Is the Lipid-Heart Model Dead?
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- Опубликовано: 1 авг 2024
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References (Copy & Paste DOI number into Search Engine)
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Dr. Brewer's Video: • Are We Ever Going To S...
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I wrote a lengthier article in the free Public Community Article Library, if you're interested in hearing some thoughts on the Oreo study, as well. Also, I'm in discussion with one of the lead researchers and pioneers of LMHR, Dave Feldman, about interviewing him for the podcast and getting into the intricacies. I hope it works out, would love to hear his perspective in more detail - I certainly respect his work and his approach. Also, I opened and analyzed most of the studies on screen, you can find those analyses here: ruclips.net/video/1t8rqfG1CMA/видео.html and ruclips.net/video/1m8D5ewuw6g/видео.html
Interviewing Dave Feldman and/or Nick Horowitz would be great!
I fit the profile precisely (well, the original one since it seems to be changing constantly). Then I developed a nasty Xanthelasma under my eye. Calcium score showed higher than average heart disease for my age and advanced lipid tests showed terrible genetics such as very small LDL particle size and high lp(a) lipoprotein…
Hearing your comments on the Oreo study would be great. Another opportunity to get clear unbiased thoughts on what I consider as just another clickbait video to attract hits while disregarding the science. I apologize in advance for my rudeness
Hi Nic - yes, I look forward to our chat. I'm hoping we can maximize the nuance and even point to some of the things that are still unknown / yet to be determined. Cheers!
@@HSLSFirsthaha. Nick norwitz is a PHD that uses the Oreo experiment to make a point. He or Dave Feldman aren't doing this for clicks. They're doing it to change the dogmatic garbage science that doctors and big pharma continue to perpetuate as fact. It will change eventually and maybe then, doctors will stop prescribing statins to everyone that walks in their office with an LDL over 100. Pure insanity!!
"Impartial, truth-seeking person" and "health influencer" don't typically coexist in the same person.
This evidence supports my diet. It is the only correct science.
They both exist in at least one person, and he is a PhD Candidate in Molecular Medicine (Cell Physiology)
Have you actually watched Dr Brewer's videos? He's fairly specific that calcified plaque is stable - so just going by LDL ApoB doesn't tell the whole story. I can be pleasantly plump with elevated levels, and at risk, BUT the risk may be mitigated if the plaque has calcified. It's the INFLAMATION from soft plaque that causes blockages and heart attacks.
@@kathryns560yes but calcified plaque can break off and you def don’t want that …
I love the phrase "integrate, don't ignore."
It's broadly applicable.
I immediately thought of Thomas Dayspring. Am I the only one?
Exactly, 1+1 = 11 (Integrate, don´t ignore ! It´s broadly applicable)
@@robert111k I´ve listen to Dayspring for hours, seems like an honest decent guy and yet he couldn't cite ONE single landmark study even if his life would depend on it. At least he admitted that one has to have diabetes/insulin resistance for the cracks in the artery walls to appear.
I went to see a cardiologist as referred by my GP. The specialist told me LDL caused heart disease and that my diabetes was a much smaller risk to CVD and I should not worry about my diabetes. This person (EDIT (removed name)) sets the Canadian food guidelines. When I noted that the publications said otherwise (as shown in JAMA cardiology), she stated that (without looking at the papers or asking to which ones I was referring), they must have been published in disreputable journals if they disagreed with her opinion. She flat out refused to look at my arteries with CCTA or CAC BUT, she insisted I WOULD die of a heart attack in 5 years. She then went on to say that she would do a CCTA AFTER my heart attack, but not before. This is from one of the "leading" specialists in Canada. I was disgusted by her rude demeanor and unhelpful meeting where she refused to discuss any science or to discuss anything for that matter (why should she bother discussing my health with me, I was just a patient). I was to follow her directions without discussion. So, if the leading researchers in your country refuse to read papers that disagree with their (50 year old) theories, then absolutely, the only way for science to progress is for these dogmatic narcissists to pass and let real scientists take over.
For the record, LDL of 482, CCTA shows zero hard and zero soft plaques. I am a lean mass person who's ldl hyper-responds on a LC ketogenic diet, but as a past diabetic, my trigs do not meet the arbitrary LMHR cut-off.
Also, I have read most if not all the papers you posted. It is BECAUSE I have read all the papers, that it is clear to me, that "cause" of CVD with respect to science and "cause" with respect to epidemiology and nutrition science have different definitions. I agree with others that LDL is in the causal pathway, but in the causal pathway does not cut it for me as a definition of a true cause. While there is a mountain of evidence showing the relation of LDL to heart disease, none of the evidence actually shows a direct causation, simply involvement.
This analogy has been used, but let's see if it applies - trees and LDL. Trees are involved in forest fires. Reducing the number of trees in a forest reduces to amount or size of a forest fire. Removing all the trees from a forest eliminates forest fires. Having a very high density of trees increases the risk of forest fires. Independently, trees are in the causal pathway of forest fires, and if you look at, camp fires, lightning strikes and arsonists, they all contribute to forest fires independently of trees. Looking at the remains of forest fires, we find the remains of trees. If we introduce a drug into the forest that kills half the trees, the size/amount of forest fires decreases. From epidemiology, we have a causal relationship between trees and forest fires, so clearly trees cause forest fires . This is the same argument you get with ldl, except apparently only an idiot who "is wrong" would argue that trees are involved in, but do not in themselves, cause forest fires. From my perspective, trees are REQUIRED but INSUFFICIENT to cause forest fires. Sound familiar? Show me a tree that spontaneously starts a forest fire, and I will change my mind. Show me proof that an LDL particle starts atherosclerosis (on it's own) and I will change my mind. So far, all I see are trees.
Fantastic reply!!!!!
Did you even watch this video? Have you even bothered looking at the evidence? Have you considered that just possibly you aren't a lot smarter and a lot more knowledgeable than your cardiologist? Do you really think that some misleading analogy invalidates a veritable mountain of evidence?
Best comment yet on this video, I like the tree analogy!
Regarding McPhearson, that sounds weird. The lipid clinic (where she is director) is all about managing risk factors, including management of diabetes.
There is probably a reason why she is not foremost known as a clinician...
Very well stated! In any case, the LMHR group are simply trying to open up discussion among all the medical and scientific community to find an answer! Recently, I had a 'discussion' with a medical consultant who wanted to put me on an 80mg statin and I was not at all pleased; but the consultant said "Well you wouldn't tell a fireman how to put out a fire, would you?" Such arrogance leads to mistrust of the medical profession - where an open mind and further research is essential!
From what I have seen and heard about LMHR, the participants involved in the study have made it very clear, that they are searching for answers and not laying down any disagreement with existing research on LDL - rather, they want an open discussion and continuing research for the benefit of everyone!
Great video
I really wish that people would not conflate “ldl level” with “apob”. They keep saying that ldl level is an independent risk factor without clearly stating that this is inclusive of divergence between ldl level and apob. Show me the study that shows high ldl and low to normal apob produces elevated CVD risk. Please.
Optimal ldl is between 50-70. APOB cannot be higher than ldl, so anything above this elevates cvd risk. You cant have high apob if your ldl is this low., Thats your answer
@@Justinegallows Optimal for what? Just for CVD prevention? I am pretty sure most studies find the lowest all cause mortality at LDL levels around 140mg/dl
@Mario-forall
Optimal for CVD prevention. That range is for primary prevention
After you have had an coronary incident , its recommended to keep your ldl under 55. That's what the European Society of Cardiology recommends
@@Mario-forall
Check out
"Optimal low density lipoprotein is 50-70 mg/ldl.
@Mario-forall
Optimal Ldl level for stroke is also 70 or less.
140 for anything is double where you should be
Interestingly, elimating animal products and ultra processed foods gets your ldl to less than 70 for most people.
But people love there meat and suffer from cognitive dissonance when it's brought up
I think that this may be a better way of explaining how ldl's role may be more complicated then we currently believe it is, without that having to disprove the lipid heart hypothesis.
The previous hypothesis was basically a straight line of cause and effect. 1. Eating saturated fat raising ldl. 2. Ldl attaches to the arterial walls. 3. Plague build up. 4. Negative health outcomes.
What we are now seeing is not showing that this can all happen without ldl, and ldl is completely innocent, but instead that ldl may not be one of the early steps, but one of the last in a much lengthier pathway. Meaning you could intervene earlier in the causative pathway or the reverse, there are other steps required for negative health outcomes after ldl, that could also be handled. For example lets say that inflammation, high blood pressure, high blood sugar and many other things all react with ldl to cause plague build up, then if you handled them, there would suddenly be no association between ldl and plague build up.
LDL not "completely innocent" yet
"No amount of experimentation can ever prove me right; a single experiment can prove me wrong." Albert Einstein
A problem with the lipid-hypothesis model is that it is overly simplistic, and it has remained so for far too long. Not enough space here to say what's wrong with it. Kudos to Dave Feldman for a strong experimental focus on LMHR. His work is instructive, but, the focus LMHR from both the critics and the supporters is a distraction. LMHR is a smaller genotype/phenotype subset of the population. The large majority of low carb practitioners are not in that group, either from not being in the BMI category or from not having a hyper-responder effect. I've been low carb for many years, and the switch from SAD resulted in a 5-point decrease in LDL, while jumping in 6 months other biomarkers to optimum or improving APOb, HDL, Trig, Glu, liver enzymes. My doc was scratching his head until I told him about my diet. There are now a lot of N=1 low carb practitioners everywhere (check the comments) who are showing the model is incomplete if not wrong. In the context of the long history of poor or false nutritional science and an old stuck-in-the-mud model, strong science-based criticisms of the model must be made.
it's lack of real data. LDL-C isn't even a real count of LDL and Apo B is just all the LDL's under a single number. the tech to collect real detailed data has existed for a long time and the people who run these studies literally ignore detailed data. dave comes from a CompSci and IT background and there the culture is to collect all the data we can.
So you mean you got your LDL-C and ApoB to optimum on low carb? If yes, what fats did you choose?
@@stellasternchen my last test LDL was a little high. but looking at the last decade of labs as my TG dropped from over 350 to around 120 my LDL increased. going back in around 6 weeks and going to eat a lot of nuts and cheese prior to increase my fat intake. maybe coconut oil in coffee too. and getting my blood drawn the morning after I run a half marathon race. looking to have a >200 LDL to get a referral for a free CCTA so I don't have to pay out of pocket. and try to get a more detailed test other than LDL-C. Lots of labs where I can do it myself but would rather just go through insurance if I can. watch dave's videos and it's probably easy to hack your LDL levels
@@burby_geek I‘ve been on his website. That does not apply to all people. This does apply to LMHR. You won‘t get your LDL up with cheese, as it has a neutral effect on LDL-C and unsaturated fat like nuts lowers it. Exercise lowers it as well. There is no evidence that high LDL-C is not harmful there.
The impression I get is that "the mountain" of data supporting the lipid heart model assumes that because LDL is in the plaque it must be the cause of heat disease. And this is where I find the theory shortsighted. LDL is part of the body's repair response and this may be a reason, or perhaps THE reason it's in the plaque. Also, there are many other factors that seem to be left out of the model. These include the effects of inflammation, insulin resistance and diabetes, all of which are potentially damaging to blood vessels and, as such, causes of heart disease.
That isn't the only argument being made. Also, the model accounts for all those aspects, as well. The studies control for all those factors, called covariates in an analysis. That said, no one is saying diabetes, blood pressure, inflammation don't contribute, because no one is saying LDL/ApoB is the only factor at play.
@@Physionic I'd love to see you do a video on the blood vessel damage and repair system at the molecular level with an eye on how these processes help us to understand heart disease.
@@PhysionicCovarients don't control anything. They smush and mangle the data as an attempt to draw associtions. They do absolutely nothing to control confounding variables.
If you wish to "control" variables with statistical adjustment then you need to create perfect knowledge of the variables affects on the event and wrap that into a magnitude. Can't supply that? Okay. Don't use regressional analysis then.
The way in which you are wording this is that you really want the LDL data to be wrong lol
Such a breath of fresh air.
Great video ! I am obsessed with magnesium, when does that video come out ?
Thank you so much for cutting through the BS and talking about the actual body of evidence! With all the misdirection and hype around this topic it's easy to get confused - and I really don't want to be confused. I have familial hyperlipidemia - my uncles and father died from ASCVD, and I want to be around for my children. I need to get this right! Your channel is a gem and has really helped provide me with clarity.
Thanks, Mark. I wish you all the best against ASCVD. :)
I truly appreciate your clear perspectives. This a rare skill in the social media world.
Don’t get me started. I get so aggravated how people pick and choose data that supports their preconceived notions and conveniently ignores or downplays data that is contrary to their beliefs.
It sort of a sign of the times that people want to kick established ideas in the nuts. I have no problem questioning established models/beliefs but they do deserve some respect and should require a preponderance of evidence to overturn it not one misinterpreted study.
Checking three of the listed studies at random I found two of the three had researchers with funding and fee relationships with statin manufacturers. It would have been better if all studies with such funding relationships were excluded. It would be a much shorter list.
I’m 70. Had high LDL for decades. Refused statin meds countless times. Calcium score 0.
Overall, I'm glad you're well, but an N=1 and using CAC alone (which does not develop in all people, regardless of their atherosclerosis progression) is a poor indicator of risk for a population.
👍
How’s your Triglyceride HDL Ratio ?
Probably good 👍
Some people can tolerate high cholesterol and not develop a lot of plaque. Throw in some smoking and high blood pressure and being overweight and I bet that high cholesterol will end up in your arterial walls.
@@Physionic
I'm 75 and in about the same situation. So now it's N=2.
And I always have low triglycerides and high HDL.
I simply ignore LDL-C as non-significant for me.
Hey I really like and appreciate your channel. I also respect Dr. Ford Brewer. I don’t know if you understand his credentials and experience. He did go overboard on the preliminary results of the LMH trials. It is way to early to make conclusions. I have CVD am 72 and have done well By my labs slowing or stopping my progression by listening to to the valuable advice that Dr Brewer has shown. He is an Epidemiologist and ran the Graduate-prevention program at John Hopkins. Yes he has monetized his channel, but I truly believe he has done that to get the message out. I still take statins ( low dose Crestor), but went low carbs along with exercise to improve my labs. Here’s the deal to me the lipid model of CVD doesn’t make sense. LDL, APOb And LPa to me aren’t causation but the body’s response to arterial wall damage. This damage seems to be from many sources and mostly slow. As almost all of the research shows insulin resistance is involve in 70-80% of the cases. A Scottish doctor theories that the LPa is a first responder to the damage and the APOB particles help the LDL stick tightly to the inflamed area to help repair the damage. All of those lipid particle are necessary and used by the body for many uses. It doesn’t make sense that they are bad. When at higher levels with metabolic disorder they indicate a problem that something is causing the damage. Standard treatment so far is to lower the lipids. Which helps slow the plaguing. But what if we are just slowing the plaguing that is trying to repair the damage? Statins have other benefits besides lowered LDLs,. Some Statins have good anti inflammatory properties and hemolytic properties that may be what is really helping the CVD. Dr Taylor’s diabetes research indicated that a fatty liver and pancreas are what is driving insulin resistance. I know I have that and am working on my HA1C. I am 5’10” and weighted 170 with mid-drift fat. I brought my weight down to 145 and all of my labs are better except HA1C. Dr. Taylor mentions something he call a fat tolerance for each individual. I may still have a fatty liver and pancreas. I attribute that to working fast paced manufacturing job and loving sugar, we had a soda machine at work and would drink 2-4 sodas a day while younger. Sodas are filled with High Fructose corn syrup . Fructose is mainly metabolizes in the liver. We have been inundated with genetically modified corn and high fructose corn syrup in our food, which is leading to a worldwide epidemic of and heart disease and diabetes. I think besides an ultrasound of everyone’s neck who may be at risk we need to scan the liver and pancreas for fat deposits and check insulin resistance. Dr. brewer is correct most doctors have not been trained to diagnose diabetes or insulin resistance. My Dr, never made and comment about my 5.7 HA1C . After listening Dr. Brewer I started checking my fasting glucose levels. That lead me to start losing weight and better exercise. Dr.Brewer claims he finds many under diagnosis patients with diabetes with a HA1C in the 5.6 range and up. No one is checking blood insulin and blood glucose is only an indicator. Back to the lipid model of causation it doesn’t explain sickle cell anemia which causes CVD… the hemoglobin has sharp edges which seem to cause damage to the endothelial cells . Most of the damage seems to start at junctions in the arteries with distended flow. So in sickle cell anemia is high LDL, Apob, LPa, the cause or a symptom of damage and attempt to repair?
The last video of yours I watched was how to reverse coronary artery disease and in that video you showed slides of the arterial walls repairing themselves with muscle growing over the plaque. I that slide tells a story. I was disappointed that some of the info I wanted to get was reserved for your insiders at a high cost. I know you need to support yourself and your , but info is too important to hide for a few at a fee. Please keep up the good work.
*Great video as always!!
Another great video. Thank you.
Thanks, Randall!
Great video, production quality is also higher than my LDL! 😊😂
I believe from my diet & a recent blood panel that I may well be one of the LMHR's. Slim, fit, good diet but every time (across 10 years) I check my LDL/APOB etc I'm told to take statins (which I never have). And yet, it still astonishes me how selective the coverage of this is. How suddenly 'I have no heart disease risk' (a leap I'm not ready to take). Great video Nic. Truth seeking is often the preserve of the 'unbeliever', aka the open-minded & rational.
Why not switch diets? No offense, but that might put you on the safe side without meds.
@@stellasternchen Eat more Oreos!
@@billchristian4918 yeah I read that 😂
@@stellasternchen I have now - so intrigued for a follow up blood panel in April to see the effect.
just eat oreos. that will lower your LDL more and faster than a statin.
The ticker tape of LDL studies while you spoke was *chef's kiss*. "Integrate, don't ignore"--well said.
Excellent as always.
As long as we keep on oxidizing our LDL through the consumption of seed oils and processed foods, yes the diet-heart model is pretty much alive. I’ve still yet to find a solid argument on why something that our body produces since the dawn of time (LDL) is something bad. In fact, if you mess with your LDL levels you’re in a world of trouble.
Exactly.
Ok. Did they measure apoB in the LMHR studies? Could they have high LDL and low apoB?
Another enlightening analysis
I think the question regarding the lmhr prospective study is whether it can disprove causality of ldl/apob and atherosclerosis, not whether they remain good indicators of potential atherosclerosis. Clearly ldl plays a role (the plaques in question are composed of it) and high ldl is a strong indicator, but if it can be shown to not be the causal factor, doctors may start actually requesting coronary scans to track people and seeing if they are actually developing plaque before pushing drugs on them.
ldl is causal to cvd in obese people, there is no doubt about that. lmhr study shows posibility that for very lean people this may not be case. lmhr does not disprove causality of ld in obese people. it just make answer more sofisticated.
@@CipovPeter that’s like saying crowbars cause broken legs because they will if swung at a person’s leg. It’s no longer causal if you need other conditions to be met. Some people would say causal but not sufficient to imply it’s part of a causal pathway but can’t do it by itself. If obesity and ldl are sufficient, what level of obesity? The point remains valid, let’s give people ct angiograms and chronicle their data over time so we can actually determine when drugs should be given instead of just giving them to everyone.
@@CipovPeter Why only in obese people. Not all people with FH are obese and getting plaques early in life.
There are fit athletic people with high
LDL-C getting MI.
How do you think that one study with no control group of one year duration can disprove the causality of LDL- a scientific consensus?
A publicaton in the New England Journal of Medicine July 2023 on Modifiable risk factors for heart disease and all cause mortality with 1.5 million subjects found:
#1 Risk factor Diabetes. #2 Smoking LDL had very low risk factor for Heart disease but not in individuals over 60 Years, and no association in all cause mortality.
If the evidence pans out a vitamin K2 deficiency will replace diabetes for the number 1 risk factor.
LDL-C is a small risk factor. Humidity where you live is a risk factor. There are so many small risk factors out there yet everyone loves to hone in on LDL instead of talking about more important risk factors. Instead LDL is emphasized like it is a primary risk factor. I'm tired of people arguing absolutes. Just because it is a risk factor doesn't make it a worthwhile risk factor.
Thanks 👍🏽 💯🔥
Content quality and way of communicating it is why I refer others to you incl medical/health care prof’ls. Be aware of funding source/industry ties etc but agree don’t ignore. Think critically/Independently. Be a student not a follower. Thx.
The sad fact is everything is confounded by the fact it is impossible to keep track of all the variables in a persons diet. How much highly processed food does a person eat, how much sugar and processed carbs, how much fried food does a person eat, how often does the restaurant you eat at change their frying oil (how oxidized is it). At least I cook most of my food so know pretty much what goes in my body.
many people use apps like macrofactor or myfitnesspal to track nutrition. many have smart watches or some other record of exercise. i don't see why people who run these studies can't buy the data. combine it with labs and that's real data
If ldl to heart link is invalidated, what HDL link is it dead too
Excellent monologue on the responsible use of science
You have two models in philosophy of science - cumulative and revolutionary . I would say that there are moments in science when the only proper way to develop it, is to start a revolution . There was no room for inclusion and cumulation for Copernicus theory. He just revolutionized previous hypothesis - because it was false. And yes, at that time there were many scientists and paper supporting the old theory and scientific consensus - still he ignored it.
thank you!
The LMHR study is not going to put the nail in the coffin of the lipid heart hypothesis. The authors of that study have stated that over and over again. But I'm still very interested in what the findings will be.
One of the problems that "conventional" cardioligists and lipidoligists have with the study is that the subset of people in the study are a very minor part of our society, so in their opinion, it really doesn't matter. I sort of agree with that statement when we are looking at today's modern society. Very few people are lean, active, eating a very low carb diet, and in ketosis most of the time. But...if we were to go back in human evolution, say 15,000 years, or a hundred thousand or a million years, how many of those humans would then meet that criteria. I would guess that it would be very close to 100%. So as far as studying humans go, the study is quite interesting and valid.
I'm 62 years old with a fair bit of atherosclerosis in my arteries from decades of living a typical western life, including consuming the processed food that was part of that life. I don't have enough time left for the world to figure it all out. I can only do what makes sense to me and since it's my life I'm dealing with, and dare say, risking, I'll do just that. If the LMHR study shows that this subset has no increase in heart disease or extremely little in spite of the extremely high LDLc, and we already know the rest of their metabolic health seems to be very good, my goal is to eat and live closer to how they live and what I assume is closer to how my evolutionary forefathers/mothers lived.
So although I don't disagree with all the studies regarding the dangers of high LDLc, I don't think those studies have much to do with extremely healthy people eating an appropriate human diet and living a healthy lifestyle, which is where my mind goes when I read these studies.
Well said. 38 million Americans are diabetic and 98 million are pre-diabetic. There's your "general population". Yes, give them statins and lower their ldl. Living a healthy lifestyle and eating like our evolutionary forefathers/foremothers seems like a better alternative.
Very well said!
Thanks!
I was wrong, I'm most of the way through Malcomb Kendricks latest book as well as listening to Nadir Ali's research; the cholesterol model of heart disease is quite dead.
"Thanks for that Nick, it seemed fairly obvious to me that they were interpreting the new data as more significant than the evidence indicates. I'm still unclear if it was through negligence or a tactic to get more viewers."
Not really. People like Feldman, Norwitz, and others, are simply asking to be included in the discussion. They have identified a specific group of individuals who exhibit an unusual response to a particular type of diet. Interestingly, these individuals, at least for the time being, do not seem to have any particularly worrisome issues stemming from their extremely high LDL-c levels. They are trying to find an explanation for this phenomenon. However, the experts in the field are outright refusing to engage in conversation with them. In my opinion, excluding any bad faith, this attitude is quite close to negligence
@@robert111k I haven't seen that at all
Dr. Spencer Nadolsky helped design the LHMR study and Dr. William Cromwell discussed the study with Dave Feldman on his YT channel for about an hour.
Some influencers are saying that the "establishment is threatened and refusing to engage", but it's simply to generate more views.
@@robert111k I don't think anyone is denying them a fair shake on their hypotheses. Norwitz almost always puts out videos where he tries to deny saturated fats' effects on heart disease risk, paints fructose as the devil, and the list goes on. He even has clickbait videos about oreos being better than statins (does it really get any worse than this?). It's ironic that you say people are ignoring them when they are putting their hands over their ears and pretending there isn't a mountain of evidence to prove that ApoB and saturated fat are significant problems.
I haven’t seen the ‘establishment’ ignoring this data. Dr. Cromwell was very forthcoming (and is an author on the Oreo study, btw!); although, I agree that Mr. Feldman, Dr. Norwitz just want to have a discussion, and they should have it, which is why I’m having Dave on the channel soon.
I was wrong, I'm most of the way through Malcomb Kendricks latest book as well as listening to Nadir Ali's research; the cholesterol model of heart disease is quite dead.@@robert111k
I agree that 130 g carb is not low carb. I had to go below 20/day to get off MDI.
Also, I'm in the majority of low carbers whose LDL and trig's went WAY down when I reversed my diabetes.
That's because you already had diabetes, you had to play a lot of catch-up. 130g of carbs is low because that's only about 500 kcal, which is like 20% of my kcal intake. Normally carbs would make up at least 60% in a non-controlled diet.
@@Leonhart_93 Isn't half the population on the road to type 2? I assume that I am per my age and how a very low carb diet influenced my weight and vision.
@@man_at_the_end_of_time There is no way you will get type 2 with like 500 kcal from carbs, and especially if those aren't straight up sugars.
They are in this situation right now because they consume 300-400+ grams of carbs, which is thousands of calories. Clearly more than 500kcal.
The responses I've heard have talked about the particle size differences within LDL where small LDL particles are the ones to worry about but you don't get that kind of breakdown in normal tests to know what percent of your high LDL is small vs. large.
Nic has a video on LDL particle size and what evidence actually shows.
@@stellasternchen ah cool. I'll check that out. Thanks!
I'm a LMHR phenotype who was glad Dave Feldman came along trying to figure out why keto send some peoples' LDL sky high. All my other labs were great. 12 years later I just started a statin, Ezetimibe, and an anti-platelet. My cardiologist recommends angiogram with possibel stent(s). My unstable angina was 97% better immediately after starting meds. Now I'm concerned about gadolinium contrast agent, arterial tear risk, and stent issues including all cause mortality and stent thrombosis. Does anybody have study titles or info?
I love when this happens. This guy does what every lier on YT does.
First he tries to degrade the integrity of the other side by lying about what they do or say. He claims the low carb side cant agree on what a low carb diet is. First of all that doesnt disprove anything about the study. Secondly, he's conflating two different things as if they were the same. To be in ketosis, you need to restrict to between 20-50 mg of carbs per day. This study isnt trying to achieve ketosis. It just talks about low carb.
What he does next is lie about people in favour of low carb saying they think that these studies are pointless. Completely not true. The entire reason the study in question was done is because they care more than people who just want to push their medications on you.
Next he claims that there is only one or two studies showing low carb is healthy and LDLs isnt as bad as its made out to be. This is a lie.
That point also goes along with what he say at the end, "why didnt they look at this and that study". The very paper he is discussing (the one with the graph). Is a called a meta-analysis. And they are a collection of every study done on the topic. Including the studies for and against the hypothesis. And the results are the accumulation of all that imformation. Its the best form of proof you can have.
Lastly, the reason everyone is agaisnt LDLs as being touted a major risk factor CVD isnt just because the evidence shows that they arent directly associated, but because the evidence showing statins which are use to lower LDLs have been show to either not be effective or to actually be harmful.
The only time high LDL counts can be bad is if you consume too many trans and unsaturated fats. Trans fats especially are very toxic as they cant be broken down by the body and immintate saturated fats. LDLs are what transport fat around your body for use along with cholesterol and other things. Therefore high LDLs and high transfat consumption is a bad thing. But with out trans fats, high LDLs is good because it transports fats for energy in low bmi or low carb people, and transports the building blocks of our body for repair.
Trans fats are the major cause of CDV as they cause inflammation and bind to cholesterol 40 time more readily that saturated fats do. Leading to plaque build up, then heart disfunction.
Good fats which you find in animal products are mostly saturated and polyunstaurated. These fats are what every cell wall in your body is made from.
Trans and unsaturated fats are in high quantities in vegetable and seed oils. Basically every take-away shop uses these because they are cheap. Thats why cooking the exact same thing at home is considered healthier. Its because at home youre more likely to use olive oil or butter to cook in. Or bake rather than deep fry.
The final thing he does is suggest that only he is doing the proper "scientific" research. Which is extremely condesending, blatantly untrue and smells a lot like narcissism.
Bravo! Well said!
The problems with “the science” is with study design, funding of the research and publication bias. I suspect there is more to the story than just high or low LDL that we need an answer to. LDL alone appears to be a much less important risk factor than metabolic disease. Thanks for the video emphasizing the importance of keeping an open, unbiased mind mind to all the research and data.
Compare the risk of cardiovascular disease of somebody with FH with somebody with diabetes. It‘s not, not statistically.
Yes. These studies are paid by..? The ones that want to sell their pills. Most of these studies are not available for independent scientist to have a look at.. Statistics are manipulated.
ONLY favorable outcomes are used and referrers to. Science these days is not science..
Explain the very healthy body builders and athletes eating high meat diets for protein that die from heart attacks before their 50's
I seriously doubt there is any data that supports that comment, and if it does, it doesn’t prove causation. Do you have any sources supporting that claim?
@@StudioRV8
Causation has been proven.
LDL fulfills the criteria of causality:
pubmed.ncbi.nlm.nih.gov/28444290/
Next, in metabolic disease, LDL is always high. It comes with high LDL particle number, just with high triglyceride rich, not cholesterol rich LDL. I do not know if the TG/HDL ratio tells you something, assessing for those particles, when LDL-C is low.
What do I mean? You can have an LDL-C of 70 mg/dl but still at elevated risk. How?
It depends how much particles are used to carry this cholesterol.
If you are metabolically healthy, your LDL particles are mostly large (pattern A) so carry larger amounts of cholesterol. So 70mg/dl of cholesterol means low particle number.
If you are insulin resistant, your LDL particles tend to be small and carry little
cholesterol. (Pattern B) In this case, standard LDL-C values do not asses risk correctly. LDL particles are harmful - not the cholesterol. This is why LDL-C goals are low in diabetics
I believe apo b is a factor and ldl when oxidated
I absolutely agree that we should all be involved in finding the truth as it is. It should not be about having our opinion be correct as a way to feel secure with our biases/choices. A healthy dose of skeptical empiricism is required.
So for the question on the title, is your answer more towards yes or no. I lost you after few minutes there, my brain just exploded.😅😅
Hi Nick. Rather than talk about LDL directly as an independent risk factor, does it make sense to posit that LDL plays a number of roles in human physiology, some of which make it a liability for heart health, but in some instances it plays a positive role (energy trafficking in LMHRs) and may not simultaneously confer risk to heart health in those roles and for those particular people?
As an aside, I myself was an LMHR who reintroduced a modest amount of carbs (less than 130g) because I didn't feel assured about the safety of my high LDL.
What are your qualifications? Would be nice to know if you’re a cardiologist… or not?
I asked my VA doc about checking apo B and he said they don't have this test .. he checked for apo A .. I was less than 10 when less than 50 is desireable .. what does this mean Pls?
Answering this question might shed some light:
What has a higher correlation with CVD, LDL or triglycerides?
I'll answer. Ldl has a 1.3 correlation with CVD whereas triglycerides have a 1.8 correlation with CVD. What's the main cause of high triglycerides? Sugar.
Why is all of the attention on LDL? Statins were the first billion dollar drug. Oh, and there is no drug for triglycerides.
Source:
Studies Relegate LDL to Lesser Role in Atherosclerotic Disease
- Is VLDL cholesterol a better prognosticator?
This has nothing to do with this topic, but I want to know if uronic acid is good or bad as in bamboo fiber
is there a mail in test or some easy way to check apo B in the Bay Area CA ?
Please consider proposing a hypothesis which is consistent with both sets of data. It doesn’t have to be perfect. Any step in the right direction would be helpful.
It seems like there is some threshold that is crossed when we transition between being fat and being lean. My guess is that it is something simple like lipotoxicity exceeding some threshold value. Your guess will probably be better than mine. Please share your guess.
Maybe Nicolas' best video.
This is the influence of postmodernism on medicine. If you think it's bad in this situation, take a look at what's happening in the mental health field in particular the treatment of gender dysphoria.
Postmodernism as practiced by those who are largely unaware of it is to dismiss the preponderance of evidence in favor of those things, which support your argument that the model is broken
Told that a hundred scientists said he was wrong, Einstein replied that if he were wrong, one would be enough.
Science is not a popularity contest. Hypotheses must explain their predictions. So the question remains, does the lipid model explain the LMHR findings (assuming they are robust, which further testing will determine)? If so, it holds; if not, it needs to be revised, at the very least.
Third year of paleo low carb, recent VA blood work; A1C 5.2, HDL 109, LDL 102, triglycerides 54... I'm 68, 30% body fat 🍻 every night.. I'm NOT concerned re heart disease or cancer. 🤞💪🙏
Maybe but have you listened to Paul mason on vegetable oils? And oxidation of ldl?
No, he’s deaf to it
I really appreciate your second looks. And I’m really pissed at people who through around the phrase “I’m a doctor” to gain influence when their training has no more relationship to the subject than their audience. Professionally criminal.
It's absolutely irresponsible for you tubers, even if they are doctors, to tell people that LDL doesn't matter if you are thin. I've seen carnivore dieters say cholesterol doesn't matter at all, even if a person is not thin. Even brag how high their LDL numbers are and how great they feel. 🙄 Maybe the science will change but for now it doesn't look that way. LDL is something to be concerned about.
The question that needs answering is whether high ldl on a low carb diet causes cardiovascular disease
Do you consider the amount of sunshine a person gets and its influence on cholesterol and vitamin D? Do any of the studies that you've read?
✌️ To be on the "safe side" , I will keep LDL below 150.
Some people are arguing that oxidation is a step in the risk pathway for high LDL causing heart problems, and without the excess omega-6 consumption in modern diets it wouldn't be as much of a problem. Are there any studies to address that? I would think most modern test subjects in industrialized countries would have very high omega-6 vs omega-3 ratios compared to our evolutionary environment unless the experiment specifically addresses that.
supposedly the O6 to O3 historical ratio was 4 to 1 and now is 20 to 1. lots of health foods have high Omega-6. seed oils is a new thing and there is evidence of CVD going back thousands of years. nutrition made simple did a recent video on it and I might disagree with his opions most of the time but he made a really good case for pollution and particulate matter being a factor and some simple google searches say it's been known for a while too. but seems to be absent from all the LDL is bad studies I see
I think yes. I think Gil from Nutrition made Simple! addressed this in a video looking at if seed oils are bad. He usually links his studies.
@@burby_geekSeed oils are not a new thing. First seed oils (sesame seed oil) probably were used in ancient Mesopotamia.
@@stellasternchen sesame oil goes back a long way but now it refers to industrial produced oils like canola or cottonseed oil. i've seen the debate about them and CVD predates modern seed oils but there is no way you can make me eat them except in rare instances
@@burby_geek It is the same omega-6 though as in the processed one.
I personally lean towards the LMHR lipid profile with ny bloodwork and can lower it significantly by eating carbs one or more nights before blood draw.. My points: 1. The LMHR influencers I follow do all seem to state that their findings in no way eliminate or disqualify the LDL-bad findings, 2. I don't think the pharma community is going to research this since it would hurt statin sales, therefore the research will be slow in developing, 3. LMHR types generally have significantly lower calculated LDL levels using the Iranian (more accurate in their case) levels than the commonly used Friedewald estimate, 4. LMHR types have outstandingly low Trig/HDL levels and would appreciate your opinion on if this is a more relevant indicator of risk than LDL itself.
All great points, Jim. Agreed. Triglycerides matter, but HDL I need to look into more.
@@Physionic Thanks for the feedback.
I think i'll get into the LMHR. type by this spring and if I can't get a more detailed labs from my dr in march i'll pay to have my own done. lots of places do it other than quest or labcorp too. i've had it done for my kids and some of the detail in those tests is insane. after the last one i spent an hour watching a youtube lecture on occludin or something like that
Over 200 million people take statins. Do the math. @@TimGautier
I don't think you're giving the new questioning of the lipid model fair credit and seem to be very surface level in your discussion. My impression is this. The lipid model is a theoretical causation to explain why there is a correlation between high LDL and heart disease (am I right so far)? People are questioning this now, because there are people being observed with very healthy healthy cardiovascular systems and very high LDL. The impression I was under, was that people were then questioning whether the proposed model of causation is correct, (they are not denying the association). The alternative model I heard made sense to me, which was that in people with CVD there was damage and inflammation within the blood vessels, causing an increase in LDL in order to help repair damage. But the damage could be the cause, not the LDL. Why is this such a bad conversation to have?
"Why is this such a bad conversation to have?" Because ot is not true and has been debunked already. LDL has been proven not only to be associated with atherosclerosis and heart disease, but to also be the cause of it along with other apoB-containing lipoproteins. Inflammation is a potential risk factor for heart disease just like many other things but it is not required for plaque to form, apoB-containing lipoproteins like LDL are the only thing required for plaque to form, if someone has high levels of inflammation but low LDL, they are not at a high risk for heart disease whereas if someone has low levels of inflammation but high LDL, they ARE at increased risk of heart disease. Don't listen to the quacks and pseudoscience-peddlers on the internet trying to spread misinformation about heart disease by saying "it's not about LDL, it's about imflammation" - it's nonsense and these people don't care about you, your health, or what the evidence actually shows, they just have a narrative they're trying to push and products and advice they're trying to sell you. These same people will also tell you that saturated fat is actually good for you (it isn't, and it has been proven time and time again over several decades to increase the risk of atherosclerosis and heart disease) and that you should avoid "seed oils" because they're "toxic" and inflammatory (which again is not true and the evidence actually shows the opposite to be true; that "seed oils" actually REDUCE inflammation and reduce the risk of heart disease as well as all-cause mortality). The internet is rampant with nutrition misinformation and pseudoscience, be very careful what you believe and who you listen to. Many of these people profit off of spreading misinformation about nutrition, don't give these frauds your attention that they crave.
And the medical community has fought Dave Feldman tooth and nail from day one! Both sides need to come together not just one.
3:31 isn’t that misleading to say only 2-3 studies? I thought one was a meta analysis of around 40 studies and to my understanding these were quite high quality studies. I could be completely wrong though!
Also, isn’t all the talk specifically around overall LDL numbers and not ApoB? The studies you referenced all seem to be focused on ApoB specifically.
What study design would the LDL doubters like to see to to show that raised LDL over decades increases risk of ascvd?
Its in the causal pathway, but there is likely an exception with this LMHR group.
We need a lot more long term data on the LMHRs. For example, compared to their lean peers with low LDLc, high HDL, low trigs - what are the caediovascular outcomes? My feeling at the moment is the LMHR is a healthy option but not optimal.
The LMHR study just proves that there can be people genetically resistant to developing plaque just like there are people which will never develop diabetes even while morbidly obese.
So what is considered low carb in the scientific literature? total percentage less than 40% carbohydrates?
Overall they say that below 150 it's low carb wich for me it's nonsense. Technically for the average American sure but that's just a healthier diet instead of going for the effects of specifically low carb.
For me a decent low carb study it's 100 g and below. Ideally 80g.
And for keto studies. At least 50g and below. Ideally 30
well that remains a big issue, and it kinda gets defined by whoever the researcher is and it lands all over the place, much to the chagrin of many. Keto dieters try to keep carbs below 20g/day or around 10% of calories because that's where you need to be more or less to stay in a ketogenic state. Most studies take a much higher number than that, because it's hard to find a significant cohort of people who are restricting carb intake to that degree. This is also true of the meta-analysis Nick mocks for defining low carb as
everyone knows low car is 20 grams to get into ketosis @@ThatFuckinGame
Yeah, it's crazy. Every time I point out in the comments that it's just about one very small specific group of people, I get flamed like crazy. This whole thing (laypeople interpreting it) feels more like religion than science.
Totally agree. I'm completely biased as a classic lmhr. I see all the data and believe it to be true. I just don't understand where the "cause" is though. There's so much I don't or can't understand, its frustrating. I like things to be more straightforward, sleep well: obvious, exercise: obvious don't eat too much: obvious. Living with uncertainty really gets to me. But the reality is that's the only way to live fully. It's ok not to have all the answers ❤
I think a lot of the doubts on LDL theory are from healthier people, myself included. What I like to see is a research on people about 50 years old with CAC=0, and follow up for 10 years to see whether LDL or ApoB levels have any significant effect on CVD events. Mortensen 2023 is in the right direction but with only 4 years of follow up.
I have high cholesterol, high triglycerides, a BMI of 31, a family history of cardiac issues (congenital). And yes, I had a cardiac episode recently and I am trying to recover. Looking at me you would say that cholesterol is predictive. I believe the usual "fat is clogging your arteries/loose weight/don't eat eggs" mantra is too simplicistic, a one-measure-fits-all not good for everyone. In the end my blood pressure is ideal, and I found out yesterday that my vitamin D is very very low.
I think that associating one factor with one disease is nonsense. You may have more or less MIs with raised cholesterol but you may have conversely more or less incidents of cancer, or liver failure or dementia etc etc. The only meaningful metric is how long your healthspan is (unless you specifically want to die from one illness or another, or you're prepared to trade off lifespan for healthspan). The fault that I find with most research is that it includes all ages, when I'd rather see it focus on people aged over 60 (like me) and the difference in the sexes. Your body changes significantly above this age. The nutrients you ingest. Your cellular efficiency etc. Many studies have shown that women with high cholesterol levels live longer (though I don't know if they are healthy in their last 10 years).
Cholesterol as the source of heart disease has been dying a slow death for decades. It's actually due to clotting, per The Clot Thickens described by Dr. Kendrick.😊
I think this is a balanced opinion, thanks.
Here's a small suggestion: using a gesture like raising a pinky finger for the thumbnail could make it resemble Dr. Berg's style. 😅
Thank you, Nic for this reality check. Finally someone provides unbiased comments about those recent videos about the lipid model in LMHR. That is what happens when so-called experts use clickbait videos to disseminate study results that should stay in the scientific realm because most people on this earth do not have the knowledge to review studies. Worst about this is that people will put their life at risk for listening at that narrative by "experts" who insinuate ground-breaking unproven discoveries.
I think that's a great idea !!! Why don't you take one of your favorite studies that support the lipid heart model and open it up for discussion face to face with a Dave Feldman or Dr Brewer or Dr Saladino who's usually open to those kinds of debates. Choose someone with an opposite view to make it a more fruitful discussion instead of having a solo discussion where your views are not being challenged or tested
I'm doing exactly that.
thank you for this video; butter is the one(LDL) which they said was harmful, sugar studies model for up to date cardiologists is more interesting. I know one professor being marginalized due to her stand on this. She also protested sugar load test during pregnancy being risky both mainstream carido and gynea attacked her(even those gygea people clueless as it is endocrinology concern)
Nic, you need to get out of the 1990's and start looking at APO B 100 glycation and oxidation. Don't forget that the APO B protein moiety of the LDL chylomicron is the key that fits in the transporter receptor in hepatic cells. If you keep your blood glucose high, that protein becomes glycated, then oxidized. After that it no longer fits into the receptor and your body has to find other ways to deal with it. Please take a look.
Interesting. Please could you cite that source. Thanks.
Cite your sources, his are linked and most are more recent than the 90s
@@ynotbegreat Look it up.
@@Vincent_Beers Look it up.
Thanks for this video. It seems based on my keto diet and my most recent LDL-C and ApoB results that I'm one of the LMHR people.
I'm taking my statins, and look forward to seeing the LDL-C and ApoB scores in 6 months.
From what I gathered the LMHR studies don't intend to invalidate the existing body of research but explain a missing piece, which according to their model, should exist. How do you study the effect of high LDL on lean people if one needs to saturate their fat stores to a certain amount before the fat cells slow down their triglyceride absorption? Well, you study people with a genetic condition - Familial Hypercholesterolemia (FH) - that causes elevated LDL even when they're lean. Studies on people with FH have established a greater risk of CVD, but the problem there is that the genetic condition does more than just elevate LDL.
These new studies aim to fill in the gap by examining people with elevated LDL who are otherwise healthy, so their contribution is non-trivial, especially if you understand the effects of what type 2 diabetes studies have termed "reaching your personal fat threshold." As a lean person who feels better on a low carb diet and is concerned about elevated LDL, I'm waiting for the results of these studies before I consider experimenting with reduced carb intake again.
I saw some interesting presentations on the subject of lipotoxicity by Dr Nadir Ali. Can you comment on that subject? Just curious on your view.
It's a pitty you didn't analyse the study. I'm really curious on your view about it.
If I got the study right, I don't believe it's an association they find (as you said in the video), since there is a comparisson with another group that was not in a low-carb diet. And they find that there is no difference in artherosclerosis between those 2 groups.
Although the LMHR may be a small group of the population, it's an important part of the low carb community, and this finding is super important for them.
2:21 that critique is non-existent because LMHR people from Dave Feldman's study took way less carbohydrates than 130g/day as they were all in ketosis.
The analysis was not on Dave Feldman's study. It used 4 studies from years ago - ketosis was not measured in all of those studies, although if it had, I agree with you.
@@Physionic fair enough. I was thinking about the latest LMHR study (Feldman/Norwitz/Budoff).
@pawel-goscicki Nic's a smart guy, I'm sure he knows most people don't pay attention and then would conflate the studies therefore driving engagement through conflict.
Really interesting. One of the researchers involved in this Nicholas Norwitz who is a LMHR ate 13 oreo cookies just as proof of concept and demonstrate that the experiment proved better lowering of LDL? So my question is he chooses a highly refined ultraprocessed carb to do this when he can easily chosen a high glycemuc complex carb like a banana or mango to show the same. While most people may be intelligent enough to understand the better choice if you want to run that experiment on themeslves, there will always be those under the false illusion that they too are LMHR, so they can start eating oreos like there is no tomorrow just to teach their doctors a lesson. Then down the line they may end up in worse condition with NAFLD and or T2D and HBP. Then their doctor will be the one to say I told you so!! While I understand and appreciate why he did that as click bait being so starved for a strong mainstream response, the fact that he runs he opts to “sugar coat” this based on his choice of a carb is something I have zero respect for as it sends a message that people may interpret the wrong way and end up doing more harm than good. Also, it’s only the oreo business that will gain the most out of this with their sales. They may use this as evidence to falsely claim that oreos are not as harmful as claimed so people should eat oreos without worry
I think you misunderstand his motives. Mainstream wisdom is that lowering your LDL is good. He is not convinced that it is necessarily a good thing and therefore he demonstrates that you can lower your LDL by eating a less healthy diet. He was being provocative but only to make a valuable point.
@@simonround2439 I totally understand but I think you misunderstood by point. His intent was actually to show that by eating oreos he could lower hos LDL even more thab a popularly prescribed statin. Whether his point or thinking is that high LDL is okay especially for LMHR and only an artificat of being an LMHR, the point is that if just consuming a super high glycemic ultraprocessed food like oreos can lower LDL better than a statin, he would have likely found the same outcome trying that experiment with a highly glycemici whole food like a banana or mango. And nutritionally there is a big diiference bettween and oreo and banana, just as there is a difference between a black bean and jelly bean. So using oreos to drsperately scream out for attention whether he gets it or not is just plain silly. It sends a message that fllys in the face of making healthier food choices regardless of what you believe.
I would LOVE to see a discussion between yourself and Nick Norwitz Phd. Im guessing you have reached out to him as you said you've reached out to Dave Feldman. I think Nick would be better to go into the weeds with you. Both of you as far as I can see are truly interested in science and aren't interested in the drama of being right and wrong that will get you likes. ...Remember "integrate don't ignore" the scientists doing great work to expand our understanding of cholesterol.
Is there any data that shows actual incidents of heart attacks are higher in people with higher LDL or Apob ? Do people with low LDL have less heart attacks? Forget the risk model. What are the actual heart attacks revealing about LDL levels? Im seeing alot saying there is actually zero correlation. High or low, same actual incidents in each group. Anybody?
Yes, there are. I have a 10 study analysis on the topic.
@Physionic
Thanx for the personal response. Im new to the channel. Ill dig in and look for your content on it. So much contradictory info out there to digest.
Nicholas, I get your frustration, but there's more to the story. Low-carb enthusiasts see recent findings as validation. Dave Feldman, once mocked widely for his stance that fit individuals on low-carb diets aren't at increased risk of heart disease, is now seeing vindication. This groundbreaking research reveals significant flaws in the 'solid evidence' you pointed out and is set to redefine the lipid-heart theory. It suggests that the risk is most likely specific to overweight, insulin-resistant subjects, regardless of their diet.
There is not enough long term data to determine healthy and fit people can get away with doing a ketogenic diet long term, and having high LDL or high APOB. It could take decades of doing a carnivore or ketogenic diet for the negative effects on ones cardio score to show. Basically there is a large study going on at the moment, and people have willingly volunteered their their health without even knowing. We shall find out in the coming decades the impactions of so many going and staying on a high fat diet.
@ryankittle3431. It's a misconception to think we need to wait decades to see the effects. Modern Coronary CTA scans are highly sensitive, capable of detecting even minor plaque buildup in arteries within weeks. The study showed participants with LDL-C levels up to 600 for nearly 5 years without any significant damage detected by Coronary CTA scans beyond their initial baseline. This challenges the assumption that a long-term ketogenic or carnivore diet automatically leads to deteriorating cardiovascular health. Essentially, ongoing research is revealing that we might not have to wait decades to understand the impact of high-fat diets on our health.
@@andreinikiforov2671 5 years is not long enough term. I would not rely on a 5 year study to make a life decision. It can take more than 5 years to develop atherosclerosis. I want to see scans in 10 years and 20 years. Show me a large body of people that have been high fat low carb for 20 years, with no atherosclerosis, and to me, that is more sufficient data.
@@andreinikiforov2671 furthermore, the lean mass hyper responder study proves one thing. It's healthy cardiovascular wise, to be lean. To have lower body fat percentage, and higher lean mass percentage. When you look at population density, most people, irregardless of their diet, do not fall under the category of a lean mass hyper responder. Someone that is low body fat, with adequate muscle, and proficient mitochondrial activity can get away with what others in the population cannot get away with.
@@andreinikiforov2671 Yes. And either the lipid-heart model can explain these findings or it can't. If the latter, it's not the whole story, maybe not the story at all, or maybe only the story for overweight people with metabolic syndrome. And why do (did?) the Scots have the highest rates of cvd in Europe when the French have (had?), much less despite a diet higher in saturated fat? How does the lipid model explain that?
Hello Nic, could you do a video on Red Light Therapy? Science seems to back it up, could you give your analysis? Thank you
What is the bias? I wish you were clear about that. What’s the bias that is driving these people to ignore the data? What’s the diet associated with the bias? Be clear about that please.
Spoken like a true scientist 🫡
Smh, a lot of these comment confirm the issue here. People are dogmatic and excessively biased, as well as unfortunately not very bright. Dunning-Kruger effect in full swing.
So I prefer to eat steak all day instead of Twinkies all day which do you prefer?
Never ate twinkies, but prefer to eat steak to a piece of dry, multi grain, obesity producing, pain causing, starvation causing toast.
There is something wrong with your body if one piece of bread causes you pain and weight gain.
The Clot Thickens by Dr Malcolm Kendrick is number one and should be read by everyone plus The Big Fat Surprise by Tina.
First of all, I am a fan of your videos. I do my own personal research in the area and I do watch videos from the Keto & Vegan "gihadists" and as well from neutral channels like yours. However, in this video you missed a critical point. I ll make an analogy. Newton's theory of gravity was getting it 99% right, right? However, Einstein proved that Newton's theory was 100% wrong even though the predictions were 99% right. Irrespective of how many researchers and how many studies have shown the association between LDL and somewhat higher CVD risk the fact will remain that if the current lipid theory cannot explain the LDL hike in LMHR when on low carb and the massive decrease in LDL when these people add more carbs to their diet, like Newton's theory of gravity, our current lipid theory is probably 100% wrong. I probably belong to the LMHR type, BMI less than 20, body fat less than 13%, walk and power walk 20 km per day, 30 mins of resistance training every day, Trigl 0.5 mmol/l, HDL 2.3 mmol/l. I am on an Omnivore true Mediterranean diet (more than 6 table spons of olive oil per day and lots of fatty fishes) and yet if I restrict my whole food carbs a bit I see wild swings in my LDL. Now I do have high Lp(a) and I am on a 5mg Rosuvastatin since I turned 50 even though I have no chronic inflammation (hs-CRP of a new born). I think the LMHR lipid energy model hypothesis provides the best explanation I heard so far for my wild LDL swings, I would love to hear more how Lp(a) interplay on all these, because after starting a statin 70% of my LDL cholesterol is actually Lp(a) 😂