I had a calcium score of 25 after eating a mixed diet all my life. I went to omad and carnivore. I became a LMHR with very high LDL. After 23 months with very high LDL my atherosclerosis did not progress at all much to the amazement of my doctor.
Calcium score increases with statins, it's called statin paradox. Studies suggests it might be the calcium density. The more dense it is the more protective. Calcium is not the major issue. The plaques are. I could imagine a lower availibility of calcium and the acidity of ketones on those diets could prevent calcification. But the actual plaques, meaning the dead immune cells with high oxidative substances and lipids inside (fome cells) reaking havoc inside the artery walls, like a wound already turning black that won't heal are the issue. It is also interesting that people with low calcium in the blood stream seem to get cardiovascular disease more often and those eating a calcium rich diet less. I'm also suprised that your cardiologist was suprised about no progression within one year. Look at studies. It is unlikely. Plaques develop and progress usually very slowly. That's why risk is calculated at minimum for 10 years.
I was supposedly in this group… low carb for years, abs at age 50, amazing trigs and HDL but quite high LDL (240). I believed I had large fluffy particles etc etc. Then I got a Xanthelasma under my eye. An advanced lipid test showed very small LDL particle size and Pattern B. It also showed high lp(a). So, my lipid genetics were horrible. Calcium score was far from zero and poor for my age. Changed to mediterranean diet and added medications. LDL is now 60.
Low carb? How low? And what's your CAC score now (or when you last got it tested)? I'm 58 and mine is 600. Fortunately, I have very low LP(a) but my LDL particles are small and Pattern B also. I'm working on it.
@@michaelhoile1369Would you agree that the jury is still out? What if it turns out that in spite of their apparently unfavorable lipid panel, that they are actually less likely to experience atherosclerosis?
@@JasonActualizationYes, let's ignore a century's worth of strong and reliable evidence that all points to the same causal marker and pin our hopes on 'what if'. SMH
In addition to HDL, triglycerides, and LDL there are a number of additional commonalities that distinguish us LMHR from our counterparts in the general public namely: lack of any metabolic dysfunction (this is true of less than 8% of the adult population), lack of any mental dysfunction such a depression, anxiety, brain fog and such, “we never felt better as a result of low carb diet”, free from all chronic diseases, ideal gut health and function (no flatulence, constipation, diarrhea), good quality sleep, not having to get up during night to pee, no need for prescription or over the counter medications, good and stable energy, we’re able to concentrate on tasks and be successful at work and at play, and there are not falling over with heart issues or strokes. The point I’m making is that obviously we LMHR are outliers in just about every aspect of healthy living. I know that I can lower my high LDL with drugs or with dietary changes but both options come with trade offs that diminish my optimal quality of life.
LMHR is the normal human state when carbs are unavailable, like 10,000 years ago. Other lipid blood work profiles are the result of abnomal carb and sugar intake.
Not it's not. The ldl of hunter gatherers and other animals in nature is less than 70 . A diet that makes your ldl double, triple and even quadruple of this is terrible And carbs were available 10,000 years ago.
But carbs WERE available 10,0000 years ago. Hell, BREAD was available 12,000 years ago or even earlier. Humans have had salivary amylase (only exists to break down carbs faster) since before we were humans. We believe that evolved in the middle Pleistocene era c. 0.8million years ago - 0.13 million years ago. And we don't know what people's lipids looked like back then, could have been terrible for all we know. We do have access to some tribes who still pre-agricultural diets, like the Tsimane. They have almsot no CVD at all. However their diet is largely carbohydrate with some hunted meats and a hell of a lot of fibre. Fibre binds to bile thus reduces the bile salts being reabsorbed by the intestines. So you make more bile salts....out of cholesterol, reducing the amount available for the liver to put into your blood stream. The teeth of early man show carbs in groves and heavy fibre wear. We believe they ate wild fruits, seeds and undomesticated grains. Modern grains have the fibre removed easily. Early grains have tiny kernals and it's really hard to do that even with grinding and winnowing. So to get those tasty carbs you get a LOT of whole grain fibre.
I'm 65 and for 25 years, have been told that my cholesterol is high (about 240 total), driven by an LDL of about 150, HDL of 75, and triglycerides of 50. These are pretty much the values I've had for 25 years. I'm in good shape, BMI of about 24, and eat what I think is a good diet that avoids most processed food and avoids most sugar and starches. I went in for a calcium test and came up with a score of 0 (this was at age 63) and did a particle size test (provider had no idea what it was) -- Despite the high LDL and Apo(b), I was low on small dense LDL (less than 10% of LDL count). Lp(a) is also low, I did a second Calcium test (at age 65) after being told I was again needed a statin and it too came in at 0. I realize I may have some (soft) plaque but assume at my age, I am not at high risk, given low CaC and good ratios based on HDL, trigycerides, etc. The MESA calculator (which accounts for CaC and uses more recent data than the standard ASCVD calculator) has me at about 2-3 % over 10 years vs the standard calculator that has me at 10 percent risk, which I could drop to 8 percent with statins (which is 20 fewer incidents per 1000 people over 10 years). I have a number of friends with similar stories - docs want statins until they see 0 CaC and see the high HDL, low tris that go withhigh LDL.
To play devil's advocate, have you tried testing for soft plaque? I met a guy last week, 10 years older than you, and had the same story roughly. CAC of 0 still to this day but after cardiac issues this year found out he was full of soft plaque that needed remediation. His plaque simply has not calcified. Definitely more rare for an older individual (CAC delivers quite a high rate of false negatives for young people due to lack of calcification) but can still happen to older individuals.
@@Donald-Putin Good point regarding the soft plaque -- could be there, but there are other markers (e.g., low monocyte to HDL ratio, low hs-crp) that suggest little inflammation that would be associated with plaque formation. Of course I could have heart trouble and it could kill me, but I think risk is relatively low (MESA that includes CaC has me at 2 percent risk for ASCVD over 10 years). Maybe I I will havecardiac issues at 75 or 80 but I'm expecting something to affect me by that point - for now, health is excellent. I'm going to keep up with good eating and moderate exercise as my mainstays.
Tbh, guidlines (European) would suggest loweing with lifestyle here and if it does not work, meds. It's not super high (LDL-C above 190) but of course higher then what is ideal. Have you also used a lifetime calculator?
Did you ever have a direct measure of cholesterol? There are studies showing that the typical Friedwald calculation that estimates LDL doesn't estimate well in people with very low triglycerides. In other words, your LDL could be much lower if you weren't getting a direct mesaure of LDL
Nick Norwitz is doing a brilliant job…with his own personal experience driving (but not distorting) his balanced, passionate research. This young man is already pushing the complex science of lipidology forward…for everyone’s future benefit.
As a flexitarian, low saturated fat, high fiber plant predominant guide, I’m fascinated with LMHR. I flexibly, pun intended, lean (no pun intended) towards Simon‘s perspective that it’s unlikely to be a long-term healthy play. But I’m also willing to buy that the risk is mitigated, and there are yet to be elucidated factors protecting against ASCVD…including the potential that Low carb induces vascular endothelium resistance to ultra large LDL particles (just throwing it out there) All that said I think there’s a weakness and simply defining the phenotype without any recognition of change from baseline. In other words, if somebody starts with an LDL of 80, triglycerides of 280 and HDL of 30 couldn’t they still be a lean mass hyper responder if their LDL ends up at 168, triglycerides 82 and HDL 62? I’m not so sure that an absolutist cut off is ultimately going to be the best way to define - but gotta start somewhere and nevertheless, still fascinated
Even if LMHR is a rare thing, it needs to be understood, for the sake of credibility of the advice people receive with regard to lipids. Currently cases like these are often used to discourage people from doing anything about their LDL levels.
I’m very interested in this because I eat a very low carbohydrate diet now. I struggled for years and years eating a mostly plant based diet but experienced gut pain that I tolerated because I believed the diet was ‘healthy’. I ended up with malnutrition, so needed to concentrate on reducing my inflammation..... low carb worked. Do I worry about my blood lipid levels???
The really important question is has and how has our diet changed in the last 100-200 years. The major changes have been increased carbs, seed oil and fructose.... and what is the impact of these on our body? Remember for most of human existence we have been primarily a meat/fish eating.
Total meat consumption is way higher now than 100 years ago. Heart disease was the biggest killer of humans back then, even worse than now. What has changed is the industrialisation of foods and the calories which are also way higher.
@@danfox8819 I didn't actually. Read what I wrote. I said heart DEATHS (as a percentage obviously). And I'm right. Did you even bother to look it up? Heart attack deaths peaked in the 50s/60s and have dropped massively since then. www.cdc.gov/mmwr/preview/mmwrhtml/mm4830a1.htm
@@danfox8819 I didn't say that. I said heart disease DEATHS are higher and they are. Go look it up. the CDC has a graph showing heart deaths as a % of the population for the last 100 years or so and it peaked in the 50s/60s and dropped to a level that is now below that of the 1920s. I looked it up before commenting. You clearly didn't.
I am 38 and have been monitoring advanced lipud panels for 13 years. About five years ago, i got caught up in the low carb craze, and after two years in that state, fit the definition of LMHR. It was brought on by the low carb eating. My trigs remained in the 40s all along, but its really the HDL-C and LDL-C that went crazy with the low carb dieting. Adter seeing my ApoB was 140+ this year which was i believe in the upper 90th percentile, i decided to stop low carb. As discussed, i am not cinvinced the evidence is there that this is a safe long term state. Within three months, my LDL-C and ApoB are reduced by 30% so it was easy to reverse. I have normal ~50 percentile Lp(a).
Normal? In a population where everyone is sedentary, obesity would probably be normal, right? Our "normal" blood values are from a population that gets a significant amount of energy from carbohydrates. We seem to assume, that this "normal" is healthy, as long as the food questionaire is "healthy". We seem to assume, that a healthy diet MUST contain fibre. It must be low in fat, saturated in particular. Not too many proteins, especially of animal sources. Still, if we look at population studies, people from Hong Kong eats the most meat and have the highest life expectancy. People from India eats almost no meat and plenty of plants, and have low life expectancy.
It is niche and he stated the science has not determined whether or what the broader significance might be. He said that in appropriate detail. If your interest is elsewhere then follow your interest.
Simon, the selective pressure is often post-reproduction, so it could persist unimpeded. Also, we do not have an understanding of any balancing selection that could provide a positive selection for LMHR. In environments where carbohydrate intake is consistently low, individuals who can efficiently metabolize fat may have a survival advantage. The LMHR phenotype could represent an adaptation to such conditions, allowing individuals to maintain high levels of physical activity and cognitive function on a high-fat, low-carb diet. The persistence of the Lean Mass Hyper-Responder (LMHR) phenotype could be due to balancing selection where its advantages, such as enhanced fat metabolism, physical endurance, and potential immune benefits, outweigh the long-term cardiovascular risks in specific environments or contexts.
For 5 years I ate a low carbohydrate diet free of saturated fat and cholesterol but it was unpalatable. Olive oil just was not for me even though I have the ApoE4 allele and cholesterol hyperabsorption mutations in my ABCG5/G8 genes. So now I eat a low carbohydrate diet with saturated fat and egg yolks and take a cholesterol lowering medication with it.
Restricting carbs too much isn’t the defacto answer. You are both right. Some humans have better cholesterol clearance than most. Oreo study might address one specific metabolic type. We need to STOP thinking that ALL humans are wired the same! We are not. Blue zone longevity does NOT point to standardized diet! lol. Put 2 different metabolic humans on the same diet and you can 100% get different results. Cancer targets certain hosts vs others, it’s that simple and complex. LMHR’s may indeed have better NATURAL RCT than the majority of us who do not……Now, whether we humans can synthetically enhance RCT definitively…..well, that’s the holy grail in CHD.
the idea that LMHR is rare and therefore mostly irrelevant is plainly false. if the hypothesis here (the lipid-energy model) is correct, then it doesn't just kick in at these extreme levels. those levels are just the clearest place to observe the phenomena. if true, the lipid energy hypothesis undercuts many assumptions of the lipid heart hypothesis.
Perhaps cholesterol alone has much lower impact on cardiovascular health compared to say smoking, diabetes, hypertension and overall obesity. And similarly on cancer. However the lack of fiber in many Keto & most carnivores still has risks with gut flora issues which includes inflammatory conditions and colorectal cancer So yes, I rather prevent my diabetes by eating whole food plant based than Keto. Both do well by avoiding UPF and reducing risk and even reversing diabetes mellitus
Cholesterol is a marker for certain particles and indeed is not considered causal. The particles are (LDL), that transport cholesterol and triglycerides and ApoB is the far superion measurment.
The number of people with this profile (LMHR) is tiny. The vast majority of people are unable to get to their actual BMI, no less than hand wringing over high LDL. Why argue about this? Time will tell whether sky-high LDL is fatal. BTW, what an obscure topic for Nick to crusade about.
@@firstchoicefarm7767 I have watched his video casts. I understand what he is doing. He is trying to get the last 50 years of research identifying high LDL / ApoB as serious markers for ASCVD risk to tell him going Keto is ok for his 'special' condition. People love good news about their bad habits. In Nick's case, he is trying to create the news. So either I am 'naive', or maybe you're just gullible.
@lophiz1945 ok, since you're so smart why don't you help him with his diet? I'm sure you're smarter than all the doctors that tried to keep him out of the hospital.
@@firstchoicefarm7767 Nick's personal situation has nothing to do with a discussion of the relevant research. Anecdotal evidence is not evidence. Nick is making a claim that does not have a body of research evidence behind it. It's all speculation and Simon is indulging Nick's fantasy because he is a nice guy with an open mind. Period.
@lophiz1945 I'm certain that Simon would disagree with you. Simon would be a phony to have Feldman and Norwitz on if he did not feel their research was of value. Again, why don't you tell Nick what he should be eating? Everyone is unique and for you to be critical of a young man fighting to survive says a lot.
Simon, why do you assume this "adaptation" is that of a survival mode of some sort and not an adaptation back to the way human's bodies were designed to operate? How can you possibly say one way or the other?
You know the bias is strong with Nick when he tries to explain how a normal person could have an LDL greater than 140. He gives multiple answers but avoid the mainstream answer, because it contradicts his world view of his love of eating fatty meat. The oreo cookie "study" is disingenuous, because any unhealthy or healthy carb consumed greater than 50 grams in a day will kick you out of your "LMHR" state. Swap the oreo cookies for healthy fruits that exceed 50 grams will do the same thing. Throwing in the statin comparison is insincere because statins operate in a different mechanism, whereas simply adding carbs back to your diet kicks you out of ketosis and your body will revert LDL levels to normal levels. This is an independent mechanism to using statins for lowering LDL and is not a valid comparison, because statins operate the same way whether you're in ketosis or not. LMHR is just a nonsense term made up by carnivore practitioners to sound like they are legitimate, but really, LMHR is just a cult term used by keto cultist to distinguish between people in ketosis who are fat vs thin. Fat keto bros have lower LDL than thin/atheletic keto bros, so the thin keto bros had to justify their extreme LDL levels (because how dare the fatsos have lower LDLs that us fitbros) with a pseudo-scientific bro term, "Lean Mass Hyper-Responders" and that the "science is not settled" whether high LDL is that bad if you worked that hard to be thin and athletic and look good in the mirror.
Just a small correction. Having watched quite a bit of Nick's content I can tell you that he doesn't have a love of fatty meat. His low carb diet was primarily based on fish with added fat coming from olive oil. This is one of the reasons he became interested in the lipid energy model. Conventional wisdom was that low carb diets inceased LDL because of large amounts of saturated fat. However, Nick's LDL skyrocketed despite him making an effort to keep saturated fats low.
We know that neither cholesterol or lipoproteins are causal for atherosclerosis. If they were then we should expect to see atherosclerosis all throughout the body seeing as cholesterol and lipoproteins travel all throughout the body. We don't see this, we only see atherosclerosis in the arteries in predictable locations. Clearly the cause is something else.
Nick Norwitz is hypocritical in my opinion. In a clever way. He adapts his tone and words to the target audience. If all would be for curiosities sake, why is he attacking people on his channel criticysing this model like Dr. Allo and Dr. Dayspring on social media instead of having a discussion. Why reject the original study design by Dr. Nadolsky and swiching to one that we can predict the outcome of? Dr. Nadolsky left then due to ethical concerns. The probability that plaque growth happens within one year is extremly low. Why the use of cherry pcked data from a study that has nothing to do with theirs as a control group instead of a real one that would not be difficult to find? Why publish two papers with data collected before the actual study with a high selection bias, performing post hoc analysis to support the claim that there is no connection between LDL-C and plaque. Nice statistical tricks. Almost all of Norwitz publications center arround the challange of the lipid heart model. And if you read them you will see his bias. He does not hide his opinion. He mentions it in his videos excitingly that their data will challange this model. He is lying here, but very convicingly.
Can you be healthy with low LDL? A question that rarely gets asked because there is no money to be made. No pill exists to raise it to a healthy level.
@@dennisward43 If large pharma cares about the money they made on statins today, they would have already switched all company vehicles to second hand gen 3 Toyota Prius. Do u know gen 3 Prius is super reliable, fuel economical and best of all, if god forbid any bumps occurred, u can get a piece of second hand panel for a super low price. Then big pharma can hand spray the bumper in their company garage. Doing it this way, it would save them at least 500 dollars every 10000 km run.
We have the answer. Mendelian randomization studies on folks who have genetically crazy low ldl-c (20 and lower) show 0 negative effects of low ldl-c. No cognitive issues, super low MACE as well. In other words, getting ApoB and ldl-c as low as possible for the longest is the ticket.
Of course you can! Watch some of Tom Daysprings talks. Infants and toddlers have LDL’s in the teens! Most of the recent research is that lower is better across the board. Many cardiologists are now treating to 50 LDL. Why? Studies show a linear decline in adverse events the lower you go! LDL is only part of the puzzle. LPa, Trigs, APO-b, NON HDL-c, and the biggie…..an NMR ldl particle count as close to 500 as possible. Also factor in low blood pressure and low inflammation markers as they too contribute to CHD risk. Lastly, good sleep and LESS STRESS! Address the above and you live the longest life possible without gene splicing and manipulation which is where we are evolving to…….
@@robertusga Not according to all cause a large scale mortality study. as seen in the BMJ. A Mendelian randomisation study is just another form of observation study which can easily be affected by bias and manipulation. Baseline LDL-C categories of 30-79, 80-99, 100-129, 130-159, 160-189 or ≥190 mg/dL. Main outcome measure All-cause mortality with follow-up starting 365 days after baseline cholesterol measurement. Results 177 860 patients with a mean (SD) age of 61.1 (8.8) years and mean (SD) LDL-C of 119 (31) mg/dL were evaluated over a mean of 6.1 years of follow-up. A U-shaped relationship was observed between the six LDL-C categories and mortality with crude 10-year mortality rates of 19.8%, 14.7%, 11.7%, 10.7%, 10.1% and 14.0%, respectively. Adjusted mortality HRs as compared with the referent group of LDL-C 80-99 mg/dL were: 30-79 mg/dL (HR 1.23, 95% CI 1.17 to 1.30), 100-129 mg/dL (0.87, 0.83-0.91), 130-159 mg/dL (0.88, 0.84-0.93), 160-189 mg/dL (0.91, 0.84-0.98) and ≥190 mg/dL (1.19, 1.06-1.34), respectively. Unlike LDL-C, both T-C/HDL cholesterol (high-density lipoprotein cholesterol) and triglycerides/HDL cholesterol ratios were independently associated with long-term mortality. Conclusions Among primary prevention-type patients aged 50-89 years without diabetes and not on statin therapy, the lowest risk for long-term mortality appears to exist in the wide LDL-C range of 100-189 mg/dL, which is much higher than current recommendations."
after listening to the whole thing, what if nick actually did go on a wfpb diet for 6 months, actually gave it a real shot, wich im sure he dident, and then see how his gut issues are. would that not be a safer appoach then going keto and running a sky high apo b and ldl. if hes honestly interested in getting to the bottom of things, removing himself from the diet wars why not do that experiment instead of this pure pointless attention grab wich was his oreo experiment
Your comment is probably not meant to be insulting or a personal attack, but it's very nieve. Nick has shared why he is on the diet he's on. Doing the oreo experiment and then taking statins were extremely difficult for him.
@@firstchoicefarm7767 nick had terrble gut issues wich only.keto could resolve.sure. if he is acutally interrested in the truth and not just going o the low carb diet gravy train like so many of fellow keto/carnivore youtubers he should do the wfpb experiment.
@cypriano8763 why do think he hasn't? Nick has experimented with many things and has clearly stated that he's researching and trying to understand the LMHR because he's stuck with it as it's the only thing he's found which is working for him. He's suggested that LMHR should really consider their options are he doesn't know if it safe/healthy. It is clear from current data that it's not the instant death sentence many think.
@@firstchoicefarm7767 one has to wonde what he was eating to achieve all these gut issues in thw first place. Its always easy to say you tried a vegan diet while eating chips and mock meats ya know
Why would anyone listen to two dudes that NEVER talk about how the physics of light, water and EMF drive the biology? Their level of understanding of circadian biology is getting a good nights sleep 🤣
@@RaveyDavey once again, refer to my original comment. The comment basically says just in case you don’t have time to read it, why would anyone listen to two guys sit around and talk about bio chemistry? When in fact, they never talk about the things that drive the biochemistry. It’s actually not a part of their vocabulary because they don’t understand physics.the point is, people that don’t understand physics have no business discussing biochemistry because essentially can’t inform on chemistry without the physics. Simon never talks about physics on any of his videos because he simply doesn’t understand it.
I had a calcium score of 25 after eating a mixed diet all my life. I went to omad and carnivore. I became a LMHR with very high LDL. After 23 months with very high LDL my atherosclerosis did not progress at all much to the amazement of my doctor.
Some have even have less coronary calcium score. Dr Ford Brewer. Soft plaque is completely gone
Because only oxidized LDL is atherogenic, not native.
Calcium score increases with statins, it's called statin paradox. Studies suggests it might be the calcium density. The more dense it is the more protective. Calcium is not the major issue. The plaques are. I could imagine a lower availibility of calcium and the acidity of ketones on those diets could prevent calcification. But the actual plaques, meaning the dead immune cells with high oxidative substances and lipids inside (fome cells) reaking havoc inside the artery walls, like a wound already turning black that won't heal are the issue. It is also interesting that people with low calcium in the blood stream seem to get cardiovascular disease more often and those eating a calcium rich diet less.
I'm also suprised that your cardiologist was suprised about no progression within one year. Look at studies. It is unlikely. Plaques develop and progress usually very slowly. That's why risk is calculated at minimum for 10 years.
@@peterwilson1038
Looking forward that you will have lower CAC score in the near future
I was supposedly in this group… low carb for years, abs at age 50, amazing trigs and HDL but quite high LDL (240). I believed I had large fluffy particles etc etc.
Then I got a Xanthelasma under my eye.
An advanced lipid test showed very small LDL particle size and Pattern B.
It also showed high lp(a). So, my lipid genetics were horrible.
Calcium score was far from zero and poor for my age.
Changed to mediterranean diet and added medications. LDL is now 60.
Low carb? How low? And what's your CAC score now (or when you last got it tested)? I'm 58 and mine is 600. Fortunately, I have very low LP(a) but my LDL particles are small and Pattern B also. I'm working on it.
That's very interesting. As an LMHR, I'm extremely pattern A. Everything my doctors have looked at say I'm metabolic healthy except for LDL.
I love Nick Norwtitz - seems like a genuine scientist. Very smart, but questions things and wants to do more research to find the answer.
Seems to me that a bunch of folk with high LDL now just claim to be ‘LMHR’ and dismiss their lipid panel results…
Yep pretty much...and it's a cope for a failed diet 😅😅😅
@@michaelhoile1369Would you agree that the jury is still out? What if it turns out that in spite of their apparently unfavorable lipid panel, that they are actually less likely to experience atherosclerosis?
@@JasonActualizationYes, let's ignore a century's worth of strong and reliable evidence that all points to the same causal marker and pin our hopes on 'what if'. SMH
There's no causal marker, if there is show us this cause and effect data please.
@@megavegan5791 It will be interesting to see how this all unravels. I hope you remain open-minded my friend.
That describes my father in law. Massive near fatal heart attack at 60. Quadruple bypass operation.
So your father-in-law had LDL, low triglycerides, high HDL, was lean and had been on a low carb diet for a number of years?
In addition to HDL, triglycerides, and LDL there are a number of additional commonalities that distinguish us LMHR from our counterparts in the general public namely: lack of any metabolic dysfunction (this is true of less than 8% of the adult population), lack of any mental dysfunction such a depression, anxiety, brain fog and such, “we never felt better as a result of low carb diet”, free from all chronic diseases, ideal gut health and function (no flatulence, constipation, diarrhea), good quality sleep, not having to get up during night to pee, no need for prescription or over the counter medications, good and stable energy, we’re able to concentrate on tasks and be successful at work and at play, and there are not falling over with heart issues or strokes. The point I’m making is that obviously we LMHR are outliers in just about every aspect of healthy living. I know that I can lower my high LDL with drugs or with dietary changes but both options come with trade offs that diminish my optimal quality of life.
you are only 100% fit and disease free. until you are not
LMHR is the normal human state when carbs are unavailable, like 10,000 years ago. Other lipid blood work profiles are the result of abnomal carb and sugar intake.
Agreed. I became a LMHR only since going low carb.
Not it's not.
The ldl of hunter gatherers and other animals in nature is less than 70 .
A diet that makes your ldl double, triple and even quadruple of this is terrible
And carbs were available 10,000 years ago.
But carbs WERE available 10,0000 years ago. Hell, BREAD was available 12,000 years ago or even earlier. Humans have had salivary amylase (only exists to break down carbs faster) since before we were humans. We believe that evolved in the middle Pleistocene era c. 0.8million years ago - 0.13 million years ago.
And we don't know what people's lipids looked like back then, could have been terrible for all we know. We do have access to some tribes who still pre-agricultural diets, like the Tsimane. They have almsot no CVD at all. However their diet is largely carbohydrate with some hunted meats and a hell of a lot of fibre. Fibre binds to bile thus reduces the bile salts being reabsorbed by the intestines. So you make more bile salts....out of cholesterol, reducing the amount available for the liver to put into your blood stream.
The teeth of early man show carbs in groves and heavy fibre wear. We believe they ate wild fruits, seeds and undomesticated grains. Modern grains have the fibre removed easily. Early grains have tiny kernals and it's really hard to do that even with grinding and winnowing. So to get those tasty carbs you get a LOT of whole grain fibre.
the normal human state is ldl of 40 -60 as seen in newborns, children and young adults before they get atherosclerosis
@@shon7507 Caused by sugar, carbs and seed oils which cause high triglycerides.
I'm 65 and for 25 years, have been told that my cholesterol is high (about 240 total), driven by an LDL of about 150, HDL of 75, and triglycerides of 50. These are pretty much the values I've had for 25 years. I'm in good shape, BMI of about 24, and eat what I think is a good diet that avoids most processed food and avoids most sugar and starches.
I went in for a calcium test and came up with a score of 0 (this was at age 63) and did a particle size test (provider had no idea what it was) -- Despite the high LDL and Apo(b), I was low on small dense LDL (less than 10% of LDL count). Lp(a) is also low,
I did a second Calcium test (at age 65) after being told I was again needed a statin and it too came in at 0.
I realize I may have some (soft) plaque but assume at my age, I am not at high risk, given low CaC and good ratios based on HDL, trigycerides, etc. The MESA calculator (which accounts for CaC and uses more recent data than the standard ASCVD calculator) has me at about 2-3 % over 10 years vs the standard calculator that has me at 10 percent risk, which I could drop to 8 percent with statins (which is 20 fewer incidents per 1000 people over 10 years).
I have a number of friends with similar stories - docs want statins until they see 0 CaC and see the high HDL, low tris that go withhigh LDL.
To play devil's advocate, have you tried testing for soft plaque? I met a guy last week, 10 years older than you, and had the same story roughly. CAC of 0 still to this day but after cardiac issues this year found out he was full of soft plaque that needed remediation. His plaque simply has not calcified. Definitely more rare for an older individual (CAC delivers quite a high rate of false negatives for young people due to lack of calcification) but can still happen to older individuals.
@@Donald-Putin Good point regarding the soft plaque -- could be there, but there are other markers (e.g., low monocyte to HDL ratio, low hs-crp) that suggest little inflammation that would be associated with plaque formation. Of course I could have heart trouble and it could kill me, but I think risk is relatively low (MESA that includes CaC has me at 2 percent risk for ASCVD over 10 years).
Maybe I I will havecardiac issues at 75 or 80 but I'm expecting something to affect me by that point - for now, health is excellent. I'm going to keep up with good eating and moderate exercise as my mainstays.
Tbh, guidlines (European) would suggest loweing with lifestyle here and if it does not work, meds. It's not super high (LDL-C above 190) but of course higher then what is ideal. Have you also used a lifetime calculator?
Did you ever have a direct measure of cholesterol? There are studies showing that the typical Friedwald calculation that estimates LDL doesn't estimate well in people with very low triglycerides. In other words, your LDL could be much lower if you weren't getting a direct mesaure of LDL
Nick Norwitz is doing a brilliant job…with his own personal experience driving (but not distorting) his balanced, passionate research. This young man is already pushing the complex science of lipidology forward…for everyone’s future benefit.
He's a buffoon. I'm surprised Simon wasted so much time & effort on this interview.
@@megavegan5791 You have every right to make that ridiculous statement, naturally!
Why call names? It is completely unnecessary and lowers the quality of the discourse.
@@keithbyrd7566 Exactly👍
@@keithbyrd7566It’s not name-calling. It’s a description of who he is as it pertains to nutritional science.
As a flexitarian, low saturated fat, high fiber plant predominant guide, I’m fascinated with LMHR. I flexibly, pun intended, lean (no pun intended) towards Simon‘s perspective that it’s unlikely to be a long-term healthy play. But I’m also willing to buy that the risk is mitigated, and there are yet to be elucidated factors protecting against ASCVD…including the potential that Low carb induces vascular endothelium resistance to ultra large LDL particles (just throwing it out there)
All that said I think there’s a weakness and simply defining the phenotype without any recognition of change from baseline. In other words, if somebody starts with an LDL of 80, triglycerides of 280 and HDL of 30 couldn’t they still be a lean mass hyper responder if their LDL ends up at 168, triglycerides 82 and HDL 62? I’m not so sure that an absolutist cut off is ultimately going to be the best way to define - but gotta start somewhere and nevertheless, still fascinated
Even if LMHR is a rare thing, it needs to be understood, for the sake of credibility of the advice people receive with regard to lipids. Currently cases like these are often used to discourage people from doing anything about their LDL levels.
I’m very interested in this because I eat a very low carbohydrate diet now. I struggled for years and years eating a mostly plant based diet but experienced gut pain that I tolerated because I believed the diet was ‘healthy’. I ended up with malnutrition, so needed to concentrate on reducing my inflammation..... low carb worked. Do I worry about my blood lipid levels???
The really important question is has and how has our diet changed in the last 100-200 years. The major changes have been increased carbs, seed oil and fructose.... and what is the impact of these on our body?
Remember for most of human existence we have been primarily a meat/fish eating.
Along with seed oils and carb intake the biggest change for humans has been our environment of light and non native EMF.
Total meat consumption is way higher now than 100 years ago. Heart disease was the biggest killer of humans back then, even worse than now. What has changed is the industrialisation of foods and the calories which are also way higher.
@@RaveyDavey you actually just said that heart disease was higher 100 years ago than now. 🤣🤣🤣
@@danfox8819 I didn't actually. Read what I wrote. I said heart DEATHS (as a percentage obviously). And I'm right. Did you even bother to look it up? Heart attack deaths peaked in the 50s/60s and have dropped massively since then. www.cdc.gov/mmwr/preview/mmwrhtml/mm4830a1.htm
@@danfox8819 I didn't say that. I said heart disease DEATHS are higher and they are. Go look it up. the CDC has a graph showing heart deaths as a % of the population for the last 100 years or so and it peaked in the 50s/60s and dropped to a level that is now below that of the 1920s. I looked it up before commenting. You clearly didn't.
I am 38 and have been monitoring advanced lipud panels for 13 years. About five years ago, i got caught up in the low carb craze, and after two years in that state, fit the definition of LMHR. It was brought on by the low carb eating. My trigs remained in the 40s all along, but its really the HDL-C and LDL-C that went crazy with the low carb dieting. Adter seeing my ApoB was 140+ this year which was i believe in the upper 90th percentile, i decided to stop low carb. As discussed, i am not cinvinced the evidence is there that this is a safe long term state. Within three months, my LDL-C and ApoB are reduced by 30% so it was easy to reverse. I have normal ~50 percentile Lp(a).
Normal? In a population where everyone is sedentary, obesity would probably be normal, right? Our "normal" blood values are from a population that gets a significant amount of energy from carbohydrates. We seem to assume, that this "normal" is healthy, as long as the food questionaire is "healthy". We seem to assume, that a healthy diet MUST contain fibre. It must be low in fat, saturated in particular. Not too many proteins, especially of animal sources. Still, if we look at population studies, people from Hong Kong eats the most meat and have the highest life expectancy. People from India eats almost no meat and plenty of plants, and have low life expectancy.
I have been in carnivore for 4 years now. Clearly keto is sustainable
yep I'm at 4 years as well and we have people eating this way for multiple decades so it's clearly no issue.
This is such a niche topic and this guy can’t seem to articulate why it’s interesting broadly.
I think it is very interesting but I am already aware of the background information. You might be correct if based just on this clip.
It is niche and he stated the science has not determined whether or what the broader significance might be. He said that in appropriate detail. If your interest is elsewhere then follow your interest.
The Oreo cookie experiment’s surprise factor seems overrated. It’s expected that adding back carbs into a keto diet will bring down LDL.
I think most people would be surprised that Oreos lowered LDL more than statins
@@Jay-it9cgexactly.
@@Jay-it9cgMost people would consider an anecdotal experiment with no control group utter nonsense.
@@PaulB_864 What cuts both ways?
Simon, the selective pressure is often post-reproduction, so it could persist unimpeded. Also, we do not have an understanding of any balancing selection that could provide a positive selection for LMHR. In environments where carbohydrate intake is consistently low, individuals who can efficiently metabolize fat may have a survival advantage. The LMHR phenotype could represent an adaptation to such conditions, allowing individuals to maintain high levels of physical activity and cognitive function on a high-fat, low-carb diet. The persistence of the Lean Mass Hyper-Responder (LMHR) phenotype could be due to balancing selection where its advantages, such as enhanced fat metabolism, physical endurance, and potential immune benefits, outweigh the long-term cardiovascular risks in specific environments or contexts.
For 5 years I ate a low carbohydrate diet free of saturated fat and cholesterol but it was unpalatable.
Olive oil just was not for me even though I have the ApoE4 allele and cholesterol hyperabsorption mutations in my ABCG5/G8 genes.
So now I eat a low carbohydrate diet with saturated fat and egg yolks and take a cholesterol lowering medication with it.
Restricting carbs too much isn’t the defacto answer. You are both right. Some humans have better cholesterol clearance than most. Oreo study might address one specific metabolic type. We need to STOP thinking that ALL humans are wired the same! We are not. Blue zone longevity does NOT point to standardized diet! lol. Put 2 different metabolic humans on the same diet and you can 100% get different results. Cancer targets certain hosts vs others, it’s that simple and complex. LMHR’s may indeed have better NATURAL RCT than the majority of us who do not……Now, whether we humans can synthetically enhance RCT definitively…..well, that’s the holy grail in CHD.
the idea that LMHR is rare and therefore mostly irrelevant is plainly false. if the hypothesis here (the lipid-energy model) is correct, then it doesn't just kick in at these extreme levels. those levels are just the clearest place to observe the phenomena. if true, the lipid energy hypothesis undercuts many assumptions of the lipid heart hypothesis.
Help finance LMHR study to extend to 5 years.
Perhaps cholesterol alone has much lower impact on cardiovascular health compared to say smoking, diabetes, hypertension and overall obesity. And similarly on cancer.
However the lack of fiber in many Keto & most carnivores still has risks with gut flora issues which includes inflammatory conditions and colorectal cancer
So yes, I rather prevent my diabetes by eating whole food plant based than Keto. Both do well by avoiding UPF and reducing risk and even reversing diabetes mellitus
Cholesterol is a marker for certain particles and indeed is not considered causal. The particles are (LDL), that transport cholesterol and triglycerides and ApoB is the far superion measurment.
ApoB best marker or if using standard Lipid profile, non-HDL closest
Be insulin sensitive (Kraft Insulin Assay Test) and be healthy regardless of your APOB/LDL. Test with Prisoners Carnivore vs Vegan
I can produly say i didn't understand anything
It's ok, neither does Nick when it comes to nutritional science.
My girlfriend has been doing a Carnivore diet on very fatty meats and her LDL hasn't moved in a year.
That’s certainly the exception not the rule.
What level is it, and what is her apo B
The number of people with this profile (LMHR) is tiny. The vast majority of people are unable to get to their actual BMI, no less than hand wringing over high LDL.
Why argue about this? Time will tell whether sky-high LDL is fatal.
BTW, what an obscure topic for Nick to crusade about.
Pretty nieve comment. Maybe learn about Nick and understand why he's on the diet he's on.
@@firstchoicefarm7767
I have watched his video casts. I understand what he is doing.
He is trying to get the last 50 years of research identifying high LDL / ApoB as serious markers for ASCVD risk to tell him going Keto is ok for his 'special' condition.
People love good news about their bad habits. In Nick's case, he is trying to create the news. So either I am 'naive', or maybe you're just gullible.
@lophiz1945 ok, since you're so smart why don't you help him with his diet? I'm sure you're smarter than all the doctors that tried to keep him out of the hospital.
@@firstchoicefarm7767
Nick's personal situation has nothing to do with a discussion of the relevant research.
Anecdotal evidence is not evidence. Nick is making a claim that does not have a body of research evidence behind it. It's all speculation and Simon is indulging Nick's fantasy because he is a nice guy with an open mind. Period.
@lophiz1945 I'm certain that Simon would disagree with you. Simon would be a phony to have Feldman and Norwitz on if he did not feel their research was of value. Again, why don't you tell Nick what he should be eating? Everyone is unique and for you to be critical of a young man fighting to survive says a lot.
Long term means what when one is 80 or 90 years old or even 70 years old !
Simon, why do you assume this "adaptation" is that of a survival mode of some sort and not an adaptation back to the way human's bodies were designed to operate? How can you possibly say one way or the other?
You know the bias is strong with Nick when he tries to explain how a normal person could have an LDL greater than 140. He gives multiple answers but avoid the mainstream answer, because it contradicts his world view of his love of eating fatty meat.
The oreo cookie "study" is disingenuous, because any unhealthy or healthy carb consumed greater than 50 grams in a day will kick you out of your "LMHR" state. Swap the oreo cookies for healthy fruits that exceed 50 grams will do the same thing. Throwing in the statin comparison is insincere because statins operate in a different mechanism, whereas simply adding carbs back to your diet kicks you out of ketosis and your body will revert LDL levels to normal levels. This is an independent mechanism to using statins for lowering LDL and is not a valid comparison, because statins operate the same way whether you're in ketosis or not. LMHR is just a nonsense term made up by carnivore practitioners to sound like they are legitimate, but really, LMHR is just a cult term used by keto cultist to distinguish between people in ketosis who are fat vs thin. Fat keto bros have lower LDL than thin/atheletic keto bros, so the thin keto bros had to justify their extreme LDL levels (because how dare the fatsos have lower LDLs that us fitbros) with a pseudo-scientific bro term, "Lean Mass Hyper-Responders" and that the "science is not settled" whether high LDL is that bad if you worked that hard to be thin and athletic and look good in the mirror.
Just a small correction. Having watched quite a bit of Nick's content I can tell you that he doesn't have a love of fatty meat. His low carb diet was primarily based on fish with added fat coming from olive oil. This is one of the reasons he became interested in the lipid energy model. Conventional wisdom was that low carb diets inceased LDL because of large amounts of saturated fat. However, Nick's LDL skyrocketed despite him making an effort to keep saturated fats low.
Hmm so basically nobody knows.
We know that neither cholesterol or lipoproteins are causal for atherosclerosis. If they were then we should expect to see atherosclerosis all throughout the body seeing as cholesterol and lipoproteins travel all throughout the body. We don't see this, we only see atherosclerosis in the arteries in predictable locations. Clearly the cause is something else.
Nick Norwitz is hypocritical in my opinion. In a clever way. He adapts his tone and words to the target audience. If all would be for curiosities sake, why is he attacking people on his channel criticysing this model like Dr. Allo and Dr. Dayspring on social media instead of having a discussion.
Why reject the original study design by Dr. Nadolsky and swiching to one that we can predict the outcome of? Dr. Nadolsky left then due to ethical concerns. The probability that plaque growth happens within one year is extremly low. Why the use of cherry pcked data from a study that has nothing to do with theirs as a control group instead of a real one that would not be difficult to find?
Why publish two papers with data collected before the actual study with a high selection bias, performing post hoc analysis to support the claim that there is no connection between LDL-C and plaque.
Nice statistical tricks.
Almost all of Norwitz publications center arround the challange of the lipid heart model. And if you read them you will see his bias. He does not hide his opinion. He mentions it in his videos excitingly that their data will challange this model. He is lying here, but very convicingly.
Can you be healthy with low LDL? A question that rarely gets asked because there is no money to be made. No pill exists to raise it to a healthy level.
@@dennisward43 If large pharma cares about the money they made on statins today, they would have already switched all company vehicles to second hand gen 3 Toyota Prius. Do u know gen 3 Prius is super reliable, fuel economical and best of all, if god forbid any bumps occurred, u can get a piece of second hand panel for a super low price. Then big pharma can hand spray the bumper in their company garage. Doing it this way, it would save them at least 500 dollars every 10000 km run.
We have the answer. Mendelian randomization studies on folks who have genetically crazy low ldl-c (20 and lower) show 0 negative effects of low ldl-c. No cognitive issues, super low MACE as well. In other words, getting ApoB and ldl-c as low as possible for the longest is the ticket.
Of course you can! Watch some of Tom Daysprings talks. Infants and toddlers have LDL’s in the teens! Most of the recent research is that lower is better across the board. Many cardiologists are now treating to 50 LDL. Why? Studies show a linear decline in adverse events the lower you go! LDL is only part of the puzzle. LPa, Trigs, APO-b, NON HDL-c, and the biggie…..an NMR ldl particle count as close to 500 as possible. Also factor in low blood pressure and low inflammation markers as they too contribute to CHD risk. Lastly, good sleep and LESS STRESS! Address the above and you live the longest life possible without gene splicing and manipulation which is where we are evolving to…….
@@robertusga Not according to all cause a large scale mortality study. as seen in the BMJ. A Mendelian randomisation study is just another form of observation study which can easily be affected by bias and manipulation.
Baseline LDL-C categories of 30-79, 80-99, 100-129, 130-159, 160-189 or ≥190 mg/dL.
Main outcome measure All-cause mortality with follow-up starting 365 days after baseline cholesterol measurement.
Results 177 860 patients with a mean (SD) age of 61.1 (8.8) years and mean (SD) LDL-C of 119 (31) mg/dL were evaluated over a mean of 6.1 years of follow-up. A U-shaped relationship was observed between the six LDL-C categories and mortality with crude 10-year mortality rates of 19.8%, 14.7%, 11.7%, 10.7%, 10.1% and 14.0%, respectively. Adjusted mortality HRs as compared with the referent group of LDL-C 80-99 mg/dL were: 30-79 mg/dL (HR 1.23, 95% CI 1.17 to 1.30), 100-129 mg/dL (0.87, 0.83-0.91), 130-159 mg/dL (0.88, 0.84-0.93), 160-189 mg/dL (0.91, 0.84-0.98) and ≥190 mg/dL (1.19, 1.06-1.34), respectively. Unlike LDL-C, both T-C/HDL cholesterol (high-density lipoprotein cholesterol) and triglycerides/HDL cholesterol ratios were independently associated with long-term mortality.
Conclusions Among primary prevention-type patients aged 50-89 years without diabetes and not on statin therapy, the lowest risk for long-term mortality appears to exist in the wide LDL-C range of 100-189 mg/dL, which is much higher than current recommendations."
@@jiashuliu9067 Of course they care about money from statins and every drug, they wouldnt last long as a company otherwise.
after listening to the whole thing, what if nick actually did go on a wfpb diet for 6 months, actually gave it a real shot, wich im sure he dident, and then see how his gut issues are. would that not be a safer appoach then going keto and running a sky high apo b and ldl. if hes honestly interested in getting to the bottom of things, removing himself from the diet wars why not do that experiment instead of this pure pointless attention grab wich was his oreo experiment
Your comment is probably not meant to be insulting or a personal attack, but it's very nieve. Nick has shared why he is on the diet he's on. Doing the oreo experiment and then taking statins were extremely difficult for him.
@@firstchoicefarm7767 nick had terrble gut issues wich only.keto could resolve.sure. if he is acutally interrested in the truth and not just going o the low carb diet gravy train like so many of fellow keto/carnivore youtubers he should do the wfpb experiment.
@cypriano8763 why do think he hasn't? Nick has experimented with many things and has clearly stated that he's researching and trying to understand the LMHR because he's stuck with it as it's the only thing he's found which is working for him. He's suggested that LMHR should really consider their options are he doesn't know if it safe/healthy. It is clear from current data that it's not the instant death sentence many think.
@@firstchoicefarm7767 one has to wonde what he was eating to achieve all these gut issues in thw first place. Its always easy to say you tried a vegan diet while eating chips and mock meats ya know
@@cypriano8763 I'm glad you're happy on your high horse. You must be very special.
Read Dark Calories
Why would anyone listen to two dudes that NEVER talk about how the physics of light, water and EMF drive the biology? Their level of understanding of circadian biology is getting a good nights sleep 🤣
Because they're talking about something else.
@@RaveyDavey yes the point is that they never talk about what drives the biology. Seems incomplete, thus lacking in application
@@danfox8819 This talk isn't about that. It's about other important information.
@@RaveyDavey once again, refer to my original comment. The comment basically says just in case you don’t have time to read it, why would anyone listen to two guys sit around and talk about bio chemistry? When in fact, they never talk about the things that drive the biochemistry. It’s actually not a part of their vocabulary because they don’t understand physics.the point is, people that don’t understand physics have no business discussing biochemistry because essentially can’t inform on chemistry without the physics. Simon never talks about physics on any of his videos because he simply doesn’t understand it.
Please stop giving this 🤡 press.