Median had mainly Very Low CHD Arterial Disease or NO Arterial Disease. Peoples above the Median have low, moderste or very very serious arterial Disease. Above the Median Both Groups have tons of peoples with CHD heart disease.

[@johnbutler3141]

You can take all those factors in determine metabolic health. If you did not start with a Fasting Insulin you are missing a trick. Insulin is a leading indicator long before HBA1C , fasting glucose or any lipid panel results that show up as a problem.

[@CvoreAthlete]

So 14 months carnivore, HDL 98, LDL 105, TG 50. I must be a lean mass HYPOresponder?

[@ingeamanda]

How is your diet ?

[@CvoreAthlete]

@@ingeamanda lion diet

[@patrice2288]

LDL 105 is not hyperresponse

[@CvoreAthlete]

@@patrice2288 duh that's why I said hypo

[@danielgage1830]

Do you drink any alcohol (red wine)

[@Dr_Boult]

Agree with Nick's observation that it would be good to look at a ratio of partical-count/SD count I'm not sure I agree with his expectation since I'd expect that the plaque score in LMHR is for life before keto, and hence, nothing in them now is really related to their TPS. the 1-year change maybe, but TPS not really. The most interesting there is Lp(a) since it does not change as much with diet (though more than was previously thought), so that there is no relation is more interesting there. Would be interesting to see if lp(a) was the "keto" version vs lp(a) prior to keto.

[@NimrodGilAd]

You've just shattered Peter Attia's "It's the ApoB/LDL-P, not the LDL-C" mantra. Let's see him squirm out of this one 😁

[@newyorkguy158]

Dr. Attia is not a lipid scientist, so there is no reason to bash him. Cholesterol is not causal for heart disease. Apob is causal. That is what world-leading lipidologists like Dr. Cromwell, Dave Feldman's friend and mentor and Dr. Sniderman have stated in their YT interviews and I don't believe they are wrong. I noted that in Dave's YT conversation with Dr. Cromwell, Dr. Cromwell identified some methodological issues with Dave's research. which he was unable to refute. I am going to review that conversation.

[@OGPedXing]

Yep, this data is a classic black swan scenario that disproves the apob hypothesis. I've never understood why Attia and friends want to stop at apob when it's clear there is a deeper issue and cause. Not knowing the true cause is harming patients.

[@realDaveFeldman]

I'd love to hear his comments on these data.

[@richardb8267]

For him to say ApoB is "causal" of Atherosclerosis is beyond malpractice!

[@newyorkguy158]

@@richardb8267 No it isn't malpractice. And I don't understand the endless bashing of Dr. Attia. He is not a lipid scientist. All of his knowledge comes from the scientists who have done the research. That Apob causes heart disease is a conclusion derived from probably hundreds of studies of every kind including, genetic, with all reinforcing each other. You will hear this on YT from world-leading authorities on lipids like Dr. Cromwell, Dr. Sniderman and Dr. Dayspring.

[@hectorviscenciobrambila3943]

Referring to the first table, the data show clearly that the null hypothesis of no correlation cannot be rejected. Even If it could be rejected, these r-values would still be weak. Am I missing something? What would be a strong r-value?

[@dahdah6668]

In the cholesterol-lowering medications group, there were similar results of the non-calcified plaque. I thought that one of the statin's protective mechanisms was calcifying the plaque, so why was there any soft plaque?

[@Julian-xs8nc]

Can someone summarise the findings?

[@sheila7814]

Ditto! I am not up on this info…. Would like a simple summary of the findings.

[@firstchoicefarm7767]

@@sheila7814 science is not simple. I quick summary would have people making false conclusions

[@CashMoneyMoore]

High LDL cholesterol in context: The study looked at people following a ketogenic diet who had high LDL cholesterol levels. Surprisingly, these high levels didn't seem to be linked to more plaque in their arteries, which is usually considered a risk for heart disease. Comparing groups: They compared the keto diet group to another group of people with normal LDL levels. Despite the big difference in LDL levels, both groups had similar amounts of plaque in their arteries. Different types of cholesterol particles: The researchers also looked at different types of cholesterol particles, including small dense LDL particles, which are often thought to be particularly harmful. However, they didn't find any connection between these particles and artery plaque in the keto group. Other markers: They examined other blood markers that are sometimes used to predict heart disease risk, like Lp(a) and oxidized phospholipids. Again, these didn't show any relationship with artery plaque in the keto group. Detailed artery scans: Using advanced imaging techniques, they measured the exact amount of plaque in people's arteries. This gave a more precise picture than traditional methods. Similar results without cholesterol medication: When they excluded people taking cholesterol-lowering medications from the comparison group, the results were still very similar. Challenging traditional views: These findings suggest that in the context of a ketogenic diet, LMHR's high LDL cholesterol might not be as risky as traditionally thought. However, this is still preliminary research and needs more investigation.

[@KristofferStenersen]

@@CashMoneyMooreis this chatgpt?

[@sheila7814]

@@CashMoneyMoore Highly appreciate the breakdown of this information for us! Thank you Thank you Thank you!

[@samuelcakar174]

When will the results of the keto study be published?

[@StyleshStorm]

What is the conclusion? Don't got 1 hour for this.

[@jamesgordon8867]

What about blood pressure and glycokalix , not to mention inflammation in arterialschlosis?

[@larrywong7834]

Dave____the LMHR n=100 observations LDL-P, smLDL-p graphs are very thought provoking. Do you have PARTICLE Count graphs for Large Diameter HDL vs TPS. Do you have PARTICLE Count graphs for small Diameter HDL vs TPS. There are literature indicating small diameter HDL's are mire Heart Artery Protective. I gather smHDL's job is to extract/remove cholestrols from the arterial wall

[@eatanelkberger]

After thinking about this, I occurred to me that I don't know what these numbers represent. Are these data from a change in plaque over the year or is it simply a snapshot in time? If a snapshot, was it the preliminary blood draw or the one at the end of the 1 yr period?

[@kennethyuman1940]

Thank you Dave for discovering this flat new world for LMHRs. The flatness sets us free.

[@EdJacobson77]

Now let's see Peter Attia give you the public apology that he owes you. Of course, it will never happen, because he is a coward.

[@ptbwinland146]

Wow that was awesome

[@kevinsmith3782]

To be honest could you make a five minute video..:this is good vs this is bad?

[@pvee-xp3sk]

This may have been stated before, but I'm noticing that most of the ppl with highest plaque are all on the left side of the graphs. (the lower end of the comparison markers.)

[@larrywong7834]

LMHR n=80. MiHeart n=80. Which group have most peoples with serious TPS total plaque score?

[@davidgifford8112]

I’m married to a PhD, I never call her doctor or introduce her to someone as doctor, there is nothing magical about a PhD except being able to successfully defend a unique thesis to your expert peer group. It provides acknowledgment of expertise within a very narrow field of study, although I confess some PhDs seem to receive a subsequent letter in the post saying “you now know everything there is to know on all subjects.” Personally I fond those “experts” less trustworthy overall”

[@alesis100]

Your point being....?

[@matthiaspriester2368]

I think this belongs to another comment. 😉

[@nicknorwitzPhD]

Didn't you notice Dave called me Nick (PhD) and Adrian "Dr Soto Mota" (MD PhD) ... tbh, I prefer Nick or "Oreo Kid" ... even when I'm an MD PhD, I think the formalities just create an intellectual power hierarchy that's not productive. In two words, I agree with you...

[@techadsr]

​@@nicknorwitzPhDIn college, I always called my Professors, Dr So and so. But in a group of friends, using first names makes it more fun. Life should be fun.

[@craigwillms61]

One of the perpetual jokes in my town is the insistence that we're all Phd's. Some people fall for it until you tell them it means Park High Diploma. It does give us license to spout off on all possible subjects with the appropriate gravitas.

[@zukiplay]

Non statin user data. Wonder if any of those used a statin a decade earlier for a short while and then stopped? That could impact the calcified results in the MIA group.

[@aky2k10]

What does density refer to in LDL and HDL!!? Can someone explain it please?

[@ElizabethMillerTX]

Huge! Thanks so much!

[@venkateswararaosunkara6571]

Non-calcified plaque is 46.4 and calcified plaque is 4.9 in MI Heart group. Av age of the group is 54.8 years. That means calcified plaque is roughly 10% of the non-calcified plaque. Only Calcified plaque could be detected in CAC score test, whereas major portion of the plaque is non-calcified type which could not be detected in CAC score test. Thought provoking data.

[@justsaying7065]

The Lipid Engergy Model is probably not correct. I believe that the large amount of cholesterol in LDL in LMHR is not from VLDL, but from chylomicron remnants. People on keto eat a large amount of fat, which means they use a lot of chylomicrons to transport the dietary fat from the intestine to the blood. After the triglycerides are removed from the chylomicrons, they are left with cholesterol and become chylomicron remnants. The remnants go back to the liver. The liver will use some of the chylomicron remnants to make VLDL, but most of them will be used to make de novo LDL. So the liver secretes a large number of LDL directly because there are so many chylomicron remnants. The liver secrets a small number of VLDL, which is consistent with low fasting triglycerides in LMHR. There are other evidences that suggest that LMHR are likely not making a lot of VLDL as proposed in the Lipid Engergy Model. In addition, LMHR do not need a lot of VLDL to supply triglycerides to the muscles because chylomicrons have already delivered triglycerides from the meals to the muscles. The triglycerides from the meals are stored in intramuscular lipid droplets, which can be used later when the person is not eating. Further, LDL receptors in LMHR are down-regulated due to lower thyroid hormones. So a combination of increased de novo LDL secretion from so many chylomicron remnants and less uptake of LDL result in high LDL in the blood. Lastly, high HDL in LMHR is also not difficult to explain. HDL usually correlates with LDL (excluding people who have insulin resistance). Because when there's so much cholesterol in the system, you need a lot of HDL to do reverse cholesterol transport (RCT). Conversely, when LDL is not high, you just don't need that much HDL to do RCT. Therefore, high HDL in LHMR is not a marker of health, but rather that there’s too much cholesterol in the system.

[@nolanwardy7409]

What is your profession. This is really well explained, so simplistic. Thank you. I would love to see a response to this.

[@justsaying7065]

@@nolanwardy7409 That's very kind of you. I'm just another citizen scientist interested in finding the truth.

[@dianavp9054]

Thank you for your comprehensible explanation.

[@nicknorwitzPhD]

Here's a question: what's the half-life of a chylomicron remn... how about for LDL? And what if you parsed ApoB48vsApoB100... what would you expect in an LMHR?

[@lls66]

Interesting. But I think that for practical purposes if the total plaque volume doesn’t correlate with ldl (subject to final publication and others studies) then I’m not sure if the theory behind this phenomenon matters to the average person who fits this profile? Would love to know if others disagree? But it is an interesting academic question!

[@Aiken47]

So seed oils, carbs, sugar, vegetable anti vitamins were never in those studied diets?

[@mrr0cksor669]

The data make total sense, since we know that you need inflamation, insulin resitance and or peroxidation for plagues to occure. It´s like banning air because of storms, you need conditions for air to be harmfull.

[@techadsr]

Or banning CO2 because it's obviously the trigger for rising global temperatures.

[@mlaroche2009]

From what I see LDL seems so far to have no impact on risk for LMHRs. However, LDL IS associated nwith plaque score in the "normal" pop in this study. The idea that while waiting for answers, LMHRs that aren't obligated to be on keto might want to eat ~100g of carbs to normalise their LDL (instead of reducing saturated fat) therefore seems weird. to me. Once you eat the 100g of carbs, you fall out of the LMHR criteria and LDL is associated with plaque in the pop he would now be. At that point, when he is no longer a LMHR, shouldn't he also try to reduce saturated fat to further reduce his LDL? From what I understand saturated fat does have an impact on LDL when you aren't a LMHR (as in you now eat carbs). Even in Nick "Low carb Data distortion", the study that claim that keto shortens lifespan, Nick points out that having carbs

[@voisinat]

There's an SSPX chapel just north of Fort Worth, about 30 minutes from the monastery. If that's their priest he doesn't have to go far.

[@BobJ357]

Very interesting. 🤔

[@drbobvs]

Ok, so basically other than glucose/insulin/A1c we don’t have any idea what to measure in the laboratory to determine someone’s cardiovascular risk. Great 👍the more we learn, the more we learn we don’t know anything.

[@firstchoicefarm7767]

Why not look at the plaque versus age of participant? Of the LMHR, how about age before beginning keto diet? I would expect that to show a correlation.

[@nicknorwitzPhD]

Of course we will be looking at this for the final analysis, along with many other things... what is shared here is very preliminary

[@techadsr]

​​@@nicknorwitzPhDObserving plaque progression would be revealing. The CAC and AI-CCTA are points in time but who knows when those plaques formed. Are they increasing or being cleared? Over time the CAC scores appear to increase, sometimes significantly with statins. But what about non-calcified plaque? Would it be cleared by the body before calcification? Are we preempting clearance by calcifying it?

[@z00011001]

Wtf you don’t include BP into the factors? That has much stronger correlation than ldl model

[@matthiaspriester2368]

Because they were studying the effects of LDL on Plaque. I agree though. BP would be interesting to see and I suspect it to have a bigger effect as well.

[@z00011001]

@@matthiaspriester2368 why study something that is totally debunked? Even big data says that LDL correlation is too noisy. There is zero reason to study it. Also, when they say percentage correlation they should also disclose noise percentage. If signal to noise ratio is too low or confounding factors are not clear they we just need to discard crap studies. Medical is mafia and only way to stop it is when "insurance" or "govt" stops paying for chronic illness. Chronic illness is not an insurance. It is pension.

[@dental9855]

This is ketogenic diet?

[@jacobmatthewseymour]

Adipocytes are causal of obesity. Shall we prevent adipogensis or lipid droplet formation?

[@patrice2288]

So maybe diet doesn't matter, nor does LDL??

[@LabelsAreMeaningless]

Diet matters, but the government suggested guidelines are harmful

[@patrice2288]

@@LabelsAreMeaningless Agreed, for me personally. But for plaque, seems our two study groups don't differ much.

[@h-man2561]

🚨 Way to many ads on this video!

[@jeffreyadams648]

Yes….an hours. Start with a 5 min summary, then go on to the data.

[@ExcelinusCom]

This video is like trying to see the forest when your face is up against one of the trees at the edge of the forest. Did not prove cause to me? Maybe a few peeks around the tree but all I saw was bark.

[@dr.julia-heyakarcic8862]

Nick, please don’t joke about “drawing pentagrams” .

[@questionasker6977]

My total cholesterol is 360 HDL 63. Triglycerides 56. LDL, NIH 291. However I recently tested Apo B and it’s 194. How can LDL be so much higher than Apo B? 😂