@@jamesalles139 And I'm glad the video didn't "scramble" your brain, nor do you feel I'm the "deviled" for implying eggs are healthy... although I know some extremists who probably want to "poach" me for my positive position on eggs. They can "fry" but they will finds it's "hard" (boiled) to take me (sunny side) down...
@@nicknorwitzPhD Isn't this all very well known already? There is an adaptation but it can't actually compensate for the dietary cholesterol consumed, so indeed eating eggs raises cholesterol in subjects with healthy LDL baseline. The studies (sometimes funded by lobbies) that seem to show no raised levels are done on people with already elevated cholesterol, where they are replacing something else with the eggs. If you gave vegans the eggs, the difference would be much clearer. ""Association between Egg Consumption and Cholesterol Concentration: A Systematic Review and Meta-Analysis of Randomized Controlled Trials": "Based on available evidence, this is the largest meta-analysis in exploring the impact of egg consumption on LDL-c/HDL-c ratio among healthy subjects and reveals that more eggs consumed per day may influence cardiovascular disease risks by increasing LDL-c and the LDL-c/HDL-c ratio. Notably, longer-term high egg-consumption may lead to higher LDL-c/HDL-c ratio and LDL-c. However, RCTs with long tern follow-up are needed to guarantee the association between egg consumption and human health"
@@yadunandanks8781 You missed the point. Eggs, especially when consumed with additional saturated fat (such as butter), cause objectively measurable increases in endothelial dysfunction, arterial inflammation, and LDL-C oxidation for hours after the meal. Feeling great doesn't change that. Some people feel great and have a heart attack in the next moment (heart disease is #1 killer in USA). A lot of people with C also feel great until they're in advanced stages. There are also genetic differences between individuals. So the point is that such personal anecdotes are not only worthless, they are actively harmful because they mislead people who don't know better.
@@xnoreq The review you are referring to (2022 www.ncbi.nlm.nih.gov/pmc/articles/PMC9437993/) investigated any type of high fat meal without fully controlling confounding factors that would be relevant here, such as the quality/type of the fats as in e.g. differing between butter and highly processed foods or the food preparation (overheating fats/oils). total caloric intake and BMI were considered in the statistical analysis, but more direct measures of precursors of metabolic syndrome as well as controlling for carb intake (indicating keto styles/fat adaptation) would be very desirable for deriving conclusions for this context here. The relationship between butter consumption and endothelial function or inflammation remains mixed, which means the effects are context-dependent. Unsurprisingly, complementary risk factors play a big role in determining the associated risks. To put it simply, people who already overeat calories and have some form of metabolic syndrome would do well to reduce their butter consumption, but for generally healthy individuals these concerns do not apply in the same way. This channel here is all about nuance. Of course you are right in saying that anecdotes have limited value for generalizing our understanding. As for another anecdote: I consume about 10 eggs a day and also butter and my bloodwork is not only fine, all my markers are optimal for longevity. That is in the context of a healthy lifestyle, not overeating calories, having a functional lipid metabolism, exercising, etc. Whatever potentially negative/transient effect I get from the fats I consume, it is apparently negligible in this context.
@@xnoreqsaturated fats never cause LDL oxidation mate, in fact provide protection against oxidation. Ox happens when your ldl is composed of USFAs esp PUFAs & if narrowed down more, from data, it's omega 6 LA metabolites, which are found in oxLDL particles.
Interesting. A TH-cam content creater just released a video on, What Happens if you eat 4 eggs a day. The study you referenced wasn't mentioned but I love when folks are on the same wavelength. The creator is Sten Ekberg a former decathelete and now a Chiropractor
I love Sten, but he spends an hour telling you sobering her could in 18 minutes and I don’t have time for that. He talks slow and repeats himself constantly.
@KidAnarky11631 some of us who are not too bright or scientifically or medically trained need that slow deliberate pace. You can always go into the video's settings and increase the speed.
Hi Nic, thank you for bringing this to our attention! I have been following your channel because you are a disruptor and lateral thinker - more of you in this world! I am a clinical physiologist and have been in private medical practice for over 40 years. Yes, way past my sell by date! I know that our clinical colleagues have no clue about basic physiology/biochemistry and how to interrogate published literature. They accept any finding in a peer reviewed study without asking “stupid” questions! “Western” Medicine is in a mess because of my generation of “learned” clinicians. I realise though, we are now in the terminal phase of this cycle because a new generation, like you, are not accepting any garbage dished up by biased scientists, clinicians and big pharma. With the help of all the new technology, of which I cannot keep up, I am of the opinion that the ills of the last 50 odd years will be corrected. Please continue on your present path because you are rocking the boat which is desperately needed. You will knock heads with the professors/deans of my generation but do not flinch - I hold them accountable for the mess our medical science is in. They are the watch dogs but have totally failed us. But the future is bright with people like you and your generational colleagues.
@@nicknorwitzPhD It's all about getting the message out to more people until the truth that science counts for much more than scientific consensus reaches a tipping point. Keep up the good work.
" I am of the opinion that the ills of the last 50 + years will be corrected". You are a sanguine soul! Big food, big pharma, big agri have heavily invented in the food pyramid with the ADA, AHA and the government on board. It is the food pyramid that's killing people. Will they allow all the $$$ investment headed to drains?
Yes, how many people have suffered health problems because of lack of knowledge? I am going back to eating eggs from happy chickens. They are expensive eggs, but the guilt and karma from eating eggs from hens suffering affects me.
@@terriem3922 "The karma from eating eggs affects me". Did you know that more than a few dozen plants eat animals? Please search TH-cam for "plants that eat animals" Some plants even eat tiny monkeys. Did you ask the plant if it knows karma?
Dr Nick, this video was a great introduction to the new-found mechanism of endogenous cholesterol synthesis. I would suggest that it took 5 decades to discover Cholesin and the pathway because someone actually wanted to find out 'why'. For years we have relied on circumstantial evidence instead of actual, repeatable scientific study. I am a family physician of 28 years and wish I knew this stuff on day-one!
Good editing. Great pacing. You got this channel dialed in. You explain complex things so we can better navigate our health journeys. You are not telling me what to do - instead, you add clarity. Perfect.
Great delivery Nick, for those of us not scientifically trained, but seeking answers. Your 'pause, rewind' advice works so well! I feel I now have an understanding of the complexity of the process as well as the simplicity of how our own biology optimises our cholesterol levels. One of your best ever! Bravo, please keep doing what you are doing.
Great video Nic! It's amazing that this new hormone (Cholesin) has just been discovered within the last year or so considering all the research that's been conducted on cholesterol over the last two centuries since its discovery. This could be a Nobel prize in medicine worthy discovery. I remember clipping a newspaper article from about 20 years ago, about a study that came out of Iowa State University if memory serves, where they empirically demonstrated that eating large quantities of eggs didn't raise cholesterol.
Fascinating, my husband is an Osteopathic physician who believes the body tries to find homeostasis. This is why many fads don't work like changing your Ph through diet
Perhaps... but the word "fad" may be tossed around too liberally for my taste... e.g. Keto is often called a fad. I argue it's a metabolic state, separate from Quest Bars ;)
It seems to me that the more we learn, the more questions we need to ask about the basic mechanisms and what changes in lifestyle might help avoid or resolve issues with metabolism, rather than what medication can be developed to address the symptoms. If the money put into pharmaceutical development were invested in basic science, maybe we wouldn't be where we are, in terms of public health. On the flip side, I don't imagine the pharmaceutical industry would be interested in funding research which eliminates the need for their products.
We can dream, can't we? "If the money put into pharmaceutical development were invested in basic science, maybe we wouldn't be where we are, in terms of public health"
If only humans could learn from the hubris of this whole egg episode that it took 60+ years to understand the mechanism of cholesterol homeostasis. Yet very firm guidelines were introduced by the AHA around egg consumption (
Don't blame young Dr. Nick... I'm not responsible for mistakes made 3 decades prior to my birth ;) ... since my mom was burn in 1965, I suppose the "egg" of me was ~3 then... ;)
There is no revalations here. It's been know for a while that body can compensate for dietary cholesterol partly, but it's also known that this mechanism is nowhere near adequate enough to compensate fully for it and even modest amounts of for example eggs raise LDL in people who start at low healthy levels. "Based on available evidence, this is the largest meta-analysis in exploring the impact of egg consumption on LDL-c/HDL-c ratio among healthy subjects and reveals that more eggs consumed per day may influence cardiovascular disease risks by increasing LDL-c and the LDL-c/HDL-c ratio. Notably, longer-term high egg-consumption may lead to higher LDL-c/HDL-c ratio and LDL-c. However, RCTs with long tern follow-up are needed to guarantee the association between egg consumption and human health"
Thank you for this one. The cholesterol debate won't go quietly. My first thought was that using medication to block a natural process is playing with fire, but at the same time, I had to check myself. All medications do that. It can be a life-saving difference.
Dietary cholesterol obviously raises LDL in most people when they start with healthy baseline. If you start at LDL 200, your LDL isn't going to go up due to eggs. That is why eggs lobby funds studies, where the study subjects already have a high LDL to begin with, so no difference is seen. It's cholesterol and saturated fat that as a combination raises LDL. "Based on available evidence, this is the largest meta-analysis in exploring the impact of egg consumption on LDL-c/HDL-c ratio among healthy subjects and reveals that more eggs consumed per day may influence cardiovascular disease risks by increasing LDL-c and the LDL-c/HDL-c ratio. Notably, longer-term high egg-consumption may lead to higher LDL-c/HDL-c ratio and LDL-c. However, RCTs with long tern follow-up are needed to guarantee the association between egg consumption and human health"
@@LawrenceAugust_ I did and the exact gene that affects the mechanism is irrelevant to the bigger picture that has been known for a long time. The claim made in the title is simply false and refuted for example in the meta-analysis of clinical trials I quoted. It's a typical claim made by the eggs lobby.
@@LawrenceAugust_ Again as my previous reply was deleted: I watched it, but the exact mechanism is irrelevant because the claim in the title is simply false.
Nice. Along with demonstrating reverse cholesterol synthesis: TG decrease as HDL increases-or lack of it depending on the individual, fasting shows how cholesterol syntheses increases.
This is already known and why lipidologists use statin and zetia together to get synergy. Doesn’t mean that either drug doesn’t lower cholesterol, just means there is some form of compensatory mechanism, we absorb little cholesterol from our diet and so maybe less effect there. Boston heart labs will show some people are cholesterol absorbers and some are synthesizers due to genetic predisposition.
Thank you for this excellent summary. I’m new to your channel and I completely understood your explanation. Question- if LDL was an issue, could they just give you the hormone in order to down regulate your liver - why would they need to also give you the drug to control absorption ? I am on the carnivore diet and my LDL has skyrocketed- but every other marker is great. My Dr wants me on a statin and so far I’ve been able to say no. Disregarding hyper-responders, now I am wondering if those of us who react to carnivore diets this way may just have a hormone issue or a liver issue. You definitely have me thinking and thanks to your great video I can head down the rabbit hole-of other TH-cam videos better prepared.
Thank you for your inquiry into all these topics and the way you put things across, I understand you a whole lot more than my GP as they are some what conditioned by “ big Pharama” and not science. Don’t get me wrong I don’t believe you just like I don’t believe my GP I just understand you a hell of a lot more than my GP. Sorry for the comparison but the topics you are mentioning are a big help to my health and my standard of living. Thank you once again.
Just yesterday I was talking about how every cell in the body makes cholesterol soooo how can it be "bad" if that is a fact? Thanks Nick ... great info for the "food fight" !
I also think it's awesome that even though we don't really actually know how little we know, our brain (when oriented correctly) can use this limited information to work (or guess) a theory of how the body operates and if correct, it would then tell us more about the secrets of life and the universe. I miss the college days in the lab working on actual EE theories and seeing how cool it was to put them to the test and get a deeper understanding of my field. We are capable of a lot but not everything because that will be our last day.
I appreciate your take on it. My only concern is whether it would be neccessary for most people to get exogenous medication for these ptoblems in the first place. Im guessing the need to speculate on these mechanisms will help those who are severely in need. Also, i love the way your illustrations have improved, now youve got the circles indicating individual parts of the diagram as youre explaining it. I hope Huberman watches your channel, coz this level of detail would of been handy in his latest vid on back pain, and explaining the McGill exercises, which luckily i stumbled across on his other channel, of him physically doing it. Still, your method is far superior, the diagrams and the anonymous guy evolving his skills on this detail is very appreciated, give him a hi five for me 👊😎
"I hope Huberman watches your channel" ... hey me too ;). We've chatted. From all our interactions, he's a really nice guy. I hope we get to interaction more, but I think my academic career will have to mature a bit more...
I did an experiment where I ate a dozen eggs a day for one month in addition to my normal diet (but only a slight caloric surplus). I ate other foods as well, including some carbs, and my cholesterol shot way up. I sort of had a LMHR response. My HDL and LDL went way up, and my triglycerides way down. Could this have been due to the saturated fat content, or a slight increase in calories and weight gain (~+3 pounds), or a LMHR type response? Inhibited Cholesin hormone?
You're probably a lean mass hyper-sterol absorber (LMHSA) meaning you probably over-absorb cholesterol. Take a cholesterol balance blood test to find out. Don't forget to get an ApoE genotype test done too. Nick wants to talk about the cholesterol balance test in his next video since he loves us LMHSAs almost as much as LMHRs. Alas, my sense of humor is an acquired test!
Eating eggs increases your cholesterol that is why your cholesterol shot up. The extent of the increase depends on the rest lf your diet beforehand obviously. Someone on keto would likely not notice that much of a different. But if you were low fat before youd likely see your cholesterol double.
This prompts the question why, if the body is working hard to maintain cholesterol in a certain range, we think it would be a good idea to take drugs designed to push the body out of that range, without fully understanding the mechanisms. Shouldn't we be working on understanding why the body sees that range as optimal before we start tinkering?
It's not very good at maintaining a tight range. I can alter my diet a bit and shift my TC by a hundred points in a few months using nothing but whole foods. Does it matter? Some argue it's the end all be all, others argue it doesn't matter at all.
@matthewtrout1440 I've been on Keto, Atkins, carnivore and the SAD during the past 20+ years, and my LDL has stubbornly maintained the same range. I know you can alter it substantially in the short-term, the Oreo experiment demonstrates that, but at least for me, diet doesn't alter it long-term.
Nick, you love LMHRs because you are one! Yet no love and no scientific interest for us lean mass hyper-sterol responders. lol. No discussion of the ApoE4 gene. I've done the cholesterol balance test. I over-absord beta-sitosterol and campesterol. I over-produce lathosterol. The interpretion is that I have increased intestinal absorption of cholesterol. I have one ApoE4 allele (E/3/E4). I love eggs and still eat one a day. But two eggs a day causes a big uptick in cholesterol. Talk about the cholesterol balance test. Nobody knows about it. Anyone can get a cholesterol balance done without needing an Rx if they know where to find it. I eat super clean and am not a diet idealogue. I'm trying to figure out whether to stop eating nuts and seeds (given the sterol content) and cut the egg out. I don't accept that ApoB can be ignored. Mine is 69. Lowered somewhat by cholestyramine (CSM) which is an old pre-statin Rx used off-label to bind mycotoxins. CSM's action is a bile acid sequestrant and I have sero side-effects from it. Only it's not a cool drug for hip cardiologists. The question is whether to cut back on sterol rich foods and the egg, continue with CSM and take low dose Rosuvastin every second day and low dose zetia every second day (an idea I heard from Tom Dayspring) to balance out absorption and synthesis as you mention. Before any diet idealogue says anything about cholesterol being unimportant because it's all about insulin resistance and inflammation; please ...stop with your religious ideological convictions. Get yourself a CIMT before you speak. It's understood that metabolic health and inflammation are top priority. But we are very far from a place of saying anyone can blow their ApoB higher without risk. I'm trying to encourage this young man to talk about more nuances. Talk about the results of a cholesterol balance test and the ApoE4 gene. We lean-mass hyper-sterol absorbers aren't getting any love. Maybe I'll cut out all eggs, all meat/saturated fats, all plant sterol food, eat a bunch of oreos and watch my cholesterol drop; then become a famous lean mass hyper-sterol absorber ;-)
It looks like Cholestyramine is similar to Ezetimibe. I recently found out that while Ezetimibe can be very effective at lowering cholesterol, it showed no benefit in lowering cardiac events. I suspect I'm a hyper absorber too, a short stint with carnivore and eggs drove my cholesterol way up, but I'm not sure a bile binder is the solution. If there is any benefit to carbohydrates (which can lower cholesterol), it may due to an entirely different pathway and cholesterol is just the red herring.
@@jenjen789 Not yet. I''m about to seek an Rx for 5mg rosuvastin and 10mg zetia but cut them in half and alternate them at this 50% low dose every other day. To flip between restricting synthesis and absorption. Still taking 2x 4mg compounded CSM powder each day (they put sucrose in the branded version, ugh). Then test again.
@@SimonHealthAction It is my understanding after listening to Dayspring’s podcast that one could take a minimum dosage statin and regular dose Zetia every day. My dad does not experience any side effects from 5 mg Rosuvastatin plus 10mg Zetia daily because the dosage of Statins is low enough. APO B is very low. No plaque progression after going low carb and taking this Rosuvastatin and Zetia combo ( now switched to 5mg Rosuvastatin and Fenofibrate combo for better control of lp(a) in addition to APO B)
Very cool. Any time a new hormone is identified it is very cool. Given the subjects that interest you most, I am surprised you aren't planning on specializing in endocrinology.
One problem however: FHC is often about cleaning up 'old' cholesterol , not about how much is created (from food or liver). Where it comes from isn't that relevant.
The liver produces around 1000mg of cholesterol in the absence of cholesin hormone. However this amount of cholesterol is okay for normal functioning. Taking additional cholesterol from diet would supress cholesterol synthesis via cholesin, but remember we still need a daily recommended value for circulating cholesterol levels. The recommended daily intake of cholesterol is around 300mg. Let's say in the absence of any dietary cholesterol, liver produces 1000mg. In the presence of 300mg of dietary cholesterol, liver would drop production to 700mg via the action of cholesin to maintain homeostasis. However exceeding the daily recommended intake value by a huge margin, say 1500mg of cholesterol is detrimental. Assuming the liver produces 0g cholesterol to make up for the absurdly huge amount of dietary cholesterol ( in this case) 1500mg. It's still going to be detrimental for health regardless of increasex cholesin production.
The human body is a Complex Adaptive System and yet….as you describe….supremely intelligent. As Donald Rumsfeld was fond of saying, there are “Unknown, Unknowns” whenever you attempt to intervene in a complex adaptive system whether it is political or biological (like homeostasis) In a nutshell, Rumsfeld wisdom almost ALWAYS means that the end result of screwing around with a complex adaptive system puts your self-interest in a worse position than before. Attempting to pharmacologically intervene in the LDL of an LMHR is case in point. Just too many Unknown Unknowns like the role LDL plays in the immune system.
The perfect example from history is bloodletting. Of course, I would guess that the doctors who performed it at the time did not give their patients (or their survivors) refunds. That pattern will probably repeat if someday it is found that cholesterol lowering drugs have been more harmful than helpful overall.
@@ArcoZakus I predict that PCSK9 inhibitors that DRAMATICALLY reduce cholesterol by irreversibly altering the liver will be shown to be much more harmful than helpful [See already: "The systematic review of RCTs of PCSK9 antibodies challenges their "efficacy breakthrough and the "lower, the better" theory" Current Medical Research and Opinion Vol 34 Issue 10 2018]
@@proper2979 No argument there. Diets do impact how your health emerges. And “emergence” is the hallmark of a CAS. When Ancel Keyes “messed” with the American Diet WHAT emerged was not what everyone involved had hoped for. What emerges from a keto diet is generally good for many sick people who try it. The emergence of sky high LDLin LMHRs in the presence of amazing health seems counter-intuitive for reasons like unknown-unknowns. Drs trying to medicate what could be a natural and beneficial phenomena in an LMHR is pretentious, IMO. We just don’t know.
Nick , your work is awesome. I am very interested in the lipid energy model. However, I want to know the full spectrum. Not just how carbohydrates and fats change it, but how carbohydrates fats, sunlight, hormones, water, and magnetism, change the lipids in the body. I have seen evidence that sunlight increases vitamin D and decreases lipids. This would play a role in different diets. And we know that people live in different latitudes for diurnal sun angle. We know that indigenous tribes typically spend more time in sunlight. And most of the time they have lower lipid levels. Even though that are on a carnivore diet. Why?
@@nicknorwitzPhD Mitochondrial Energy and hormone changes with light. Sunlight and artificial light. Deuterium, water and grounding to the earth providing electron balance for the mitochondria. Have you heard of this?
Umm... you may be getting something from this video that wasn't said... please work with your physician. This is a mechanistic explanation. Also, to be crystal clear, the compensation to Zetia re cholesin/endogenous synthesis is not complete.
@@nicknorwitzPhD fair enough, I will listen again, of course I declined before you made the video so you didn’t influence the decision, she is uncomfortable with my 388 LDL amongst otherwise perfect numbers and sees no need for a CT angiogram. I scored a 16 on my CAC so I am curious, but curiosity was not valid in her opinion. I am in search of other opinions 😃 Thanks for the clarification 👍🏻
I see a multi billion dollar market opening up: cholesin 'enhancer' or something like that, new patents combining it with existing cholesterol medications...
Another great point i can rais when cardiologists try to tell my clients that they need to eat less cholesterol heavy foods in order to decrease harmless LDL levels. It doesnt help that tests for actual oxidated-vLDL´s have to be financed privately in our already heavily taxed state healthcare system in germany. You wouldnt believe just how many Cardiologists dont even know about OX-LDL at all...
on another podcast I believe they stated that the cholesterol we ingest is a larger molecule and can't be used by the body. That seems incorrect based on this video. Can you help me understand if there is a big difference on how you body uses external dietary cholesterol and what our liver makes. ( non-scientist asking and trying to learn)
That's why I won't take cholesterol meds now. When Crestor first came out my Dr. put me on it. It lowered it, then about 3 years later it started climbing again. In my mind that says my level is where my body wants it. Felt better after I quit taking it too. Didn't realize all the side effects it was giving me. Sigh.
The mechanism you describe is interesting. Your title might be better put to say "Dietary cholesterol does not cause serum cholesterol increase". There are numerous studies showing an increase in serum cholesterol from eating eggs. How? Sat fat? A 2020 meta-analysis by Mah-Yun Li et al, "Consumption and Cholesterol Concentration: A Systematic Review and Meta-Analysis of RCT's" shows this.
@@billdublewhopper3064 The meta-analysis I mention above was not based on studies of vegans, so a carnivore/vegan interpretation doesn't really apply there. They simply found that in these various randomized controlled trials, eating eggs raised cholesterol significantly. As I said, a likely mechanism is saturated fat, known to raise serum cholesterol.
Nick, My understanding is cholesterol doesn't cross the blood brain barrier so it would make sense that cholesin doesn't either otherwise the down regulation of cholesterol production would be bad (like some statins apparently do). Do you know anything for sure? Hope you do a video on this aspect. Thanks, Bill
It’s interesting but I’m not a fan of trying to bypass your system. I try to find ways to increase health within the system. If there was a dietary pattern to follow to get results that has more value to me. But it is valuable to understand the mechanisms.
I switched to a Keto then carnivore diet. My cholesterol definitely went up. But the type(s) that went up arent necessarily bad, LDL and HDL, while Trig went DOWN. Then in subsequent testing cholesterol LDL has been declining over time, while HDL went up further, then leveled off. SO... I went from 234lbs 39.5" waist 26%BF to 178lbs 15%bf 32" waist. Whos healthier the lower cholesterol obese me, or the higher (LDL) cholesterol me? I can workout again because autoimmune issues are at bay, and fatty liver and anemia etc are resolved. Did I mention my testosterone almost doubled, my thyroid level increased? EVERY marker across the board in improved unless you count LDL as a negative
One of the things I hear the vegan docs say is that the studies that show animal fat doesn’t raise cholesterol are taking diets they consider high in fat already and add a little more so the raise in cholesterol isn’t statistically significant. If you take some eating plant based low to no fat adding eggs will raise cholesterol. I don’t know what the truth is. What I do know is I ate a proper “healthy “ vegan diet and my physical health slowly declined. Eating high meat carnivore/ketovore has restored my physical health very quickly and I feel the best I have in decades. I feel like a healthy 20 year old at 47.
I believed that babbling BS for DECADES about eggs .. then as I changed my life style (what some call diet) I had the wakeup call that eggs are really, really good for you. Thanks for this ... love the details, i.e. FACTS
Definitely cool, Nic. It poses many more questions. Cholesin works with eggs to inhibit blood cholesterol so can we assume it will work for all dietary cholesterol? And what % of dietary cholesterol is inhibited? 100%? 50%? Is all dietary cholesterol the same? And what other factors - such as weight, stress, lack of sufficient sleep , exercise, genes, etc - may be factors in making blood cholesterol and ldl rise?
"Cholesin works with eggs to inhibit blood cholesterol so can we assume it will work for all dietary cholesterol?" - Yes. Was just using eggs and an example food and for SEO. In terms of %, I think there is near complete compensation, although may differ by individual.
@@nicknorwitzPhD Super interesting, but, your liver maxes out at producing around 1g of cholesterol per day. So if you exceed 1g of cholesterol intake via the diet (5 eggs), then cholesin presumably can't limit any more than that 1g. What happens to the cholesterol then?
Nick, thank you for this video, but I want to make sure I got this correct...sounds like you said the more Cholesin is activated the lower your Cholesterol? I've watched it about 3 times, maybe I need another 3 watches.
Still thinking this through... Ok, the cholesterol in eggs doesn't raise cholesterol levels, but what about the saturated fat in eggs?? Honest question.
Eggland’s Best seems to be funding all the best science on diet these days. Do you know of any other studies they have funded showing that eggs are healthy?
this is great Nick... love your work (and eggs!!) so a double whammy. I just wondered if you a a tendency towards a diet outline for someone with APOE4 polymorphism (so a tendency for super High T Chol and LDL)?
@@nicknorwitzPhD all SREBP are suspicious.... and these are connected. it's because cholesterol synthesis and DNL are connected in function and regulation and of course a dyslipidaemia comes usually with both, high LDL-C and TG rich VLDL....
My Grandma ate 2 eggs a day and had low cholesterol. She didn't pig out, ate moderately. I have higher cholesterol no matter what I eat, and have avoided eggs for years. Genetics.
So could we just take Cholesin directly instead of statins if we need to lower cholesterol in people who's 'cholesterol balancing' mechanism obviously errors on the high side? Or maybe a gut probiotic that generates more Cholesin per gram of dietary cholesterol absorbed?
@@nicknorwitzPhD Reporting back after 10 weeks on Ezetimibe: LDL dropped from 337 to 147. 53y/o male on carnivore diet for migraines. Lab results before and after 10 week trial: TC: 428/231, Trig 102/83, HDL 75/70, LDL 337/147, ALT 28/56, AST 21/29. This is about double the reduction in LDL I was hoping for. I'm a little concerned in the rise in ALT. No adverse symptoms other than smelly pee. I am not an LMHR by the cutoffs (close sometimes), but became lean on a low-carb diet and LDL went from 135 to 335.
Great content as always! Could you please look into Citrus Bergamot as claimed by some people to be one of the best natural way to decrease LDL and Trig while raising HDL? Thanks.
Ok, so there are 3 forms of SREBP: "SREBP-1c regulates transcription of genes involved in FAs, such as acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), two crucial DNL regulation enzymes, and triacylglycerol synthesis, whereas SREBP-1a stimulates both FAs and cholesterol synthesis. SREBP-2 regulates transcription of genes that control cholesterol synthesis. All these pathways interact and overlap in a complicated fashion" (Na Li et al. "SREBP Regulation of Lipid Metabolism in Liver Disease, and Therapeutic Strategies" ...) So SREBP2 is indeed different from SREBP1-c - BUT I think it would really be worth it looking at what Cholesin doesn to the other SREBP variants and how it affects de novo lipogenesis (DNL). I would bet that Cholesin would suppress DNL as well which would mean that EATING cholesterol is beneficial from a metabolical point of view (you don't really want your DNL upregulated!)...
Help me understand why this means eating eggs doesn't increase cholesterol. This hormone regulates cholesterol produced by the liver, but surely cholesterol from eggs also gets absorbed. If you eat enough eggs surely that will outweigh the reduced cholesterol production by the liver
How many eggs that would be? The title is phrased that way because that's what's practical. People are worried about eating eggs because they think they will overflow on cholesterol.
I think there needs to be a big rethink in public health - the body needs to be studied as a system of systems, rather than a collection of isolated parts. Cholesterol is used to produce other hormones, so how can it be bad for the body? When cholesterol is out of whack, why? That points to a problem in the feedback mechanism, but not a why.
So, and yet another consequence: PKA a) inhibits glycolysis and b) activates gluconeogesis in hepatocytes. Which means eating cholesterol does the exact opposite. In other words makes you more insulin sensitive...
@@nicknorwitzPhDCould eating too many eggs, like going overboard, simply push this system beyond its ability to maintain homeostasis? It was a joke, but in all seriousness, what if someone did eat 12 eggs a day for 10 years. Wouldn’t that just be too much cholesterol? Not that any sane person would eat that many eggs a day, but I would think that there would be some number of eggs that you’d overwhelm this mechanism, like anything else, there’s always a tipping point. For myself, I eat 3 eggs a day, every day, for breakfast. Sometimes with half an avocado, and/or half a cup of full fat cottage cheese.
Then of course there are tons of people with this homeostatic/ self-compensatory mechanism all screwed up from the get go. So unless they have constant steatorrhea as means of getting rid of excess dietary fats/cholesterol, their excess dietary cholesterol WILL increase their blood cholesterol levels eventually, and cause the myriad of vascular problems (atherosclerosis). Therefore, I think it is wrong to interpret these new studies by generalizing and promoting the “it’s fine to keep eating food high in cholesterol because it’s not the cause of your high cholesterol” when over the years we’ve seen the majority of patients with moderate high chol levels can and will lower them by just modifying the diet. No medication involved. So yes, generalization via sensationalism is bad.
However the danger from increased cholesterole is not the Chol per se, but the debris in the damaged epithelium. So cholesin or not the issue is not that
Nick, I hated chemistry during my highschool, now this video made me hate it even more. Why can't you say directly eating more than one egg will not kill me. My doctor said the oposite. Who do I trust my doctor, who gave me statin for last 20 years or this kid may not be even 20 years old yet?
My 21yo son is vegan and has total cholesterol of 95. If he eats 3-4eggs a day he will double his cholesterol and you know this. The question is what is the risk of elevated cholesterol.
Though for some people, i'm guessing they will synthesize cholesterol even if their intake is moderately high due to an error in the process somewhere down the line...hence high LDL numbers regardless of intake. but for the majority this process works well? also love the karate kid reference hehe...'Sweep the leg' 'BUT SENSEI'
So, considering this information, how does this model describe the situation when familial hypercholesterolemia occurs? Is it a cholesin deficit that is the proposed cause given this model? Also, do I understand that the CPC1L1 receptor is on the PSCK9 protein? Do I have the correct? Thank you for explaining this research. 🙂
"So, considering this information, how does this model describe the situation when familial hypercholesterolemia occurs?" In most cases it doesn't describe FH at all. The mechanism how FH (which is a set of very different genetic mutations) cause high LDL is the same how eating sugar causes high LDL: It is all mediated by mitochondrial dysfunction. The inability of mitochondria to fully "burn" the substrate for energy leads to the activation of the citrate shuttle by which the mitochondria tries to protect itself. A large amount of citrate is pushed out of the mitochondria and converted to AcetylCoa in the cytosol. Coseqeuntly, AcetylCoa is converted either into fatty acids (triglycerides) and mostly exported out of the liver in a VLDL particle - or converted through the HMGCoa-pathway all down into cholesterol and also mostly pushed out of the liver as again VLDL. VLDL then looses it's TG cargo and is converted into LDL...
Help me here. So cholesin tries to keep the cholesterol levels in our blood/body in a homeostasis state? If that is true, why do people have high levels on cholesterol? Is the cholesin not able to do it job?? Now I do eat a lot of meat, avocado, ghee which has put my total cholesterol at 317, Non hdl= 245, Tri=79, ApoB=148, LDL small=393, LDL medium=668. According to my dr, my bloodwork is a train wreck. I am 5'0" and weigh 105, not taking any cholesterol meds and won't. As I write this, maybe my take away from this video is about the meds we shouldn't take and not if cholestin is able to keep the bad cholesterol from becoming too high? I'm a bit confused. Can someone dumb this down for me? Sorry and thanks
i read an article in T NATION nearly 10 years ago that said dietary cholesterol doesnt directly effect blood levels . it never mentioned this hormone though
My friend Dr Nick, do you know what the real problem is? I will tell you. They say that In order to have a Coronary Disease you have to have over a 50% stenosis. Then probably you should follow guidelines. Most of us perform a CT Coronary angiography and find that there are plaques around 30% to 40% infarction to two or three arteries without having any other serious problems (HOMA IR = 1 , Triglycerides to HDL ratio 1 ...etc). AND the serious decision arises: should we take a Lowering LDL Drug or not , since we are on keto diet and we have Total Cholesterol around 250 and LDL around 180. I would appreciate your thoughts on this topic (without ofcourse taking them as a medical advice).
Dr. Nicholas - I took Zetia for two months and asked my Dr. for a lipid panel as I was curious how the lipids where at. I suffer from high trigs, not high total cholesterol. Anyway, the results came in, and sure, my LDL was lower, but also my HDL went from 48 DOWN to 36. I quit the drug immediately and went back to fenofibrate. Could you explain this effect on HDL?
The TH-cam nutrition space seems to be hyper fixated on LDL. Despite so many statements that LDL is not a killer for most. Likely due to decades of pharma and statin promotion. I see many statements about how LDL is much less important to lipid health than previously thought, but then followed by endless discussion of LDL control. I debate with my doctor regarding his insistence that I take a statin, If I do take a statin my HDL goes too low. Never-mind the slightly elevated LDL. I'm focused on a best possible triglyceride to HDL ratio.
@@proper2979 I am of the understanding that one must differentiate between LDL and HDL. HDL being beneficial, LDL having little impact on CVD and mortality. I'm increasingly understanding that triglyceride to HDL ratio is the most useful blood test result.
@@dr.coole. You have been misled. LDL is the key risk factoe (apoB technically but LDL is a good marker for apoB) for CAD and HD. All these ratios are stories told by people trying to sell you good news about your bad habits.
@@dr.coole. I have to agree with the other guy who responded to you. There is strong (but not definite) evidence that high LDL (specifically ApoB) causes atherosclerosis. There are some caveats here - what about specifically for LMHRs? We don't know, maybe high LDL among lean, healthy people is not a problem. For now, to the best of our knowledge, there is good reason to be concerned by high LDL levels. This concern only gets stronger if you are overweight and inactive.
![[ TEASER ] เงาะป่า - วงL.กฮ. | TMG RECORD](http://i.ytimg.com/vi/M4ObdFfcPww/mqdefault.jpg)
Dr. Nick one of the MOST helpful 10 minutes on Cholesterol ever. Thanks this was great
You're very welcome! But you could have called it "egg-cellent" ;)
@@nicknorwitzPhD I see what you did there LoL
thanks
@@jamesalles139 And I'm glad the video didn't "scramble" your brain, nor do you feel I'm the "deviled" for implying eggs are healthy... although I know some extremists who probably want to "poach" me for my positive position on eggs. They can "fry" but they will finds it's "hard" (boiled) to take me (sunny side) down...
@@nicknorwitzPhD 🥚An egg a day keeps the doctor away, but that might have been a bit egg-cessive. 😜
@@nicknorwitzPhD Isn't this all very well known already? There is an adaptation but it can't actually compensate for the dietary cholesterol consumed, so indeed eating eggs raises cholesterol in subjects with healthy LDL baseline. The studies (sometimes funded by lobbies) that seem to show no raised levels are done on people with already elevated cholesterol, where they are replacing something else with the eggs. If you gave vegans the eggs, the difference would be much clearer.
""Association between Egg Consumption and Cholesterol Concentration: A Systematic Review and Meta-Analysis of Randomized Controlled Trials":
"Based on available evidence, this is the largest meta-analysis in exploring the impact of egg consumption on LDL-c/HDL-c ratio among healthy subjects and reveals that more eggs consumed per day may influence cardiovascular disease risks by increasing LDL-c and the LDL-c/HDL-c ratio. Notably, longer-term high egg-consumption may lead to higher LDL-c/HDL-c ratio and LDL-c. However, RCTs with long tern follow-up are needed to guarantee the association between egg consumption and human health"
I eat 4 eggs (cooked in butter) for breakfast and 6 eggs (cooked in butter) in the evening !! Done it for years , feeling great at 76 years old !😊
So what? There are 80 year old smokers that feel great too.
@@xnoreqthey might be eating better
@@yadunandanks8781 You missed the point.
Eggs, especially when consumed with additional saturated fat (such as butter), cause objectively measurable increases in endothelial dysfunction, arterial inflammation, and LDL-C oxidation for hours after the meal. Feeling great doesn't change that. Some people feel great and have a heart attack in the next moment (heart disease is #1 killer in USA).
A lot of people with C also feel great until they're in advanced stages.
There are also genetic differences between individuals.
So the point is that such personal anecdotes are not only worthless, they are actively harmful because they mislead people who don't know better.
@@xnoreq The review you are referring to (2022 www.ncbi.nlm.nih.gov/pmc/articles/PMC9437993/) investigated any type of high fat meal without fully controlling confounding factors that would be relevant here, such as the quality/type of the fats as in e.g. differing between butter and highly processed foods or the food preparation (overheating fats/oils). total caloric intake and BMI were considered in the statistical analysis, but more direct measures of precursors of metabolic syndrome as well as controlling for carb intake (indicating keto styles/fat adaptation) would be very desirable for deriving conclusions for this context here.
The relationship between butter consumption and endothelial function or inflammation remains mixed, which means the effects are context-dependent. Unsurprisingly, complementary risk factors play a big role in determining the associated risks. To put it simply, people who already overeat calories and have some form of metabolic syndrome would do well to reduce their butter consumption, but for generally healthy individuals these concerns do not apply in the same way. This channel here is all about nuance.
Of course you are right in saying that anecdotes have limited value for generalizing our understanding. As for another anecdote: I consume about 10 eggs a day and also butter and my bloodwork is not only fine, all my markers are optimal for longevity. That is in the context of a healthy lifestyle, not overeating calories, having a functional lipid metabolism, exercising, etc. Whatever potentially negative/transient effect I get from the fats I consume, it is apparently negligible in this context.
@@xnoreqsaturated fats never cause LDL oxidation mate, in fact provide protection against oxidation. Ox happens when your ldl is composed of USFAs esp PUFAs & if narrowed down more, from data, it's omega 6 LA metabolites, which are found in oxLDL particles.
Interesting. A TH-cam content creater just released a video on, What Happens if you eat 4 eggs a day. The study you referenced wasn't mentioned but I love when folks are on the same wavelength. The creator is Sten Ekberg a former decathelete and now a Chiropractor
I love Sten, but he spends an hour telling you sobering her could in 18 minutes and I don’t have time for that. He talks slow and repeats himself constantly.
@KidAnarky11631 some of us who are not too bright or scientifically or medically trained need that slow deliberate pace. You can always go into the video's settings and increase the speed.
I just watched it!
Thanks, my Dr fixates on cholesterol which I don't think is bad at 278 overall. Least he wants me on is ZETIA. Seems counter to me?
@@carolj.3175If you exercise ,you could eat a sweet potatoe each day for less ldl , and it will not affect your ketogenesis very much.
YAY! I eat 6 -10 eggs a day. This is thrilling news. And, now I know WHY my cholesterol is not affected!! Thank you! 😊
Hi Nic, thank you for bringing this to our attention! I have been following your channel because you are a disruptor and lateral thinker - more of you in this world! I am a clinical physiologist and have been in private medical practice for over 40 years. Yes, way past my sell by date! I know that our clinical colleagues have no clue about basic physiology/biochemistry and how to interrogate published literature. They accept any finding in a peer reviewed study without asking “stupid” questions! “Western” Medicine is in a mess because of my generation of “learned” clinicians. I realise though, we are now in the terminal phase of this cycle because a new generation, like you, are not accepting any garbage dished up by biased scientists, clinicians and big pharma. With the help of all the new technology, of which I cannot keep up, I am of the opinion that the ills of the last 50 odd years will be corrected. Please continue on your present path because you are rocking the boat which is desperately needed. You will knock heads with the professors/deans of my generation but do not flinch - I hold them accountable for the mess our medical science is in. They are the watch dogs but have totally failed us. But the future is bright with people like you and your generational colleagues.
Love THIS: "we are now in the terminal phase of this cycle because a new generation"... I hope you're right!?
@@nicknorwitzPhD It's all about getting the message out to more people until the truth that science counts for much more than scientific consensus reaches a tipping point.
Keep up the good work.
" I am of the opinion that the ills of the last 50 + years will be corrected". You are a sanguine soul! Big food, big pharma, big agri have heavily invented in the food pyramid with the ADA, AHA and the government on board. It is the food pyramid that's killing people. Will they allow all the $$$ investment headed to drains?
Yes, how many people have suffered health problems because of lack of knowledge?
I am going back to eating eggs from happy chickens. They are expensive eggs, but the guilt and karma from eating eggs from hens suffering affects me.
@@terriem3922 "The karma from eating eggs affects me". Did you know that more than a few dozen plants eat animals? Please search TH-cam for "plants that eat animals" Some plants even eat tiny monkeys. Did you ask the plant if it knows karma?
Dr Nick, this video was a great introduction to the new-found mechanism of endogenous cholesterol synthesis. I would suggest that it took 5 decades to discover Cholesin and the pathway because someone actually wanted to find out 'why'. For years we have relied on circumstantial evidence instead of actual, repeatable scientific study. I am a family physician of 28 years and wish I knew this stuff on day-one!
Good editing. Great pacing. You got this channel dialed in. You explain complex things so we can better navigate our health journeys. You are not telling me what to do - instead, you add clarity. Perfect.
Thanks! That's what I aim to do!
Great delivery Nick, for those of us not scientifically trained, but seeking answers. Your 'pause, rewind' advice works so well! I feel I now have an understanding of the complexity of the process as well as the simplicity of how our own biology optimises our cholesterol levels. One of your best ever! Bravo, please keep doing what you are doing.
Thank you! Deeply appreciate this!
Great video Nic! It's amazing that this new hormone (Cholesin) has just been discovered within the last year or so considering all the research that's been conducted on cholesterol over the last two centuries since its discovery. This could be a Nobel prize in medicine worthy discovery. I remember clipping a newspaper article from about 20 years ago, about a study that came out of Iowa State University if memory serves, where they empirically demonstrated that eating large quantities of eggs didn't raise cholesterol.
Thank you. Another great explanation that I can understand. I wouldn't want to be tested on it, but my knowledge is increasing bit by bit.
Amazing overview of the new science. Nick - please just keep being Nick!
I don't think I have a choice! That's great news to some people... but not all 😉
@@nicknorwitzPhD LOL!
Fascinating, my husband is an Osteopathic physician who believes the body tries to find homeostasis. This is why many fads don't work like changing your Ph through diet
This even applies to blood pressure or blood sugar.
If parameters like BP or BS are off it means the regulation is dysfunctional...
Perhaps... but the word "fad" may be tossed around too liberally for my taste... e.g. Keto is often called a fad. I argue it's a metabolic state, separate from Quest Bars ;)
It seems to me that the more we learn, the more questions we need to ask about the basic mechanisms and what changes in lifestyle might help avoid or resolve issues with metabolism, rather than what medication can be developed to address the symptoms. If the money put into pharmaceutical development were invested in basic science, maybe we wouldn't be where we are, in terms of public health. On the flip side, I don't imagine the pharmaceutical industry would be interested in funding research which eliminates the need for their products.
We can dream, can't we? "If the money put into pharmaceutical development were invested in basic science, maybe we wouldn't be where we are, in terms of public health"
I look forward to that day.
If only humans could learn from the hubris of this whole egg episode that it took 60+ years to understand the mechanism of cholesterol homeostasis. Yet very firm guidelines were introduced by the AHA around egg consumption (
Don't blame young Dr. Nick... I'm not responsible for mistakes made 3 decades prior to my birth ;) ... since my mom was burn in 1965, I suppose the "egg" of me was ~3 then... ;)
There is no revalations here. It's been know for a while that body can compensate for dietary cholesterol partly, but it's also known that this mechanism is nowhere near adequate enough to compensate fully for it and even modest amounts of for example eggs raise LDL in people who start at low healthy levels.
"Based on available evidence, this is the largest meta-analysis in exploring the impact of egg consumption on LDL-c/HDL-c ratio among healthy subjects and reveals that more eggs consumed per day may influence cardiovascular disease risks by increasing LDL-c and the LDL-c/HDL-c ratio. Notably, longer-term high egg-consumption may lead to higher LDL-c/HDL-c ratio and LDL-c. However, RCTs with long tern follow-up are needed to guarantee the association between egg consumption and human health"
Fascinating! Thank you, I love a paper like this with my morning tea.
Yes! Me too!
I learn something new every day. Thank you.
You're welcome!!!
Thank you for this one. The cholesterol debate won't go quietly. My first thought was that using medication to block a natural process is playing with fire, but at the same time, I had to check myself. All medications do that. It can be a life-saving difference.
Hearing you on Stemtalk gave you ALOT of credibility in my book! I wish some of the more well know " experts" would have you on their shows.
Thanks! Was a fun time... in due time I'm sure...
I find it fascinating too. Thank you for explaining this!
Welcome 😁
Dietary cholesterol does not increase blood levels of cholesterol. (Any food, not just eggs).
Ya, but eggs have better SEO
Dietary cholesterol obviously raises LDL in most people when they start with healthy baseline. If you start at LDL 200, your LDL isn't going to go up due to eggs. That is why eggs lobby funds studies, where the study subjects already have a high LDL to begin with, so no difference is seen. It's cholesterol and saturated fat that as a combination raises LDL.
"Based on available evidence, this is the largest meta-analysis in exploring the impact of egg consumption on LDL-c/HDL-c ratio among healthy subjects and reveals that more eggs consumed per day may influence cardiovascular disease risks by increasing LDL-c and the LDL-c/HDL-c ratio. Notably, longer-term high egg-consumption may lead to higher LDL-c/HDL-c ratio and LDL-c. However, RCTs with long tern follow-up are needed to guarantee the association between egg consumption and human health"
@@cyberfunk3793 Tell us you didn't bother to watch the video.
@@LawrenceAugust_ I did and the exact gene that affects the mechanism is irrelevant to the bigger picture that has been known for a long time. The claim made in the title is simply false and refuted for example in the meta-analysis of clinical trials I quoted. It's a typical claim made by the eggs lobby.
@@LawrenceAugust_ Again as my previous reply was deleted: I watched it, but the exact mechanism is irrelevant because the claim in the title is simply false.
That was "eggcellent"! Thanks!
Glad it didn’t scramble your brain
@@nicknorwitzPhDToo late, my brain is already scrambled, but I try to keep a "sunny side up" attitude. 😂
@@frankenz66 lol
Nice. Along with demonstrating reverse cholesterol synthesis: TG decrease as HDL increases-or lack of it depending on the individual, fasting shows how cholesterol syntheses increases.
Amazing content brother 👏👏👏
🙏🏻🙏🏻🙏🏻
This is already known and why lipidologists use statin and zetia together to get synergy. Doesn’t mean that either drug doesn’t lower cholesterol, just means there is some form of compensatory mechanism, we absorb little cholesterol from our diet and so maybe less effect there. Boston heart labs will show some people are cholesterol absorbers and some are synthesizers due to genetic predisposition.
Thank you for this excellent summary. I’m new to your channel and I completely understood your explanation. Question- if LDL was an issue, could they just give you the hormone in order to down regulate your liver - why would they need to also give you the drug to control absorption ? I am on the carnivore diet and my LDL has skyrocketed- but every other marker is great. My Dr wants me on a statin and so far I’ve been able to say no. Disregarding hyper-responders, now I am wondering if those of us who react to carnivore diets this way may just have a hormone issue or a liver issue. You definitely have me thinking and thanks to your great video I can head down the rabbit hole-of other TH-cam videos better prepared.
Thank you for your inquiry into all these topics and the way you put things across, I understand you a whole lot more than my GP as they are some what conditioned by “ big Pharama” and not science. Don’t get me wrong I don’t believe you just like I don’t believe my GP I just understand you a hell of a lot more than my GP. Sorry for the comparison but the topics you are mentioning are a big help to my health and my standard of living. Thank you once again.
I’m glad you feel my content is helpful and easy to understand:)
Brilliant Nick. Thanks for sharing.
You're welcome!
Just yesterday I was talking about how every cell in the body makes cholesterol soooo how can it be "bad" if that is a fact? Thanks Nick ... great info for the "food fight" !
I like how when you said "take a step back", you took a step back...😊
I also think it's awesome that even though we don't really actually know how little we know, our brain (when oriented correctly) can use this limited information to work (or guess) a theory of how the body operates and if correct, it would then tell us more about the secrets of life and the universe.
I miss the college days in the lab working on actual EE theories and seeing how cool it was to put them to the test and get a deeper understanding of my field. We are capable of a lot but not everything because that will be our last day.
Thank you, Nick!
You are very welcome Robyn
Thank you, Nick. Fabulous info!!!
you're very welcome!
I appreciate your take on it. My only concern is whether it would be neccessary for most people to get exogenous medication for these ptoblems in the first place. Im guessing the need to speculate on these mechanisms will help those who are severely in need.
Also, i love the way your illustrations have improved, now youve got the circles indicating individual parts of the diagram as youre explaining it. I hope Huberman watches your channel, coz this level of detail would of been handy in his latest vid on back pain, and explaining the McGill exercises, which luckily i stumbled across on his other channel, of him physically doing it.
Still, your method is far superior, the diagrams and the anonymous guy evolving his skills on this detail is very appreciated, give him a hi five for me 👊😎
"I hope Huberman watches your channel" ... hey me too ;). We've chatted. From all our interactions, he's a really nice guy. I hope we get to interaction more, but I think my academic career will have to mature a bit more...
I did an experiment where I ate a dozen eggs a day for one month in addition to my normal diet (but only a slight caloric surplus). I ate other foods as well, including some carbs, and my cholesterol shot way up. I sort of had a LMHR response. My HDL and LDL went way up, and my triglycerides way down. Could this have been due to the saturated fat content, or a slight increase in calories and weight gain (~+3 pounds), or a LMHR type response? Inhibited Cholesin hormone?
You're probably a lean mass hyper-sterol absorber (LMHSA) meaning you probably over-absorb cholesterol. Take a cholesterol balance blood test to find out. Don't forget to get an ApoE genotype test done too. Nick wants to talk about the cholesterol balance test in his next video since he loves us LMHSAs almost as much as LMHRs. Alas, my sense of humor is an acquired test!
Eating eggs increases your cholesterol that is why your cholesterol shot up. The extent of the increase depends on the rest lf your diet beforehand obviously. Someone on keto would likely not notice that much of a different. But if you were low fat before youd likely see your cholesterol double.
@@SimonHealthAction thank you for the reply!
This prompts the question why, if the body is working hard to maintain cholesterol in a certain range, we think it would be a good idea to take drugs designed to push the body out of that range, without fully understanding the mechanisms. Shouldn't we be working on understanding why the body sees that range as optimal before we start tinkering?
Fabulous point!
It's not very good at maintaining a tight range. I can alter my diet a bit and shift my TC by a hundred points in a few months using nothing but whole foods. Does it matter? Some argue it's the end all be all, others argue it doesn't matter at all.
Too right
@matthewtrout1440 I've been on Keto, Atkins, carnivore and the SAD during the past 20+ years, and my LDL has stubbornly maintained the same range. I know you can alter it substantially in the short-term, the Oreo experiment demonstrates that, but at least for me, diet doesn't alter it long-term.
Depends... are we optimizing for the same outcomes that natural selection optimized for?
Absolutely fantastic video
Thank you very much!
Love your diagram
Thanks. The figure in the video is from the paper. The thumbnail was made by a friend, Andrew, and using a Zack S. Photo, with permission from Zack
My Dr. flagged my higher LDL.
I mentioned cholesin.
He said ‘What’s cholesin?’
I said ‘Exactly’ and left.
good job! keep the bar high. Here's a mechanism for you; If you treat people like they are stupid then they will respond that way.
Good one! Really... love this... I'm "borrowing" it
Many thanks Nick ,interesting. I think not vilifying Ldl or putting Ldl on a pedestal is to be considered. Stay curious
I appreciate your breakdown of these papers. I have been trying to study why biologics cause weight gain and my head is 😵💫
Nick, you love LMHRs because you are one! Yet no love and no scientific interest for us lean mass hyper-sterol responders. lol. No discussion of the ApoE4 gene. I've done the cholesterol balance test. I over-absord beta-sitosterol and campesterol. I over-produce lathosterol. The interpretion is that I have increased intestinal absorption of cholesterol. I have one ApoE4 allele (E/3/E4). I love eggs and still eat one a day. But two eggs a day causes a big uptick in cholesterol. Talk about the cholesterol balance test. Nobody knows about it. Anyone can get a cholesterol balance done without needing an Rx if they know where to find it. I eat super clean and am not a diet idealogue. I'm trying to figure out whether to stop eating nuts and seeds (given the sterol content) and cut the egg out. I don't accept that ApoB can be ignored. Mine is 69. Lowered somewhat by cholestyramine (CSM) which is an old pre-statin Rx used off-label to bind mycotoxins. CSM's action is a bile acid sequestrant and I have sero side-effects from it. Only it's not a cool drug for hip cardiologists. The question is whether to cut back on sterol rich foods and the egg, continue with CSM and take low dose Rosuvastin every second day and low dose zetia every second day (an idea I heard from Tom Dayspring) to balance out absorption and synthesis as you mention. Before any diet idealogue says anything about cholesterol being unimportant because it's all about insulin resistance and inflammation; please ...stop with your religious ideological convictions. Get yourself a CIMT before you speak. It's understood that metabolic health and inflammation are top priority. But we are very far from a place of saying anyone can blow their ApoB higher without risk. I'm trying to encourage this young man to talk about more nuances. Talk about the results of a cholesterol balance test and the ApoE4 gene. We lean-mass hyper-sterol absorbers aren't getting any love. Maybe I'll cut out all eggs, all meat/saturated fats, all plant sterol food, eat a bunch of oreos and watch my cholesterol drop; then become a famous lean mass hyper-sterol absorber ;-)
It looks like Cholestyramine is similar to Ezetimibe. I recently found out that while Ezetimibe can be very effective at lowering cholesterol, it showed no benefit in lowering cardiac events. I suspect I'm a hyper absorber too, a short stint with carnivore and eggs drove my cholesterol way up, but I'm not sure a bile binder is the solution. If there is any benefit to carbohydrates (which can lower cholesterol), it may due to an entirely different pathway and cholesterol is just the red herring.
Have you tried ezetimibe plus 5 mg Rosuvastatin?
@@jenjen789 Not yet. I''m about to seek an Rx for 5mg rosuvastin and 10mg zetia but cut them in half and alternate them at this 50% low dose every other day. To flip between restricting synthesis and absorption. Still taking 2x 4mg compounded CSM powder each day (they put sucrose in the branded version, ugh). Then test again.
@@SimonHealthAction It is my understanding after listening to Dayspring’s podcast that one could take a minimum dosage statin and regular dose Zetia every day. My dad does not experience any side effects from 5 mg Rosuvastatin plus 10mg Zetia daily because the dosage of Statins is low enough. APO B is very low. No plaque progression after going low carb and taking this Rosuvastatin and Zetia combo ( now switched to 5mg Rosuvastatin and Fenofibrate combo for better control of lp(a) in addition to APO B)
Very cool. Any time a new hormone is identified it is very cool. Given the subjects that interest you most, I am surprised you aren't planning on specializing in endocrinology.
I am...
One problem however: FHC is often about cleaning up 'old' cholesterol , not about how much is created (from food or liver). Where it comes from isn't that relevant.
The liver produces around 1000mg of cholesterol in the absence of cholesin hormone. However this amount of cholesterol is okay for normal functioning. Taking additional cholesterol from diet would supress cholesterol synthesis via cholesin, but remember we still need a daily recommended value for circulating cholesterol levels. The recommended daily intake of cholesterol is around 300mg. Let's say in the absence of any dietary cholesterol, liver produces 1000mg. In the presence of 300mg of dietary cholesterol, liver would drop production to 700mg via the action of cholesin to maintain homeostasis. However exceeding the daily recommended intake value by a huge margin, say 1500mg of cholesterol is detrimental. Assuming the liver produces 0g cholesterol to make up for the absurdly huge amount of dietary cholesterol ( in this case) 1500mg. It's still going to be detrimental for health regardless of increasex cholesin production.
The human body is a Complex Adaptive System and yet….as you describe….supremely intelligent.
As Donald Rumsfeld was fond of saying, there are “Unknown, Unknowns” whenever you attempt to intervene in a complex adaptive system whether it is political or biological (like homeostasis)
In a nutshell, Rumsfeld wisdom almost ALWAYS means that the end result of screwing around with a complex adaptive system puts your self-interest in a worse position than before.
Attempting to pharmacologically intervene in the LDL of an LMHR is case in point. Just too many Unknown Unknowns like the role LDL plays in the immune system.
Well stated!
The perfect example from history is bloodletting.
Of course, I would guess that the doctors who performed it at the time did not give their patients (or their survivors) refunds. That pattern will probably repeat if someday it is found that cholesterol lowering drugs have been more harmful than helpful overall.
Makes no sense. Human diets inherently mess with that "complex adaptive system." Everytime you eat your messing with it.
Sounds super pretentious.
@@ArcoZakus I predict that PCSK9 inhibitors that DRAMATICALLY reduce cholesterol by irreversibly altering the liver will be shown to be much more harmful than helpful [See already: "The systematic review of RCTs of PCSK9 antibodies challenges their "efficacy breakthrough and the "lower, the better" theory" Current Medical Research and Opinion Vol 34 Issue 10 2018]
@@proper2979
No argument there. Diets do impact how your health emerges. And “emergence” is the hallmark of a CAS.
When Ancel Keyes “messed” with the American Diet WHAT emerged was not what everyone involved had hoped for.
What emerges from a keto diet is generally good for many sick people who try it. The emergence of sky high LDLin LMHRs in the presence of amazing health seems counter-intuitive for reasons like unknown-unknowns. Drs trying to medicate what could be a natural and beneficial phenomena in an LMHR is pretentious, IMO. We just don’t know.
Nick , your work is awesome. I am very interested in the lipid energy model. However, I want to know the full spectrum. Not just how carbohydrates and fats change it, but how carbohydrates fats, sunlight, hormones, water, and magnetism, change the lipids in the body. I have seen evidence that sunlight increases vitamin D and decreases lipids. This would play a role in different diets. And we know that people live in different latitudes for diurnal sun angle. We know that indigenous tribes typically spend more time in sunlight. And most of the time they have lower lipid levels. Even though that are on a carnivore diet. Why?
Nick that was awesome. That just proves we don’t know much. How about quantum biology?
I think I might be quantum entangled with Dave Feldman and Adrian Soto Mota in a nerd trio
@@nicknorwitzPhD Mitochondrial Energy and hormone changes with light. Sunlight and artificial light. Deuterium, water and grounding to the earth providing electron balance for the mitochondria. Have you heard of this?
would be interesting to have you on Huberman
I mean... I'd say yes...
Yes, this information is very cool because eggs are one of the best foods for us to eat. Thank you. :)
They are egg-cellent!
That was awesome, my cardiologist tried to prescribe Zedia 😃 now I know why I declined 😃
Umm... you may be getting something from this video that wasn't said... please work with your physician. This is a mechanistic explanation. Also, to be crystal clear, the compensation to Zetia re cholesin/endogenous synthesis is not complete.
@@nicknorwitzPhD fair enough, I will listen again, of course I declined before you made the video so you didn’t influence the decision, she is uncomfortable with my 388 LDL amongst otherwise perfect numbers and sees no need for a CT angiogram. I scored a 16 on my CAC so I am curious, but curiosity was not valid in her opinion. I am in search of other opinions 😃 Thanks for the clarification 👍🏻
I see a multi billion dollar market opening up: cholesin 'enhancer' or something like that, new patents combining it with existing cholesterol medications...
Another great point i can rais when cardiologists try to tell my clients that they need to eat less cholesterol heavy foods in order to decrease harmless LDL levels. It doesnt help that tests for actual oxidated-vLDL´s have to be financed privately in our already heavily taxed state healthcare system in germany. You wouldnt believe just how many Cardiologists dont even know about OX-LDL at all...
on another podcast I believe they stated that the cholesterol we ingest is a larger molecule and can't be used by the body. That seems incorrect based on this video. Can you help me understand if there is a big difference on how you body uses external dietary cholesterol and what our liver makes. ( non-scientist asking and trying to learn)
Interesting (but it was a Nic Norwitz video so that is hardly a surprise).
AWEEE!
BTW, the MAPK/ERK pathway is linked to tumorigenesis as well.
Does it mean that eating cholesterol would suppress cancer?
That's why I won't take cholesterol meds now. When Crestor first came out my Dr. put me on it. It lowered it, then about 3 years later it started climbing again. In my mind that says my level is where my body wants it. Felt better after I quit taking it too. Didn't realize all the side effects it was giving me. Sigh.
That’s cool I thought we didn’t know. I would ask so tell the system that shows eating unsaturated fats increases cholesterol.
The mechanism you describe is interesting. Your title might be better put to say "Dietary cholesterol does not cause serum cholesterol increase". There are numerous studies showing an increase in serum cholesterol from eating eggs. How? Sat fat? A 2020 meta-analysis by Mah-Yun Li et al, "Consumption and Cholesterol Concentration: A Systematic Review and Meta-Analysis of RCT's" shows this.
@@billdublewhopper3064 The meta-analysis I mention above was not based on studies of vegans, so a carnivore/vegan interpretation doesn't really apply there. They simply found that in these various randomized controlled trials, eating eggs raised cholesterol significantly. As I said, a likely mechanism is saturated fat, known to raise serum cholesterol.
Nick, My understanding is cholesterol doesn't cross the blood brain barrier so it would make sense that cholesin doesn't either otherwise the down regulation of cholesterol production would be bad (like some statins apparently do). Do you know anything for sure? Hope you do a video on this aspect. Thanks, Bill
It’s interesting but I’m not a fan of trying to bypass your system. I try to find ways to increase health within the system. If there was a dietary pattern to follow to get results that has more value to me. But it is valuable to understand the mechanisms.
I switched to a Keto then carnivore diet.
My cholesterol definitely went up.
But the type(s) that went up arent necessarily bad, LDL and HDL, while Trig went DOWN.
Then in subsequent testing cholesterol LDL has been declining over time, while HDL went up further, then leveled off.
SO... I went from 234lbs 39.5" waist 26%BF to 178lbs 15%bf 32" waist.
Whos healthier the lower cholesterol obese me, or the higher (LDL) cholesterol me?
I can workout again because autoimmune issues are at bay, and fatty liver and anemia etc are resolved.
Did I mention my testosterone almost doubled, my thyroid level increased?
EVERY marker across the board in improved unless you count LDL as a negative
One of the things I hear the vegan docs say is that the studies that show animal fat doesn’t raise cholesterol are taking diets they consider high in fat already and add a little more so the raise in cholesterol isn’t statistically significant. If you take some eating plant based low to no fat adding eggs will raise cholesterol. I don’t know what the truth is. What I do know is I ate a proper “healthy “ vegan diet and my physical health slowly declined. Eating high meat carnivore/ketovore has restored my physical health very quickly and I feel the best I have in decades. I feel like a healthy 20 year old at 47.
I believed that babbling BS for DECADES about eggs .. then as I changed my life style (what some call diet) I had the wakeup call that eggs are really, really good for you. Thanks for this ... love the details, i.e. FACTS
Eggs are so packed with nutrients, they’re like nature’s vitamin pills
Definitely cool, Nic. It poses many more questions. Cholesin works with eggs to inhibit blood cholesterol so can we assume it will work for all dietary cholesterol? And what % of dietary cholesterol is inhibited? 100%? 50%? Is all dietary cholesterol the same? And what other factors - such as weight, stress, lack of sufficient sleep , exercise, genes, etc - may be factors in making blood cholesterol and ldl rise?
"Cholesin works with eggs to inhibit blood cholesterol so can we assume it will work for all dietary cholesterol?" - Yes. Was just using eggs and an example food and for SEO. In terms of %, I think there is near complete compensation, although may differ by individual.
@@nicknorwitzPhD Super interesting, but, your liver maxes out at producing around 1g of cholesterol per day. So if you exceed 1g of cholesterol intake via the diet (5 eggs), then cholesin presumably can't limit any more than that 1g.
What happens to the cholesterol then?
Nick, thank you for this video, but I want to make sure I got this correct...sounds like you said the more Cholesin is activated the lower your Cholesterol? I've watched it about 3 times, maybe I need another 3 watches.
Still thinking this through... Ok, the cholesterol in eggs doesn't raise cholesterol levels, but what about the saturated fat in eggs?? Honest question.
Eggland’s Best seems to be funding all the best science on diet these days. Do you know of any other studies they have funded showing that eggs are healthy?
Of course they do.
this is great Nick... love your work (and eggs!!) so a double whammy. I just wondered if you a a tendency towards a diet outline for someone with APOE4 polymorphism (so a tendency for super High T Chol and LDL)?
pubmed.ncbi.nlm.nih.gov/33921683/
It's always the SREBP2 regulator, never trusted that thing from day 1 🤔😂 But seriously Doc, thanks for the details.
Glad to help
@@nicknorwitzPhD all SREBP are suspicious....
and these are connected. it's because cholesterol synthesis and DNL are connected in function and regulation and of course a dyslipidaemia comes usually with both, high LDL-C and TG rich VLDL....
Nick please do a video on LMHR and taking ezetimibe, I take it and my LDL went from 103 to 51. That an incredible 50% reduction.
My Grandma ate 2 eggs a day and had low cholesterol. She didn't pig out, ate moderately. I have higher cholesterol no matter what I eat, and have avoided eggs for years. Genetics.
Why you should always use ezetimibe with a low dose statin or red yeast rice
So could we just take Cholesin directly instead of statins if we need to lower cholesterol in people who's 'cholesterol balancing' mechanism obviously errors on the high side? Or maybe a gut probiotic that generates more Cholesin per gram of dietary cholesterol absorbed?
I guess I ll have to watch that again a few times.
Yes my little brain stops listening right away lol I dont know why I watch these videos haha I dont need to know why, just the good news lmao
Do it! Do it now!
Include CIMT in LMHR to detect soft plaque with high LDL
Using CCTA atm
@@nicknorwitzPhD
The presentation did not report on soft plaque
Definitely interested to hear your thoughts on LMHR and Ezetimibe.
Hypothesis: will punch above it's weight in terms or LDL-C reduction vs general population
@@nicknorwitzPhD Reporting back after 10 weeks on Ezetimibe: LDL dropped from 337 to 147. 53y/o male on carnivore diet for migraines. Lab results before and after 10 week trial: TC: 428/231, Trig 102/83, HDL 75/70, LDL 337/147, ALT 28/56, AST 21/29. This is about double the reduction in LDL I was hoping for. I'm a little concerned in the rise in ALT. No adverse symptoms other than smelly pee. I am not an LMHR by the cutoffs (close sometimes), but became lean on a low-carb diet and LDL went from 135 to 335.
Great content as always! Could you please look into Citrus Bergamot as claimed by some people to be one of the best natural way to decrease LDL and Trig while raising HDL? Thanks.
BUT that would also mean that eating cholesterol supresses de novo lipogenesis WHICH WOULD BE A REALLY GOOD THING!
Ok, so there are 3 forms of SREBP:
"SREBP-1c regulates transcription of genes involved in FAs, such as acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), two crucial DNL regulation enzymes, and triacylglycerol synthesis, whereas SREBP-1a stimulates both FAs and cholesterol synthesis. SREBP-2 regulates transcription of genes that control cholesterol synthesis. All these pathways interact and overlap in a complicated fashion" (Na Li et al. "SREBP Regulation of Lipid Metabolism in Liver Disease, and Therapeutic Strategies" ...)
So SREBP2 is indeed different from SREBP1-c - BUT I think it would really be worth it looking at what Cholesin doesn to the other SREBP variants and how it affects de novo lipogenesis (DNL).
I would bet that Cholesin would suppress DNL as well which would mean that EATING cholesterol is beneficial from a metabolical point of view (you don't really want your DNL upregulated!)...
Help me understand why this means eating eggs doesn't increase cholesterol. This hormone regulates cholesterol produced by the liver, but surely cholesterol from eggs also gets absorbed. If you eat enough eggs surely that will outweigh the reduced cholesterol production by the liver
How many eggs that would be? The title is phrased that way because that's what's practical. People are worried about eating eggs because they think they will overflow on cholesterol.
So there could be an evolutionary sense to keep cholesterol in a specific range.
But there are other pathways which have an effect on cholesterol synthesis
I think there needs to be a big rethink in public health - the body needs to be studied as a system of systems, rather than a collection of isolated parts. Cholesterol is used to produce other hormones, so how can it be bad for the body? When cholesterol is out of whack, why? That points to a problem in the feedback mechanism, but not a why.
So, and yet another consequence: PKA a) inhibits glycolysis and b) activates gluconeogesis in hepatocytes.
Which means eating cholesterol does the exact opposite. In other words makes you more insulin sensitive...
So you are telling me that my eating a dozen eggs a day for decades did not make me more likely to have a heart attack? That's too bad!
Sorry to disappoint
@@nicknorwitzPhDCould eating too many eggs, like going overboard, simply push this system beyond its ability to maintain homeostasis? It was a joke, but in all seriousness, what if someone did eat 12 eggs a day for 10 years. Wouldn’t that just be too much cholesterol? Not that any sane person would eat that many eggs a day, but I would think that there would be some number of eggs that you’d overwhelm this mechanism, like anything else, there’s always a tipping point.
For myself, I eat 3 eggs a day, every day, for breakfast. Sometimes with half an avocado, and/or half a cup of full fat cottage cheese.
Then of course there are tons of people with this homeostatic/ self-compensatory mechanism all screwed up from the get go. So unless they have constant steatorrhea as means of getting rid of excess dietary fats/cholesterol, their excess dietary cholesterol WILL increase their blood cholesterol levels eventually, and cause the myriad of vascular problems (atherosclerosis). Therefore, I think it is wrong to interpret these new studies by generalizing and promoting the “it’s fine to keep eating food high in cholesterol because it’s not the cause of your high cholesterol” when over the years we’ve seen the majority of patients with moderate high chol levels can and will lower them by just modifying the diet. No medication involved. So yes, generalization via sensationalism is bad.
However the danger from increased cholesterole is not the Chol per se, but the debris in the damaged epithelium. So cholesin or not the issue is not that
Nick, I hated chemistry during my highschool, now this video made me hate it even more. Why can't you say directly eating more than one egg will not kill me. My doctor said the oposite. Who do I trust my doctor, who gave me statin for last 20 years or this kid may not be even 20 years old yet?
My 21yo son is vegan and has total cholesterol of 95. If he eats 3-4eggs a day he will double his cholesterol and you know this. The question is what is the risk of elevated cholesterol.
Eating 4 eggs will change his cholesterol from 95 to 190? Really? That’s unusual
Though for some people, i'm guessing they will synthesize cholesterol even if their intake is moderately high due to an error in the process somewhere down the line...hence high LDL numbers regardless of intake. but for the majority this process works well?
also love the karate kid reference hehe...'Sweep the leg' 'BUT SENSEI'
So when’s the egg & Oreo study coming out?
Icky... I had one Oreo omelette during that expt and that gave my tongue PTSD
So, considering this information, how does this model describe the situation when familial hypercholesterolemia occurs? Is it a cholesin deficit that is the proposed cause given this model? Also, do I understand that the CPC1L1 receptor is on the PSCK9 protein? Do I have the correct?
Thank you for explaining this research. 🙂
"So, considering this information, how does this model describe the situation when familial hypercholesterolemia occurs?"
In most cases it doesn't describe FH at all.
The mechanism how FH (which is a set of very different genetic mutations) cause high LDL is the same how eating sugar causes high LDL: It is all mediated by mitochondrial dysfunction.
The inability of mitochondria to fully "burn" the substrate for energy leads to the activation of the citrate shuttle by which the mitochondria tries to protect itself.
A large amount of citrate is pushed out of the mitochondria and converted to AcetylCoa in the cytosol.
Coseqeuntly, AcetylCoa is converted either into fatty acids (triglycerides) and mostly exported out of the liver in a VLDL particle - or converted through the HMGCoa-pathway all down into cholesterol and also mostly pushed out of the liver as again VLDL. VLDL then looses it's TG cargo and is converted into LDL...
Help me here. So cholesin tries to keep the cholesterol levels in our blood/body in a homeostasis state? If that is true, why do people have high levels on cholesterol? Is the cholesin not able to do it job?? Now I do eat a lot of meat, avocado, ghee which has put my total cholesterol at 317, Non hdl= 245, Tri=79, ApoB=148, LDL small=393, LDL medium=668. According to my dr, my bloodwork is a train wreck. I am 5'0" and weigh 105, not taking any cholesterol meds and won't. As I write this, maybe my take away from this video is about the meds we shouldn't take and not if cholestin is able to keep the bad cholesterol from becoming too high? I'm a bit confused. Can someone dumb this down for me? Sorry and thanks
I want to see Nicholas debate one of these vegan gurus maybe Neal Barnard or Michael Greger.
Me not. Those quackers should be completely ignored...
Great content. Any thoughts on CETP inhibitors (e.g.- obicetrapib), particularly in the context of ApoE4?
i read an article in T NATION nearly 10 years ago that said dietary cholesterol doesnt directly effect blood levels . it never mentioned this hormone though
My friend Dr Nick, do you know what the real problem is? I will tell you. They say that In order to have a Coronary Disease you have to have over a 50% stenosis. Then probably you should follow guidelines. Most of us perform a CT Coronary angiography and find that there are plaques around 30% to 40% infarction to two or three arteries without having any other serious problems (HOMA IR = 1 , Triglycerides to HDL ratio 1 ...etc). AND the serious decision arises: should we take a Lowering LDL Drug or not , since we are on keto diet and we have Total Cholesterol around 250 and LDL around 180. I would appreciate your thoughts on this topic (without ofcourse taking them as a medical advice).
Ah, another biochemistry fix. Thanks Nic.
Thank you for your thank you!
Dr. Nicholas - I took Zetia for two months and asked my Dr. for a lipid panel as I was curious how the lipids where at. I suffer from high trigs, not high total cholesterol. Anyway, the results came in, and sure, my LDL was lower, but also my HDL went from 48 DOWN to 36. I quit the drug immediately and went back to fenofibrate. Could you explain this effect on HDL?
The TH-cam nutrition space seems to be hyper fixated on LDL. Despite so many statements that LDL is not a killer for most. Likely due to decades of pharma and statin promotion.
I see many statements about how LDL is much less important to lipid health than previously thought, but then followed by endless discussion of LDL control.
I debate with my doctor regarding his insistence that I take a statin, If I do take a statin my HDL goes too low. Never-mind the slightly elevated LDL.
I'm focused on a best possible triglyceride to HDL ratio.
high cholesterol is the cause of heart disease and is a major cause of mortality in the united states.
@@proper2979 I am of the understanding that one must differentiate between LDL and HDL. HDL being beneficial, LDL having little impact on CVD and mortality.
I'm increasingly understanding that triglyceride to HDL ratio is the most useful blood test result.
@@dr.coole. You have been misled. LDL is the key risk factoe (apoB technically but LDL is a good marker for apoB) for CAD and HD. All these ratios are stories told by people trying to sell you good news about your bad habits.
@@dr.coole. I have to agree with the other guy who responded to you. There is strong (but not definite) evidence that high LDL (specifically ApoB) causes atherosclerosis. There are some caveats here - what about specifically for LMHRs? We don't know, maybe high LDL among lean, healthy people is not a problem. For now, to the best of our knowledge, there is good reason to be concerned by high LDL levels. This concern only gets stronger if you are overweight and inactive.
@@proper2979By what mechanism?