Dave Feldman: When Cholesterol doesn’t cause Heart Disease
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- čas přidán 12. 09. 2024
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References (Copy & Paste DOI into Search Engine)
[1] doi:10.1161/JAHA.121.023690
[2] doi:10.1016/S0140-6736(20)32233-9
[3] doi:10.3390/ijerph19148272
[4] doi:10.5935/abc.20180063
[5] doi:10.3390/metabo12050460
[6] doi:10.1161/CIRCULATIONAHA.117.031951
[7] DOI: 10.1056/NEJMoa054013
[8] doi:10.1016/j.jacc.2012.09.017
[9] doi:10.1001/jamacardio.2021.5083
[10] doi:10.1001/jama.2016.14568
Mr. Feldman's video: • New Heart Scan Data fo...
Mr. Feldman's Presentation: • Dave Feldman presentat...
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#leanmasshyperresponders #heartdiseaseawereness #heartdiseaseprevention
**1 NOTE &* *1 AMENDMENT BELOW*
*NOTE:* Hi - I recorded this video before the Miami Heart data presentation by Dr. Budoff, so I’d like to mention a few things to consider with this new information, for those of you in the know:
Dr. Budoff (one of the lead authors) recently gave a presentation wherein the LMHR baseline data (the study I was describing in the video) was compared against the baseline data of an unrelated study (people who were not LMHR); so, they compared 80 participants from the LMHR study vs 80 non-LMHR participants from the MiamiHeart study. They ended up showing that there was no difference in coronary plaque progression compared to these MiamiHeart participants.
There are a number of issues with this data that no one has pointed out and I think are critical for us to look at this from a proper scientific lens:
A. This is still not a proper control. This is a comparator, yes, but it is not a proper control. Here is what a proper control would have been:
2 Prospective Conditions:
1. LMHR + Ketogenic Diet
2. Non-LMHR Normal Weight + Ketogenic Diet (High Saturated Fat)
Condition 1 is the main treatment condition, so the condition being studied.
Condition 2 is to see if plaque progression would occur in the same time frame in people who are not LMHR - this is critically important to make sure the experiment has run long enough to detect differences (a critique I brought up in the video). Yes, saturated fat increases LDL particles; however, the magnitude of the effect is lower than LMHR (I have analyzed many studies showing this). If possible, although likely not very feasible, adding weight gain would supercharge the effect.
B. There were multiple differences at baseline between the LMHR cohort and the MiamiHeart cohort; for example, higher inflammatory markers in the Miami cohort, higher bodyweight, 1/3 of the participants were on lipid lowering drugs, etc.. The point being that while it is nice to see there are no differences between groups, it seems premature to attribute that to LDL when there are multiple factors different. Additionally, the results were largely ‘null’, so this does not provide evidence that the experiment was sensitive to changes in the first place.
C. This is still associative. This data is still not based on double blind, controlled study design.
Overall, I think it would be really cool (from a selfish perspective) and highly beneficial (for those LMHRs) to detect a true nuance in the LDL theory of heart disease. If you’ve been following Physionic for a time, you know I live for the nuances, but those nuances should be well controlled and be backed by substantial, high-quality evidence. This LMHR study is a step in the right direction, but it simply falls short of making any changes in my interpretation of the LFL theory, because it fails to address key points that I hope will be addressed in the future. I am open to changing my mind, as always, but I need to see concrete, irrefutable data, which we currently do not have and this study will not provide (yet!).
*AMENDMENT:* @rashoff pointed out that a ketogenic diet does not include pizza and hamburgers as seen in illustration @8:22 - that is true. My illustrator through those in as 'high fat' foods based on my general directions, but I should have corrected it. Sorry about that - those are not representative of the typical keto style nutrition. Thank you for the correction.
I eat healthy, thin but still blood work shows my LDL is higher than normal !!! So weird, none of my family members ever had cholesterol issues!
Thank you for the work you put into this! Very very interesting and hopefully more well designed studies can shed more light on the issue
Why is there no correlation between LDL and plaque in Miami? Wasn't a correlation to be expected? If expected, then could that indicate a weakness in the LMHR study? (edit: I guess Miami did their own measuring of plaque, so I dunno...)
Thanks for the elucidation.
So people need to be obese for years in keto in order to be a good control group.
Very hard, nearly impossible.
Keto diet generally will make people lose weight.
I was a LMHR. Was on strict keto 2years and very active and great cardio shape. Just had major heart attack 2 months ago! Be careful out there!
I'm glad you're on the mend, Thomas.
My worry is that folks who are not “lean responders” will come to the conclusion that high LDL is no problem, esp. if they combine this with the fluffy/small dense line of argument, and then they may have bad outcomes. Have you done a video on that whole issue?
Lota of that going around. It has nothing to do with LDL. You know that.
@@ivermekten2293 Separate meta analysis of over 200 prospective cohort studies, Mendelian randomisation studies and randomised trials including more than 2 million participants with over 20 million person years of follow up and over 150,000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of the exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. There is more evidence for high LDL-C/high apoB being causative of cardiovascular disease than almost anything else in all of nutrition science.
@@Barbara-ch3qf There isn’t a good reason to be confident that LDL/apoB being causative of cardiovascular disease doesn’t apply to lean mass hyper responders either. It would be like people being unsure if smoking causes lung cancer in lean mass hyper responders/thinking lean mass hyper responders are the exception to smoking causing lung cancer. Both are incredibly dangerous viewpoints, except the view for cardiovascular disease is even more dangerous due to how unbelievably more common deaths from cardiovascular disease are compared to deaths from lung cancer and with LDL levels above 200 having an even higher risk of cardiovascular disease than people who have LDL levels of 100, who have a lower but non zero risk of cardiovascular disease as LDL levels of 100 are still enough to cause cardiovascular disease in some people. Going below 100 decreases the risk of cardiovascular disease even more. But having LDL levels of over 200 is not good for your health.
"Here at Physionic, we integrate, not ignore." I love it!
Thanks for recognising the great work conducted by Mr. Feldmen and contributing to his study.
As someone with a BMI of 21 and normal cholesterol levels yet have required six heart angiograms in six years due to Hypohomocysteinemia Accelerated Atherosclerosis I can personally testify that elevated homocysteine is a major risk factor for accelerated atherosclerosis, and actually leads to lipid and glucose processing dysfunctions. One pathway elevated homocysteine leads to atherosclerosis is by causing increased oxidation of LDL cholesterol. If you have high LDL and low homocysteine then no oxidation, but if you have high LDL and high homocysteine then the increased oxidation promotes atherosclerosis. Homocysteine also suppresses nitric oxide and increases coagulation. You should look into the work of Dr Kilmer S. McCully, undoubtedly the global expert on elevated homocysteine and atherosclerosis.
I find this subject fascinating, particularly as a person on a low carb diet with high LDL. I think what we hope will be discovered through this and other research is whether LDL is a significant risk factor for heart disease when all other risk factors are low. I, for example, have a good BMI, excellent blood pressure, high HDL and low triglycerides, I work out regularly and I have no family history of heart disease. I also scored zero on a CAC scan. My doctor has prescribed statins but I am not keen to take a strong drug with potentially serious side effects unless I know I am at risk. Hopefully we are a little further down the line to finding this out.
That's a great assessment, Simon. Clearly, in all other metrics, you'd be considered low risk. I would caution exclusively using CAC as a metric of progression, however - a good minority of people do not develop calcium and still develop atherosclerosis (see attached study in description on that). Still, no doubt you would be at lower risk than many others with elevated risk factors. Ultimately, it is a personal choice, even if the science indicates LDL is an independent risk factor.
Why would you choose though to be on a low carb diet (high in saturated fats I presume) that usually leads to high LDL, when we know that this raises risk for CVD among other things? Why not choose another diet?
@@CharlieFaderbecause he wants to?
@@CharlieFaderIn my case, I tried vegetarian, vegan, etc, but too much plants tend to give me GI issues. I had IBD symptoms but immediately went keto. It immediately fix that. I have DNA SNPS that makes me gluten sensitive and might have a higher than normal risk to have Celiac, Crohns disease, etc. So, no wholewheat heart healthy diet or a mountain of salad for me.
@@matijagrguric6490 he has the right to smoke and drink alcohol too if he wants to, but I would still wonder why he would want to, when we know these practices raise the risk for a number of diseases.
The key point they are making is as follows: There isn’t any research indicating that LDL cholesterol is linked to or causes cardiovascular diseases when it's elevated due to healthy physiological reasons. In every existing study, high LDL levels are attributed to factors such as genetics, lipid system dysfunction, or other causes. In these scenarios, it's evident from research that high LDL is correlated with an increased risk of cardiovascular diseases. However, the LMHR (Lean Mass Hyper-responders) population presents a unique case. In this group, LDL levels are high (along with elevated HDL and low triglycerides) due to a very specific reason. This population practices carbohydrate restriction, leading to depleted glycogen reserves in the liver. As a result, fat becomes the liver's primary energy source for export. An increase in VLDL (Very Low-Density Lipoprotein) secretion is only necessary in individuals with minimal body fat. If there was abundant fat throughout the body, the liver wouldn't need to send out VLDLs, which eventually convert into LDLs, because muscles and other organs already have access to an energy source stored in adipose tissue. Therefore, this population, which exhibits high LDL levels, does so for reasons that are both healthy and logical, as described in the LEM paper.
I know this is a simplification of a more complex discussion but this is the most I can compreend.
Kind of where I am. High total cholesterol (543), high LDL (low 400s), HDL of 86, trigs 56, low insulin, low Homocysteine. I'm 65. How long I live mattered when my kids were young. Now I'm a granddad, enjoying whatever remains of my low carb/keto life. I have books on the subject because I'm curious and a little mad about the decades of nutrition and pharma lies we have been told.
How about addressing September's Swedish study of individuals with exceptional longevity. Health markers of 40,000 65 year old people were followed for life up to the age of 100. Less than 3% lived to be centenarians but those who did had the highest cholesterol and the lowest heart disease. Those who became centenarians also had low blood glucose and low uric acid.
@@whiznot3028 Evident, since deadly diseases lower cholesterols.
I continue to put you in my S-tier for health info on CZcams. Thank you for all the work you put into your channel
1) I love that you approached it with great curiosity and an open mind.
2) Why don't you join the team in future trials? Your critical mindset could help the study designs so that they have few holes. Am sure they would welcome your skills and expertise on the team... 😊
Nick is supposed to be open minded ? He criticized Paul Saladino who claimed what this study just revealed ! He said one has to have metabolic disfunction in order for cholesterol to cause harm !
@@usernwn7qe doesn’t have to be metabolic dysfunction. You can have high blood pressure or be a smoker which damages endothelium and then cholesterol can become harmful in excess.
@@felixcat9455 High blood pressure IS a metabolic dysfunction in 9 out of 10 cases.(you can obviously have some rare exotic morbidities but for most individuals it comes down to metabolic syndrome. (Which is, as the name suggest not a clearly defined illness - hence most individuals will never be diagnosed)
Good point that this study is after all also "just" association not a RCT, but (and this is important) the findings are completely unambiguous i.e. they point in one direction only. This makes the result much more compelling and clinically significant than the association studies we normally see in this field. Great study!!
I love how thoughtful and unbiased your reviews are. Especially when they contradict my nonexpert opinions, which several of your other videos have. Keep up the good work!
I wonder if it's the combination of high fat and high sugar that causes calcification.
It is. U should never eat carbs with fat. Because the body burns the carbs military in a panicky effort to throw rhem out. That means, the meat fat is being stored which isn't good. If u eat meat alone then the body uses it as fuel without waiting for carbsto be burnt first.
I am 46 yo. My total cholesterol was always around 300, often above. TG always low and HDL high. I am constantly refusing taking statins. I just got yesterday cartoid ultrasound and report says
0 plaque. Why I am not surprised - 30 years of regular training (weights, cardio 5 times a week), intermittent faating, and keeping my body fat around 18% max - mainly by cutting carbs, when I start gaining unwanted weight. I think metabolic syndrom is way more dangerous than high cholesterol.
I think one reason Mr. Feldman started this is because too many doctors are so quick to throw the statins suggestion at you, and will even dump you as a patient, if you refuse them solely based on elevated LDL levels. Thanks! I had the LMHR response to eating this way myself, but my question is how good of an idea is it to do this if you have high CAC levels already when you started? Like myself.
@@Feed_Bleed_Read how so?
@@Feed_Bleed_Read I listened to Feldman early on he spoke of the things I spoke of. I never said he had had a bad experience he is a very curious person. Docs will send you packing in some cases if you won't do their drugs. It isn't common but it does happen. They see you as uncooperative. Otherwise, you are just running your mouth on my time and have no idea.
I just recently started Keto (again) and my thinking is to get a CAC test for baseline and after a few months of being on Keto with presumably a high LDL, re-test to determine if there's progression of plaque and if not, continue marching on. If there is progression of plaque, then I will consider abandoning Keto but I have no intention of changing my diet until I've established a clear correlation between Keto and an increase in plaque.
@@frankenz66I suspect health insurance companies would be alarmed buy a high LDL
@@billkimura4512 if the CAC score was high before keto, the correlation would not be between keto and increasing hard plaque, unless the build up had accelerated after keto
Yep. I have high LDL. Not as high as in the study. My HDL is always over 70 and triglycerides are under 70. Fastest insulin is under 2.5 the past 3 years. I want to have an esthetic breast lift and needed cardiac clearance. So I had a Bruce protocol stress test with echo before and after. The cardiologist said my heart was exceptional !!! I’m cleared for my surgery!
Yes I have been keto for 3 years
Afaik ( i might be wrong), you can´t see coronary plaques in an echo. I also don´t think, clear coronary arteries are , what define cardiac-fitness before a surgery.
What's even more fascinating is that saturated fat is not necessary to be a lmhr. You just need to be low carb lean and active , vegan or carnivore doesn't matter. I'm a classic lmhr and flipflop between thoughts. I appreciate the content. Just be careful, nuance breaks the internet 😊❤
That's right. One of the investigators, Nick Norwitz, has spoken about how his LDL skyrocketed when he went low carb even though he deliberately avoided saturated fat.
That is fascinating!
@@Physionic He also published a case report on various changes to the saturated fat content and LDL. With Diet trials. End result, it matters, a little, but an order of magnitude less than low carb
@@simonround2439I saw an interview on Plant Chomper CZcams channel with Dave and Nick. Plant chomper said he had an lmhr phenotype as a vegan when he was competing for a triathlon in his younger days.
@@simonround2439 And Oreo cookies brought it down, fast.
why is there always a presumption that everyone has a physician
If you don't have one, you should still find one to consult when you make major diet choices. Or just to check your health status every now and then.
What doc? Are you kidding me. What ❓ to ask anyways....
I haven't seen a doctor in over 7 years and I would never bother asking a doctor for nutritional advice.
They are from the US
@@health9818 i don't ask doctors for nutritional advice either, but I go every 5 years or so to check my blood markers. You could have deficiencies or excesses that you have not quite noticed yet, but that could mean a lot for your health long term.
Wait till you see the Statin to 12 oreo a day test about lowering the so call LDL cholesterol ....
LDL May be a risk factor, but is dwarfed in relative risk terms by insulin resistance and type 2 diabetes
I have been on an LCHF lifestyle for over 10 years. Got lean and stayed lean. Have high HDL and high LDL. Feel great and my bloodwork are «great» as my doc say.
Nick I can't thank you enough for what you do and how much insight you share with public in a language most can understand despite nuances in science esp in regards to cardiac risks. I heard too many videos on cardiac risks from Carnivor groups who minimize risks of LDL-C and often times misinterpret the data. You analyse the data in a way people can understand and decide for themselves. Truly can't thank you enough.
Great video! Thank you! Appreciate the unbiased view as opposed to the large number of internet doctors rejecting Dave Feldman's research - because it did not agree with what they had been saying for years that LDL is dangerous. The solutions to bring LDL down are, presumably, equally as dangerous. Looking forward to future studies as well as to the time when we understand the cause of plaque buildup without the association. My favorite analogy is the firefighter analogy where seeing firefighters is associative of fires but not causative. Thanks for the great content!
Nick, Checkout Jim Fixx, author of The Complete Book of Running. He started the Running Craze but died of a heart attack at 52. However, he had significantly outlived his parents. There's a genetic variation in the number of Cholesterol Receptors on human cells. The Fixx family had basically None.
I know his story well
I believe that Jim Fixx smoked 🚬 ..?
Heart failure can be congenital, it is not always atherosclerosis.
I'm a lean mass hyper-responder, on Keto, but I'm taking Repatha which keeps my cholesterol numbers in the middle of the healthy range. I plan to stay on Repatha unless and until the LMHR study eventually shows that it's important for LMHR people to keep their cholesterol numbers high. As a confounding factor in my case, I have autonomic dysfunction, with the symptom of erratic blood pressure -- often too high and too low in the same day, so I can't take BP meds to lower my highs or the low would go extremely low. I'm eager to learn, with certainty, the mechanisms of action regarding LMHR cholesterol.
Thanks for chiming in!
As always, it's a great video. I love your delivery of information and humor. Need a study on humor and laughter impacts on well-being and human health. Im sure your brilliant mind is coming up with humor all day as you work😅
Not sure about all that, but thank you
I find this question really interesting and i'm excited to see what this study finds. However, the number of low carbers out there who believe they're at a low risk of ASCVD despite having high ApoB or LDL-C is very worrying. This data is not conclusive and at this stage it would violate parsimony to assume high ApoB is not a risk factor within the context of a healthy BMI, high HDL and low Triglycerides. It is possible for many individuals to be low carb or Keto whilst not raising LDLC. Just ensure your total Saturated Fat is within 10% of tota daily calories.
Since reviewing some of your content, I felt satisfied to Subscribe to your Channel.
Love the emphasis on life extension and the many factors that are important like understanding nutrition.
THANK YOU!
you could do a selfie test by getting all your cholesterol numbers, do a no real no calories three or more days fast then retest yourself ( I bet it's much higher after the fast) then trying and explain it in a video without cognitive dissonance since no fat has been consumed. My # when eating lots of carbs stupidly learning to bake bread for a year & eating way too much bread only ( and getting fat!!!) 165#(by 20#) 150t/50 HDL &140 trigs, doctor perfectly fine with that!? now four years later low carb OMAD last October tested and weigh 145# Total 306, HDL 77, Trig 60, doctor sending panic message DYSLIPEDEMIA!! you're dying!!! inside ten years for sure!!! except I'm feeling and looking far better and stronger than last twenty years, daily morning wood no meds. Daily blood pressure 110/70 usually- down from ~ 130/90, insulin 4. I should have signed up for the study as I live five miles from the where the study was done but they would have rejected me cause I'm 69. It's so obviously to me a physiological response to carb restrictions and leanness. Also don't forget all the data out there with two clicks on google you can find it that shows "high" cholesterol=longer life in folks over 60, reverse causality is clown🤡 explanation don't go there.
No control? Why was the control group of n=80 from the Miami Heart Study dataset used in this analyis not a control group?
Please read the pinned comment
the LMHR group isn't actually defined by leanness, that just happens to come with the territory. LMHR is defined by the ranges of (high) HDL, (high) LDL, and (low) Triglycerides
My understanding is leanness is a prerequisite.
@@Physionic Nope its just an observed association that went into the label. I don't believe leanness was a prerequisite for the study cohort either, just x years on keto and with high ldl/hdl and low trigs and the bloodwork to prove it
Great video, thanks. But my reality is Doctor sees LDL over 190, demands I take statin drugs. Statin drugs make me feel bad, raise my blood sugar level and.....I cannot find enough evidence to convince me that lowering my LDL from ~220 to far below 190 does anything at all for my length of life. Physionic means well; but ignores the fact that most Doctors are handing out statins like mint candy. Plus the side effects of statins, like fatigue, are far worse than the 220 LDL because it reduces my exercise. And to be blunt; I think high cholesterol does not causes heart disease. Just the reverse; high cholesterol levels are the body's response to other damage from something else (high sugar levels, high insulin levels, bad diet, no exercise, no sunlight so no Vitamin D, etc.). Then there are claims of lowering cholesterol levels causing senile dementia. Bottom line: statin drugs are going to be proven a huge mistake. These lean mass hyper responders walking around with LDL far over 300 for the NEXT five years with zero plaque growth are just the beginning. Thanks
I was checking some old bloodwork from back when I was 40 or so and eating high carb and low fat and my trigs were over 300 and LDL only 115 or so. No doctor ever said anything. 2 years ago after a few years on low carb i go to the doctor again and my LDL is 140 and trigs under 200 and he's all worried and all. I'm finally down to body fat in the teens and next time I'll go for blood work i'll just laugh at the high LDL. For sicker people I think it's some kind of defense mechanism from the body because some of the recent science i've seen says high LDL risk for CVD drops off the older you get
Hey John, that makes sense. I discuss the science, but that doesn't mean I'm immune to the personal effects. It's difficult to just blanketly state that lowering LDL is important and then hear a story like yours and not try to get into the nuances. Your doctor should be listening to you and how you feel, just as you should listen to them - unfortunately, some doctors aren't great at listening. As for cholesterol causing heart disease - I'd just encourage you to check out my 10 study analysis on the topic, it goes into detail on all of it.
Looking forward to your follow through on these studies
THANK YOU for your valuable attention!
I think there is something important that you might not have considered - and that is are we ALL LMHR - or at least most of us - under the right conditions. To say this is a "small" group might not be correct in the sense that PERHAPS this group reflects how we should all be eating. When I think of the ancestral evolution of homo sapien, the vast majority of our diet was likely meat, fish and some fowl ... and a smattering of berries/tubers, for 100s of thousands of years prior to the onset of agriculture (say 10,000 years ago), which has only been a very small % of our evolutionary time and I suspect evolved because supplies of meat and fish were becoming more limited (likely for lots of reasons). Our ancestors killed mastadons and woolly mammoths and huge deer/elk (lots of evidence of that) as recent as 30,000 years ago and mostly consumed meat ...we have been evolving for a million years, so 10,000 years of agriculture is nothing in the scheme of things. I think agriculture was a stop gap to prevent famine when meat/fish were low. It makes sense because fat provides more joules of energy than carbs do per unit volume ... and nature is, if nothing else, is hugely economical and efficient and would default to the process that would most likely sustain life i.e., use fat as its critical energy source.
I don't speak to ancestral points, because it's not an area I'm educated in. However, I would disagree we are all LMHR.
that's what I think. LMHR is just your average pre younger dryas human. you need muscles to lift heavy megafauna body parts to carry back to cook. and your plant foods were high fiber plant foods unlike today. and you can jog for 20 miles or so for your hunts
@@Physionic I think as the research unfolds, we are going to find that the % of LMHR is higher than we initially thought, but even if it turns out to be only 25-30% of the population that is hugely significant. And, it would further explain the rather tepid response that cholesterol-lowering drugs has in preventing heart disease. Frankly, I would have expected much more from these drugs in preventing CVEs if lowering cholesterol was truly that effective.
Maybe the study should be done over 10-20 years?
The non calcified plaque (soft plaque) is more dangerous. CAC score is not enough
What does cause heart disease...?
SUGAR.
30 seconds in and im like, aiight, good pitch, tell me more!
Always good to see an Physionic upload.
Probably the most neutral and unbiased study ever launched! Bravo to the people taking control.
A thought:
Take 1000 people who are healthy and set their blood sugar to 300 nonstop for five years. Group A
Take 1000 people who are healthy and set their LDL to 300 and their ApoB to 150 for 5 years. Group B.
We already know that every single person in group A has serious damage being done to their body the entire time. We also know that not everyone in group B has progression in heart disease more than they would have if those numbers were lower. There are many real-life examples of this of people doing say carnivore for more than a decade and the lack of progression in this study.
People are claiming LDL and ApoB increase risk in isolation, that's just as associative in practice. High blood sugar is directly causative. Medicine tries to claim this type of causation is the same for both groups. Clearly not.
At the end of the day the most likely contributor to both heart disease and type 2 diabetes when it comes to our diet is the combination of high levels of fat and carbohydrates in the same meals over and over. Humans didn't evolve to eat anything that has equal portions fat and carbs with the exception of breast milks, something designed by nature for growing young bodies.
There is a big difference between a pizza and a plate of sweet potatoes salmon and avocado. But both of these meals have never been able to be consumed the way we consume them except in the last 100 years or less. People in the jungle didn't stockpile their carbohydrates before they got their proteins and fats ready. They ate when it was available. We have never combined these macronutrients in the quantities that we do in all of history until now outside of breast milk.
5 years is not a long time for CVD, we need decades. But also, what do you mean by setting healthy people’s blood sugar to 300? Also, what do you consider meaningfully lower LDL? Is it 130 or 50? What about blood sugar?
@@CharlieFader I have a T2D client whose blood sugar runs average of 226. HIs time in range, with the range being the far too high of 70-180, is 22%. He is not motivated to change his diet as needed.
Nearly 24 hours a day, his body is literally burning away. When you blood sugar stays above 110 for extended periods of time, your body is in hyperglycemia and every moment is burning away tissue. This is a fact for all humans. If someone is running at 400+ blood sugar, the damage is compounded drastically. Above 700 and you risk sudden death.
The same fact in the same way does not apply to all humans with elevated LDL. There are people walking around with 300 LDL or above not getting the same level of heart disease progression or heart disease at all.
If a doctor sees an elevated LDL and first response is prescribe a statin, they are making a false assumption about elevated LDL in the exact same way they are making a true assumption about elevated blood sugars. They are not the same, not everyone with elevated LDL is developing heart disease faster, and not everyone with sky high LDL's is developing heart disease faster. To assume otherwise is ignoring all existing data.
Very morbidly obese friends in my past would say why should I exercise or eat properly if I can just take a statin? The reason is because on Lipitor's website it even mentions "when diet and exercise are not enough" but our world has the shortcut mentality. I'm fighting this mentality especially about lipids and CVD.
@@Sheikdaddy you’re not addressing my questions. Try again.
@@CharlieFader I answered them. By you saying meaningfully lower LDL, you are making the false presumption that all cases of high LDL need to be lowered. You can't just put a single number on LDL for all humans, the same way you can for blood sugar above say 200 to make it clear. It is not a fact that having LDL 200+ accelerates heart disease in all humans in all contexts the same way it is a fact having blood sugar being 200+ harms all humans regardless of context.
We aren't even talking about ApoB either, but same logic applies.
@@Sheikdaddy you just said lower, that’s why I asked for clarification. Lower than 300 could be anything. On the other hand we know what the ideal levels are. You may choose to disagree, but that’s what the data shows.
Cardiac and CT angiograms only detect plaques that restrict the size of the lumen. However, plaques develop and progress inside the walls of the arteries for years before they protrude into the lumen (see ‘Glagov’s Coronary Remodeling Model’). Also, according to one of the original study designers (Dr. Nadolsky, who has a whole thread about this on X), Dave and Nick excluded people with confirmed positive CAC scores at baseline.
Do you have a link to that thread? I did not know this.
A more accurate description would seem to be that the glycocalyx is injured first. How else would the intima be injured? As it (the glycocalyx) breaks down, then you have irritation to the intima. Then you have inflammation under the intima, then remodeling. Then just plug in the effects of metabolic disease in this scenario and it's pretty obvious where things go. Here's a little hint to go further, it's the excess carbohydrates only that cause the poor lipids. Then again, some people still hang on to elevated LDL being a negative, even when NNR shows that its pattern A. You can only move the goalpost so far before it falls off the cliff of obscurity.
@@randomdiyguy1883The arterial wall does not need to be damaged or inflammed for LDL particles to pass through. That's common knowledge for anyone who understands atherosclerosis.
That exclusion is common practice like when anyone with an adverse event in the first 3 months of the original statin trial was excluded from the trial.
I’ve been following Dave and Nicks work very closely and this is the first I’ve heard that they excluded people with positive CAC. Pretty sure that is made up but if you really have evidence of this please provide.
Im reading The Clot Thickens by Dr. Kendrick. Im wondering if you are familiar with it and if his conclusions are accurate/correct? Thanks, great video
Im whipping a dead horse here but systemic inflammation seems to disrupt HDL (types) it seems that you need both elevated LDL and depressed HDL to really develop damage to the glycocalyx precipitating plaque no?
Good analysis. LDL is like the nasty child who does not behave without HDL putting it in its place.
Obviously it’s limited and early science but the goal of Feldman’s study was to show that in his subset of healthy people LDL is a poor predictor of CVD as a single variable and I think they did it pretty well
Oh, I know their aim - it would be cool to see, but I disagree they've done so beyond doubt. I mean, we have such a high burden of proof people seem to need to show LDL is linked to heart disease, but then people cite a single associative study and call it a job well done, case-closed. The hypocrisy is high as a sky scraper. Haha.
Yup, and this isn't the only study to indicate this. LDL might be required for certain CVD, but that doesn't mean it is the root cause, no more than rubber is the root cause of tire punctures, or that removing the rubber makes the ride better. David Diamond goes through some of them here: czcams.com/video/dOzgrhG0xKI/video.html
@@defeqel6537 after watching his videos I think it's more like the body can't absorb the sugar you're feeding it and needs nutrition and creates more LDL as a survival mechanism.
The study result is actually not that surprising. From what we know of LDL - it is the LDL oxidative damages that lead to CVD. Hence, it is less likely that you'll see CVDs in people who are in energy equilibrium - especially young people. One probably would not see such a result in elderly and/or are gaining weight.
@@burby_geek I don't think there is any indication that people with FH have trouble utilizing dietary glucose
Interesting. Thanks for the update. It's very exciting, that we're starting to actually answer these questions now!
I suspect that a diet without carbohydrates changes your metabolism in fundamental ways. Findings that apply under this condition (free of carbohydrates) can provide important input for understanding metabolism - but these findings cannot be applied to a metabolism that functions using a Western diet. I've also been on a ketogenic diet for about a year. I follow a very strict diet consisting exclusively of meat and animal fat. The caloric ratio of fat to protein is 80 to 20. So it is a ketogenic carnivore diet. Although two of the LMHR type parameters apply to me (my HDL increased from under 50 to over 80 and my triglyceride decreased from 160 to under 70), I am not affected by an increase in LDL. My LDL level has even dropped slightly to just over 100. However, I was overweight at the start of this diet and have now reached my normal weight. I'm eagerly awaiting the next blood test to see whether my normal weight now has an impact on my LDL level. According to the LMHR hypothesis, my LDL level should now increase. PS: All other symptoms of metabolic syndrome, such as blood pressure, long-term blood sugar, visceral fat, triglycerides and HDL, have improved significantly and returned to normal - that is very meaningful for me.
It would be great if they could continue the study for the rest of their lives with regular scans. If they never develop any atherosclerosis I would be very surprised.
Budoff says with their high LDL, only one year is needed for follow up after baseline. The authors have said over and over that their hope is that this study will open up dialog and further experiments, it is not a scientific done deal that seems to be the current view in medicine. Congratulations on recognizing being LMHR evolves a triad not just high LDL, many "reviewers" of the results don't even recognize it.
I would love to see more studies on it. It would be really cool to find an exception in the LDL idea of heart disease.
Not just only one year is needed, but one year is standard. But they've said they want to do longer term ones too.
@@Physionicit's crazy that LMHR are the 'exception' when it comes to CVD and LDL.
They should be the norm, it's just that the majority of people are not metabolically healthy today so our perception of normal has been warped.
8:22 isn't an accurate representation of the keto diet. They normally will not have burgers or pizza, those both have more carbs than the allowable amount per day.
That's fair. You're right. I didn't correct it with my illustrator, which is my fault. I wouldn't imply pizza is part of a healthy keto diet. I'll add an amendment to the video. Thank you.
Added a correction - thanks
Association isn't proof FOR something, but lack of association can disprove a previous theory
As someone who eats keto and does not fall into the LMHR group I'm tuned into this also. I'm still not sure that high LDL (which I have but not at LMHR levels) is good, bad or inconsequential for me. My HDL is great along with my triglycerides. I wish the science would catch up with the times. Money , greed and integrity are at stake when it comes to how the current guidelines were made and changing them. I thought in science there is no shame in having a wrong hypothesis but in this instance it seems to be the opposite. I hope they can figure this out sooner than later.
Good grief. There is no debate among cardiovascular disease researchers about LDL cholesterol. It is a REQUIREMENT for Atherosclerosis. Without significant LDL/APOB levels in your blood it is IMPOSSIBLE for plaque to build up in your blood vessels. If it were possible to lower your LDL very low you would never develop Atherosclerosis no matter what. Even if you smoke, are fat, have diabetes, and are chronically inflamed!
Great breakdown and very sensible position. Good on you for sharing the information !
I know a couple of thin long distance runners that had to have heart stents. Diet is most important.
Great content. I would be curious if sugar in the diet was recorded in this study. I doubt it, but it would be good to know.
they were low car or keto eaters therefore less than 30 grams of carbs per day including sugar if any,
@@DGE123 Right, got that. But was the carb intake recorded? I'm curious about how low the carbs sugar went.
I’m new to the channel so may have been done. But Physionic should do a video on the best non I ndusrty study on stains ( or industry funded if it’s that good) showing the positive benefits and results. Explaining and equating for abousolte risk vs relative risk also which can be confusing.
Go into the details of it as studies for the lay person can be hard to understand.
Would be great to have an in depth of both sides.
Great video! All I can say Mr Feldman, follow up your particpants over 30* years then check back. High LDL is a life time exposure risk factor when it comes to plaque build up It can take 30+ years before you may in all liklihood you will end up with a cripppling heart attack or stroke. Given there may be a few genetically blessed that may escape the bullet, that is the exception but not the norm. Also while I agree with you that obesity is an independent risk factor for many major cardiometabolic and cardiovascular issues, you have to be careful. As someone who is lean at 13% body fat and who regularly does cardo and resistance trains and tracks all my calories, macros, I could easily hit all my calories and macros on a all twinkie, high saturated , junk food diet, then if and when my LDL shoots through the roof, I can say hey I am still 13% body fat, so it means nothing.I am nothing more than a lean mass hyper responder, case closed. As long as I continue to exercise, don’t overeat, manage my 13% bf level, it is irrelevant. All my other metabolic blood markers and blood pressure is normal so I am good bro! Then when I get a crippling heart attack or stroke after 30+ years, I may say it’s all bad genetics bro vs my diet given I took really good care of myself!
i've also recently heard about studies from the Nordic countries that higher LDL results in longer lifespans. It might be a risk factor but only because the number comes up high but i've never heard of any real proof that LDL particles turn into plaque.
@@burby_geek at least by itself
@@burby_geek You've never seen the numerous Mendelian randomization studies on this exact subject?
@@burby_geek Population studies in and of themselves are weak in the hierarchy of studies.
@@azdhan RCT's are supposed to be the gold standard but when you have hundreds or thousands of them on a specific subject and many of them say the complete opposite of each other then someone is lying or doing things like selecting participants for the ending they want. Don't do carnivore but was kind of shocked when I looked up studies done around it and none showed anything bad after a year
Blood pressure should be taken care along with coronary calcium score.
In addition eating meat won't kill you.
Quote from Note: "Additionally, the results were largely ‘null’, so this does not provide evidence that the experiment was sensitive to changes in the first place." Very good, critical response (in the video and in the notes below the video). I saw other 'science' channels who seem to just try to get new subscribers and don't mention any critical response (for example Brad Stanfield's video about this study).
'continue working with your doctor' 🙉 are we all patients? I'm 57 and don't 'have' a doctor.
Same with supplements. I read many times 'ask your doctor' but 1. I don't 'have one' and 2, if i had, I'm sure he wouldn't have time for all kind of medical questions.
I am 59 and like you I don't have a doctor besides I would not bother asking a doctor for nutritional advice.
This is really amazing. I think this is how my body operates. I'm getting a calcium scoring test to see if I'm right
that last part prevented me from ordering pizza
I'm sorry
Incredible channel you have... thank you for this!
First of all congratulations on your work. I really enjoy your content, not only for presenting the data but also providing a deeper analysis, opinions from someone with a very good depth of knowledge on the subject, peppered with some humour and a healthy portion of sarcasm. What's there not to like?
I'm slowly going through some of your past work and not too long ago I listened to your analysis on Paul Saladino's assertion on pretty much the same subject. Obviously there's a study with data in this instance but the idea is more or less same here, don't you think?
If anyone wanted to know how Nic conducts himself I would show them this video. He’s not a “follow the science” robot. He’s a “do the science -and keep doing it !” practitioner.
in a society of cargo culters and posers and fakes and metoo’ers, . Nic is in a rare cadre of people who *integrate* new data, not just shoot it down.
Full disclosure, I’m a pretty big skeptic of Pharma-funded studies and have been following Feldman with interest for years. The guy is a *true* pioneer and the type of scientist you almost never hear about in our current era…. I am extremely happy this landed on the Physionic radar and Nic handled it perfectly.
Thanks! Not perfect, but trying to be open minded within the confines of what the data allows.
It could simply be that exercise and leanness are such powerful risk modifiers that the LDL is simply not sufficient to cause atherosclerosis. If so, a meaningful behaviour hierarchy could develop in conjunction with meds to allow patients ultimately choice control. As the authors state, this is just the first step.
Plaque still ended up progressing in the keto group so LDL is still sufficient to cause ASCVD.
No doubt there are ways of mitigating some of the negatives of heart disease even with high LDL, but I wouldn't be quick to assume LDL still wouldn't lead to progression, even if heart disease were slower to form.
What about endurance athletes who carb load, train 20+ hours a week, and still get CVD?
That's a fascinating situation. There's actually several reasons why (heart scarring, damage to the arteries, etc.). I'll cover it in future content.
@@defeqel6537I think blood sheering it’s called. Basically micro damage by the blood 🩸 but I’m not sure if that is the same as blood clumping.
The study is not using a CAC only. As per their website...
"We are seeking to help provide wide spectrum blood panels and cardiovascular testing such as CT Angiogram, Carotid Intima Media Thickness (CIMT), and Coronary Artery Calcium (CAC) score to this phenotype of interest where we likewise confirm no genetic Familial Hypercholesterolemia."
Yes, I said that.
Now study show that high LDL levels Actually, can cause to lower death.
The study was 22 years withs over 170000 participate
I would love to see your comment about this❤ thank you 🙏
What this says to me - is those on plant or say mediterranean diet can benefit too - ie not by taking up your LDL ( no keep that low as possible ) but lose weight - come off simple carbs , and high sugar ( obviously no added sugar ) - the same ultra processed food everyone should cut - and eat lots of nuts etc to increase HDL ( as from a video the other day - maybe there is a reason high HDL reduces cardiac events - ie helps clean up lipids released by LDL not take up ),. So low LDL , high HDL and low triglycerides - obviously hard to have really low carb diet as lots of plant stuff has carbs - but a low blood sugar diet - ie learn how to dress carbs , order of food , soak up blood sugar ( exercise , having some muscles etc )
Keep up your great work! Much appreciated.
I think i will stick to my regular old ordinary omnivorous diet that contains carbohydrates. As someone who's basic biology is within the 'normal' group aka no mutations in these areas I don't see how I would be better off doing something like keto. Nevermind its hard to maintain and stick to. As for CAC scores since those are typically end stage and the damage is done i ignore those because really the damage is being done before you register calcium and your in the too late group.
All great points, Pixel.
if you look at the nutritional value of non-keto carbs like rice or wheat it's essentially zero and you're just eating sugar to fool your body into thinking you've eaten. at least the keto carbs have nutritional value. some of these foods like corn or white rice didn't even exist in their current form until maybe 200 years ago and white rice is still a manufactured food.
We know that LDL is present in plaques and high LDL is associated with higher risk of plaques. But is high LDL necessary AND sufficent for the formation of plaque ?
My hypothesis is that only dysfunctional LDL (and APO B) partiucles tends to accumulate in plaques. The LMHR study could show that a metabolicly high level of undamaged LDL is not causal of plaque formation if there is no other CVD risk factors like HF , T2 diabetes, insuline resistance, smoking, chronic inflamation, oxydative stress...
funny how when we feed our bodies what it evolved to use it suddenly operates better an gets healthier. Its almost like evolution iterates an organism to be the best version of what it can be with whats in its environment.
Physionic; do you have a video explaining the Randal Cycle? Which study proves that LDL ia causetive of CVD, not preponderance of “evidence”?
No. I wrote a lengthy article on the Randle Cycle a long time ago, but I haven't made any videos. I have lengthy videos dissecting the data across many studies on LDL and heart disease - check out the channel.
1:19 - "I love the idea of the public directly funding a study"
**WINK** **WINK**
So I have been following a lower carb diet for a year or two. Not keto but just drastically lower carb than my normal. Higher fat and animal protein. I wouldn’t consider myself lean but I’m not fat either. My cholesterol has went from 174 in 2021 to 291 this year. My ldl was 105 to 198. My triglycerides from 47 to 59. My HDL from 60 to 77. So this is all interesting to me. I’m having additional test ran to follow up on bloodwork.
good luck with your GP... they will probably try to force you on statins.
A ketogenic diet is not just high saturated fat, it is very restricted carbs/glucose. It can also be restricted carb/sugar and high protein such as the carnivore diet.
An issue with scientific studies is they refer to high fat diets and do not consider the carb/sugar content.
If you do not restrict carb/sugar the diet is not ketogenic.
So I take it that he hasn't figured out that LDL is healthy... and only after oxidative damage and damage from carbohydrates does oxLDL uptake free radicals and deliver them throughout arteries to cause oxidative damage.
thanks for taking time to review the study. I appreciate your nuanced videos and you taking a measured approach considering nutritional science remains very dogmatic.
Few points: reading through the literature I feel LDL-C is a risk factor if vascular health is compromised one way or the other. Cholesterol in itself cannot initiate damage to blood vessels. Not many studies have looked into this salient distinction. Oxidization of cholesterol when a person is experiencing high bodily inflammation is a dangerous situation, however, ketogenic diet has showed that if you are in good metabolic health, then LDL-C level doesn't present in itself a risk factor.
Also, can you indicate to me few articles which talk about saturated fat being a risk factor in people who are metabolic healthy and what's the mechanism? Because again long chain fatty acids (breakdown product of saturated fat) in itself don't present a cardiac risk, except some inconsistent thrombotic risk has been associated with them.
Look at the paper, "the complex and important cellular metabolic function of saturated fatty acids". Looking forward to hearing back from you. Ty.
What is annoying to me is the public’s interpretation of this study calling it the death knell of the cholesterol hypothesis of CVD. So far this study is pointing towards the fact that metabolically healthy people can tolerate high cholesterol. For someone that has a propensity towards plaque formation as a result of genetics or lifestyle having high cholesterol is only likely to increase progression of the disease.
Dont blame cholesterol for what the bad lifestyle have done.
Well done. IMO (one of billions) given the depth/breadth of intelligence/complexity of the human body and health (even w/century plus of studies and writings from before then) nuance vs absolute would be a given. Crazy? Much respect for staying open minded and (fairly) patient on controversial or highly debated topics like this. Take time off over the holidays to just enjoy and eat too much. : )
Curious if they measure and track ApoB of all the participants? That seems to have a stronger correlation with cardiovascular risk.
You ve just missed the release a few hours ago of their preliminary data with a matching control group. impressively the keto group have less plaque than the control group who have similar CVD risks except LDL.
Covered in the pinned comment - it isn't a matched control group, on multiple levels.
IIRC the difference in plaque was not statistically significant
Is Feldman's study published yet? If so, where can I find it? Thanks.
I agree, LDL is only one of the indicators, and not the best one at that also, I'd say. I think Triglycerides, ApoB (as you mentioned), the ratio of Triglycerides over HDL, etc., might be more nuanced and accurate.
The public is just getting that eating egg yolks isn't bad for you, so there may be lots of things to be unlearned and learned.
I'm watching this closely. I have celiac so I've eaten lower carb my whole life. I'm also a cyclist, with excellent health metrics. Low triglycerides, good muscle mass, low blood pressure, great a1c, low resting heart rate, high VO2 max, lean muscle mass...
... and high cholesterol.
What is important to analyze is the Lipoprotein particle size. Also when you are on carnivore diet your mineral intake is better. Also K2 and D3 vitamins are important factors to keep the pipes clean…
Particle size is completely irrelevant to CVD, unless you’re at a Carnivore money-making convention.
Not sure what the carnivore diet has to do with anything here, but as for your second point - particle size matters in so much that it contributes to particle number, mostly. Particle number matters far more. I have videos showing the data on that, too, if interested.
@@PhysionicBecause it's a common talking/selling point in that realm that particle count is irrelevant if particle size is mostly large/fluffy.
@@Physionic What do you think about turnover rate? I would hypothesize that LMHR have an increased receptor count as well as dispatch for LDL, so they spend less time individually in circulation.
Either way, I'm hedging my bets on real food, strength training, zone 2, and sprints for health and longevity.
@@Physionic I just saw a video by a doctor yesterday saying how the size matters and it had nice graphs and an explanation how you want to see a specific curve of particle sizes and numbers by each and why
Cholesterol is a rate limiter on protein and branch chain amino acid metabolism, and also rate limits lifespan in high protein diets.
One year without a control is unconvincing. I suspect this will be a big waste of money.
you don't really need a control if the aim is to disprove a theory, in this case the theory that extremely high LDL necessarily causes plaque build up and thus CVD
Not for Dave. He'll be cashing-in big time on the lecture circuit.
1 year is not enough.
@@defeqel6537
YES, it's heart disease risk on a high carb diet. Triglycerides, are raised when the body burns glucose, but when the body is used to using fat as fuel, the triglycerides lower. Using a ratio of cholesterol to triglycerides and hdl, you'd get a better picture of your risks in heart disease. That article you showed, if you look at the participants, they would show high triglycerides ALONG with high cholesterol. I believe it's the triglycerides that shows inflammatory issues happening, which diabetics ALL have high triglycerides..
FWIW I see the issue of ASCVD as a one-two punch, or like a binary explosive.
For atherosclerosis to develop, it _requires_ BOTH the vascular endothelial glycocalyx to be washed out for long periods of time (high blood sugar)
AND oxidized LDL / Small, dense LDL / apoB / other toxins to be present in large quantities in the blood stream. Enter the ultra-processed American diet, with plenty of the requisite seed oils.
thank you.
What were the Lp(a) in these patients?
No idea, yet
It's not people that are the exception it's the conditions they are in ie the way they eat and their energy balance
I would be interested to see what the risk of a ket diet is for those with different ApoE variants. Does Feldman's study account for such genetic traits?
In Feldman's own presentation he answered that. He accounted for it.
"oxidized LDL" may be key in the answer to the cholesterol question
And what oxidizes LDL? CARBS.
@@aurapopescu1875Do you have any links to studies that show this? Genuinely interested
The only place where there's a "question" about cholesterol is on the Internet.
@@profd65and all the studies that show people with high cholesterol live longer.
Great! I've been waiting for a response to this.
No, no, ironic is, if you arguing with epidemiology study with food questionnaire 1x per 2-3 years and then arguing we do not know what this study participants ate :D .
Irony should be the next flavor of LMNT. 😂
If you have high blood pressure, insulin resistance, chronic inflammation and sedentary, high LDL may be an issue, and also may not be.
If the above conditions doesn’t apply then it doesn’t really matter.
Some of the point he wanted addressed have been I think also, the cardiologist running the scans explained that 1 year would be enough between to have an indication
Also they kinda had a
Control group with the Miami heart study, or maybe I’m wrong on that?
Great content!
Great video.