Lol, such an eyelash-curling episode Simon! It's been very significant for me because I'm now 20 years older than my father who died at 52 while running before work. He had atherosclerosis at post mortem. I became vegetarian at 12 when he told me why a few hundred cows were gathered closely together in a paddock next to an abattoir on a Sunday drive in the countryside. He stopped smoking when I begged him at 8 to stop so he wouldn't die. He went cold turkey that night and i became vegetarian on the day of the Sunday drive. It was before I knew about Pritiken, and before the digital revolution. But more significantly re my still much missed father, he ate steaks with a green salad most work nights once my brother and I went to university, and he was also in a stressful high-powered job. My mother was a terrible cook so had no positive effect in the family food dynamic except as an accomplished nag with big globs of judgement. This episode was a cholesterol masterclass. Am about to have my annual blood lipids tested, but I didn't know to ask my doc about ApoB. But, I've had “good cholesterol” overall as a vegan for many years now. Am now a bit more educated about it all and about my genetics still being a possible factor. Lots of vegan food for thought. I have so many friends my age who think of me as eccentric. Funnily enough no one ever questioned my vegetarianism over many decades but being vegan/WFPB seems much more challenging for people. Unlike a commenter below I think I succeeded in catching the point of the episode. Thanks as always Simon. Your ability to help these specialists communicate the important info is always appreciated : )
If you’re in the USA ask your Dr to use the CardiaciQ blood panel at Quest. Or pay out-of-pocket and try the online testing lab mentioned in this episode at time stamp 2:05:03. They have a “Premium Heart Health” test for $150. And while you’re at it the “Cholesterol Dx” test is excellent information too as mentioned in this video.
@@christinawheeler6209 Confirmation bias. Clearly 90% of Americans have metabolic diseases which is the common denominator. Healthy Insulin sensitive Lean Mass Hyper Responders have zero Coronary Calcium Score
what a gold lecture. i have read a few books on topic, lot of biochemistry and it gets partially outdated in a year. it is hard to keep up with so many actors. love to hear new stuff to deep dive in.
WOW! What an episode! I've got to be honest, much of this went right over my head. However, I'm definitely going to have my ApoB checked after listening to this.
If I ever be able to learn Dr. Dayspring 's lecture by heart, I will tell it my future grandchildren at the age of about 10 and make it a modern fairytale and hope they will get curious enough to become cardiologists and solve this atherosclerosis mystery for the future generations.
@@TheProofWithSimonHill Simon, always enjoy your "balanced interviewing", but just fyi Tom Dayspring (as you'd be aware) copped a mention in Peter Attia's book as having bad glucose/insulin resistance. Peter guided him to fasting to help improve his risks. Bottom line the overall picture matters...even for experts.
Thank you for this! I've heard other episodes about lipids and I am always left with the same question: how to choose a statin? I don't want to go to a doctor and simply get on what he recommends blindly. I'd like to have more info on this so I can at least make the right questions when addressing the matter with a cardiologist... Both my LDL and ApoB are high and dietary changes haven't worked for the past 5 months...
Simon, could you invite Chris Masterjohn to your podcast? His insights on the antioxidant system and other topics would be incredibly valuable to the listeners
As one who suffered his first cardiac event twenty years ago I've tried to follow this stuff for quite awhile and I always appreciate those sharing this info. But I still at times get frustrated. What I was told to keep an eye on years ago now seems irrelevant...which makes me wonder if that I hear now will be irrelevant 10 years from now. Nevertheless it's all we can do. The effort to maintain a healthy lifestyle doesn't change regardless of what the info says.
Can't wait to get through this. Would love to see a long-form debate on LMHR and CVD risk. Akin to what you did with Feldman and Cromwell, but with a bigger panel including the likes of Dayspring, Attia, Norwitz, Budoff.
I'd like to hear Dayspring's interpretation of the match analysis results from the LMHR study, specifically why there was no evidence of rapid plaque accumulation despite 5 years of extremely high LDL-C.
@@gray45374 I think part of the reason is that they excluded anyone with any calcium score > 0 OR any sign of heart disease .. so - they basically started off with people they knew had no heart disease, not exactly representative.
@jp7357 I get where you are coming from, but even under those terms, the lipid hypothesis would predict significant plaque development detectable via CCTA given the magnitude of exposure in the 5 year timeframe. The principal investigator Matt Budoff has said that even one year should be sufficient to detect plaque progression in patients with LDL-C at that level. The technique is highly sensitive. Yet we don't see that in LMHRs. That's the part I don't understand. It's not consistent with the lipid hypothesis. Dave might be wrong. We don't know for sure yet. But the emerging evidence continues to line up with his model, so further research and discussion should be encouraged.
@@gray45374 indeed. I’m a big fan of cctA. However, if you exclude all the lmhr phenotypes that showed soft/calcified plaque you are just left with the ones that are genetically gifted. if one watches this lmhr stiuf, one may conclude that ALL lmhr are going to be free of plaque, which, due to the exclusion is simply not the case. I went for 50 years with ldlc > 200 and apoB > 160 .. yet ct.angiogram showed zero calcified plaque and “no vessel,disease” .. doesn’t mean I won’t start getting plaque buildup .. just means mine is slower. I had a cIMT scan which did show thickening of the carotid arterial wall .. so .. the soft plaque buildup process is happening just not detectable (right now) with a CT or CT.A. 6yrs ago I went plant based and take a statin .. my ldlc is now in the low 30’s and the soft plaque buildup in my carotids has reversed.
It's nice to hear the conventional ideas on cholesterol. It would also be nice to have somebody like Malcolm Kendrick as a guest on your show. I have watched a number of your interviews and it does 😢seem like a lot of them are vegan perspective on dieting.
When Dr. Dayspring show that 4 different LDL molecules, according to size and lipid content, I got one doubt. He says the smaller is the most feared and then shows a comparison for people with the same LDL-c. However, if we are measuring apob in mmol/dl (quantity, not mass), for two people with the same ApoB, we already know that they have the same amount of LDL-c molecules (simplification that all apob is LDL-c, instead of 90-95%). With that being said, wouldn't it be worst, in this case, to have the larger, normal lipid concent, with more cholesterol?
The study PMID: 38219649 said, "choose cooking oils, liquid margarine and soft margarine over hard margarine and butter." It was also funded by many Pharma, so if you take their advice you might destroy your health.
The Health/Integrity of the endothelial lining of blood vessels and the glycocalyx which protects it....are the two most important factors in preventing CVD. The lipids are transport molecules. Lowering your LDL will not protect your endothelial lining, and that's why people with low LDL still have heart attacks. That's also why focusing on lowering LDL has not lowered CVD. The lipid hypothesis for heart disease is just that ... a theory pushed by Big P. It's time to turn our attention to the actual cause of CVD - which is....anything that damages the glycocalyx and subsequently the endothelial lining. Things like: smoking, pollution, seed oils, glyphosate, sugar, heavy metals....etc.etc.etc.
Have you studied how inactive Matrix gla protein plays a central role in the calcification of the arteries? "Association of the Inactive Circulating Matrix Gla Protein with Vitamin K Intake, Calcification, Mortality, and Cardiovascular Disease: A Review". Journal: International Journal of Molecular Sciences Volume: 20 Issue: 3 Article Number: 628
The Spike Protein from SARS-Coronavirus or 💉 also caused inflammation of the endothelial cells. This has caused a huge spike in heart attacks and CVD. But central to the mechanism is damage to the lining of blood vessels. The idea that high LDL causes damage independently is currently being challenged by the LMHR study and thousands of people on the Carnivore diet who have no heart disease. Time will tell.
@@DrJK-wm9ec The most direct cause of damage and calcification of the arteries is inactive Matrix Gla Protein. Mice have it. Knock out the gene and they all died between 6 to 8 weeks from the calcified arteries bursting. 149 research studies have been published on MGP and calcification of arteries. Association of the Inactive Circulating Matrix Gla Protein with Vitamin K Intake, Calcification, Mortality, and Cardiovascular Disease: A Review". Journal: International Journal of Molecular Sciences Volume: 20 Issue: 3 Article Number: 628
@@DrJK-wm9echigh LDL is causal, but that doesn’t mean that it’s the only cause. That’s why you may find some people with low LDL having a CVD event. Although, they probably didn’t have ideal levels for life. Still, it’s very clear that having low LDL dramatically lowers your chance of having a heart-attack.
I heard Dr Dayspring say (at 1:20:45) that we can simply subtract HDL from total cholesterol and that gives us ApoB? So we don't need to bother with an ApoB test? (thanks for this great compilation, Simon!) ~ Marian
I’m in deep trouble. My APoB is 168, was 198 in last September. But otherwise I’m healthy. Exercise and always have a lot of energy. No high blood pressure. No insulin resistance (fasting insulin 3). Triglycerides 49. HS CRP 0.15. CAC scores zero at age 58. Do I really need to get on statins 😢🤔
Yes, long term you are at very high risk of developing CVD. You could trust the LMHR clowns ofcourse. Unfortunately they don't have any long-term hard outcome data to show those are safe. But go ahead, don't take ldl-c lowering therapy if Russian Roulette is your jam.
Your trigs are impressive. I also have a CAC score of zero, but at age 64. Apparently, they are a better assessment of risk from the age of 70 onwards since they only show hard plaque (it's been there a while) versus soft plaque. Think the tip of an iceberg hiding underwater. The tip being the older harder stuff that indicates it's been there some time. The softer plaque hidden in the arteries that doesn't show up on the scan. My APoB is, well, I will know later today, but my LDL is 158 and trigs are, also will also know later today. If I remember, will come back and report the findings of my bloodwork.
At 43:50 and 44:30 he seems to be saying it's the ApoB that's the problem, and inflammatory conditions are not required for atherosclerosis. If I understood him correctly.
Would inflammation be relevant in the context of having a causal negative effect, weakening/damaging the endothelium making intrusion of the wall easier?
@@biodieseler1 And you are most likely healty? And so you know you don't messure colesterol but Lipoproteins the carrier of colesterol. And there is only one colesterol. Not good and bad. Just good!
@simon what I was thinking about for some time now is the following, and maybe you have an answer or at least some thoughts about it: Apo(B) is the key metric to assess the likelihood for a heart attack. But can we predict with it the "time" of getting a heart attack as well? Let's say someone has a value of 1.80 (which would be above the reference range). What does it mean? Would that person get a heart attack in the next 10 days, 10 months, 10 years?
Yes sort of. We know people get symptomatic after about 4,000 mg/dl years. So multiply your ldl-c by years of exposure. Once over 4,000 mg/dl that’s generally when we start seeing symptomatic CVd at a population level
the explanation as to why peter and mary are treated differently was not satisfying. seemed full of conjecture and failed to establish that the mere presence of ldl/apo-b is to blame for foam cell creation - ie, “aggregation” explains the how, not the why (eg, the precursors that lead to mutase changing the phospholipids). also, no mention of glycation of apo-b. i can’t help but sense a bias and/or blind spot. if we don’t understand the full causal chain, then we should remain agnostic as to the risks posed by apo-b levels.
So I have done keto the last 7 months and dropped 35 pounds, which is good and I did this in attempt to reduce my A1C. Went from 5.7 to 5.6. I had my ApoB tested and it’s at 145, as is my APOa-1. Is it fair to say that if I switch to cutting the red meat and replace with chicken to reduce sat fat, and go to more Mediterranean, I will reduce these numbers? I’m 53, and CRP was also low at less than 2.
@@chriscoffey6667 There is scant difference between 5.6 and 5.7. One might have been 5.64 and the other 5.68. Barely any difference. Even at a full tenth the difference is slight and might change in a day. It’s trivial. Losing weight is significant.
@@nicmartI understand, I just figured cutting the carbs and losing the weight, it would have been lower. It’s a three ish month average, so the only thing I can come up with is at the end, when I’ve lost the weight, I’d have maybe a beer a week, and chips with salsa once a week as well. Literally that is all. For this next three months, cutting that out as well. I don’t understand otherwise what would cause this. I meal prep and eat the same daily. 8 eggs, one yolk pasture raised, at the time of this last test, lots of grass fed organic burger and steak, now I’ve replaced that with chicken and maybe twice a week eat the red meat, then later in the day I’ll eat more chicken, and maybe and egg or salmon. I know also add olive oil on top of my chicken, and I added a few fermented things like sauerkraut, kefir, and I’ll add broccoli and or arugula to my salad. It’s pretty simple.
@@chriscoffey6667 Don’t sweat the numbers. Part of it is genetic. If you a1c is good, your Lp(a) can be crap. The most important thing is to live it to the fullest.
In the context of the LMHR study, ApoB being causal is thrown out the window along with LPa. In the context of the general population which are 80+% metabolically unhealthy, yes it (ApoB) is causal because of the presence of damaged lipoproteins. We need to look at it through 2 different lenses. Fat burners vs glucose burners. It’s a simple way to put it. Fat burner meaning the Lipid Energy Model as proposed by Nick Norwitz and Dave Feldman explains the conundrum of it not being causal to this group.
You are running far ahead of the evidence here. Neither Nick nor Dave claim that ApoB or Lp(a) are "thrown out the window", nor is there any substantial evidence that those described as LMHRs are at no elevated risk from their high-ApoB / LDL. The physiological hypotheses posited by the Lipid Energy Model (LEM) are interesting and worthy of discussion, but physiological explanations do not write-off the potential for pathology. In fact, we can already explain how or why LDL-receptor expression is reduced in response to dietary factors, but that this physiological response exists or is explainable does not make it inherently "good" nor exempt from causing pathology. There's nothing wrong with testing hypotheses, but you have taken these hypotheses and turned them into something they're not. Ultimately, you can do what you want as an individual, but you have to appreciate that the establishment of guidelines & recommendations is about a lot more than just hypotheses. To date, the conclusion best supported by the body of evidence is that elevated ApoB / LDL increases risk, and that this risk is still likely to occur in a state of metabolic health, even if not to the same extent as that of metabolic ill-health (which I'm sure most agree is a reasonable conclusion given what we know about other contributing factors).
@@DrGaryMcGowan They don't "caim" that but they employ the classic demagogic trick of "just askin'". All of the LMHR work is special pleading, which the meat community has extrapolated massively. Feldman and Norwitz know that they are inflaming the issue, as evidenced by their (particulary Norwitz') click-baity titles. Their calls to honest debate ring hollow.
@@classicgameplay10 Just as for others it’s wishful thinking that it is! Tribalism needs to stop and Simon is at least open minded and becoming ever more so.
@@robertusga 2022 study title: Small Dense LDL: Scientific Background, Clinical Relevance, and Recent Evidence Still a Risk Even with ‘Normal’ LDL-C Levels. This explains everything you need to know that the man in the video hid from the public because he can sell all the statins to lower LDL but it won't effect the sdLDL which is more important and having higher HDL levels is also more important but he can't sell meds for that. He only promotes what he can sell but what does that have to do with your overall health?
@Jeffs60 please share outcome data where lowering ApoB did not reduce risk related to particle size. The idea of particle size being important has been long debunked. RIsk follows particle number, not particle size.
Your guest gives a masterclass on how the body efficiently makes and uses lipid carriers and how LDL is more involved in returning cholesterol to the liver than HDL. Inexplicably then says states too much apoB will cause atherosclerosis. Then states kids don’t have much lipid issues or didn’t before ultra processed food was ubiquitous. When will we realize, it’s not the lipids that’s the problem. It’s the damage we do to ourselves with the unnatural substances we keep ingesting in copious amounts. Even the science expert is influenced by “common knowledge” of high LDL causes atherosclerosis. SMH
Enjoyed the talks very much. Very little recognition of Lp(a) which from my research is by far the most atherogenic particle. Dayspring completely dismissed the question of all cause mortality. He came across as knowledgeable but an arrogant know-it-all and these sort of people are the most unlikely to ever change their mind or admit they are wrong. Too much certainty in his delivery for a topic that clearly is not completely understood. And my last comment, isn’t there evidence that a macrophage will only react to an oxidised LDL or glycated LDL particle but won’t react at all to a healthy LDL particle?
Your level of Lipoprotein(a) which is in your genetics for a reason means nothing as there are people over age 100 who have had lifetime elevated levels for longevity and people with low levels that get heart attacks at a young age.
Hmmm, not so sure Jeff. Just because something is in your genetics doesn’t mean it’s a benefit. It would have been a benefit for most of humanity because it’s used to increase the bodies ability to deal with wounds. Not really essential anymore. I personally have very high Lp(a). For the majority of my life I followed the ‘low fat’ way of eating and for all that time I had very low LDL. Admittedly I didn’t know my apoB. But after 50 years of that i discovered I had a positive calcium score so something wasn’t working. Then found out about my sky high Lp(a).
@@stevemc2626 Your Lp(a) level is not the cause, you have to find out what the real cause is. What were you eating most of your life and what is your BMI? Low fat diet causes friction in the body. Who told you to eat low fat and what was that persons credentials?
BMI 22. I’ve never had a bit of fat on me. Who told me to eat low fat? The bloody food pyramid that I grew up with. I’m certainly not eating that way now and haven’t for the last 3 years but unfortunately that leaves 49 years of eating an overload of carbs. I’m scared to think of what my carb count was back in the day when I ate bread like it was about to go out of fashion and juicing fruits and veggies every day.
Does the concordance or discordance that person might have between non LDL cholesterol and ApoB particles stay more less the same during a lifetime or does it change? If the concordance is genetic and stable then you would only need one measure of both once to check if they correlate and after that non LDL measurements would be enough to check the ApoB.
It changes depending on whether the LDLs are cholesterol-rich or cholesterol-depleted - mostly related to coexisting IR and TG enrichment of LDLs (which may have no relation to serum TG)
Age 68. Oh,oh Apo b: 75 APLa: 37 Triglycerides: 55 … and a overproducing platelet disorder A1c: 5.7 Coronary Calcium Score :zero, 2. 1/2 yrs ago. I am starting to feel I should be on a statin
I see we are gradually moving away from LDL as a predictor of heart disease....as predicted by me a while back. I've never bothered about my high LDL I don't have heart disease. 0 CAC score every five years and my diet is the same. I get a lot of exercise and eat a real food diet including dairy eggs and animals but no seed oils. My doctor is very happy with me, despite higher LDL I have no inflammation and no blood sugar issues or insulin resistance or high platelets or anything that would indicate clotting risk - in fact I'm very healthy for an old fart. I've never had my ApoB tested, just the standard cholesterol tests but because my triglycerides are always very very very low I'm always 'good to go'. I get a script for statins though but I only use them if I'm sick as that increase clotting factors and as the doctor says because of my higher LDL he has to prescribe. I want my co enzyme q10 though so why would I reduce that by taking statins! that's the energy for the body. The PURE investigators found that saturated fat was not associated with risk of myocardial infarction or cardiovascular disease mortality and was significantly associated with lower total mortality as well as lower risk of stroke [34]. I don't worry about it, if you eat real food and don't eat tons of adulterated junk your intake should be just in the foods you eat, nuts, olive oil, lean meat, dairy = not high levels in a normal diet.
@@tdayspring I always learn something from you ... and Ive been paying attention for a long time. Today it was circulating apoA1 collect cholesterol and become HDL .. I always figured small HDL were made "somewhere" (liver) and got bigger ... I'm less dumb than I was 2 days ago - thank you.
All cells produce all the cholesterol they need. "All somatic cells, including astrocytes and oligodendrocytesin the brain, make cholesterol through the same pathway that the liver utilizes, and can obtain some from High-Density Lipoprotein (HDL). Even when LDL-C is extremely low, there is no impairment of cellular cholesterol production and utilization within the brain because the brain produces its own pool of cholesterol , as do all cells in the body. No tissues depend on cholesterol transfer from LDL-C" www.sciencedirect.com/science/article/pii/S2666667722000551?via%3Dihub
Every LDL study shows a hockey stick graph but these guys explain it away. Why do studies if you’re just make excuses for results you don’t agree with??
- switches to a cheese / bacon diet - looses weight, this is nice - LDL goes to the 200's but some youtubers say its gud - ends up with a cardiac event and arteries of a 90 100 year old - * surprised pikachu *
41:35 " the endothelium it's going to get stuck there that apob protein on the surface of at the particle has great affinity for connective tissue molecules uh uh glycoproteins that bind the apob particle and it's like a flies on fly paper it's stuck now sometimes it's just stuck there nothing ever happens who cares very few of them break free and can leech out again back into the plasma perhaps a minuscule number but once they crash there they're stuck in the arterial wall so as they're bound to these prot glycans in the arterial wall they can just be bound there forever and like a mummy it'll they'll just ultimately shrink up add to the connective tissue and they're of no consequence because for atherosclerosis to develop uh apob cholesterol containing particle has to be ingested by a maccrage that is in the arterial wall connective tissue how did the maccrage get in there a monocyte left the bloodstream it passes through the endothelium there receptors that pull it in and it transforms into a maccrage in the arterial a maccrage is basically a white blood cell capable of Scavenging eating things so what makes some of the retained apob particles a substrate for receptors on maccrage is that they will internalize them and now if that maccrage keeps internalizing humongous numbers of apob cholesterol carrying particles before you know it the macroy BEC super cholesterol Eng Gorge they're called foam cells because they look foamy if you look at them in a microscope and that if you get a maccrage that turns into a foam cell and you get a few billion of those maccrage that is plaque initially a fatty streak in the artery wall after that more localized collections of cholesterol and over time they get bigger and bigger and bigger most of the disease early on is in the wall of the artery it's notobstructing the arterial wall loom in it all sooner or later bad things can happen but the million dooll question is after the apob particle goes through the endothelium why do some get ingested by macrofagos and others do not a word first about what you said the transendothelial passage transcytosis of the apob particle that can occur with perfectly healthy endothelial cells you do not need an flame Disturbed endothelium for that particle to pass right through it cavoli and there's other receptors that just pull those particles through there is a little gap between endothelial cells a perivascular sort of Channel they can sneak throughthat these are very very small particles you know 20 micrograms 21 micro Nan grams uh Mill millimeters excuse me they get in so but they certainly can get in with greater frequency if the endothelium happens to be disturbed or inflamed and most of the inflammation ofendothelium and atheros scerotic disease is because those macres I told you about they start ingesting the particles they."
54:33 " it's mostly ldls the vldls have a plasma resonance time of a few hours kyom microns less than an hour idls an hour LDL several days so when you measure apob 90 to 95% of your apob nparticles are ldls so yes a vldl or colam Micron Remnant can make its way into the ottery wall but it's like you know 95% of the Army is LDL particles that are doing The Invasion "
@@TheProofWithSimonHill so ApoB and lipoproteins are not a natural function of the body.And only when compromised by glycation and oxidation is it a problem.
Dayspring needs to just stick to speaking about the proven mechanistic science of the lipoprotein system and forget about his belief in the associational data. When it comes to ApoB causing cvd, it’s just his ‘opinion’ and nothing else.
Wow, it took 55 minutes to get to LDL is 95% of Apob. Then we get LDL is causal in atherosclerosis a then back the old genitics theroy. This is way out dated theroy. I am personally very pleased that with a excellent HDL and Trigs and great ratieo, and an excellent metabulism, LDL classed as high by the likes of this doctor is a great longevity marker. Judgeing by his questions I think Simon knows this. The doctor is stuck in the 1970's. Science has moved on, so should the doctor.
@@bobhill4364 I try to maintain an open mind and keep learning. You’re mistaken if you believe science doesn’t evolve or change (sometimes radically). I refuse to be over-influenced by UA-camrs with any “agenda”, though some from both “camps” are prepared to listen and learn…as Simon Hill is.
@@bobhill4364 If "science" does not change it is not science but propaganda, narrative, opinion or dogma. Science continuously evolves as we continuously learn.
@@murraypooley9199 It's shocking how you guys butcher this and I agree with your statement. If something is no longer open to being challenged, then it is not science. New studies have been done and they still align with the old data and that suggests that a diet high in fiber(fruits, vegetables, whole grains, beans) are best for longevity, with high saturated fat foods showing the opposite effect. Science is not supposed to change, it is supposed to be open to challenge. But social media influencers asserting an all meat diet is healthiest is not evidence lol. And trust me, I would love for the evidence to show you can eat whatever you want for optimal health but it is what it is.
@@joshuachia504 It's sad. Now a lot of the low carbers are eating loads of fruit and honey. Lol so now carbs are ok as long as they taste nice. I don't know how this isn't so obvious. Adults rebelling like they did as kids because they were made to eat the mushy veggies they didn't want.
@@bobhill4364 Excuse me but a confused LLM might think that fruit & honey are low-carb. What I mean is that you can have high LDL despite eating large amounts of vegetables especially when on a low-carb diet.
@@joshuachia504 Low carb and carnivore doctor Paul Saladino now eats tons of fruits and gallons of honey. You can certainly have high ldl if you have a genetic disposition, but more frequently, it's the loads of saturated fat low carbers tend to eat.
Don’t forget that the majority of humanity are omnivorous. Just because two opposing “Tribes” are constantly at each other’s throats doesn’t mean they speak for that vast majority. Let both extremes carry-on believing they have found “The Panacea”!
What I learned from ex-vegans is not to go vegan because of some health benefits. I agree with that sentiment, it takes more than simply going vegan to get guaranteed health benefis. What I have not heard from ex-vegans however, is why not to go and stay vegan for the animals. They are innocent and deserve better, imho.
Ironic name of "longevity coach" and not promoting the vegan or heavily plant based diet, while presumably being more meat based which is not longevity confering. Also the current context of Apo-B is not vegan propaganda, not sure how that's even relevant to the current video.
@@stisca well, I have some salads growing but now hundreds of animals are coming to eat them. So, should I kill all those hundreds of animals to eat salads for few weeks or should I kill one of my cows to have food for the next six months or longer?
@bobhill4364 You are deluded but even if you are right and I was to get heath problems some time in the future, as I test regually any problems arising would be picked up on and lifestyle adjusted. Meanwhle I will continue to enjoy excellent health and vitality. Meanwhile I am willing to bet my health and future outlook is far better than you and most if not all of the sick people on this channel.
Lol, such an eyelash-curling episode Simon! It's been very significant for me because I'm now 20 years older than my father who died at 52 while running before work. He had atherosclerosis at post mortem. I became vegetarian at 12 when he told me why a few hundred cows were gathered closely together in a paddock next to an abattoir on a Sunday drive in the countryside. He stopped smoking when I begged him at 8 to stop so he wouldn't die. He went cold turkey that night and i became vegetarian on the day of the Sunday drive. It was before I knew about Pritiken, and before the digital revolution. But more significantly re my still much missed father, he ate steaks with a green salad most work nights once my brother and I went to university, and he was also in a stressful high-powered job. My mother was a terrible cook so had no positive effect in the family food dynamic except as an accomplished nag with big globs of judgement. This episode was a cholesterol masterclass. Am about to have my annual blood lipids tested, but I didn't know to ask my doc about ApoB. But, I've had “good cholesterol” overall as a vegan for many years now. Am now a bit more educated about it all and about my genetics still being a possible factor. Lots of vegan food for thought. I have so many friends my age who think of me as eccentric. Funnily enough no one ever questioned my vegetarianism over many decades but being vegan/WFPB seems much more challenging for people. Unlike a commenter below I think I succeeded in catching the point of the episode. Thanks as always Simon. Your ability to help these specialists communicate the important info is always appreciated : )
Do you think anyone cares about what you eat ?.
If you’re in the USA ask your Dr to use the CardiaciQ blood panel at Quest. Or pay out-of-pocket and try the online testing lab mentioned in this episode at time stamp 2:05:03. They have a “Premium Heart Health” test for $150. And while you’re at it the “Cholesterol Dx” test is excellent information too as mentioned in this video.
@@kenadams5504 yes, we do. Case closed.
This doctor is brilliant, love his passion on the subject.
@@christinawheeler6209
Confirmation bias. Clearly 90% of Americans have metabolic diseases which is the common denominator. Healthy Insulin sensitive Lean Mass Hyper Responders have zero Coronary Calcium Score
what a gold lecture. i have read a few books on topic, lot of biochemistry and it gets partially outdated in a year. it is hard to keep up with so many actors. love to hear new stuff to deep dive in.
Glad to hear that!
WOW! What an episode! I've got to be honest, much of this went right over my head. However, I'm definitely going to have my ApoB checked after listening to this.
Happy ApoB at 60! Amazing series of interviews
If I ever be able to learn Dr. Dayspring 's lecture by heart, I will tell it my future grandchildren at the age of about 10 and make it a modern fairytale and hope they will get curious enough to become cardiologists and solve this atherosclerosis mystery for the future generations.
@@orchidmuse
Glucose to ketone index of less than 2 may do the trick for reversal of at least the soft plaque
He is great! So enthusiastic ❤
Passionate and lots of information
Thanks for having him
What a fantastic presentation b y Dr. Daysprings. I was so intrigued !
Glad you enjoyed it!
@@TheProofWithSimonHill Simon, always enjoy your "balanced interviewing", but just fyi Tom Dayspring (as you'd be aware) copped a mention in Peter Attia's book as having bad glucose/insulin resistance. Peter guided him to fasting to help improve his risks. Bottom line the overall picture matters...even for experts.
Thank you for this! I've heard other episodes about lipids and I am always left with the same question: how to choose a statin? I don't want to go to a doctor and simply get on what he recommends blindly. I'd like to have more info on this so I can at least make the right questions when addressing the matter with a cardiologist... Both my LDL and ApoB are high and dietary changes haven't worked for the past 5 months...
Amazing and wonderfully informative episode. Thank you.
Glad you enjoyed it!
Simon, you have a very soothing voice.
Amazing guests, Simon. Kudos to you. 👏👍
Please do a podcast about Lean Mass Hyper Responders 🙏
Simon, could you invite Chris Masterjohn to your podcast? His insights on the antioxidant system and other topics would be incredibly valuable to the listeners
Is this a troll post?
@@CM-ss7yy Why would you think that?
Masterjohn is a conspiracy theorist wacko.
@Krunch2020 I think differently. He seems balanced, rational, and has good points on many aspects
As one who suffered his first cardiac event twenty years ago I've tried to follow this stuff for quite awhile and I always appreciate those sharing this info. But I still at times get frustrated. What I was told to keep an eye on years ago now seems irrelevant...which makes me wonder if that I hear now will be irrelevant 10 years from now. Nevertheless it's all we can do. The effort to maintain a healthy lifestyle doesn't change regardless of what the info says.
Can't wait to get through this.
Would love to see a long-form debate on LMHR and CVD risk. Akin to what you did with Feldman and Cromwell, but with a bigger panel including the likes of Dayspring, Attia, Norwitz, Budoff.
I suspect it would be a blood bath, I get the feeling saying LMHR to Dr Dayspring would be a red flag to a seriously enraged bull.
I'd like to hear Dayspring's interpretation of the match analysis results from the LMHR study, specifically why there was no evidence of rapid plaque accumulation despite 5 years of extremely high LDL-C.
@@gray45374 I think part of the reason is that they excluded anyone with any calcium score > 0 OR any sign of heart disease .. so - they basically started off with people they knew had no heart disease, not exactly representative.
@jp7357 I get where you are coming from, but even under those terms, the lipid hypothesis would predict significant plaque development detectable via CCTA given the magnitude of exposure in the 5 year timeframe.
The principal investigator Matt Budoff has said that even one year should be sufficient to detect plaque progression in patients with LDL-C at that level. The technique is highly sensitive.
Yet we don't see that in LMHRs. That's the part I don't understand. It's not consistent with the lipid hypothesis.
Dave might be wrong. We don't know for sure yet. But the emerging evidence continues to line up with his model, so further research and discussion should be encouraged.
@@gray45374 indeed. I’m a big fan of cctA. However, if you exclude all the lmhr phenotypes that showed soft/calcified plaque you are just left with the ones that are genetically gifted. if one watches this lmhr stiuf, one may conclude that ALL lmhr are going to be free of plaque, which, due to the exclusion is simply not the case. I went for 50 years with ldlc > 200 and apoB > 160 .. yet ct.angiogram showed zero calcified plaque and “no vessel,disease” .. doesn’t mean I won’t start getting plaque buildup .. just means mine is slower. I had a cIMT scan which did show thickening of the carotid arterial wall .. so .. the soft plaque buildup process is happening just not detectable (right now) with a CT or CT.A. 6yrs ago I went plant based and take a statin .. my ldlc is now in the low 30’s and the soft plaque buildup in my carotids has reversed.
This guy is brilliant
What a beautiful, uplifting message. Thank you for sharing. ❤
Are you psycho?
This guy is the only Doc I've seen, saying hdl amount doesn't matter .
This was a fantastic listen.
It's nice to hear the conventional ideas on cholesterol. It would also be nice to have somebody like Malcolm Kendrick as a guest on your show. I have watched a number of your interviews and it does 😢seem like a lot of them are vegan perspective on dieting.
When Dr. Dayspring show that 4 different LDL molecules, according to size and lipid content, I got one doubt. He says the smaller is the most feared and then shows a comparison for people with the same LDL-c. However, if we are measuring apob in mmol/dl (quantity, not mass), for two people with the same ApoB, we already know that they have the same amount of LDL-c molecules (simplification that all apob is LDL-c, instead of 90-95%). With that being said, wouldn't it be worst, in this case, to have the larger, normal lipid concent, with more cholesterol?
Please share link to study confirming LDL receptor down-regulation from the consumption of saturated fatty acids.
PMID: 38219649
The study PMID: 38219649 said, "choose cooking oils, liquid margarine and soft margarine over hard margarine and butter." It was also funded by many Pharma, so if you take their advice you might destroy your health.
Thanks for another great episode!
Great video Simon, et al.!
Great podcast 🙌🏽
The Health/Integrity of the endothelial lining of blood vessels and the glycocalyx which protects it....are the two most important factors in preventing CVD. The lipids are transport molecules. Lowering your LDL will not protect your endothelial lining, and that's why people with low LDL still have heart attacks. That's also why focusing on lowering LDL has not lowered CVD. The lipid hypothesis for heart disease is just that ... a theory pushed by Big P. It's time to turn our attention to the actual cause of CVD - which is....anything that damages the glycocalyx and subsequently the endothelial lining. Things like: smoking, pollution, seed oils, glyphosate, sugar, heavy metals....etc.etc.etc.
Have you studied how inactive Matrix gla protein plays a central role in the calcification of the arteries? "Association of the Inactive Circulating Matrix Gla Protein with Vitamin K Intake, Calcification, Mortality, and Cardiovascular Disease: A Review".
Journal: International Journal of Molecular Sciences
Volume: 20
Issue: 3
Article Number: 628
The Spike Protein from SARS-Coronavirus or 💉 also caused inflammation of the endothelial cells. This has caused a huge spike in heart attacks and CVD.
But central to the mechanism is damage to the lining of blood vessels. The idea that high LDL causes damage independently is currently being challenged by the LMHR study and thousands of people on the Carnivore diet who have no heart disease.
Time will tell.
@@DrJK-wm9ec The most direct cause of damage and calcification of the arteries is inactive Matrix Gla Protein.
Mice have it.
Knock out the gene and they all died between 6 to 8 weeks from the calcified arteries bursting.
149 research studies have been published on MGP and calcification of arteries.
Association of the Inactive Circulating Matrix Gla Protein with Vitamin K Intake, Calcification, Mortality, and Cardiovascular Disease: A Review".
Journal: International Journal of Molecular Sciences
Volume: 20
Issue: 3
Article Number: 628
@@DrJK-wm9echigh LDL is causal, but that doesn’t mean that it’s the only cause. That’s why you may find some people with low LDL having a CVD event. Although, they probably didn’t have ideal levels for life. Still, it’s very clear that having low LDL dramatically lowers your chance of having a heart-attack.
@@CharlieFader it is not all that clear, really. 🤔
I heard Dr Dayspring say (at 1:20:45) that we can simply subtract HDL from total cholesterol and that gives us ApoB? So we don't need to bother with an ApoB test? (thanks for this great compilation, Simon!) ~ Marian
Not quite - gives us a close proxy known as NON-HDL-C.
@@TheProofWithSimonHill Ah, yes, got it! And ApoB is even more accurate than non-HDL-C so get ApoB if we can. Thanks!
I’m in deep trouble. My APoB is 168, was 198 in last September. But otherwise I’m healthy. Exercise and always have a lot of energy. No high blood pressure. No insulin resistance (fasting insulin 3). Triglycerides 49. HS CRP 0.15. CAC scores zero at age 58. Do I really need to get on statins 😢🤔
Just change your diet.
If you listen to these guys you’ll probably get dementia and forget about how healthy u r
Yes, long term you are at very high risk of developing CVD. You could trust the LMHR clowns ofcourse. Unfortunately they don't have any long-term hard outcome data to show those are safe. But go ahead, don't take ldl-c lowering therapy if Russian Roulette is your jam.
You need to consult a lipidologist as your apoB is > 95th population percentile cut point
Your trigs are impressive. I also have a CAC score of zero, but at age 64. Apparently, they are a better assessment of risk from the age of 70 onwards since they only show hard plaque (it's been there a while) versus soft plaque. Think the tip of an iceberg hiding underwater. The tip being the older harder stuff that indicates it's been there some time. The softer plaque hidden in the arteries that doesn't show up on the scan. My APoB is, well, I will know later today, but my LDL is 158 and trigs are, also will also know later today. If I remember, will come back and report the findings of my bloodwork.
At 43:50 and 44:30 he seems to be saying it's the ApoB that's the problem, and inflammatory conditions are not required for atherosclerosis. If I understood him correctly.
Would inflammation be relevant in the context of having a causal negative effect, weakening/damaging the endothelium making intrusion of the wall easier?
The True Believers are out in full force in the comments.
To be honest, it looks like a orchestrated effort. Bots perhaps ? Aí generated comments ?
@@classicgameplay10 there is a theory that the majority of comments in the internet are made by bots and trolls. Kind of "dead internet".
Agreed…from both sides of “The Divide”!
yup, they remind me of flat-earthers
@@veganfortheanimals6994 Kind of like the anti seed oil crowd. They'll just make things up about seed oils based on no evidence at all.
My non-HDL cholesterol is 395. I wonder what percentile I'm in ...
99.9 population percentile - lethal over time Change your diet and seek care
@@biodieseler1 And you are most likely healty? And so you know you don't messure colesterol but Lipoproteins the carrier of colesterol. And there is only one colesterol. Not good and bad. Just good!
@simon what I was thinking about for some time now is the following, and maybe you have an answer or at least some thoughts about it: Apo(B) is the key metric to assess the likelihood for a heart attack. But can we predict with it the "time" of getting a heart attack as well? Let's say someone has a value of 1.80 (which would be above the reference range). What does it mean? Would that person get a heart attack in the next 10 days, 10 months, 10 years?
Yes sort of. We know people get symptomatic after about 4,000 mg/dl years. So multiply your ldl-c by years of exposure. Once over 4,000 mg/dl that’s generally when we start seeing symptomatic CVd at a population level
@@TheProofWithSimonHill thanks, that interesting. But that refers to LDL-C. What about Apo(B)? Or is it the same?
@@KolinSchunckalmost the same. For example, the cutoff for LDL is around 70 and for ApoB is 80.
Great content. Thanks you
He never answered the question about target levels for ApoB.
50 mg/dl for those at high risk of cvd. 80 mg/dl if low risk
@@TheProofWithSimonHill Thank you! Greatly appreciate all of your work.
@@TheProofWithSimonHill
Sez who? Normal range is 46-174. I just had a test.
@@nicmart My test range shows
the explanation as to why peter and mary are treated differently was not satisfying. seemed full of conjecture and failed to establish that the mere presence of ldl/apo-b is to blame for foam cell creation - ie, “aggregation” explains the how, not the why (eg, the precursors that lead to mutase changing the phospholipids). also, no mention of glycation of apo-b. i can’t help but sense a bias and/or blind spot. if we don’t understand the full causal chain, then we should remain agnostic as to the risks posed by apo-b levels.
I agree!
Can chylomicrons get trapped in the spaces
In the lymphatic system causing fibrosis or lipomas?
So I have done keto the last 7 months and dropped 35 pounds, which is good and I did this in attempt to reduce my A1C. Went from 5.7 to 5.6. I had my ApoB tested and it’s at 145, as is my APOa-1. Is it fair to say that if I switch to cutting the red meat and replace with chicken to reduce sat fat, and go to more Mediterranean, I will reduce these numbers? I’m 53, and CRP was also low at less than 2.
5.7 to 5.6 could be a lab variation or just a fraction of a fraction difference. Means nothing.
Well I’ve cut carbs to max 30 a day, and most days maybe 5-10, and lost 40 pounds. So, little confused on how that’s even possible.
@@chriscoffey6667
There is scant difference between 5.6 and 5.7. One might have been 5.64 and the other 5.68. Barely any difference. Even at a full tenth the difference is slight and might change in a day. It’s trivial. Losing weight is significant.
@@nicmartI understand, I just figured cutting the carbs and losing the weight, it would have been lower. It’s a three ish month average, so the only thing I can come up with is at the end, when I’ve lost the weight, I’d have maybe a beer a week, and chips with salsa once a week as well. Literally that is all. For this next three months, cutting that out as well. I don’t understand otherwise what would cause this. I meal prep and eat the same daily. 8 eggs, one yolk pasture raised, at the time of this last test, lots of grass fed organic burger and steak, now I’ve replaced that with chicken and maybe twice a week eat the red meat, then later in the day I’ll eat more chicken, and maybe and egg or salmon. I know also add olive oil on top of my chicken, and I added a few fermented things like sauerkraut, kefir, and I’ll add broccoli and or arugula to my salad. It’s pretty simple.
@@chriscoffey6667
Don’t sweat the numbers. Part of it is genetic. If you a1c is good, your Lp(a) can be crap. The most important thing is to live it to the fullest.
So much fantastic info! Thank you👏👏👏
What’s a bad apob number?
Download the pdf at theproof.com/lipidseries
In the context of the LMHR study, ApoB being causal is thrown out the window along with LPa. In the context of the general population which are 80+% metabolically unhealthy, yes it (ApoB) is causal because of the presence of damaged lipoproteins. We need to look at it through 2 different lenses. Fat burners vs glucose burners. It’s a simple way to put it. Fat burner meaning the Lipid Energy Model as proposed by Nick Norwitz and Dave Feldman explains the conundrum of it not being causal to this group.
Except that there is no evidence that is not causal in this group, for now is just wishful thinking.
Special pleading.
You are running far ahead of the evidence here.
Neither Nick nor Dave claim that ApoB or Lp(a) are "thrown out the window", nor is there any substantial evidence that those described as LMHRs are at no elevated risk from their high-ApoB / LDL. The physiological hypotheses posited by the Lipid Energy Model (LEM) are interesting and worthy of discussion, but physiological explanations do not write-off the potential for pathology. In fact, we can already explain how or why LDL-receptor expression is reduced in response to dietary factors, but that this physiological response exists or is explainable does not make it inherently "good" nor exempt from causing pathology.
There's nothing wrong with testing hypotheses, but you have taken these hypotheses and turned them into something they're not. Ultimately, you can do what you want as an individual, but you have to appreciate that the establishment of guidelines & recommendations is about a lot more than just hypotheses. To date, the conclusion best supported by the body of evidence is that elevated ApoB / LDL increases risk, and that this risk is still likely to occur in a state of metabolic health, even if not to the same extent as that of metabolic ill-health (which I'm sure most agree is a reasonable conclusion given what we know about other contributing factors).
@@DrGaryMcGowan They don't "caim" that but they employ the classic demagogic trick of "just askin'". All of the LMHR work is special pleading, which the meat community has extrapolated massively. Feldman and Norwitz know that they are inflaming the issue, as evidenced by their (particulary Norwitz') click-baity titles. Their calls to honest debate ring hollow.
@@classicgameplay10 Just as for others it’s wishful thinking that it is! Tribalism needs to stop and Simon is at least open minded and becoming ever more so.
I just read the article which was written in 2019. Looks like K2 supplementation (MK7) up-regulated MPG- a powerful natural calcification inhibitor.
Some studies say the most important blood test is the sdLDL test and not ApoB.
Lol. "Some studies say". Uhuh.
@@robertusga 2022 study title: Small Dense LDL: Scientific Background, Clinical Relevance, and Recent Evidence Still a Risk Even with ‘Normal’ LDL-C Levels.
This explains everything you need to know that the man in the video hid from the public because he can sell all the statins to lower LDL but it won't effect the sdLDL which is more important and having higher HDL levels is also more important but he can't sell meds for that. He only promotes what he can sell but what does that have to do with your overall health?
@Jeffs60 lol. He does not sell statins. Go ahead, ignore all outcome data showing ApoB causal in CVD. Free country.
@@robertusga ApoB is important and statins can lower the level but won't help if your sdLDL is not optimal.
@Jeffs60 please share outcome data where lowering ApoB did not reduce risk related to particle size. The idea of particle size being important has been long debunked. RIsk follows particle number, not particle size.
Wondering what will be the MENDELIAN RANDOMIZATION for INSULIN RESISTANT individual and INSULIN SENSITIVE Individuals?
Capitol letters are metabolic death.
The man who knows too much, meaning Mr. Dayspring.
Your guest gives a masterclass on how the body efficiently makes and uses lipid carriers and how LDL is more involved in returning cholesterol to the liver than HDL. Inexplicably then says states too much apoB will cause atherosclerosis. Then states kids don’t have much lipid issues or didn’t before ultra processed food was ubiquitous. When will we realize, it’s not the lipids that’s the problem. It’s the damage we do to ourselves with the unnatural substances we keep ingesting in copious amounts. Even the science expert is influenced by “common knowledge” of high LDL causes atherosclerosis. SMH
Nope you just didn’t understand what he explained
Is not LDL is the quality of the collagen simple
Enjoyed the talks very much.
Very little recognition of Lp(a) which from my research is by far the most atherogenic particle.
Dayspring completely dismissed the question of all cause mortality. He came across as knowledgeable but an arrogant know-it-all and these sort of people are the most unlikely to ever change their mind or admit they are wrong. Too much certainty in his delivery for a topic that clearly is not completely understood.
And my last comment, isn’t there evidence that a macrophage will only react to an oxidised LDL or glycated LDL particle but won’t react at all to a healthy LDL particle?
Your level of Lipoprotein(a) which is in your genetics for a reason means nothing as there are people over age 100 who have had lifetime elevated levels for longevity and people with low levels that get heart attacks at a young age.
Hmmm, not so sure Jeff. Just because something is in your genetics doesn’t mean it’s a benefit. It would have been a benefit for most of humanity because it’s used to increase the bodies ability to deal with wounds. Not really essential anymore. I personally have very high Lp(a). For the majority of my life I followed the ‘low fat’ way of eating and for all that time I had very low LDL. Admittedly I didn’t know my apoB. But after 50 years of that i discovered I had a positive calcium score so something wasn’t working. Then found out about my sky high Lp(a).
@@stevemc2626 Your Lp(a) level is not the cause, you have to find out what the real cause is. What were you eating most of your life and what is your BMI? Low fat diet causes friction in the body. Who told you to eat low fat and what was that persons credentials?
BMI 22. I’ve never had a bit of fat on me. Who told me to eat low fat? The bloody food pyramid that I grew up with. I’m certainly not eating that way now and haven’t for the last 3 years but unfortunately that leaves 49 years of eating an overload of carbs. I’m scared to think of what my carb count was back in the day when I ate bread like it was about to go out of fashion and juicing fruits and veggies every day.
Does the concordance or discordance that person might have between non LDL cholesterol and ApoB particles stay more less the same during a lifetime or does it change? If the concordance is genetic and stable then you would only need one measure of both once to check if they correlate and after that non LDL measurements would be enough to check the ApoB.
It changes depending on whether the LDLs are cholesterol-rich or cholesterol-depleted - mostly related to coexisting IR and TG enrichment of LDLs (which may have no relation to serum TG)
Thank you
What was the one test?
ApoB
well done...
Age 68. Oh,oh Apo b: 75
APLa: 37
Triglycerides: 55
… and a overproducing platelet disorder
A1c: 5.7
Coronary Calcium Score :zero, 2. 1/2 yrs ago.
I am starting to feel I should be on a statin
I see we are gradually moving away from LDL as a predictor of heart disease....as predicted by me a while back.
I've never bothered about my high LDL I don't have heart disease. 0 CAC score every five years and my diet is the same. I get a lot of exercise and eat a real food diet including dairy eggs and animals but no seed oils.
My doctor is very happy with me, despite higher LDL I have no inflammation and no blood sugar issues or insulin resistance or high platelets or anything that would indicate clotting risk - in fact I'm very healthy for an old fart.
I've never had my ApoB tested, just the standard cholesterol tests but because my triglycerides are always very very very low I'm always 'good to go'.
I get a script for statins though but I only use them if I'm sick as that increase clotting factors and as the doctor says because of my higher LDL he has to prescribe. I want my co enzyme q10 though so why would I reduce that by taking statins! that's the energy for the body.
The PURE investigators found that saturated fat was not associated with risk of myocardial infarction or cardiovascular disease mortality and was significantly associated with lower total mortality as well as lower risk of stroke [34].
I don't worry about it, if you eat real food and don't eat tons of adulterated junk your intake should be just in the foods you eat, nuts, olive oil, lean meat, dairy = not high levels in a normal diet.
Good luck!
.clever of you to predict that apoB would take over from ldlc and not get an apoB test. Almost clairvoyant.
@@jp7357 haha, yep
Your doctor needs remedial study
@@tdayspring I always learn something from you ... and Ive been paying attention for a long time. Today it was circulating apoA1 collect cholesterol and become HDL .. I always figured small HDL were made "somewhere" (liver) and got bigger ... I'm less dumb than I was 2 days ago - thank you.
5:13 arent micelles basically soap? 😭
What about the role cholesterol plays in immune function. At what point does lower cholesterol levels negatively impact your immune system???
All cells produce all the cholesterol they need.
"All somatic cells, including astrocytes and oligodendrocytesin the brain, make cholesterol through the same pathway that the liver utilizes, and can obtain some from High-Density Lipoprotein (HDL). Even when LDL-C is extremely low, there is no impairment of cellular cholesterol production and utilization within the brain because the brain produces its own pool of cholesterol , as do all cells in the body. No tissues depend on cholesterol transfer from LDL-C"
www.sciencedirect.com/science/article/pii/S2666667722000551?via%3Dihub
Bingo - it is why the lipophilic statins can damage your brain/memory via blocking the brain's ability to make cholesterol
Cholesterol circulating in plasma has no relation to immunity
@@tdayspring Sure thing
Thanks to both of you for addressing the question.
Every LDL study shows a hockey stick graph but these guys explain it away. Why do studies if you’re just make excuses for results you don’t agree with??
- switches to a cheese / bacon diet
- looses weight, this is nice
- LDL goes to the 200's but some youtubers say its gud
- ends up with a cardiac event and arteries of a 90 100 year old
- * surprised pikachu *
My ApoB is fine, my Lp(a) is too high. My calcium score is too high. Not a damned thing can be done about it yet.
Pauling protocol?
fluffy buffy LOL
41:35 " the endothelium it's going to get stuck there that apob protein on the surface of at the particle has great affinity for connective tissue molecules uh uh glycoproteins that bind the apob particle and it's like a flies on fly paper it's stuck now sometimes it's just stuck there nothing ever happens who cares very few of them break free and can leech out again back into the plasma perhaps a minuscule number but once they crash there they're stuck in the arterial wall so as they're bound to these prot glycans in the arterial wall they can just be bound there forever and like a mummy it'll they'll just ultimately shrink up add to the connective tissue and they're of no consequence because for atherosclerosis to develop uh apob cholesterol containing particle has to be ingested by a maccrage that is in the arterial wall connective tissue how did the maccrage get in there a monocyte left the bloodstream it passes through the endothelium there receptors that pull it in and it transforms into a maccrage in the arterial a maccrage is basically a white blood cell capable of Scavenging eating things so what makes some of the retained apob particles a substrate for receptors on maccrage is that they will internalize them and now if that maccrage keeps internalizing humongous numbers of apob cholesterol carrying particles before you know it the macroy BEC super cholesterol Eng Gorge they're called foam cells because they look foamy if you look at them in a microscope and that if you get a maccrage that turns into a foam cell and you get a few billion of those maccrage that is plaque initially a fatty streak in the artery wall after that more localized collections of cholesterol and over time they get bigger and bigger and bigger most of the disease early on is in the wall of the artery it's notobstructing the arterial wall loom in it all sooner or later bad things can happen but the million dooll question is after the apob particle goes through the endothelium why do some get ingested by macrofagos and others do not a word first about what you said the transendothelial passage transcytosis of the apob particle that can occur with perfectly healthy endothelial cells you do not need an flame Disturbed endothelium for that particle to pass right through it cavoli and there's other receptors that just pull those particles through there is a little gap between endothelial cells a perivascular sort of Channel they can sneak throughthat these are very very small particles you know 20 micrograms 21 micro Nan grams uh Mill millimeters excuse me they get in so but they certainly can get in with greater frequency if the endothelium happens to be disturbed or inflamed and most of the inflammation ofendothelium and atheros scerotic disease is because those macres I told you about they start ingesting the particles they."
54:33 " it's mostly ldls the vldls have a plasma resonance time of a few hours kyom microns less than an hour idls an hour LDL several days so when you measure apob 90 to 95% of your apob nparticles are ldls so yes a vldl or colam Micron Remnant can make its way into the ottery wall but it's like you know 95% of the Army is LDL particles that are doing The Invasion "
no mention of APO little a !
LP(a) ? Dedicated episode to that coming
Love your work Simon, but please lose the cap.
So hanging his hat on apoB and ldl lowering .its like saying lets kill the fireman who fights the fire
Not really! As fireman don’t start the fire. ApoB containing lipoproteins damage the endothelium and can start inflammation themselves
@@TheProofWithSimonHill so ApoB and lipoproteins are not a natural function of the body.And only when compromised by glycation and oxidation is it a problem.
@@patrinaandrew7763 ApoB levels in the blood matter.
The mechanism of that damage was not explained, or did I miss it? He said it would give him a headache or something. @@TheProofWithSimonHill
Best predictor is Kraft Insulin Assay Test. Worst insulin resistance the higher risk for heart attack and stroke
Thank you Doctor!
Is it just me, or does Dr Dayspring looks like a mobster from an old Jimmy Cagney movie!
Just you. He definitely looks Jewish though, and there were some Jewish mobsters.
Who is the big man speaking? He seems unhealthy?
Just for interest Peter Attia helped him with his terrible insulin resistance and fasting glucose levels, despite his heart expertise
@@timh-c7186 and who helped Peter Attia with his cholesterol issue? What is your point?
Please invite Lean Mass Hyper Responders
You mean like this? theproof.com/is-high-cholesterol-on-a-keto-diet-a-problem-dave-feldman-and-william-cromwell-md/
Dayspring needs to just stick to speaking about the proven mechanistic science of the lipoprotein system and forget about his belief in the associational data. When it comes to ApoB causing cvd, it’s just his ‘opinion’ and nothing else.
Sure. Totally. If you ignore all RCTs and Mendelian randomization studies and every other line of evidence showing high ApoB causal in CVD.
@@robertusgaall of which are correlation studies.
@adaswichura1335 Lol. Show me you don't have a clue about Mendelian randomization and "correlation studies" without telling me.
Wow, it took 55 minutes to get to LDL is 95% of Apob. Then we get LDL is causal in atherosclerosis a then back the old genitics theroy. This is way out dated theroy. I am personally very pleased that with a excellent HDL and Trigs and great ratieo, and an excellent metabulism, LDL classed as high by the likes of this doctor is a great longevity marker. Judgeing by his questions I think Simon knows this. The doctor is stuck in the 1970's. Science has moved on, so should the doctor.
Social media influencers have moved on, but the science hasn't changed.
@@bobhill4364 accurate
@@bobhill4364 I try to maintain an open mind and keep learning. You’re mistaken if you believe science doesn’t evolve or change (sometimes radically). I refuse to be over-influenced by UA-camrs with any “agenda”, though some from both “camps” are prepared to listen and learn…as Simon Hill is.
@@bobhill4364 If "science" does not change it is not science but propaganda, narrative, opinion or dogma. Science continuously evolves as we continuously learn.
@@murraypooley9199 It's shocking how you guys butcher this and I agree with your statement. If something is no longer open to being challenged, then it is not science.
New studies have been done and they still align with the old data and that suggests that a diet high in fiber(fruits, vegetables, whole grains, beans) are best for longevity, with high saturated fat foods showing the opposite effect.
Science is not supposed to change, it is supposed to be open to challenge. But social media influencers asserting an all meat diet is healthiest is not evidence lol.
And trust me, I would love for the evidence to show you can eat whatever you want for optimal health but it is what it is.
Lol jokes
All of this nonsense because grown adults want to act like kids and not eat their fruits and veggies.
You can be a LMHR from eating meat & vegetables on a low-carb diet, with high LDL. Did you mean "carbs" instead of "fruits and veggies"?
@@joshuachia504 It's sad. Now a lot of the low carbers are eating loads of fruit and honey. Lol so now carbs are ok as long as they taste nice. I don't know how this isn't so obvious. Adults rebelling like they did as kids because they were made to eat the mushy veggies they didn't want.
@@bobhill4364 Excuse me but a confused LLM might think that fruit & honey are low-carb. What I mean is that you can have high LDL despite eating large amounts of vegetables especially when on a low-carb diet.
@@joshuachia504 Low carb and carnivore doctor Paul Saladino now eats tons of fruits and gallons of honey. You can certainly have high ldl if you have a genetic disposition, but more frequently, it's the loads of saturated fat low carbers tend to eat.
Don’t forget that the majority of humanity are omnivorous. Just because two opposing “Tribes” are constantly at each other’s throats doesn’t mean they speak for that vast majority. Let both extremes carry-on believing they have found “The Panacea”!
Vegan propaganda. If you are vegan, you better talk to ex vegans as soon as possible. Maybe it’s not to late.
What I learned from ex-vegans is not to go vegan because of some health benefits. I agree with that sentiment, it takes more than simply going vegan to get guaranteed health benefis.
What I have not heard from ex-vegans however, is why not to go and stay vegan for the animals. They are innocent and deserve better, imho.
Haha what? Did you even listen to?
Ironic name of "longevity coach" and not promoting the vegan or heavily plant based diet, while presumably being more meat based which is not longevity confering. Also the current context of Apo-B is not vegan propaganda, not sure how that's even relevant to the current video.
This guy made no sense whatsoever with this comment. Nothing to do with this video lol
@@stisca well, I have some salads growing but now hundreds of animals are coming to eat them. So, should I kill all those hundreds of animals to eat salads for few weeks or should I kill one of my cows to have food for the next six months or longer?
@bobhill4364 You are deluded but even if you are right and I was to get heath problems some time in the future, as I test regually any problems arising would be picked up on and lifestyle adjusted. Meanwhle I will continue to enjoy excellent health and vitality. Meanwhile I am willing to bet my health and future outlook is far better than you and most if not all of the sick people on this channel.
Very nice!!! 😄