I’m a retired internist who was motivated by Tom to become certified in lipidology through the National Lipid Association. Tom is a national treasure, who as Simon indicated has a selfless passion to educate and the skill to communicate a very complex molecular mechanism. I’m also plant based as is Simon - interestingly without rosuvastatin and ezetamibe my apo B is at the 75th percentile for Americans. This interview series is one of Simon’s best (which is saying a lot. I sat at the feet of Tom through high free website updates and podcasts. This is Tom at his expert fluid best. I love you man (both of you) - as you are both examples of a mensch par excellence.
I agree. These interviews were amazing. I learned so much. I’ve been transitioning to a Whole Foods plant based diet over the last 7 years or so. I’ve had my lipids checked every couple years over this transition period. My total cholesterol started at 230 and has dropped to 165. However, by LDL started at 35 and is now 113. I’m not sure how this can be going in the opposite direction. I have always exercised regularly.
@@jasonsmith8651 I heard with of the same doctor I believe that if we get the HDL cholesterol(the good one) TOO HIGH is eventually rise the LDL too The question is how high is HDL good helper??
Simon, I have worked out 6 days a week my whole life and have always stayed between 12 to 14% body fat. Thought I was in incredible shape until I had a coronary calcium score of 550 and my Apob was off the charts of 189. Found out I was a walking time bomb. So crazy. I am now on an extremely low fat whole foods plant based diet with a small does statin and dropped my cholesterol and Apob dramatically. So happy I had my Apob tested. Thanks for all the great content you create.
@TheSavior888 Patrick, you should get your Lp(a) level tested....if elevated, it could explain in part your CAC score. It would not change your treatment (although with high Lp(a) you might want to be more aggressvie with ApoB lowering talk to your cardiologist) but more importantly, since it is genetic, you should have siblings/cousins/children tested too so they can see if they are at increased risk too. The sooner you know and treat, the better.
@joek9339 I was on the SAD diet, but I never over ate and worked out a lot to stay in shape. I never took PEDs. Feel so much better now that cleaned up my diet. Less aches and pains and a lot more energy. I'm 55 now so I'm getting up there. A good whole foods diet is so important
I've heard Dr. Dayspring before and he's always entertaining and so knowledgeable. My Dad has 3 stents from a lucky duck finding with some anginal pain and while he didn't infarct, he had a 99% Left Main, 95% LAD and 75% LCx. He had borderline lipids for years that went untreated. His Dad died at the age of 47 with MI in bed while my father and my Grandmother stood by helpless. I am passionate about my risk reduction and have pushed hard for ApoB and Lp(a) labs much to the dismay of my PCP. I am a nurse practitioner and have the labs drawn regardless. Thank you for your education and willingness to share.
Why doesn’t anyone talk to Robert C Williams has been the leading researcher in cholesterol and the heart for over 60 years,he’s now 90 and still going strong?
This was fantastic. Thank you both so, so much. I am currently having "discussions" with my doctors regarding my LDL and am undergoing investigations as we speak and this has helped me immensely.. plus as an ex clinical chemist/biochemist I found it excellent and stimulating. Really can't thank you both enough.
Loved this podcast! So important. Please,I hope you will ask about dietary saturated fat. I've eaten a vegan diet for years and was shocked to find out my TC was rising and my ApoB was slightly above optimal. I've had zero dietary cholesterol for over 10 years BUT plenty of vegan foods that have coconut and palm oil. Currently trying to turn this around with a WFPB diet.
Perhaps the plants were the issue. Cut it out or reduce it aggressively and I can almost guarantee you that all your health markers will improve. Just be sure to eat lots of fatty meat.
I also wondered why saturated fat was not discussed- but on a second viewing I heard him say at about 1:47:00, in response to Ketogenic promoters, that high (saturated) fat is detrimental because it shuts down the liver's LDL receptors needed to capture and then metabolize LDL-c
Yep, WFPB for the win! Not only are you avoiding sat fat/cholesteroI, but the detrimental animal protein itself, plus Arachidonic acid, Endotoxins, Carnitine - > TMAO, Neu5GC, Heme Iron, PAH'S/HCA's, Hormones, Antibiotics, etc.
I’m almost half-way through this and just wanted to say it’s BRILLIANT. I had zero knowledge of the lipid mechanisms in the body. Will definitely watch all the rest of their conversation. Just want to understand why my cholesterol is high for the first time ever and whether I need to do something about it! Thank you so much, Simon!
Do NOT take Statins toxic & cause cancer, FDA warns of confusion & memory problems, permanent muscle damage. 👉All for what = a 1% absolute risk reduction. Risks higher than any meager benefit. ✅Solution = Magnesium acts as a natural statin Without destroying everything down the Mevalonate pathway. 👉 Read "Poisoned" by Hannah Yosephs MD
Very good details explanation of mechanism but unfortunately lacking logical conclusion. Brushing off inflammation and blood pressure in conjunction with ApoB does not make sense. If halving ApoB is makes dramatic improvements as claimed but inflammation and blood pressure increases to double the amount of place building ApoB mathematically it doesn’t make sense to me it is a useful solution to only focus on reducing ApoB if the measure increases the inflammation and blood pressure. Tons of study on impact of ApoB abut do we have any that compensates for inflammation factors?
Interesting yet misleading conversation. Scientific data shows that elevated LDL cholesterol reduces the risk of heart disease. It also enables better health of nerves, muscles including the heart, tendons, and a stronger immune system. Data shows that heart disease risk positively correlates with artery calcium increase rates and with activation of clotting mechanism genes. Why would one try to lower LDL ???
No. The lower the Apo B, the lower the heart disease risk. If Apo B is low enough, risk is essentially 0. Clotting does play a role, and it is likely that clotting is why omega 3’s reduce heart disease, as they prevent such clotting. But to say that LDL doesn’t cause heart disease is just wrong.
1:34:00- ApoB due to genes or lifestyle? Polygenic risk vs monigenetic risk PCSK9- gene Secondary causes: Renal desease Liver desease Hypothyroid Keto diet Genetic - hypo absorber? If yess- avoid dietary CL and phytostirols. If so- than ezetimibe, bcs statin make CL absorbtion worse.
He said - High fat diets shuts down your LDL receptors you stop clearing LDL particles (so LDL goes up) then when asked about saturated or unsaturated fat consumption he talks about cholesterol-sensing genes and doesn't answer the question about which is up regulating and which down regulating LDL receptors. Ha! He doesn't know, calls them damn diets.
@@TheProofWithSimonHill I don't think he does or he wouldn't be saying what he's saying. He has the physical appearance of not understanding it as well.
I listened to the podcast first. I've now watched the whole interview again, written 6 pages of notes, and am astonished at the brilliance of both of you taking a complex subject and making it so accessible to us non-medical folk. Simon, what can I say? Am so grateful for you and your podcast.
I wish I was impressed but I was not. More or less he said only the progression of heart disease could be stopped and that it would always be there. He should look at me. As a 200 point 30% reversal of my CAC isn't likely an error. I did like the talk of what happens when Doctors go against the grain and their careers go flat. The people that speak out I have a lot of respect for. Like Dr. Linus Pauling and Dr Thomas Levy.
@@SET12DSP I do have very high respect for Dr. Linus Pauling not only for his scientific work, but also for his contribution to peace. Please tell me how did you manage to reverse Coronary artery calcium (CAC). I am 53 years old, and I have been diagnosed with CHD advanced stage. All the main corona arteries of my left heart, 70 % and the arteries of my right heart 80 % are clogged and my CAC is above 1000. I am a born vegetarian, Non-smoker, BMI of 22.7. My physician should have advised me long ago and put me on a statin, but now I am so worried. I am scared even to go to bed because I have a heart attack or stroke. I have a family history (my mum died at the age of 39 as a result of a stroke) and I think I carry the gene 9P21. Now I am taking ASS 100 mg and statin along with Omega-3, Vitamins D3, K2 and magnesium
This is absolutely fantastic. I've been on a mission to understand LDL and my risk. I think Dr. Dayspring is a ROCK STAR. Thank you for asking really great questions. Well done!
Does accumulation of fat in the liver is started by high blood LDL levels? Does accumulation of fat in pancreas, kidney and visceral region in general is started by high blood LDL levels? Does accumulation of fat in muscle is started by high blood LDL levels? Does accumulation of fat in the rest of the body is started by high blood LDL levels? From the little I have learnt, the answer seems to the be: No. What I know is that all this fat accumulation in the many organs mentioned is a consequence of metabolic syndrome. And all these are signs of metabolic problems in different tissues. Then why accumulation of fat in arteries and heart is assumed to be started by high blood LDL levels and not by metabolic syndrome? (I understand that many many years ago the plumber hypothesis of pipe clogging made sense, but it is already 2023! And we all know this is an alive biology system!) For me, clogging from blood content makes no sense. It makes much more sense that metabolic syndrome expresses itself in the cardiovascular system as accumulation of fat in arteries and heart. Health status of US population does not help to elucidate the root problem, as 95% of their population lives with metabolic syndrome. Then doctors correlate high LDL with cardiovascular disease, but the root of CVD is in the metabolic illness and not in the high LDL. And even worse are their solutions of using statins instead of stopping the nasty plan of the Food & Beverage Industry sickening humans (and dogs).
@@TheProofWithSimonHill thanks a lot. I really appreciate your passion and honesty. But there are other theories (with scientific publications) out there and a lot more to say from other points of view. Please bring on to the discussion Norwitz & Feldman to have a chat about the Lipid Energy model. And Dr. Subbotin, with whom I agree about sick arteries expressing their metabolic syndrome by getting fat themselves. Dr. Volek, D'agostino & Paul Mason also have a lot to say in this topic. Healthy discussion about the topic would be much more nurturing than turning your channel into an echo-chamber.
I think that in a past life Dr Dayspring was a macrophage who died becoming a foam cell and now he redeemed himself by helping people and macrophages avoid the common enemy. Ahah. Love him, great masterclass.
Best treatment for atherosclerosis: Vitamin C Why do only coronary arteries clog with cholesterol and not veins or small capillaries? Scurvy = No vitamin C in your diet. Symptom: Your blood vessels break and you bleed to death. Think of the sailor of the past. Scurvy of the heart = Just enough vitamin C from food. Symptom: Arteries around the heart are not strong enough to resist high blood pressure. Damage is repaired with cholesterol LP(a) to prevent worse. After years of repair, your arteries become clogged. Enough vitamin C supplement of at least 3000 mg. per day gives strong and flexible arteries. Cholesterol is not needed as a repair agent. Cholesterol in your coronary arteries is broken down and burned in your liver. Source TH-cam: - Cardiovascular disease and vitamin C (Dr. Rath Foundation) - Ending the Cardiovascular Epidemic by Natural Means - Dr. Matthias Rath
Can someone please tell me what to eat? I've got familial cholesterolemia and a CT calcium score of 600, I'm a 50 year old male. I haven't eaten in three days since I found out my CT score. I've watched a thousand videos about what to eat, and it seems like not one of them give a straight answer
You should take a look at Dr. David Diamond’s lectures. He speaks about people with familial hypercholesterolemia and the main risk factors associated with it. To put it simply you should focus on clotting factors and fibrinogen among inflammation markers. Try to drive them down as much as possible preferably with a low carb diet.
It was a true masterclass.! I think this info will outweight knowledge of many "qualified" doctors in my country :) Cant wait to see remaining 2 episodes. Simon thanks a Ton
Excellent! He's so entertaining to watch. One thing that I don't get: SF inhibits LDL-R through these transcription factors, as he says, because "the liver doesn't want more lipids". But, aren't LDLs made by the liver in the first place (directly or through VLDLs)? So the lipids (which ones? Triglicerides?) in these LDLs are coming from the liver itself? Are the lipids/TG secreted by the liver in VLDLs coming from dietary fats or from de novo lipogenesis? As far as I understand, fatty acids (TG) from diet would mostly be packed into chylomicrons and be directly absorbed by others cells (eg muscle), am I right? So overall I don't see how SF from the diet would end up in the liver inhibiting LDL-R, whose function is to capture LDLs that served their purpose (according to Dr. Dayspring) of "bringing back cholesterol to the liver". Of course it's impossible to summarize lipid metabolism in a 2h podcast, but I'm confused and it's hard see how all these pieces fit. Thanks for a great podcast!
Wow, what an amazing interview. Yes a bit high level, but wow to have this level of expertise in an interview anyone can watch on TH-cam. That’s a true public service. Thank you Simon.
Fantastic discussion. Key points: - ApoB is most important biomarker and should be less than 80 mg/dL assuming there are no other risk factors. For risk factors it needs to be even lower. Below 40-50 mg/dL no atherosclerosis occurs. - ApoB levels of 40-50 mg/dL are not harmful to overall health, despite what some may claim. Babies and children have these levels and have healthy development. - Inflammation is not necessary for the ApoB particles to enter the endothelium. The keto/carnivore crowd incorrectly believes inflammation (mainly caused by insulin resistance) is the driving factor in atherosclerosis whereas it is actually ApoB concentration. Inflammation from a wide number of causes does exacerbate the problem though. - ApoB particles entering the endothelium do not cause plaque by themselves, they must be absorbed by a macrophage such as a monocyte. It is not known what causes this to happen and what can be done to reduce it. - There is a plethora of studies to support elevated ApoB levels causing atherosclerosis. No serious person believes otherwise, but genetics can affect this as some people with high ApoB never develop athersclerosis. - Saturated fats are harmful, but mono and polyunsaturated fats are not. - ApoB can be lowered with medication or diet, but trying to lower with only medication may be difficult but worth a try. - In general dietary cholesterol does not affect ApoB or atherosclerosis unless you are a cholesterol hyperabsorber.
This is the first time I have heard this doctor. I have been following Dr Robert Lustig, Dr Ali, Dr M Kendrick, Dr Paul Mason and others who say cholesterol is not the culprit of atherosclerosis but sugar is I am confused now.
So ApoB particle and a macrophage walk into a bar and meet a gang of aggreggated LDLs.... What a wonderful discussion with great slides. Those aggregated LDLs the coolest thing I learned about. Looking forward to his coverage of lp(a) , my personal risk factor. Thanks Simon and your team, great work.
“The alternative hypothesis is that blood clots, and blood clotting, are the key players in cardiovascular disease. “ Dr Malcolm Kendrick, author of the Clot Thickens. Can you get a representative of this school of thought. It’s becoming confusing to me as a sufferer. This hypothesis explains why such things as smoking are far more causal than cholesterol. Dr Kendrick also seems as humorous as Dr Dayspring.😊
It's absolutly rubbish what this man starts his video with! apob can't just penetrate the endothilial wall. Unless the prossess of bloodcloting happens! 1 min of rubbish, and the rest is not worth listening to.
Very informative video, thanks! I had elevated cholesterol levels but changed my diet towards a more plant-based diet or pescatarian-diet avoiding saturated fats from meat and dairy products. I decreased my cholesterol levels just within the reference intervals. But my HDL-levels was very low, 0,5 mmol/ L = 30 mg/dl, so I tried the LCHF-diet. My cholesterol skyrocketed, but my HDL. After this I wanted to lower my cholesterol levels to the same levels as before with the Pescatarian-diet. But now I can't reach the same low levels. It that because of the fewer LDL-receptors caused by the LCHF-diet? And if so, how long does it take for the liver to start producing these LDL-receptors?
It's odd that Ivor Cummins has never had Dr Dayspring or Dr Peter Attia on his Fat Emperor Podcast despite them being low-carb doctors as well. Is it because he doesn't want low-carb doctors showing the dangers of a high LDL on a high saturated fat diet? He is an LDL deniar after all.
Wow, this video is a game-changer! 🌟 The life-saving information you've shared is invaluable and has the potential to make a significant impact on so many lives. The content of the conversation is top-notch, meticulously presented, and easily digestible. Kudos to Simon for compiling such high-quality questions and visuals! 👏 And let's not forget the speaker - absolutely phenomenal! 🎤 Dr. Dayspring's eloquence, enthusiasm, and ability to convey complex ideas with clarity and passion are truly impressive. It's evident that he cares deeply about the subject matter, and that energy is contagious. Bravo! 👌 This interview is a masterpiece that deserves all the praise and recognition! Keep up the fantastic work! 🙌🎉
This is the clearest, simplest explanation of the lipid transport system and atherogenesis I've ever heard. The idea that the purpose of LDL is to return cholesterol to the liver, not deliver it, is amazing.
Probably the youngest generation doesn't understand this but, 20 years ago, in order to receive as much information as you can get in this 2 hours podcast, you'd have to spend at least 1 year at the library, everyday.
What a great Interview! I think I listened to Dayspring first on Peter Attia’ Podcast and it was fascinating and very educational! The illustrations you inserted in yours helped a lot ( I watched it on my big TV-screen) to follow his great explanations. (And who else would think of cholesterol molecules having sex and change their type/identity by that😂 other than TD). Thank you again very much for this video and please never be afraid of long episodes to explain certain topics!
A lousy conversation. Simon can ask a generic question here and there but simon lacks the biochemistry acumen to really challenge anything Dayspring says - and so we let the lipid doctor ramble on. Dietary cholesterol or any kind of dietary fat has zero impact on what is going on in the body. All this talk or pathways and Chylomicrons etc. is moot null and void due to the psychical fact (fact of physics, laws of physics) that these exogenous molecules were already broke down prior to eating. Decay of cow, begins this process, then exposure to light and oxygen, heat, cooking (do you really think there is an intact cholesterol molecule post frying pan?).
Extremely informative podcast regarding cholesterol flux. It would be great for you to interview Malcolm Kendrick who is also a luminar in this field. His opinion debunks some of Tom's theories. By the way your interview was brilliant, you covered some areas of lipidology which help me fill in some of the missing pieces of the puzzle.
@@TheProofWithSimonHill Care to elaborate on why you weren't? I'm doing the best a lay person can in trying to figure thus all out but it is SO difficult as there are many "experts" and many conflicting information. I have lost nearly 100lbs, now have no hbp, no pre diabetes but have extraordinarily high cholesterol. Like 618 total, 492 ldl, 86 hdl, 86 triglyceride.
Very intresting talk, but what I want to know, is the health of the ldl particles and the sise of them matter ? and that about lean hyper responders with extremely hi level of ldl and hdl, but low triglycerides, being healthy with 0 plack
Hi Quick request. I subscribe to your Podcast on Spotify but often come across podcasts on TH-cam of yours that I want to listen to on Spotify while driving/running etc. It would be great if on your videos you could add a link to the specific Spotify podcast (and other podcast providers that you are on) rather than just to the channel. It would make it easier to find a particular podcast. Thank you. Kind regards Michael. BTW can’t wait to listen to this one in full and the subsequent ones in the series.
Vitamin E, omega 3, vitamin D ....especially k2 doses of 230mcg a day will reduce arterial plaque by 51% in 6 months and 31% in 3 months. The vitamin E and omega 3 will help take care of the inflammation there .What is your opinion about this?
The information given on comparison between high saturated fat consumption and heart disease has been proven wrong over and over again. It was repeatedly proven by both research and anecdotal evidences that Metabolic Syndrome and insulin resistance is the main driver of atherosclerosis. Can the doctor please put forth some research with randomized control trials that proved consumption of 'low carb high saturated fat' diet has a direct relationship to heart disease? Also high LDL is not a matter of concern but the particle size and Trygliceride to HDL ratio is what matters ?
Really interesting. Both my parents had high cholesterol and so do I despite being plant based vegan and this helped explain things. I would have thought diet would have played a greater role but seems not. Thank you so much.
Diet does play a massive role, namely carbohydrates, sugar, not fat. I study this subject and beleive his guys way outdated views and advice are highly influential in causing the huge rise in hart events. The interviewer askes the right questions but he ducks around them. Why is this guys decades long approach not working? Because it is wrong. Doctors Cywes, Diamond, Paul Mason, Ken Berry, Anthony Chaffee, Bikman, Huberman, Sayfried, Ekburg, Shawn Baker. All these doctors and many more would strongly disagree on many of the points he makes.
Love your show and especially this episode - except in the section near the end (1:53) when he states that dietary intake of cholesterol has "nothing to do with coronary outcome..." Dr Gregor's video posted today (Apr 5) reiterates that dietary cholesterol raises blood levels and increases CVD risks, including a statement to that effect by Kim Williams What gives? Your guests assertion that it "has nothing to do with" seems to undercut his credibility.
I'm trying to learn everything I can about health. Trying to put together all I'm learning. If dietary cholesterol does not cross the blood brain barrier but statins drugs do, taking statins can't be a good thing for our brain's cholesterol needs???
You have the answer here in this 2015 article title: "Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms." Written by Japanese scientists living in a no profit healthcare system so no reason to mislead their own people who already have the highest life expectancy in the world.
The brain makes its own cholesterol, and instead of lasting for weeks it lasts for years. This has been extensively studied, and statins do not affect the brain’s cholesterol production or brain health.
A lousy conversation. Simon can ask a generic question here and there but simon lacks the biochemistry acumen to really challenge anything Dayspring says - and so we let the lipid doctor ramble on. Dietary cholesterol or any kind of dietary fat has zero impact on what is going on in the body. All this talk or pathways and Chylomicrons etc. is moot null and void due to the psychical fact (fact of physics, laws of physics) that these exogenous molecules were already broke down prior to eating. Decay of cow, begins this process, then exposure to light and oxygen, heat, cooking (do you really think there is an intact cholesterol molecule post frying pan?).
At 1:53:30 he mentions phytosterols, and states the body would NOT want to see that. On my low carb diet, the plants of choice are all on the top in regards to phytosterols. Various nuts, flax seed, broccoli, brusselsprouts, spinach. If the normal range is to absorb 55%, then maybe these preferred foods are not that good anyway? Pretty sure I eat more of these, than eggs or even beef and butter. Could it be, that the "lean mass hyper responders" he dismisses so fast, might be hyper-absorbers? That despite doing what is often referred to as clean keto, still have LDL that is drastically elevated? Despite a lot of research being done here in Denmark, the only lipid panel that is routinely offered, is HDL, LDL-C and trigs. Not unless you fork out a buttload of money on a private hospital, can you get a detailed panel.
Nurse told me about a patient who had an LDL of 800! Both her parents died in their 30's. Pretty obvious she was genetically predisposed. I don't know her outcome or how old she was when the nurse had her as a patient.
Should get Ron Krauss on as a guest. Though he is essentially in agreement with Dayspring, his take is a lot more nuanced, especially where it comes to the role of particle size in determining cvd risk.
Brilliant episode - WOW! It's rare to find an expert who can distill his decades of experience with such clarity while being so personable and humorous. I loved Dr. Lipid. He cut through all the popular misconceptions and made me smile in the process.
Loving the level of detail here, I was surprised to hear him say in general the level of dietary cholesterol has little to do with systemic level of apoB and cardiac outcomes (except for genetics), therefore would the main benefit of lowering dietary cholesterol be that in eliminating those foods you are usually also eliminating saturated fat which is the real issue (at least in terms of dietary input)? Can’t wait for the next one, thanks Simon
It’s a hyperbolic curve. If your ApoB is already low and you consume zero cholesterol and then add a few eggs to your diet you will see a significant increase in blood ApoB. They should have clarified this. Nutrition Made Simple has a video about this.
@rf9612.......Sorry, but enthusiasm does not always equate into scientific accuracy. Please investigate into alternate theories which scientifically and biologically challenge the current lipid theory of CVD. This mainstream theory only makes sense on the surface, but looking critically you see the pathways embraced do not actually exist in the body. Cell wall integrity and tight junctions between cells will not allow LDL in unless it has provided receptors for entry. Also, cholesterol found within plaques is pure cholesterol crystals, found abundantly only in red blood cell membranes. The other type of LDL found in circulating blood cannot form such crystals. But supposing LDL could enter why not also the entry of most everything else in circulation, many of which are way smaller than LDL. And, being that same blood supply but with less oxygen also flows in veins why does the LDL not cause plaque and arteriosclerosis within veins? It does rarely happen in a few places but not common except in veins grafted in the position of a bypass (CABG). Higher BP, and higher levels of mechanical damage is the main reason for that,.......but if LDL were actual cause of CVD it would happen in both arteries and veins and would be occurring uniformly the same on all surfaces, not just in selected spots. For more info please view You Tube videos of Malcomb Kendrick interviews. Specifically view this video around the 1 hr mark. th-cam.com/video/wRjQCG4NU-Y/w-d-xo.html
So DR. Statin saying there is no role in insulin resistance / metabolic disease and atherosclerosis? Because the prevalence of this disease is a relatively recent phenomenon in human history beginning at the same time as high-carb and processed food became our mainstay. Does he have any idea what the average ApoB score was in the 20's and 30's. I'm sure he has no clue.
It's not a recent phenomenon. Check out a study in the Lancet called Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations
I get it modified the LDL , obviously with Statins. My question is, I personally know people, because I am old, that been on Statins for decades, lower their LDL , yet still have bypass surgeries. . Lowering LDL for decades,, didn't stop thier arteries from getting plague.
That is why an OGTT test is the only test to determine if you have IR, which is common once you reach 65 and older. Go find the root cause that is creating soft plaque thereby its potential danger for causing thrombosis.
Try looking through the eyes of a 2-time Nobel Prize winner Dr. Linus Pauling and Dr Thomas Levy who expanded on Pauling 's work. The real issue is arterial scurvy. I have lowered my CAC said to be not reversible from 660 to 458. Sam is very right here!
@@darrendigiacomo6889 I agree, not only that they narrow the arteries even further all in the name of stabilization of Plaque but after the stabilization and a much narrower artery a piece of Plaque comes along and boom heart attack. I prefer Linus Paulings approach and belief that the problem is localized vitamin C deficiency which Lp-a arrives first on the scene to start the Plaque and calcium process of shoring up the arteries holes and cracks from the mechanical stress of the arteries close to the heart depleting vitamin C. The RDA of C is not enough. Standard medicines approach to calcium and plaque build-up is a backwards approach IMO as well as others such as Dr. Thomas Levy Cardiologist. How do I know because I am using Paulings and Levy's solution and my heart disease is reversing with a CAC of 458 down from 660.
This guy is amazing. I could listen to him all day. He is very skilful at explaining the anatomy and physiology of the subject matter without bamboozling you or boring you. He's one of the best I've heard so far. Outstanding.
Hello Friends, I'm keen to find out which part of our chat you found most enlightening. Should you have any further questions on this topic, do please post them beneath this comment. I shall endeavour to include them in our next discussion.
I’m a retired internist who was motivated by Tom to become certified in lipidology through the National Lipid Association.
Tom is a national treasure, who as Simon indicated has a selfless passion to educate and the skill to communicate a very complex molecular mechanism.
I’m also plant based as is Simon - interestingly without rosuvastatin and ezetamibe my apo B is at the 75th percentile for Americans.
This interview series is one of Simon’s best (which is saying a lot.
I sat at the feet of Tom through high free website updates and podcasts. This is Tom at his expert fluid best.
I love you man (both of you) - as you are both examples of a mensch par excellence.
I agree. These interviews were amazing. I learned so much. I’ve been transitioning to a Whole Foods plant based diet over the last 7 years or so. I’ve had my lipids checked every couple years over this transition period. My total cholesterol started at 230 and has dropped to 165. However, by LDL started at 35 and is now 113. I’m not sure how this can be going in the opposite direction. I have always exercised regularly.
Yes, indeed, he is brilliant
@@jasonsmith8651
I heard with of the same doctor I believe that if we get the HDL cholesterol(the good one) TOO HIGH is eventually rise the LDL too
The question is how high is HDL good helper??
Simon, I have worked out 6 days a week my whole life and have always stayed between 12 to 14% body fat. Thought I was in incredible shape until I had a coronary calcium score of 550 and my Apob was off the charts of 189. Found out I was a walking time bomb. So crazy. I am now on an extremely low fat whole foods plant based diet with a small does statin and dropped my cholesterol and Apob dramatically. So happy I had my Apob tested. Thanks for all the great content you create.
@TheSavior888 Patrick, you should get your Lp(a) level tested....if elevated, it could explain in part your CAC score. It would not change your treatment (although with high Lp(a) you might want to be more aggressvie with ApoB lowering talk to your cardiologist) but more importantly, since it is genetic, you should have siblings/cousins/children tested too so they can see if they are at increased risk too. The sooner you know and treat, the better.
I'm so glad you got this information and were able to avoid a bad health outcome. Thanks for sharing your story!
Why statins? They have nothing to do with your calcium score being high
Good for you, man. Your example fits the nuances Tom spoke to.
@joek9339 I was on the SAD diet, but I never over ate and worked out a lot to stay in shape. I never took PEDs. Feel so much better now that cleaned up my diet. Less aches and pains and a lot more energy. I'm 55 now so I'm getting up there. A good whole foods diet is so important
I've heard Dr. Dayspring before and he's always entertaining and so knowledgeable. My Dad has 3 stents from a lucky duck finding with some anginal pain and while he didn't infarct, he had a 99% Left Main, 95% LAD and 75% LCx. He had borderline lipids for years that went untreated. His Dad died at the age of 47 with MI in bed while my father and my Grandmother stood by helpless. I am passionate about my risk reduction and have pushed hard for ApoB and Lp(a) labs much to the dismay of my PCP. I am a nurse practitioner and have the labs drawn regardless. Thank you for your education and willingness to share.
Why doesn’t anyone talk to Robert C Williams has been the leading researcher in cholesterol and the heart for over 60 years,he’s now 90 and still going strong?
This was so informative and educational. Many thanks to you and your host for this, much appreciated!
This was fantastic. Thank you both so, so much. I am currently having "discussions" with my doctors regarding my LDL and am undergoing investigations as we speak and this has helped me immensely.. plus as an ex clinical chemist/biochemist I found it excellent and stimulating. Really can't thank you both enough.
I love his energy. It makes it even easier to learn. 😀
Loved this podcast! So important. Please,I hope you will ask about dietary saturated fat. I've eaten a vegan diet for years and was shocked to find out my TC was rising and my ApoB was slightly above optimal. I've had zero dietary cholesterol for over 10 years BUT plenty of vegan foods that have coconut and palm oil. Currently trying to turn this around with a WFPB diet.
Perhaps the plants were the issue. Cut it out or reduce it aggressively and I can almost guarantee you that all your health markers will improve. Just be sure to eat lots of fatty meat.
I also wondered why saturated fat was not discussed- but on a second viewing I heard him say at about 1:47:00, in response to Ketogenic promoters, that high (saturated) fat is detrimental because it shuts down the liver's LDL receptors needed to capture and then metabolize LDL-c
Yep, WFPB for the win! Not only are you avoiding sat fat/cholesteroI, but the detrimental animal protein itself, plus Arachidonic acid, Endotoxins, Carnitine - > TMAO, Neu5GC, Heme Iron, PAH'S/HCA's, Hormones, Antibiotics, etc.
This is SO fascinating. Thank you for this.
Some good information, but it sounds like an infomercial for pharmaceuticals.
Thank you so much for sharing your knowledge with us. Tony 🇬🇧
I’m almost half-way through this and just wanted to say it’s BRILLIANT. I had zero knowledge of the lipid mechanisms in the body. Will definitely watch all the rest of their conversation. Just want to understand why my cholesterol is high for the first time ever and whether I need to do something about it! Thank you so much, Simon!
Do NOT take Statins toxic & cause cancer, FDA warns of confusion & memory problems, permanent muscle damage.
👉All for what = a 1% absolute risk reduction.
Risks higher than any meager benefit.
✅Solution = Magnesium acts as a natural statin Without destroying everything down the Mevalonate pathway.
👉 Read "Poisoned" by Hannah Yosephs MD
If you want the actual mechanism, look up Dr Malcolm Kendrick. He has it nailed. This guy is a Dinosaur!!
Man, REALLY GOOD 🎉
Thank you
Great episode!
Beautiful man
Very good details explanation of mechanism but unfortunately lacking logical conclusion. Brushing off inflammation and blood pressure in conjunction with ApoB does not make sense. If halving ApoB is makes dramatic improvements as claimed but inflammation and blood pressure increases to double the amount of place building ApoB mathematically it doesn’t make sense to me it is a useful solution to only focus on reducing ApoB if the measure increases the inflammation and blood pressure. Tons of study on impact of ApoB abut do we have any that compensates for inflammation factors?
Interesting yet misleading conversation. Scientific data shows that elevated LDL cholesterol reduces the risk of heart disease. It also enables better health of nerves, muscles including the heart, tendons, and a stronger immune system. Data shows that heart disease risk positively correlates with artery calcium increase rates and with activation of clotting mechanism genes. Why would one try to lower LDL ???
No. The lower the Apo B, the lower the heart disease risk. If Apo B is low enough, risk is essentially 0. Clotting does play a role, and it is likely that clotting is why omega 3’s reduce heart disease, as they prevent such clotting. But to say that LDL doesn’t cause heart disease is just wrong.
A track playing in the background in your Intro ❤ What's it?
1:34:00- ApoB due to genes or lifestyle?
Polygenic risk vs monigenetic risk
PCSK9- gene
Secondary causes:
Renal desease
Liver desease
Hypothyroid
Keto diet
Genetic - hypo absorber? If yess- avoid dietary CL and phytostirols.
If so- than ezetimibe, bcs statin make CL absorbtion worse.
Can people survive if they do not take in any cholesterol from food?
stearic acid got no imapct on ldl
kind regards
@@TheProofWithSimonHill i thnik it is more nuansed, like gent said phytosterols are not very welcomed
kind regards
Nothing on triglycerides?
@@TheProofWithSimonHill I heard Dr. Alo say that people with hypertriglyceridemia can’t rely on a standard blood lipid panel to assess ASCVD risk.
He said - High fat diets shuts down your LDL receptors you stop clearing LDL particles (so LDL goes up) then when asked about saturated or unsaturated fat consumption he talks about cholesterol-sensing genes and doesn't answer the question about which is up regulating and which down regulating LDL receptors. Ha! He doesn't know, calls them damn diets.
Why you do not have many more subscribers….I do not understand.
The whole point is in the title. The fats eat a lot of cholesterol. Now I don't have to watch the video.
So high fats are good??
This Dr. never heard of The Randle Cycle? He loses all credibility for either not knowing that or not understanding it.
@@TheProofWithSimonHill I don't think he does or he wouldn't be saying what he's saying. He has the physical appearance of not understanding it as well.
Good job spreading false info by a statin-based misanthropist. Really good job
I listened to the podcast first. I've now watched the whole interview again, written 6 pages of notes, and am astonished at the brilliance of both of you taking a complex subject and making it so accessible to us non-medical folk. Simon, what can I say? Am so grateful for you and your podcast.
Agree wholeheartedly!!!
I wish I was impressed but I was not. More or less he said only the progression of heart disease could be stopped and that it would always be there.
He should look at me. As a 200 point 30% reversal of my CAC isn't likely an error.
I did like the talk of what happens when Doctors go against the grain and their careers go flat. The people that speak out I have a lot of respect for. Like Dr. Linus Pauling and Dr Thomas Levy.
@@SET12DSP I do have very high respect for Dr. Linus Pauling not only for his scientific work, but also for his contribution to peace. Please tell me how did you manage to reverse Coronary artery calcium (CAC). I am 53 years old, and I have been diagnosed with CHD advanced stage. All the main corona arteries of my left heart, 70 % and the arteries of my right heart 80 % are clogged and my CAC is above 1000. I am a born vegetarian, Non-smoker, BMI of 22.7. My physician should have advised me long ago and put me on a statin, but now I am so worried. I am scared even to go to bed because I have a heart attack or stroke. I have a family history (my mum died at the age of 39 as a result of a stroke) and I think I carry the gene 9P21. Now I am taking ASS 100 mg and statin along with Omega-3, Vitamins D3, K2 and magnesium
@@SET12DSPplease tell me how you achieved that 30% decrease in CAC
@@ronniekirby5406 I'll get back to you after I get to the person above you that I somehow missed..
This is absolutely fantastic. I've been on a mission to understand LDL and my risk. I think Dr. Dayspring is a ROCK STAR. Thank you for asking really great questions. Well done!
Does accumulation of fat in the liver is started by high blood LDL levels? Does accumulation of fat in pancreas, kidney and visceral region in general is started by high blood LDL levels? Does accumulation of fat in muscle is started by high blood LDL levels? Does accumulation of fat in the rest of the body is started by high blood LDL levels? From the little I have learnt, the answer seems to the be: No.
What I know is that all this fat accumulation in the many organs mentioned is a consequence of metabolic syndrome. And all these are signs of metabolic problems in different tissues.
Then why accumulation of fat in arteries and heart is assumed to be started by high blood LDL levels and not by metabolic syndrome? (I understand that many many years ago the plumber hypothesis of pipe clogging made sense, but it is already 2023! And we all know this is an alive biology system!) For me, clogging from blood content makes no sense. It makes much more sense that metabolic syndrome expresses itself in the cardiovascular system as accumulation of fat in arteries and heart.
Health status of US population does not help to elucidate the root problem, as 95% of their population lives with metabolic syndrome. Then doctors correlate high LDL with cardiovascular disease, but the root of CVD is in the metabolic illness and not in the high LDL. And even worse are their solutions of using statins instead of stopping the nasty plan of the Food & Beverage Industry sickening humans (and dogs).
@@TheProofWithSimonHill thanks a lot. I really appreciate your passion and honesty.
But there are other theories (with scientific publications) out there and a lot more to say from other points of view. Please bring on to the discussion Norwitz & Feldman to have a chat about the Lipid Energy model. And Dr. Subbotin, with whom I agree about sick arteries expressing their metabolic syndrome by getting fat themselves. Dr. Volek, D'agostino & Paul Mason also have a lot to say in this topic. Healthy discussion about the topic would be much more nurturing than turning your channel into an echo-chamber.
I think that in a past life Dr Dayspring was a macrophage who died becoming a foam cell and now he redeemed himself by helping people and macrophages avoid the common enemy. Ahah.
Love him, great masterclass.
Best treatment for atherosclerosis: Vitamin C
Why do only coronary arteries clog with cholesterol and not veins or small capillaries?
Scurvy = No vitamin C in your diet.
Symptom: Your blood vessels break and you bleed to death. Think of the sailor of the past.
Scurvy of the heart = Just enough vitamin C from food.
Symptom: Arteries around the heart are not strong enough to resist high blood pressure. Damage is repaired with cholesterol LP(a) to prevent worse. After years of repair, your arteries become clogged.
Enough vitamin C supplement of at least 3000 mg. per day gives strong and flexible arteries. Cholesterol is not needed as a repair agent. Cholesterol in your coronary arteries is broken down and burned in your liver.
Source TH-cam:
- Cardiovascular disease and vitamin C (Dr. Rath Foundation)
- Ending the Cardiovascular Epidemic by Natural Means - Dr. Matthias Rath
Can someone please tell me what to eat? I've got familial cholesterolemia and a CT calcium score of 600, I'm a 50 year old male. I haven't eaten in three days since I found out my CT score. I've watched a thousand videos about what to eat, and it seems like not one of them give a straight answer
You should take a look at Dr. David Diamond’s lectures. He speaks about people with familial hypercholesterolemia and the main risk factors associated with it. To put it simply you should focus on clotting factors and fibrinogen among inflammation markers. Try to drive them down as much as possible preferably with a low carb diet.
Eat: fruits, vegetables, whole grains, beans, lentils, peas, nuts, seeds, herbs, spices. Avoid: All animal sourced foods, coconut oil, palm oil.
@@reason3581he should do the opposite of what you said.
It was a true masterclass.! I think this info will outweight knowledge of many "qualified" doctors in my country :) Cant wait to see remaining 2 episodes. Simon thanks a Ton
Excellent! He's so entertaining to watch. One thing that I don't get: SF inhibits LDL-R through these transcription factors, as he says, because "the liver doesn't want more lipids". But, aren't LDLs made by the liver in the first place (directly or through VLDLs)? So the lipids (which ones? Triglicerides?) in these LDLs are coming from the liver itself? Are the lipids/TG secreted by the liver in VLDLs coming from dietary fats or from de novo lipogenesis? As far as I understand, fatty acids (TG) from diet would mostly be packed into chylomicrons and be directly absorbed by others cells (eg muscle), am I right? So overall I don't see how SF from the diet would end up in the liver inhibiting LDL-R, whose function is to capture LDLs that served their purpose (according to Dr. Dayspring) of "bringing back cholesterol to the liver". Of course it's impossible to summarize lipid metabolism in a 2h podcast, but I'm confused and it's hard see how all these pieces fit.
Thanks for a great podcast!
Wow, what an amazing interview. Yes a bit high level, but wow to have this level of expertise in an interview anyone can watch on TH-cam. That’s a true public service. Thank you Simon.
I was going to the same thing... wow, what a great video. Thank you Simon, and thank you Dr. Thomas Dayspring.
Fantastic discussion. Key points:
- ApoB is most important biomarker and should be less than 80 mg/dL assuming there are no other risk factors. For risk factors it needs to be even lower. Below 40-50 mg/dL no atherosclerosis occurs.
- ApoB levels of 40-50 mg/dL are not harmful to overall health, despite what some may claim. Babies and children have these levels and have healthy development.
- Inflammation is not necessary for the ApoB particles to enter the endothelium. The keto/carnivore crowd incorrectly believes inflammation (mainly caused by insulin resistance) is the driving factor in atherosclerosis whereas it is actually ApoB concentration. Inflammation from a wide number of causes does exacerbate the problem though.
- ApoB particles entering the endothelium do not cause plaque by themselves, they must be absorbed by a macrophage such as a monocyte. It is not known what causes this to happen and what can be done to reduce it.
- There is a plethora of studies to support elevated ApoB levels causing atherosclerosis. No serious person believes otherwise, but genetics can affect this as some people with high ApoB never develop athersclerosis.
- Saturated fats are harmful, but mono and polyunsaturated fats are not.
- ApoB can be lowered with medication or diet, but trying to lower with only medication may be difficult but worth a try.
- In general dietary cholesterol does not affect ApoB or atherosclerosis unless you are a cholesterol hyperabsorber.
This is the first time I have heard this doctor. I have been following Dr Robert Lustig, Dr Ali, Dr M Kendrick, Dr Paul Mason and others who say cholesterol is not the culprit of atherosclerosis but sugar is
I am confused now.
Both are bad.
They all are experts but they all have opposite ideas what’s ideal go figure
Simple and/or excess Carbs , sugar, seed oils. Avoid those. Done. You're good.
And lose weight/visceral fat with diet/lifestyle, exercise, build some muscles, rest. No stress.
So ApoB particle and a macrophage walk into a bar and meet a gang of aggreggated LDLs....
What a wonderful discussion with great slides. Those aggregated LDLs the coolest thing I learned about. Looking forward to his coverage of lp(a) , my personal risk factor. Thanks Simon and your team, great work.
What a darling man-an expert and yet so loving; clearly hanging on every word of the story of Simon’s father.
“The alternative hypothesis is that blood clots, and blood clotting, are the key players in cardiovascular disease. “ Dr Malcolm Kendrick, author of the Clot Thickens. Can you get a representative of this school of thought. It’s becoming confusing to me as a sufferer.
This hypothesis explains why such things as smoking are far more causal than cholesterol. Dr Kendrick also seems as humorous as Dr Dayspring.😊
Dr. Dayspring is a living legend.
It's absolutly rubbish what this man starts his video with! apob can't just penetrate the endothilial wall. Unless the prossess of bloodcloting happens! 1 min of rubbish, and the rest is not worth listening to.
Very informative video, thanks!
I had elevated cholesterol levels but changed my diet towards a more plant-based diet or pescatarian-diet avoiding saturated fats from meat and dairy products.
I decreased my cholesterol levels just within the reference intervals.
But my HDL-levels was very low, 0,5 mmol/ L = 30 mg/dl, so I tried the LCHF-diet. My cholesterol skyrocketed, but my HDL.
After this I wanted to lower my cholesterol levels to the same levels as before with the Pescatarian-diet. But now I can't reach the same low levels.
It that because of the fewer LDL-receptors caused by the LCHF-diet?
And if so, how long does it take for the liver to start producing these LDL-receptors?
1:47:00 Why do saturated fats down regulate LDL receptor but polyunsaturated fats up regulate it?
It's odd that Ivor Cummins has never had Dr Dayspring or Dr Peter Attia on his Fat Emperor Podcast despite them being low-carb doctors as well.
Is it because he doesn't want low-carb doctors showing the dangers of a high LDL on a high saturated fat diet?
He is an LDL deniar after all.
Wow, this video is a game-changer! 🌟 The life-saving information you've shared is invaluable and has the potential to make a significant impact on so many lives. The content of the conversation is top-notch, meticulously presented, and easily digestible. Kudos to Simon for compiling such high-quality questions and visuals! 👏
And let's not forget the speaker - absolutely phenomenal! 🎤 Dr. Dayspring's eloquence, enthusiasm, and ability to convey complex ideas with clarity and passion are truly impressive. It's evident that he cares deeply about the subject matter, and that energy is contagious. Bravo! 👌
This interview is a masterpiece that deserves all the praise and recognition! Keep up the fantastic work! 🙌🎉
This is the clearest, simplest explanation of the lipid transport system and atherogenesis I've ever heard. The idea that the purpose of LDL is to return cholesterol to the liver, not deliver it, is amazing.
Probably the youngest generation doesn't understand this but, 20 years ago, in order to receive as much information as you can get in this 2 hours podcast, you'd have to spend at least 1 year at the library, everyday.
@@Mrgasman1978 exactly, that too depends on the quality of books they keep in those usual libraries.
The issue is not with dietary cholesterol, but with saturated fat, which really can affect the LdL levels, as far as I understand it.
So, how much animal products can you eat while keeping ApoB in a non atherogenic range? Not much, I’d guess.
What a great Interview! I think I listened to Dayspring first on Peter Attia’ Podcast and it was fascinating and very educational! The illustrations you inserted in yours helped a lot ( I watched it on my big TV-screen) to follow his great explanations. (And who else would think of cholesterol molecules having sex and change their type/identity by that😂 other than TD). Thank you again very much for this video and please never be afraid of long episodes to explain certain topics!
A lousy conversation. Simon can ask a generic question here and there but simon lacks the biochemistry acumen to really challenge anything Dayspring says - and so we let the lipid doctor ramble on. Dietary cholesterol or any kind of dietary fat has zero impact on what is going on in the body. All this talk or pathways and Chylomicrons etc. is moot null and void due to the psychical fact (fact of physics, laws of physics) that these exogenous molecules were already broke down prior to eating. Decay of cow, begins this process, then exposure to light and oxygen, heat, cooking (do you really think there is an intact cholesterol molecule post frying pan?).
Does drinking MCT & extra-virgin olive oil increase triglycerides in the blood? Thanks in advance!
I probably missed it, but I have a question. What determines how many LDL and VLDL particles the liver produces?
Extremely informative podcast regarding cholesterol flux. It would be great for you to interview Malcolm Kendrick who is also a luminar in this field. His opinion debunks some of Tom's theories. By the way your interview was brilliant, you covered some areas of lipidology which help me fill in some of the missing pieces of the puzzle.
@@TheProofWithSimonHill Care to elaborate on why you weren't? I'm doing the best a lay person can in trying to figure thus all out but it is SO difficult as there are many "experts" and many conflicting information. I have lost nearly 100lbs, now have no hbp, no pre diabetes but have extraordinarily high cholesterol. Like 618 total, 492 ldl, 86 hdl, 86 triglyceride.
@@TheProofWithSimonHillI've read Kendrick's book also and one of only two people who've given it 2 stars on Amazon. I'm with you.
How come all these people on carnivore diets aren't having heart attacks left and right??
Very interesting!!! But no answer forthcoming
Very intresting talk, but what I want to know, is the health of the ldl particles and the sise of them matter ? and that about lean hyper responders with extremely hi level of ldl and hdl, but low triglycerides, being healthy with 0 plack
Hi Quick request. I subscribe to your Podcast on Spotify but often come across podcasts on TH-cam of yours that I want to listen to on Spotify while driving/running etc. It would be great if on your videos you could add a link to the specific Spotify podcast (and other podcast providers that you are on) rather than just to the channel. It would make it easier to find a particular podcast. Thank you. Kind regards Michael. BTW can’t wait to listen to this one in full and the subsequent ones in the series.
Vitamin E, omega 3, vitamin D ....especially k2 doses of 230mcg a day will reduce arterial plaque by 51% in 6 months and 31% in 3 months. The vitamin E and omega 3 will help take care of the inflammation there .What is your opinion about this?
The information given on comparison between high saturated fat consumption and heart disease has been proven wrong over and over again. It was repeatedly proven by both research and anecdotal evidences that Metabolic Syndrome and insulin resistance is the main driver of atherosclerosis. Can the doctor please put forth some research with randomized control trials that proved consumption of 'low carb high saturated fat' diet has a direct relationship to heart disease? Also high LDL is not a matter of concern but the particle size and Trygliceride to HDL ratio is what matters ?
Really interesting. Both my parents had high cholesterol and so do I despite being plant based vegan and this helped explain things. I would have thought diet would have played a greater role but seems not. Thank you so much.
I was basing this on the ‘eat your eggs if you want to ‘ comment. Good to know diet can help.
Diet does play a massive role, namely carbohydrates, sugar, not fat. I study this subject and beleive his guys way outdated views and advice are highly influential in causing the huge rise in hart events. The interviewer askes the right questions but he ducks around them. Why is this guys decades long approach not working? Because it is wrong. Doctors Cywes, Diamond, Paul Mason, Ken Berry, Anthony Chaffee, Bikman, Huberman, Sayfried, Ekburg, Shawn Baker. All these doctors and many more would strongly disagree on many of the points he makes.
Just read Malcolm Kendicks ‘The Clot Thickens’ and you might be able to work out why this video is out of date…
Do omega-3 supplements raise LDL, regardless of the source (fish/algae)?
1:47:10 In Star Wars terminology, one would say that the nuclear transcription factors sense a disturbance in the Force.
Thank you so much for your content. I subscribed. I'm extremely interested in your guests and all that they share. ❤
Love your show and especially this episode - except in the section near the end (1:53) when he states that dietary intake of cholesterol has "nothing to do with coronary outcome..." Dr Gregor's video posted today (Apr 5) reiterates that dietary cholesterol raises blood levels and increases CVD risks, including a statement to that effect by Kim Williams What gives? Your guests assertion that it "has nothing to do with" seems to undercut his credibility.
I'm trying to learn everything I can about health. Trying to put together all I'm learning. If dietary cholesterol does not cross the blood brain barrier but statins drugs do, taking statins can't be a good thing for our brain's cholesterol needs???
@@TheProofWithSimonHill Thank you.
You have the answer here in this 2015 article title: "Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms." Written by Japanese scientists living in a no profit healthcare system so no reason to mislead their own people who already have the highest life expectancy in the world.
The brain makes its own cholesterol, and instead of lasting for weeks it lasts for years. This has been extensively studied, and statins do not affect the brain’s cholesterol production or brain health.
None mentioned how heat/cold can thicken/thin the cell membrane by regulating lipid molecules.
You mean hot weather is good ..in Scotland we don't even have warm weather?
This was SUPER informative and DENSE!!! Will definitely be re-listening and eagerly anticipating the rest of this series!
A lousy conversation. Simon can ask a generic question here and there but simon lacks the biochemistry acumen to really challenge anything Dayspring says - and so we let the lipid doctor ramble on. Dietary cholesterol or any kind of dietary fat has zero impact on what is going on in the body. All this talk or pathways and Chylomicrons etc. is moot null and void due to the psychical fact (fact of physics, laws of physics) that these exogenous molecules were already broke down prior to eating. Decay of cow, begins this process, then exposure to light and oxygen, heat, cooking (do you really think there is an intact cholesterol molecule post frying pan?).
@@oliverleslie7382 Do you have any links you can provide to support your assertions?
Very confusing, wish there were more illustrations. Also, how do we reverse atherosclerosis?
At 1:53:30 he mentions phytosterols, and states the body would NOT want to see that. On my low carb diet, the plants of choice are all on the top in regards to phytosterols. Various nuts, flax seed, broccoli, brusselsprouts, spinach. If the normal range is to absorb 55%, then maybe these preferred foods are not that good anyway? Pretty sure I eat more of these, than eggs or even beef and butter.
Could it be, that the "lean mass hyper responders" he dismisses so fast, might be hyper-absorbers? That despite doing what is often referred to as clean keto, still have LDL that is drastically elevated?
Despite a lot of research being done here in Denmark, the only lipid panel that is routinely offered, is HDL, LDL-C and trigs. Not unless you fork out a buttload of money on a private hospital, can you get a detailed panel.
Nurse told me about a patient who had an LDL of 800! Both her parents died in their 30's. Pretty obvious she was genetically predisposed. I don't know her outcome or how old she was when the nurse had her as a patient.
Should get Ron Krauss on as a guest. Though he is essentially in agreement with Dayspring, his take is a lot more nuanced, especially where it comes to the role of particle size in determining cvd risk.
Read Malcom Kendrick who ,awesome considerably ,ore sense,
Enjoyed this....thank you to both of you. Learned so much. From a Pattern B small dense LDL guy.
I’ve been searching 5+ years for the answer at 1:10:49. Thank you both! ❤
My dad died of a heart attack on Thanksgiving 1972
Brilliant episode - WOW! It's rare to find an expert who can distill his decades of experience with such clarity while being so personable and humorous. I loved Dr. Lipid. He cut through all the popular misconceptions and made me smile in the process.
The next time a carni tells you we need LDL, show them 45:50
Thanks to you Simon and Dr Dayspring.
Very complicated, unfortunately!
I haven't understood half of these but still appreciates the podcast as it is wonderful to know about the World of Lipids.
Based on your explanation whe re doe s e ndothelia
Injury and repaired come in? Wh doesn't this occur in veins, Are you at all fa
It occurs in veins when you put them in the arterial system as grafts
does niacin lower apob??
Wow, super-loaded, informative conversation. Gotta listen to it a few times. I don't mind though, Dr. Dayspring is a gem :).
Loving the level of detail here, I was surprised to hear him say in general the level of dietary cholesterol has little to do with systemic level of apoB and cardiac outcomes (except for genetics), therefore would the main benefit of lowering dietary cholesterol be that in eliminating those foods you are usually also eliminating saturated fat which is the real issue (at least in terms of dietary input)? Can’t wait for the next one, thanks Simon
It’s a hyperbolic curve. If your ApoB is already low and you consume zero cholesterol and then add a few eggs to your diet you will see a significant increase in blood ApoB. They should have clarified this. Nutrition Made Simple has a video about this.
That makes sense, thanks
@@reason3581 Yes, I was surprised this was not mentioned. It must be an advantage to not have this rise happen?
Yeah, cholesterol aside, eggs are 28% saturated fat...well above the 8-10% recommended range.
@@megavegan5791 Yes, most people probably don't limit the rest of their daily saturated fat intake enough to make room for eggs.
What an enthusiast doctor ,,,and nice person sharing his great knowledge
Thanks a lot !!
@rf9612.......Sorry, but enthusiasm does not always equate into scientific accuracy. Please investigate into alternate theories which scientifically and biologically challenge the current lipid theory of CVD. This mainstream theory only makes sense on the surface, but looking critically you see the pathways embraced do not actually exist in the body. Cell wall integrity and tight junctions between cells will not allow LDL in unless it has provided receptors for entry. Also, cholesterol found within plaques is pure cholesterol crystals, found abundantly only in red blood cell membranes. The other type of LDL found in circulating blood cannot form such crystals. But supposing LDL could enter why not also the entry of most everything else in circulation, many of which are way smaller than LDL. And, being that same blood supply but with less oxygen also flows in veins why does the LDL not cause plaque and arteriosclerosis within veins? It does rarely happen in a few places but not common except in veins grafted in the position of a bypass (CABG). Higher BP, and higher levels of mechanical damage is the main reason for that,.......but if LDL were actual cause of CVD it would happen in both arteries and veins and would be occurring uniformly the same on all surfaces, not just in selected spots. For more info please view You Tube videos of Malcomb Kendrick interviews. Specifically view this video around the 1 hr mark. th-cam.com/video/wRjQCG4NU-Y/w-d-xo.html
This is a masterclass on the lipids
Thank you Simon. A lot of it went over my head, but I’m so glad I stayed with it. So very detailed and interesting. Greg - Australia
So DR. Statin saying there is no role in insulin resistance / metabolic disease and atherosclerosis? Because the prevalence of this disease is a relatively recent phenomenon in human history beginning at the same time as high-carb and processed food became our mainstay. Does he have any idea what the average ApoB score was in the 20's and 30's. I'm sure he has no clue.
It's not a recent phenomenon. Check out a study in the Lancet called Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations
This episode is brilliant 👌👏. Thank you . I have learnt so much more and feel way more informed to help clients I see.
So what foods are good ? Diet?
I get it modified the LDL , obviously with Statins. My question is, I personally know people, because I am old, that been on Statins for decades, lower their LDL , yet still have bypass surgeries. . Lowering LDL for decades,, didn't stop thier arteries from getting plague.
Maybe that's because sugar damages the endothelial and the repair mechanisms inadvertently cause the plaque to begin.
That is why an OGTT test is the only test to determine if you have IR, which is common once you reach 65 and older. Go find the root cause that is creating soft plaque thereby its potential danger for causing thrombosis.
Try looking through the eyes of a 2-time Nobel Prize winner Dr. Linus Pauling and Dr Thomas Levy who expanded on Pauling 's work. The real issue is arterial scurvy. I have lowered my CAC said to be not reversible from 660 to 458.
Sam is very right here!
Statins don’t reduce heart disease in primary prevention
@@darrendigiacomo6889 I agree, not only that they narrow the arteries even further all in the name of stabilization of Plaque but after the stabilization and a much narrower artery a piece of Plaque comes along and boom heart attack. I prefer Linus Paulings approach and belief that the problem is localized vitamin C deficiency which Lp-a arrives first on the scene to start the Plaque and calcium process of shoring up the arteries holes and cracks from the mechanical stress of the arteries close to the heart depleting vitamin C. The RDA of C is not enough. Standard medicines approach to calcium and plaque build-up is a backwards approach IMO as well as others such as Dr. Thomas Levy Cardiologist. How do I know because I am using Paulings and Levy's solution and my heart disease is reversing with a CAC of 458 down from 660.
Great info on lipids. Thank you Simon
My LDL and cholesterol went up after taking a high dose fish oil.
Fascinating conversation. Thanks! I was wondering if Nitric Oxide play a part in being protective of the endothelial cells?
Why don't people answer?
100% it does. It's a vaso dilator and immensely important. Insulin resistance in the endothelial cell will down regulate it's ability to produce it
Where does nitric oxide come from
I love how this gentleman delivers his knowledge! I would have enjoyed his lectures/ transfer of knowledge!! Awesome video.
Glad you enjoyed it!
This guy is amazing. I could listen to him all day. He is very skilful at explaining the anatomy and physiology of the subject matter without bamboozling you or boring you. He's one of the best I've heard so far. Outstanding.
Hello Friends,
I'm keen to find out which part of our chat you found most enlightening. Should you have any further questions on this topic, do please post them beneath this comment. I shall endeavour to include them in our next discussion.
It would be great to debunk or confirm the LMHR hypothesis.